2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

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2'.2'3.4-Dichlorobenzene (p-Dichlorobenzene.4'.1-Trichloroethane (Methyl chloroform) 1. The process for selection is described at http://www.html. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2'.4'.4’.4.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1. Table 1.3.3'.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.5.2'.4’.3.4.6'-Hexabromodiphenyl ether (BDE 154) 2.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .2-Dichloroethane (Ethylene dichloride) 1.2'.3.6'-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 2.4.2-Trichloroethane Trichloroethene (Trichloroethylene) m.4.2-Dichloropropane 2. Paradichlorobenzene) 1.3’.3.5.2-Dichloroethene trans-1.5'-Tetrachlorobiphenyl (PCB 49) 2.4.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.1.1.2’.2-Dichlorobenzene (o-Dichlorobenzene) 1.2'.5’.5.2-Dichloroethene Dichloromethane (Methylene chloride) 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 (2.5'.4'-Tetrabromodiphenyl ether (BDE 66) 2.1.2'4.1-Dichloroethene (Vinylidene chloride) cis-1.5'-Hexabromodiphenyl ether (BDE 153) 2.3-Dichlorobenzene (m-Dichlorobenzene) 1.5-Pentabromodiphenyl ether (BDE 99) 2.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.4.4. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.2.cdc.5.1-Dichloroethane 1.4'.4'-Tribromodiphenyl ether (BDE 28) 2.4-Tribromodiphenyl ether (BDE 17) 2.4.1.3-Tetramethylbutyl] phenol) Triclosan (2.2'.What’s New in this Report What’s New in this Report In this Fourth Report.gov/exposurereport/chemical_selection.4'-Tetrabromodiphenyl ether (BDE 47) 2.2'.5'-Tetrachlorobiphenyl (PCB 44) 2.6-Heptabromodiphenyl ether (BDE 183) 2.4.4'-Pentabromodiphenyl ether (BDE 85) 2. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4'.2'.4'.2'.6-Pentabromodiphenyl ether (BDE 100) 2.4.4.6.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4.

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

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

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

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

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

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

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

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

Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. and in some cosmetics.6-104) 82.3) 86.4) 57.1) 101 (95.4) 100 (89.1) 62. gels. Recently.7 (63.1-64.1 (73.6-66.S.7) 54. drinking water. 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.0.2 (75.6) 71. 2005).S.6 (81. Survey Geometric mean (95% conf.4-83.5) 58.7) 75th 79. EPA. the main source of exposure is from the diet.. Polyacrylamides are useful water-compatible polymers used in water treatment. Tareke et al.0-58. FAO/WHO.7-64.4-60. 2004).S.8 (81. pulp and paper production. and is either metabolized to the reactive epoxide. These estimated intakes are hundreds of times lower than occupational exposures. Estimated intakes in children are about twice that of adults (DiNovi and Howard. Fennell et al.0) 57.5 (52.S.3) 70. but can covalently bind to form adducts with proteins.3) 63.1) 46. 2005).9 (60. 2005.3-71.1-64. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U..0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.6-61.8 (52. in some sealing grouts. People may be exposed to acrylamide from foods.2) 57.6) 50.7) 73.6 (51.8 (91. 2006). Animal studies indicate that acrylamide is well absorbed. Since acrylamide has limited volatility and high water solubility.0-66.8-55.2-70. and binding agents. 1990. smoking.1 (83. but are generally above the U.9 (54. are heated at temperatures used for frying and baking.9) 58.S.9-52.Acrylamide Acrylamide CAS No. 2004. In the general population. Acrylamide is not thought to accumulate in the body at environmental doses.1) 55. acrylamide is synthesized and used in the production of polyacrylamide polymer. soil conditioners.9-61.0 μg/kg for adults (FAO/ WHO. it was discovered that acrylamide is formed when starch-rich foods. such as potatoes and some grains.2-114) 163 (147-191) 96.2 (58.6-108) 61.5-80.2 μg/kg/day (U.4-76. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. see Data Analysis section) for Survey year 03-04 is 3.1) 53.7) 96.0 (53. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.0 (67.2) 57.2-59. and from dermal contact with products that contain residual acrylamide.9) 57.5 (44. and in the synthesis or compounding of dye materials.3-2.4 (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 61.5 (79. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. 1994).2 (62. or to glutathione conjugates (Calleman et al. Natural substances in the food are converted to acrylamide.1 (52.4-89.4-60.6) 90.2-67. and well below doses known to cause nerve damage or carcinogenicity in animals. 2005).5-85. (NTP-CERHR.5 (74.2-118) 98. 2005). 2002). population from the National Health and Nutrition Examination Survey.8-57.1-57.7-64.9) 75. mineral processing.6-65.0 (57. widely distributed in tissues.9 (69.5) 66.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.. and cosmetics (NTP-CERHR. EPA.9-105) 86.0) 85. glycidamide.4) 57. interval) 61. FDA.2-77. in permanent press fabrics.6-75.4 (54. as an absorbent in disposable diapers. ocular and dermal irritation from direct contact with acrylamide containing materials.4) Selected percentiles ( 95% confidence interval) Sample 95th 192 (168-217) size 7101 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 54.8 (57. Fourth National Report on Human Exposure to Environmental Chemicals 11 . 217 million pounds of acrylamide were produced commercially in the U.0 (69.4 (59.1 (88.0-108) 152 (139-175) 126 (111-142) 108 (86. Commercially.0-49. acrylamide has produced upper airway irritation following inhalation of high levels. Elimination occurs mainly in the urine as mercapturic acid conjugates.7 (58. 2006.7) 58.3 (55. In 1997. EPA reference dose of 0.6) 73.2-93.9) 63.3 (53.7-60.1-61.1 (47.7 (55.7 (65.4 (53.6 (56. In humans. and an average daily intake is estimated as 0. 2005).2-91.4 (54.

9-62.4-98.S. Hagmar et al...5-66.4 (90. 2005) and sperm DNA adducts (Xie et al.9-78. 2005.who.3 (56.1 (56.5) 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.2) 55.Acrylamide occupational exposures. 2005. and cancer (mammary.7 (84.2 (63.3-101) 95.4 (57.1) 56.. Axonal degeneration.5-94.S.3) 59. Additional information is available from U..4) 53.5-64. reproductive effects (reduced litter size. 2005. 1997.. Schettgen et al.6-64.0-103) 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. In addition. 2009).0) 94. Survey Geometric mean (95% conf. 2005.4 (56. EPA. presynaptic nerve terminal binding (LoPachin.9 (57. 2005) have been demonstrated in animals. and other sites) (FAO/WHO. 2005).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..0) 118 (103-126) 121 (112-134) 113 (94.0-93.6 (66. Klaunig et al.1) 60. 12 Fourth National Report on Human Exposure to Environmental Chemicals .4) 46. 2005). 2005.7-64..7-86. 2005).5 (42. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.2-68. and neuronal DNA reactivity (Doerge et al. 2005.. Puppel et al.7) 61. After exposure ceases. 2002. Puppel et al. fetal death.. uterine..5) 75th 85.8 (44.4) 83..0-62.4-65. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al. thyroid.5 (59. IARC classifies acrylamide as probably carcinogenic to humans. Vesper et al.3) 59.. adrenal.5) 71.8-61. see Data Analysis section) for Survey year 03-04 is 4. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.1) 62. respectively) are markers of integrated acrylamide exposure over the preceding few months..S. most non-smokers had levels less than about 100 pmol/gram hemoglobin.7) 74.1-70. 2004. EPA at: http://www. AHA levels have been shown to increase with dietary intake (Hagmar et al.0 (75. U. scrotal. probably through its epoxide metabolite..9-76.9 (58. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. 2005. dominant lethality). 2003. 2005). 2005. 2006). altered gene expression in testicular tissues (Yang et al..8) 45.4-103) 79.2-90.4 (51. 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. 2004). Maniere et al.1 (82.2) 65.0.9) 59.0 (80. 1997.3-78.6-90.. EPA...7 (87. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.2-91.7 (61. Glycidamide has been shown to react with DNA (Doerge et al. Acrylamide is clastogenic and can produce dominant lethal mutations.1-56. 2006.7) 90.8) 60.pdf.6 (90.8-48. although different analytic methods can affect results.2 (72. 2005.4 (61. 2002.6-62.2) 87.3) 85.0 (52.1 (57. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.9) 87.9-64.8-49.9) 65. population from the National Health and Nutrition Examination Survey.1-62. Schettgen et al.9 (81.7-62. 2006) have been demonstrated after acrylamide dosing.0 (70. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.5) 87. 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.4 (81. 2005. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.5-92.9-77. male germinal cell injury.4-59. 2006).S. glycidamide (NTP-CERHR.7) 60. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.int/ ipcs/food/jecfa/summaries/summary_report_64_final.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.2 (56. Animal studies have shown that acrylamide can cause nerve damage (neuropathy). 2001). interval) 59. 2008).8 (51. 2008).5 (83.7 (57.1 (70.1-60. Vesper 2005) and smoking (Bergmark.9) 75. 2005.9-138) 143 (130-159) 96. NTP-CERHR. Rice. Mucci et al. U...5 (56.1 (66.epa.3) 59.

National Toxicology Program.cfsan. Wu Y. Nordander C.pdf. Available at URL: http://www.10(1):78-84. Wirfalt E.580(1-2):131-141. Toxicol Sci.580(1-2):157-165. Food and Drug Administration (FDA). 6013-6019. Toxicol Sci 2005. Duale N. 2001). Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . gov/~dms/acrydata. Bjellaas T. Perez et al. 1994). Alexander J. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Illinois. The Updated Exposure Assessment for Acrylamide. April 13-15.561:21-37. Mutat Res 2005. Cheong HK. et al. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Paulsson B. Bergmark E. Magnusson AL.Toxicol Appl Pharmacol 1994. Becher G. Tornqvist M. Wilson KM. Costa LG.html#u1004. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Human exposure and internal dose assessments of acrylamide in food. Finding a measurable amount of acrylamide or glycidamide hemoglobin adducts in blood does not mean that these levels of acrylamide or glycidamide hemoglobin adducts cause adverse health effects. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al.int/ipcs/ food/jecfa/summaries/summary_report_64_final. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Italy. Acrylamide intake through diet and human cancer risk. Haugen M. 1993. Mechanisms of acrylamide induced rodent carcinogenesis. smoking habits and gender. Bergmark E. Scand J Work Environ Health 2001. Beland FA..gov/chemicals/ acrylamide/Acrylamide_Monograph. Rome. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). 2/3/09 Perez HL. 2001. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Fennell TR.27(4):219-226. 2009 Jan 8. 2004. Burgess J. et al. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. 2/3/09 Klaunig JE. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. 054472. Granath F. Summer SCJ. Axmon A. Adv Exp Med Biol 2005. Toxicol 2005. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes.43:365–410. morphological and molecular endpoints in animal models. Calleman CJ. Mutat Res 2005. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. and Research Strategies. Chem Res Toxicol 1990. He F. Acrylamide neurotoxicity: neurological. Tornqvist M. Hagmar L. 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. Churchwell MI. 1999).pdf. Malmberg B. Maniere I. da Costa GG.Acrylamide In occupational settings. Snyder RW. Osterman-Golkar S. July. Laurentie M.126(2):361-371. He F. Bridson WE. Guffroy M. Costa LG.3:406-412. February. Rosen I. J Agric Food Chem 2008. Andersen M. Doerge DR. Chicago. Available at URL: http://www. [Epub ahead of print] Dybing E. Aprea P. Adv Exp Med Biol 2005. Joint FAO/WHO Expert Committee on Food Additives. Bergmark E. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Twaddle NC. 2005. Godard T. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Survey data on acrylamide in food: individual food products. et al. NIH Publication No. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al.. Chem Res Toxicol 1997 Jan. CFSAN/Office of Plant and Dairy Foods.nih. Uncertainties. Hagmar et al.who.. Toxicol Appl Pharmacol 1993. Food Chem. Fennell TR. Farmer PB. 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. Mucci LA. 8-17 February 2005. Calleman CJ. Kamendulis LM..120(1):45-54. et al. Mutat Res 2005.85:447-459. Doerge DR. Calleman CJ. In another study. Kautiainen A. References Bergmark E. Spicer R. 2/3/09 Hagmar L.. 2006.561:49-62. McDaniel LP. Yang JS. 64th Meeting: Summary and Conclusions (FAO/WHO). Tian G.56. Metabolism and hemoglobin adduct formation of acrylamide in humans. Bruze M.niehs. Zhang S. LoPachin RM. Paulsen JE. smokers and nonsmokers. DiNovi M and Howard D. Available at URL: http://cerhr. et al. Churchwell MI.fda.580(1-2):119-129.

561:89-96. Myers GL. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. et al. 1994.Acrylamide glycidamide by gas chromatography-mass spectrometry. Analysis of acrylamide.S. Smith A. Acrylamide. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Tornqvist M. Ingham L. Anal Biochem 1999. Ding X.20(6):959-64. Eriksson S. Xie Q. Drexler H.htm. Office of Pollution Prevention and Toxics.134(1-3):65-70. Letzel S. Lee SH. Toxicol Lett 2006.163(2):101-8. Liu Y. Toxicol Lett 2002. Schettgen T. Fueller F. Tareke E. U. J Agric Food Chem 2002. Puppel N.gov/chemfact/s_acryla. propylene oxide. Marko D.207(6):531-9. Weiss T. Choi JH.epa. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Rydberg P. Schettgen T. EPA).580(1-2):71-80. Meyers T. Han CH. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Yang HJ. Environmental Protection Agency (U. Rice JM.epa. Benetou V. Mutat Res 2005 Feb 7.S. The carcinogenicity of acrylamide. a carcinogen formed in heated foodstuffs. Kutting B. Tjaden Z. Licea-Perez H. Adv Exp Med Biol 2005. 2/3/09 Vesper HW. Chae C. Hallmans G. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Vesper HW.19(4):527-34. U. Environmental Protection Agency (U. Ospina M. Angerer J. Agudo A.50(17):4998-5006. Vesper HW.206(1):9-14. Meyers T. Ospina M. September.txt. Fu D. Rossbach B. Slimani N. Hemoglobin adducts of ethylene oxide. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Angerer J.56(15):6046-53. 2/3/09. Gray JG.gov/iris/subst/0286. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Jin Y. Schettgen T. Drexler H. Karlsson P. Int J Hyg Environ Health 2004. Rapid Commun Mass Spectrom 2006. revised 1/3/06. Sun H. Han DU. Toxicological effects of acrylamide on rat testicular gene expression profile.S. Available at URL: http://www. Drexler H. Broding HC. Washington (DC).580(1-2):3-20. Available at URL: http://www. Chemical Summary for Acrylamide.274(1):59-68. EPA). Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Reprod Toxicol 2005. Lee MH. Tjønneland A. et al. Integrated Risk Information System (IRIS). J Agric Food Chem 2008. Int J Hyg Environ Health 2003. Liu K. Angerer J. Mutat Res 2005. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany.S.

Survey Geometric mean (95% conf.350-.087) < LOD < LOD .930 (.201) .540 (.110-.23 (.84-3.S.54 (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.23 (2.21-1.39) 3.260-1.12) 1. and various other disorders (U.070 (<LOD-.960-1. 1998).26-1.110 (.34 (1.93) .63-2.630 (.96 (1.726) .02 (.040-.180) .077) .570-1.167 (.150) .110 (.66) 1.710 (.164 (.28-1. and exacerbated asthma (U.089) Age group 3-11 years 99-00 01-02** 03-04 .32-2.790) .Cotinine Cotinine CAS No.950-1.104-.88 (1.061) < LOD .900-1.131 (.163) .070) .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.310-1.430-1. stroke.910-1.062 (.62) 2.160 (..77 (1.059-.50-4. Children exposed to ETS are at increased risk for sudden infant death syndrome.05.310-1.50) 3.060 (.95) 1.153-.020-.70-2.85 (1. 2004).23-2.124 (.140-.050) .070) .860 (.110-.19) .059-.142-.071) .14) .570 (.99) 2.120 (.32) 1.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .49) 1.030-.02) 1. ear problems.96) 2.94) 1.084) .139) * .54 (1.080 (.800 (.57) 2.063) .14) .770) . Fourth National Report on Human Exposure to Environmental Chemicals 15 .280 (. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.820) .44 (1.058 (.92 (1.090-. cardiovascular disease.66 (1.20-2.S.230 (.130 (.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * . DHHS.073) < LOD .050 (<LOD-.990 (.164 (. 2006).770-1.76 (1.080-.160-.850 (. and 17% had an LOD of 0. 83% of measurements had an LOD of 0.088-.02) 1.22) 2.070-.040 (.213) .730 (.500 (.043-.20 (.066-.580) .188) .43 (1.44) 2.230) . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.42 (1.030-.620-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.83-2.220) .076-.17 (.030 (.120 (.150) . Cigarettes contain about 1.145) .5% nicotine by weight (Kozlowski et al.63 (2.175 (.S.55 (1.148-.14-1.240 (.35 (2.23 (1.30) * .120 (.510 (.55-2.100-.180 (.075 (. ** In the 2001-2002 survey period.090-. respectively.01 (1.310) 90th 1.15 (2.066) .38-2.060) .75) 1.950 (.621-1.48-3.00) .060-.05 ng/mL.126) .310) .234) .110 (.110) .66-3. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.65 (1.320) .68) 2.187) .45) 1. population from the National Health and Nutrition Examination Survey.190-.09-3.080) < LOD .68 (1.19) 1.42-4. see Data Analysis section) for Survey years 99-00.130) .047-. DHHS.050 (<LOD-.060-.193) .015 ng/mL. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease. which may vary for some chemicals by year and by individual sample.110 (.140 (.180) .094) .144 (.670) .160) .410) .068) .050-.066 (.89) 1.77 (2.49) 1.20) .220) .16) .200) 1.220-.086 (.620 (.040-. emphysema.120-.62 (2.20 (1.81-2.108) * .920 (.210 (.154-.137 (.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 .77 (1.052 (<LOD-.50 (1.520 (.630 (.260) 1.505 (.533-.28) .137-.09-3.580 (. and 0.40) .052 (<LOD-. 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.040 (.180 (.44 (2.180) .015.580-1.50-1. 2004).060 (<LOD-.470-.190-.047-.087-. acute respiratory infections.080-.302) .080 (.740-1.506 (.053 (<LOD-.690 (.600-1.198) * .080) < LOD < LOD .60-2.110) .197) .12-4.300) . < LOD means less than the limit of detection.312) .21-1.090-.050 (<LOD-.68) .180) .350 (.770) .050) .057-.480-1.030-.400-.350-.080-.11) .04 (1.990) .060 (<LOD-.87-3.12 (2.068) .308 (.09-2. maternal exposure during pregnancy can result in lower birth weight.216 (.997-3.070) 75th .160 (.370-.47-3.160 (.087 (.32-2.140 (.12 (1.79) 3.120) .88 (.060 (.54) 1.01) 3.120 (.70) 2. acute respiratory illness.15) 2.077) .050 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.540-.428-.33-2.480-.120 (.660) .30) 2.450-.054 (.106-.180) .080-.96-4.360) .840) 3.18-3.110-.140-.53 (1.120-.163 (. and 03-04 are 0.630 (.040 (.060-. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.17 (1.050 (.19-2.53-4.00) 1.160) .115-.190-.625) .20) 1.110 (.071 (.111-.05) 1.44) 2.39 (1.99) 2.78) 2.30) 2.48-2.050-.740-1.17) .21 (.

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

Available at URL: http://monographs. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Pirkle JL. Herrera B. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey.63:139-43.291(3):1196-1203. Exposure of the U.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Soliman S. U. IARC Monogr Eval Carcinog Risks Hum. and the United States. Benowitz NL.S. June. et al. et al. 4/13/09 National Cancer Institute (NCI). Pechacek TF. Ethnic differences in N-glucuronidation of nicotine and cotinine. Warner K.56:483-493. Vol 83. Herrera B.94(2):314-320. U. cigarette smokers: the Third National Health and Nutrition Examination Survey.gov/library/ secondhandsmoke/. 4/13/09 U. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Etzel RA. Available at URL: http://monographs. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Sosnoff CS. Pickett MA. Brody DJ. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary.gov/ntp/roc/eleventh/profiles/ s176toba. Giovino GA.15:302-307. U. International Agency for Research on Cancer. National Institute for Occupational Safety and Hygiene (NIOSH). Modin G.niehs. Mowery PD.7:369-375. Flegal KM. Centers for Disease Control. Strauss WJ. Bernert JT. National Center for Chronic Disease Prevention and Health Promotion. Department of Heath and Human Services.cancer.fr/ENG/Monographs/ allmonos90. 1999. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace.gov/eid/rmca/critdocs/ criteriadoc/33.php. Turner DM. Am J Public Health 2004. Respiratory nicotine absorption in non-smoking females during passive smoking. Absorption and metabolism of nicotine from cigarettes. Atlanta (GA): 2005. Centers for Disease Control and Prevention. Benowitz NL. Benowitz NL. Pirkle JL. DHHS). Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Tob Control 1998. National Toxicology Program (NTP). population to secondhand smoke: 1988-2002. JAMA 1998. Office on Smoking and Health [online] 2006. Dollery CT. 1999-2002.S Department of Health and Human Services (U.S Department of Health and Human Services (U.niosh. In Report on Carcinogens. Houseman TH. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Curtin LR. Centers for Disease Control and Prevention. Caudill SP. Pharmacol Rev 2005. Tob Control 2006. Benowitz NL. BMJ 1975. Caraballo R.S. Trends in the exposure of nonsmokers in the U. 4/13/09 Iwase A. Bernert JT. Schwartz SS. Coordinating Center for Health Promotion. Lewis PJ. Pechacek TF.pdf. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Epidemiol Rev 1996. Summary of Data Reported and Evaluation [online] 2004. JAMA 1998. Tobacco Smoke and Involuntary Smoking.cdc. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Third National Report on Human Exposure to Environmental Chemicals. Jacob P III. Schober SE. JAMA 1996. Perez-Stable EJ.S.iarc. George CF. Summary of Data Reported and Evaluation [online] 1986. Kira S. Jacob P.php. Metabolism and disposition kinetics of nicotine.57(1):79115.gov/tcrb/monographs/10/.4:313-316. Available at URL: http://ntp. Tobacco Smoke. Sweeney CT. Jacob P III. Giovino G. Vol 38.S. Jacob III P. Available at URL: http://www.114(6):853-858. DHHS).fr/ENG/Monographs/allmonos90. Maurer KR.pdf. Tobacco related exposures. Environ Health Perspect 2006. 4/13/09 International Agency for Research on Cancer. Hukkanen J. IARC Monogr Eval Carcinog Risks Hum. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.S. iarc.275:1233-1240. J Pharmacol Exp Ther 1999. Coordinating Center for Health Promotion. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Jarvis MJ. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Fong I. Smoking and Tobacco Control Monograph 10 [online]. Racial/ethnic differences in serum cotinine levels among adult U. Clin Pharmacol Ther 1994. Kozlowski LT.surgeongeneral. available at URL: http://mtn. Vogler GP. Mehta NY. Pollack HA. 1988-1991. References Armitage AK. Cotinine as a biomarker of environmental tobacco smoke exposure. Aiba M.280:135-140.nih. 1988-1991.280:152-156. 1991. Benowitz NL. [online].S. the United Kingdom. Int Arch Occup Environ Health 1991. Available at URL: http:// cancercontrol. Brody DJ. 11th ed. Department of Heath and Human Services. 4/13/09 Perez-Stable EJ. 4/13/09 Centers for Disease Control and Prevention (CDC). 2004. Nicotine metabolism and intake in black and white smokers.S. Richter PA.18:188-204.

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

180 (.1.140-..N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.140) < LOD . Survey Geometric mean (95% conf. Its use is recommended for prevention of several vector-borne diseases.140 (.130 (. DEET is not registered for use on agricultural commodities. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.140) < LOD .100-.S.250) < LOD .N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.130-.S.160) < LOD . DEET is not a developmental or reproductive toxicant in animals (U.220 (.170 (.120-. DEET has low acute toxicity.520) < LOD . and it has not been rated by IARC or NTP with respect to human carcinogenicity.110 (.EPA. 2003).449 and 0... Sudakin and Trevathan.100-.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 .100 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .130) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 19 .130 (. DEET is also used in combination with dermal sun screens (U.180 (.130-.100-. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. 2002). General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.S.S.S. 1998).S.210 (.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 .130 (.170 (. 1995. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110 (<LOD-. population from the National Health and Nutrition Examination Survey.270) 688 678 518 700 598 956 Limit of detection (LOD.140) < LOD . DEET is not genotoxic. One survey detected DEET in 74% of sampled streams in the U.110 (.180 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.130) < LOD . Urinary N.150) < LOD . Neurological effects in humans.190) < LOD . EPA.EPA. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .100-. and they range in concentration from 4% to 100%. Additional information is available from U. 134-62-3 General Information N.110-.120-.EPA at: http://www. (Kolpin et al. which may vary for some chemicals by year and by individual sample. including seizures and encephalopathy.240) < LOD .100-.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 .110 (<LOD-.130-.N-Diethyl-meta-toluamide (DEET) N. < LOD means less than the limit of detection.110-. 2003). 1998).180) < LOD . There are over 225 insect repellents brands containing DEET. After absorption. (U.130-. 2002). have been reported as result of self-poisoning by ingestion or excessive dermal application.N-Diethyl-meta-toluamide (DEET) CAS No. DEET can be applied to clothing and the skin to repel biting insects.110 (. 2005). About 3-8% of dermally applied DEET is absorbed.100-.epa.110 (.gov/pesticides/.N.560) < LOD .

S.410 (. 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-. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.S.190-.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 . 1992).390-.190 (<LOD-.320) < LOD .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.320 (.300 (.350-. Urinary DEET levels as high as 5. In this survey period.280-1.230-. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.240) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .230-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .270-.490) < LOD . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.410-.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.330 (.N. 2007). population from the National Health and Nutrition Examination Survey.270 (.280 (.640 (.290-..270) < LOD .250) < LOD .440) < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2005).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 . Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.240-.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.630) < LOD .410 (. Survey Geometric mean (95% conf.150) < LOD . DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.93) < LOD .330 (. representative subsamples from NHANES 2001-2002.190 (.350) < LOD .500 (.480 (.130 (<LOD-. Urinary N.270 (<LOD-.370) < LOD .190 (.250-.. 20 Fourth National Report on Human Exposure to Environmental Chemicals .350) < LOD .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 .170-.250 (.200 (.230) < LOD .370-.

Int J Toxicol 2002. hormones.S.S. Barber LB.S. Zaugg SD.25:95-100. 4/9/09 U.gov/teach/chem_summ/ DEET_summary. Lowry LK. Furlong ET. Toxicity and Exposure Assessment in Children’s Health. Absorption. Selim S. Smallwood AW. Osimitz TG. U.41(6):831-839. metabolism.EPA.S.epa. Tapia J. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Chemical Summary. U. EPA 738-R98-010. EPA.S. DeBord KE. and excretion of N.36(6):1202-1211. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Washington (DC): U. Schoenig GP.N. Environ Health Perspect 2007. et al. Veltri JC. Diethyltoluamide (DEET).N-Diethyl-meta-toluamide (DEET) References Arcury TA.epa. Fundam Appl Toxicol 1995. 2005.115(8):1254-1260.gov/oppsrrd1/REDs/0002red. Sudakin DL. Available at URL: http://www.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. J Toxicol Clin Toxicol 2003. September 1998. Hartnagel RE Jr. Thurman EM. Third National Report on Human Exposure to Environmental Chemicals. Trevathan WR.16(1):10-13. Environmental Protection Agency (U. Environmental Protection Agency (U. 1-118. pp.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers.S. Pharmaceuticals. Human exposures to N.S.2:341352. Environ Sci Technol 2002. Meyer MT. Centers for Disease Control and Prevention (CDC). Bell JW. streams. 1993-1997.N-diethyl-mtoluamide following dermal application to human volunteers.EPA). Chen H. Quandt SA. Gabriel KL. 1999-2000: a national reconnaissance. and other organic wastewater contaminants in U.pdf. Atlanta (GA). Reregistration Eligibility Decision (RED): DEET. Grzywacz JG. J Anal Toxicol 1992.EPA). N. 2005 Kolpin DW. Page BC. Available at URL: http://www. pdf. Barr DB. DEET: a review and update of safety and risk in the general population.

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

Needham LL.pdf . Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Available at URL: http://ecb.eu/ health/ph_risk/committees/sct/documents/out156_en. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Environ Sci Technol 2002. Kawamura N.Environmental Phenols References Akingbemi BT. Caudill SP. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. National Institutes of Health. Lynch BS. U. Thurman EM.149:988-994. McConnell EE. and Hardy MP. Harazono A. Hanaoka T.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Watanabe C.nih. T. In vitro and in vivo interactions of bisphenol A and its metabolite. Shin HC. 2002. Imai H. Brine DR. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Thomas BF.. Italy. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents.59(4):403-408.gov/chemicals/bisphenol/BPAFinalEPVF112607. Available at URL: http://cerhr. Cha SW.jrc. Timms BG.S.pdf. November 26. and other organic wastewater contaminants in U. Yoshinaga J. Barr DB. 4. Klinefelter GR. Hara K. Endocrinology 2008. Life Sci 2001. Endocrinology 2004.145:592-603. National Institute of Environmental Health Sciences. et al. Kroes R. Koh WS. Bisphenol A. et al. Environ Health Perspect 2008. Keimowitz AR. and Hajszan. Sottas CM. Occup Environ Med 2002. Tyl RW. Howdeshell KL.Scientific Committee on Toxicity. Kim YH. Ikka T. Leranth.europa. Brussels. Gray GM. et al. Human Health. Watanabe S. Exposure of the U. National Toxicology Program. Biochem Biophys Res Commun 2003. Rat two-generation reproductive toxicity study of bisphenol A. Bradley S.312(2):441-448. Ye X. An evaluation of the possible carcinogenicity of bisphenol A to humans. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Richter CA. Fujii S.gov/chemicals/bisphenol/bisphenol.nih. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Environ Health Perspect 2005.pdf.pdf . Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Wong LY. MacLusky. Rubin C. Barber LB. Szigeti-Buck. hormones. Zacharewski TR. Tsugane S.35(2 Pt 1):238-254. Kim CS. C. Regul Toxicol Pharmacol 2002. Yang M. Twomey K.780(2):365-370. Nippon Eiseigaku Zasshi 2004. with estrogen receptors alpha and beta. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Joint Research Centre Institute of Health and Consumer Protection. Reidy JA. niehs. 2/4/09 Fujimaki K. Matthews JB. May 22. Needham LL.68(1):121-146. Barton L. 2003.10:875-921. August 2001. Kim JC.S. Hum Ecol Risk Assess 2004. Ekong J. Serizawa S. 2/4/09 European Commission. 1999-2000: a national reconnaissance. Chem Res Toxicol 2001. Joskow R. DirectorateGeneral Health and Consumer Protection. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Calafat AM. Calafat AM.pdf. European Commission. Myers CB.102(19):7014-7019. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Research Triangle Park. N. Reprod Toxicol 2001.14(2):149-157. Ema M. September. Cunha G. niehs. Hughes C. Ispra. K. Kiguchi M. 2008. Gender differences in the levels of bisphenol A metabolites in urine. J Am Dent Assoc 2006.nih. Furlong ET. Arakawa C. Cohen JT. Park S.S. Doull J. Department of Health and Human Services.36(6):1202-1211. Kuklenyik Z. 2/4/09 Ouchi K. vom Saal FS. Kolpin DW. streams. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).113(4):391-395.J. J Chromatogr B Analyt Technol Biomed Life Sci 2002.. Munro IC. Proc Natl Acad Sci USA 2005.69(22):2611-2625.niehs. Marr MC. Meyer MT. Han SS. Needham LL. Koulova AI.116(1):39-44. Barr JR..59(9):625-628. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Calafat AM. Available at URL: http://cerhr. Zaugg SD. Available at URL: http://ec. Toxicol Sci 2002. Ecotoxicity and the Environment (CSTEE). Reidy JA. Belgium. NC. Available at URL: http://ntp. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). 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. Han SY. Haighton LA. bisphenol A glucuronide.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Furukawa M. Pharmaceuticals. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. 2007. Rhomberg et al. 5: 505-523.137(3):353-362. Chung MK. Hlywka JJ. Pyo MY.

Chem Res Toxicol 2002. Vom Saal FS. vom Saal FS. Witorsch RJ. Yang M.40(7):905-12. Kawamoto T. III. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Chang SS. and nonylphenol at home and daycare.44(4):546-51. Arch Environ Contam Toxicol 2003.147(6 Suppl):S56-69. Wilson NK. Environ Res 2007. Lordo RA. Environ Health Perspect 2005.15:12811287.Environmental Phenols Volkel W. Dekant W. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Large effects from small exposures.113(8):926-33. et al. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment.103(1):9-20. bisphenol-A. Lee SM. Biological monitoring of bisphenol a in a Korean population. Chuang JC. Kim SY. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Morgan MK. Nagel SC. Welshons WV. Hughes C. Filser JG. An observational study of the potential exposures of preschool children to pentachlorophenol. Csanady GA. Endocrinology 2006. Food Chem Toxicol 2002. Colnot T. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Jang JY. Sheldon LS.

have demonstrated estrogenic effects particularly when injected at high doses in animals. Indoor and to a lesser extent.1.50 (1.S.30 (1.5% of 139 U.10 (1.20-2.60-3. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol)...500) 75th .600) 1. and through manufacturing waste streams (Warhurst. to shorter chain alkylphenol ethoxylates.500) . These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. 140-66-9 General Information 4-tert-Octyphenol.268-. including 4-tert-octylphenol.20) 1. 2003. is used to manufacture alkylphenol ethoxylates. textiles.600-1. Urinary 4-tert-Octylphenol (4-[1. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.40) 1.30) 90th 1. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. < LOD means less than the limit of detection.10 (.60) 613 652 1092 Limit of detection (LOD.400 (..507) * < LOD .600-1.500 (. an alkylphenol.70 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. Several alkylphenols..g.274-. Blake and Boockfor.900 (.. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.80) 2.600-1.300-. and impaired spermatogenesis (e. and was quickly eliminated from the blood (Certa et al.. altered estrus cycles and reproductive outcomes.600) .700-1. 1996). fish) and drinking water. 2004).900 (.60-3.300 (<LOD-.00 (1.50-3.369 (.70 (1.60-3.000 tons of alkylphenol ethoxylates were produced annually worldwide.200-. 4-octylphenol monoethoxylate was detected in 43.900 (. streams in 30 states (Kolpin et al. and the polyethoxy chain may consist of up to 50 ethoxy units. which are anionic surfactants used in detergents. Bian et al. 2002).357 (.400 (.40 (1.60) 1. testicular atrophy.40) 2.300 (<LOD-. 34 Fourth National Report on Human Exposure to Environmental Chemicals . 1995.50) 1.20) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2000.20 (1. altered neonatal sexual development.20-2.30 (. the various alkylphenols have also been used as emulsifiers and modifiers in paints.00 (.50) 1. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. see Data Analysis section) for Survey year 03-04 is 0.400) 1.80 (1.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60-3. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. In 1999-2000. and some personal care products.60) .00 (.10) 2. During the 1980s and 1990s.70 (1.30-2. through sewage.. Less frequently..300 (<LOD-. pesticides.800-1.500) .20-2.600-1.10-2.400 (.g.500-1.80 (1.600) .900 (.299-. Saito et al.20) 314 715 1488 03-04 03-04 * * .20) 2.40) 2. leading to inhalation as another potential exposure route (Rudel et al.20-2.40) * 03-04 03-04 03-04 . and emulsifiers.3.50) ..40) 1.00) 1229 1288 03-04 03-04 03-04 * . Disposition in humans has not been studied sufficiently.70 (1.500) .497) * . The alkylphenol ethoxylates enter the environment through human use of products containing them. 1997.900 (.Environmental Phenols 4-tert-Octylphenol CAS No.30) 2. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. population from the National Health and Nutrition Examination Survey.30) 1.200-.10 (. 2002).300 (<LOD-.477) . Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. Survey Geometric mean (95% conf. Ying et al.90) 2. In the 1990s. and from contact with some personal care products and detergents. and to alkylphenoxycarboxylates. Katsuda et al.S.389 (.30 (1.500-1.600) .60-3. did not bioaccumulate.90) 2.300 (<LOD-.50) 1.50) .. orally administered 4-tert-octylphenol was well absorbed. Laws et al.80 (1.300-. impaired steroidogenesis. In rats. The alkylphenols can bioaccumulate in some fish. which may vary for some chemicals by year and by individual sample. over 500.2.50-2. 2006.20-2.30 (1. and some of their degradation products are toxic to aquatic life.30 (1. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.10) 1.600-1. 2000. industrial cleaners.20-2.600-1.60-3.

570) .71) 2. Calafat et al. 2001).62) .81 (1.380 (<LOD-. 2004.24) 612 651 1091 < 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. 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. or their corresponding ethoxylates with respect to human carcinogenicity. Fourth National Report on Human Exposure to Environmental Chemicals 35 . 2004).03-6.276 (.260 (<LOD-.. population from the National Health and Nutrition Examination Survey.460 (. In a small number of adult Japanese volunteers. 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.. Survey Geometric mean (95% conf.740 (.349) * < LOD .43-3. IARC and NTP have not rated octylphenol.17 (.03 (1.08) 1.850 (.470-1.64 (. Kawaguchi et al.33) 3.59 (1.68) 2.43) 1.31 (1.15) 1.470) 75th .640-1.3.96-4. nonylphenol. 2001.43) 1.450) .02-4.22) .03 (1.00) 2.370 (<LOD-.435 (.76 (2.40-4.85 (1.170-.36-3.910 (. Sweeney et al.41) .25) 90th 1.33 (2.320 (<LOD-.11) 1.25) 2.Environmental Phenols Myllymaki et al.67-2..770 (. It is unclear if estrogenic or other effects occur in animals through oral dosing.500-1.59) 1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al..384) * . 1999).207-.05-2.11-2.20 (1. 2005. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.06 (2.199-.S.78) 3. 4-tert-Octylphenol is not considered directly genotoxic.00) 2.31-2.18-4.740 (.470-1. Tyl et al. Urinary 4-tert-Octylphenol (4-[1.610) .620) ..890-2.270 (.410 (.78) 1228 1286 03-04 03-04 03-04 * .270 (.160-.337-.420) . at lower or environmentally relevant doses (Blake et al. 2003.60 (1.68-2.620-1.630-1.62 (1..00) 1.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.300 (<LOD-. 2000.730-1.540-1.270-. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.14) 314 713 1487 03-04 03-04 * * .73) 2.62 (1.530) .560) .00 (.65-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.53-3.50 (2.860 (.269 (.25-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400) .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 .11) 2.54) * 03-04 03-04 03-04 .10-2.450) 1.280-.550-1.78 (1. Yoshida et al.00 (. representative subsample of NHANES 2003-2004.40 (1.29) 2.1. Nagao et al.

Toxicol Lett 2001. Ferrell JM.co. Needham LL. Kawaguchi M. Brooks AN. Arch Toxicol 1996.28(3):215-226. Sakui N.37(20):4543-53. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Takai N.165(3):217-226. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Nair-Menon JU. Carey SA. Okada F. et al.54(1):154-167.121(1):21-33. Biol Reprod 1997. Wiegand HJ. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Regul Toxicol Pharmacol 1999. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Environ Int 2002. Toxicol Appl Pharmacol 2005. 2/4/09 Ying GG. Boockfor FR. Watanabe G. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol.14(5):325-332. Ono H. Ye X. Environ Health Perspect 2008. Thurman EM. et al. Watanabe G. and sertoli cell number. 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. Korn LR. Ito R. and other organic wastewater contaminants in U. Nicol L. Raychoudhury SS.30(2 Pt 1):81-95. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Wang X. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Maekawa A. An environmental assessment of alkylphenol ethoxylates and alkylphenols.pdf. polybrominated diphenyl ethers. Rudel RA.141(7):2667-2673. Katsuda S. Endocrinology 2000.foe. Two-generation reproduction study with para-tert-octylphenol in rats. Food Chem Toxicol 2006. Tyl RW. testis size. McCoy GL. Indoor air pollution by alkylphenols in Tokyo. Reidy JA. Brine DR.uk/resource/reports/ethoxylates_alkylphenols. Wong LY. Myllymaki SA.799(1):119-125. Toxicol Appl Pharmacol 2000. alkylphenols. Environ Sci Technol 2003.207(1):59-68. Barber LB. Sweeney T. Inoue K. Pharmaceuticals. Yoshida M. Chen J. Nakagomi M.Environmental Phenols References Bian Q. Seely JC. Camann DE. Taya K. Boockfor FR. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Makino T. Reprod Toxicol 2004. Myers CB. streams. Fedtke N. and testosterone. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. et al. Millette CF. Calafat AM. Kookana R.116(1):39-44. Bodman GJ. Saito I. Maekawa A. 36 Fourth National Report on Human Exposure to Environmental Chemicals .15(6):683-692. Fail PA. Haavisto TE.folliclestimulating hormone. Spengler JD. Saito Y. J Chromatogr B Analyt Technol Biomed Life Sci 2004. prolactin. Xu L. Certa H. Meyer MT. Kolpin DW. Horie M. Seto H. Muller AM. Blake CA. Bolt HM. Inoue K. Anal Chim Acta 486:41-50. Nagao T. and other endocrine-disrupting compounds in indoor air and dust. Toppari J. Blake CA.S. Williams B. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. et al. Environ Sci Technol 2002. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Karjalainen M. 1995. Estrogenic activity of octylphenol. Taya K. Song L. Marr MC. nonylphenol. Yoshimura S. Izumi S. Katsuda S. Toxicol Sci 2000. Paranko J. Warhurst AM. Cooper RL. Laws SC.S. Exposure of the U. Brody JG.36(6):1202-1211. Yoshimura Y. Indoor Air 2004. Onuki A. pesticides. Usumi K.71(1-2):112-122. 2003. Toxicokinetics of p-tert-octylphenol in male Wistar rats.18(1):43-51.44(8):1355-1361. Qian J. hormones. bisphenol A and methoxychlor in rats. Roche JF. Reprod Toxicol 2001. Phthalates. Available at URL: http:// www. Takenaka A. Kawaguchi M. 1999-2000: a national reconnaissance.57(2):255-266. Furlong ET. Zaugg SD. Yoshida M.

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

5-14.2 (37.90-10. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.80 (5.0) 49.0-15.5 (11.3-15.6-65.0 (36.6) 10.1-39.7 (39.1) 7.2) 13.16 (6.1) 9.92-12.4-19.2-58.Environmental Phenols Urinary Triclosan (2.8-112) 30. Urinary Triclosan (2.55 (4.3 (26.3-67.89-11.43-13.6-37.1) 13. interval) 12.8-127) 37.4) 317 (231-433) 144 (96.22-10.2 (25.10-9.6 (12.8 (21.6 (30.8-60.9 (8.3 (8.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.10) 84.1 (45.45 (5.1) Selected percentiles ( 95% confidence interval) Sample 95th 368 (294-463) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.9-61.4-18.7) 123 (36.7 (14. see Data Analysis section) for Survey year 03-04 is 2.6-20.2 (27.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 (15.70-16.2-14.6) 39.0 (34.8-85.1) 14.11-11.72-13.3.7) 10.5) 11.0) 65.2-58.S.6) 31.86-12.8) 9.29-12.6 (10.0 (11.9 (50.3) 10.6-14.40-17.32-14.4) 357 (225-456) 203 (87.60 (8.6) 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 9.9) 7.50-10.4 (38.6-15.1) 50.20-13.20-10.1) 9.0 (8. interval) 13.74 (5.0-213) 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 (13.7 (11.5) 20.S.8) 14.0 (26.3 (11.38-18.00 (4.3) 47.4) 7.5) 66.40-11.4) 25.6) 90th 212 (172-241) 03-04 03-04 03-04 9.2-46.60 (6.8-63.1) 11.6-111) 33.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.93 (7.30-14.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.2 (10.3-35.4 (11.54 (8.4.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.0-73.4.7 (28.20-11.20 (7.4) 90th 249 (188-304) 03-04 03-04 03-04 8.4 (32.9) 8.45-13.3-31.21 (6.6-14.48-10.3) 6.1) 9.6 (9.0-19.1) 9.5-86.0) 9.94 (7.9) 32.9 (11.7) 292 (151-432) 132 (78.00-8.9) 75th 47.50) 10.4) 75th 43.2) 9.4) 73.7 (9.8) 116 (39.82 (8. Survey Geometric mean (95% conf.4) 51.4 (12.8) 7.6) 12.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.1 (8.48 (8.9 (33.20 (7. population from the National Health and Nutrition Examination Survey.0-15.45-10.18 (5.2) 12.2 (11.9-236) 193 (90.5) 13.3 (9.

Windham G. Kolpin DW. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Erratum in: Aquat Toxicol 2007. et al. Percutaneous penetration and dermal metabolism of triclosan (2. Barber LB. Ferrer I. Wong LY. Mar Environ Res 2000. Bhargava HN. The oral retention and antiplaque efficacy of triclosan in human volunteers. Calafat AM.24(3):209-218. Br J Clin Pharmacol 1987.. Furlong ET. Anal Chim Acta 1004. Teitelbaum SL. Hirano M. Chemosphere 2007. Osachoff H. Williams PE. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Veldhoen N.23(5):579-583. Pilot study of urinary biomarkers of phytoestrogens. Kaneshima H. Pharmacokinetics of triclosan following oral ingestion in humans. Skirrow RC. Gilbert RJ. Environ Health Perspect 2008. Williams FM. phthalates. Kanetoshi A. Howes D. Clapson DJ. Levy SB. Benson WH. and phenols in girls. J Toxicol Environ Health A 2006.36(6):1202-1211. Toxicology of 2.7/2. Matsumura N.38(2):64-71. hormones. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Environ Sci Technol 2002. Furia T. Lyman FL. Wigmore H. Watanabe N. Pharmaceuticals. Aguera A. Adolfsson-Erici M. Bodey GP. Ishibashi H.80(3):217-227.38(4):361370. J Invest Dermatol 1976. Gunderson MP. Hong HC. Foran CM. Needham LL. Thurman EM. Developmental evaluation of a potential non-steroidal estrogen: triclosan. streams. Aranami K. Shiratsuchi H. Katsura E. Mezcua M.Environmental Phenols References Aiello AE. Wolff MS. Triclosan: applications and safety. Am J Infect Control 1996. Larson EL.83(1):84. Fernandez-Alba AR. Okui T. Readman JW. Ekstrand J. Photolytic degradation of triclosan in freshwater and seawater.50(1-5):153-156. Evidence of 2. Urinary concentrations of triclosan in the U. Aquat Toxicol 2006. 4’-trichloro-2’-hydroxydiphenyl ether. et al.S.67(4):532-537. et al. Odham G. Bennett ER. Britton JA. Chelimo C.4’-trichloro-2’hydroxydiphenyl ether).116(3):303-307. Arch Environ Contam Toxicol 1988. Ebersole R.4. IMS Ind Med Surg 1969.28(9):1748-1751. Zaugg SD. Pinney SM. Hernando MD. Nagao Y. Ogawa H.115:116-121.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007.17(5):637-644.69(20):1861-1873. Sandborgh-Englund G.524:241-247. 4.66:1052-1056. Gomez MJ.45 Suppl 2:S137-S147. population: 2003-2004. Meyer MT. et al. Food Chem Toxicol 2000. 1999-2000: a national reconnaissance.S. Reidy JA. Moss T. Biol Pharm Bull 2005. Ye X. Leonard PA. and other organic wastewater contaminants in U. Environ Health Perspect 2007.

500-2.350-1.390 (. < LOD means less than the limit of detection.350-.350-.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .98 (1.350 (.350 (.350 (.350) < LOD .350) < LOD .350-.75) 2. PCP is degraded by sunlight and metabolized rapidly by microorganisms. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.350-.S. and it is used primarily as a preservative for wood to be used outdoors (e.350) < LOD < LOD 75th .350) < LOD .10) 1. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.90) 2.860-2.350-.00 (.480-2.350-.350 (.65 (.510-5.01 (<LOD-1.90 (1.650 (. Effects including hyperthermia. PCP use in the U.350-1.58-2.60) 1.350-.350) < LOD .980 (.62 (. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350-2. algaecide and insecticide.91 (1. 1976.350-.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .25 and 0.76) . To-Figueras et al.30) 1. 1986). along with small amounts of tetrachlorohydroquinone and conjugates.530) 1.50) 1. water and sediments because of the large amounts that were produced and used historically. In the environment. Human exposure to PCP has become less common.350-2. hypertension.09) .850-2.350-2.33) . 1997). population from the National Health and Nutrition Examination Survey.65 (.60) 1.350-1. which may vary for some chemicals by year and by individual sample. Since 1984.04) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. PCP has been detected in soils.10 (<LOD-1. After a single dose.45-2. plants.94 (1. After absorption.350) < LOD .48-2.680-1.5. General population exposure to PCP may occur by inhalation of contaminated air..350 (.350-.890 (.350 (.30 (.350-.90) 1.990-2. other polychlorinated benzenes..350-.37) .73 (1.650) 1..350 (. 2002. and metabolic acidosis were observed in CAS No.350-2.10 (.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 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.350 (.390 (.67) 1.350-.350-. with repeated or chronic exposure.350-. air.350 (.350) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.990 (<LOD-2. bactericide.350 (.350 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.53) size 1994 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th . and dermal contact with PCP-treated products.47-5.350-.83 (2.76) 1.47-3.33-2. The parent compound and conjugates.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.960) 1.350 (. utility poles and fence posts). herbicide. has been restricted.30) .94 (1.78) 1.350-.350) < LOD .350-. Acute.510-3.770 (.70) .350) < LOD .40 (. 1979). ingestion of contaminated food or water.350) < LOD .18 (<LOD-1. are eliminated in the urine.350 (.42) 696 680 521 696 603 951 Limit of detection (LOD.80) .350-2.00) 1.350-.350 (.37 (.350) < LOD .350 (.30 (1.350 (. 40 Fourth National Report on Human Exposure to Environmental Chemicals .51) 1.350-.10 (1.58-2. the elimination half-life may be a week or more (Uhl et al. so it is relatively non-persistent.10) 1.350-.32 (.350) 90th . PCP is distributed to most tissues and is not extensively metabolized.08-3.350 (. mollusicide.350) < LOD . Kohli et al.350) .350 (.54-2.660 (.. and possibly of lindane (IPCS.350) < LOD .890-1.350) < LOD .23 (.350 (. PCP is absorbed rapidly and well by all exposure routes.350) < LOD .00) 1.350) < LOD .64) 1. Survey Geometric mean (95% conf.350 (.30) 1..00) 2.630 (.70) 2.350 (.590-1.30 (. and animals.350-.350-1. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.48 (.350) < LOD .350-. PCP is eliminated over a few days (Braun et al.g.S. PCP cannot be used on wood in residential or agricultural buildings.

55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .67-3.920 (.800) < LOD 1. OSHA has established an occupational standard.67 (1.290-.94 (1.590-1.95) 3.52 (1.69 (1.360 (.19) 2.75) 1.67 (1.82) 1.630 (.730) < LOD .35) 1.580-. and the FDA has established a standard for bottled water.S..26 (1.e.320) < LOD < LOD 75th .30 (.25-2. chronically administered high doses of PCP were hepatotoxic.760 (.780) < LOD .330-.48-2.16-1.250 (.35-2. 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.84-4..gov/ pesticides/ and from ATSDR at: http://www.440 (.950-1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.950-1. Biomonitoring Information In NHANES 1999-2000 the median urinary PCP levels among children aged 6-11 and 12-19 years were as much as thirteen times lower compared to a sample of German children aged 6-14 years in 1990-1992 (4.9 mg/L.82 (1.470 (.18 (1.epa.500-.10 (1.650) 90th 1. Fourth National Report on Human Exposure to Environmental Chemicals 41 ..67-3.08 and 5.gov/ toxpro2.710-1.84 (1..S.430) < LOD .560-.370 (. 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 (1.560) < LOD .cdc.300 (.310-.350) < LOD . EPA has developed standards for PCP in drinking water and the environment.S.67 (1.0 mg/L.40) 1.360-.320 (.16 (.500 (.36) .650 (.990 (.300 (..21-2.320) < LOD .340-.40) 1.94-3.73 (1.18) . 2003).610 (. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.700-2. EPA at: http://www.25-1.00) 1. Death can result from seizures and cardiovascular collapse.94 (1.21 (..290-.90) 1.35) 1. More information about external exposure (i. 2004.09) 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 .29-3. environmental levels) and health effects is available from the U.09 (<LOD-2.56) 1.25 (1.400 (.25) 1. respectively) (Seifert et al.250 (.800-1.52) 1.950-1.900-1. Among adults in the NHANES 1999-2000 subsample.84) 1. Pentachlorophenol is not mutagenic or teratogenic. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.79) 1.. 2003).850 (.240-. children in the 1980’s.40) 1.57 (.52 (<LOD-1.30-2.11) 2.830) < LOD .Fungicides adults and children severely exposed to PCP through ingestion.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .S.atsdr.30) 1.30) 1.570 (.06-3. and adversely affected thyroid function (U.09-1.html.57 (1.51) 1.00-1. carcinogenic.06) 1.26 (1.78) 1.280) < LOD .270-.300 (. 1991).S.910-1.490) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.83 (1.290) < LOD .310) < LOD .52 (<LOD-1.420) < LOD .19) 2.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .78) 1. inhalation. respectively) (Becker et al. 2000).25-2. Survey Geometric mean (95% conf.220-. or skin absorption. In NHANES 2001-2002 subsamples.6 and 14. 1989). The U.00-1. In animals.67 (1.19 (1.06 (. Urinary PCP levels at the 95th percentile in this Report are approximately half the corresponding 95th percentile values found in German adults evaluated in 1998 (Becker et al. Urinary 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. In a small sample of U. van Raaij et al.560) < LOD .92) 1. population from the National Health and Nutrition Examination Survey.10-2.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.75 (<LOD-2.430-.590) < LOD .25 (1.510-.67-2.13 (.55) 1.40) 1.510-.380-.35-2.320) < LOD .19) 2.EPA.650 (.500-1. 1989).260 (..220-.40) 1. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.780-1.270-.34 (. 1995).40-2.

Hill RH Jr. J Expo Anal Environ Epidemiol 2000.S. References Becker K. Environ Health Perspect 1997. Blau GE. Chenoweth MB. Toxicology 1991: 67(1):107-16. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Pesticide residues in urine of adults living in the United States: reference range concentrations. U. 4/21/09 Kohli J. Schulz C. Bailey SL. EPA). hair. 42 Fourth National Report on Human Exposure to Environmental Chemicals .10:552-65. Rodamilans M. Helm D.18(4):469-474. available at URL: http://www. Arch Environ Contam Toxicol 1989. Fast DM. Schmid P. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Kaus S. Arch Environ Contam Toxicol 1989. Int J Hyg Environ Health 2003. htm. Arch Toxicol 1986. PCP: Human Risk Characterization [online].org/documents/jmpr/jmpmono/2002pr08. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. r e g u l a t i o n s . The metabolism of higher chlorinated benzene isomers. 206:15-24.105(1):78-83. Barrot C. International Programme on Chemical Safety (IPCS). urine. et al. Phillips DL. Notten WR. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Lindane. drinking water and indoor air. Safe A. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Braun WH. Bragt PC. Environ Res 1995. 11/30/2004. Hill RH.71:99108. Gregg M. Needham LL. 4/21/09 van Raaij JA. Santiago-Silva M. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.58:182-186. Head SL. Schulz C. Engel R. Jones D. Can J Biochem 1976.4:289296. van den Berg KJ. 2002. Krause C. Holler JS. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Pharmacokinetics of pentachlorophenol in man. Seifert B. Available at URL: h t t p : / / w w w. g o v / f d m s p u b l i c / c o m p o n e n t / main?main=DocketDetail&d=EPA-HQ-OPP-2004-0402. Seifert B. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Seiwert M. Schlatter C. et al. Environmental Protection Agency (U. To-Figueras J. Otero R.S. Hill RH Jr.54(3):203-208. Seiwert M. Sala M. Dev Toxicol Environ Sci 1979. Smith SJ. Becker K. Shealy DB. et al. 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. Cline RE.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect.18:475-481. To T. house dust. Baker S. Uhl S. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Needham LL.inchem.

Survey Geometric mean (95% conf.550-1.30) < LOD 1.EPA.03) 1.00) < LOD . Workers who manufacture.10) .30) < LOD 90th 1.00) . Most agricultural food applications have been revoked.364-.402-.Fungicides ortho-Phenylphenol CAS No. OPP is considered to be moderately toxic after acute oral doses in animal studies.00 (1.40-5. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.23) 695 680 520 695 603 953 Limit of detection (LOD..33 (.610-1.570 (.50) . leaving the chemical residue OPP.600-1.836) * .860) * 99-00 01-02 99-00 01-02 99-00 01-02 .90 (1.30-2. 1989).50) < LOD .88) 1.638) * .610 (.770 (.30 (1.490 (<LOD-. 90-43-7 General Information Ortho-phenylphenol (OPP.450 (<LOD-.624) * . SOPP is applied topically to the crop and then rinsed off.90) 1.S.567 (.540-2.30) < LOD . < LOD means less than the limit of detection.50) < LOD .490 (<LOD-.10) 1.600) < LOD .10) .600) < LOD 1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.590-2. 2002.00 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.890 (.690-1. OPP is still used as a disinfectant fungicide for industrial applications.S. Estimated human intakes have been below recommended intake limits (U.50-2.466 (.690) < LOD .00 (1.20) 2.490 (<LOD-. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.890) 1. formulate.40-2.880-2. Fourth National Report on Human Exposure to Environmental Chemicals 43 . Both chemicals degrade within hours to weeks in the environment (U.76) 1.970 (. on ornamental plants and turfs.60 (1.20-3. In the past. and it has limited water solubility.00 (1.636) * .621) * .370-.570-1. 1998).386-.S.389-.20 (1.92 (.00) .349-.490 (<LOD-. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley. such as fruits and vegetables. Cnubben et al. and sanitizers.50 (1.780) < LOD .61) 2.50 (1.28 (.10) 2.. it was used in home sanitizers for surfaces.508 (.10) 1.40-7.696) * .770 (. General population exposure can occur via dermal.07 (.60 (1.710) 3. in paints. 1998.570 (.EPA.00-2. are antimicrobial agents used as bacteriostats.10 (1.370-. Available evidence suggests that OPP does not accumulate in the body.950) < LOD . 2006).750-2.22 (.498 (.390-.860 (.85) 2.890 (.800-3.30-7.10-1.600) < LOD 75th .790) 2.34) 1.710-2.930 (.500-2.389-.520 (.600-1.20 (.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 . fungicides.830 (.570-2. inhalational. or apply these chemicals may be more highly exposed than the general population.580-1.17 (.850 (.50-4..3.80) 1. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.630) < LOD . Timchalk et al.450 (<LOD-.480-1.20) < LOD 2.S.50) < LOD .840-1. whereas SOPP is not volatile and is more water soluble.645) * .20 (1.50) 1. which may vary for some chemicals by year and by individual sample.90) 2.496 (.10-2. EPA.450 (<LOD-.820 (.20) < LOD 1.433-.60 (1.497 (.470 (<LOD-.410-.552 (.493 (.90 (1.90) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350-1.560-8.740 (. 2006).3 and 0.600-1. 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.09) 2. 2006).80 (2.22) 2. and as a wood preservative.10) .40 (.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .370-.80-3. Both have been used in agriculture to control fungal and bacterial growth on stored crops.60-3. or 2-phenylphenol) and its water-soluble salt. interval) .509 (.19 (.640) < LOD .20-2.490 (<LOD-.60-2.50-3.570-. 2006).30) 1. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.14 (<LOD-3. but OPP and SOPP are still used on pears and citrus (U. OPP is volatile.600) < LOD . sodium ortho-phenylphenate (SOPP).10 (1.90) . however.670) 2.742) * .50 (1. population from the National Health and Nutrition Examination Survey.760-2.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .420 (<LOD-.40-5.80) 1.02) 1.28-3.27 (.

59) 1.610) < LOD 1.4) 3.270-.05-2.550-.750 (.440 (. U. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.11 (.. 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.52 (.880-1.248-.840 (.38-3.06-4. Nakagawa et al. Bomhard et al. 1999.950) < LOD .455-. Smith et al.656) * .08-2. population from the National Health and Nutrition Examination Survey.43 (1.473) * .560-2.93) .444 (.570) < LOD 1.51-3. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.380 (.47) .620-1.770-2.S.S.13) 1.09-3.89 (1.420 (<LOD-.353-.81) 1. Ito et al. less likely.311-. 2002.410 (<LOD-.28 (<LOD-4.590) * . 1997.21) 1.750-2.11) 4.27) < LOD .470) < LOD .21-2.0) 1.410 (<LOD-. 1984.514 (.EPA at: http:// www. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.670) < LOD . 2005). 1999.75 (1.750 (.06-5.910 (.791) * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. or developmental toxicity was observed (Bomhard et al. 44 Fourth National Report on Human Exposure to Environmental Chemicals .96 (1.860 (.670 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. but no neurologic.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.11-1. U.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .43) 3.17) 2.650-1.93 (1.403-.00 (. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect. leading to production of two metabolites. Additional information is available from U.96-4.EPA 2006).00 (1.43-2.28 (2.550 (. Biomonitoring Information Urinary OPP levels reflect recent exposure.980 (<LOD-1.59) .24-2.780 (.08-1. CDC.666) * .33-2.360 (<LOD-.550) < LOD .31) < LOD .24-2.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.500) < LOD .09-6.. 1993. or.510 (<LOD-. Survey Geometric mean (95% conf.08) 1.800-1.508) * .33) . and it has classified OPP as not classifiable with respect to human carcinogenicity.12-2.382 (.74 (1.11) < LOD 90th 1.32) 3.25-6.21 (.291-.329-.gov/pesticides/.640-1.93) 1.860 (.04-4. Detectable levels were seen in over half the U.670 (.453 (.40-13.43-2..Fungicides anemia.93) .61 (. Zhao et al. 2005.12) < LOD 1. Volunteers exposed to 0..32) 1.484) * .900) < LOD .940-2.69 (1.810-1. 1998.620-1.01) 1. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. 1992..epa.910-1.990) < LOD .61 (1.600-1.88-4. Murata et al.61 (2.53) 1. 2005).385 (. Kwok et al. Brusick.11 (. 1984.62) .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.96 (1.38) 1.420 (<LOD-. 1986).20) < LOD 3.460-.17 (.75 (1.18) 2.970) 1.46) < LOD 1. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2002. OPP was not found to be mutagenic.560) < LOD 75th .44 (1.96) 1.480-.568) * .07) 2..510-. Pathak and Roy.361-.S.470 (<LOD-.980 (..91 (1.810) < LOD . reproductive.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .26) 1.38) 2.58) 2.780-14.33) 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 . 2002).910 (<LOD-1..78 (2.17 (.29) 1.06 (1. In high dose animal studies.84 (1.64 (2.02 (.496 (. 2000.900-1. interval) .EPA 2006).580) < LOD .09 (1.S.690 (.97 (2.580-1.29) 1.343 (.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .301-.320 (<LOD-. by possible genotoxic mechanisms (Hagiwara et al. ortho-phenylhydroquinone and ortho-phenylbenzoquinone..S. IARC has classified SOPP as a possible human carcinogen.86 (1..

March 1986. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Cnubben NH.35(2 Pt 1):198-208.28(6):579594.43(7):14311437. Leser KH. Coelhan M. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Herbold BA. Sangha GK. Buchholz BA. Hirose M.17(8):411-417. Shirai T.gov/ntp/htdocs/LT_ rpts/tr301. Timchalk C. 1989.22(10):809-814.45(5):460-481.S. 90-43-7) in Swiss CD-1 mice (dermal studies). Vogel JS. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. EPA). rat and man. Murata M. Moriya K.EPA). Narang A. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats.. Cano M. Turteltaub KW.pdf. Imaida K. Bomhard EM. National Toxicology Program (NTP). The carcinogenicity of the biocide ortho-phenylphenol. Bormett GA. Xenobiotica 1998.50(11):3351-3358. Roberts AL.703(12):97-104. Hum Exp Toxicol 1998. Tayama S. Bartels MJ. Elliott GR. EPA 739 R-06004. Environmental Protection Agency (U. Arch Toxicol 2000. Kwok ES. Richter M. July 28. et al. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Roy D. Regul Toxicol Pharmacol 2002. U. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Selim S. Stanley JS. IARC Sci Publ 1984. Bartels MJ. Gierthy J. Zhao S. Eastmond DA. Smith RA. McNett DA. Bartels MJ. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. van de Sandt JJ. Office of Toxic Substances. Christenson WR. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Environ Mol Mutagen 2005. et al.S.(56):399-407.niehs. Pathak DN.54(16):5731-5735. Hagiwara A. J Agric Food Chem 2002. 4/9/09. Brzak KA. Arnold LL. Comparative metabolism of orthophenylphenol in mouse. Third National Report on Human Exposure to Environmental Chemicals.nih. Bartels MJ.286(2):309-319.74(2):61-71. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Mendrala AL. Carcinogenesis 1999.S. Available at URL: http://ntp. Kawanishi S. J Agric Food Chem 2006.159(1):18-24. Brusick D.150(2):402-413.S. Food Chem Toxicol 1984. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Hakkert BC. Inoue S. Drugs. 2006. Biochem Pharmacol 1992. Environmental Protection Agency (U. Hagiwara A. Nakagawa Y. St John MK.epa. Moldeus P. Mutat Res 1993. Meuling WJ. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Toxicol Appl Pharmacol 1999. Crit Rev Toxicol 2002.Fungicides References Appel KE. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Available at URL: http://www.20(5):851-857. Sangha G. 4/13/09 Onstot JD. Fukushima S. Freyberger A. EPA-560/5-89-003. 2005.pdf. Centers for Disease Control and Prevention (CDC). Ito N. Shibata M. Moore GA. Toxicol Appl Pharmacol 1998. Timchalk C. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Ito N. U. Bromig KH. Brendler-Schwaab SY. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Glas K.gov/oppsrrd1/REDs/ phenylphenol_red. Identification of SARA compounds in adipose tissue. J Chromatogr B Biomed Sci Appl 1997. Atlanta (GA). Eadon G.32(6):551-625. Christenson WR. Fukushima S.

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

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

which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.S. 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. see Data Analysis section) for Survey year 01-02 is 0. < LOD means less than the limit of detection.1.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 48 Fourth National Report on Human Exposure to Environmental Chemicals .Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 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. 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. Survey Geometric mean (95% conf. Survey Geometric mean (95% conf.

Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Jefferies PR. Green T. Linhart SM. Kier L.html. Quistad GB. Davison KL. Bravo R. Dialkylquinonimines validated as in vivo metabolites of alachlor. Environ Sci Technol 2005.S. et al. Tinwell H. Camann DE. Xenobiotica 1994. Burkhardt MR. Occurrence of sulfonylurea. Fourth National Report on Human Exposure to Environmental Chemicals 49 . and metolachlor herbicides in rats. Olsson AO.S.108(12):1151-1157. Barr DB. Deddens JA. Hodgson E. Available at URL(non U. Sanderson WT.248(2-3):115-122. Hines CJ. EPA).S. Feng PCC. et al. Kolpin DW.Herbicides References Ashby J. 5/30/06 U.pdf.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Environ Health Perspect 2003. Lefevre PA. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Battaglin WA. Peter CJ. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. J Expo Sci Environ Epidemiol 2007. Atlanta (GA). 2000. reservoirs and ground water in the Midwestern United States. Whyatt RM. Andrews HF. Thurman EM. Kinney PL. Barr JR. Linderman R.37(4):10881093. Comparative metabolism and elimination of acetanilide compounds by rat. sulfonamide. epa. Barr DB. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry.cce. J Expo Anal Environ Epidemiol 2005. Hsiao JJ.S. 1998. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Furlong ET. Barr DB.24(10):1003-1012. Alavanja MC. Volume 65. Hum Exp Toxicol 1996. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Sci Total Environ 2000. imidazolinone. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.EPA): http://pmep. EPA 738-R-00-009. Hladik ML. Environmental Protection Agency (U.cornell. 5/30/06. et al.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Environmental Protection Agency (U. Reynolds SJ. Hein MJ. EPA).248(2-3):123-133. 2005. Heederik D. Environ Health Perspect 2000. Wilson AG. Striley CA. Larsen GL. Rose RL. Ward EM. March 2006. Casida JE. Curwin BD. J Agri Food Chem 1989.39(17):6561-6574.15(9):702-735.11(4):353359. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Centers for Disease Control and Prevention (CDC). pages 3682-3690. Federal Register: January 24.111(5):749-756. Third National Report on Human Exposure to Environmental Chemicals. U.S. Feil VJ. Acetochlor (Harness) Pesticide Petition Filing 1/00. Roberts AL. Coleman S. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Number 15. Chem Res Toxicol 1998. Available at URL: http://www.17(6):559-566. acetochlor. Sci Total Environ 2000.15(6):500-508. and other herbicides in rivers. Wratten SJ.

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

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

Ann Occup Hyg 2003. Third National Report on Human Exposure to Environmental Chemicals. 2007. Hines CJ. Sci Total Environ 2000. Camann DE. et al.37(4):10881093.S. revised February 15. Mutat Res. Brown MA. Peter CJ. Shealy DB.epa. Alachlor in Drinking-water. Clark JM. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor.gov/oppsrrd1/ REDs/0063. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.11(4):353359. sulfonamide.43(9):2504-2512. Furlong ET. reservoirs and ground water in the Midwestern United States. Hill RH Jr. DNA adduct formation by alachlor metabolites. Environ Sci Technol 2005. Bull Environ Contam Toxicol 1996. 2005.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Barr DB. WHO/ FAO Data Sheets on Pesticides.111(5):749-756. Martens MA. Tessier DM. Centers for Disease Control and Prevention (CDC).org/documents/pds/pds/pest86_e. 98-4245 (by Barbash JE. Geological Survey (USGS). Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Casida JE. Brown KK.htm. Identification of a major human urinary metabolite of alachlor by LC-MS/MS.56(6):853-859. Heydens WF. Striley CA. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. World Health Organization. Deddens JA. Linhart SM.Herbicides References Battaglin WA. Sacramento. 1999. Hull RD.int/water_sanitation_health/dwq/chemicals/en/alachlor. Kier LD. Available at URL: http://water. An evaluation of the carcinogenic potential of the herbicide alachlor to man.47(6):503-517. U. Quistad GB. Comparative metabolism and elimination of acetanilide compounds by rat. acetochlor.39(17):6561-6574. Am Ind Hyg Assoc J 1995.248(2-3):115-122. 2003. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Hill AB. MacKenzie B. Hines CJ. Thake DC. Feng PCC. Circular 1291. et al. California. Andrews HF. Casida JE. International Programme on Chemical Safety (IPCS). Dialkylquinonimines validated as in vivo metabolites of alachlor. Burkhardt MR. Biagini RE.44(18):1325. World Health Organization (WHO). Casida JE. Shoemaker DA.43(25):2087-94.php. and other herbicides in rivers. EPA 738R-98-020.pdf. Chem Res Toxicol 1998. who. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . 1997. 1998. Quistad GB. Environmental Protection Agency (U.S.56(9):883-889. J Ag Food Chem 1995. Henningsen G. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. J Agri Food Chem 1989. Geneva. Sci Total Environ 2000. Tolos W. Kimmel EC. Available at URL: http://www. Thurman EM. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Background document for development of WHO Guidelines for Drinking-water Quality. Roberts AL. Supplemental Technical Information (available on-line only). EPA). Life Sci 1988. Feil VJ. Thelin GP. ALACHLOR. Jefferies PR. Atlanta (GA).S. Lau H. Hsiao JJ. Larsen GL. and metolachlor herbicides in rats. December 1998. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Xenobiotica 1994.24(10):1003-1012. Kinney PL. March 2006. Available at URL: http:// www. Hladik ML. Available at URL: http://www. Kolpin DW. Occurrence of sulfonylurea. 1999.pdf. Kolpin DW. 2/27/09 U. Sanderson WT.usgs. imidazolinone. Erratum in: Life Sci 1989. Driskell WJ. 1992-2001. Davison KL.S. Hum Exp Toxicol. Biagini R. Geological Survey (USGS). 86. Wratten SJ. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Gilliom RJ). Barr JR.395(2-3):159-171. No. Wilson AG. Environ Health Perspect 2003. Reregistration Eligibility Decision (RED) Alachlor.18(6):363-391. 4/2/09 U. 1996.248(2-3):123-133. 2/27/09 Jefferies PR. Whyatt RM.inchem.

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

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

atsdr. Mendoza M. J Toxicol Environ Health 1994. Gillis JH. et al. International Programme on Chemical Safety (IPCS).inchem. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Cottica D. Wetzel LT. diamino-S-chlorotriazine and hydroxyatrazine. Saiz SG.htm.109(6):583-590. Deddens JA. Stoker TE. Hines CJ.30(2):244-247. 2005).47(6):503-517.99(8):5476-5480. Curwin BD. 1993). Barr DB.69(2):217-222. 1996. Collins A. Available at URL: http://www.cdc. Biagini RE. Lucas AD. Wetzel LT. Aldous CN.gov/toxprofiles/tp153. References Adgate JL. Toxicol Sci 2000. J Agric Food Chem 1982. Tapia J. Toxicol Sci 2000. In small studies of Maryland residents in 19951996 (MacIntosh et al. Bersani M. Available at URL: http:// www. Reynolds SJ. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L.61(4):331-355. 2005). Goldman JM. 2001 [online]. Quandt SA. et al. 3/11/09 Arcury TA. 2007). Ferrell JM. 2003. Sanderson WT. Perry et al. Hein MJ.org/documents/pds/pds/pest82_e. Barr DB. et al. In a small number of field workers.. Stevens JT. Centers for Disease Control and Prevention (CDC).64(9):672-678. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Fleenor-Heyser DG.76(1):190-200. Shoemaker DA. Environ Health Perspect 2001. Moseman RF. In a study of 60 farm worker children. Hayes TB. Schmid J. Steroids 1999. Toxicol Sci 2003. Agency for Toxic Substances and Disease Registry (ATSDR). 2000). Pfeifer KF.. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. et al. Eberly LE. Pest Manag Sci 2005. Cooper RL. Carr WC Jr. J Toxicol Environ Health 1994. Ann Occup Hyg 2003. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. WHO/ FAO Data Sheets on Pesticides.43(2):155-167. Lioy PJ.. 2001).115(8):1254-1260. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Extrom PC. Sanborn JR. The geometric mean of urinary atrazine mercapturate was 1. Biological monitoring of human exposure to atrazine. Striley CA. Chen H. Simpkins JW. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence.. Brown KK. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. J Expo Anal Environ Epidemiol 2005. Cooper RL. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.15(6):500-508. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Maroni M. Environ Health Perspect 2007. Cooper RL. McElroy WK. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect.53(2):297-307. Toxicol Lett 1993. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Freeman NC. Blewett C. Geneva. Jones AD. Gillis JH. Barr DB. 3/11/09 Laws SC. Eldridge JC. Lee M. In the NHANES 2001-2002 subsample. Clayton CA. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . et al. Atlanta (GA).Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. et al. Catenacci G. No. Laws SC. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Seiber JN. Bradway DE. 2005. Barbieri F. atrazine was detected in only four children (Arcury et al. Goodrow MH. Eldridge JC. ATRAZINE. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Gammon DW. 82..html. Tyrey L. Ferioli A. Heederik D. A risk assessment of atrazine use in California: human health and ecological aspects. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Noriega N. Toxicological profile for atrazine. Stoker TE.58(2):366-376.43(2):155-167. Third National Report on Human Exposure to Environmental Chemicals. Grzywacz JG. levels of atrazine mercapturate were generally not detectable (CDC. Vonk A. 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. Breckenridge CB.. Proc Natl Acad Sci USA 2002. Ferrell JM. World Health Organization. Hermaphroditic. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Stoker TE. Stuart AA.

EPA). Chem Res Toxicol 1993. Toxicol Sci 2000. Langvardt PW. Breckenridge CB. EPA Office of Pesticide Programs. Tortorelli J.S. Dagenhart D. Boerma J.67(2):198-206.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. May 2003a. 6/1/09 U. Laws SC. Environmental Protection Agency (U. Interim Reregistration Eligibility Decision For Atrazine. Wood C. Timchalk C. White paper on potential developmental effects of atrazine on amphibians. Environmental Fate and Effects Division. Dryzga MD. Washington (DC).usgs. Ann Epidemiol 2000. Toxicology 1990.S. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Christiani D. Toxicol Appl Pharmacol 2004. Kastl PE. Stoker TE.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. March 2006. Perry M. Sanderson JT. Toxicol Appl Pharmacol 2002. Stevens JT.S.epa. EPA). Hammerstrom KA.58(1):50-59.61(1):27-40. Singzoni B. Rayner JL. Supplemental Technical Information (available on-line only). 0062. Cooper RL. Cooper RL. revised February 15. A review of epidemiologic studies of triazine herbicides and cancer. 3/11/09 U.pdf.Herbicides development of a biomarker of exposure. Osborne DW.56(2):69-109. Pesticides and Toxic Substances. Toxicol Sci 2002. Office of Prevention. Available at URL: http://www. U. Ryan PB.S. Pesticides in the Nation’s Streams and Ground Water.182(1):44-54. MacIntosh DL. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . A longitudinal investigation of selected pesticide metabolites in urine.epa. Needham LL. Delzell E. Guidici DL.195(1):23-34. Laws SC. The Quality of Our Nation’s Waters.php. Circular 1291.10(7):479. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Available at URL: http://water. J Toxicol Environ Health A 1999. 2007. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Fenton SE. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Case No. Wetzel L. Sathiakumar N. A risk characterization for atrazine: oncogenicity profile. Available at URL: http://www. van den Berg M. Geological Survey (USGS). 1992-2001. J Expo Anal Environ Epidemiol 1999. 2003b. Environmental Protection Agency (U. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells.gov/oppsrrd1/REDs/ atrazine_ired. Stoker TE.pdf. Urinary biomarkers of atrazine exposure among farm pesticide applicators.27(6):599612.9(5):494-501. Guidici DL. Lansbergen GW. Crit Rev Toxicol 1997.S.6(1):107-116.

General population exposure to 2. but at higher levels they are herbicidal. At low levels. Human health effects from 2.EPA in 1948.55 (1.48) < LOD 1.08) < LOD . although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.230-. MCPA. < LOD means less than the limit of detection. myotonia. dizziness. and delayed Urinary 2.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. 2004).16) < LOD . headache.230 (<LOD-.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2. in 2001 (U.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .51 (1.37) size 1977 2413 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 57 . Similar to other chlorophenoxy herbicides. It is not well absorbed through the skin.4-Dichlorophenoxyacetic Acid CAS No.490) < LOD < LOD < LOD . agricultural.210-.27 (. It was first registered with U.952 and 0. 1977).2. and aquatic environments.670-1.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .S.890 (.560-.40) 1.310) < LOD .4-D is rapidly absorbed via oral and inhalation routes.13) < LOD . hypotension.10) < LOD 1.EPA.05-2.350) < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms. 2005).20 (.610 (.07 (.4-D have been below recommended intake limits (U. It is rarely detected in ground waters (USGS. 4-D. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Recent estimates of chronic intakes of 2.930 (.27-2.490 (.70) 1.440-1. 2. As much as 62 million pounds of 2.910) 1.690 (.910) < LOD .4-D) controls broadleaf weeds in residential. by direct contact with agricultural and residential areas after applications.210 (<LOD-..960-1.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .4-dichlorophenoxyacetic acid (2. 1974.27 (1. population from the National Health and Nutrition Examination Survey.610-. Once absorbed. It is poorly bound in soils. 2007). 1989.930-1.30 (<LOD-2.740 (. these herbicides can enhance plant growth.21) 1.680-1.00-2.420-. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. Kohli et al.550-1.S. 2.320) 90th . renal and hepatic injury.Herbicides 2. abdominal pain.02-1.810-1.410) < LOD .250 (<LOD-.420) < LOD . 94-75-7 General Information Widely used throughout the United States. 2.4-D or exposed for prolonged periods.370-. which may vary for some chemicals by year and by individual sample.560-1. nausea.4-D can be applied either as an aqueous salt or as oil-soluble esters.24 (..10 (<LOD-1.250 (<LOD-.690 (.S.4-D has low acute toxicity. with a half-life of several days to several weeks.4-D were used in the U.330 (.80) 1. it acts as a plant growth hormone. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.20 (<LOD-1..32 (1. 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.310 (.400) < LOD .43) 1.690 (.260 (<LOD-.730 (.03) 695 659 520 668 589 892 Limit of detection (LOD.4-D may occur during residential applications.S.540-.60) 1.66) < LOD 1.EPA. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.22) < LOD . and mecoprop). Survey Geometric mean (95% conf.890) < LOD . the chlorophenoxy herbicide 2.760 (. Sauerhoff et al.660) 1.10 (<LOD-1.690-1.

. developmental.3.920) < LOD 1.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.670 (<LOD-1. population (Hill et al. 2000).13 (.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.700 (. 58 Fourth National Report on Human Exposure to Environmental Chemicals .780) .26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .gov/pesticides/. 2003. Average post-application urinary levels of 2.590 (<LOD-1.73) .4-D are eye irritants.560-. 2005.740 (. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.930-1..14 (.610-. 1992). 1996.670 (.05) .590 (<LOD-1.27-1.EPA. 2005).EPA 2005)..380 (<LOD-.380 (<LOD-. Biomonitoring Information Urinary levels of 2. eyes.EPA. 1985.13 (.41 (1.19) . IPCS. It is unclear whether these associations are related to the chlorophenoxy herbicides.S.660) < LOD ..Herbicides neuropathy (Bradberry et al.. 2004).580-. 2.EPA. Kolmodin-Hedman and Erne. 2001. other exposures.S.340 (. IPCS.4-D production plant workers and a few forestry workers spraying 2.39) < LOD 1. Pearce and McLean.670 (. 2005). 2002. adrenals and gonads (NTP. 2005. 2005).720 (. 2005. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. or to contaminants in the herbicide formulations (specifically 2.560-. 2006.980) < LOD 1. Survey Geometric mean (95% conf. 2. U.780-1.35) < LOD . 2005. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.24) 1.17 (.790) < LOD . In previous samples of the U.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.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.270 (<LOD-.S. 1995). and of adults and children (Baker et al. or teratogenic effects in chronic rodent studies (Charles et al. 1995.32 (<LOD-2.S. and evidence of histological injury to the kidneys. U.350 (<LOD-.470) < LOD . Frank et al. U. thyroid.S.S.660 (.480 (. 1980.16) 1.440 (. population from the National Health and Nutrition Examination Survey. Additional information is available from U. liver. 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.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 . U.780 (. urinary 2.550-.410 (<LOD-. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 1989).29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . IOM.640 (.490 (. CDC.epa.330-.790) 1.7. 2.810-1.990-1.680) < LOD . 1994). Hill et al. in small samples of children (Hill et al.620-.410) 90th .4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.380-. 1996.270-.4-D does not have significant reproductive.. 1996. 2005).890) < LOD 1.08 (..S.4-D levels were detectable in less than a quarter of the individuals studied.56) ..4-D reflect recent exposure. Kutz et al.610-.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Post-application levels in farmers and home gardeners were dependent on Urinary 2.390) < LOD < LOD < LOD .810-1.820-1.410) < LOD 1.EPA at: http://www. 2002. The acid and salt forms of 2. myotonia.08 (.380) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. Knopp et al.08 (.850) < LOD . Acute high doses administered to laboratory animals produced ataxia. IPCS.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.340-..570) < LOD .410) < LOD < LOD < LOD .520-.890-1. Epidemiological studies have reported associations of several types of cancer..

4.4-Dichlorophenoxyacetic Acid). Review of 2. Barr DB. Garabrant DH. Biomonitoring studies of 2.4-D).4-dichlorophenoxyacetic acid (2. Baker BA.27(1):23-38. Fast DM. Curwin BD. Ripley BD.4-D than levels found in the general population. Pesticide residues in urine of adults living in the United States: reference range concentrations. Available at URL: http:// www. Gupta BN. J Expo Anal Environ Epidemiol 2005 Nov.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Tandon JS.. 2005). 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Wilson RD.gov/index. Chapman P. Cook BT. Kohli JD. Veterans and Agent Orange: update 2002. Sirons G J. Brody D.org/documents/jmpr/jmpmono/v96pr04.4-dichlorophenoxyacetic acid in man.4:97-100. et al. Environ Res 1995. Crit Rev Toxicol 2002. Frank R.51(3):152-159. International Programme on Chemical Safety-INCHEM (IPCS). References Arbuckle TE. Selected pesticide residues and metabolites in urine from a survey of the U. 3/17/09 Knopp D. Kolmodin-Hedman B. Arnold EK. 2003. J Expo Anal Environ Epidemiol 2000. Tables.31 Suppl 1:90-97. Philbert MA. Exposure of homeowners and bystanders to 2. Available at URL: http:// www. Baker S. Occup Environ Med 1994. Finding a measurable amount of 2. TOX-63: TOXICITY REPORT CURVES.4-D in urine does not mean that the level of the 2. Assessment of exposure to 2. the amount of pesticide applied.31(2):121-125. Barr DB. Toxicol Sci 2001.18(4):469-474. Bailey SL. Arch Environ Contam Toxicol 1989. Developmental toxicity studies in rats and rabbits on 2. geometric mean urinary levels of 2.4 dichlorophenoxyacetic acid (2. Hein MJ. Hill RH Jr.nih.4-D) epidemiology and toxicology. Washington (DC): National Academies Press. 2005.60(1):121-131. Alexander BH. 2005 Charles JM. In farm families. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Harris et al. Acquavella JF.32(4):233-257.edu/catalog. Forestry workers involved in aerial application of 2. Beeson MD. Arch Toxicol Suppl 1980.niehs. Scand J Work Environ Health 2005.71(2):99-108. Holler JS.10(6 Pt 2):789-798.inchem. Hill RH Jr. general population.. Solomon KR. 2. National Toxicology Program (NTP). the number of acres to which it was applied (Curwin et al. Gregg M. Needham LL.. Scand J Work Environ Health 2005. Third National Report on Human Exposure to Environmental Chemicals. Biomonitoring for farm families in the farm family exposure study. van Ravenzwaay B. 2006. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. 3/17/09 Institute of Medicine (IOM). Biomonitoring of herbicides in Ontario farm applicators. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.nap. Reynolds SJ. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. and the use of protective clothing or equipment (Arbuckle et al. Harris SA. Needham LL. Board on Health Promotion and Disease Prevention.php?record_id=10603. Hanley TR Jr. Carter-Pokras OD. Ritter L.4:318-321. Pesticides residues in food: 1996 evaluations Part II Toxicology.. Xenobiotica 1974. Honeycutt R.4-D will result in an adverse health effect. Updated March 7. Mandel JS. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Dichlorophenoxyacetic acid. J Environ Sci Health B 1992. Absorption and excretion of 2.4-D): exposure and urinary excretion. Heederik D. Driskell WJ. 2005).htm.4-.4-D and 2. 2005. Sircar KP. J Toxicol Environ Health 1992.4-dichlorophenoxyacetic acid (2. Shealy DB.4-D. Baker SE. Mandel et al.15(6):500-508. Kutz FW. Stephenson GR. Available at URL: http://ntp.5-T). Murphy RS.Herbicides the time since application. To T.4-dichlorophenoxyacetic acid and its forms.31 Suppl 1:98-104. Dhar MM. Khanna RN. Arch Environ Contam Toxicol 1985. Cole DC.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. Bus JS. TOX-63 Peroxisone Project (2. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. 1992). Smith SJ. Head SL. Centers for Disease Control and Prevention (CDC). et al. Estimation of occupational exposure to phenoxy acids (2. Vet Hum Toxicol 1989. Atlanta (GA). 914. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.4:427-435. Sanderson WT. Beasley VR. Survival and Growth Curves from NTP Toxicity Studies. et al. Campbell RA.4-D were highest in the farmers who applied the 2.37(2):277-291.S. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Erne K.

S. May. Supplemental Technical Information (available on-line only).EPA. 2007.php.S.S. The fate of 2.4-D) following oral administration to man. EPA 738 F-05-002. gov/oppbead1/pestsales/01pestsales/market_estimates2001. The Quality of Our Nation’s Waters. S. 2.pdf.EPA).2000 and 2001 market estimates.4-D RED Facts. 1992-2001.8:3-1U. Environmental Protection Agency (U. June 2005. Office of Prevention Pesticides and Toxic Substances.Herbicides Sauerhoff MW.epa. Pesticides in the Nation’s Streams and Ground Water. 3/17/09. Environmental Protection Agency (U. 4/2/09 U. 60 Fourth National Report on Human Exposure to Environmental Chemicals . 2004. Braun WH. Available at URL: http://www. Washington (DC): U. Available at URL: http://www.S. Available at URL: http://water. Blau GE. Circular 1291.epa. Geological Survey (USGS).4-dichlorophenoxyacetic acid (2.gov/oppsrrd1/ REDs/factsheets/24d_fs.EPA).S. 3/17/09 U. March 2006. Toxicology 1977. Pesticide industry sales and usage . Gehring PJ.usgs.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.htm. revised February 15.

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

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 .200 (<LOD-.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.670 (<LOD-.440 (<LOD-.S. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 01-02 is 0.240) 679 701 957 Limit of detection (LOD.2.740) 679 700 957 < 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.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.500) < LOD 1192 1345 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 .S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-.

Barr DB. J Agri Food Chem 1989. Jefferies PR.S. Andrews HF.gov/nawqa/ pnsp/pubs/wrir984245/text. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. World Health Organization (WHO). Available at URL: http://water. Third National Report on Human Exposure to Environmental Chemicals. Striley CA.S. 4/2/09 U. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . 2005. Feil VJ. Sci Total Environ 2000.37(4):10881093. J Expo Anal Environ Epidemiol 2005. EPA 738R-95-006.41:3409-3414. Feng PCC. Alavanja MC.15(6):500-508. Curwin BD. Environ Sci Technol 2007. 2007.gov/nawqa/pnsp/pubs/files/051507. Casida JE.S. reservoirs and ground water in the Midwestern United States.pdf 3/30/09 Hines CJ. Background document for development of WHO Guidelines for Drinking-water Quality.pdf. Burkhardt MR.int/water_sanitation_health/dwq/chemicals/ metolachlor. Ann Occup Hyg 2003. March 2006. Comparative metabolism and elimination of acetanilide compounds by rat. Gillion. Thelin GP. Sanderson WT. Camann DE. Larsen GL. Kolpin DW. streams and groundwater. Heederik D. 2003. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. 6/1/09 Whyatt RM. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.111(5):749-756. Peter CJ. revised February 15.248(2-3):115-122. Pesticides in U. Metolachlor in Drinkingwater.php. Hein MJ. Hodgson E. Chem Res Toxicol 1998. imidazolinone.11(4):353359. Atlanta (GA).gov/oppsrrd1/ REDs/0001. et al. and other herbicides in rivers. Available at URL: http://www. sulfonamide. Environ Health Perspect 2000. et al. acetochlor.ESTfeature_gilliom. Deddens JA.47(6):503-517. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.who. Brown KK. Biagini RE. Xenobiotica 1994.html. Available at URL: http://www. Coleman S.248(2-3):123-133. Hladik ML. 1999. Davison KL. Environ Sci Technol 2005. EPA).S. 1998. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Barr DB.epa.39(17):6561-6574. 98-4245 (by Barbash JE. 1992-2001.usgs. Rose RL. Centers for Disease Control and Prevention (CDC). Linhart SM.usgs. Furlong ET. usgs. Dialkylquinonimines validated as in vivo metabolites of alachlor. Kinney PL. Shoemaker DA. Thurman EM. 3/26/09 U. Kolpin DW. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Reregistration Eligibility Decision (RED) Metolachlor.108(12):1151-1157. U. Hsiao JJ. Geological Survey (USGS). Ward EM. Available at URL: http://water.24(10):1003-1012.pdf. Roberts AL. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Environ Health Perspect 2003. Environmental Protection Agency (U. California. Reynolds SJ. and metolachlor herbicides in rats. Supplemental Technical Information (available on-line only). Gilliom RJ). Circular 1291. Sci Total Environ 2000. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Sacramento. Barr JR. R. Occurrence of sulfonylurea. Linderman R. Available at URL: http://water.S. Geological Survey (USGS). April 1995. Quistad GB. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Wratten SJ.Herbicides References Battaglin WA.

2. Mohammad and St. 1989. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. with an elimination half-life of approximately 19 hours (Arnold et al. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. Epidemiological studies have reported associations of several types of cancer.5-Trichlorophenoxyacetic Acid CAS No. < LOD means less than the limit of detection.4. dizziness.. and concern about contamination with 2. Nelson et al. nausea. which may vary for some chemicals by year and by individual sample. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. Survey Geometric mean (95% conf.4. Omer.5-Trichlorophenoxyacetic acid (2. 2.7.5-T in soil varies with conditions. 1974). Human health effects from 2.5-T and 2.5-T was once applied as either an aqueous salt or as an oil-soluble ester.5-T degrades to 2. 64 Fourth National Report on Human Exposure to Environmental Chemicals .2 and 0. these herbicides can enhance plant growth.4. 93-76-5 General Information 2.5-T has been rarely detected in ground waters (USGS..4. 1986.4. Chlorophenoxy herbicides act as plant growth hormones.5-trichlorophenol and other degradates.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States..4.4-D were used as defoliants in the Vietnam War (e.Herbicides 2.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.4. 2007).4.4.4. 2004). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD. myotonia.g. headache. Agent Orange).5-T (Holson et al.4. abdominal pain..5-T use as a herbicide in 1985.4.1. 1992). renal and hepatic injury.4. 2. Given the commercial unavailability of 2. population from the National Health and Nutrition Examination Survey. the general population is unlikely to be exposed to it. hypotension.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S..4.5T is rapidly absorbed via oral and inhalation routes.5-T is eliminated mostly unchanged in the urine. it is not well absorbed through the skin.4. 1992.4.3. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. Although 2. 2. The half-life of 2. and delayed neuropathy (Bradberry et al.5-T. ranging from several weeks to many months. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. Ester forms of 2. Once absorbed into the body. At low levels.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Kohli et al. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. but higher levels are herbicidal.

Survey Geometric mean (95% conf.5-T were generally below the limit of detection. 2. It is unclear whether these associations are related to the chlorophenoxy herbicides. 1980). Urinary 2.4.3. Additional information is available from U. Fourth National Report on Human Exposure to Environmental Chemicals 65 .Herbicides or contaminated herbicides. 2005.EPA.4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.5-T does not mean that the level will result in an adverse health effect.4.4.EPA at: http://www.4. Pearce and McLean. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biomonitoring studies on 2. 1992). in which urinary levels of 2. 2005). 1996.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. 2003. population from the National Health and Nutrition Examination Survey.5-T also were below the limit of detection (Kutz et al. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. 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..5-T reflect recent exposure. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7. Mean urinary levels of 2. 2002.4.epa.5-T itself is not mutagenic.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2.4. 2004).5-T than levels found in the general population. U.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. or to contaminants in the herbicide formulations (specifically 2. urinary levels of 2.S. IPCS. other exposures. Biomonitoring Information Urinary levels of 2. similar to results of NHANES II (19761980). IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.4. Finding a measurable amount of 2.4.S.gov/pesticides/. IOM.

Vale JA. II. McCallum WF. Sheehan DM.31 Suppl 1:1825. Environmental Protection Agency (U.4. Selected pesticide residues and metabolites in urine from a survey of the U.19(2):286-297.epa. Erne K. Gaines TB. Agricultural exposures and non-Hodgkin’s lymphoma. Murphy RS.EPA). Board on Health Promotion and Disease Prevention. Pesticide industry sales and usage .2000 and 2001 market estimates. Poisoning due to chlorophenoxy herbicides. Beasley VR. Crit Rev Toxicol 2002. Multireplicated dose-response studies with technical and analytical grades of 2.4. Arch Toxicol Suppl 1980.inchem. Pearce N. Gaylor DW. Absorption and excretion of 2. Vet Hum Toxicol 1989. 2005. 914. Cook BT. Pesticides residues in food: 1996 evaluations Part II Toxicology. Proudfoot AT.5-T). Office of Prevention Pesticides and Toxic Substances.4-D/2. Kutz FW. et al.S. Developmental toxicity of 2.4. Atlanta (GA). 3/17/09 Kohli JD. Sircar KP. Carter-Pokras OD.S.Herbicides References Arnold EK. I.5-t mixture. 2. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .5-trichlorophenoxyacetic acid (2. Developmental toxicity of 2. 210:250-255. Fundam Appl Toxicol 1992. Dhar MM. Khanna RN.edu/catalog.5-T).8(5):551-60.5-T in four-way outcross mice. May. Available at URL: http:// www. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4. Mohammad FK.htm. Washington (DC): National Academies Press.37(2):277-91.4-D) epidemiology and toxicology.nap. Neurobehav Toxicol Teratol 1986. International Programme on Chemical Safety-INCHEM (IPCS).4-. Bradberry SM.4. Available at URL: http:// www. 2003.4-dichlorophenoxyacetic acid (2. Wolff GL. Behavioral and developmental effects in rats following in utero exposure to 2. et al.S. Estimation of occupational exposure to phenoxy acids (2. Nelson CJ.4. Tandon JS. Kolmodin-Hedman B.4. Veterans and Agent Orange: update 2002. Washington (DC): U.4-D and 2. Available at URL: http://www. general population.pdf. discussion 5-7.4. 3/17/09 Institute of Medicine (IOM).5-T). Scand J Work Environ Health 2005. Garabrant DH. J Toxicol Environ Health 1992.4:318-21.5-trichlorophenoxy acetic acid in man. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Fundam Appl Toxicol 1992.5-trichlorophenoxyacetic acid (2. LaBorde JB. Arch Int Pharmacodyn Ther 1974.19(2):298-306. Review of 2. Holson JF.32(4):233-257. Gaines TB. Holson JF.31(2):121-125. Brody D. Philbert MA. S. Third National Report on Human Exposure to Environmental Chemicals. Centers for Disease Control and Prevention (CDC). McLean D. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. St Omer VE. U. Toxicol Rev 2004.php?record_id=10603. Dichlorophenoxyacetic acid.EPA. LaBorde JB.23(2):65-73. Gupta BN.org/documents/jmpr/jmpmono/v96pr04. Nelson CJ. 2004. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.

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

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

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

070) .5 and 7.190) .8-25.103 (.6 (15.109-.120-.120 (.130) . see Data Analysis section) for survey years 01-02 and 03-04 are 10.1) 15.2) 12.150 (.090 (<LOD-.7 (15.9-38. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110) .9 (12.10 (<LOD-16.100-.4) < LOD < LOD 16.4) 20.1) 10.1 (13.0-21.5 (16.2) 11.9-23.130 (.7 (<LOD-15.5-17.101) .110) .8-17.0) 19.080) .103 (.100 (.6) 16.150 (.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.6) 9.170) .1) 20.4-17.0 (11.060) .062-.110-.140) .4) 95th 20.058) < LOD .8 (11.190) .70 (7.138) .7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.1) 15.090-.1-19.117) < LOD .120) .202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.6 (14.064 (.60-10.4 (12.180) .00-14.8-17.00 (8.059 (. 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 (13.4-18. which may vary for some chemicals by year and by individual sample.055 (.1 (18.4) 19.070 (<LOD-.100) .098 (.8 (18.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.2) 14.4) 21.130) .120 (.110 (.069) < LOD < LOD .6-33.30 (8. which may vary for some chemicals by year and by individual sample.3 (18.4 (12.080 (.062 (.8) < LOD 8.9 (13.138 (.139 (.089 (.3-21.109 (.8.6-24.5) 21.0-25.9-22.6-24.130-.116) .0 (15.062 (.2-15.3 (18.102 (.3 (13.S.2) 15.054-.4) 14.088-.056-.1) 14.077 (.1) 13.120 (.077-.090-.090-.8) 15. population from the National Health and Nutrition Examination Survey.80-10. population from the National Health and Nutrition Examination Survey.0 (10.113 (.054-.100-.30 (8.160 (.048 (<LOD-.5) 15.160) .130-.8) 14.5-17.4) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.090 (. 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 9.112) 95th .160 (.9 (12.7) 15.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .100-.140-.6 (15.8 (9.100) .3 (19.50) 15.7-19.130) .1-16.149) . Survey years 01-02 03-04 Geometric mean (95% conf.242) .S.1-18.40-9.90) 90th 15.1-24.049-.3 (14.6) 19.063-.7-22.080-.070-. 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.073-.083-.7 (14.124) .158) .8-19.0) 21. < LOD means less than the limit of detection.096-.108-.054-.8-24.147) 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 .112-.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .130-.084-.5) 19.110 (.139 (.064) 90th .0 (10.80-9.80 (<LOD-10.075) < LOD .109-.50 (8.1) < LOD 9.9 (14. Survey years 01-02 03-04 Geometric mean (95% conf.4) 539 456 484 487 980 885 Limits of detection (LOD.086-. Fourth National Report on Human Exposure to Environmental Chemicals 79 .053 (<LOD-.110 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.180) .0) < LOD 9.093) .5 (<LOD-11.40-10.140 (.147 (.5-15.

91(1):122-126. Narahashi T. 2 Classes of Pesticides. Needham LL. Carlson JN.109(Supp1):113-139. Kanthasamy AG. 6/1/09 Ward EM. Available at URL: http://www. 1991.66(4):229-234. Available at URL: http://pubs. 1989. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Toxicological profile for aldrin/dieldrin [online].9:1357-1367. pp. toxicology.html. In Hayes WJ. 4/21/09 Hoyer AP. Serrano FO. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures.59:229-234.352:1816-1820. J Toxicol Environ Health 1989. Lancet 1998. Exp Neurol 1998. et al. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Edwards JW. Sonnenschein C. Cox. Psychopharmacology (Berl) 1987. Roy ML. Grandjean P. September 2002. Daniel SE. Neurotoxicol 2005. Tully DB. David VL. Song S. Vol.64-65 Spec. Soto AM. Garrett N. Organochlorine exposure and risk of breast cancer.gov/ circ/2005/1291/. Rosellini RA. Finley B. Academic Press. J Toxicol Environ Health. Corrigan FM. 731-915.usgs.cfsan. Ellis H.html. Jr. Cancer Epidemiol Biomarkers Prev 2000. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.103(Suppl 7):113-122. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. McIntosh LJ. International Programme on Chemical Safety (IPCS). VT.54:1431-1443. 1992-2001. Revised Feb. Chlorinated Hydrocarbon Insecticides.150:263-271. bioaccumulation. PA. plasma dieldrin. Pesticides in the Nation’s Stream and Ground Water. Brock JW. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Kitzazwa M. Turner W. 2007 [online]. United States Geological Survey (USGS).27:405-421. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Demographic and seasonal influences on human serum pesticide residue levels. Available at URL: http://www. Sanchez-Ramos J. Chung KL. are nonestrogenic in transfected HeLa cells. Six high-priority organochlorine pesticides. Grajewski B. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Jr and Laws ER.26:701-719. Chapin RE. 4/21/09 Bates MN.atsdr.14:95-102. 4/21/09 Jorgenson JL. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. New York. Kanthasamy A. Shore RF. Inc. Environmental Health Criteria 91.fda. Mumtaz MM. Aldrin and Dieldrin [online]. 15. Toxicol Lett 1992. Basit A.cdc. Environ Health Perspect 2001. August 2008. Jorgensen T. and lymphocyte sister chromatid exchange. Reprod Toxicol 2000. Teta MJ.inchem. Food and Drug Administration (FDA). Patterson DG Jr. Eds. 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. Smith AG. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Li AA. Fernandez MG. Environ Health Perspect 1995.org/documents/ehc/ ehc/ehc91. Mann D. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Olea N.gov/toxprofiles/ tp1. Facca A. Available at URL: http://www. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Wienburg CL. Int Arch Occup Environ Health 1994.gov/~dms/ pesrpts. Schulte P.47:1059-1087. Patterson DG Jr. Mink PJ. Stehr-Green. Priestly BG. Ginsburg KS. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Handbook of Pesticide Toxicology. J Occup Environ Med 2005. Chemosphere 2004. Part A 2000. References Agency for Toxic Substances and Disease Registry (ATSDR). Andersen A. either singly or in combination.htm. and epidemiology in the United States. Hartvig HB. No:429-436.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Buckland SJ. Anantharam V. Frey JM. et al. 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.

9) 23.5-44. heptachlor use has been limited to treatment of fire ants near power transformers.7) 19.1 (25.2 (41. and 03-04 are 14.9-40.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8 (42.5) < LOD < LOD < LOD < LOD 13.8.2) * 12.8) 18.8-33.7 (43.2-28.7 (19.9-21. respectively. see Data Analysis section) for Survey years 99-00. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9) 39.0-13.5-65.9 (15.7 (17. 2007).7-12.1) < LOD < LOD < LOD < LOD < LOD 8.8-32.3 (21.3 (26.8) 52.9) 11.5-41.2) 34.7-70.3) 10.5-42. which may vary for some chemicals by year and by individual sample.3 (25.0) 75th 20.1-50. 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.2-21.5) 21.2 (10. Chlordane is not currently produced or used in the U. the technical grade product of each chemical contains 10%-20% of the other chemical.4) 18.6) 36. 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.4 (22.9 (26.0 (<LOD-12.9) 13.2-56.7) 31.Organochlorine Pesticides Chlordane CAS No.9 (17.1 (44. 1994). 2007).0-12. chlordane was used to kill termites and other insects on agricultural crops.6) 49.70 (<LOD-10.5-13.5 (<LOD-12.6 (9.4) 12.0) 27.37 (8.1 (<LOD-12.6-24.4 (10.4 (31. 1994.8) 53.5-32.20-11.0) 37. fish.1 (17.1) 30.4 (35.82-11. 01-02.89-10.1) * 11.7) 35.6) 9.2) 46.3 (<LOD-19.9 (26. < LOD means less than the limit of detection.6) < LOD 11.3 (11.69-10.9 (31.1 (<LOD-12.7-56.5 (41.9) 10.3-24. and in soil.20-10.3-43.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.8-31.7 (<LOD-32.1-25.0 (37.5-38.2 (39.2 (37.36-11.10 (8.6 (25.7-39.2 (36. Technical grade chlordane had contained 7% trans-nonachlor.4) 29.8-23.0 (32.1-25. and 7.9 (21.9) 11.8) 27.7 (34.5.8 (10.7 (<LOD-13.8-73.0 (20.3-49.2) < LOD 11. Fourth National Report on Human Exposure to Environmental Chemicals 81 .S.6) 11.3 (9.7 (34.5) 56.2) 36.1 (40.4 (30.5) 38. and dairy products are the usual sources of exposure to these chemicals in the general population.0-33.5-43.6-18.9) 31.9-21.0 (26.1-51. 10.7-14.3-45.8 (10.6-24.9) 36.4 (30.2) 33.3) 37.3) 18.3 (20.9 (15.2) 22.0) 20.4-51.5) 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 * * * * 11.6-12.7 (42.9) 23.4) 22.6) 23.5 (33. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.8 (17.3-45.7 (10.1 (<LOD-12.8-61.7) 42.8 (40.8 (18.5 (31.1) 90th 34.2-49. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.1 (27.6) 48.0-25.2 (21.1-65.7 (32.S.S.5 (34.8) 44.9) 17.6) 9. Since 1992.3 (28.9 (11.3) 18. in addition to trace amounts of numerous other related compounds (ATSDR.7-25.1) 22.6) 8. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.30-11. 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.3) 41.7) 9.9 (18.4-21.4-40.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.1 (16.3 (27.9-42.6 (43. 57-74-9 Heptachlor CAS No.9) 37. Consequently.2) < LOD 11. buildings. foods high in fat such as meat.5-47.2 (9.2 (28.1-15.6 (9.6) 20.3-32.8) 52.4 (<LOD-12.0) 31.8-43.0-67. lawns.6-53.90 (8.1 (15.2-49.7) 19.5) 9.5) 37.4) 39.8-33.8-20.6-45.63 (8.9-38.0) 21.9 (36.9 (29.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.1) 30. population from the National Health and Nutrition Examination Survey.5) 10.4) < LOD 11.2-26.1 (11.6) 48.9 (11.2) 37.8-42.4) < LOD < LOD < LOD 23.4-45.4) 37.6 (16.6) 39.1 (20.5) < LOD < LOD 9.0-61.4-14.7) 28.. Survey Geometric mean (95% conf.10-18. As a result of the manufacturing process.0) 41.1-19.0-18.1) 16.1) * 11.0 (16.10-11.3) 10.9) 47.74 (<LOD-10.20 (<LOD-11.5. Until 1988. from the early 1950’s until the mid-1980’s. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.5 (8.5-40.8 (17.5) 44.

150-.310 (. dermal.160 (.450) .130-.140 (.100 (<LOD-.140 (.430) .310) .210 (. and alterations in immune function of offspring. 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. 82 Fourth National Report on Human Exposure to Environmental Chemicals .140 (. The U..119 (.280-.210-.220-.160) .063 (.130-.310) . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.250 (.150 (.080) . and inhalation exposure.230) .230 (.079) .140) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.280-.225 (.203-.049 (<LOD-.048-.180) . population from the National Health and Nutrition Examination Survey. Chlordane and heptachlor are absorbed after oral.077) .130-.190-.350 (.150 (. chronic doses of heptachlor have produced liver enlargement and injury.091) .260-. neonatal mortality.100-.300 (. 1986).070 (.126) .310) .380) .302) . IARC.290) .067 (. which is also persistent in the body (ATSDR.140-.510) . 2002. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.199-.260 (.074-. heptachlor.115-.050 (<LOD-.050-. Elimination of all these chemicals from the body occurs over months to years.060 (<LOD-.075 (.130 (.057) * .220 (.258 (.069 (<LOD-. 1977b.062) < LOD .053-.S.227) < LOD . EPA has established environmental criteria for chlordane and heptachlor.063-.126 (.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .200 (.066-.290-.410) .077) .280 (.208 (.146) < LOD < LOD .055-.063) * .258-.216-.245-.286 (.066-.140 (.300) .320) .S.400) .360) .066 (.065-.240-.240-.110-. Takahashi et al.063 (.373) .220-.120-. 1986). No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.160) .068) .180-.223) . characterized by seizures and paralysis.170) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .110 (<LOD-.104-. The major metabolite of heptachlor is heptachlor epoxide.077) .240 (.148) .320 (.120-.230 (.230-.260 (.170) . which may vary for some chemicals by year and by individual sample.056 (. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP. Shindell and Ulrich.112 (.070-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.149 (.057-. 2007.070 (<LOD-.070-. 1996. OSHA has established occupational exposure criteria. Le Marchand et al..168-.061-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.430) .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .070) .280-.560) .165-.315 (.280 (.077) .150) .320 (.286 (.058 (.063) .066 (<LOD-.063 (. 2007).350) .080 (.290) .246-.204 (.287) .320) .440) .450) .189-.120 (.270 (.271 (.058-.083) .070 (<LOD-.068) 75th .269 (.148-.160) .300) .290-.340) .090) .310-.370 (.207 (. to heptachlor.230-.189 (.207) . FDA established allowable residues of chlordane. Acute.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 * * * * .170) .180) .115 (.100-.090) .180-. Smith.068-.130-.090-.073) < LOD < LOD < LOD < LOD .070-.076) < LOD . 1977a.083 (.213) * . and breast milk is a major excretion route in lactating women.300-.200-.100 (.300) . and heptachlor epoxide in foods and bottled water.080) . Chlordane is metabolized primarily to oxychlordane and to a lesser extent.300) .080 (.348) .230-.071 (.290-.063 (.170-.133) 90th .070 (<LOD-.S.073 (.242-. Rogan. Survey Geometric mean (95% conf.130) .320 (.270 (.280) . 2006).070 (<LOD-.190-.128 (.079) < LOD < LOD < LOD .104) .250 (.140-.082 (. 1991.290 (.200-.092) .106-.080) .250-. 1991).Organochlorine Pesticides (Dallaire et al.320 (. In laboratory animal studies.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.057 (.146) .200-. 2001.120-.370 (.330 (.170) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130) .210 (..190-. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.047 (<LOD-.070) < LOD < LOD < LOD < LOD < LOD . 1981).340) .130 (.064) < LOD .087-.053-.150 (.270 (.240) .136) .170) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350 (.253-.058-.370 (.108-. and the U.130-.260 (..231) .130 (.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .400) .

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

2 (<LOD-16.8 (13.3) 23.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.6) 14.6 (11.3 (<LOD-25.2) 15.8 (18.40) 15.9) 15.8) 13.4) 21. respectively.6 (16.8 (18.9-29.50) < LOD < LOD < LOD 17.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8. which may vary for some chemicals by year and by individual sample.2) 20.3) 18.1-16.90 (<LOD-9.8) 19.9-23. population from the National Health and Nutrition Examination Survey.0 (15.8. 84 Fourth National Report on Human Exposure to Environmental Chemicals .5 (10. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.20 (<LOD-9.2-16.3-18.8) 14. 10.6 (16.9-25.4 (11.6 (13.8-24.8) 19.6-17. and 03-04 are 14.0) 13.0-17.5) < LOD 14.6) < LOD < LOD < LOD 27.8) 13.5 (11.8) 16.8-24.4 (15.5) 19.0 (11.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3) 18.3) 16.8) 20.7-18.2-27.9 (15.7-19. see Data Analysis section) for Survey years 99-00.6) 22.2 (<LOD-25.S.7-25.3) 10.6 (14.2 (18.1 (19.8-46.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.6.2 (<LOD-62.4 (11.7 (16.3) 18.4) 18.0-17.9 (12.2) 13. and 7.8 (<LOD-23. Survey Geometric mean (95% conf.2) 26.1-38.8 (13.8) 21.1 (16. 01-02.5 (18.3) 22.1) 13.8) 14.8-24.1-15.1-29.0-16.6 (<LOD-27.4 (<LOD-19.0) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.0-19.3 (13.7 (10.2-17.4 (<LOD-54.2-27.5 (11.5 (<LOD-32.3) 27.5) 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 7.6) 13.1) 23.6 (12.8) 15.1) 20.6-21.8 (15.9-29.6 (8. < LOD means less than the limit of detection.10-13.8-23.5 (<LOD-21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9-16.0-54.7 (13.5.

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-88.5 (13.8 (11.2 (19.9-35.5) 36.5) 22.4) 59.8 (28.5) 14.9 (51.2 (14.4 (12.3-50.0) 18.0-68.5) 14.8-19.8-19.5-87.4-52.8-21.70 (<LOD-12.7) 52.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.8 (<LOD-20.3) 15. see Data Analysis section) for Survey years 99-00.8 (30.0 (13. respectively.4) 107 (84.5-36.4) 20.7 (11.1 (22.2-17.6-66.2-37.8 (26.6-82. 01-02.1-34.7-18.3 (17.1-126) 67.9) 14.0-38.0 (60.2 (36.7-17.1) 18.1) 17.1 (48.5) 77.8 (15.8-41.7) 15.6) 10.9) 14.7) 17.0) < LOD < LOD 8.9-45.8-16.9 (19.9 (29.0 (15.1) 17.5-20.6 (50.0 (13.0-24.1-16.0-123) 74.5-95.9) < LOD < LOD < LOD 20.9-40.4-23.8 (28.1 (41.1-34.2 (15.2-16.8-79.7 (35.0-59.2 (64.7-22.3 (14.3) 32.3) 25.3 (45.5-69.4) 48.S.0 (29.5 (45.8-77.1) 78.0-113) 68.8 (12.1) 17.8 (13.7) 56.5) 78.5) 48.6 (57.4 (67.5) 20.2 (27.3-57.1-20.3) 36.6 (12.6) 56.3-32.7 (30.7) 59.6 (52.7-160) 86.0-37.8 (49.1 (10.9) 51.3-39.0-22.5 (44.4-36.0) 75th 31.2) 19.1-16.7-38.2) 34.2) 17.4-62.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.1 (17.9 (47.7) 28.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.0 (42.8 (26.5) 19.3) 18.2 (25.6-22.5.1 (65.1-51.0) 33.1) 14.3) 30.8) 51. 86 Fourth National Report on Human Exposure to Environmental Chemicals .5-111) 68.6) 34.9-65.6) 82.0 (16.4 (28.7) 73.1-22.2) < LOD 10.7) 78.1 (47.1) 31.2-21.0 (16.7-23.7) 35.4-22.1) 17.8.0) 49.7-35.6 (<LOD-14.1) 32.7-32.9 (15.6) 56.8-90.7 (28.0 (42.7 (74.5) 90th 55.9-89.8 (16.10 (<LOD-11. 10.0-23.2-18.3) 19.3 (16.5.9 (16.2) 59.9-69.7) 78.3-86.6) 54.9-64.8) 80.3) 16.9-20.3) 18.4 (45.8-90.0-20.6-54.2) 20.9 (51. and 03-04 are 14.2) 30.5 (15.1) 17. Survey Geometric mean (95% conf.1-18.1) 17.0 (62.7 (59.9 (<LOD-14.0-93.2 (14.8 (19. population from the National Health and Nutrition Examination Survey.0 (48.9-58.4 (30.0) 13.7 (16.2 (26.8-67.8 (26.6 (32.5-19.8 (13.2) 39.7-77.2 (7.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 (13.4-18.6 (56.4-35.8 (42.0-93. which may vary for some chemicals by year and by individual sample.6) 13.2-18.4) 55.2-88.5 (25.1) 16.7 (59.8 (17.5) 26.8) 19.3-74.7-20.8) 47.6 (16.9-22.3) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.7-29.6) 84.5-17.2 (60.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.7) 14.9-36.7-21.8 (71.4) 16.5) 9.6-19.5) 30.3 (56.86-13.1) 17.0-143) 112 (68.1) 18.0 (19.5 (15.9 (28.8 (45.4 (11.1-55.7 (18.8 (28.8-16.9 (15.9 (66.4 (16.4) 19.6 (56.0) 19.3 (49.7-113) 68.3 (58.0) 40. < LOD means less than the limit of detection.2-23.1-28.9) 51.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.6-20.9 (36.3) 30.0 (15.2 (59.3-30. and 7.6 (15.1) 78.0-23.6) 60.3-21.3-58.1) 62.3 (14.7-34.9-65.0 (14.8-129) 74.4-67.5) 35. interval) 18.3) 32.8-110) 59.6) 25.1) 30.

310) .390 (.220 (.112 (.470 (.320-.100-.220 (.240) .684) .540) .580 (.100 (.096-.119) < LOD < LOD < LOD .310-.460) .240) .089 (.080 (.134) .270-.079-.500) .090-.800) .301-.062 (.079-.093-.830) .290-.210 (.098) .186 (.186-.440) .380 (.173-.460) .20) .125 (.080) .071 (<LOD-.600 (.130) .098-.099-.090 (<LOD-.170 (.080-.211) 90th .410-1.041 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 87 .100-.210) .141) .414 (.420 (.127) < LOD < LOD .390 (.330-.096-.098 (.131) .286-.078 (.111-.080-.830) .395) .210 (.220 (.470 (.128 (.104 (.112 (.360-.090-.420) .220 (.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 .400-.092 (.360-.110 (.450) .285-.180-.330 (.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.430-.110 (.470-.120) .640 (.108) .094 (.350-.440-.120-.300-.390 (.310-.220 (.124) .090-. which may vary for some chemicals by year and by individual sample.317 (.497-.930) .130) .760 (.590 (.130 (.099-.461 (. population from the National Health and Nutrition Examination Survey.510 (.103 (.084-.100-.120-.120) .098 (.116 (.395-.520) .558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .458 (.180-.250) .190-.220 (.690) .100-.220 (.367) .630) .090-.324 (.116-.630) .260) .110 (.390) .106 (.090 (.190-.047-.230 (.590) .202 (.390) .250) .161) .400-.108 (.594) .288 (.120 (.060-.470 (.210-.210) .093) .122) .240-.091-.092 (. Survey Geometric mean (95% conf.260) .840) . interval) .210-.110-.130) .590 (.565) .237) .310-.559) .080-.242) .210) .651) .490) .111 (.114) .060) .161-.116) .350 (.108) 75th .410-.600) .288-.085-.171-.100 (.109 (.106 (.070 (.160-.400 (.130) .085-.240 (.183 (.120-.082) .091) .409-.122) .120 (.680 (.103 (.580 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .110) .093-.119) Selected percentiles ( 95% confidence interval) Sample 95th .095-.113) < LOD .126) .190-.158-.106 (.520 (.097) .690) .430-.081 (.390-.330-.240) .390 (.069) .120) .370 (.343 (.470-.340-.054-.490 (.109 (.130 (.110 (.090-.371) .145-.220) .550 (.630) .061-.110 (.405) .081-.140) .090) .180-.580 (.113) .078-.300) .191 (.430-.141) .960) .130) .510-.205 (.320-.130) .210 (.490-.340-.237) .400) .220 (.S.355 (.272-.120 (.085-.417 (.055 (<LOD-.150) .460-.280) .190-.310-.397-.190-.090-.480) .135 (.150) .104-.490 (.279-.370 (.069-.068-.096) .310 (.120) .190-.234) .520 (.250) .110 (.087 (.177-.060 (<LOD-.129) .093-.400 (.573 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.232) .080-.327 (.105 (.117) .160 (.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .130) .680) .125) .Organochlorine Pesticides Serum trans-Nonachlor (whole weight) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.340) .

In Hayes WJ. Barker J.atsdr. Gilman A. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Available at URL: http://www.html. et al. 1963-1967. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Jr. gov/toxprofiles/tp12. Academic Press. Hansen JC. Chlordane and heptachlor [online]. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Bioassay of heptachlor for possible carcinogenicity. Handbook of Pesticide Toxicology. Available at URL: http://ntp. Circumpolar maternal blood contaminant survey. Takahashi W.niehs.8:1-123. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Siegel BZ. Drews K. Environ Health Perspect 2003. LeMarchand L. Bioassay of chlordane for possible carcinogenicity. Organochlorines in Swedish women: determinants of serum concentrations. Available at URL: http://www. Bjerselius R. Inc. Vol.pdf. Head SL. Environ Health Perspect 2002. Hertz-Picciotto I. Toxicological profile for heptachlor and heptachlor epoxide [online]. Wong L. Keller JA. Sci Tot Environ 2006. 1993. Available at URL: http://www. Odland JO. Smith AG. Voorspoels S. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Senie R. Jaraczewska K.org/ documents/cicads/cicads/cicad70. Wohlleb JC. Loo S. Saidein D.41:145–148. A Report to the Hawaii Heptachlor Research and Education Foundation. Ayotte P. Available at URL: http://www.gov/ntp/ htdocs/LT_rpts/tr008.pdf. Lawrence River (Quebec. August 2007. Aune M.htm. Covaci A. Organochloride pesticide residues in human milk in Hawaii. Van Oostdam JC.org/site/foundation/ research/projects2. Toxicological profile for chlordane [online].htm.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Environ Health Perspect 2002. Arch Pediatr Adolesc Med 1996.259(3):374-377. Available at URL: http://ntp. JAMA 1988. Bleiweiss IJ.50(3):108-118. 9/25/07 International Programme in Chemical Safety (IPCS). 2006. 6/1/09 National Toxicology Program (NTP). KalubaSkotarczak A. 1991 pp. 79. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.28:497501. 1986. et al. Takei G.110(8):835-838. J Occup Med 1986. Vol. Sci Total Environ 2004.110:617-624.cdc. 2 Classes of Pesticides. Hawaii Med J 1991. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Shindell S and Ulrich S. May 1994.inchem.330:55-70. 2001. et al.html. 6/1/09 Rogan WJ.nih. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Dewailly E. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Dewailly E. Distribution of polychlorinated biphenyls.gov/toxprofiles/tp31. International Agency for Research on Cancer (IARC). Laliberte C.html. Bull Environ Contam Toxicol 1981:27:506-511. Darnerud PO. maternal serum and milk from Wielkopolska region. Environ Res 2000. Baker DB.9:1-109. Concise International Chemical Assessment Document 70 Heptachlor [online]. Available at URL: http://www. Chashchin V. Tartter P.inchem. Brower S. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). New York. Arch Environ Health.84:151-161.niehs. Granath F. 1994-1997 organochlorine compounds. Berkowitz GS. Atuma S.nih. 731-915. 4/21/09 James RA. 4/21/09 Baker DB. Chlorinated Hydrocarbon Insecticides.cdc.Summaries & Evaluations. Charles MJ. 4/21/09 Dallaire F. Mortality of workers employed in the manufacture of chlordane: an update. Royce W.atsdr. Muckle G. Willman E. Poland. Organochlorine exposures and breast cancer risk in New York City women.org/documents/iarc/ vol79/79-12.gov/ntp/ htdocs/LT_rpts/tr009. International Agency for Research on Cancer (IARC) . Kolonel LN. Stehr-Green P. Dendle WH. Jr and Laws ER.150:981-990. Glynn AW. Lulek J.372:20-31. Pollutants in breast milk. National Toxicology Program (NTP). 1979-1980. Eds.111:349355.heptachlor. et al. Canada). Wolff MS.

DDT usually refers to the technical product.3) 22. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR. resulting in fetal exposure.1’-dichloro-(2.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (18.6 (9. It is still used in some countries.5 (14. including 1.5 (23. see Data Analysis section) for Survey years 99-00.p'-Dichlorodiphenyltrichloroethane (DDT) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.0 (21.1 (23.5 (15. which may vary for some chemicals by year and by individual sample. Gunderson.7-16.0) 19. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Smith.9 (10. or dermal exposure.S.8) 36.2 (11.4) < LOD < LOD < LOD 61.9) 17. 2002.2 (<LOD-40.2) 155 (59.7) < LOD 18.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. DDT and DDE can cross the placenta.0 (18. DDT can be absorbed after ingestion. Fourth National Report on Human Exposure to Environmental Chemicals 89 .9 (10. and water.00 (<LOD-10.5 (23.3-590) 293 (104-541) 48.9 (10.5) < LOD < LOD 9.0-27.7) 12.3) 28. 1988).0 (10.7.0-37.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.70 (8.10-13. as well as in plant and animal tissues.1 (33.90 (<LOD-12.6 (31.9) 29.3-16.0) 26. depending on conditions.1-71. p.7 (15.0-155) 83.4.10 (<LOD-12.9) < LOD < LOD 9.8) 15. In the general U. population from the National Health and Nutrition Examination Survey. The biodegradation half-life of DDT in soil varies from 2 to 15 years. DDT was used at one time as a treatment for head and body lice.6 (25. DDT is converted to DDE and several other metabolites.3 (27.1) 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. air.4 (23. In the body. and trace amounts of several related compounds.2-65.8-26. and 7. although DDT and DDE intakes have decreased over time (FDA.9-34.9) 14.p’-DDD (4% or less). sediments. Both Serum p.8-23.3) 21. particularly meat. and dairy products. particularly for endemic vector and malaria control. 17. 1991). and 03-04 are 20.8.8-17. when virtually all use of it was banned. which is a mixture containing p.1 (<LOD-39.8) 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 8.3 (<LOD-21. food.8-39.2) 30.5-54.0-15. Only a small proportion of DDT is metabolized and excreted (Smith. 1991).2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.0-53.9 (21. Survey Geometric mean (95% conf. population. o. It was produced and used in the U.50-11.7 (19.2-bis(p-chlorophenyl) ethane (DDD).2) < LOD < LOD 9. < LOD means less than the limit of detection.6 (22.1’-(2.3-236) 24.0) 20.0) 40.S.9-28. 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.p’-DDT (65%-80%). interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.9 (<LOD-20.5) 23.6 (<LOD-25.1-27. These chemicals are highly persistent in soil.4) < LOD 17.1) 31. 01-02.0-35.5-36.S. DDT is converted in the environment to other more stable chemical forms.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. continues to be the primary source of DDT exposure. inhalation.p’-DDT (15%-21%).3 (<LOD-31.5) 25. after World War II until 1972.6-33. 2008. fish.3) 21.2-95. respectively.8) 30. Food imported from countries that still use DDT may contain the chemical or its residues.

2004.180) .120-.250-1.200 (.146 (. fertility.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 . It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. 2006).260) . Gladen and Rogan.098-. In laboratory animals. tremor.p’-DDD and p..Organochlorine Pesticides chemicals are excreted in breast milk.106-. In high dose.132-.106) .00) .203) .084 (. resulting in exposure to nursing infants (Rogan. Jusko et al.190-1.160-..180) . 2000.189-. Hayes et al.400 (.150 (<LOD-.150 (<LOD-.180 (.150-.071-.g. 2002. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. premature delivery.201 (.086 (...00 (..p’-DDE can produce anti-androgenic effects (Gray et al.170) . 2001). and duration of lactation. have not been consistently demonstrated (Beard.570-4... reproductive organ abnormalities. Studies of DDT exposure and pancreatic cancer.240 (. 2001).128 (. Survey Geometric mean (95% conf.130 (<LOD-.240) . 2002.p'-Dichlorodiphenyltrichloroethane (DDT) (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.142 (. Jusko et al.080-. Beard.065-. 2006.420) .071 (.207) 799 1073 959 880 1232 1006 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .170-.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 .078 (.343) < LOD . which may vary for some chemicals by year and by individual sample. Snedeker.063 (<LOD-.180-. DDT may bind to estrogen receptors (Chen et al. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. A workplace standard for DDT has been established by Serum p. and seizures. 2006. and leukemia have also been inconclusive (ADSDR.530 (.069) .180 (. Gray et al.130 (<LOD-.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.150-. 1998).190 (. 1956).140-.230) . and altered behavior after neonatal exposure (Eriksson and Talts. 90 Fourth National Report on Human Exposure to Environmental Chemicals .530) .106) < LOD < LOD .048 (<LOD-.120 (<LOD-. other organochlorines.. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. 2001). 1995.105-. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. 1996).130-.230) .068-.051 (<LOD-.130 (<LOD-.. overt signs of acute human toxicity include vomiting. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. 2002.061) < LOD < LOD < LOD .059-. and o.150) .146 (. 2001).167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .078-. accidental exposures.. population from the National Health and Nutrition Examination Survey.170 (.054-. Mariussen and Fonnum. 2006).. 2002.220) .190 (.095) < LOD .34) .S.330-4. polychlorinated biphenyls.. lung cancer. 2006).075) 1.143) < LOD < LOD .250 (.112 (.140) .62 (. Animal studies reported reduced fertility.290) .220) .087 (. Calle et al. Reproductive effects in humans affecting birth weight. 1997).114-.079) < LOD < LOD .064 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.313 (.627) . Longnecker et al.01) .074-.26) 1. Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR. 2006.400) . dioxins and furans).108 (.

for males and females in the NHANES 19992000 subsample (Pavuk et al. 1989). Declining DDE levels over time have also been observed in the German population. Link et al.atsdr. Biomonitoring Information DDE persists in the body longer than DDT. 1998.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.. 2003). In general.. More information about external exposure (i. Survey Geometric mean (95% conf.e.. IARC classifies DDT (p.. Smith. 2004). mean serum levels of DDT and DDE in the U. 2002. 2004).epa.. interval) 260 (226-298) Selected percentiles ( 95% confidence interval) Sample 95th 1830 (1410-2300) 2320 (1830-2780) 1860 (1400-2380) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 226 (184-278) 251 (228-278) 203 (163-275) 75th 537 (476-631) 598 (521-699) 509 (376-655) 90th 1150 (976-1350) 1410 (1210-1500) 1170 (836-1570) 295 (267-327) 238 (195-292) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 118 (102-135) 124 (106-146) 105 (84. 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. Compared to females in the NHANES 1999-2000 subsample. and 03-04 are 18. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.. NTP considers DDT as being reasonably anticipated to be a human carcinogen. Fourth National Report on Human Exposure to Environmental Chemicals 91 . population declined by about fivefold to tenfold. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.gov/ toxpro2.6 (81. 2002. respectively. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al.p’-DDT) as a possible human carcinogen. 2003.3. Stehr-Green. Heudorf et al. environmental levels) and health effects is available from the U. population from the National Health and Nutrition Examination Survey. 01-02.6.8.. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. 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. Since the 1970’s. 2005).S.S. 8. see Data Analysis section) for Survey years 99-00.gov/ pestcides/ and from ATSDR at: http://www.cdc.html.Organochlorine Pesticides OSHA and a guidance established by ACGIH. respectively. EPA at: http://www.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. and 7. In a population-based sample of men and women from eastern Slovakia. 1991). the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.7-119) 113 (100-140) 93.. compared to levels observed in this Report (Anderson et al.

01-11.57-3.11-1.71 (5.45 (1.516 (.25 (.1) 7.01) 1. considerably higher than levels in this Report (Smith.34-11.47) 3.92 (3.39-2.54) 8.80) 3.55-9.07) 1.860 ng/L) and DDE (about 14.19-14.10-1.27-1.6 (17.2) 26.12-1.3) 10.69 (2.12 (.25-14.7) 13.06) 1. 1991).18-1.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.59 (1.57 (1.25-16.600) .534-.93 (7.40-4. less than one percent had detectable serum levels of o.71) 32.4) 13.61-2.9) 7.9-38.03-4..88 (2.2 (9.77 (1.17-3. o.28) 1.635) 1.41 (1.37-16.1) 12.8 (14.4 (12. Finding a measurable amount of p..26-2.730) .30 (1.8) 15. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.80) 1.p'-Dichlorodiphenyldichloroethene (DDE) (whole weight) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.32) 1.32-1.680-1.29 (1.6) 12.20 (.430-.12 (6.15-4.49) 8.37-4.22) .84-3. In the NHANES 1999-2000.23 (7.59) 3.41-12.66) 1.68 (2.611-1.81 (1.54 (1.31-12.05 (3. 2001-2002 and 2003-2004 subsamples.55 (2.46 (1. Survey Geometric mean (95% conf.48 (6.7) 9.54-7.79) 4.4) 14.11 (2.19) 4.4 (8. High mean levels of whole blood DDT (about 3.34) 6.02) 1.419-.07 (5.75) 1.04 (6.82 (1.30-1.1) 40.36-11.6) 8. Serum p. 2004).5) 10.38 (1.64-2.58) 75th 3.05) 1.34) 2.3 (9.00 (.5) 7.870 (.5) 22.26-10.22-1.66) 4.0 (12.71) 12.01-11.40 (3.82) 1.17 (3.2 (6.7) 16.561 (.57 (3.0) 2.40-4.385-.16 (2.90) 22.52 (1.97 (3.75 (4.56-3.57-2.16-1.85-10.10) .9 (26.57) 2.14 (1.45 (1.51) 1.520 (.963-1.32-1.63 (6. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.21) 3.66-2.51-8..18 (6.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.66-4.99) 1.4) 9.49 (1.820-1.59 (4.88-35.75) 2. 2004).02-8.34-3.726) .50 (2.43-8.p’-DDT (Stehr-Green.557) 1.646) .7-20.68) 2.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.24-17.43 (5.32 (1.26) 3.Organochlorine Pesticides nearby agriculture (Botella et al.6) 9.65 (1.87-16.90-8.9) 5.18-4.p’-DDT.31 (1.6) 9.49 (6.6 (8.91 (6.32-9.92 (3.85 (1.9 (15.03-1.97-4.59 (1.2-32.53-15.6 (9.10) 2. population from the National Health and Nutrition Examination Survey.69) 4.63 (1.2 (19.76) 1.53) 7.13) 4.6) 9.500-.36-1.63 (1.71 (6.56-6.36 (3.590 (.6) 9.70) 1.51 (1.01-1.66) 3.61 (1.965-1.58) 1.47 (1.50-17.60-13.01-15.7 (8.27) 3.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.18) 1.44) 1.6) 11.51-49.46-2.91-2.39-1.81-18.51) 3.01-5.72) 1.00 (6.84 (3.14) 2.33-1.5) 16.1 (9.1 (8.96) .81-5.69) 8.39) 1. interval) 1.69 (.13 (1.40-8.53) 1.70-3.91-3.52 (3.9-17.8 (9.81) 11. In a subsample of NHANES II (19761980) participants.22 (7.37-10.30-1.76) 1.8 (13.02 (2.09-1.68-4.p’-DDT were below the limits of detection.77 (1.p’-DDT.13-2.00) 7.24 (1.76 (2.796 (.25) 8.83 (1.56) 2.06) 3..07) 1.04-1.58) 1.59) 6.3) 16.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .57 (1.66) 1.994-2.39 (3.78 (4.76-3.5) 5.6) 13.21) 90th 7.0) 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 . 1989).62-6.4-19.01-1.456 (.14) 2. 309 versus 268 ng/g lipid.80) 1.81 (7. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.623 (.36) 3.6 (7.37 (1.56-2.3 (8.2 (9.96) 1.38 (1.75) 6.3) 13.48-4.14-1.37-1.92) 1.87 (5.2) 19.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.43-4.8-90.3-43.57-13.25 (1. or p.65) 1.14-9.890-1.7-19. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.8 (13.64) 3.35) 1.66-17.36-2.25) 1.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect. 2005).0 (9.18-1.85-4.00-1.7-48.51-15. 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.18-3.53 (2.S.52-6.69 (1.75 (8.26 (1.63-15.32 (1.43-4.10-5.31-2.34 (7.80 (2.91) 3.01) 1.30 (1.72) 1.46 (1.24) 1.488-. serum levels of o. 1971).49 (1.

7. Fourth National Report on Human Exposure to Environmental Chemicals 93 . which may vary for some chemicals by year and by individual sample.S. respectively.Organochlorine Pesticides Serum o. and 7. 01-02. < LOD means less than the limit of detection. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and 03-04 are 20. 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. see Data Analysis section) for Survey years 99-00.8. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.4.

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

Hum Reprod Updat 2001. Environ Res 2004. 4/21/09 Anderson HA. Olea-Serrano MF. Kaus S. Gray KA. Eriksson P. Link B. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. et al.111:349355. and DDD [online]. Greenfield TA. Brock JW. FDA total diet study. Kashyap R. Gabrio T. Environ Health Perspect 1998. et al. Int J Hyg Environ Health 2002.58:1185-1201. Int J Hyg Environ Health 2003. Saiyed HN. Olson JR. Gray LE Jr. Klebanoff MA. Patterson DG Jr. Gunderson EL. and HCB residues in human blood in Ahmedabad. India.17(6):692-700. Needham LL. Ellis H. selected elements. Drexler H. Cueto C. Gladen BC.97(2):178192. et al. hypospadias. Chemosphere 2004. dichlorodiphenyldichloroethylene. Bloom MS. Falk C. Moysich KB. Needham LL. Glynn AW. Piechotowski I. Lepom P. Zhou H.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Heudorf U. Am J Public Health 1995. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Jr. JAMA 1956. Beard J. Katz SH. April 1982 to 1984. Baker RJ.html. Zoellner I. Organochlorines in Swedish women: determinants of serum concentrations. Wolf CJ. Savitz DA. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Olea N. Longnecker MP. Vorojeikina DP.106(5):279-289. Sci Tot Environ 2006. Lancet 2001.71(6):1200-1209. Zhou H. Klebanoff MA. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.atsdr. Needham LL. Rivas A. et al. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Notides AC. Talts U. Burse VW. Fourth National Report on Human Exposure to Environmental Chemicals 95 .53(8):1161-1172. Olson J. Available at URL: http://www. Henley SJ.7(3):248-264.cdc.21(1-2)37-48.gov/~dms/ pesrpts. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Atuma S. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Environ Res 2005. The Great Lakes Consortium. Charles MJ.1-dichloro2. Botella B. Am J Epidemiol 2002.206:485-491. Effects of environmental antiandrogens on reproductive development in experimental animals. Darnerud PO. Crespo J. Biomonitoring of persistent organochlorine pesticides. Klebanoff MA. Bull Environ Contam Toxicol 2004. Swanson MK. 4/21/09 Gladen BC. dietary intakes of pesticides. Maternal DDT exposures in relation to fetal and 5-year growth. lindane (g-HCH). and other chemicals. Seiwert M. Chemosphere 2005.85:504508. Profiles of ortho-polychlorinated biphenyl congeners. Bjerselius R. Hediger ML. Granath F. Calle EE. Epidemiology 2006. et al.355:7889.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Longnecker MP. The effect of known repeated oral doses of chlorophenothane (DDT) in man. et al.96:34-40. hexachlorobenzene. Food and Drug Administration (FDA). Schulz C. Garrett N. Neurotoxicol 2000. and polythelia among male offspring. Hurd C. Brock JW.358:110-114. Rogan WJ. DDE and shortened duration of lactation in a northern Mexican town. Chen CW.72:261265. Ostby J. Angerer J. Biochem Pharmacol 1997. Kulkarni PK. Environ Health Perspect 2003.52:301-309. Organochlorines and breast cancer risk. Frumkin H.gov/ toxprofiles/tp35. Parks L. and dichloro(diphenyl)ethylene (DDE). Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Durham WF. DDT and human health. et al. Levels of DDT. Jr. Koepsell TD. Maternal serum level of 1. Jusko TA.cfsan. DDE.fda.155(4):313-322. August 2008. Aune M. Thun MJ. CA Cancer J Clin 2002.. Furr J. Zaidi SS. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP).54:1431-1443. Willman EJ. Barr DB. Davis MD. Buckland SJ. Vena JE. et al.html.162:890-897. Hanrahan L. Arnold SF. Environ Health Perspect 2004. Krause C. Toxicological profile for DDT. Bhatnagar VK. Hayes WJ. et al. HCH. Lambright C. Available at URL: http://www. Herrman T. J Assoc Off Anal Chem 1988. Exposure of women to organochlorine pesticides in Southern Spain. Becker K. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Cerrillo I. Paepke O. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. September 2002. Bates MN.112(17):1761-1767.205:297-308.

Rey AA.27:405-421. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Chlorinated Hydrocarbon Insecticides. DDE. DDE.150:981-990.36:253-589. et al. Pesticides and breast cancer risk: a review of DDT. 1991 pp. Arch Pediatr Adolesc Med 1996. New York. Astolfi E. Comparative pharmacodynamics of CYP2B induction by DDT.54:1509-520.53:455-477. Vol. Cerhan JR. Snedeker SM. Pavuk M. 2 Classes of Pesticides. children and newborn infants. J Toxicol Environ Health 1989. Lynch CF. Academic Press. Schecter A. Inc. Jr and Laws ER. et al. 731-915. Reddy AB.109:35-47. Nims R. Environ Health Perspect 2001. Jones CR. and dieldrin. Chovancova J. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Lubet R. Jr. Toxicol Appl Pharmacol 1971. Pollutants in breast milk. Smith AG. 96 Fourth National Report on Human Exposure to Environmental Chemicals .Organochlorine Pesticides Mariussen E. Eds. Crit Rev Toxicol 2006. Petrik J.20(2):186-193. Rogan WJ. Deichmann WB. In Hayes WJ. Fox S. Demographic and seasonal influences on human serum pesticide residue levels. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Thomas PE. PA. and DDD in male rat liver and cultured rat hepatocytes. J Toxicol Environ Health Part A 1998. Chemosphere 2004. Stehr-Green. Handbook of Pesticide Toxicology. Fonnum F. Radomski JL.

Because it is metabolized so rapidly.40-5.S. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. In the body.S. EPA. 72-20-8 General Information Endrin. 1992).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.. or from contact with contaminated soils and sediments in areas where endrin was applied. population from the National Health and Nutrition Examination Survey. Endrin was used as an insecticide. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. a stereoisomer of dieldrin. 1996.20 (<LOD-5.S. Over time.S.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. An epidemic of acute endrin poisoning. endrin has been detected with declining frequency in U. total diet surveys (FDA. fatty infiltration.10 (<LOD-5. manufactured. 1987). endrin can persist for years. 1991). At high doses. Ketoendrin is a major photodegradation product (IPCS. endrin usually is not detected in serum of exposed individuals. 2008). 1979. 1992.8. IPCS. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.. Serum Endrin (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. unlike aldrin and dieldrin. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. Endrin is absorbed rapidly after ingestion.40 (<LOD-6. Endrin has been detected in soils. Fourth National Report on Human Exposure to Environmental Chemicals 97 .20 (<LOD-5. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown.30) < LOD 5. Endrin does not accumulate in body tissues (IPCS. inhalation or dermal exposure routes. Kavlock et al. anti-12hydroxyendrin. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. 1981). All uses of the pesticide in the U.Organochlorine Pesticides Endrin CAS No. endrin is converted rapidly to its major metabolite.S.50) < LOD 5. Depending on soil conditions. have been cancelled by the U. rodenticide and avicide. 1991).30 (<LOD-6. unless the dose is high and the exposure is very recent.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. 1992). < LOD means less than the limit of detection. or discarded.60 (5.. is no longer manufactured in the U. Endrin was not widely used as a termiticide. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. Smith.09 and 7.10 (<LOD-5. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals.50) < LOD < LOD < LOD 5. and occasionally at low levels in sediment and surface waters.. Hepatic effects of endrin exposure have included necrosis. 1992).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. and inflammation (Smith. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.

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

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

Urinary metabolites include pentachlorophenol (PCP).1 (17.6 (24.1 (14.9 (14.8) < LOD < LOD 27. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.2 (17.7-16.6-33.4.4.3) < LOD < LOD 29.0) < LOD < LOD 24.7 (15.9) < LOD < LOD 19.8 (15. 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. and elimination occurs by renal and fecal routes..7 (27. 2. and foods with a high fat content.0. particularly by consuming fish.9) 19.4) < LOD < LOD 33. 31.9-15.5-trichlorophenol (2.7-29.5 (13.7) < LOD < LOD 24.8 (22.9) < LOD < LOD 28.7-21. respectively.2 (14.3 (16. Although it is not manufactured as an end-product in the U.0 (25.3 (22.9-17.9 (25.6 (21.S.9-20. 2008.9-30. wildfowl.. 2005).. 2002).6-44.3) < LOD < LOD 20.2 (24. which may vary for some chemicals by year and by individual sample.7-22.4) < LOD < LOD 22.5-33.1-16. EPA cancelled its use in 1984.3-22.6-TCP) (To-Figueras et al.5-TCP) and 2.9) < LOD < LOD 20.1) * * 15.3-20.9) < LOD < LOD 20.3 (20. The general population may be exposed to HCB through diet.8. or game taken from areas with HCB contamination. Survey Geometric mean (95% conf.3) 24.6) < LOD < LOD 14.1) < LOD < LOD 15. primarily as a fungicide and seed treatment until the U.9) < LOD < LOD 16.S. Gunderson.1-20. breast milk is an additional route of elimination in nursing women.4-16. and 03-04 are 118. HCB is well absorbed after oral administration.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3 (12.4. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.4.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.4) < LOD < LOD 14.5-18.9-32.9-24.4.3 (14. air.0-16.2-31.9 (25. 1988).6 (23.7-16.5 (13.3) * * 15.0) < LOD < LOD 15.0) < LOD < LOD 15. Therefore.2) < LOD < LOD 29. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4 (18.0 (18.3 (22. water.6) < LOD < LOD 26. 1976). 01-02.5-14. 1997).5-14.4) < LOD < LOD 23.4 (11. and has been detected in soil.7 (15. The FDA dietary surveys have shown that over time.0-25.7-15.7 (19.6-32.0) * * 15. and accumulates in fatty tissues where it persists for years.6) < LOD < LOD 26.2) < LOD < LOD 13.6) < LOD < LOD 25.2-15. population from the National Health and Nutrition Examination Survey.1 (14.2 (13.9) < LOD < LOD 15.6) < LOD < LOD 24.8 (26.Organochlorine Pesticides Hexachlorobenzene CAS No. distributes widely throughout the body.S. HCB has been detected in fewer foods since the 1980s (FDA.0-28. see Data Analysis section) for Survey years 99-00. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR. and sediment (Barber et al. measuring HCB in serum is a specific indicator of exposure to the parent Serum Hexachlorobenzene (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.4) < LOD < LOD 18.1 (13.5-15. 100 Fourth National Report on Human Exposure to Environmental Chemicals . and 7.6-trichlorophenol (2.6-19.6-26.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.4 (18.S.0 (14.5-15.8-15. < LOD means less than the limit of detection.0-19.7-30..4 (22.5 (14.2-15.7) * * 14.0 (18.3-26.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13. HCB is slowly metabolized. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.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 * * 14.4) < LOD < LOD 19. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.4-15.5) < LOD < LOD 18.9 (23. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.2 (14.7-26.

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

but overall. April 1982 to 1984. Environ Health Perspect 2002. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Laliberte C. 2002). IARC Sci Publ 1986. et al.. Lackmann GM. Schulz C. In a representative sample of the 1998 German adult population.cdc. Bradman A. dietary intakes of pesticides. Darnerud PO. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. respectively. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lawrence River (Quebec. 2005). Gunderson EL. Available at URL: http://www. Santiago-Silva M. 102 Fourth National Report on Human Exposure to Environmental Chemicals . German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. more HCB levels were quantified. 2002.349:144. Bertram HP. Biomonitoring of persistent organochlorine pesticides..135(4):400404. 2002) and among children (Link et al. 1999). Kemper FH. Toxicological profile for hexachlorobenzene update [online]. Sala M. HCB detection in serum also was proportional to age. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Kohli J. only 4. Safe A. Bryan GT.. Environ Health Perspect 2003. 2003). Available at URL: http://www. Int J Hyg Environ Health 2002.. Canada).58:1185-1201. 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. Seiwert M. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Bertram et al. Hexachlorobenzene in the global environment: emissions. Lepom P. Can J Biochem 1976. Sci Tot Environ 2005. Ozalla D. Muckle G. 1989). Lecha M. Herrero C. Organochlorines in Swedish women: determinants of serum concentrations. et al.gov/ toxprofiles/tp90.81(2):82-85. Jones KC. Sweetman AJ. 2005. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Atuma S. distribution. Becker K. van Wijk D.gov/~dms/ pesrpts.9% of participants had quantifiable levels (Stehr-Green. In the 1976-1980 NHANES subsample. Schwartz JM.111:349355. Granath F. 2002. Peters HA. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. 2002..html.17:388–399. Gocmen A. 2006).71(6):1200-1209. Biol Neonate 2002. Arch Neurol 1982. Muller C. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. 1986. 2002. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. August 2008..fda. Zoellner I. Dallaire F. FDA total diet study. Jones D. Otero R. J Assoc Off Anal Chem 1988. Link et al. Over the past two decades. and the geometric mean concentration of HCB in whole blood was 0.77:173182.205:297-308. Herrman T. Paepke O.54(3):203-208. J Exp Sci Environ Epidemiol 2007. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. levels. FDA Pesticide Program Residue Monitoring 1993-2006 [online].cfsan. trends and processes.110(8):835-838. As a result of the lower limit of detection in NHANES 2003-2004. Arch Dermatol 1999.. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. 4/21/09 Barber JL. Link B.. Fenster L. 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.atsdr. et al.. 2005). The metabolism of higher chlorinated benzene isomers.. selected elements. however. Holland NT. HCB levels were directly related to age. References Agency for Toxic Substances and Disease Registry (ATSDR). Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Eskenazi B. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. et al. Gabrio T.44 mg/L. Bradman et al. Aune M. In Spain. Cripps DJ. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. September 2002. Krause C.39(12):744-749. Dewailly E.html.. Lackmann. Lackman. Barr DB. Piechotowski I. Chemosphere 2005. Food and Drug Administration (FDA). declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Ayotte P. Kaus S. 4/21/09 Glynn AW. Dogramaci I. Glynn et al. Reference values updated. Bjerselius R. and other chemicals.

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

4 (11.1-27.4) 21.5 (24.7) 10. 2005).4 (8.7 (29.68 (<LOD-10. exists in several isomeric forms. and have been used either as fungicides or to synthesize other chemicals.5 (8.6 (10.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.9-81.9-51.70 (6.80 (6.4-50. which may vary for some chemicals by year and by individual sample.6) 35.8 (9.8) 39.60-13. see Data Analysis section) for survey years 99-00.7 (13.5) 29.9 (32. formerly referred to as benzene hexachloride.2-87.9) 15.0) 71.4) 11. the U.7-96. and 03-04 are 9.9-178) 48.0-34.2-22. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice. In 2006.5 (14.1) 71.9-14. It is no longer produced or sold in the U. However.1 (21.7 (30.6) 18.9-56. See the section “What’s New” at the beginning of this Report for details.2) 62.6-62.8.1 (27.7) 97.5) 11. General population Serum beta-Hexachlorocyclohexane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.7-20.36.4) 10.9 (11.50) 8.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.3-38.6 (17.6-47.7) 18.9 (50.0-23.4) 901 1067 952 992 1224 1007 Females 11.8 (10.8 (21.90) 7.9-21.3 (26. and sediment as a result of historic production and use.30-11.90-8.0 (35. and delta.6) 47.2-20.9) 45. each result has been multiplied by 1.1) 12.6-37.0 (14.2 (50.6 (40.1 (11.4 (52.2-46.S. 58-89-9 General Information Hexachlorocyclohexane (HCH).0 (8.3-56.7 (53. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.5 (16.2 (29.1 (30. HCH isomers.6-20.3) 34.8-19.2) 13.2-98.7) 10. 319-85-7 gamma-Hexachlorocyclohexane CAS No.89 (<LOD-9.2 (9.4) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD 21.1-32.4) 44.4) 51.8) 52.7) 23.8) 7.1) 13.0 (37.3-85.1 (16. interval) 9.87 (9.1-32.2 (34.8) 95th 68.5) 90th 42.3 (13.90-8.1 (18.5528.6-14.7) 32.66-12.3) 37.2) 9. environmental levels declined.7-96.1 (9.5-123) 49.4 (50. gamma.2) 36.20-16.5 (43. 01-02.0-70.4) < LOD < LOD < LOD 46. particularly alpha and gamma have been detected widely in air.5-29.70-19. water. Technical grade HCH is a mixture of all four isomers.7 (62.46-11.2) 142 (99.9) 81.76.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.04-10.6) 653 758 589 1240 1533 1370 20 years and older 10. Lindane has a half-life of about two weeks in soils and water. EPA cancelled agricultural uses of lindane (ATSDR.9) 17.5) 22.2-55.3) 25.61-12. soil. including alpha.2-17.2 (31.7-26. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-199) 134 (85.5 (11.8-87.2-67. As pesticide applications of HCH were increasingly restricted or eliminated.0-21.8) 27.Organochlorine Pesticides Hexachlorocyclohexane CAS No.6 (33. **In survey period 2001-2002. 608-73-1 beta-Hexachlorocyclohexane CAS No. commonly known as lindane.1) 31.2 (48.1-37.4-73.7 (<LOD-16. 104 Fourth National Report on Human Exposure to Environmental Chemicals . 6.1-15.3 (42. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.6-42.0-111) 70.8 (17.1-49.7) 56.3 (42.6-18.5) 67. 2005).0-70.7-166) 70.0) 17. containing about 64% alpha and 10%-15% gamma isomers.7-69.8 (32.43 (<LOD-9. population from the National Health and Nutrition Examination Survey.4 (12.5 (37.2-52. and 7.2 (18.7) 27.1) 12.8 (33.3) 51.4-111) 84.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.0 (<LOD-12.6) 16.9 (40.8 (23. HCH isomers are lipophilic.0) 7.70 (8.7-69.4 (16.7 (35.8) 12.6 (22.8-16.0) 8.0 (33.2-42.8) < LOD 10. The gamma isomer.8) * * * * * * 15.4-45. so they can accumulate in fatty tissues of animals. respectively.0 (19. < LOD means less than the limit of detection.3) 14.S. beta.5) 14.8 (64.5) 40.6-89.9-24.0) 35.9 (9.6) 50.7) 73.5) 16.1 (12.7 (25.0-20.S.56-12.1 (9.4) 27.6) 36.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.1-36.8-54.4) < LOD 9.9 (62.70-12.0) 41.9 (30.6-135) 69. The other isomers can be formed during the synthesis of lindane.9 (26.3 (62.6 (16. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.80 (<LOD-14.8-68.1-16.

160) . 2002).814) .062 (.098 (.290 (.190) .587) 653 758 589 1240 1533 1370 20 years and older .620) . Distribution is mainly to fatty tissues.480 (.600) .110) .01 (. Saxena et al.480 (.390 (. HCH crosses the placenta and is also excreted in breast milk (Radomski et al. and memory loss (Nigam et al. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.250 (.840) .222 (.140) .570 (.710) .090-.065 (.160 (.420-.070-.090 (. each result has been multiplied by 1.200-.100-.360 (.410) . paresthesias.191-.480) .100-.058 (<LOD-. for lindane.120-.062 (.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 .220-. and nephropathy developed (IPCS. ataxia.412 (.Organochlorine Pesticides exposure to HCH is through the diet.250 (.175 (. ingestion.059-. 1981).081-. After dermal application of lindane 1% lotion.501) .470 (.072 (.37) 1.460) .057 (<LOD-.450 (.260) .214) .170-.250-.070-.350) .065 (.260-.521 (.077) < LOD . Workers who directly handled HCH have complained of headache.100 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.110-. resulting in a half-life of about seven years.350 (.110) .064 (.580 (.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .051 (<LOD-.047-. population from the National Health and Nutrition Examination Survey.450) .056-.270 (.174) .083 (.360-.100) . interval) .131-.067 (.140) .050 (.190-.661) 901 1067 952 992 1224 1007 Females .057-.091) .057-.410) . U.310 (. When animals were chronically fed lindane at high doses.090 (.060) .620-1. 1983). Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.680) .140) .220 (..056-.070 (.382-.330-.120 (..118 (.290 (.5528.090 (.110) . Fourth National Report on Human Exposure to Environmental Chemicals 105 . 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.220) .260) .310) .050) .244-.150-.S.210-.080) .050 (. which may vary for some chemicals by year and by individual sample.120) .240 (.120 (.118-. probably by blocking inhibitory neurotransmitters in the central nervous system.250-.400) .32) .070 (.073-.200-.05) .050-.310) .320 (.080-.139 (. See the section “What’s New” at the beginning of this Report for details.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.089-.690) .078 (. Rogan.125) < LOD < LOD < LOD .370-.080 (.S. hepatic enzyme induction.120 (.080 (.070-.080-.510) .080) * * * * * * .050-. or dermal exposure. and seizures.280-.400) .040-.450-..096) .240-.210) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .051-.146-.064) .404) . and FDA has established a bottled water standard and food residue tolerances for lindane.910 (.080-.144 (.221-.069) . the serum half-life was about 20 hours among children (Ginsburg et al.190) .580-1. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.160-.390-.234 (.068-. The U. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.700) .216 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.100-.070) .048 (<LOD-.319) .173-. Gunderson 1988).130-.281 (..360) ..210 (. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.220-.200 (.230-.331 (.380 (.050-.250 (.410-.120-.067) .130) .057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .560 (.294-.210 (.305) .308-.050 (<LOD-.191-.050 (<LOD-. 2008. OSHA and ACGIH have established workplace standards and guidelines.254) 95th .250) .150) .442 (.119) .130 (.150 (.560) .100) .092 (. enlarged livers.290) .167 (. respectively.290 (.372 (.330 (. EPA has established a drinking water standard.470) .460 (.089) .297-.340-.180-.103 (.120) .300-.124-. **In survey period 2001-2002. 1986).150) . HCH isomers are absorbed after inhalation.190-1. tremors.287 (. 1996. 1971. 1977).100 (.S.103) 90th .290) .083) .086) < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170-.340) . The beta isomer accumulates in fatty tissues and is metabolized more slowly. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.410 (.120-.077) < LOD .103-.050-.140 (.280-.

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

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

Radomski JL. gov/toxprofiles/tp43. The Great Lakes Consortium. International Programme on Chemical Safety (IPCS). Hanrahan L. Environ Health Perspect 2003. Olea N. children and newborn infants. and HCB residues in human blood in Ahmedabad. August 2005. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Siddiqui MKJ. Granath F. India. et al.96:34-4Food and Drug Administration (FDA). Atuma S. et al. Majumder SK.111:349355. Schulz C. Link B. Int Arch Occup Environ Health 1983. Rogan WJ. Pollutants in breast milk. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Available at URL: http://www. Int Arch Occup Environ Health 1986. Maass R. Toxicological profile for hexachlorocyclohexanes update [online]. Rivas A.71(6):1200-1209.54:1431-1443. Bottimore DP. Placental transfer of pesticides in humans. Needham LL. et al. Visweswariah K. Demographic and seasonal influences on human serum pesticide residue levels. Stehr-Green. Toxicol Appl Pharmacol 1971. April 1982 to 1984. selected elements. Krishna Murti CR. Ellis H.9(4):417-424. FDA total diet study. Bai KM. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Aune M. Seiwert M.106(5):279-289. Rothman N. Wood PH.58:1185-1201. Raju GS.cfsan.91:998-1000. org/documents/jmpr/jmpmono/2002pr08. Nigam SK.27:405-421. Garrett N. Chemosphere 2005. Saxena MC. Kutty D. Int J Hyg Environ Health 2002. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Karnik AB.57(4):315-320. Patterson DG Jr.fda.html. Piechotowski I. Bhargava AK. Rev Environ Contam Toxicol 1991. Potischman N. Burse VW. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Falk C.120:1-82. Krause C. Lindane. Heinrich R. Bhatnagar VK. Kaus S. Darnerud PO. Exposure of women to organochlorine pesticides in Southern Spain. Levels of DDT. Paepke O.cdc.72:261265. Herrman T. et al. available at URL: http://www. Sturgeon SR. VI. Bjerselius R. Kashyap R. Metabolism of gammahexachlorocyclohexane in man.htm. J Toxicol Environ Health 1989. August 2008. Saiyed HN.html. Lepom P. 4/21/09 Ginsburg CM. Available at URL: http://www. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Brinton LA. and other chemicals. Bates MN.20(2):186-193. Biomonitoring of persistent organochlorine pesticides. Lowry W. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States).52(1):59-67. Zaidi SS. Bull Environ Contam Toxicol 2004. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.atsdr. Deichmann WB. Chemosphere 2004. 108 Fourth National Report on Human Exposure to Environmental Chemicals .205:297-308. et al. Rey AA. Angerer J.150:981-990. J Assoc Off Anal Chem 1988. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Needham LL. Kulkarni PK. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Environ Health Perspect 1998. Olea-Serrano MF. Cancer Causes and Control 1998. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Becker K. Buckland SJ. Occupational exposure to hexachlorocyclohexane. Gabrio T. PA. dietary intakes of pesticides. Cerrillo I. Absorption of lindane (g benzene hexachloride) in infants and children. et al.gov/~dms/pesrpts. et al. 2002.48:127-134. Olson J. Glynn AW. Astolfi E.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).inchem. Needham LL. Arch Pediatr Adolesc Med 1996. Gunderson EL. Zoellner I. Botella B. 4/21/09 Anderson HA. HCH. Reisch JS. 4/21/09 Kutz FW. Environ Res 2004. Crespo J. J Pediatr 1977. Brock JW. Organochlorines in Swedish women: determinants of serum concentrations. Arch Toxicol 1981.

1991).1 (13.S. (Kutz et al.70-24. after which it is widely distributed in the body and stored in fat. sediments.5.4) < LOD 15.6 (<LOD-108) 9.5 (<LOD-115) 153 (30.3) 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) < LOD 66.4) < LOD 63. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.8 (<LOD-73.0) * * * 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 19.7 (<LOD-47.7 (12.4 (8. Survey Geometric mean (95% conf.S.0-374) 11.3 (15.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Occupational exposure is limited to workers at sites where mirex contamination is present. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. In studies conducted in the 1970’s and 1980’s.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. especially those from persons living in the southeastern U. 1985. 10.5-291) 11.8 (12.40 (<LOD-13.5-425) 40. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. animals.10-37. water. Some states and the U. Mirex is not metabolized in the body.6. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. Mirex binds strongly to soil.8. and 03-04 are 14.2-230) 13.3 (15..5-82..3-225) 15.1 (8.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. 01-02. and foods.8) < LOD 15.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. see Data Analysis section) for Survey years 99-00. soil. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. since 1977.0 (12.S.S.6-305) 15.0 (<LOD-108) < LOD < LOD 50. Mirex has been detected in air.6) < LOD < LOD < LOD < LOD 71. Mirex is absorbed through the skin and from the gastrointestinal tract. aquatic organisms. 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.2) 51. it is a highly persistent chemical in the environment.5 (<LOD-42.6 (<LOD-31.Organochlorine Pesticides Mirex CAS No.2 (7. The most likely sources of human exposure to mirex are eating fish from contaminated water or living in areas with soil contaminated by historic mirex manufacturing.5 (9.7) 8.1) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 16.S. or pesticide application. and 7.70-40. Fourth National Report on Human Exposure to Environmental Chemicals 109 . where it was applied directly to soil and by aerial spraying. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. respectively. 2385-85-5 General Information Mirex has not been produced or used in the U.0 (14. Mirex can cross the placenta and be excreted in breast milk. Formerly.1 (<LOD-65.6 (<LOD-23. disposal. 1995). where it has a half-life of 12 years.90-29. mirex was detected in human adipose samples.4-230) 18.70 (<LOD-15. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. which may vary for some chemicals by year and by individual sample.10 (<LOD-15.6) 9. resulting in exposure to newborns and nursing infants.

430 (. population from the National Health and Nutrition Examination Survey.102) < LOD < LOD < LOD < LOD .090-1.059 (<LOD-.170-3.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .370 (. which may vary for some chemicals by year and by individual sample.080-1. 1995.73) .112 (.054 (<LOD-. reproductive toxicity included decreased fertility and testicular damage.093 (..110 (<LOD-.S.470) .7 ng/g of lipid.100 (<LOD-.79) . 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.08 (.268) < LOD . and 4.8. 1989). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .064 (<LOD-. 110 Fourth National Report on Human Exposure to Environmental Chemicals .220) . In addition.690) .106) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .cdc. 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.S.055-. environmental levels) and health effects is available from the ATSDR at: http://www.256 (.92) .410 (.052-. Smith. as well as in a subsample of NHANES II (1976-1980) participants. 1991).108 (.html.080-1. and 2003-2004 subsamples..470) .240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . More information about external exposure (i. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. serum mirex levels were generally below the limits of detection (Stehr-Green. Survey Geometric mean (95% conf.077 (<LOD-. 7.37) .41) . IARC classifies mirex as possibly carcinogenic to humans.450) 1.100 (<LOD-.610) < LOD < LOD < LOD < 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 . The U.090-1.310 (. 2005).106 (.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.. In samples obtained between 1994 and 1997.79) .atsdr.e.635) < LOD .090 (<LOD-.090 (<LOD-.140 (<LOD-.gov/toxpro2. 2001-2002.02) .470 (.090-1.450 (.510) < LOD < LOD . 2004). EPA has established environmental standards for mirex.062-. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.170) < LOD .089-.053-.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 . and NTP classifies mirex as reasonably anticipated to be a human carcinogen.070-1.Organochlorine Pesticides exposures are unknown. 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.079 (<LOD-. 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.220 (<LOD-. The geometric mean mirex levels of the Inuit mothers were 8. Laboratory animals fed high doses developed liver enlargement and liver tumors. Biomonitoring Information In the NHANES 1999-2000.090 (<LOD-.

html. Environ Res 2005. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. References Agency for Toxic Substances and Disease Registry (ATSDR). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Strassman SC.atsdr. Odland JO. Kutz FW. Smith AG. Olson JR. August 1995. In Hayes WJ. 4/21/09 Bloom MS. Leininger CC. Handbook of Pesticide Toxicology. New York. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Profiles of ortho-polychlorinated biphenyl congeners. 731-915.330:55-70. Van Oostdam JC. Vol. Jr. Kutz FW. Toxicological profile for mirex and chlordecone [online]. Chashchin V. Bottimore DP. Stehr-Green.97(2):178192. 1994-1997 organochlorine compounds.Organochlorine Pesticides effect. dichlorodiphenyldichloroethylene. 2 Classes of Pesticides. Chlorinated Hydrocarbon Insecticides. Demographic and seasonal influences on human serum pesticide residue levels. Swanson MK.cdc. Gilman A. Wood PH. J Toxicol Environ Health 1985.gov/toxprofiles/ tp66. J Toxicol Environ Health 1989. Academic Press. Jr and Laws ER. Watts DL. The human body burden of mirex in the southeastern United States. Vena JE. Eds. Rev Environ Contam Toxicol 1991. 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. PA. hexachlorobenzene. Inc.15:385-394.27:405-421. et al.120:1-82. Carra JS. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Hansen JC. et al. Moysich KB. Circumpolar maternal blood contaminant survey. Stroup CR. Sci Total Environ 2004. Dewailly E. 1991 pp. Available at URL: http://www.

40 (1. are metabolites of several organochlorine chemicals. 1999). soils.50) < LOD 1.0) 2. and sediments. Survey Geometric mean (95% conf.6-TCP in any of the samples (U.10-3.60 (. usually at herbicide production or waste incineration facilities.42 (<LOD-8.0) < LOD 5.40 (.5-trichlorophenol (2. Both chemicals have been detected in air.40 (2.4.19 (<LOD-6.60-18.30) < LOD 4.40 (2.72) < LOD 1.80 (1.20) < LOD 90th 5.60 (4. 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.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30-27.0) 2.4.27) 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 1.7) 24.4.Organochlorine Pesticides 2.5TCP and 2.0 (5. public drinking water systems did not detect 2. other organochlorines.0) < LOD 5. Formation of 2.40 (2.71 (<LOD-8.60 (2.80-41. recent sampling of U. 2.50-25.50 (2.30-44. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.0) < LOD 11.6-TCP).80 (2.20) < LOD 5.S.40 (2.30-27.30) < LOD < LOD < LOD < LOD < LOD 1.S.980-3.920-3.40) < LOD 4. 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16. hexachlorobenzene.20 (4.60-8.00-3.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.0) 5.4.31 (<LOD-9.0) 2.940-3.30 (.57 (<LOD-15.4.0 (8.9 (<LOD-121) 9.0 (3.4.6-Trichlorophenol CAS No. EPA.30-40.5-TCP) and 2.6-TCP were used as intermediates in the production of certain pesticides. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.9 and 0.4.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .00-8.0 (3.40 (1.90-33. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. including hexachlorobenzene and hexachlorocyclohexanes.20) < LOD 1.0) 2. population from the National Health and Nutrition Examination Survey.60) < LOD 8.900-2.4.9.40 (.03) 9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR. may occur by inhalation or dermal routes.0) 2.20-71.50 (.40-11. surface water. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.40) < LOD 6. Such workers would probably Urinary 2. 1976).0 (4. Historically. Occupational exposures.42 (<LOD-12.0) < LOD 11.0 (4.980-3.4..0 (4. 112 Fourth National Report on Human Exposure to Environmental Chemicals .71 (<LOD-8. Exposure to trichlorophenols also may result from metabolism of lindane.30-27.30-11. which may vary for some chemicals by year and by individual sample.40-18. Trichlorophenols are no longer manufactured commercially.27) 696 661 521 696 603 939 Limit of detection (LOD.80) < LOD 1.50-63. and polychlorinated benzenes (Kohil et al.00-3.63) 18.8) 21.30-3. however.4.3.00 (3.5-Trichlorophenol CAS No.0) 14.50 (1.0) 2.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.6-trichlorophenol (2. 2.00 (2.7.0) < LOD 5.S.0) < LOD 21.20-36. 1999).4.5-trichlorophenol.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. 2006).50-16. 95-95-4 2. < LOD means less than the limit of detection.4.950 (<LOD-1.40) < LOD 1.

88-16. environmental levels) and health effects is available from ATSDR at: http://www.33) < LOD < LOD < LOD < LOD < LOD 2.80 (1. Among 6-11 year old children in NHANES 1999-2000..05-8.4.78) < LOD 1.. More information about external exposure (i.19-12.00-29.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2. Survey Geometric mean (95% conf.1) 2.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). Human health effects from 2.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.32) < LOD 4.15) < LOD 2.75 (3.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al. However.6) 4. 2003).37) 16.37-11.36 (1. Urinary 2.4) < LOD 3.4. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. leukemias. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.4.68 (<LOD-8..9) 12.62-20. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.4.4. IARC classifies combined exposures to polychlorophenols.6-TCP as reasonably anticipated to be a human carcinogen.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . the 95th percentile urinary 2.67 (1.20-6.49 (1.820-2.8) 4.6-TCP. The 95th percentiles for 2..24 (3. as being possibly carcinogenic to humans.2) 2.7 (4. the 95th percentile urinary 2. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.920-2.5-TCP and limited for 2. At lower doses.html.6) 4.93-11. in addition to dioxins.4.43 (2. furans. 1995) were similar. In the same 2-6 year old children. which includes trichlorophenols.atsdr. Laboratory animals chronically fed high doses of 2.4.29 (1.50) < LOD 2.19-4.8) < LOD 9.00) < LOD 4.57 (<LOD-7.3 mg/L reported in German adults aged 18-69 years (Becker et al.Organochlorine Pesticides be exposed to mixtures of chlorophenols. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.16) < LOD 90th 5.5) 11. animals showed hepatocellular abnormalities. 1995) and up to 19 times higher than the 95th percentile value of 1.gov/toxpro2.81 (<LOD-9...86 (3.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.69-18.4.6-TCP had increased rates of hepatic tumors.6-TCP level was approximately eight times higher than the corresponding percentile in a small group of 2-6 year old children living near an herbicide manufacturing facility: 33 versus 4 mg/L (Hill et al.05-17.4.9 (5.68-4.90 (4.. Neither 2.53-3. Radon et al.5) < LOD 12.1 (<LOD-58.95 (3.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.cdc.44 (1.00-19. 2004).55 (4.8 (5.53-3.4.0) 7.5-TCP.44 (.24) < LOD 6.16 (.74) 11. 1989). Fourth National Report on Human Exposure to Environmental Chemicals 113 .2 (2.4.28-25..79-4.60-3.31) < LOD 2.57 (<LOD-7.46 (1.24) < LOD 1.13-13.17) 9.980 (<LOD-1.43) < LOD 12. NTP classifies 2.64 (4.4) 5.5-TCP or 2..4. population from the National Health and Nutrition Examination Survey. 2003.78 (3.47-8.6-TCP levels at the 95th percentile were up to eight times higher than 3. 7. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.02) < LOD 7.27-17.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.4 (6. 2003).0 mg/L.67 (1.11) 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 2.2) < LOD 5.78-19. and other chlorinated compounds.3 (5.73 (<LOD-8.57 (3. urinary 2.75 (<LOD-6.6) 4.02-3.5-TCP nor 2.4.82 (<LOD-32.e.83-12.24-11.24) < LOD 5. 1989).69 (2.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4) < LOD 3. and lymphomas.

1998).0 (12.0 (8.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.32) * 3.1) 16.95 (4.30-2.0) 19.80 (2.70) 3.4 (8.5-TCP and to the median 2.53) 2.45-9.6-17. 2003).0 (7.78 (2.0) 7.20) 4.55-3.60) 6.0) 17.90 (4.50 (2.91-4.4.4.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.84) 2.0-41.5-TCP and 2.6-22. In harbor workers exposed to chlorophenol-contaminated river silt.4.0-38.0 (6.6-TCP level.40) 4.1-25.54) 6.31 (3.80 (2.00 (4.10-2.23-2.4. which may vary for some chemicals by year and by individual sample.95-6.59-6.70) 5.26 (2.5-TCP (0.50-5..6-TCP (0.74 (2.0) 19.45 (2.87-14.65) 15.98-11. for males in NHANES 19992002 (Agramunt et al.6 mg/g creatinine) and 2.6) 21.4 (10.5-TCP or 2.68 (<LOD-2.2) 25.79 (5.30) 4.45) < LOD 11.60-21.3 (11.70-3.5-TCP or 2.76) 3.0-37.7-3.36 (1.4.3-26.57 (<LOD-2.0 (15. Urinary 2.10) 2.9 (11.14 (2.4 (17.80-25.01-6.23) 3.80 (3.0 (6.52-3.0 (11..5-TCP level of 0.5 mg/g creatinine) were similar to the limit of detection for 2.6TCP causes an adverse health effect.5-TCP and 2.40) 2.4.9) 694 677 519 696 602 931 Limit of detection (LOD.4.0) 14.6-19.5-TCP or 2.0 (9.10 (5.20 (3.00-21.0) 15.0) 11.36 mg/g creatinine.60 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-3. 1991).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.4.0 (20.49 (6.45 (5.99) 6.0) 9.0-50.1 (8..06) * 2. interval) 2.0) 7.80-20. respectively. Survey Geometric mean (95% conf.0-18.4. 114 Fourth National Report on Human Exposure to Environmental Chemicals .5-46.0) 13.58-3.60) < LOD 5.0 (14.0 (20.0) 6.2-0.4-17.70-6.60-37.70-6.0) 10.73-9.30-11.70 (2.60-3.9 (13. < LOD means less than the limit of detection.67) 4. was about six times lower than the median urinary levels for males in this Report (Radon et al.0-54.0 (15.9) 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 2.28) 24.35-3. Mean values of 2.8-24. Biomonitoring studies on levels of 2.6 (12.2) 12.90-8.40-7.5-TCP or 2.0 (8.4.2 (14.7) 33.40 (2.7) 21.8-15.70) 1.60 (3.70) 5. Urinary 2.09-7.89-6.40-4.56 (3.0-43.10-3.53) 4.80-7.07 (<LOD-3.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.24 (2.3-17.4.25-11.92 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.00-4.80) 1.46-3.7 (13.78 (2.4.4.08 (2.47 (3.1 (10.48-26.0) 10.4.0 and 1.7 (9.6TCP values.4.4.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.18-3.59) 4.40) 2.20-3.66 (8.6-TCP than are found in the general population.0) 13.85) * 3.32-4.0 (14.20-23.6-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 (14.40-14.0-44.6-TCP exposure and health effects.0) 13.23) 2.0) 9.3) 37. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.30-33.7 mg/L.6 (11.85 (2.40-2.0-68.32) 3. 0.65 (5.31) * 2.40 (2. Finding a measurable amount of 2.8-13.3.74-3.30-2.72-10.80-6.69 (3.89 (3.6) 26.0) 17.44) 75th 4.0) 12.0-38.33-4.00 (2.0) 13.20-6.4.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.9) 13.60 (2.98-7.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.63) 90th 15.70 (2.51-12.0 (4.0 (6.0 (13.3) 20.75 (8.4. Biomonitoring data will also help scientists plan and conduct research about 2.4.3 (11.04) 2.00 (1.95) 3.90) 2.. 2004).40-32.20 (3.02) 2.0) 14.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8) 18.3) 23.4.0) 11. the median urinary 2.12) 2.40-2.6-TCP in urine does not mean that the level of 2.S.36-5.90 (3.09) 15.40) 3.52 (2. population from the National Health and Nutrition Examination Survey.58 (1.7-16.4 (9.0 (16. similar to the limit of detection for this Report (Anderson et al.28) * 2.67-12.8 (9.10) 6.8) 32.

02) 3.75) 75th 4.91-2.14-2.67-17.81) 2.56 (7.10-9.25 (3.29-4.13-6.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.82-2.52) 2.65) 18.1-21.9) 8.15 (1.7-36.25 (3.16-10.22 (1.17) 13.99-2.43 (2.1 (8.51) 18. population from the National Health and Nutrition Examination Survey.6 (12.6 (22.4) 8.76) 2.51-21.32-19.15 (6.6 (10.42 (2.63-13.17) 2.9) 19.8 (8.9 (9.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.33) * 2.53) 4.00) 4.50 (2.00 (2.50-8.87-6.94-13. interval) 2.83-5.19-5.88) 4.01 (3.3-23.10 (6.87) * 2.51 (2.88) 5.88 (2.87 (3.65-2.3 (9.27-9.00 (3.53-11.0 (11.2 (8.6 (9.6) 8.70-9.43-7.25-17.9) 8.43 (<LOD-2.4) 4.5) 12.14-13.90) 2.65) 2.9 (9.83-6.5-28.77) 2.1) 11.68) 2.05 (6.82 (3.81-9.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2 (12.7 (14.9-34.32 (2.10) 4.6) 12.9-29.73) 5.58 (4.56) < LOD 11.0 (9.77-4.11) 10.22 (<LOD-2.83 (3.6 (6.33-2.91 (3.79-17.4 (11.5) 8.52 (5.13 (1.7) 25.52 (3.2) 19.5 (10.5) 9.63 (2.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.83-6.78) 90th 12.60-2.78) 2.5) 11.33 (1.20-2.88) 1.68) 2.25-2.04-16.17-4.3) 8.05 (3.21-11.72) 32.6 (9.2 (7.98 (1.26 (6.0) 10.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.71 (3.62-15.65-21.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.8) 11.76-8.6 (5.63 (<LOD-2.90 (1.87-7.66-4.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.96) < LOD 4.76) 1.95-2.59 (2.60 (4.09-3.26-13.0) 8.Organochlorine Pesticides Urinary 2.06) 11.63-15.9-32.22-2.40 (2.52) 2.46-14.72-16.8 (7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1-32.24 (1.38 (4.0 (6.23) 4.73-22.38-5.23 (1.4.06) 4.8) 19.5) 11.41-6.55-2.63) * 4.22-9.18-4.22 (3.98) 10.88) 4.18-2.91 (7.9-64.53) * 2.82 (8.6-31.33 (7.35 (3.3-37.2 (13.4 (12.1 (13.00) 4.29-4.7) 6.5 (8.38) 22.63) 4.56-5.40 (7.53 (3.30-2.S.48-2.25-15.5 (7.54 (2.92) 4.88-7. Survey Geometric mean (95% conf.8) 12.88) * 2.78 (2.04-2.89) 10.02 (1.76) 4.9) 7.06-2.49) 4.38 (2.28-4.6) 13.44 (3.8) 21.82) 2.89-2.47-5. Fourth National Report on Human Exposure to Environmental Chemicals 115 .41 (3.49-3.87) 2.1) 14.08-2.42) 2.4) 9.29 (6.

Wegner R. Baker S. Poschadel B. et al. S. Anderson HA. Can J Biochem 1976. Int J Hyg Environ Health 2003. Aitio A.63:57-62. Toxicological profile for chlorophenols [online]. Kohli J.18(4):469-474. 4/21/09 Agramunt MC. 206:15-24. Pesticide residues in urine of adults living in the United States: reference range concentrations.pdf. et al.146:83-91. Baur X. Needham LL.106(5):279-289. Am J Ind Med 2004. Jones D. Shealy DB. Safe A. Seiwert M. Available at URL: http://www. Int Arch Occup Environ Health 1991. Domingo A. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Kaus S. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Fast DM.EPA). Heinrich-Ramm R. Environmental Protection Agency (U. December 2006 Draft. U. Pekari K. Falk C. Domingo JL. et al. Hill RH Jr. Environ Res 1995.gov/toxprofiles/tp107. Urinary excretion of chlorinated phenols in saw-mill workers. Toxicol Lett 2003. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. 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]. Radon K. Hill RH Jr.cdc. Olson J. Corbella J. July 1999. Environ Health Perspect 1998. Bailey SL. The metabolism of higher chlorinated benzene isomers. Gregg M. Head SL. Available at URL: http://www.71:99108.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).54(3):203-208. Burse VW.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport.45:440-445. Holler JS. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Needham LL. Luotamo M. Jarvisalo J. Chlorophenol exposure in harbor workers exposed to river silt aerosols.atsdr.S. Szadkowski D. Lindroos L. Arch Environ Contam Toxicol 1989. Smith SJ. To T. Becker K.epa. Seifert B. html. Schulz C. Hanrahan L. The Great Lakes Consortium. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.

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

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

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

40-5.0) 5.2-20.0 (7.16) 4. which may vary for some chemicals by year and by individual sample.44 (2. 01-02.40-19.0) 10.10) < LOD < LOD 4.7 (14.50-36.27-3.5) 15.93-24.98-12.90-4.32 (.8) 11.13 (2.840-1.39 (3.830 (<LOD-3.61) 4.7 (12.30-4.90 (1.44-38.29) * * 1.40-16.37 (3.42) . respectively.80 (2.02) 4.71-9.700-1.1-23.981 (.80-22.34-3.47) 5.623-1.0) 11.3) 17.95) 5.60-18.12-19.08 (<LOD-2.80-4.860-2.8) 19.17-3.20 (.08-15.970-2.57-7.30 (2.8 (9.52-11.97) 8.00-12.80) 2.70 (4.90) 2.20 (.19) 9.0 (9.0-28.80-24.40-11.30-6.60) < LOD < LOD 4.1 (10.74 (8.0 (5.8 (12.1) 10.56 (4.20 (.60) .80) 2.33 (5.4 (7.0) 7.21) 9. population from the National Health and Nutrition Examination Survey.56-13.5-16.60-25.83 (5.8) 7.2 (7. 120 Fourth National Report on Human Exposure to Environmental Chemicals .0) 20.71 (2.33-18.717-1.0 (6.35-11.10 (2.13 (2.46) 10.07-10.42-3.0) 15.11 (.954 (.16 (2.52) 6.0) 6.35-16.40-1.20-30.9) 14.780) < LOD 3.757-2.8-32.43-12.32) 1.00-27.955 (.76 (2.96-3.79-7.30 (2.2) 471 576 308 664 822 701 814 1122 922 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.4) 17.82) 10.70 (2.0) 11.1-17.2) Sample size 1949 2520 1931 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0) 10.0) 10.58 (5.80) 2.45 (2.740-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6) 7.10 (.60 (5.80) .55-8.600 (<LOD-1.9) 8.50 (2. and 03-04 are 0.00 (4.60-11. 0.85 (3.80 (4.0) 10.5-17.4 (9.0 (9.5) 20.70-19.63) 1.58 (2.26-6.99 (5.14) * * .94) 3.68-7.2) 14. < LOD means less than the limit of detection.4 (9.35-12.620-1.50 (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.48-7.7) 11.82-12.8 (8.2.27-15.13-2.04) < LOD 1.9-18.21 (.0 (8.2.86-15.97) 90th 7.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.20 (2.89) 9.0 (7.38-5.5 (8.6) 18.44-3.0) 12.8 (14.3-15.530 (<LOD-2.79 (5.2 (7.70) .00-7.94) * * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.01) * * 1.810-1.0 (7. and 0.58 (3.0 (8.47) * * 1.34-7.00) 3. see Data Analysis section) for Survey years 99-00.81) 1.52) * * 1.2 (11.2) 16.80) 4.70) < LOD < LOD 75th 3.9) 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 1.490-2.03 (.890 (<LOD-2.40 (.0) 11.20-7.26 (5.23-5.22 (.0) 6.67) 3.10) < LOD .86 (1.599-1.08-2.3) 16.12) 4.39 (8.55-6.73) * * .72) 5.4) 20.0 (7.05-7.40-14.0 (12.1.90-5.2 (14.51) 2.70-11.0) 5.9 (8.0) 9.10 (.54 (3.80) 11.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.50) 2.56 (1.00-27.28) 1.80) .56 (6.00) 3.0) 5.10-7.3) 14.81) 11.81) 11. interval) 1.290 (<LOD-1.61 (3.0 (8.0-27.26-8.758-1.66) * * 1.670-1.80) 3.00 (5.0) 6.0) 11.750-1.579-1.20 (.90) 3.50-5.74 (8.00 (1.20-4.15) 14.00-19.70-23.1) 95th 13.8) 7.93 (4.36-4.02-5.2 (9.53) 4.91) 4.1 (9.60 (1.50 (.2) 16.10 (2.0 (4.1) 13.S.00-12.2 (9.70) < LOD < LOD 1.4) 18.98-5.0) 10.2 (14.30 (4.2 (7.290 (<LOD-.5 (11.70-14.0 (6.15-12.4 (7.

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 .95) 2.71-2.773-1.87 (1.29) * * .920 (.1 (7.3) 5.23 (4.8 (10.30) 2.92-2.05) .09) 2.04 (1.6 (9.9 (9.818 (.75) 14.47 (3.4 (9.88-15.80) 9.40-3.73 (1.5-16.00-17.0) 7.960 (<LOD-2.5-20.75) 2.34) * * .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 1.69) 4.61 (1.18 (.15-10.5) 8.42 (3.80 (6.10-13.1-15.31 (3.00 (4.36) * * 1.6) 13.52) 4.40-28.924 (.85 (6.67-19.20-8.93) 9.780 (<LOD-1.8) 16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.28 (2.00 (4.11-6.03 (7.87-5.72) 11.883 (. population from the National Health and Nutrition Examination Survey.9) 16.40) 4.5) 11.1) 4.75 (7.25) 6.76) < LOD .94 (2.2 (10.6) 8.35) < LOD < LOD 3.54) .67) 4.02-2.47) 2.95 (3.710 (<LOD-1.7) 12.46-5.77 (6.3) 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 1.6) 11.8) 7.41) Selected percentiles ( 95% confidence interval) Total * * 50th .3) 15.94-23.75-7.93-9.57 (6.78 (2.570-1.03) 2.430-1.57) 4.566-1.23) 4.5) 12.9) 12.28 (5.54-15.68-4.5 (4.35 (1.S.996 (.37-5.04-6.84 (5.64-5.80 (7.98-22.6) 9.5-13.82-14.1 (10.71) 10.560-1.820 (.2 (8.1 (9.83 (7.80 (2.25) < LOD .32-12.44 (2.67) 1.10 (3.98) .53 (6.28) 10.93-5.2) 5.87 (3.53) 9.68) < LOD < LOD 3.650-1.58) * * 1.66-15.76-4.74) 4.890 (<LOD-1.07 (.7 (8.21-23.9 (9.62-5.82-26.60-9.41-12.40-12.37 (4.38 (1.81 (1.61-13.66 (1.39 (2.890 (<LOD-1.02 (7.98) 9.960 (.0 (8.05 (.84) 7.90-5.2) 7.13) 4.81-5.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.60) 2.47) * * .40-14.1 (11.88) 2.0) 6.30 (1.540-1.855 (.79-3.56-13.46) 2.40 (3.34 (6.3) 16.830-1.94-22.69-10.06-2.57-10.24-3.8) 8.29 (2.45-5.43 (.6 (10.14 (3.61 (1.89-3.74) 90th 7.54-2.549-1.4 (4.43) 2.620-1.2) 5.56) 4.2) 8.00-13.56) 7.2) 95th 12.82-6.8) 12.05 (1.89) * * 1.02-14.51-5.1 (6.900 (.7 (10.92-5.03 (2.82-14.37 (5.2) 13.932 (.00) 8.3) 12.60) * * .02 (2.90-8.38) .5) 7.40-5.37-3.1 (8.42) 12.440 (<LOD-2.66 (5.40) < LOD < LOD 75th 2.94-10.31-14.41) .7 (9.34) < LOD < LOD .9 (5.9) 11.2) 9.03) 2.69) 2.57 (4.500-1.94 (4.88 (5.37) 9.2 (6.98-5.19 (4.1) 4.09 (.34 (6.7) 18. Fourth National Report on Human Exposure to Environmental Chemicals 121 .9-28.55-20.860 (.5) 7.83) 8.62) .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.54-4. interval) .69 (4.54-11.66-34.75 (3.4) 4.7) 5.28 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.533-1.56) .28-9.27) < LOD 2.09-11.45-5.98) .4) 13.750 (<LOD-1.4) 4.790 (.43 (3.94-9.88-10.47 (1.608-1.47 (3.26) * * .870-2.53-11.85) 2.8) 6.633-1.574-1.98 (3.45-11.03-6.5-32.79-9.66 (2.00-19.510-1.61-29.01-2.50) 7.

0) 23.31-12.22) 8.92) 9.3) 22.0) 19.5 (8.1) 11.6 (10.01 (2.00-4.8 (12.0 (8.3 (11.75 (3.8 (12.37 (3.80) .8-20.62-17.7 (11.00-9.74) * * * * * 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90-9.98-9.31) 1.90-31.5) 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 * * * * * * .82) 8.88) 3.4 (10.8) 8.89 (2.2) 14.9) 16.9-14.63-14.00-18.14 (6.70) 2.00) 3.73) 7. 122 Fourth National Report on Human Exposure to Environmental Chemicals .80 (2.34 (6.9 (7.41-5.5 (9.740 (<LOD-1.9) 10.95 (2.80-12.5 (8.50) 3.1-23.89) 2.80 (2.16-1.6) 18.35 (6. respectively.7) 16.90 (2.90 (6.10-10.0-19.46-4.0 (14.20-8.6-41.00) 7.5-26.0-33.6) 11.5) 21.00) 3.80-14.9) 9.0 (9.6 (10.41) 3.67) 3.58 (1.15-2. 0.8) 9.0) 13.40 (2.20-18.0) 14.99 (3.580-2.22-12.8) 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 1.24 (2.46-28.6) 14.27) 4.60) < LOD < LOD 2.66) 4.35-3.27) .3 (7.95-9.20 (<LOD-2.96) 90th 7.80) .00 (.4-17.670 (<LOD-1.90-15.80-4.30) 3.70 (8.30) < LOD < LOD 4.78) 5.84-4.77-3.60 (2.3) 8.75 (2.59-3.30) 3.25 (2.90) 4.90-15.0 (10.3 (9.0) 9.95 (5.7) 15.20) 3.5.40) < LOD < LOD 75th 2.4) 7.17 (7.10 (.0) 18.0 (7. and 0.90 (5.1 (10.0 (15.18) * * * * * * * * 1.15-6.0 (9.9-17.80 (5.97-4.3) 10.67-10.90 (2.50-5.45 (3.27) 9.4 (10.06 (2.70-9.10) 6.10-15.27 (3.20) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.52 (6.10-4.8-17.0-24.22 (6.2 (7.51) < LOD 1.34-10.50) 5.22 (6.7) 14.9 (12.64) 10.92-17.04 (3.790 (<LOD-1.0) 12.00) < LOD .00) 8.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.53 (3.35) 4. population from the National Health and Nutrition Examination Survey.49-4.00-16.6) 14.90 (2.70-8.7-19.0) 12.3) 14.67) 4.4) 11.10 (<LOD-1.81-6.66-13.33-11.40 (2.9-15.7) 22.0) 13.3 (9.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80-6.77-14.00-18.0) 12. 01-02.0) 7.50-4.30) < LOD < LOD .0) 11.61-32.0) 6.29) < LOD < LOD < LOD < LOD 3.88) 10.39 (5.7 (10.910 (<LOD-2.0) 14.58.29-4.8-21.6-19.6) 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 * * * 1.7-21.0 (5.34-3.1 (10.11-6.30) 8.3) 20.670 (<LOD-1.61 (3.0) 9.70-5.18 (3.80-8. and 03-04 are 0.80-3. which may vary for some chemicals by year and by individual sample.42 (1.00-4.37) 2.0-29.96) 3.7) 10.0) 11.20-4.80-21.31-7. < LOD means less than the limit of detection.72) 2.2 (9.5.90 (6.70-9.12 (4.34-5.S.0 (10.0 (13.27 (7.3 (6.9) 95th 14.28 (7.90 (6.680 (<LOD-1.3 (12.39-13. see Data Analysis section) for Survey years 99-00.0-24.20) 3. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .4 (14.70 (1.970 (<LOD-2.47-6.86-10.650-1.50) .80) 5.8-20.90 (6.90 (1.60 (6.90) 8.24-5.670 (<LOD-1.60 (5.670 (<LOD-1.

7) 14.89-3.32) 2.74-19.67 (1.09-11.01-5.68) .21) * * * * * 1.950) .86) 9.99) 2.6) 7.82-8.9) 19.16 (3.5-17.3-15.6) 12.9) 16.5 (9.5) 10.9 (9.27-13.7) 9.25 (4.2) 16.94-14.06 (<LOD-1.8 (8.5 (15.61 (2.8) 11.3 (7.890-2.89 (2.00) 2.78 (6.3-17.83 (7.6 (11.93 (6.00 (2.77) 3.2) 10.850 (<LOD-1.38) 1.72-4.34) < LOD < LOD < LOD < LOD 3.15) < LOD < LOD 75th 2.97) < LOD .4-15.38 (.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.4) 16.6) 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 1.89 (3.7 (11.45) 6.5 (11.5 (8.03 (6.27) < LOD .48 (2.20-3.7-23.77 (2.53-8.27) 5.9 (9.6 (13.6 (11.07 (5.29 (5.88 (1.71 (1.0 (11.68-19.4) 6.00 (<LOD-1.07) 2.940) < LOD < LOD 1.7 (8.50 (6.79-6.6) 13.02-4.4) 15.2) 15.33-10.45) 3.2) 12.37) 3.12 (7.1) 13.11 (5.2 (9.64-11.9 (9.91) 3.68-4.75-3.4) 7.96-10.00 (5.00 (<LOD-1.3) 6.29-2.14 (2.690 (.93 (<LOD-2.29 (2.93-10.07-3.87 (3.780-1.7) 15.55) 16.67 (7.95) 90th 8.5 (10.04) 9.38-13.6 (10.0 (8.32-8.06) .3) 12.0 (13.6) 14.55 (2.28 (1.23-3.1 (19.34-18.00 (7.38 (2.4-16.2) 19.6) 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 * * * .54 (7.27) 1.82-11.52-3.21-21.810 (<LOD-1.86-3.42-19.78-10.6) 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 * * * * * * .S.30) 2.3) 9.74-4.12) < LOD < LOD 4.25-9.81 (7.43 (2.973 (.3-17.760 (<LOD-1.41 (7.73 (5.78) 4.80) 3.6) 6.0-19.8) 14.9-25.28) 6.93 (2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .78 (4.5) 22.69-11.89-10.44-6.03 (2.39-17.05-3.0 (10.8 (10.27) * * * * * * * * 1.63 (6.7-19.89-13.6) 95th 16.89-3.18) 2.03) 3.7 (10.54-5.92 (5.6 (12.58 (4.1) 10.11-3.3-34.94 (5.6 (13.79-9.51-10.2-30.28-12.9-17.51-7.2) 8.2) 12.0) 14.8) 16.00 (3.3-21.15 (1.71) < LOD < LOD 2.55) .91-9.1 (13.1 (8.4-16.3) 8.59-3.5) 13.2) 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.590 (<LOD-.85-8.530-1.6-19.38 (1.00) 8.2) 12.89) 5.70-35.42) 8.88-7.33) 3.86 (3.1) 20.85-17.4) 9.7) 14.7) 12.16-14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.42) 7.47-9.95) 3.72) 4.77 (2. Fourth National Report on Human Exposure to Environmental Chemicals 123 .7 (10.30) 8.99 (4.37-5.5) 8.4 (11.4) 7.30-5. population from the National Health and Nutrition Examination Survey.29) 3.910 (<LOD-1.97-4.70-2.83 (6.4-18.75-3.30) 7.36 (2.920 (<LOD-1.07) 2.2-15.19) 3.50-17.54) 9.620 (<LOD-.63 (2.09-11.2 (9.96-11.68-10.0-21.92) 3.4) 7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.95 (2.

950) 90th 1.700) .680-1.60-4.840 (.34) 2.48 (2.453 (.560-.14 (1.78) Sample size 1949 2519 1905 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .20) 3.73 (2.353-. 0.80 (1.30-3.587) * * .76-6.80) 2.20 (1.10-1.20) 2.70-2.700) .550 (.13) .780 (.303-.398-.49) .11-3.490 (<LOD-.55 (3.350-.31) 95th 2.60) 2.83) 1.570) * .50 (1.70 (1.570 (.86) 3.592) * .18 (.77 (1.73-5.860) < LOD < LOD .45 (1.46 (1.54 (2.73 (1.41-5.505 (.30) 4.95 (2.37-2.40 (1.910 (.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 * .50 (1.74-5.98) .570 (<LOD-.980) 1.40 (1.960 (.618) * .80) 5.940) < LOD .54) .30 (.89) .32 (1.400) .30-3.810) .690-1.48 (1.780 (.50-2.45 (1.570-1.83 (2.380-.09. 124 Fourth National Report on Human Exposure to Environmental Chemicals .740 (.96-3.710 (.690-.970) .720-1.94 (2.820 (.25-1.390-.585) * * .65 (2.41 (2.46-3.580-.570 (.60 (2.36-4.80 (2.380) .57 (2.850) < LOD .13) 2.47 (1.720 (.930) 1.592-.20 (1.80) 3.94) .16-3.30 (.390-.30-1.960) .710) .38) 1.20) 3.70-7.01) .570 (<LOD-.89) 1. which may vary for some chemicals by year and by individual sample.910) 1.960) 1.15) 2.740 (.30) 2.70 (1.340-.970) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.88) 1.70 (1.20) 2.80) 3.930-1.720-1.1.960) .45 (2.17-4.90) 2.584) .740-1.580-1.2.10) 1.600-1.23-3.46) 1.30) 1.42-2.31-3.657) * * .79) .60) 3.350-.450 (<LOD-.26) .600-.880) < LOD .820 (.14-1.05-2. respectively.31-3. < LOD means less than the limit of detection.750) 1.650-.22-3.20-1.21) 3.20-3.10-1. and 0.460-.54-2.592) * 50th .500 (<LOD-.160 (<LOD-.336-.359-.34) 2.45-4.510 (.26 (2.425 (.20) 1.50 (1.86 (1.01-1.22-3.95-5.50) 1.455 (.990-1.343 (.04) 1.790 (.20-2.90-4.910-1.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .780) .260 (<LOD-.690 (.16) 2.510 (<LOD-.949) .98 (2.S.10) 1.00-4.59-6.449 (.960-1.75 (2.08 (2.57 (1.98-3.39) 2.380-.620-1.50-2.930) < LOD . and 03-04 are 0.750-1.467 (.35) 1.457 (.64 (1.30) 4.201-.83) 2.880) < LOD 75th .690) .680-1.17) 1.459 (.27 (2.94 (3.710 (.210 (<LOD-.19-1.00-2.78) .91) 2.20-2.388-.08 (2.61 (1.15) 2.63 (1.759) * .80) 2.32-1.01-3.90) 3.760 (.00) 2.76 (1.50 (1.58 (1.590-.280-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) 1.18 (1.20 (1.240 (<LOD-.32) 3.79) .11-3.33-2.83) .47) 2.382-.90 (1.50 (1.31) 2.00 (1.22-2.17) 1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.549 (.800 (.77-2.05-3.90) 2.22 (1.20) 1.600 (<LOD-.880 (.04) .89-6.00) 1.29) 1. see Data Analysis section) for Survey years 99-00.69-4.49) 2. 01-02.03) 1.75-2.20 (2.550 (.670) .29-2. interval) Selected percentiles ( 95% confidence interval) Total * .22-8.80) 3.83 (2.87-3. population from the National Health and Nutrition Examination Survey.27 (3.96-5.09 (.46 (2.540 (.30 (.730) .830 (.68-5.95) 2.97 (2.597) * .749 (.740-.16) 1.440-.930 (.74) 3.10) 3.30 (1.59-2.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.

97 (1.07) 1.840) 1.640 (.08 (.62 (1.950-2.08-3.78) 3.36) 3.390) .25-3.41 (.740) < LOD 1.320-.28 (1.89-3.58) 3.45 (2.32 (.23) 3.58-6.06) 4.92 (1.710 (.88 (1.57 (3.72-4.84-6.90) 2.447 (.23) 2.47 (1.34 (1.77 (3.22-2.05) 1.440-1.830 (.07) 5.350) .70 (3.740) .84 (2.16-2.234 (.510 (.91 (1.08-2.17) 2.670 (.680 (.60 (1.08-3.30-2.97 (1.690) < LOD < LOD .597) * .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.05) < LOD .05-2.22) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.77-4.57 (1.32) 2.390-1.92-8.580 (.03-2.57-4.136-.790) .38-3.42) .368) * .02-3.88) .11-2.750 (.550-.33) .250 (<LOD-.800) < LOD .98) 1.80) 2.00-1.72 (2.43) 1.55-3.372 (.320-.403) .18-2.13 (1.42 (.47 (1.55 (1.66) .22) 1.62 (2.60 (2.560 (.76) 1.00 (3.87 (2.60) 1.67 (1.75 (1.480) .38 (1.550-.560-.75 (2.23) 1.64 (2.940-1.530 (.82 (2.590 (.81) 2.71) .444-.900) 1.33 (1.82) 2.550) .280 (<LOD-.750 (.520-.61-3.20) 1.04) 95th 2.310 (<LOD-.830) 90th 1.69 (3.02-6.42-6.73-3.50) 1.39) 2.05 (1.32-1.79) 1.710 (.720-1.49-4.850) 1.990-1.500-.44) 2.92) 3.790 (.448 (.370-.71 (1.67) 1.58 (1.742) * * .470 (<LOD-.930-1.412-.460-1.560-.920) .53) .14 (2.80) 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 * .19 (1.30) 3.00-3.270-.590-1.710 (.840) .840) 1.453 (.75-3.43) 2.180 (<LOD-.300 (<LOD-.11 (.73 (2.08) 1.760) .75) 6.310-.61) 2.510 (.77-3.94) .07) 1.06-2.460 (.22) .515) * * .880) 1.330 (<LOD-.300-.760) < LOD 75th .07-3.335-.39 (1.630) * .17) 2.400-1.07 (.348-.22-3.17-2.07) 1.870) .61-3.330-.97) 2.65) 2.02-3.44-2.11) 1.540-.99) 2.16-1.63 (1.645) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20-7.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.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 * .61 (3.253-.08-2.04-1.305 (. interval) Selected percentiles ( 95% confidence interval) Total * .460) .509 (.43 (1.23) 2.47-4.250 (<LOD-.510-.485) * * . population from the National Health and Nutrition Examination Survey.49 (1.720 (.66 (2.08-3.380-.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 * .42-8.310 (<LOD-.700 (.69 (1.739) * .99) 1.24) 4.730) .520 (.03-1.910) < LOD .23 (.870 (.09) .820) .640 (.470) .640 (.32) 5.45 (1.57-2.285-.400) .64 (2.38 (2.08-2.52) 3.552 (.89 (1.79 (1.04-5.29-4.480-1.72 (1.380) .07-2.377-.580-.43) 2.270-.550-1.688) * .535 (.32) 1.820) 1.580) .318-. Fourth National Report on Human Exposure to Environmental Chemicals 125 .52 (1.490 (.16) 1.70 (2.22-3.95) 1.700 (.08-3.980-1.591 (.590) * 50th .10) 2.97) 1.72) 1.393 (.230 (<LOD-.08 (2.270 (<LOD-.31-1.S.50 (1.08) 2.60) .700 (.05-4.67 (1.71) 2.22 (2.67-3.380-1.20-2.660-.800-1.67) .471-.

830-4.52 (4.18) 6.19) 2.18) 20.0-43.11) 2.8) 62.2) 31.0 (26.70 (1.4.2 (19.0-92.05) 1.29-9.2-62.13 (1.40-4.32 (2.0) 15.83-2.93-3.97) 6.13 (1.4) 19.46-6.70) 5.7-22.0-62.96) 5.0-41.64-8.10) .530-4.53) * 2.2-26.3) 31.10-13.90) 11.41-4.0-110) 34.0) 3.9 (19.0-110) 42.0 (6.600-2.80) .5) 69.610 (<LOD-1.0) 3.8) 32.3) 26.7 (12.2-33.80) 1.88) 1.0) 30. and 03-04 are 0.10-4.85 (1.5-40.26) 75th 11. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0 (13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 45.3) 38.0-49.0) 19.05-3.49-2.5-20.0) 28.3 (14.0-39.58) 16.98) * 2.20 (2.83 (3.69) 2.2-39.91 (4.0) 31.50-2.72 (1.40) < LOD 2.14) 5.90 (1.85) * 2.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.2-27.9) 17.00-24.29-4.0) 4.9-51.4) 38.0) 4.30) 11.2-47.21 (1.0 (38.0 (37.1) 95th 48.95 (5. population from the National Health and Nutrition Examination Survey.74-2.10 (1.58-2.0 (19.1) 18.80-18.79 (1.0) 20.3 (24.0) 13.40) 50th 2.1) 140 (46.0 (20.3) 28.80) < LOD 1.8) 41.53 (1.1 (26. and 0.0 (8.0) 8.26 (.0 (21.53) 40.6 (11.99 (2.33 (5.4-22.80) 90th 38.4 (19.46-2.6 (9.0 (38.30-14.64-3.0-62.36-2.12 (3.8 (26.0 (8.16) * 1.00 (.0 (38. respectively.7) 20.86-3.5 (24.67 (1. interval) 1.10 (7.6-22.57-2.0) 3.18) 14.3 (12.7 (28. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 6.4-76.31-6.0-69.0-58.7-41. which may vary for some chemicals by year and by individual sample.830-3.70 (1.470 (<LOD-1.41) 1.8-24.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.0-52.60 (2.0 (38.0 (33.94 (1.00 (.82 (1.42) 1.02 (2.0) 17.6-27.7) 47.1) 38.0-260) 34.27-6.44) 2.3 (12.90 (1.3 (10.6) 52.0 (38.2-27.0) 18.21 (4. see Data Analysis section) for Survey years 99-00.44) 3.75-14.0) 28.30 (.60) < LOD 1.5-27.0 (24.9 (10.70) 1.9-21.66-5.48-2.48) 5.81-2.0 (7.81-3.70 (7.0-41.40-16.90-8.61-2.50-17.3 (23.05) * 2.65 (4.92-5.70-6.0) 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 2.09 (4.10 (1.10) 39.06) * 2.4 (15.11 (4.59 (1.0) 3.8) 39.76 (2.23-2.53) 1.8 (12.0) 32.1 (10.0-39.17-2.1 (22.21 (3.86 (1.1-47.71 (4.6 (26.0 (8.40) < LOD 1.41) 1.1) 38. 01-02.70) 1.13) 12.76 (2.690-3.0 (17.54 (1.79 (2.0-41.54 (3.50-5.5) 30.30) 4.20-4.41 (1.83 (1.71) 5.0) 16.0 (20.0 (11.50-7.57-2.06 (1.1 (25.44) Selected percentiles ( 95% confidence interval) Total * 2.0 (32.2) 16. 0.0 (25.0-29.1-19.23-2.1 (11.77) 38.83-2.0-58.92) * 2.04 (<LOD-2.9) 48.77 (1.1-40.0-230) 35.660-2.7 (12.9 (23.8 (22.5.50-20.6-45.35-6.0) 42.45) 2.0) 20. < LOD means less than the limit of detection.4 (10.0) 5.1-25.04-8.88) 3.0) 4.0) 17.2-80.8 (12.44-7.9) 38.50 (2.80-2.70 (.6 (15.63-6.0-50.8-21.20) 1.0-53.0) 15.12) 1.78 (1.3) 33.16) 2.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.0 (38.1-46.18.19-2.71-2.25-3.9 (19.0-31.9 (27.1 (25.10 (1.48-2.59 (1.0 (40.87-7.1-20.78) 9.9) 18.2 (12.04) 3.45) 2.0-47.5-74.61 (1.07-5.23) 9.S.70-17.43-7.41) 5.0) 16.0 (38.0-53.29) 2.5-45.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.46 (.79-2.10 (1.6-54.0) 33.98 (1.

52 (1.54-15.0 (23.0 (6.86) * 3.0 (25.47 (1.03) 1.0) 30.38-1.6) 3.6-51.2-34.S.94-20.90 (.51) .22 (.3-22.94) 19.0-70.0-118) 29.16 (1.01 (.5) 27.71-2.3 (20.25-3.64 (1.0 (17.6) 19.1) 27.5 (34.23) < LOD 2.1) 15.870-3.29-5.7-37.26-4.0) 13.2) 33.40 (5.2) 41.00) 6.06) 75th 9.1) 25.2) 13.56 (2.27 (6.79 (2.1) 13.9 (10.7 (18.3 (8.9) 24.2 (16.95 (2.3 (9.7) 30.71 (1.3-27.7 (18.07-2.62) 4.45 (1.4-39.8) 15.6) 11.34) * 1.2) 13.9 (26.0) 48.36) 10.38-5.57) 4.82) 1.96) 2.899-2.2 (8.7) 61.16 (1.6 (27.8) 23.8-37.888-1.46-5.7) 95th 51.19 (1.18) 3.03-2.79-17.33) < LOD 1.27) 10.2 (22.69-5.2-38.69-18.48) 1.26-2.6) 23.58-2.20-5.80-8.7 (11.8) 32.6) 7.88 (4.17) 2.09 (5.88 (1.0) 10.28 (1.28) 1.43-12.66 (1.1) 13.08) 1.6-32.0) 25.0-71.5 (15. interval) 1.2 (15.4 (19.43-2.08 (1.00-16.7-38.9-52.27-3.0 (23.8) 31. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.870-3.4-34.7-19.68 (1.5 (15.67 (1.38 (3.5 (17.33-5.18) * 2.6-38.5-190) 30.0) 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 1.9-95.2) 671 678 497 509 694 578 595 947 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2) 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 1.67-16.2) 36.75 (1.14-8.83) .12 (1.95) 90th 32.24 (1.60) 4.35) 1.16-2. population from the National Health and Nutrition Examination Survey.54-2.1 (50.45-1.83 (.6-49.30) 28.53) 1.860 (<LOD-1.40-7.22 (2.6 (11.0 (14.84-13.37-2.67 (1.9) 24.4 (9.33) 1.59-15.5 (13.6 (7.3) 13.4) 12.5 (8.2 (21.8 (7.59-2.2) 4.1) 36.9 (7.1 (34.0-40.3-19.1-60.99-4.71) 8.2-70.0 (19.37 (1.02) * 1.27) 50th 2.51) < LOD 1.88 (1.91 (6.23-1.19-14.63-5.68) 47.16 (1.61-2.22-3.7) 34. Fourth National Report on Human Exposure to Environmental Chemicals 127 .20) Selected percentiles ( 95% confidence interval) Total * 1.88 (4.4 (11.5 (6.5-43.3 (10.36-13.22-2.7-47.35) .18-1.7 (24.9-18.70-4.55 (2.07) 9.56) 1.4) 3.8) 3.33) 2.46) 1.4-21.41 (2.6) 3.4 (25.4-71.4) 14.39 (1.61 (1.1-22.58-17.80 (1.7-20.750 (<LOD-1.8-45.1) 27.9-37.9 (19.67-3.21 (4.66 (1.32 (3.60 (.6) 112 (40.76-2.38) 5.36 (4.32-3.96-16.59-2.94) 1.5-97.1 (39.9 (39.5-36.75-6.19) 5.50 (2.7) 23.75 (1.8-34.4 (12.40-4.95-16.00) 1.0) 3.15 (.06) 1.47 (3.4 (25.8) 11.9-41.06) 1.9) 3.1 (25.48 (4.70 (1.50-5.9 (13.93) 5.1) 52.00 (4.8-43.31) 2.2 (9.72) 2.930 (<LOD-1.61-22.0 (39.75) * 1.7) 66.670-1.3 (10.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.7) 26.9-36.1 (33.5 (41.52-4.66) 8.680-4.4 (21.91-2.47-17.44) 9.82 (2.890-4.86) * 2.6 (24.1-63.0 (32. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.11-2.3-42.7 (10.06-1.95-16.1) 17.02 (.07-2.0) 47.870-3.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.1) 25.4-67.1 (12.9) 54.3) 28.2-28.7) 15.97 (1.57 (6.7-109) 22.19-6.5) 70.9) 12.11) < LOD 1.40 (2.19) 5.46-22.2-47.23) 37.17-3.9) 3.7-43.14 (.4) 12.62 (2.43) * 2.12) 3.8-26.02) 1.4 (5.46-6.35 (2.

130) . and 0.570) .140) .130 (.990) .240 (<LOD-.220 (<LOD-.130-.680-1.730) . which may vary for some chemicals by year and by individual sample.050-.S.090 (<LOD-.470 (. and 03-04 are 0.610 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.200) < LOD < LOD .830 (.440-1.12 (.660 (.380-.120 (<LOD-.350) .780) < LOD 1.30) .650) .05.120-.370-.090 (<LOD-.42) .00) .190 (.870 (.600 (.360-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.460 (.220 (.380-.270 (.190 (.630 (.430 (.720 (.090 (<LOD-.640) .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 .150 (<LOD-.30) .450 (.162) * * * * * .850 (.310 (.650-1. 0.540) .940 (.540 (<LOD-.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 * * * * * * * * * .870 (.160) .180) .730-.084-.700-1.900 (.58) .10 (.990 (. 01-02.330-.870 (. population from the National Health and Nutrition Examination Survey.290) < LOD < LOD < LOD < LOD 90th . < LOD means less than the limit of detection.080 (<LOD-.60) 1.620 (. see Data Analysis section) for Survey years 99-00.090 (<LOD-.080 (<LOD-.740) < LOD .160) .120-.680-1.490 (.830) < LOD .540) .850) < LOD .640) . 128 Fourth National Report on Human Exposure to Environmental Chemicals .390) < LOD < LOD .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.100 (.460-.360-.290) < LOD < LOD < LOD < LOD .20) .700-1.650) .760) < LOD .300-.310) < LOD < LOD < LOD < LOD .720-1.820 (.230) .930 (.110-.680) .420-.40) .720) .860-1.610-1.410-.140-.150) .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.700-1.860) .36) .870 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .410-1.10) .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 * * * * * * .380-.390 (.400-.640 (.1.560 (.990) .550) .310) < LOD < LOD < LOD < LOD .850 (.870 (.770 (.450 (.170-.610-.430-.530-.650 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .820 (.03) .130-.260 (.130) .640-1.190 (.870) < LOD .15) .630 (.610 (.450 (.140-.830 (.320 (.310-.840) .210 (.280) < LOD < LOD < LOD < LOD .370-.510-1.770) < LOD 95th .099-.700-1.090 (<LOD-.117 (.310 (.300-1.140-.090 (<LOD-.830) .650-1. respectively.410-.470-1.840) .171) * * .10) .42) .690-1.560 (.680 (.30) .210 (.350) < LOD < LOD < LOD < LOD .410) < LOD < LOD < LOD < LOD .13) .10) .130-.32) .1.230-.290 (<LOD-.160-.320-.

730 (.320 (<LOD-.760) .580-1.210 (.60) .057-.120) .330-.450) .140-.540 (.12) < LOD .080 (.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.600) .260) .100-.720 (. population from the National Health and Nutrition Examination Survey.66) 1.970) .300-.700) .500) .100 (<LOD-.750) < LOD 95th .660-1.940) .470 (<LOD-.360) < LOD < LOD < LOD < LOD .580) .730) .080) .270) < LOD < LOD < LOD < LOD .080 (<LOD-.380-1.140-.110) .330-.780 (.410 (.78) .700 (.03) .280) < LOD < LOD < LOD < LOD .600-1.084-.230-.230 (<LOD-.390-.170) < LOD < LOD .62) 1.380 (.410-.780) < LOD 1.240-.20) 1.02) .58) 1.110) .880-1.740 (.650) < LOD .330-.03 (.00) < LOD .070 (<LOD-.310) < LOD < LOD < LOD < LOD .870) .850 (.200 (.670 (.01 (.140-.150-.510-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.540 (.700 (.410-.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 * * * * * * * * * .330 (.570-.730) .110-.400) .070 (<LOD-.29 (.500 (<LOD-.990) . Fourth National Report on Human Exposure to Environmental Chemicals 129 .400 (<LOD-.220 (.300 (.670 (.120) .580 (.110) .570-1.090 (.460 (.410 (.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.290) < LOD < LOD < LOD < LOD 90th .740) < LOD 1.520-.070 (<LOD-.050 (<LOD-.14) 1.200 (.990) .540) .720 (.940) .03 (.410) .330 (.161) * * .360-.890 (.550 (.03 (.450 (.86) .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 . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .960) .250-.190 (.640-1.190-.610-1.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .880 (.S.340-.810 (.230) < LOD < LOD < LOD < LOD .19 (.170 (.670-1.170 (.370 (<LOD-.24) .38) 1.730) .440-1.800-1.36 (1.220) < LOD < LOD < LOD < LOD .180-.111) * * * * * .650-1.860 (.67) .500-1.24 (.570 (.116 (.490-1.43) .270 (.86) .140-.09) .390-.550 (.070 (<LOD-.380-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.580) < LOD .560 (.260-.710-1.300-.380-.140-.060-.110) .440 (.360-.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 * * * * * * .02-1.580 (.140) .700-1.860 (.360 (.860-2.410) < LOD < LOD .380-.090 (<LOD-.190 (.

400-1.31) .610 (.07 (3.70-3.0 (17.86) 4.0) 5.620-1.0 (4.12) * * * * * * * * .26 (2.080-1.32-9.0-38.0) 2.20-4.48) 13.0) 4.0) 2.74) 5.S.840 (<LOD-1.690 (.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 * * * * * * .0) 3.48 (2.00) .0-40.50) .0 (6.0 (5.20 (1.40-8.00 (.80 (4.40 (1.83-3.21) 3.425-1.32 (1.28) 1. population from the National Health and Nutrition Examination Survey.21-3.0) 2.67) .53) 20.20 (1.53 (2.11) 13.49 (1.66) 4.99) 11.330 (<LOD-1.0) 4.40 (1.10-3.07 (1.90-37.840 (.49) 17. 0.33 (4.0) 4.600 (.70) 2.370-.90) .63 (3.30-6.750-1.99) 19.36-3.0 (5.90-28.36-3.62-8.20-17.83) 2.15) 14.0) 2.43-4.0 (7.1.90) .96 (1.05 (2.40-20.730 (.590 (.90-20.250 (<LOD-. see Data Analysis section) for Survey years 99-00.190-1.610) < LOD < LOD < LOD < LOD < LOD 2.870) < LOD < LOD .55-4. and 03-04 are 0. and 0.14) 2.800-4.380-.350-.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.00) .0 (17.42) 2.00) 1.70-17.00-17.90-9.07) 1.0) 5.07 (3.30-3. 01-02.52 (1.39) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.51-8.640 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.10-3.01) 5.70-30.24-7.740 (.52 (1.90 (1.10 (3.08.40) 2.480-.12-1.750-2.691 (.30) .53-7.40-4.11) .30 (2.20-4.11 (1.800) 90th 13.770 (<LOD-1.14-5.40-7.67 (1.0 (5.960 (.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.42) .49 (1.30) 95th 19.05-3.0-39.87) 12.88-3.0 (17.00-17.37) .59-5.0-38.840-3.35-10.47 (3. 130 Fourth National Report on Human Exposure to Environmental Chemicals .30 (1.30 (1.61 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) < LOD < LOD < LOD < LOD < LOD 1.07-3.170-1.0 (13.94-8.10 (.03 (.0 (3.60) 1.830 (.0 (5.90 (2.0-38.3) 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 * * * * * * * * * .15) 19.0-40.800) 17.0) 2.97) 20.0 (16.28-9.68) 2.05 (3.70-7.260-.94 (1.51 (2.880) 5. < LOD means less than the limit of detection.0 (17.0-44.67 (2.580 (.83-3.210-1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 7.70-50.31-10.35) 11.720) 2.60) .6) 5.40) 1.900 (.63) 32.28) .0) 4.0) 5.85-3.0) 2.0 (5.99 (1.350-.35) 5.1.110 (<LOD-.82-4.94-3.910) 2.29-10.960 (<LOD-1.74 (3.65) 1.10-9.13 (3.30 (1.770) 2.850) 16.16) Sample size 1949 2518 1930 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .0 (17.38-3.30 (.52) 5. which may vary for some chemicals by year and by individual sample.0) 5.39 (2.890 (.14) .0) 2.640 (.50) 2.87) 5.10 (3.90) .97) 20.30-7.00 (1.46 (1.510-.0 (4.360-1.55-8.23-6.18) 1.45 (2.07-3.76 (1. respectively.

4) 2.96-8.890 (.40) 1.71 (.33 (3.48 (4.650 (.S.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 * * * * * * .2-38.40 (.7) 5.590) 2.940-4.55) 21.69) 2.91) 2.25 (1.90-6.18) 95th 21.8) 7.5 (11.340 (.800-2.56) .53) .8) 1.45 (1.14 (1.25-9.88-3.560 (.360 (.67) 1.47-10.08) .51-44.580) 16.67-6.8 (20.64) 30.330-1.55 (3.650) 90th 10.35 (.31) .01 (1.83 (4.310-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8) 4.540 (.748 (.81-17.03) 16.41 (4.44) .04-16.0 (4.340-.5) 2.86 (3.59 (1.340-.970-3.40-12.830-3.12 (4.3) 3.10-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.340-.56) 2.57) 1.07-21.00) .14-6.22) 2.15) 9.710 (<LOD-1.1 (7.89 (2.580) 1.9 (11.29-4.31) .04 (1.370) < LOD < LOD < LOD < LOD < LOD 1.57) 8.5) 2.250 (<LOD-.7) 4.96) 2.50) .25-38.80) 3.56 (1.67 (2.8-33.740-1.5) 7.60 (1.62-17.55) 21. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.50 (4.820) .7 (12.450 (.5 (8.580-1.44-11.24) 3.49-2.02 (.500 (.700) 6.9) 5.270 (<LOD-.730-3.18) 1.470 (.67) 2.13 (2.02-4.57 (.03) 2.820 (.31-18.65 (2.47) 5.37) 4.4 (4.43) .660) < LOD < LOD .96-25.00-19.1 (5.52 (.88) 17.88 (.02) .09-3.57-40.690-5.61) 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 .12-4.83-11.23-7.6) 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 * * * * * * * * * .33-3.5-40.9) 6.62 (1.86) .66-47.630-1.88 (2.17) 5.79 (.32-6.75) 5.390-.21-3.64-4.830 (.11) .22-27.670 (.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.540-1.370 (.27 (2.06 (.150 (<LOD-.98 (4.7) 6.92 (2.11-5.33-5.370-1.47) .0 (9.53) 27.4-34.17 (1.39) 20.8) 7.31-7.260-. Fourth National Report on Human Exposure to Environmental Chemicals 131 .29 (4.33-4.80 (.600 (<LOD-1.7 (6.860-2.240-.10 (2.73 (4.8) 2.0) 4.41) 18.5 (9.71 (2.10) 2.82-11.960 (.07 (2.260-.3) 2.2 (8.8) 2.38 (2.50 (2.620-3.1) 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.36 (.97) .320-1.74 (2.770) .18) * * * * * * * * .47-10.40-2.85-3.84) 9.77 (.69-7.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.91-4.850-3.840-3.270-.780-4. population from the National Health and Nutrition Examination Survey.85 (1.430) 1.190-1.33 (1.48-7.30 (4.7) 3.430 (<LOD-.580 (.32) 9.790 (.28-6.1) 2.700) < LOD < LOD < LOD < LOD < LOD 1.48-42.51-4.05) .930) .02 (1.790) 11.50) 11.474-1.

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Wickremasinghe AR. O’Malley M. Ames RG. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Office of Prevention Pesticides and Toxic Substances. Rohlman D. Steenland K.38(4):546-563. Smit LA. Johnson C. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Rothlein J. Robson MG. Environmental Protection Agency (U. Jamal GA. Masala G.114(5):691-696.52(2):190-195. Visuthismajarn P.52(10):648-653. Weerasekera G. Tumino R. Calvert IA. Berry H. National Academy of Sciences. Narang A. Daniell WE. Eskenazi B.43(1):38-45. Santana J. Pesticide industry sales and usage . Buchanan D. Irish RM. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities.26(2):199-209.58(11):702710.68(3):209-227 Maizlish N. Pesticides in the Diets of Infants and Children. Ruberu DK. Keefe TJ.pdf. EPA. Rosenstock L. Jenkins B. Neurotoxicology 2005. Neurotoxicity among pesticide applicators exposed to organophosphates. Buccafusco JJ. Russo J. Lu C. vibration sense and tremor among South African farm workers. Bradman A.nap. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. U. Pilkington A. low-level exposure to the organophosphate diazinon. Caltabiano LM.332(1-3):71-80. Lancet 1995. Neurotoxicol Teratol 1998. Kidd M. Muniz J. Claypoole K.2000 and 2001 market estimates. J Occup Environ Med 2002. Bravo R.345(8958):11351139. and spatial learning in monkeys and rats. May. Chronic neurological sequelae to organophosphate pesticide poisoning. Frasca G. and cholinesterase status of date dusters and harvesters in California.edu/ openbook.12(2):134-141. Lancet.20(2):115-22. et al. Occup Environ Med 2001. Stokes L. Am J Public Health 1994. Weisskopf C. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Sci Total Environ 2004. Barr DB. Washington (DC): U. London L. Muniz J. Keifer M. Myers JE. Marshall E.24(1):18-29. Phillips J. et al.epa. Rodnitzky RL. van der Hoek W. Hansen S. Available at URL: http://books. metabolite clearance.113(4):504-508. Scherer J. National Research Council (NRC). et al. Prendergast MA. Effects of chronic. Gillham R. Spurgeon A. low-level organophosphate exposure on delayed recall. Thompson ML. 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. EPA). 1993 [online].S. Mounce LM. Lambert WE. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. 2004.S. Dinoff TM. Burcar PJ. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Lasarev M. 1991. discrimination. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Terry AV Jr. Schenker M. Salvini S. Samuels S. 1/12/09 Peiris-John RJ. McConnell R. Saieva C. Vitayavirasak B. Nell V.30(2):98-103. Takamiya K. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Heaton RK. et al. Malathion deposition. Lewis JA.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI.php?record_id=2126&page=1. A behavioral evaluation of pest control workers with short-term. Environ Health Perspect 2005. Arch Environ Health 1975. Savage EP. Stark A. Available at URL: http://www. 4/7/09 Young JG. Environ Health Perspect 2006. Rothlein J. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Am J Ind Med 1987. Effects of long-term organophosphate exposures on neurological symptoms. Hore P. Chrislip D. Levy LS.84(5):731-736. Aprea C. Petchuay C. Occup Environ Med 1995. Pedersen L.12(2):153-172. et al. Scand J Work Environ Health 1998. The Pesticide Health Effects Study Group.338(8761):223-227. Bull Environ Contam Toxicol 1994. Lasarev M. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Int J Occup Environ Health 2006. Gladstone EA. Arch Environ Contam Toxicol 2000. Washington (DC). J Toxicol Environ Health A 2005. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. McCauley L. Stephens R.44(4):352-357. Seiber J. S. Arch Environ Health 1988. Beach J.

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

01) 1.50 (2.00) 2.97) 2.17 (1.98-15.32-1.77 (1.00) 1.79-2.37 (4. chlorpyrifos was no longer registered for indoor residential uses in the United States. 2005).80) 1.0) 12.13-3.20 (4.0) 8.10) 2.6) 7.30) 4.67 (2. For instance.40-13. It has low leachability.00) 3.99-4.95 (4.30) 4.0 (7.S.63 (2.37 (1.70 (1.4.000 pounds are used per year.47-13.50-14.66-4.51 (1.90-2.20-4.30-5. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.80 (1.0) 10.50 (2.20) 10.80) 4. and dust. Fourth National Report on Human Exposure to Environmental Chemicals 135 .4 and 0.70-5. 1999.83) 1.25) 1.04-10.02 (1.90-8. interval) 1.0) 8. and inhalation routes.5.20) 2.60-3.0) 6.90 (1.40-2.5 (8.and post-construction structural applications for termite control were to be phased out by 2005 (U.77-15.71 (2.94 (4.46-2.40 (6.80) 2.63 (8. 2002).05-5.47 (4.50-2.40 (5.40-26.29-1.67 (1. and on plants for days to several weeks.00-24.51-2.91 (1.03) 1.0) 14.50 (2.40) 9.19 (1.0 (13.30-1.10 (4.30 (2.55-5. 2921-88-2 Chlorpyrifos-methyl CAS No.66-15.30) 5.76 (1.0 (7.90-7. 2007).71 (1.1) 5.9 (7.44-5.63 (1.47) 1.38 (3.0) 11.8) 10.50-4.0) 18.0 (7. The general population may be exposed to chlorpyrifos via oral.22 (1. Exposure can also result from contact with contaminated surfaces.50 (1.20-11. Approximately 21-24 million pounds per year were used domestically from 1987-1998.60) 5.22) 2. After 2001.50 (1.8-15.25) 3.4 (10.59-2.50-4.10 (3.45 (1.7) 8.28-3.60 (5. USGS.9 (9.19-3.20-2.S.39) 4. applied to structures to kill termites.36 (4.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.72-4.20-3.64) 3.60 (4.92 (1.0 (7.71 (6.50-5.37) 5.90 (2.9) 697 660 521 701 602 947 Limit of detection (LOD. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.40-10.10-17.76 (1.5) 7.4-15.00-8.81-2.68 (7. Chlorpyrifos is Urinary 3.0 (10.05) 1.40) 2. It also has been applied directly on animals to kill mites.0-28.43-2.61-7.72) 2.5-24.20) 4.60-2.30-11.52-12. and sprayed to kill mosquitoes.51) 1.70-16.28) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.04-10. dermal.77-6.0) 9.0) 12.35) 1.44 (3.80-10.30-9.60-4.70-11.31-2.32) 2.0) 12.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.87-6.5.3) 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.EPA.34) 1.86) 4.68-2.96) 3.62-2.90 (1.70 (1.89 (2.20-16.10 (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.80) 12.59) 2.31-2.70-17. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.97-7.30-12.8) 9.09 (2. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.89-2.1-16.15 (1.74 (1.97) 2.3 (11.60-3. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use. but can be detected in streams receiving runoff from application sites.7) 13.24-1.90) 7. pre.20-14.0) 12.84) 1.9-18.7) 9.20) 2.0 (7.0) 12.30 (2.30 (4. Estimated intakes from diet and water have not exceeded recommended intake limits.10 (5.27 (7.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.S.43-2.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.26) 7. in 142 urban homes and preschools in North Carolina.7-23.13 (1.61 (1. population from the National Health and Nutrition Examination Survey.70) 1.47-11.90 (6.2 (10.9 (10.90 (3.02 (7.61) 75th 3.21) 3.52-2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.80 (7. air.60 (2.29) 90th 7.4 (8.39-2.97) 7.20 (2.24-3.70-15.09 (3. 2002). and is infrequently detected in ground water (IPCS.4 (9. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.3) 8.30-2.80-8.0) 10. Survey Geometric mean (95% conf.74-9.35) 2.50-8.47-9. staying bound to soil particles.78 (7.57 (2.3 (10.50-2.53 (1. 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.67 (2.40 (5.02) 1.EPA.88 (1.0) 15.0) 7. Chlorpyrifos is degraded in agricultural soils with a half-life of several months. Approximately 80. 5598-13-0 General Information The chemical 3.10) 6.0 (9.90) 3.77) 1.97) 4.9) 11.0) 10.95) 7.90-4.44-2.16) 2..3 (8.91) 16.

neurotransmission.87-3.49-2.57) 9.05) 3.50 (4.70-4.57-2.57-2.12) 1..95 (3..68) 1. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.37 (1.43-10. 2005.91 (3. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.00-13.20-1. 2006. Based on animal data and human cholinesterase monitoring during occupational exposure.47 (1.20 (2.66) 1. TCPy is more persistent in the environment than chlorpyrifos itself (U.98 (7.71) 3..59) 3.27-1.82) 8.22 (6.S.1-21.5.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .92) 3.80-11.45 (1.39 (4.92 (1. Howard et al.53-5.0) 12.63 (5. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.14-8. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.05-1. 2000).80-4.86 (1.09-3.49-2.64-7.44 (6.88 (1.8) 9.27-7.11 (2.25-11.3) 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 1.56-2. Metabolic hydrolysis leads to the formation of TCPy. interval) 1.58) 5. Once absorbed..22) 1.19) 6. Thus.19-2.3) 9. and seizures. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure. 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.17-4.57) 2.24-1.25-1.81 (3.69 (1. vomiting.42 (6.41 (1.4) 4.65-11.0) 10.. and other metabolites. TCPy can also occur in the environment from the breakdown of the parent compounds.47 (5.1 (7.91-13.11-9.3 (7.85) 1.64-2.21-1. Slotkin et al.54) 5.24) 5.66 (1.09 (1.. weakness.96) 3. Ricceri et al.56 (1.65-15. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.75) 6.39 (2.24-24.02) 7.80) 3.38) 3.26-14.01) 99-00 01-02 99-00 01-02 99-00 01-02 3. Survey Geometric mean (95% conf.91) 1.94-12.85) 4.62) 90th 5.63 (4. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.88-8.82 (3.33 (.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.11) 7.31-1.49-2.58 (4.06-4.84-6.07) 1.95 (1.00) 1.30-4. cholinergic effects.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.60-3.0) 16.28) 2. resulting in excess acetylcholine at nerve terminals. 2006b).63-2.0) 6.45-1.66-11.85 (2.44 (1.23-1.83-11.36) 1.43 (4.91 (4.29 (3.46 (2.06 (5.S.9 (12.77) 1.68) 6.73 (1.93 (4.23) 14. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).2) 6.31) 1.93) 2.76 (2.93 (2. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.97 (2.58-5.34-1.35) 2.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.12-1.940-1.33) 2.17-4.44 (5.81) 2.00-8.99-8. 2005.31-4.79-13. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.88-10.93 (1.14) 1.02 (5. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.33 (5.48 (1.60 (1. In pesticide applicators.35-1.15 (4.58) 1.93) 5. population from the National Health and Nutrition Examination Survey.83-2.85 (3.05-4.99) 1.16 (4.40) 1.19-1.22-6.62-7.64 (1. 2006a.21-6.72) 1.39-1.88-9.62) 1.39) 6.08) 6.EPA.09-1.05-3.16) 6.19) 3.07) 5.35) 1.88 (1.00 (7. Betancourt et al.1 (10.97) 3.76 (3.51 (1.88-8. 2005.82 (2.97-3.97 (3.25-12. 1984). Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.5) 5.7) 7.47-2. Roy et al.82-4..98 (6.03) 1.24-4.01) 1.2 (7.24-5.89) 4.53 (2.75 (1. and producing acute symptoms such as nausea.3) 8.30-1.72) 2.11 (2.1-38.44 (1.28) 2.91-4. 2002).72-2.90-9.97) 3. Urinary 3.22 (4.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.55 (1.32) 1.56) 2. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.54 (2.85-4.58 (1.3) 8.12-3.42 (5. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.91) 10..55) 1.86 (1.83) 1.33-7.24) 75th 2.56 (4.71 (1. paralysis.91) 2.06 (1.33 (1.74) 1.6) 10.78 (1.58 (1.52 (5.46 (1.01) 3.44-6..80-6.01) 3.49 (1.24 (1.09-2.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.88) 6.55 (4.47 (1.6) 9.91) 1.44 (5.05-8.56) 5.92-2.42-2. 2006.86 (3.48 (2.59-2.94-14.5 (6.

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

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Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Ryan PB. Meeker JD.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Sanderson WT. Barr DB. Seidler FJ.31 Suppl 1:98-104. J Expo Anal Environ Epidemiol 2005. 1999.6-trichloro 2-pyridinol in their everyday environments. Chlorpyrifos. Cometa MF. Irish R. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Barr DB. Chlorpyrifos: pharmacokinetics in human volunteers. et al. 2921-882. Reid TM. Barr D. Pesticide residues in urine of adults living in the United States: reference range concentrations. Bruun D. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Adgate JL. 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Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Jett DA. Weltzien E. Available at URL: http://ntp.93(1):105-113. Bravo R. Nolan RJ. Bucelli R.nih. Yang D. Ricceri L. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Hines CJ. Available at URL: http://www. J Expo Anal Environ Epidemiol 2000.9(5):494-501. Curwin BD.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. 4/7/09 Koch HM. 4/7/09 Perera FP. Environ Health Perspect 2006a. Baker S. Barr DB. Tate CA.111(2):201-205. chlorpyrifos. Seidler FJ. Environ Health Perspect 2006.51(1):53-65. J Expo Anal Environ Epidemiol 2005.niehs. et al. Ryan L.org/documents/jmpr/jmpmono/ v99pr03.207(2):112-124.112(10):1116-1124. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Kinney P.inchem.10(4):327-340. 2005.5. Hill RH Jr. Scand J Work Environ Health 2005. MacIntosh DL.108(4):293-300.73:8-15. gov/ntpweb/index. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Zhang J. Executive summary of safety and toxicity information. Toxicol Sci 2006. Environ Res 1995. Alexander BH.

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

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

< LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 141 . see Data Analysis section) for Survey year 01-02 is 0.210) < 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 .670 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.2. 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 .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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (<LOD-.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.200 (<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 .S. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.270) < LOD 659 701 920 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.380 (<LOD-.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.

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

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. Fourth National Report on Human Exposure to Environmental Chemicals 143 . population from the National Health and Nutrition Examination Survey.45 (<LOD-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1842 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. and particularly when it was ingested in granular form. 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. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. Most granular formulations. Inhalational and dermal routes of exposure can be significant for pesticide applicators.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).S. 2007). 2004). 1998. in some pest strips. diazinon produced wild bird kills before use restrictions were in place. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. It is toxic to birds. 1998). 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. Diazinon is not well-absorbed through the skin. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. Survey Geometric mean (95% conf. USGS. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. which may vary for some chemicals by year and by individual sample. an organophosphorus insecticide that is used to control insects on nuts. Once absorbed. in the past. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. Estimated intakes from diet and water do not exceed recommended intake limits (U. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. and other metabolites. < LOD means less than the limit of detection. aerial. 2004). diazinon cannot be sold for residential use.7. vegetable. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. fruits.EPA. but is rapidly absorbed orally (IPCS.S. since 2004. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. diazinon was widely used in residential and garden application. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. and forage crops. Before these restrictions.S.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. but these uses have been phased out.EPA. seed and foliar applications are planned to be phased out (U.49 (<LOD-2. Prior to 2000.2 and 0. It is also used for cattle ear tag applications to control flies and ticks and.

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

1992-2001. International Programme on Chemical Safety-INCHEM (IPCS). Barr DB. Liu F. Drobnis EZ. Diazinon. Geological Survey (USGS). Third National Report on Human Exposure to Environmental Chemicals. 2006). The Quality of Our Nation’s Waters. Rajendra W. References Anthony J. Environmental Health Criteria 198. Olsson AO.S. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Drug Chem Toxicol 1986. 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. Barr DB. Ann Occup Hyg 2006. Needham LL. 2007 [online].111(12):1478-1484. EPA 738-R-04-006.50(5):505-515. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids.gov/circ/2005/1291/. Interim reregistration eligibility decision (IRED. May 2004. Biochem Pharmacol 1992. Environ Health Perspect 2003. Centers for Disease Control and Prevention (CDC). 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . 1998..10(6 Pt 2):789-798. Noisel N. Available at URL: http://pubs.Organophosphorus Insecticides: Specific Metabolites 2005). 1/14/09 U.usgs. Sadowski MA. Available at URL: http://www. Oloffs PC. Cocker J. Anal Bioanal Chem 2003.9(2):117-131. et al. Atlanta (GA). Environ Health Perspect 2006. Pewnim T.gov/ oppsrrd1/REDs/diazinon_ired.S. U. Seifert J. Barr DB. Brunet RC. March 2006.134(1-3):105-113.inchem. EPA). 2006). Banister EW.44(11):2243-2250.htm. In a small number of men visiting fertility clinics in Missouri and Minnesota. Banister E. Carrier G. Jones K.114(2):260-263. Semen quality in relation to biomarkers of pesticide exposure. Effect of sublethal levels of diazinon: histopathology of liver. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al.S. Mason HJ. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects.37(4):501-507.376(6):808-815. Fenske RA. Nguyen JV. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Toepel K. 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.. Bouchard M. J Expo Anal Environ Epidemiol 2000. 4/7/09 Lu C. Redmon JB. Bravo R. In 23 children. Dumas P. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Swan et al. Swan SH. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Kruse RL. Diazinon. Study for Future Families Research Group. Beeson MD. Bull Environ Contam Toxicol 1986. Barr DB. Environmental Protection Agency (U. Pesticides in the Nation’s Streams and Ground Water. 2005. revised February 15. Toxicol Lett 2002.pdf. Available at URL: http://www. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Irish R. Garfitt SJ.org/documents/ehc/ehc/ehc198. Oloffs PC. Driskell WJ. Baker SE.epa. In 54 Canadian greenhouse workers.

S. gardens. see Data Analysis section) for Survey year 99-00 is 2. Once they are absorbed. and other metabolites. malathion has low acute toxicity. phosphorothioates such as malathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticide. Metabolism of malathion leads to the formation of malathion monocarboxylic acid. 2003).S. In addition to being a metabolite of malathion. 2006). 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. cholinergic effects. as well as lawns. 2000). malathion dicarboxylic acid. 146 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf. and producing acute symptoms such as nausea. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). 2006). It is moderately to highly toxic to fish.Organophosphorus Insecticides: Specific Metabolites Malathion CAS No. which is an organophosphorus insecticide that is used on a wide variety of agricultural crops. Human health effects from malathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. About 31-35% of oral doses of malathion are excreted in the urine as malathion monocarboxylic acid (Krieger and Dinoff. Most of the estimated 15 million pounds used annually are applied to cotton (U. inhalational. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. It is highly toxic to aquatic invertebrates and rare fish kills have been reported from wide area applications onto surface waters and runoff into waters. which may vary for some chemicals by year and by individual sample. usually only a small fraction of the crop is treated. resulting in excess acetylcholine at nerve terminals.80 (<LOD-5. Compared with other organophosphorus insecticides.EPA. malathion and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. Malathion is rapidly eliminated from the body within 12-24 hours (Bouchard et al.64.S. in fruit fly control. Malathion is slowly absorbed through the skin.EPA. weakness. or oral routes (U. and in government programs such as the USDA’s Boll Weevil Eradication Program. but is more rapidly and efficiently absorbed via ingestion. Limited general population exposure occurs through the diet. 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. 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. depending on the species. the detection of malathion dicarboxylic acid in a person’s urine may also reflect exposure to the environmental degradate. 2007). and seizures. shrubs. 121-75-5 General Information Malathion dicarboxylic acid is a metabolite of malathion. vomiting. ornamental trees. Malathion is infrequently detected in groundwater sampling (USGS. Thus. < LOD means less than the limit of detection.. malathion dicarboxylic acid can also occur in the environment from the breakdown of the parent compound. paralysis. It is registered for use in public health mosquito control. Pesticide applicators and agricultural workers can have higher exposures via dermal. and plants. It has a short halflife in soils and water and is not considered persistent in the environment. Malathion is also used medically in lotion form (0.5%) to kill body lice. population from the National Health and Nutrition Examination Survey. At high doses. When malathion is used on food or feed crops.

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

15(2):164-171. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Available at URL: http://www. Irish R. Arch Environ Contam Toxicol 2000. 4/7/09 Kissel JC. Weltzien E.Organophosphorus Insecticides: Specific Metabolites References Adgate JL.S. Am J Epidemiol 1990.445(2):275-283. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Samuel O. Environmental Protection Agency (U. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Harley K. Mutat Res 2002. Flessel P.S. Jewell NP. EPA 738-R06-030.22(1):7-17. htm. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Geological Survey (USGS). Lu C. Pluth JM. Cancer Res 1996. Malathion (addendum). Neutra R.77:1009-1010.org/documents/jmpr/jmpmono/v2003pr06. Brunet RC.132(4):794-795. et al. Environ Mol Mutagen 1993. Ryan PB. Centers for Disease Control and Prevention (CDC). Atlanta (GA). Pesticides in the Nation’s Streams and Ground Water. Prasad SB. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Environ Health Perspect 2006.usgs.514(1-2):223231. Reproductive outcome in women exposed to malathion. Environ Health Perspect 2004. 6/1/09 U. Freeman NC. Hooper K. Bouchard M. Third National Report on Human Exposure to Environmental Chemicals.73(1):182-94. Eberly LE.inchem. Petitti D.gov/oppsrrd1/REDs/ malathion_red. Available at URL: http://pubs. O’Neill JP. Clayton CA. Kedan G. March 2006. Toxicol Sci 2003 May. Jaloszynski P. The Quality of Our Nation’s Waters.gov/circ/2005/1291/. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Hammerstrom KA. Nicklas JA. Needham LL. Quintana PJ. Eskenazi B. Available at URL: http://www.38(4):546-553.109(6):583-590. Barr DB. revised February 15.epa. Barr DB. J Expo Anal Environ Epidemiol 1999. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Bradman A. Hertz-Picciotto I. Bravo R. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Gosselin NH. Erratum in: Toxicol Sci 2003 Aug. Szyfter K. Rappaport E. Lioy PJ. Albertini RJ. MacIntosh DL. Giri A. Griffith W. Grether JK. A longitudinal investigation of selected pesticide metabolites in urine. Barr DB. Reregistration eligibility decision (RED) Malathion. International Programme on Chemical Safety-INCHEM (IPCS). Carrier G. Environ Health Perspect 2001.pdf. Toepel K. Malathion deposition.74(2):following table of contents. 2007 [online]. Harris JA. Blasiak J.S. Krieger RI. July 2006. Am J Public Health 1987. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. U. Dumoulin MJ. Dinoff TM. Lu C.9(5):494-501. et al. Curl CL. Giri S. Barr DB.114(2):260-263. 2005. Fenske RA. EPA).56(10):2393-2399. Mutat Res 1999. metabolite clearance. Thomas D.112(10):1116-1124. Genetic toxicity of malathion: a review. Swan SH. et al. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. 1992-2001. J Expo Anal Environ Epidemiol 2005. Goldhaber M. Sharma GD. and cholinesterase status of date dusters and harvesters in California. Trzeciak A.

first registered in 1948.60-5.0) 3.10) 4.47) 2. and to a lesser extent.70) 2.90-11.57-4.91-3. was once a restricted-use insecticide with limited applications on certain agricultural crops.44) 2.20 (<LOD-2.28 (1.61) < LOD 1.8 and 0.10 (3.26 (1.298-00-0 Ethyl Parathion CAS No. and eliminated rapidly from the body after absorption (Kramer et al.860 (<LOD-1.0) 3..S.50 (1. 2000).58) 3.20 (2.22-3. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.46 (3.10-11. It had been applied to cotton.50) 3.12) < LOD < LOD 1.00 (2. and aquatic invertebrates.57) 1.27) 2. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. Fourth National Report on Human Exposure to Environmental Chemicals 149 .50) 2. 2003).45) 5.S.01) 4.60) 1.910) < LOD < LOD < LOD 1.92-2. < LOD means less than the limit of detection. 2006).30-3.40-4.02-6.15-3.32 (1.70 (<LOD-3.60-24. Increased risk of exposure via dermal.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .50-14.30 (2. 2007).40) 4.32-1.50) 3.70-6.21 (2. Morgan et al.70-3.13-1.0) 2.28-4.72 (3.80 (1.90 (1.85 (2.S.40) 1.16) < LOD 1.37) 2.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.0 (3. In the 1990s. with limited applications in agriculture.28 (1.69 (2. binds tightly to soils resulting in low leachability.40-4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.62 (1.EPA.50 (1.48) 90th 2.70-6.10 (3.69) 4.71 (3.50) 1. and oral routes can occur in pesticide and agricultural workers (Muttray et al.05) 4.71 (2.18-3.37-4. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate. Estimated intakes from diet and drinking water have been below recommended limits. Methyl parathion has low water solubility.11) 2. all registered uses were voluntarily cancelled (U. which may vary for some chemicals by year and by individual sample..790 (<LOD-.37-2.70) 2.30 (1. fish.770 (. pulmonary. on cereal grains. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.21-1.80) 2.09-1.1.70 (3.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .730 (<LOD-.10 (<LOD-6.00) 3.66 (2.10-1.11-4. population from the National Health and Nutrition Examination Survey.990-1.60 (4.90-9.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . Methyl parathion use is highly restricted. more slowly absorbed through the skin.0) 3.32-1.92) 5.40-3.70-3.60-19. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS. Both are toxic to birds.41-4.01) 695 660 518 679 603 941 Limit of detection (LOD. Methyl parathion is not registered for residential use in the United States.50 (2. methyl parathion was rapidly absorbed after ingestion.50-9.70-6.50 (1.10) 22.33) 2.45 (1. peak domestic use was as high as 5-6 million pounds per year.0) 3.89 (2.910) < LOD < LOD .70 (2.50 (2.34 (3..70 (2.80 (2.30-5.0) 3. ethyl parathion. In animal studies.32-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1977). and has a short half-life in soils and on plants.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. Methyl Parathion.40 (1.74) 5.910) < LOD . but by 2003.20-5.37-4.20) 5.36-1.850) < LOD . Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.50 (1.67) < LOD 1. Survey Geometric mean (95% conf. and of the chemical nitrobenzene.EPA.33 (1.49 (1. Ethyl parathion. 2002. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.67 (1.700 (<LOD-.80 (2.79) 4. Given its limited use.61) < LOD 1. Once absorbed.19 (.30-16.70 (2.300-.01-4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.40) 2.940 (<LOD-2.60-36.0) 4. Many previous registered agricultural uses of methyl parathion have been cancelled (U.00 (2.70) 2.

9) 1.400 (<LOD-.970 (.84) 3.30-1. but lists ethyl parathion as a possible human carcinogen.35-3.44-3.17) .60) 2.38-3. U.01-3. EPA at: http://www.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .790-1. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. 1995.67 (3.97 (<LOD-4.. paranitrophenol.25 (2.16-4.14-3..21-21.43) 4.790-.930 (.39) 1.680 (<LOD-1. Jaga and Dharmani.640) < LOD < LOD 1. Zurich et al.530) < LOD < LOD < LOD . 2006.89 (2.26) 17.04 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07) 2.850-1.15) 3.S.930 (. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS. teratogenic.05) 4.500) < LOD < LOD .78-2.87 (1. and other metabolites.78 (2.55 (<LOD-3.25) 1.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . 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.540) < LOD .04) 1.08 (1.20) .00 (1.71) 1.720-1. vomiting.96 (1.59 (1.31-3. Lores et al.89 (2.48-4.S.720 (<LOD-.93 (2.29 (2.cdc. The metabolite.33-6.72-2. Karanth and Pope et al.830-1.33-3.13-12.. population from the National Health and Nutrition Examination Survey.80 (1. gov/toxpro2..61) 4.97 (2. 2006.56-2.310-. 2005. accidental exposure.30) 3. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.10) 90th 2.950) < LOD . 1991).78) 2.. ethyl parathion. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. In large doses. 1990.88 (1. 1978.94-47.3) 2. WHO.01 (.S. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.07 (1.26 (1.15-10.08-3. resulting in excess acetylcholine at nerve terminals.21) 1. Additional information about external exposure (i.97-10. 2004).01 (2.92 (2.730-1. Slotkin et al.11) 1. In addition to being a metabolite of methyl and ethyl parathion..57-2.html and from U.39 (1. 2003. weakness.20 (3.35-3.880 (.08) < LOD .55) 2.2) 2.Organophosphorus Insecticides: Specific Metabolites Metabolites”). and unintentional acute or chronic high-level occupational exposure (Hill et al.17-4.00 (1.690-1.91) 1.70) 3.77-7.98-7.870) < LOD . Orsorio et al.82) < LOD .980 (.epa.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.82 (2.79 (1. does not inhibit acetylcholinesterase enzymes.430 (.840 (.57) 6.2) 2.940 (<LOD-1.33-3.440 (<LOD-. and producing acute symptoms such as nausea.73 (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 .10 (1.60 (1.09) 2. Thus.90 (1.370 (<LOD-.86 (2. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.41-2.7) 3.94-4.31) < LOD . and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. and seizures.00) 2. environmental levels) and health effects is available from ATSDR at: http://www.970 (.800-1.57-7. gov/pesticides/.78-2.80 (1.29) 1.23) 1.96 (1.60-2.1) 2. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS. cholinergic effects.67-2. 2004). Methyl Parathion.atsdr. Survey Geometric mean (95% conf.11-4. 1995). Methyl parathion is not considered genotoxic.83 (1.13) 4.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.91 (1.71 (1. At high animal doses of methyl parathion. Parathion and methyl parathion have high acute toxicity in animal testing.20) 3. paralysis. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.37-1.4 (3..29) 2.76-14.88) 1..e.EPA considers methyl parathion unlikely to be carcinogenic to humans.44-3.79) 1.95) 1. 150 Fourth National Report on Human Exposure to Environmental Chemicals . methyl parathion.

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. J Expo Anal Environ Epidemiol 2005. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Rev Environ Health 2006. A study of 13 children from an agricultural region of Washington State reported median levels that were more than threefold higher than median levels in the NHANES 1999-2000 subsample (Kissel et al.25(5):599-606. Dharmani C. Arch Environ Health 1978. Role of individual susceptibility in risk assessment of pesticides. Giordano G. Pesticide residues in urine of adults living in the United States: reference range concentrations. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Jewell NP.. Clark JM. 2002. Eskenazi B.. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Barr DB. Baker SE.110 Suppl 6:1075-1078. Hill et al. Karanth S. Leng G. Wellman SE. Lores EM. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. 2004). Centers for Disease Control and Prevention (CDC). 1995. Bradman A. Moseman RF. Toxicology 2005.. 2002.112(10):1116-1124..org/documents/jmpr/jmpmono/v95pr14. 2005. Lewalter J. 2005. J Anal Toxicol 1990. Shealy DB. Parathion-Methyl (addendum).21(1):5767. Laboratory investigation of a poisoning epidemic in Sierra Leone. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.110 Suppl 6:1085-1091. Kedan G. Head SL.S. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.15(2):164-171.. Environ Health Perspect 2004. Runkle KD. 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. Environ Health Perspect 2002. Griffith W. and many residents were symptomatic (Barr et al. 2002). McClure PC. population (Olsson et al. Chicago area methyl parathion response. Pesticide workers may have much higher levels following pesticide applications. Turner WE. 1995). Arch Environ Contam Toxicol 1977. DiPietro E. and levels were similar or slightly lower that those in a small convenience sample of the U. Bradway DE. Fourth National Report on Human Exposure to Environmental Chemicals 151 . et al. 2005). Methyl parathion: an organophosphate insecticide not quite forgotten. Pope C. Rubin et al. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Kramer RE. Third National Report on Human Exposure to Environmental Chemicals. CDC. Alley CC. Moomey CM.71:99108. Atlanta (GA). Pathak S. McCann et al. Barr DB.inchem. Curl CL. Weltzien E. Baker RC. et al. et al. Occup Environ Med 1999. Available at URL: http:// www. Rockhold RW. Baker S. Hryhorczuk DO.6(2-3):159-173. 2005).9:311-320.33(5):270-276. J Biomed Sci 2002. Cline RE. Costa LG.14(4):213-216.. Lu C. 1999). Environ Res 1995. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. et al. Gregg M. Guizzetti M. Barr JR. 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. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. et al. Hill RH Jr.215(3):182-190. 2005. McCann KG. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Bailey SL.56(7):449553. Neurotoxicol Teratol 2003. Morgan DP. Head SL. References Barr DB. International Programme on Chemical Safety-INCHEM (IPCS). Harley K. In a study of workers who handle parathion.. Kissel JC. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. a range of values several hundred times higher than levels found in the U. 4/7/09 Jaga K. Needham LL. Hetzler HL. Ashley DL. Lin LI. oral or dermal administration.5 mg (500 µg)/g creatinine for workers at the end of shift. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Environ Health Perspect 2002. ACGIH recommends a BEI of 0.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure.S. Hill RH Jr. Barr DB.htm. Slach EF. general population (CDC.

Rubin C. Kieszak S. et al.162(2-3):219-224. Toxicol Appl Pharmacol 2004. 1992-2001. 5/19/09 Zurich MG. Toxicol Lett 2006. Esteban E. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Investigation of a fatality among parathion applicators in California. Environmental Protection Agency (U.usgs. Available at URL: http://pubs. Anal Bioanal Chem 2003.pdf. 1/14/09 U.S.epa. Available at URL: http://www. WHO/SDE/WSH/03. EPA).114(10):1542-1546.Organophosphorus Insecticides: Specific Metabolites Muttray A. Environ Health Perspect 2002. Levin ED. EPA). Available at URL: http://www. Backer G. U. 6/1/09 World Health Organization (WHO). Sadowski MA. Jung D. Dunlop B. Mengle DC.epa.S. Schilter B. Honegger P. Environ Health Perspect 2006. EPA-738-FOO-009. September 2000.110 Suppl 6:1047-1051. 2004. revised February 15.pdf. Hill RH Jr. Hill G. 2007 [online]. Pesticides in the Nation’s Streams and Ground Water. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Environmental Protection Agency (U. Case No.04/106. March 2006. Seidler FJ. gov/oppsrrd1/REDs/methylparathion_ired.S. R. Ryde IT. 0153.20(4):533-546. Rosenberg J. May 2003. 1995-1996. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. The Quality of Our Nation’s Waters.E. Nguyen JV. Am J Ind Med 1991. Methyl parathion in drinking water.S. Slotkin TA. 1/12/07 U.gov/oppsrrd1/REDs/factsheets/0155fct. Barr DB. 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. Ames RG. Facts. pdf.int/water_sanitation_health/dwq/chemicals/ methylparathion.S.gov/circ/2005/1291/. Ohio. Osorio AM.D.376(6):808-815. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Tate CA. External and internal exposure of wine growers spraying methyl parathion.who. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Yacovac R. Geological Survey (USGS). Costa LG. Ethyl parathion. Monnet-Tschudi F. Letzel S. Available at URL: http://www. Olsson AO.201(2):97-104.

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

610 (<LOD-1.2.780 (<LOD-1.210-.15) < LOD . Survey Geometric mean (95% conf.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .760 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.840) 669 687 929 Limit of detection (LOD.210 (<LOD-.470 (.410 (<LOD-1.00) 669 687 929 < 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.670 (<LOD-1.430 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . < LOD means less than the limit of detection.17 (.300-1.07) .27) .580-1.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .700-1. 154 Fourth National Report on Human Exposure to Environmental Chemicals .840 (.21) < LOD .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .210-1.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200-.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.780 (.94) .850 (.820) < LOD < LOD .780 (.250 (<LOD-.31) .780 (<LOD-1. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .740-1. see Data Analysis section) for Survey year 01-02 is 0. which may vary for some chemicals by year and by individual sample.950) < LOD < LOD 1.55) .500 (. Survey Geometric mean (95% conf.64) .680 (<LOD-.770) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .700-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .740 (. 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.S.

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

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

Kunimatsu T. Zhao RC. Int J Hyg Environ Health 2002. Caudle WM. J Reprod Dev 2004. Lee SJ. Ranft U.1/15/09 Aziz MH. Varoli FM. Kunimatsu et al.300(3):161-165.cdc. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Biochem Biophys Res Commun 1998. Moniz et al.atsdr. Richardson JR. Go V. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays.. Bull Environ Contam Toxicol 1999.205(6):459-472. 2003. 2006. Cruz-Casallas PE.50(2):245-255. References Agency for Toxic Substances and Disease Registry (ATSDR). Kim IY. epa. 2002). Leng G. 2001. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Lewalter J. Adhami VM.27(12):1273-1283. Song L. et al.8(1):197-202. Sunami O. Lazarini CA. Wieseler B.gov/toxpro2. 2001. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Shin JH. In developing rodents. Shukla Y. EPA at: http://www. 1999. Yang J.. Salzgeber SA. 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.108(1):78-85. Kamita Y. Fredriksson A. 2004. WHO. Pauluhn J. Garey and Wolff.. Berger-Preiss E. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Go et al. Kim HS. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. motor activity. Elwan MA. Leng A. and permethrin) in the Hershberger and uterotrophic assays. Moniz AC.gov/pesticides/ and from ATSDR at: http://www.html.27(4):609-614. Yamada T. Available from URL: http://www. Levsen K.. bioallethrin and deltamethrin. Neurotoxicol Teratol 2005.251(3):855-859. Elwan et al.. Miller GW.107(3):173-177. 2000. 2003. Garey J. 2005). Okuno Y. 2005). Kim et al. hypersensitivity. Agrawal AK. Bernardi MM. and seizures (ATSDR. et al. Wang SL. Idel H. Additional information about pesticides is available from U. Eriksson and Fredriksson. 1991. Leng G.. Regul Toxicol Pharmacol 2002. Shaw IC. Toxicol Appl Pharmacol 1991. Lazarini et al. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Ray et al. Florio JC. Ose K. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate.atsdr. cdc.. Neurotoxic effects of two different pyrethroids. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Lemonica IP. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Sugiri D. Hu JY.S. Pyrethroid pesticide-induced alterations in dopamine transporter function.211(3):188-197. neurochemical changes in cholinergic. 2003. Eriksson P. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO.gov/toxprofiles/ tp155. salivation. 2002.8(1):18-21. Idel H. Seth PK. Shafer.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. and striatal dopamine levels in male and female rats. 2003.. Kim TS. Bernardi MM. Hu et al. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Neurotoxicol Teratol 2001. Xenobiotica 1997. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. 2006. Toxicological profile for pyrethrins and pyrethroids. Leng G. et al. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. In California. Generally. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Indoor pyrethroid exposure in homes with woollen textile floor coverings. 2005).. 2005). September 2003.23(6):665-673. Pogo BG..html. tremor. choreoathetosis. Environ Health Perspect 1999. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Kang IH. Chen JH. Thomson BM.. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al.. Toxicol Appl Pharmacol 2006. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Soderlund et al. dopaminergic. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Kuhn K.. McCarthy AR. Neurosci Lett 2001. Kuhn KH. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Estrogenicity of pyrethroid insecticide metabolites. Guillot TS. McCarthy et al. Spinosa HS. Garey J. fenvalerate. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Wolff MS. 2002). et al. Abell AD. 2006). 1998.62:101-108. J Environ Monit 2006. Wolff MS.35(2 Pt 1):227-237.

who. Forshaw PJ.htm. Toxicology 2002.usgs. Revised February 25.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Marsh JR. Sheets LP. June 2006a. Pyrethroid illnesses in California. Available at URL: http://whqlibdoc. Pyrethroid insecticides: poisoning syndromes. Geological Survey (USGS).S. June 2006b. Pesticides in the Nation’s Streams and Ground Water.S. Environ Health Perspect 2005. World Health Organization (WHO). EPA). Available at URL: http://www. 19962002. Xenobiotica 1992. Laird WJ. 2005. Permethrin.S.10. Crofton KM.22(8):983-991. Available at URL: http://www. EPA).gov/oppsrrd1/REDs/ factsheets/permethrin_fs. resmethrin. March 2006.113(2):123-136.epa. and therapy. Reregistration Eligibility Decision for Cypermethrin.S. Clark JM.Pyrethroid Pesticides Ray DE.epa. Environmental Protection Agency (U. 5/26/09 Woollen BH. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). Piccirillo VJ. 5/26/09 U. April 2002.gov/oppsrrd1/REDs/cypermethrin_red. synergies.htm. EPA).38:95-101. Mullin LS. et al. Rev Environ Contam Toxicol 2006. Available at URL: http://pubs.S. J Toxicol Clin Toxicol 2000. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Shafer TJ. 1992–2001. Environmental Protection Agency (U. Environmental Protection Agency (U. U. Soderlund DM.pdf. 5/26/09 U. Available at URL: http://www. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.gov/ circ/2005/1291/.S. O’Malley M. 2007.171:3-59.S.epa. Spencer J. Lesser JE. Pesticide and Evaluation Scheme. Safety of pyrethroids for public health use. Sargent D. sumithrin synthetic pyrethroids for mosquito control.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Meyer DA. pdf.186:57-72. 5/26/09 U. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .

Pyrethroid Pesticides Cyfluthrin CAS No. 2001) showed that urinary levels of 4-fluoro-3-phenoxybenzoic acid at the 95th percentile ranged from either slightly higher or lower than the detection limit in the U. Thus. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002. 2003). Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0.. Cyfluthrin is rapidly metabolized and eliminated from the body. 2004). 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. 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. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment. Leng et al.. most of which were dermal and respiratory irritations (Spencer and O’Malley. representative 2001-2002 NHANES subsample (CDC. 2006). 2005.68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin.2 μg/L) in the U...S. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. 2003). 2006) and 1177 urban adults and children (Heudorf et al. Following an indoor application exposure. Studies in Germany of 396 children and adolescents (Becker et al. 2005). Urinary levels for adults and children in these studies were similar (Heudorf et al. 2005). the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. representative subsample in NHANES 2001-2002 (CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.95 µg/L... 2003). 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. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. Baker 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. 2001. Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. Fourth National Report on Human Exposure to Environmental Chemicals 159 .

2.S. Survey Geometric mean (95% conf.2 and 0. which may vary for some chemicals by year and by individual sample.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. < LOD means less than the limit of detection. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 160 Fourth National Report on Human Exposure to Environmental Chemicals .

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. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 . population from the National Health and Nutrition Examination Survey.

Int J Hyg Environ Health 2006. Centers for Disease Control and Prevention (CDC).Pyrethroid Pesticides References Baker SE. Kolossa-Gehring M. Berger-Preiss E.46(3):281-288.206(2):85-92. Hoppe HW. et al. Bernard CE. Heudorf U. Sugiri D. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Pyrethroid illnesses in California. Int Arch Occup Environ Health 2004. Olsson AO. O’Malley M. Int J Hyg Environ Health 2003. Schulz C.109(3):213-217. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.186:57-72. 19962002. Becker K. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Atlanta (GA). Barr DB. Seiwert M. Angerer J. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. 2005. Heudorf U. Arch Environ Contam Toxicol 2004. Environ Health Perspect 2001. Int J Hyg Environ Health 2006. Rev Environ Contam Toxicol 2006. Angerer J. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Leng G. J Expo Anal Environ Epidemiol 2003.209(3):221-233. Heudorf U. Ranft U. Drexler H. Ball M. Williams RL. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.13(2):112-119. Krieger RI. Third National Report on Human Exposure to Environmental Chemicals. Angerer J. Idel H.77(1):67-72. Hadnagy W. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Angerer J. Spencer J. Butte W.209(3):293-299.

730 (.and trans-isomers.2-dichlorovinyl)-2.580) 1.680-3.80) .220-.600-1. trans-cypermethrin.270 (.340-.370-.2-dichlorovinyl)-2. which may vary for some chemicals by year and by individual sample.2-dichlorovinyl)2. The presence of cis-3-(2.570 (.890 (.440 (. Survey Geometric mean (95% conf.68) .240) .270 (.or trans-3-(2.300-.250-.210-.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.280-.740) 1.790-1.610) .790-1.340) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. population from the National Health and Nutrition Examination Survey.140 (.960 (.120-.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . cis-permethrin.640 (.11) .600) .280 (.510 (.880 (. The chemical trans-3(2. and trans-cyfluthrin.160 (.210) .43) .730 (.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.68 (.200) .220) .650-1.2dichlorovinyl)-2.680 (.820 (.53) .Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.300-.700) .380) .780) .740-1. 1985. cis-cypermethrin.670-1.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.200 (.490-.1 and 0.08) .260 (.200) < LOD < LOD < LOD .460 (.670-2.570-.710) .2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.15) . Fourth National Report on Human Exposure to Environmental Chemicals 163 .270 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .180 (.200-.210) 90th .2-dichlorovinyl)-2.110 (<LOD-.. < LOD means less than the limit of detection.920) 1.630) . In the body. trans-permethrin.160 (<LOD-. Kuhn et al. but can also reflect exposure to trans-3(2.2-Dichlorovinyl)-2.510 (. 1985.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.910-5.250 (.1.35) .54) .330 (.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.490-1.670 (.400-.430-.120-.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .44 (. transcypermethrin and trans-cyfluthrin.550) .230) .340) .950-2.110-.35) 1.770-1.630-.2-dichlorovinyl)- CAS No. 52315-07-8 CAS No.380 (.120-.140 (<LOD-.68359-37-5 Cypermethrin Permethrin CAS No.330) .170 (.150 (.12 (.710-1..740-2.21) .155-.460-1.300 (.180) . more of the trans-metabolite than Urinary cis-3-(2.580-1.470-1.790) . cis-3-(2. Generally.770) . 1999).S.110-.530 (.890 (.50) .28) 671 680 518 701 591 957 Limit of detection (LOD.47 (.410) .350) .13 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.77 (.220-.460-.68) .262) * * * < LOD < LOD .900 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 1999).240) .2dichlorovinyl)-2.740 (.120-. the presence of trans-3-(2.490-.510 (.370 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-.470 (.500 (.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis. ciscypermethrin and cis-cyfluthrin.07 (.500 (.410) .32) .300 (.200-.160 (.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.220-.600 (. but it can also reflect exposure to cis-3-(2.610) .200) . Similarly.24) 1.790 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.380-.220-.420-. Biomonitoring Information Urinary levels of cis.202 (.270-.490-1.520) . Cyfluthrin.110-.630 (.730 (.850 (.380-.380-.310) . Kuhn et al.690) .670-1.10) 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 .870) 1. and ciscyfluthrin.630) .

290-.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .S. representative NHANES 2001-2002 subsample (CDC.780) 1.170 (. Studies in Germany of 396 children and adolescents (Becker et al. 2004).340-.67) .640-. 2006).250 (<LOD-.11) .590 (. 2002).250) .2-dichlorovinyl)-2.230 (.530 (.370-.530 (.540) .300) .2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.150-. median urinary levels of trans-3-(2.180 (. post- Urinary cis-3-(2. Lu et al.240 (<LOD-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2001) showed urinary levels of cis.33) .920 (.420 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.750 (.600 (.200-.350 (. Schettgen et al.270-..37) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In these volunteers. Other studies have provided evidence that urinary levels of cis. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.260-.900 (.840 (.280 (.390-.250-.250) . Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.300) .160 (<LOD-.130-.430-.370-.260 (.340) . 2005).33 (.680-1.250) 90th . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.440-.550) .250-.220 (.440 (.080-.104-.2-Dichlorovinyl)-2.. 2005).700-2.320) .380-.370-. urinary levels of cis-3-(2.220) ..260 (.190) .710-3.300 (. 2006.. 2001.290) .12-2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.680 (.300-.400 (.640-1.560) .340) .170 (.640 (.710 (.180-.31) . 2005) In a small group of indoor pest-control operators.290 (.150-.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al...640-1.560) 1.120 (.59) .182) * * * < LOD < LOD .190 (.200) .550-1.580) .11 (.200-.230-.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 .280-.170) < LOD < LOD < LOD .250-.890 (. 2002).Pyrethroid Pesticides 2.260 (.430-1.21) .200 (.440-.138 (.49) .12 (.750-1.360-1. 2006).450-.210-.150-.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.270) . 2005)..11) 1. In a study of urban residents in Germany (Berger-Preiss et al.810 (. In a study of volunteers. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .390-.2dichlorovinyl)-2. 2004. 2006.220 (.690-1.270 (.03) 1. 2003).and trans-3-(2.300 (.380) . 2005).700) .and trans-3(2.880) ..2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.640) 1.890) .580-1.550) . urinary trans-3-(2.290) .320-.260) .230-.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.29 (. In the same residents..S.80) .2-dimethylcyclopropane carboxylic acid did not increase.230-.190) .470-1.24) . Survey Geometric mean (95% conf.140-.11) .830) .67 (.430 (.590) .2-dichlorovinyl)-2.780 (.550-1.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.410) . the median and 95th percentile of urinary levels of cis-3-(2.800 (.. Cyfluthrin.450-1.510-1. 2006) and 1177 urban adults and children (Heudorf et al.380 (.540 (.500 (.59) .350) .550 (.400-1.840 (.2-dichlorovinyl)-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.540 (.270) .2-dichlorovinyl)-2.440 (.2dichlorovinyl)-2. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.570) . 164 Fourth National Report on Human Exposure to Environmental Chemicals .390 (.450 (. 2003).700) .59 (1. population from the National Health and Nutrition Examination Survey..680-1.

66) 691 680 518 690 595 954 Limit of detection (LOD.420 (<LOD-.81) 2. The maximum post-application urinary levels.94 (1.460-.810-1.410 (<LOD-.59 (1.54 (1.410-.2dichlorovinyl)-2.610) 1.14-2.830-1.820) .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 .670) .03-1.700) .23 (. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.48) 4.940 (.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .400-.11-2.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.08) 1.90) 1.560 (.22 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.39-5.68) 1.37 (1.55-5.20 (.470 (.97-11.95) 3.840-1. population from the National Health and Nutrition Examination Survey.26 (.60) .85) 4.500-.560 (.560 (.550 (.64-4. which may vary for some chemicals by year and by individual sample.77) 2.50 (1.470 (<LOD-.11-1.19) 1.42 (2.800-1.520) .19 (3.910-1.60-4.570) 90th 1.77 (1.68-2.63) 1.27 (1.400 (<LOD-.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .4.39 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.700-1.14-6.91 (1.08-6.07 (1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.35) 1.55-4. Urinary trans-3-(2.56) 2.730) .Pyrethroid Pesticides application median urinary levels of summed cis.69 (1.680-1.2-Dichlorovinyl)-2.12-6.970 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.710 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.25 (1.01 (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.440 (<LOD-.17 (.460-.20 (. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.620) < LOD 2. 2005).03-1.4 and 0.69) 1. Finding a measurable amount of cis.660) 1.670) .58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .S.2-dichlorovinyl)-2.07-3.68) 1.49-3. Fourth National Report on Human Exposure to Environmental Chemicals 165 . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3. trans-Cypermethrin.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.860) .10) 2. however.60) 1.530) .89 (2.77) 1.410 (<LOD-.76-3.5) 2.500) .68-3.520-.49-3.17 (. < LOD means less than the limit of detection. Biomonitoring studies on urinary levels of cisor trans-3-(2.or trans-3-(2. Survey Geometric mean (95% conf.62 (1.500 (.76-4.54) 4.84 (1.23) 2.410-.68) 2.25-3.and trans-3-(2.95) 2.16) 1.2-dichlorovinyl)-2.55-3.580 (.17-1.28 (1.43) 2.760) .41 (1.56 (1.01) 4.14) 1.490 (<LOD-.42) 1.08-4.49-5.850-1.7) 2.480-.09 (.13) .920-1.40 (1.490-1.41-14.780 (.66) .63) 1.910-1.56 (1.56) 2. 2005).750) .28 (2.20 (.19 (2.87 (1.

30-6.34-3.570-.670) .Pyrethroid Pesticides Urinary trans-3-(2.540) .12-1.08 (.75 (1.60) 2.22) 1.70 (.56-5.55 (2.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .19) .750) .87-3.55 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.45-2.970 (.98 (1.41) 1.40-2.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.35) 1.20-2.19 (1.15-3.07) 2.760 (.37 (1.930-1.440-.770) < LOD 2.570 (<LOD-.530 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.61) 1.00-5.31 (2.470-.89) 2.22-2.86 (2.33-2.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .64 (1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.00) 1.00 (1.850) 1.56 (1.29) 1.87) 1.15) 3.07) 2.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .47-2.700 (.07-1.60) 2.740) .00) 5.880 (<LOD-1.640) .480-.27-2.81 (2. trans-Cypermethrin. population from the National Health and Nutrition Examination Survey.36 (1.500-.580 (.55 (2.26 (1.780) .07-2.80) 1.S.720-1.87-8.39 (1.900 (<LOD-1.91) 1.850) .720-1.31) 1.42) 1.20 (1.520 (<LOD-.530 (<LOD-.74) .15-3.45 (1.27-2.700-.31 (.68) 3.00) 1.800-1.30-3.60 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.87 (1.850-3.700 (.44) 2.65) 1.13) .580) .91-11.560 (.74) 2.780) 90th 1. Survey Geometric mean (95% conf.780 (<LOD-.15) 2.33-1.07-3.570 (.47-2.410-.22-1.36) 2.610-.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.91 (1.57) 3.12 (.13) 1.15-3.28) 2.15 (1.11) .800-1.820-2.08 (.67 (2.48-2.56-2.730) .470 (.87) 1.39) 1.57 (1.42 (.02-1.720 (<LOD-.880-1.47 (1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .3) 2.33 (1.34-4.16 (1.48 (1.2-Dichlorovinyl)-2.65 (2.660) .35 (1.880 (.

Ranft U. Atlanta (GA). Sugiri D. Int J Hyg Environ Health 2006. Third National Report on Human Exposure to Environmental Chemicals. Schettgen T. Levsen K. Drexler H.209(3):221-233.62:101-108. Biological monitoring of workers after the application of insecticidal pyrethroids. Int Arch Occup Environ Health 2003. Butte W. Sugiri D. et al.206(2):85-92. Ranft U. Drexler H. Bravo R. Seiwert M. Int J Hyg Environ Health 2002. Angerer J. Pearson M. J AOAC 1985.76(7):492-498. Barr DB. Idel H.134(1-3):141-145. Heudorf U. Wieseler B. Int J Hyg Environ Health 2006. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Heudorf U. Bull Environ Contam Toxicol 1999. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides.77(1):67-72.109(3):213-217. Idel H. Permethrin and its two metabolite residues in seven agricultural crops. Leng G. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Berger-Preiss E.205(6):459-472. Int J Hyg Environ Health 2003. Hadnagy W. Heudorf U. George DA. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.68(6):1160-1163. Berger-Preiss E. Kolossa-Gehring M. Hoppe HW. Ball M. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Angerer J. Angerer J. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Angerer J. Int Arch Occup Environ Health 2004. Angerer J. Bartell S. Leng G. Heudorf U.209(3):293-299. Environ Health Perspect 2001. Idel H. Angerer J.114(9):14191423. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Leng G. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Schulz C. 2005. Centers for Disease Control and Prevention (CDC). Kuhn K. Environ Health Perspect 2006. Lu C.Pyrethroid Pesticides References Becker K. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Hardt J.

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

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

S. Survey Geometric mean (95% conf.Pyrethroid Pesticides Urinary cis-3-(2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 830 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 700 527 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 170 Fourth National Report on Human Exposure to Environmental Chemicals .2-Dibromovinyl)-2.

Deltamethrin. and genotoxicity in exposed children. Hoppe HW. et al. 2005. Int J Hyg Environ Health 2006. Angerer J. Fourth National Report on Human Exposure to Environmental Chemicals 171 .org/documents/ehc/ehc/ ehc97. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Atlanta (GA). Centers for Disease Control and Prevention (CDC). Drexler H. toxicokinetics. Butte W. Carranza C. Environ Health Perspect 2001.209(3):221-233.Pyrethroid Pesticides References Becker K. Int J Hyg Environ Health 2006. Ball M. Angerer J. Environmental Health Criteria 97. Torres-Dosal A. Kolossa-Gehring M. Heudorf U. Schulz C. Int Arch Occup Environ Health 2004.113(6):782-786. et al. [online] 1990. Heudorf U. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Angerer J.htm. Heudorf U. Lopez-Guzman OD. Environ Health Perspect 2005. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.209(3):293-299. Seiwert M.109(3):213-217. Angerer J.inchem. Available at URL: http://www. 5/26/09 Ortiz-Perez MD. Third National Report on Human Exposure to Environmental Chemicals. Grimaldo M.77(1):67-72. International Programme On Chemical Safety (IPCS). Batres LE. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.

Baker et al. 2003. 52645-53-1 Tralomethrin CAS No. Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al. 2004).52315-07-8 CAS No. In the New York City study. 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.... 2006). Hardt and Angerer. 2003). Thus.. 2005).. 68359-37-5 Cypermethrin Deltamethrin CAS No. 2002. representative NHANES 2001-2002 subsample (CDC. (2004) reported geometric mean levels of 3-phenoxybenzoic acid that were approximately sixfold higher than levels for adults in the NHANES 2001-2002 subsample (CDC. 2005). Following residential spraying with deltamethrin for malaria protection in Mexico. 2003. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. 2005). 2005. CDC. 39515-41-8 CAS No. CDC. Fenpropathrin Permethrin CAS No. 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. Saieva et al. In one study of 145 urban residents in 80 private homes in Germany.S. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. Biomonitoring studies of 3-phenoxybenzoic acid provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of pyrethroids than levels found in the general population. Urinary levels of 3-phenoxybenzoic acid in children were found to be related to residential pesticide 172 Fourth National Report on Human Exposure to Environmental Chemicals . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. 2006. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. CDC. 2005).. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. Becker et al.. 2005). A study of 396 German children (Becker et al. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 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. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. 2005. 52918-63-5 use and house dust levels (Lu et al. 2005). In a small group of indoor pest-control operators.Pyrethroid Pesticides Cyhalothrin CAS No. 2005)..

27-11.374) 99-00 01-02 99-00 01-02 99-00 01-02 .253-.267 (.53-3.520 (.990) .36) 1.26-2.42-2.93 (1.340) 75th .34-6.56-5.292 (.63-3.16) 1.336 (.273 (.38 (2.266-.25 (2.38 (2.02-6.83-11.277-.180-.364) .35 (2.430-.230-.630) .25 (2.210-.760 (.45 (2.13) . interval) .530-.590-.33 (2.260-.247-.570-1.233-.311 (.840-1.34 (2.340) 1.25-1.27-2.190-.03 (3.820) .230-.30 (1.29-1.73) 1.680 (.417 (.362) .610) .960 (.41-2.41-3.48-2.44) 5.46) .1.16-1. Deltamethrin.440) .353 (.595) .295) .210-.800 (.750) .78) 6.750-1.12) 4.30) 3.450 (.90) 1.230-.240 (.50 (2.52-5.45-5.810) 1.04-5.280 (.387) .160-.670 (. Fourth National Report on Human Exposure to Environmental Chemicals 173 .72 (1.79) 3.507 (.650 (.39) 2.240 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.384) .30 (.160-.14-6.35) 2.53) 1.320) .314) .328 (.320) .51-6.76 (1.01 (1.49-2.81 (1.190-.315 (.300) .200-.250 (.12) .434) .62-8.420) .820) .830-2.49-2.260 (.75 (1.05) 1.86 (1.62-6.940) 1.300 (.48-2.78) 1.530-.250 (.1) 3.330) .32 (1.49 (1.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .26) 2.710 (.321 (.227-.246-.200-.49 (1.870 (.60) .8) 3.510-.71 (1.427) .850) .230 (.360) .63 (3.490) .34) 8.276-.250-.320) .52-4.560-1.373) .740 (.700 (.560-.33 (1.340) .270) .740 (.710 (.780) 4.69) 3.800) 1.265-.43) 3.41 (1.12 (.23 (2.490-.330) .292-.190-.260 (.1) 3.750) .370) .640 (.35 (1.290 (.390) .230 (.35) 2.620-1.32 (2.33) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.470-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.314 (.730 (.226-.51-3.46) 2.550-.355) .55 (1.320) .18 (2.190-.454 (.325 (.250 (.25) size 1998 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .428-.600 (.300 (.300 (.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .271-.830) 90th 1.260 (.35) 1.05) .89-71.560-.04) .54) 1.590 (.238-.65-2.S.586) .200-.220-.700-1.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.510-.430-.1 and 0. Survey Geometric mean (95% conf.78) 1.69 (1.288 (.298 (.26) 2.320 (.25-4.350-.78 (1.64) 697 680 524 701 603 957 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.406) .601) .270 (.32-21.570-.25-7.41) 3.21 (2.369) .65 (1.850) .62) 5.27-2.13 (.297 (.288-.92-3.28) 1.352-.1) 3.18 (1.

271-.63) 1.10 (2.96 (1.17-1.07) 2.234 (.240-.280) .730) .49 (1.264 (.27) 1.490 (.440-.610 (.60-4.500) .06-3.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .200-.16-4.190-. interval) .53 (1.440-.560 (.67 (1.300-.480-.590) .740) .860 (.330) .335-.43 (2.530-.02-1.640 (.380 (.261 (.670) .36-6.55) 3.216-.250 (.74) 3.190-.401) .240-.S.35-3.329) .91-4.480 (.328) .261-.240-.580) .25-2.43) 1.410) .309) .321-.0) 3.19) 2.250) .83 (1.370-.21 (1.35) 1.210 (.860-1.73) 1.49-2.75-8.720) 90th 1.15-2.44 (1.91) 9.91) .330 (.13-1.240 (.550 (.52 (1.35) .64-5.372) .730-1.280-.677) .750-1.19 (2.650) .270 (.490-.720 (.270) .323 (.290) .390-.40) 2.590-1. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.73-4.400) .95) 1.35 (1.178-.365) 99-00 01-02 99-00 01-02 99-00 01-02 .400-.510 (.11 (.03 (.02 (2.760) .52) 2.00) 1.440-.510 (.274-.840-1.90) 3.88) size 1998 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .19-6.960-1.62) 1.225-.310) .88-5.387) .240 (.86 (1.84 (1.67) 1.450 (.590) .570) .09 (.63-3.21-4.320) .49) 1.700-1.17 (.48 (1.200-.550 (.230-.13-1.278) .230-.400-.05-3.311 (.590) .290-.640 (.200-.62) .72 (1.534) .446) .510 (.309 (.930) 1.226-.362 (.83) 1.25) 2.238-.51-7.04 (3.240 (.41-4.67 (1.49) 3.460-.22 (1.44) 2.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.280) .299-.300-.210 (.09) 3.730) .55 (1.190 (.330) .810) 1.540 (.202-.253) .380-.437) .150-.550 (.43-64.490 (.25-5.36 (1.61-2.580 (.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .270) .330) 75th .04 (.32 (2.240 (.41) 1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.270 (.39) 1.460-.37 (1.220-.330) 1.370 (.11 (.272) .200-.220 (.312 (.670) 3.00) 5.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.60) 1.270-.210-.350) .09-2.13 (.173-.240-.91 (2.280 (.410-.530-.274 (.37) 1.40 (1.930) .229-.860-1.224-.316 (. Deltamethrin.250 (.00) 1.230) .43 (1.357) .03-1.80) 4.329) .420-.94 (1.350 (.160-.227 (.630) .423 (.290) .280 (.272 (.280 (.246 (.07-5.54 (1.81 (1.378 (.275 (.09-2.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .

Lu C. Int J Hyg Environ Health 2003. Atlanta (GA). Ranft U. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Grimaldo M. Torres-Dosal A. Arch Environ Contam Toxicol 2004. Ranft U.205(6):459-472. Carranza C. Becker K. Bravo R. Berkowitz GS. Berger-Preiss E. Godbold J. urban cohort. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Lapinski R. Leng G. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Int J Hyg Environ Health 2006.111(1):79-84. Ball M. Seiwert M. Barr DB. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Kolossa-Gehring M. Int J Hyg Environ Health 2002. Third National Report on Human Exposure to Environmental Chemicals. Idel H. Angerer J. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Barr DB. Obel J.206(2):85-92. Angerer J. Int Arch Occup Environ Health 2003. Ortiz-Perez MD. Sugiri D. Olsson AO. toxicokinetics. et al. 2005. Pearson M. Deych E. Hoppe HW. Centers for Disease Control and Prevention (CDC).209(3):221-233.Pyrethroid Pesticides References Baker SE. Environ Health Perspect 2005. Environ Health Perspect 2006. Environ Health Perspect 2003. Biological monitoring of workers after the application of insecticidal pyrethroids. Hardt J. et al.113(6):782-786. Exposure to indoor pesticides during pregnancy in a multiethnic. Leng G.76(7):492-498. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. et al. Hadnagy W.46(3):281-288. and genotoxicity in exposed children. Sugiri D. Berger-Preiss E. Bartell S. Batres LE.114(9):14191423. Liu Z. Levsen K. Lopez-Guzman OD. Idel H.

320) Total .210) .080) .161) .130) < LOD .120) .430 (.130-.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 .131-.350-.280 (.160) .180 (. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.108-.440) .300) . The absorption.320 (.200 (.126-.184) .460 (.070 (<LOD-.120 (.400) .160 (.119-.130 (.190 (.310-.170 (.170) .250) .210) .080-. and as a fire-retardant in textiles and plastics.250-.150-.430 (. population from the National Health and Nutrition Examination Survey.270) .100-. < LOD means less than the limit of detection.130 (.200 (.220-.260-.122 (.120-.095-.140 (.350-.310 (.150) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.180) .164-.390) .154) .145) Selected percentiles ( 95% confidence interval) 50th .150-.154-.390 (. interval) .140) .330) .240 (.390-.240 (.120) .330) .070-.130-.105 (.280) .200) .176 (.290-.160) .115-.280) .170-.230) .132 (.440 (. +3.140) .180-.390-.130) .150 (.260) .390) .190-. and pewter.330 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3.530) .197) .410) .134 (.410) .180 (.070 (<LOD-.360) .137) .160) .250-.150 (.100 (. 7440-36-0 General Information Antimony is found in ores or other minerals.200-.128 (.142) * Sample size 2276 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .430 (. castings.130 (.230 (.210) .150) .088-.210 (.290-. People are exposed to antimony primarily through food and.570) .310 (.470) .240 (.126 (.470) . enamels.460) .250 (.310 (.080) .130-. Dermal contact with soil.220-.490) .270) .330) .110-.079-.125 (.300 (.120-.150) 90th .200 (.260-.350) .117-. solder.390) .090-.420) .144) .150-.135) * .500) .510) .280-.100-.360-.310-. 0. water.270 (.350-.200 (.080 (<LOD-.120 (.180 (.350 (.136) * .190) .175 (.300-.220-.400 (.400) .123 (.210 (.190) . Workplace exposures can occur at smelters.400-.190 (.260) .114) .280) .230-.260) . and excretion of antimony vary depending on its oxidation state.300-.04.087-.490 (.220 (.130-. and 03-04 are 0. 176 Fourth National Report on Human Exposure to Environmental Chemicals .330-.110-.230-.140) .143 (.300) .210-. and +5.300) . respectively.230-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.330 (.130 (.117-.230 (.120 (.180-.280-. It is used in metal alloys.280-.130 (.150-.280 (. ammunition.130 (.190-.142 (.370-.220) 95th .410-.120-.170-.120) .210-.310) .280-.130) .148-.190 (.350) .04.120-. It is also used in paints.119) .157) .160-. ceramics.180-.Metals Antimony CAS No.141-.240-.130 (.360 (.190-.140 (.220-.133) * .108 (.250-.160) . and refuse incinerators that process or release antimony.400 (.140) .250-. to a lesser extent.180) .112-.154) .170-.170 (.350 (.220) .134-.190) .190) .140 (.270 (.160-.120 (.110-.200-.158 (.090) 75th . Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.120-.270 (. Antimony enters the environment from natural sources and from its use in industry.099 (.180 (.150) .136-.280) .230) .180 (.130-.090 (.160) .200) . and glass.169 (.090 (<LOD-.250 (. 0. or other substances containing antimony is another means of exposure.160-.320) .170-. metal bearings.150-.220) .340) .200 (.132 (.390-.350 (.130) .128 (.350) .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.156-.140) . fireworks.200) .330-.350 (.340 (.370) . from air and drinking water.320-.140) .250 (.178) .115) .120-.260 (. sheet and pipe metal.145 (.090-.710) . storage batteries.400 (. and 0.320-.100) .340 (.207) .100 (.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 .200-.190) .290 (.230) .110-. Stibine is a metal hydride form of antimony used in the semiconductor industry.400) .S.310 (.180-.180-.260 (.280-.109-. which may vary for some chemicals by year and by individual sample.300-.150 (.330 (.210) .230-.350) .360 (. 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.120-.110 (.230-.360) .220-.310) .110) .460 (.600) .210) .460 (.140 (.098-. coal-fired plants.103) .180 (.320-.140-.200) .120-.190 (.200-.240 (. distribution.230 (.120 (.07.190-.240 (.350 (.470 (.220) .160 (.160-.130-.200 (.130 (.320-.270 (.170-.190-.330) .320 (.120-. 01-02.270-.220-.440) .160 (.137) .240) .220 (.240-.260 (.300 (.500) .093 (.120) .560) .095 (.146 (.390) .130-.190 (.160) . see Data Analysis section) for Survey years 99-00.

103-.241-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.130) .114 (.192) .170 (.173) .137 (.333) .315) .127) .159-. Histopathologic inflammatory and degenerative changes in the lung.150-.176 (.167 (.148-.298 (.085) .159-.147) .107-.. abdominal pain.106-.444) .500) .135) .148) * .150-.153 (.417) .352 (.162-.250) .257) .352) .343 (.471) . and ulcers (Werrin.321) . 1953).391) .195-. diarrhea.185 (.116 (.235-.115) .156 (. Acute antimony poisoning may cause a metallic taste.175 (.280 (. Ming-Hsin et al.269 (.191 (.099-.068-.208-.126-.089) .203) .127) . and gastrointestinal symptoms such as vomiting.430) .138-.069-.107-. Fourth National Report on Human Exposure to Environmental Chemicals 177 .115-.192-.385 (.261) .146-.313-.447 (.160 (.122 (.203) .123) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.143 (.245) .320) .208 (.228 (.161) .082 (<LOD-.068 (.30) .338 (.310) .320-.250-.318-.272) .113-.149) .471 (.741 (.320 (.130 (.200-.230-.391) .357) .119 (.338 (.200-.131) .173 (.276 (.425) .310) .Metals than for trivalent compounds (Elinder and Friberg.295 (.278 (.164 (.176-.078 (.196 (.120 (. 1986).081 (<LOD-.124) .213 (.318-.138 (. liver.333 (. interval) .205-.127) .126 (.364 (.225 (.071-.104-.178-.119-.100 (.224 (.. 1944).188) .087) . 1986).172-.267) .310 (.124-..081) .357-. and eyes.153-.200-.131-.178 (.300 (.109 (.229-.161) .181) .181) .140) .125 (.167-.102-.308) .124 (.095-.211) .118 (.108-.266 (.204-.444) .288 (.727) ..082) .125-.429 (.333) 787 682 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.333-.159-.112 (.111 (.106-.061-.117-.123 (.238 (.115 (.333 (.135 (.259 (.105-.236 (.417) .228 (.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 .193) .129) .118 (.193 (.143) 90th .074 (.082) .120 (.248) .373) .277 (.121 (.250 (.111-. 1988.132) .086 (.371 (.220) .143) .129) * .144-.151) .187) .233 (.173 (.263 (.233-.233) .079 (<LOD-.099-.227-.278) .146-.333-.130) .167 (.124-.075 (.195-.164-.146) .108-.114 (.098) . population from the National Health and Nutrition Examination Survey.181) .130) .136) .250 (.152) . 1962).077) .182 (.131 (.333-.164) .098-.300) .121) .135) .250-.199-.143) Selected percentiles ( 95% confidence interval) 50th .129 (. myocardium.120 (.244-.333-1. 1958) and occupational exposures (Briegner et al.147-.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 .338) .239-.173-.115-.103-.113-.183) . Inorganic antimony salts irritate the mucous membranes.265-.185 (.230) 95th .133) .080 (.255) .109 (.206-.308-.271-.317) .194-.192 (.400 (. resulting in hemolysis with abdominal and back pain (Dernehl et al.209-.115 (. species.209) . 1954).143) .139 (. 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.075 (.140) < LOD .127 (.281-.112-.280-.108 (.253 (.117-.207) .149-.255-.317) .120 (.222 (.086) 75th .163 (.152) .113) .250-. and route of exposure (Elinder and Friberg.405) .132 (.333 (.242-.241-.116-.179-.226 (.320 (.248-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.076-. and kidney have been demonstrated in high dose animal studies depending on the dose.S.084) .198) .364 (.429) .294) Total .096-.146-.265 (. 1973). The toxicity of stibine after acute inhalational exposure is similar to that of arsine.163 (.485) .167 (.126) .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 .176 (.119-.250-.154-.121 (.228-.263-.256 (.253-.267-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.148-.127) .109-.135 (.421) .268) .080 (<LOD-.238) .138) * .741) .209 (.092-.115 (.186) .156-.217 (.098-..214) . 1995).238) .480) .069-.076-.108-.200) .129 (.128-.414) .188-.145) .209) .438) .267 (.112 (.195 (.189 (.247) .139 (.114 (.380 (.092) .286 (.097-.300) .185-.317) .104-.320-.171) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.134) .102-.122 (.107-.135) . skin.138-.117-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.225) .095-.

New York: Elsevier.e. 1994) have reported values slightly higher than those in this Report. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Pozzoli L.cdc. Alimonti A. Arch Dis Child 1997. Mahieu P. 20012002. Paschal et al. gov/toxpro2.. Elinder CG. J Trace Elem Med Biol 2002. Buchet JP.16: 33-39. Nordberg GF. Stasney J. Rev Infect Dis 1988. Cordasco EM. Bolten C. Review of elements in blood. Cullen A. Ho C-K.67:119-123..13:361-362. Yang C-Y. 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. 1995. Biological assessment of exposure to antimony and lead in the glass-producing industry. plasma and urine and a critical evaluation of reference values for the United Kingdom population. O’Regan M. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Caroli S. et al. Third National Report on Human Exposure to Environmental Chemicals. Chemotherapy for leishmaniasis: Biochemical mechanisms. Ludersdorf et al.S. Antimony in blood and urine of infants.76:432436. Fuchs A. Stocks J. Dernehl CU. Arsine. 1998. Sci Total Environ 1994. Vouk VB. and antimony in optoelectronic industry workers.html. 2004. Gebel TW. Skulsukai G. Urinary antimony in infancy. stibine. which may be due to methodologic. VI. Industrial antimony poisoning. Wade A. Chest 1973. J Clin Pathol 1998. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. 1986.158:165-190.. Costeloe K. Apostoli P. even when exposure levels were below workplace air standards (Bailly et al. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Pilgrim L. 26-42. Br J Ind Med 1991. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Kentner et al. 2nd ed. 1991. population. arsenic. Pietra R. Mayer P. and hydrogen sulfide. J Occup Environ Med 2004. Schacke G. Kiberd B. Schaller KH. Weltle D. Shao-Chi C. Chia-Yu H. Delves HT. Information about external exposure (i. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Ju-Sun P. Centers for Disease Control and Prevention (CDC). Int Arch Occup Environ Health 1987. Antimony. Handbook on the toxicology of metals. eds.76(2):103-115.521-523. EPA. Roland H. et al. Carelli G. Semisch CW. Stone FD. Antimony trioxide is rated by IARC as a possible human carcinogen.10(3):560-586. 2002. Earlier measurements in general populations (Minoia et al.46:931-936.Metals to antimony have been established by OSHA and ACGIH. clinical efficacy... Mayne P. Element reference values in tissues from inhabitants of the European community. et al. Cheng-Wei L. gallium. Chin Med J 1958. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Industrial Medicine and Surgery (Dec. Dezateux C. 2005.48:93-97. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Hamilton EI. Suchenwirth R. 1998). Briegner H. Environ Health Perspect 1998.atsdr. indium. External and internal antimony exposure in starter battery production. Lenert G. or exposure differences. Trace element reference values in tissues from inhabitants of the European community I..64(2):182-185.51:238-240. Delves HT. Sabbioni E. Biomonitoring of a worker population exposed to low antimony trioxide levels. Lauwerys R. Luedersdorf R... Ming-Hsin H. Liao Y-H et al. and future strategies. Matthews T. Friberg L. Int Arch Occup Environ Health 1995. Stead FM.106:33-39. and a drinking water standard has been established by the U. 1997). Chen J-R. and 2003-2004. Leinemann M. Wu M-T. Iavicoli I. Dunkelberg. Dezateux et al.. Petrucci F. Liao Y-H. 1990. Industrial Medicine 1944. In: Friberg L.. Sabbioni E. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. environmental levels) and health effects is available from ATSDR at: http://www.)1954. Atlanta (GA). Biomonitoring Information Levels of urinary antimony reflect recent exposure. 1987).59:469-474. Piatnek DA... HH. Yu H-S. pp. Kuo-Juie Y. Konings J. respectively. Van der Venne MT. Nau CA. Iavicoli et al. Bailly R. Kentner M. Gallorini M. Biological monitoring of exposures to aluminum. References Berman JD. Pulmonary edema of environmental origin. 1998) or compiled reference ranges (Hamilton et al. Minoia C.

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

6-35.8) 7. lead. trimethylarsine oxide. mostly for use in wood preservation (ATSDR. 2001).1 (32.3-111) 78.1) 1281 1276 03-04 03-04 03-04 9.74. to a lesser extent.5) 41.5-178) 46.90-8.08 (5. Arsenic trioxide is approved to treat acute promyelocytic leukemia. see Data Analysis section) for Survey year 03-04 is 0. and gray forms). copper arsenates.80 (5.4 (24.0 (43.29 (8.30 (6.2 (41. the smelting of copper. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.1-18. Since the 1940s.84) 8.57) Selected percentiles ( 95% confidence interval) 50th 7.2) 46.Metals Arsenic CAS No.90 (7.90-11. Survey years 03-04 Geometric mean (95% conf.4 (7.9-34. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.4) 40. and play sets.0 (14. meats.4) 60.0-19.4-65. and as a cosmetic to lighten complexion.70 (6.70) 8. arsenic as elemental metalloids may be used in some ammunition. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.77) 6.8) 29. Various arsenic compounds were used in paint pigments and for tanning animal hides.2-93. arsenites. retaining walls.8) 30. In the last century.3-15. referred to as inorganic arsenic compounds.5) 43. and arsenates (oxidation states of -3. gaseous hydride manufactured in small quantities for use in the semiconductor industry. Arsenic is measurable in most soils. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.02-8.25-9.9) 68.80) 6.80-9.70-9.7 (11. Arsenic trioxide (As2O3.0 (11. solders. In nature.1) 7.5 (14. and produce. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.27) 9.90-8.2-61. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.1-40. The United States no longer produces arsenic from mining but imports about 22.2 (13. arsenocholine. or rarely as elemental metalloids (yellow.1) 15.8-77.6 (13.90-7.10-7. cacodylic acid. ocean and fresh waters.30) 17.41 (7. +3 and +5).34-9. and as homicidal poisons. 180 Fourth National Report on Human Exposure to Environmental Chemicals . and indium arsenides are used in the semiconductor industry.19-9.5 (23. and. 2005).66-8.8) 17.9-46.5) 66.6-43. and arsenosugars.8-61. interval) 8.1) 290 725 1542 03-04 03-04 9.5-52.3) 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. it is found in over 200 crystalline or mineral forms.6 (32.5 (36.00 (6.10-10.9-62.5-19. particularly arsenic trioxide.6-141) 53. Also.55 (7.97) 8. aluminum.6) 618 722 1074 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey. Water sources contain mostly inorganic arsenate.6 (9.10 (6.50 (8. from coal burning.6) 11. Before the 20th century.5) 95th 65.8 (48. sodium arsenite. psoriasis.34-10.0-60. grain.12 (6. Arsenic and its compounds have had many uses in the past and present as medicines.0 (22. though in some locations arsenite may be prevalent (WHO. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. as alloy in metal bearings. and in lead-acid storage battery grids.84) 8.S.0 (15.90 (7.7) 24. General population exposure to inorganic arsenic can occur through consumption of drinking water and.1 (38. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.9 (17.90) 75th 16.90 (5.3) 10.30 (7.3-19.4 (31.2) 15.90) 16. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.9) 21. were used as treatments for syphilis.5 (34.5-41.8) 7. cancers.7-95.2-20.7) 90th 37. lead hydrogen arsenate.5 (40.000 metric tons annually.40) 7. Gallium.90-14. semiconductors. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. such as arsenopyrite (FeAsS) and realgar (As4S4).4) 13.4 (26.50-14.8) 34.2-17. Arsine (AsH3) is a reactive.2 (12. black.4 (48.2 (51. arsenic compounds.7) 65. pesticides. mental disorders. and foods.00-9.10) 10.12-10. alloys.9 (8.20 (8.8) 33. Although it is still widely used in the United States.6 (15.7-83. and other metals.13-8. to a lesser extent.

66 (7. 2001.04) 7.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .8) 27.4 (11.64 (7. 2001.5) 17.. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.3-53. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.4 (26.1-36.1) 58.S.0) 1281 1276 03-04 03-04 03-04 8.1) 6.20-9. NRC. Chowdhury et al.7-34. 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. Extremely high groundwater arsenic levels.8 (21.41) 6.8-62.99-9. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.4 (42.1 (14. trimethylarsine oxide (TMAO).7-17.. so exposure to the general population is extremely limited.8-75. 2007.93-8. Gamble et al.11 (5.3 (27.7-18.13) 8.33 (6.66-8. Fish. Arsenate is reduced in the body to arsenite (oxidation state +3).44-11. and some other seafood can contain organic forms of arsenic including arsenobetaine.10-8.25 (6.4-64.8) 22. 2001). Tseng. population from the National Health and Nutrition Examination Survey.3-41.1) 7. Though modest bioconcentration occurs in some aquatic life. inorganic arsenic is widely distributed within the body.59) Selected percentiles ( 95% confidence interval) 50th 7.0) 12..12-10.6-17.2-15.51) 75th 14. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.06 (4.10-16.9-56.5 (9.0 (31.6 (35.7 (9.40) 8.. are used in enclosed ultraclean operations within the semiconductor industry.6 (10. but is poorly absorbed dermally (WHO.24 (7. and arsenosugars.38-10. 2001).75 (5.0 (17.. though some reduction may occur in the gut prior to absorption. The semiconductor dopants.7-188) 27.32 (5. 2001).0) 42.0-38.7-35.6 (17.5) 290 725 1542 03-04 03-04 8.01) 7..S. Steinmaus et al.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.8 (27. After absorption.96) 12. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. 2006.93-9.2) 40. 2007.66-8. organic arsenic can be converted back to methylated and inorganic arsenic. In aquatic organisms. have caused clinical arsenic poisoning.0-69.5-17.7 (11.44) 6.2) 90th 30. 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.31 (6. selenium. interval) 8. kelp. dose level. 1988).2 (12. Smoking tobacco is also a source of inorganic arsenic.47 (7.3) 9.5-120) 40. U.7 (25.33-10. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC. Inorganic forms of arsenic demonstrate high acute toxicity. mine tailings).8 (20. arsenocholine.45) 5.86-17. age.0) 26.8 (12.88) 7.35) 7. 2001).9) 13.4) 32. and contact with CCA-preserved wood structures.58-10.01) 11.25-9.1 (11. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. as observed in Bangladesh where millions of people have been exposed.3 (24. shellfish.4) 54.1) 8.3) 6. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.S.81-9.23-7.18 (5. and folate status (Chen et al.8 (11.4 (40.9 (45.88 (5.07-9. Direct exposure to DMA and MMA may result from use of the two pesticides.1) 24.47 (6. WHO.6) 45. 2001). 2001). 2007.75) 13. 2001).2-46.00 (6.g.0-18.4 (24.7) 28.3-64.9) 53. Children may have additional exposures from ingestion of contaminated soils (e.28-7.0) 14. arsenic does not show biomagnification in the food chain (WHO. EPA’s maximum contaminant level (Hughes. EPA.04 (5.47-6. dust. 2001). cacodylic acid and monosodium methyl arsenate.7) 95th 50.4 (12.0-26. 2006. Survey years 03-04 Geometric mean (95% conf.8-32. WHO.76 (6.2) 15. gallium arsenide and indium arsenide. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.61 (7. In aquatic sediments.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) 33.30-9. 2003.50 (6.3-62.

. gluconeogenesis. which may vary for some chemicals by year and by individual sample. Taiwan. arsenic trioxide) includes hemorrhagic gastritis with nausea. vomiting. population from the National Health and Nutrition Examination Survey. drinking water have not been associated with increased cancer rates (Schoen et al. 2006.g. 2001). apoptosis. Survey years 03-04 Geometric mean (95% conf. 2004).50) 621 725 1078 Limit of detection (LOD.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. The U. 2007.. which can lead to dehydration and shock.20 (<LOD-1. substitution in phosphate metabolism.10 (<LOD-1. 2007). see Data Analysis section) for Survey year 03-04 is 1.0. 182 Fourth National Report on Human Exposure to Environmental Chemicals .30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Bangladesh. noncirrhotic portal hypertension. 2001). 2006. Chronic elevated arsenic intakes have been associated with diabetes.50) 1. 2001).60) 1. hepatotoxicity.. Cellular glucose uptake. Chronic arsenic exposure in humans is considered to be a cause of skin. and altered gene expression. and production of glutathione may be affected as well. 2000. 2007. WHO.. hyperkeratosis. increased oxidative stress. Studies of arsenic at levels typical of U. 1998. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. including inhibition of numerous enzymes. and hyperpigmentation of the skin (NRC. Cardiac arrhythmias. cytotoxicity. leading to a decrease in adenosine triphosphate energy production. but additional or confirmatory research is needed (Kapaj et al. and it also will inhibit succinate dehydrogenase.80) 1. lung. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. cell transformations.S. U.S.20 (<LOD-1. including drinking water sources with elevated arsenic levels (e. Cohen et al. NRC. Laboratory studies using inorganic arsenic have shown chromosomal aberrations.g. and by uncoupling oxidative phosphorylation (NRC. 2006) or when exposure occurs in smokers (Chen et al. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. can cause peripheral sensorimotor neuropathies.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. 2004. hematocytopenias. respectively. renal failure. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 1. food residue. and endothelial injury (Kumagai and Sumi..20 (<LOD-1.10 (<LOD-1. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. 2001).30) 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.EPA has established drinking water. WHO. 2004).. NRC.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. The organic forms of arsenic occurring in seafood have little known toxicity. Bredfeldt et al..10 (<LOD-1. 2001)..EPA. 2001. 2001.. interference in signal transduction pathways. fatty acid oxidation. < LOD means less than the limit of detection. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide.20 (<LOD-1. and diarrhea.10 (<LOD-1. Raml et al. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. 2001). WHO. WHO. and childhood neurodevelopmental effects in observational human studies. and DNA repair inhibition (Cohen et al.. Chile).60) 1.S. Chronic human intake of arsenic at less than acutely toxic doses. Such actions may lead to decreased energy production. hypertension.10 (<LOD-1. and bladder cancer (IARC. peripheral vascular disease. Acutely. Arsenic has many actions demonstrated in cellular studies. 2006..S. With chronic exposure.. some of these effects may take years to develop. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. Although arsenate is reduced in the body to arsenite.

environmental levels) and health effects is available from ATSDR at: http://www. 1992.. Caldwell et al. In a Nevada town where groundwater levels were naturally elevated. Pellizzari and Clayton. Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al.S... 2006). Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.. Caldwell et al. had decreased since the prior 1990– 1992 survey. WHO.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.e. 2000. gov/toxpro2..89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.00) 1. but generally only at maternally toxic doses (WHO. 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. In animal studies. Levels of total urinary arsenic in the U. 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.33 (<LOD-3. Fourth National Report on Human Exposure to Environmental Chemicals 183 . and the FDA has established a bottled drinking water standard. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. Meza et al.S.. 2008). 2001). Calderon et al. arsenic has been fetotoxic and teratogenic. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.Metals compounds. Pellizzari and Clayton 2006).41) 3.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2001). population (Rubin et al. although urinary arsenic levels were not associated with CCA contact (Shalat et al.. 2007... 2004.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2..04 (<LOD-3. population from the National Health and Nutrition Examination Survey. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. 1999). Consequently.18) 3. 1999. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. 2006). Offergelt et al. Josyula et al.. Pellizzari and Clayton. Shalat et al. 2004. 2007.50) 1.. Shalat et al..S.69 (<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. 2008).50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2006.75 (<LOD-2. 1999.html. DMA produced bladder cancer in some chronic rat studies (Cohen et al.33 (<LOD-3..S. Compared with this Report.80 (<LOD-4.61 (<LOD-3.. population in NHANES 2003–2004 (Schulz et al.. 2006).19) 3. Several studies have shown that urinary arsenic levels are not correlated with low levels of arsenic measured in house dust or in washings taken from hands (Hysong et al. 2006.. Valenzuela et al..18 (<LOD-3. Survey years 03-04 Geometric mean (95% conf. 2001).75 (<LOD-2.atsdr. urinary arsenic levels have been accepted as a good biomarker of dose (WHO.. 1986). 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. median urinary total arsenic levels in 4052 adults varied with seafood intake. Vahter et al. 2006).cdc. and were about two-fold lower than those for the U. 2003. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. Additional information about external exposure (i. 1998. In the German Environmental Survey III of 1998. 2000). 2008. 2006...

05) < LOD .3 (21.e. Valenzuela et al. geometric mean levels were about 70-fold higher than for the U. 2008).871-1.800-1.55 (1.6 (13.. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine. 2001. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.700-1.20-25. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.800-4.70-21. arsenocholine.5) 32. 2001).. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. which may vary for some chemicals by year and by individual sample.50-6.800) 1..0 (26.4-35.00) 3. 2006).8-40. and two methylated metabolic products. Caldwell et al..83) Selected percentiles ( 95% confidence interval) 50th 1.0-23.6 (25. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.50) .90-29.7) 15.8 (12. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-38.80 (3.20-190) 31.00-12. in NHEXAS 1995–1996.60) 1.17-1. arsenite. when seafood organic arsenic is subtracted)..1-94. methylation capacity.g. population from the National Health and Nutrition Examination Survey. 2005. Tseng et al.80 (. Some noncancer effects of arsenic (e. 1985.1-25.700-1. population in the NHANES 2003–2004 subsample. When seafood intake is avoided.. 2000. These associations are stronger at higher urinary levels. arsenocholine.30) 10.20 (2..6 (11.8) 35.1) 45.5) 29.00-6.50) .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 * * 1.29 (1.10) 8. Individually measurable species resulting from inorganic arsenic exposure are arsenate.6-44.50) 90th 16. For residents of Inner Mongolia.6.900-1.2 (6.00-4. 2005.43-1. and TMAO. 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.S. vasospasm. In the residents of a Chilean town who consumed water with high levels of arsenic.3% of a representative sample of the U.5 (14. The higher percentiles of total urinary arsenic levels in the U.60-3.30 (2.4) 23..600 (.Metals other areas of the world (Ahsan et al. and duration of exposure are also considered important. 2008).3) 95th 35.0) 29.6.3) 1284 1284 03-04 03-04 03-04 1.70) 6. In the late 1980s.20 (4. 2003).1-51. MMA.20) 7. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. arsenobetaine.20 (1..80-5..S. see Data Analysis section) for Survey year 03-04 is 0.7-22. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.9 (7.8-50. DMA and MMA.S. population (Sun et al. 2007). After recent seafood ingestion.400-.74 (1.70 (3. 2000.5) 292 728 1548 03-04 03-04 1. and TMAO were detected in only 7.800 (.10) 4. Aposhian et al...70 (5. 2005.500-1.9 (6.30 (1. 2008. and other factors such as nutrition. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.00 (. China.80 (4. 2008).70-21. 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7 (13.62) 2. and 0.. Also.00 (1.3 (9. respectively.3-39. Sun et al. Arsenate. 2000.68) .93) 1.4) 31. WHO. 1990.. 2008).80) 1.45 (1. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.20) 3.3) 35.00-1.8. population showed a higher contribution of arsenobetaine (Caldwell et al.20-3. < LOD means less than the limit of detection.11-1. with DMA. Caceres et al.S.7) 13. arsenite.19 (... interval) 1.0 (27.0) 4.2-35. dermal keratosis.4.. 1.40-7. 2008.9-23.31-1.66 (1.48-2. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.40) 5. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.S.7 (21.8 (17. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.37 (1..1) 18. 184 Fourth National Report on Human Exposure to Environmental Chemicals . arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. Caldwell et al. 1996.90-7.4 (16. Caldwell et al.40-6.5) 621 725 1078 Limit of detection (LOD.28) 1.40) 75th 5. Measurable organic arsenic species in this Report are three biologically generated environmental forms. population (Ahsan et al.5 (26.9) 13. Blom et al.900 (. Survey years 03-04 Geometric mean (95% conf. 2007) with higher levels of arsenic in the drinking water.20 (. Chowdhury et al. Pellizzari and Clayton..30) 2.20) 18. In most human studies.10 (4.800 (..

6-29..44 (1. Sun et al.2 (4.45) 1.30) 1.9 μg/L.51) 5.50-15.786-1. 2001).05 (.37-2.67) 1.25 (.70) 5.00 (3.73-6.76-27.638) 1.8) 29.40) 1. 2007).68 (1.43) 75th 5.6-46..2 (12.15-4.Metals as with DMA.938-1.82) 4. 2008).1 (26.531 (.0 (9.80-153) 17.6) 19. 2008).14 (1.61-6.54 (1.91 (4.S.7) 9.833-1.9-18.39-3.82) Selected percentiles ( 95% confidence interval) 50th 1. 2003.4 (11.25-7.29-14.3 (10. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..9) 14.. WHO.1-18. Fourth National Report on Human Exposure to Environmental Chemicals 185 .50-7.877 (.65 (1. not to imply a safety level for general population exposure.11 (.2 (12.51-2.4) 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 * * 1.93 (1.3-24.S.13-39. interval) 1. 1992.83) 2.47 (1.4) 32. 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. 2001).28) 1.83) 8.4-82. Offergelt et al.79 (1.4) 13.909-1.4-28.9) 32. Survey years 03-04 Geometric mean (95% conf.29 (4.88 (5.5) 17.15-1.80) . Vahter et al.62-6.6 (6.40 (1.30-1. which is below the ACGIH BEI (Caldwell et al.1) 26.400-.9 (25. population from the National Health and Nutrition Examination Survey.1-36.4 (24.81 (4. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. Information about the biological exposure indices is provided here for comparison.5 (18. population for the sum of inorganic related species was 18.55) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..88) 2.15-1.78 (3..58 (3.91) 90th 16.9 (13.47 (2. 1998..12) < LOD .67) 4.3) 95th 29. The 95th percentile of the U.10 (.53 (. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.21) 5.16 (.959-1.5) 26.18-1. Biomonitoring studies of urinary arsenic can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of arsenic than are found in the general population. 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. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.05) 1.6-32.4) 292 728 1548 03-04 03-04 1.2 (13.901-2.3 (10.5-20..0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.612-1.4-21.5 (18.43) 14. Caldwell et al. In recent years.72) 12.36) 2.32-7.78-5.00 (1.3) 1284 1284 03-04 03-04 03-04 1.0-36. 1986.7) 30.6 (9. 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.7) 17. occupational monitoring and research studies have focused on the sum of inorganic-related species (arsenate + arsenite + DMA + MMA) as a measure of inorganic arsenic intake.64-29.19-2. 2006.

S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey years 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Metals Urinary Arsenocholine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < 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. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection. see Data Analysis section) for Survey year 03-04 is 0. 186 Fourth National Report on Human Exposure to Environmental Chemicals .S.6. 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. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.00 (<LOD-3.76) < 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.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.95 (<LOD-2.00) 1. Fourth National Report on Human Exposure to Environmental Chemicals 187 .2. Survey years 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00 (<LOD-2.80) < LOD 621 725 1078 Limit of detection (LOD.08 (<LOD-4. see Data Analysis section) for Survey year 03-04 is 1.40 (<LOD-1. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample. Survey years 03-04 Geometric mean (95% conf.44) 2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.S.20 (<LOD-1.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

0 (8.7 (10.6 (9.3 (8. see Data Analysis section) for Survey year 03-04 is 1.00-9.0) 16.00-7.0) 12.52) 3.16-11.8) 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 3.00-4.70 (3.0-18.81 (5. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0 (9.71 (3.00-4.8) 7.7.61-16.34) 3.98) 4.20-12.86 (2.05) 10.7) 1284 1284 03-04 03-04 03-04 4.17-6.57 (3.00-3.03 (3.82-9.0 (10.85 (3.32 (8.71-4.00 (5.00 (3.17-4.0 (12.65-6.80-5.61-11.0) 9.00) 3.74) 90th 9.00) 4.91) 75th 5.73) 6. interval) 3.90) 2.13-4.9 (11.27-2.14) Selected percentiles ( 95% confidence interval) 50th 3.00-7.27 (2.59 (6.69-3. interval) 3.55 (2.89 (3.00 (3.50 (4.27-5.4 (7.0) 13.60-4.00) 4.00 (3.0) 14.24) 3.7) 13.92-12.95-3.9) 5.00-4.00-15.9 (7.25 (4.00 (3.6) 1284 1284 03-04 03-04 03-04 4.00 (6.70-4.70) 5.0-12.S.00-11.0) 13.50-5.24-4.42) 3.0) 11.0) 17.0-19.00 (5.80-6.00-15.31) 4.3 (7.S.11 (3.38 (3.0) 11.34-4.65-8.45) 8.0 (13.0) 17.50-15.80 (4.1 (8.9) 12.67) 9.0) 95th 16.0 (10.5) 12.00-11.8) 7.12-4.00-10.15) 4.49) 10.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00-12.92) 3.00-4.0) 9.70-3.00 (3.0 (14.0-17.86-21.0 (9.44) 5.94-3.22) 4. Survey years 03-04 Geometric mean (95% conf.5) 95th 13.00 (6.11) 4.34 (3.0-16.29-4.00) 3.60-3.69-6.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .0) 10.0 (8.30 (7.49-4.00) 7.32-10.16 (2.00 (5.71 (4.00) 9.57-5.0-16.71) 3.0-25.74 (2.33) 3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.48 (3.18 (6.0 (12.00-7.00) 6.84-18.6) 292 728 1548 03-04 03-04 3.37 (3.06) 5.95-4.00-3.00-12.03-6.1-18.00-13.80) 7.1-22.00 (5.95 (4. population from the National Health and Nutrition Examination Survey.95-6.1-15.00-15.10) 3.82-5.2) 10.78) 4.33-4.37 (2.34 (3.0) 9.12 (3.00-5.00 (4.34-4.20-4.00) 75th 6.00) 90th 11.17 (2.78 (4. population from the National Health and Nutrition Examination Survey.0 (11.70-12.00 (7.00-8.77 (3.88 (4.05) 3.69 (3.60-7.00-4.00) 12.20) 11.0-17.00 (7.9) 13.28) 2.09 (7.00) 6.00 (6.9) 11.14) 3.10) 6.80) 2.00-22.0 (10.00-11.0) 16.0 (13.00) 6.16 (4.31-4.39-3.48 (2.0) 621 725 1078 Limit of detection (LOD.90 (3.86-7.6-18.5 (11.73 (3.97-3.7-16.67) 8. Survey years 03-04 Geometric mean (95% conf.84-8.44 (2.94) 3.00-4.19) Selected percentiles ( 95% confidence interval) 50th 3.00) 6.82) 3.0 (10.3 (8.72 (4.79 (3.80-3.46 (4.0) 292 728 1548 03-04 03-04 4.69 (3.00 (3.62) 4.00 (5.30) 3.00-7.0 (9.90) 5.7) 12.32 (4.00) 5.27 (3.45) 3.05) 5.45 (8.08 (2.60-6.

30 (1.50 (1.S.46-2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.77) 1.30) 90th 1.86 (2.17) 2.10 (.40-2.40 (2.10-1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.82-2.10) 2.60 (1.28 (1.45) 3.62) 2.10-3. < LOD means less than the limit of detection.S.73-2.20 (1.58) 2.10 (<LOD-1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1. Survey years 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.70-2.30 (1.43-3.90) 1.11-1.40) 2.00 (2.36) 1.85) 2.70-2.16 (2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.61) 2.31 (1.07-3.00-2.90 (2.96-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.88-2.50) 621 725 1077 Limit of detection (LOD.00-2.50) 1.30-1.00-1.20-3.10 (1.18-1.81) 1.53-2.36 (1.60) 1.46 (1.00) 1.30 (2.30-2.20 (1.07 (1.816 (<LOD-.40-3.22) 3.40-2.985) 1.20 (1.70) 2.60 (2.33 (1.80) 1.90) 2.853-1.88 (1.00 (1.10) 95th 2.50 (<LOD-1.20) 2.34) 2.90) 2.80-2.00-4.52 (2.30) 2.50 (1.80 (1.57) 95th 2.80 (1.30-1.00 (<LOD-1.15-1.20 (1.80 (1.00) 2.10 (.00) 1.70-2.86) 2.86 (2.30) 1.50-2.28 (1.79) 2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.18-1.900-1.31-3.60) 2.88 (1.10-1. Survey years 03-04 Geometric mean (95% conf.33 (1.00) 1.50 (2.90 (1.53 (1.71-2.70-2.9.70-3. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.80) 1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .60) 2.93) .10 (1. which may vary for some chemicals by year and by individual sample.00 (2.85) 1.20-1. population from the National Health and Nutrition Examination Survey.54) 90th 2.80 (2.07) 2.35-3.37 (1.00 (<LOD-1.05-1.30) 1.40 (1.61-3.22 (1.00-1.80 (1.63 (<LOD-1.20 (1.20 (1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.86) 3.30 (1.84-3. see Data Analysis section) for Survey year 03-04 is 0.60-2.00) 2.40-3.40) 1.23) 1.14-1. 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 1.82-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) 1.80-2.

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

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10-4. such as brazil nuts.70-5.87 (6.70) 3.93 (4. interval) 1.19-1.46-1.67) 6.50 (1. Barium salts have also been available as rodenticides.49) 4.49 (1.30) 3.52 (4.42 (1.30-3.36 (1.11 (3.25 (1.40) 3.Metals Barium CAS No.95 (4.90) 4.71) 95th 6.20-1.31 (2.78-2.14-6..71-9.41-1.56 (1.20-8.70-3.12) 6.50 (5.63) 1.38 (1. 7440-39-3 Medically.50 (1.43 (1.20) 2.81-2.21 (1.00) 1.12 (2.16) 5.93-2.39-1.20-8.87-9. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).78) 1.39) 4.03 (1.51) 7.40) 7.70) 1.68 (1.8) 9.39 (1.40 (4.71 (2.35-1.73-5.51) 2.62) 1.1) 9.66) Selected percentiles ( 95% confidence interval) 50th 1.88 (5.37-1.80) 6.86-4.33 (1.87-14.55-3.90) 2.01-7.95-6.57 (5.97 (1.05% of the earth’s crust.32-7.70-8.90-13.40-13. respectively.71) 1.00) 1.70 (5.g.12-1.73) 3.93-8.69 (1.00) 4.74) 3.19) 2.28-1.45 (1. such as barium chloride. it combines with other chemicals such as sulfur or carbon and oxygen.11 (2.54-8. Fourth National Report on Human Exposure to Environmental Chemicals 193 .64 (1.09 (1.70 (1.18) 3.43) 6. fireworks.24-1.02 (7.38 (1.00-3.09 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50) 1.81-2.43) 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 1.12) 7.06-2.54) 1.10 (2.60) 1. Some barium salts are freely soluble in water.57) 3.49) 11. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.86 (4.30) 2.37 (4.66 (4.20-5.26) 5.20-1.50 (3.62 (1. population from the National Health and Nutrition Examination Survey.44-2.15 (2.8) 5.60-6.45) 7.35-1.15-11.40 (1.65-8.50-1. rubber. barium sulfate and barium carbonate).10-5. and ceramics.80-3.64-3.10) 3.25-11.50) 2.53-5.37) 5.54 (6.86-5.14-1. and 03-04 are 0. Barium compounds are used by the oil and gas industries to make drilling muds.30) 5.85) 1.54) 2.80 (2. bricks.72) 4.27) 2.26) 2.73 (5.29) 5.54) 1.78) 1. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10) 5.60-2.55-7.47-1.65-5.48-4.32) 8.46) 1. 01-02.08 (6.70-2. see Data Analysis section) for Survey years 99-00. and 0.63) Total 1.20-6.80-5.70) 5.50) 4. 2001).50 (1.70) 1.34) 2.17-1.85) 1.30) 5.75) 2.30) 8.39 (1.48 (6.38) 2.80-7.73) 1.65 (5.22-1.46) 1.92) 2.63 (1.15-1.63 (8.82) 1.30 (2.90) 1. soluble forms of barium. In single dose animal studies.05-2.88) 4.56 (6.10 (3.30 (5.30) 5. Certain foods.77 (3.60) 1.88) 7.11 (3.61 (1.94-6.34 (1. glass.12 (2.08-8.62) 1.99 (4.20 (3.50 (1.40 (5.65) 1.27 (1.64) Sample size 2180 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.8 (6.54 (2.99-5.32-1.90 (4.22-1.40 (1.70-6.00) 6.50-6.30 (3.56) 4.51) 1.29-5.61 (2.57-7.65) 3.35 (3.52 (1.91) 6.40 (1.72) 75th 3. whereas others are practically insoluble (e.22) 6. depilatories.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 1.56 (1.77) 1.00-8.82-6.80-2.43) 2.76 (3.12.30-2.87 (5.11-1.30-2.12.90-2.16 (1.01 (4.43 (1.24-1. tiles.25-1.34 (2.4) 9.20 (4.00 (2.40 (5.70-2.30 (5.21 (1. The general population can be exposed to low amounts of barium in air.65-1.48) 1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.62 (1.15 (6. Workers employed by industries that make or use barium compounds can be exposed to barium dust.47-1.78-3.27 (1.80 (1.50-6. 0.59-11.80 (5.24 (4. are high in barium (Genter.70) 7. and food.35) 5.60-10.56 (2.50 (4.39) 1.90 (1.41-3.9) 5.36) 5.86 (4.86) 6.20-1.90 (6.50 (1.56) 1.61 (5.40 (5.65) 1.74-2.31.34 (1.63 (2. water.35-4.49) 2.35 (2.20-8.80 (1.18 (6.20 (1.74-3.31-2.37) 1.48) 1.00 (1.76-2.75-3.63) 1.87-3.40) 7.60) 4.04-6.15 (1.76) 1.43 (5.88) 1.61-8.84) 5.21-2.60-3.54-1. Barium compounds are also used commercially in paint.85 (2.29-1.30-1.50 (6.96-2.50) 2.98) 1.49-1.59) 3.80) 1.35 (1.76-7.77-3.00-76. Small amounts of barium can be released into the air during mining and other industrial processes.37-8.14 (6.91 (2.41) 1.80) 7.72) 1.26-1.44 (1.50-1.4) 7.15-1.53) 1.49) 8.60 (1. In nature.26-7.38) 8.90-9.15) 5.18-1.30-1.51 (1.20-1.87) 7.10 (4.82) 2.53) 2.4) 6.90) 2.60) 3.80 (2.76-3.07 (2.81-3.61 (1.61 (3.36-1.91) 2.73 (6.50 (2.50 (4.71) 2.87-7.36-1.49-9.28) 90th 5.80 (1.2) 6.36 (4.30 (1.44-5.54-1.70) 4.06-1.S. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.60-6.47) 4.63 (5.30-5.30) 4.60 (2.48-4.04-2.50 (4.21-8.

10) 6.59) 1.49-1.31 (4.34-5.00) 6.82) 1. in urine.79-5.81-7. interval) 1.881 (.75) 1.19-1.0) 5.67-6.47) 4.82) 1.46) 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.49-1.55) .03-1.32) 2.72) 6.65 (5.39 (3.58-6.45-1.59) 1.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.00 (3.91 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60 (2.38-1.02 (3.40 (1.64 (1.58) 1.29-7.72) 4.48 (1.32 (1.84-5.97 (5.60) 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 2.86) 5.06) 2.13-3.20-2.23-1..52-4.31-1.58 (2.48-3.20) 4.50) 1.45 (3.88 (2.26-1.34-3.60 (1.43) 1.51) 4.37 (1. Barium is not rated for human carcinogenicity.832-1. Insoluble barium salts.35-1.59-7.39-1.40 (1.76 (2.41) 5.51) 4.89 (2.08-1.52) 2.34) 1.45-1.41 (1.41 (1.77) 5.96) 4.62) 2.38 (1. Chronic high doses in animals resulted in kidney damage (McCauley et al.23-2.62 (1.97 (4.4 (5.19-1.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.32 (2.51 (1.22-4.710-1. 1994.63-4.29-1.68 (3. 2001).38) 4. vomiting.38-5.27) 7.915 (.03) 2. 1989).69-9.39-1.36-2.74 (5. chemical form.50) 2.22-1. Following intravenous injection in animals.68) 3.96) 4.28-6.34-1.76) 2.80) 4.703-1.26-1.70) 10.16) 11.26-1.01) 1.86-7.52) 7.99 (2.37-2.30 (1.45) 1.55 (5.921 (.33-4.38 (1.61 (4. paralysis.76) 1.24-6.96) 7.Metals was eliminated primarily in feces and to a lesser extent. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.15-4.36 (1.90-2.24-1.37 (1.47) 1.43-6. weakness.05-1.24) 3.37-1.00) 4.29-4.96-6. Wones et al.36-1.47 (2.38) 1.25) 4.77) 1.27-1.42) 1.29) 1.36 (3.33 (5.39 (2.26-4. NTP.73) 2.47-8.2) 5.45 (1.51) 6.58) 4.03) 1.91) 2.39-5.33 (1.44-2.49 (1.24-6.38-7.01 (4.00-1.55 (4.33) 1.16-1.71 (5.59 (1.56 (1.99 (4.80-6.35-1.68 (2.83) 3.38 (4.24 (5.2) 6. The health effects of exposure to barium compounds depend on the dose.24-11.44-2.24-3.58 (4.02) .0) 6. population from the National Health and Nutrition Examination Survey.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 .06) .75) 2.38) 1.35-3.13-2. 1986).51-3.2 (3.78 (2.74) 1.02) 4. a benign condition that may occur among barite ore miners.57-5.00 (2.55 (1. 1990). such as those used in medical radiographic procedures.89) 90th 4.91 (3. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.24-1.41 (2.33 (1.84) 2.60 (5.22-2.47) 1.880-1.58) 75th 2.92 (4.21 (1.46 (2.76 (3.73-4.57 (6.61) 2.03-1.10 (6. hypertension.54 (1.75) 1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.45-8.77) 1.52-10.87) 1.76 (4.46) 2.905 (.26) 4.41) 4.42) 1.97-4.85-5.20-8.76) 2.29 (3.77-5.70) 4.46-22.30) 2.28-1.68) 1. Symptoms following acute high dose include perioral paresthesias.36 (1.32 (1.53) .68-3.04) 5.39-10.88 (6.04 (2.25-11.26-1.75-3.31-1.31-1.47) 10.891 (.20-1.11) .51 (1.54 (2.36 (5.754-1.28 (1.54) 2.98 (2.77) 1.33-1.63) 1.75-22.97-3.37) 2.31 (1.00-7.25 (1.20 (1.48) 2.59) 2.49-1.54) 1. and cardiac dysrhythmias.69 (5.79) 1.77) Total 1.0) 7.81-6.48-1.64) 7.22-1.24 (3.39) 4.31) 5.96) 4.66 (1.49 (1.75) 2.11-2.56) 4.40-1..19-1.62 (2.28-7.4) 5.76-3. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.70) 1.51 (3.73-2.52) 1.56 (1.36-1.99) 1.27 (2.18 (1.3 (6.963 (.55-6.68 (3.45) 95th 6.45-6.57-10.28-11.53 (2. Toxicity from soluble barium salts is rare.64) 7.00 (5.62 (4.29-4. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.59 (1.91-2.64 (1.53-21.09) 6.52 (3.68-3.86 (2.55-5.44 (1.50 (4.08-2. 1984.18 (1.56) Selected percentiles ( 95% confidence interval) 50th 1.11) .01 (5.777-1. water solubility.64 (1.40 (1.28) 5. and route of exposure.29-3.33) 6. 1985.30 (1.32) 2.80) 3.48 (1.81-6..84 (3.10) 3.84-2.39 (2.16 (1.64 (1.10-2.60 (2.92) 2. are not absorbed when administered.72 (2.48 (1. diarrhea.83) 2.57-7.03) 3.39 (2.10-1.29 (1.00 (3.55 (1.27-3.14-2.S.74) 1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.57) 2.8) 4.97) 1.65 (2.48-5.34 (1.19-2.02-5.00) 1.00) 4.96 (4.42 (4.96 (4. Perry et al.50) 1.36 (3.23-5.47 (5.3) 6.60 (1.12) 2.04) 1.38 (4.46) 3.56-3.

and 2003-2004 (CDC. Princeton (NJ): Princeton Scientific Publications. eds. p. Biomonitoring Information Levels of urinary barium reflect recent exposure. Kopp SJ. 2001. 1985. 2005.. Minoia et al. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). and serum of Italian subjects. patient population and literature reference intervals for urinary trace elements. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. 1990. Paschal et al. Gallorini M. et al. p..html?charset=iso-88591&url=http%3A//ntp. Ting BG.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. Magnesium. Pirkle JL. p.html. 5th ed. 2005. Wones RG. Barium. calcium. 4/8/09 Paschal DC. New York: Elsevier. Third National Report on Human Exposure to Environmental Chemicals.. Levy. Investigations into the effect of drinking water barium on rats. 84-94. Howerton K. Reeves AL. Perry EF.nih. Apostoli P.niehs.76(1):53-59. Advances in modern toxicology. ed. 1994.gov:8080/cs.. Jr.. Environ Res 1998. et al. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. 1986.64(1):13-23. Douglas BH. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. Perry HM. Comparison of representative ranges based on U. In Friberg L.197210. Minoia C. Frohman.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. and radium In: Bingham A. 2nd Ed. Stadler BL. Pietra R. 1998). strontium. Sabbioni E.85:355-359.. Centers for Disease Control and Prevention (CDC). 221-252 Komaromy-Hiller G. Fourth National Report on Human Exposure to Environmental Chemicals 195 . Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. Pozzoli L. Handbook on the Toxicology of Metals. PS. et al. In: Inorganics in drinking water and cardiovascular disease.e. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. New York: John Wiley & Sons.nih. Weltle D. pp.. [online].95:89-105. and a drinking water standard has been established by U. Cohressen B. Schaller KH. Information about external exposure (i. et al. 2001-2002. J Toxicol Environ Health.. Morrow JC. A study of 46 elements in urine.gov/ntp/htdocs/LT_rpts/tr432.296(1-2):71-90. Lack of effect of drinking water barium on cardiovascular risk factor. LA. Nordberg GF. blood. Int Arch Occup Environ Health 1992. 1992). barium. NTP. McCauley PT. Powell C.S. eds. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. In: Calabrese EJ. the welders had no obvious adverse clinical effects (Zschiesche et al. Princeton NJ: Princeton Scientific Publications. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Vouk VB. 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. Epidemiological study of barium in Illinois drinking water supplies.niehs. Exposure to soluble barium compounds: an interventional study in arc welders. Trace metals in urine of United States residents: reference range concentrations.cdc. References Brenniman GR. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Genter MB. Jackson RJ. Inc. 2000) to levels in NHANES 1999-2000 and 2001-2002. ed. Sampson EJ.S. Trace element reference values in tissues from inhabitants of the European community I. Patty’s toxicology. 231-249..gov/toxpro2. environmental levels) and health effects is available from ATSDR at: http://www. Atlanta (GA). Environ Health Perspect 1990. Ash KO. National Toxicology Program (NTP).atsdr. Available at URL: http://ntp. Sci Total Environ 1990. Laurie RD.28(3):373-388. 1989. Vol 2: Specific Metals. Costa R. 1984. Calabrese EJ. Clin Chim Acta 2000. Zschiesche W. EPA.

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response.346 (<LOD-.. 2003.391) < 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. Maier.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 . or berylliosis. respectively. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. and drinking water and environmental standards have been established by U. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. 2002). Fourth National Report on Human Exposure to Environmental Chemicals 197 . Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. based upon excess lung and central nervous system cancers in studies of workers. S. IARC has classified beryllium as a human carcinogen. EPA. including contact dermatitis and subcutaneous nodules. NTP considers beryllium to be a known human carcinogen.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 .Metals days has been calculated for beryllium elimination from the human skeleton (IPCS.S. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.281 (<LOD-. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Skin exposure can result in delayed hypersensitivity reactions. 1990). Chronic beryllium disease.231 (<LOD-. which produces pneumonitis. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .

Ash KO. A study of 46 elements in urine.inchem. 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. Morrow JC. International Programme on Chemical Safety (IPCS).13 μg/L.S. Paschal et al. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.e. et al. Sci Total Environ 1994. population were generally undetectable in NHANES 1999-2000. environmental levels) and health effects is available from ATSDR at: http://www. Sabbioni E. and 2003-2004. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. and serum of Italian subjects. Sci Total Environ 1990. population are lower than levels in workers.158:165-190. Andrew M. Van der Venne MT. 2001). Hamilton EI. less than 0. Ting BG. Am J Epidemiol 2003.. Schaller KH. Pietra R.org/documents/ehc/ehc/ ehc106. Costa R.S. Minoia C. it is likely that urinary beryllium levels in the U. Given these results. Available at URL: http://www. Clin Chim Acta 2000..12 to 0.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Third National Report on Human Exposure to Environmental Chemicals. Beryllium [online]. Element reference values in tissues from inhabitants of the European community. 1990. McCanlies EC. 106. HLA-DPB1 and chronic beryllium disease: a HuGE review.74:162-166.htm. Comparison of representative ranges based on U.atsdr. Trace metals in urine of United States residents: reference range concentrations. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Howerton K. Levels of beryllium in urine for the U. which approximate this Report’s limit of detection. and the 95th percentile for males in NHANES 2001-2002. In other studies.76(1):53-59. 20012002. Int Arch Occup Environ Health 2001. Minoia et al. 2000.cdc. Centers for Disease Control and Prevention (CDC). Review of elements in blood. Hamilton et al. Pirkle JL. Genetic and exposure risks for chronic beryllium disease. 1990. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Gallorini M. Atlanta (GA) 2005.95:89-105. Environ Res 1998. 0.gov/toxpro2. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Paschal DC. et al.. Weston A. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Apostoli P.. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. They reported urinary beryllium levels ranging from 0. References Apostoli P. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i.23:827-839. blood.S.157:388-398.. Sampson EJ.Metals (i. Pozzoli L. and the fact that most NHANES participant levels were undetectable. Clin Chest Med 2002.1 μg/L). patient population and literature reference intervals for urinary trace elements.html. 1998). 3/27/08 Komaromy-Hiller G. VI.296(1-2):71-90. Sabbioni E. Maier L. Kriess K. Trace element reference values in tissues from inhabitants of the European community I.e. Environmental Health Criteria. Jackson RJ.

500-.40) 1.00-1.200-.300-.300) .300 (<LOD-.300 (.20-1.362-.20-1.400-.376-.398) < LOD < LOD < LOD < LOD < LOD < LOD .50) 1.300 (. Since 2001.300) . < LOD means less than the limit of detection.500-.600) .500-.200-.40-1.378-.30) 1.00 (1.600 (.300 (.283 (.400 (.368-.400-.500) .50 (1.300 (.10 (1.382 (.900-1.400 (.400 (.500-.00) .400-.50 (1.309-.400-.200 (.300-.300 (.00-1. 7440-43-9 General Information Cadmium is a soft.500 (.60) Total * .326 (.300) .600) .300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) 1. Cadmium also may be emitted into the air from zinc.500 (.400) .500 (.400-.600 (.300) .600-.400) < LOD .00-1.500 (.400) < LOD .460) .700) .600) .400 (.600 (.50 (1.400-.600-1.700) . or copper smelters (U.304 (.600 (.3.300-.400) .421 (.500-.300 (.900-1.00 (.400-.300) .359-. as zinc sulfide) and to a lesser extent.449) Selected percentiles ( 95% confidence interval) 50th .400) .300-.300 (.Metals Cadmium CAS No.300) .300) .400 (.400) .300-.70) 1. lead.400) .20-1.331) .400 (.400 (.300-.400) .400 (.300) .30 (1.10 (.500 (.300 (.3.304-.10) 1.300-.300-.500) .20) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.500 (.00-1.300 (.500 (.50) 1.600) 90th 1.400 (.333 (.400) .usgs.80 (1.40) 1.500 (.600) .400-.00 (.00 (.304 (.600 (.10) 1. population from the National Health and Nutrition Examination Survey.403) .400 (.600) 1.50-1.80) 1.600 (.289-.800-1.10) 1.337) .700) .266-. respectively.500-. coatings and plating.400 (.10) 1.400) .700-1.700 (. which may vary for some chemicals by year and by individual sample.900-1.900 (.90) 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 .600 (.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.412 (.60 (1.300 (.378 (.500-.S.50-1.700) .300 (.300 (<LOD-.400 (.900-1.20 (.300 (.300 (.300) .600 (.235 (.20) 1.20-1.20) 1.60) 1.00 (1.10 (1.30-1.20) .424) * .600) .200 (<LOD-. The predominant commercial use of cadmium is in battery manufacturing.800-1.452) .40 (1.40 (1.gov/minerals/pubs/commodity/cadmium).30) 1.10 (1.393 (.30) .700) .441) * .50-1.427) * .600 (.10) 1.300-.00-1.800) .470) * .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 * * * * * * .216-. see Data Analysis section) for Survey years 99-00.00-1.366) * * .10) 1.60 (1.20-1.400) .60) 1. cadmium use has declined in response to environmental concerns (http:// minerals.50-1.70) 1.400-.40 (1.600 (.300 (<LOD-.60-1.00-1.20) 1.403 (.386-. during refining of lead and copper from sulfide ore.60) 1.20-1.200 (<LOD-.500 (.425 (.395 (.300-. malleable.300 (.900-1.500-.S.30-1.20 (1.20) 95th 1.275-.500) .200-.200 (.400) < LOD .500) .S.700) .600) .300) 75th .30-1.500-.10 (1.60 (1.30-1.700) .300) 1.600 (.400) .00 (.500) .700-1.800) . and nonferrous alloys.00) .200 (.296-.600-.60 (1.300-.20-1.70) 1.400-. and 03-04 are 0. Other uses include pigment production. plastic stabilizers. and 0.200) .900-1.900-1.900-1. and incineration of municipal waste materials.500-.500-.400 (. EPA.500-.30-1.30) 1.40 (1.800 (.00-1.90) 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 . interval) .900-1.00 (.367-.400 (.420 (. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.600 (.500-.300) .300) .20) .513) .600) .20) 1.500-.10 (1.300-.60 (1. Fourth National Report on Human Exposure to Environmental Chemicals 199 .400-. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.361-.255) . bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.300 (<LOD-.200-.400) . U.468 (.00 (.00-1.00 (.700) 1.344) .00 (.40 (1.40 (1.600 (.600-.700-1.300-.500-.10 (1.20) 1.800) 1.900 (.400 (.00 (.900-1.400) .500-.70) 1.400) < LOD < LOD < LOD .300-.14.20) 1.300-.300-. 01-02.50) 1.800 (.500) .400) .500-.80) 1.300) . 0.400) .300-.600) .00 (.313 (.200-.10) 1.40-1.50 (1.426-.10) 1.500-.300-.300) .500) .400 (.10 (1.200) .300-.300-.300-.600) .400 (.40 (1.600 (.700) .

251) .255) .194-.520-.17) .15) 1.295) .519) .107-. however.350 (.200 (.381-.550 (.13) .148) .230 (.260-.440-. wheat.265 (.203) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210 (.308) .280 (.310 (.596) .06) .191 (. To a lesser extent.13 (.201 (. Renal tubular and glomerular damage.366-.200-.390-.273 (.232) .680 (.220-.07-1. Cadmium absorption may be increased with iron deficiency (Berglund et al.208-.060-.989-1.322 (.354) .790 (.09-1.990) .479) .466 (. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.03) .530 (.065-.83) 1.450 (.221 (.818 (. 01-02.06.237-.233) .223 (.52 (1. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.41 (.886-1.74) 1.733) .20 (1.490) 1.480) .510-.167-.284) .372) .940-1.141 (.229) .230) .313) . The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.120 (.430-.222) . About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.249) .580) .445 (.30-1.130 (.187 (.440 (.265) .128 (.387) .806) .972 (.713) .360) .226) .366) .175 (. 2003).279 (.38) . drinking water is a source for cadmium intake.38) 1. and 0.37) 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 .207-.800 (.190-.121 (.240-.610) . including many food crops such as cereal grains.551) .447 (.135 (.36) 1.977) .980-1.875 (.38) .51 (1.210) .160) .476-.151-.193 (.277 (.38) 1.01) .169-.282 (.412) .32 (1.135-.870) .490) .493-.393-. and various seeds.153-.189) .134) .886) .339) .109 (. interval) .918-1.114-.310) .963-1.199 (.34) 1..730-.210) .241) .184-.081) .820 (.191-.481) .500) .101) .210 (.090) .890 (.875) .227 (.330-.221) .171-.28-1.800-. 2003.S. and 03-04 are 0.390-.892 (.748-1.633-1.20 (1.400-.623) .231) .980) .43) 1.220-.980) .078 (.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 .150) .25) 1.206) .067-.239 (.272-.210 (. potatoes.06-1.238) .456-.980-1.175 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.261-.206 (.196-.426 (.240) .220) .919) .229-. Diamond et al.25 (1.190-.204 (.233) .216 (.20 (1.960) 1. 200 Fourth National Report on Human Exposure to Environmental Chemicals .243-.200-.302 (. calcium.510) .260-.191-.351-.540) .202-.820) 1.Metals 2000)..733-.892-1.150-.700-.475 (.06.192-.160-.433-.246) .067-.445 (. 2003).462 (.15) .263) .790 (.04 (.238-.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .115-.181 (.633 (.192-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * . respectively.157) .717-.198) .980 (.170 (.705-.390 (..820-1.72) 1.219 (.15 (.336) .13-1.06..753-.289-.270 (.519) .22 (.177-.02-1.700-.640) .210 (.47) 1. Horiguchi et al.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.087-..160) .270 (.180 (.366-.220) Selected percentiles ( 95% confidence interval) Sample 95th 1. For nonsmokers who are not exposed to cadmium in the workplace. rice.498-.700-.763-. an inducible metal binding protein.22 (1..470-.455 (.214-. 2004a.686-.388-.209 (.960 (.17 (.200 (.836-1.160 (.220 (.** Survey Geometric mean (95% conf.165-.092) .170-.24) 1.01-1.092 (. Cadmium is absorbed via inhalation and ingestion. 2001).436-.202 (.126) .741-1.362) .229) .257-.855-1.327 (.17 (.320) .482) .235) .82) 1.551 (. 0. 2003).860) 1.178-.100-.210 (.080 (. With chronic exposure.06-1.817 (.262) .232 (.110-. zinc.061-.173) .234 (.300 (.20) 1.28) 1.203 (. Cadmium in soil is absorbed by plants.607) .189-.219 (.257) .500) 90th .57) 1.299) .219 (.193-. whose body burdens of cadmium can be approximately twice that of nonsmokers.061 (<LOD-.394-.589 (.189-.539) .423-. see Data Analysis section) for Survey years 99-00.249-.848 (. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.326) .813 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers.247) .440 (.458 (.01 (.316 (.109-.858 (.430) .450 (.714-1.077 (.766 (.290-. 1999.306 (.140 (. copper) and protein. Kikuchi et al.329 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.492 (.507) .283 (.195-. ingestion through food is the largest source of exposure. population from the National Health and Nutrition Examination Survey.890-1.255) .559 (.880) .04 (.10 (1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.20-1.530) .255) .545 (.112-.28 (1.183-.077 (.48 (1.17 (.190-.452 (.179-.843-1.300) .261-.157-.211 (. 1994).136) .839 (.400-.285-.817 (.281 (.19) 1.090) .253-.230) 75th .12-1.170-.148-.211-.810-1. **All results are corrected for molybdenum oxide interference in the ICP-MS method.260 (.12 (.

Jarup et al.S.166 (.253) .225) .318 (.666-.238-.865 (.144-.140-.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .093 (.201-.143) .255-.094) .154-.098) .163 (.690-.729 (.263 (.136-.906) .267 (.07) .446) .247-.826-1.137 (.687-. population from the National Health and Nutrition Examination Survey.078-.08) .687 (. 1999).090 (.404) .292) .421 (.647-.484 (. 1996.387 (.537-.481 (.617 (.336-.091) .224 (.223) .985 (.830-1.700) .722-.176 (.414-.266-.783) .281) .297) .196 (.199-. 2004).998) .208-.181-.181) .143-.209) .827) .146-.757) .688-.321) .16) .438) 90th .232) .438-.757 (.335 (.404 (.38) ..175-.678 (.444-.185 (.850) .183) .607) .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 .206-.927-1.802 (.074-.10) 1.163) .168 (.767 (.212 (.490 (.533) .690-.101) .296 (.784) .311) .137-. 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...189-.209) Selected percentiles ( 95% confidence interval) Sample 95th .208 (.423 (.449) .218) .156-.432 (.00 (.795) 1.562-.078 (.130-.686 (.191) . 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.650-.282 (.199 (.154 (.140-.273 (.207) .157-.182) .288-. 2002.501 (.917) .283 (.630-.221 (.05) 1.177) .112) .631) .174-.227-.12) 1.175 (..839) .123-.247-.818) .288) .239-.207-.178-..382) .192) .818) .667) .077-.491-.979 (.234-..754) .123-.316 (.191-.240) .767) .551) .220 (.234) .266) .274) 1.769 (.198) .708-1.433-.300-.096) .085-.176 (.725-1.147 (.235) .162 (.289) . a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.245 (.700 (.431) .418-.187-.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.210 (.185) .252 (.07 (. 2002.826-1.187) .391-.084-.182) .16) 1.962) .261-.182) .268 (.228-.538) .929) .473 (.216-.941 (.415) .678-.159 (.190 (.156 (.716-.175 (.487 (.178) .158-.779 (. 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.159 (.418) .233 (.381-.204-. most often a result of occupational exposure (Roels et al.364) . At lower environmental exposures.331 (.157-.350) . 2004b). However.343-.426-.097) .168-.281) .783 (.340) .148 (.500-.200 (.440) .075-.06 (. 2002.107) .663 (. 1999).789 (.308) .293-.278) .261) .884) .516-.09 (.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .850) .308 (.352) .591 (.191 (..091 (.833-1.197-.828) .219 (.950) .229) .250) .147-.856 (.940-1.173-.181 (.236-.434 (.472) .718 (.** Survey Geometric mean (95% conf.412 (.316) .289) .338 (.00 (.304-.727-.222-..131-.559-.813-1.674-1.210 (.106) .171-.170-.104) . 2003.170 (.712 (.280 (.377-.874-1.719 (.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 .696-. 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.545) .100 (. 2000.388-.830) .184-.126 (.423-.253 (.873 (..184-.263-.261 (.085 (.221-.161-.242) .398-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.740 (.940 (.690 (.507-.086 (.240) .806-1.476) .303) .919 (.414 (.091 (.653) .668-.917 (. Olsson et al.387-.541) .716) .304) .382-.691-.693 (. 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.084 (.792 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.205 (. can result from high dose chronic exposure.909-1. 1999).17) .531 (.183 (.215 (. interval) .181 (.210) .645-.190 (.219 (.104) .288 (.083-.136-. Fourth National Report on Human Exposure to Environmental Chemicals 201 .067-.202 (.267 (.470) . Horiguchi et al.051-.02 (.536 (. During the 1950’s and 1960’s.329 (.614) .211 (.479 (.518) .234 (.256-. Staessen et al.122 (.232) .622 (.440) .156) .560-.241) . Noonan et al.247-.813-.150-.075 (<LOD-.470) .135) .147-.226) 75th .876-1.270 (.931 (.143-.168-.071 (.111-.194-.184) .441-.325 (.113-..13) .856) .173 (.063-.238) .225) .

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

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64 (4.93 (4.4 (9.87 (4.7) 10.30-5.05) 5.80 (8.88 (8.1-12.00) 6.40-5.0 (9.05) 5.8) 11.40-5.42) 7.2-13.59-5.7 (8.2.99) 7. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5-14.26) 7.62 (5. respectively. scintillation counters.10 (6.8 (11.87 (4.89) 5.31-8.4 (10.7 (10.3-13.2-13.17-6.8) 12.70) 5.3) 9.26-11.71 (4.33 (5.61) 7.70 (5.97 (7.80 (4.90-10.95 (3.60-7.70 (4.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.40-11.37) 7.53-11.08) 7.5-13.79 (4.40-5.72) 4.70) 7.01-6.74 (4.3) 10.35-5.32) 4.25 (3. see Data Analysis section) for Survey years 99-00.80-10.14.3) 12.10-9. nausea.90 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2 (9.50 (4.9) 11.42) 6.30 (6.7 (10.43-8.04 (4. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.14 (4.17 (6.9 (11.35 (4.20) 5.55 (4.99-11.90-10.9 (11.13 (8.87) 5. For absorbed cesium salts.40-11.99-6.35 (4.20) 4.16-6.63-4.97) 4.54-11.70) 5.10 (8.8) 9.70 (6.8) 12.6) 11.7) 11.5 (8.0) 11.6) 10.01-8. and high-power gas-ion devices.0-15. interval) 4.02 (4.27-5. 2004). Whether cesium compounds are carcinogenic is unknown.7 (9.4 (9.04) 7.92-13.90) 7.6 (9.5-14.70-8.77-8.23-4.21 (4.2 (9.81) 4.34) 9.94) 4.81 (4.90-8.59-5.12-5.0 (10.3) 10.49) 4.45-5.47-8.00) 7.7 (11.30-10.40) 5.14.90) 9.70 (9.60 (8.98 (7.12) 5.59) 7.40) 7.49 (4.4) 12.03 (4.44 (8.90) 5.20) 8.56 (4.70 (8.30 (6.94 (4.40-7. population from the National Health and Nutrition Examination Survey.60-6.54) 4.4) 10.8) 9.89) 4.40-5. although cesium was generally of low toxicity when given to animals.50 (6.63) 6. and as polymerization catalysts.22-4.73-5.00-4. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.50) 5.6 (9.00 (7.37) 5.50 (4.3) 10.5-16.0-13.00-10.15-8.10-5.10-7. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4) 12.9) 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 4.00-9.Metals Cesium CAS No.00-8.87-7. 01-02.80-13.49 (5.40) 5.90-12.55-11.1) 9.80 (8.81) 9.27) 4.70 (8.00-8. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.67 (4. and 03-04 are 0.9 (10.9) 8.91 (7.10 (8.46) 7.05-5.95-4.59-5.9 (11.9) 12.9) Total 4.6 (11.82-4.2) 11.60-5.13 (5.6 (9.94 (4.64-5.36 (3.0) 12.74) Selected percentiles ( 95% confidence interval) 50th 4.26 (3.9 (10.23) 9. Most human exposure to cesium occurs through the diet.20-7.8-13. and cardiac arrhythmia (ATSDR.61-6.3-13.64) 4.38) 5.03-4.56-11.4) 9.32 (3.10 (6.50 (4.1 (9.80-11.50 (7.26) 4.52) 7.21) 90th 9.84) 8. semiconductors.32-5.60 (7.0) 11.80) 7.8) 11.36) 3.43 (5.25) 4. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.7) 10.2) 12.5) 12.81-14.10-8. Little is known about the health effects of this metal.81) 4.71-5.77 (9.90) 4.90 (6.80 (4.33 (6.29 (4.20) 7.49) 75th 7.0) 9.6 (11.70-5.30) 7.1-13. diarrhea.60-7.9 (11.3 (8.60) 7.86-12.62) 4.12 (4.1 (10.2-12.0) 12.56) 5.08 (7.42-7.7) 11.62 (5.96 (6. Fourth National Report on Human Exposure to Environmental Chemicals 205 .4) 11.64-10.98 (7.09) 5.30) 5.71) 4.95) 5.90-10.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1) 10.20 (6.17) 4.68) 9. and clay.6 (9.71-8.5 (10.73-11.80 (8.7 (10.12-11.09-5. photographic emulsions.50) 9.08 (6.77 (4.53 (6.82) 5.60-6.86-11.87 (4. and 0.80-10.45-8.80-10. infrared lamps.4) 95th 11.86 (7.40 (4.83-4. 0.52-9.84-9. Radioactive 137Cs has been used medically to treat cancer.0) 12.5) 10. However.71 (8.71-9.39) 7.20 (4.22 (4.77 (9.68 (7.90-12.3 (8.20-5.8) 12.63 (4.3-15.76-6.55 (7.50-7.1 (11.20-4.1) 11.69-6.70 (6.99) 9. soil.99-11.00) 4.7 (9.80-6.01) 7.29) 4.08-5.07-11.27 (7.13-8.89-5.84-5.84 (4.97-7.34 (4. cesium hydroxide is corrosive and irritating at high concentrations.1) 9.60-12.7-14.47-4.59 (5.24) 4.2-13.0) 10.6) 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 (10.20-8.1-12.66 (7.84) 5.39-4.7 (9.91-8.4) 10.13 (7.90) 5.64) 5.08-5.83) 6.3) 10.5) 9.25-5.33-5.4-13.94-4.57-5.16-6.8 (10.05-5.60) 7.56 (4.36 (6.74-5.1) 11.60) 5.80 (4.S. the body half-life is estimated to be 70-109 days based on 137Cs exposures.2-14.72-7.64) 5.07) 4.03 (4.

13 (3.22-11.S.63 (6.38 (3.58) 3.47) 6.96 (4.2) 11.58) 8.74-11.41) 4.54 (5.7) 10.30) 10.91 (5.04-11.79) 6.74 (4.04) 6.43-11.05) 6.16-5.17 (6.79 (5. Biomonitoring studies on levels of cesium can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cesium than are found in the general population.88-10.60 (3. population results shown in this Report (Alimonti et al.74 (5.13-9.53 (4.03) 6.51 (4..71) 6.99-4.59-8.07) 8.35) 3.10 (5.13) 7.51) 4.56) 4.47 (4. population.0) Total 4.07 (5.02-4.66-6.20-4.31 (4. 2004).60-10.07-4.18 (7.7) 10.91-9.17-4.89-4.90-8.29) 4.79) 4.66 (5.22 (3.42 (5.28) 7.02 (5.43 (4. (2000) found urinary cesium levels that were slightly lower than those reported for the U.51 (3.98) 5.12-6.62) 5.06 (3.00-5.14 (6.17) 9.95 (5.29) 4.38) 10.21-3.84-11.54 (4.09) 8.03) 5.24-4.20-4.3-15.92) 3.05-3.08) 4.39) 5.5) 7.33-3..42-6.37) 4.7-12.91) 5.91 (5.96) 4.51 (7.53 (6.9) 10.31-6.12) 3.87 (5.S.05) 3.50 (7.00-4. 1990).73-4.46) 6.38-7.63 (7.15-11.08) 3.3 (8.12 (3.48-6. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.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 5.49) 3.47 (7.44-9.71 (7.68-11.94 (5.95-6.91) 5.98) 5.87-4.92 (5.97-5.8) 5.74) 75th 5.6 (9.43 (3.14-7.42 (4.1) 11.84-7.28) 8.5) 9.27 (8.95-12.95) 8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.44-5.40-5.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.3) 11.8 (9.96) 4.21 (2.79-5.28 (4.97-4. Minoia et al.16-8.16-8.56) 4.85) 5.39) 8.66 (6.22) 6.36-3.4) 10.21-5.0) 7.77 (6.30 (4.43-6. interval) 4.90-3.33 (5.14-6.62-8.11 (5. population from the National Health and Nutrition Examination Survey.07) 8.63) 6.0) 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 .00-8.2 (8.55-5.10 (3.36-10.29-3.98 (7.99-9.70) 6.30 (7.58-5.43) 8.84-7.3) 9.96-4.99-9.40) 7.41 (5.34 (5.5 (9.56-10.15-4.53) 3.50 (5.56) 3.06) 4.68) 6.81 (4.00 (8.20) 5.29-3.57) 3.99 (3.70) 7.78) 4.96-4.43 (4.60 (5.55) 4.64) 9.3) 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 3.60-20.14) 4.31-4.06 (5.67) 5.28 (5.95) 4.48) 7.47) 6.81 (4.76-9.84-9.58 (6.65 (6.16) 5.08 (3.63-6.85) 4.61 (7.95) 10.10) 7.6 (9.78) 4.84-9.31 (4.64) 4.27-6.93-7.65-4.75 (6.05 (4.01-8.27-4.47) 4.67 (5.09 (4.77 (4. Two small studies of European populations reported urinary cesium levels similar to U.3 (10.58 (4.05-3.83-6.46-8.41-4.27) 4.56 (4.27 (6.26-6.33 (5.8) 6.6) 6.95 (3. 2005.08-7.26 (4.50-5.60) 3.41 (8. and were also roughly similar to those in this Report.35 (4.87) 5.68) 3.03-6.76-6.78 (3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.64) 5.14-4.75-11.98 (6.99) 4.05-4.83-7.48) 90th 7..78 (3.64 (4.30-4.04-5.37-3.8) 10.10 (3.97) 8.82-4.30) 10.43 (8.9 (9.46 (7.50 (6.20-4.44 (4.24-10.25) 4.73 (3.09) 4.66 (5.25) Selected percentiles ( 95% confidence interval) 50th 4.38-12.08-3.83) 8.30 (3.91-7.00) 6.63-6.77) 4.63 (4.00-5. Komaromy-Hiller et al.19-6.08 (5.36-6.00-9.42-4.68) 4.33-8.45-6.50) 4.88-4.94) 7.47) 7.5) 9.10-4.00-10.42-4. Using clinically submitted specimens.0 (7.82) 7.18-6.51 (3.20-8.19-3.74) 3.65-3.54 (3.11 (5.35 (3.06) 5.68 (4.72 (4.2 (8.41) 9.77 (7.90 (7.91-6.03-5.44 (8.08 (6.41-7.50) 8.23 (7.52-5.61-3.17) 4.53) 6.41 (4.50) 4.75 (7.9 (10.15) 95th 8.59) 4.18-7.14) 4.50) 4.26 (3.46 (8.35-7.24 (3.54 (4.08) 4.15 (7.90-8.55 (3.79) 9.18) 8.51 (4.44) 3. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.45 (4.27 (6.64-6.35-11.S.29) 5. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.3 (9.70 (7.40) 6.77-5.64 (8.13-9.2) 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 3.46-4.93-9.04) 5.85-4.21-4.30-4.72) 4.67 (6.39 (5.91) 4.72-5.38 (3.86 (4.80) 6.

Spezia S.296(1-2):71-90. Centers for Disease Control and Prevention (CDC). and serum of Italian subjects. et al.html.cdc. Available at URL: http://www.95:89-105.atsdr. Costa R. Ronchi P. Sewell CM. Third National Report on Human Exposure to Environmental Chemicals. Rapid Commun Mass Spectrom 2005. 4/8/09 Alimonti A. Wood CM.14:120-128.gov/toxprofiles/tp157. Comparison of representative ranges based on U. Mincione G. Gallorini M. 2000. New Mexico. Sci Total Environ 1990. Gatti A. Toxicological profile for cesium. A study of 46 elements in urine. et al. Paschal D. cesium. et al. Clin Chim Acta 2000. Wolfe MI. J Expo Anal Environ Epidemiol 2004. patient population and literature reference intervals for urinary trace elements. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. Sabbioni E. blood. Voorhees RE.S. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Pozzoli L. Ash KO. Trace element reference values in tissues from inhabitants of the European community I. antimony and tungsten. Pietra R.19:3131-3138.2004 [online]. Atlanta (GA) 2005. Howerton K. Mott JA. Assessment of urinary metals following exposure to a large vegetative fire.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Forte G. Komaromy-Hiller G. Apostoli P. Minoia C.

640) .960-1.427-.06 (.340) . 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.33-1. 208 Fourth National Report on Human Exposure to Environmental Chemicals .64) 1.03) .379 (.410 (.730) 1.480 (.370-.430-.25-1.04) 1.23-2.330) .700) .26-2.520 (.920) 1.460 (.44) 1.417) .950-1.660) .12) 1. population from the National Health and Nutrition Examination Survey.09 (.870 (.890-1.50 (1.07-1.04-1. varnishes.520-.375 (.520 (.04-1.580 (.390 (.399) .03 (.15-1.32 (1.550) 90th .450) .13) 1.32 (1.00) .430 (.04 (.404) .316-.73) 1.550-.670-. shiny.14-1.840) .01-1.380 (.270-.461 (. interval) .370 (. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.07 (.46 (1.590 (.367 (.285 (.26) Total .820 (.14) .470) .500 (.570-.580 (.410) .740-.750 (.530) .463-.380-.610-.460-.460) .03) 1.950 (. The cobalt used in U.67) 1. hard metal or in combination with other elements.05 (.810-. blue-colored pigments.339 (.17-1.330-.333-.06-1.39) 1.510) 1.520) .830-1.520 (. automobile airbags.420) .750-.53) 1.430) .22 (1.640) .950-1.81) 1.12) 1.610) . and in synthesizing polyester and other materials.930) .450) .414) .502) .460 (.379 (.420) .790) .28 (1.32) 1.26) 1. Usual human exposure is from food sources.08-1.370-.850-1.300 (.540-.850-1.450) .348-.S.52 (1.47) 1.372) . Cobalt occurs naturally in airborne dust. and fertilizers.380 (.16) 1.02-1.33 (1.530 (.369 (.680) .920-1. and magnetic recording media.820 (.388-.24 (.380-.700) .68 (1. and soil.670 (.340-.670 (.310-.418 (.670 (.430) .04-1.980-1.352 (.540-.550 (.820 (.47 (1.28 (1.09 (.32-2.355-.92) 1.760 (.42) 1.50) 1.410 (.600) . diamond-polishing wheels.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 .99) 1.760) .60 (1.420 (.930 (.690-.21) 1.450-.398) .410 (.470 (.564) .640) .405-.740-.540) 1.940-1. 01-02.590-.22-1.280-.320 (.520) .810) .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 .490-.620-.670-.16-1.16-1.400-.610 (. see Data Analysis section) for Survey years 99-00.08) .630-.340 (. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.630 (.890) .340-.348-.19) .294 (.910-1.48) 1.900) .520-.81) 1.590-.343 (.690 (.900) .37-1.940 (.460) .15 (1.680 (. and 0.430 (.790 (.890-1.800-. and kitchenware.16 (1.01-2.305-. Cobalt is used as a drying agent in paints.390-.450) .428-.410 (. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.880-1. large appliances.360-.310 (.515 (.410-.48) 1.07.364-.600-. Cobalt compounds are used as catalysts in producing oil and gas.334) .398 (.394) .290-.434 (.500) .327-.03 (.370) .620) .416) .540-.47) 1.424) .543) .465) .570-.419) Selected percentiles ( 95% confidence interval) 50th .390) .496) .487) . steel-belted radial tires.570) .710) 1.65) 1.24 (1.28-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.359 (.680) .454 (.540-.590) .330 (.291-.410-.350-.259-.270-.890) 95th 1.08. and inks.373-.390 (.581) .680 (.570) .56) 1.930-1.26-1.386) .660) .900) .07-1.05) 1.350 (.380 (.301 (.59 (1.16) 1.660-.800) .36) 1.440-.520 (.519 (.07. respectively.371 (.469-.410-.900-1.870-1.900-1.350-.710) .460) .17 (1.610) .03-1.800-.620-.850) 1.980) .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 .452 (.480 (.22) 1.750 (.23) .870 (. seawater.28 (1.583) .374 (.480-.740 (.410) .300-.Metals Cobalt CAS No.06 (.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.430 (.47 (1.16 (.370-.03) 1.373) .331-.308-.32) 1.360-.520-.450-.350) 75th .810) .435 (.860 (.770) .523) . hard metal (alloys of cobalt and tungsten carbide).360-.16 (1. It is also a component of porcelain enamel applied to steel bathroom fixtures.530-.319) .790-.270-.29 (1.01 (.75 (1.600 (.340) .940-1.333-.520-.05 (.630 (.950 (. Cobalt compounds are also used in manufacturing battery electrodes.316 (.490-.350-. It is emitted into the environment from burning coal and oil and car and truck exhaust.650 (.890-1.17 (1.850) .880 (.499 (.650-.17 (.09) .20 (1.01 (.390 (.45 (1.560 (.570 (.313) . and 03-04 are 0.950) .580 (.410 (.710 (.338-. 0.431) .750 (. industry is imported or obtained by recycling scrap metal that contains cobalt.431) .650 (.690-.336-.620-.377-.S.393-.

428-.303-.736-.33) 1.297) .582-.911-1.434-. 1994). an essential human nutrient.700 (.476-.329 (. 1979).740-1.471 (.393-.457) .297-.461) .753-.274-.10 (.895-1.513-.361 (.833-1.248-.03-1.723 (.215-.821 (.289) .83) 1.932-1.792 (.57) 1.425-.606 (.750) .426 (.550-.376 (.328) .462) .667-1.365) .251-.335 (.964 (.792-1. population from the National Health and Nutrition Examination Survey.365-.247 (.513) .523 (.00) .396) .595) .352 (.626-.737 (.861 (.60) 1.487-.421) .616-. 1972).479) .378 (.. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.744) 1. using hard metal cutting tools.471-.35) 1.328 (.368 (. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.313 (.481) 90th .279 (..727 (.591 (.848 (.700 (.562) .Metals fabricated from cobalt alloys (Lhotka et al.879-1.73) 1.337 (.505) .508-.963) .358 (. Cobalt is absorbed by oral and pulmonary routes.547 (.673-.774 (.435-.562) .694) .503-.467-.19) . A portion of cobalt retained for long periods is concentrated in the liver.391 (.00 (.304) .00 (.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 .425) .02 (.644 (.317 (.29) . A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.634-..400 (.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 .857-1.291 (.27) 1.442-.387) .286) .259-.331-.683-.256-.599) .850 (.513 (.640) .50) 1.250) .15) 1.826-1.10) 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .393 (.378-.380-.750-.738 (.11-1.598 (.10) .290 (.534 (.04-1.660-.662) .368) .298 (.310) .301) .296-.300) . Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.728) .268 (.560-.937 (.600-.29 (1.469-..248-.630-. 2003).00 (.257-.237-.439) .785) .333-.777-.487-.963-1.533 (.952 (.449) .352) .635 (.333-.756 (.552 (.438) .829) .898 (.457-.313-.27) 1.938) .278 (.09) 1.386 (.281) .850-1. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.632-.407) .234 (.333 (.630-.384) .593) .435 (.25 (.829-1.388 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.900-1.417) .16 (.272-.861-1.29 (1.35) .574-.319-.55) .12 (.290 (.50) 1.S.728 (.955) .344-.523 (.282-.404-.280-.983-1.611) .275-.468) . Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.00-1.239-.708) .33) .14 (.529 (.342-.329-.313-.50 (1.444 (.585) .11-1.457 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).409) .429) 1.348) .313-.381) .402 (.983) .362 (.257 (.353 (.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 .362) . cobalt is excreted predominantly in the urine.475 (.290 (.495 (.03 (.548 (.500 (.488) . Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.04 (.54) 1.563-.328 (.419) .990) .372) .804) 1.361 (.691 (.534-. Smith et al.23 (1. Once absorbed and distributed in the body.394) .327 (.667-1.537 (.851 (.277-.301-.392 (.561) .316 (.06 (.275-.594) .368) .608 (.781) 95th 1.929) .36) 1.963) .259) .396) .960 (.326-.25 (.327-.786-.963-1.378-.917) .17) .872 (.679-.339-.938-1. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.669) .369 (.279) .306 (.842) .955) .259 (.689 (.433) .830 (.243-.452-.00) .24) .615) . 1972).905) .304-.847) .407 (.611) .760-1.821-3.382-.449-.306) 75th .296) .824 (.408 (.60) 1.309) .500-.990-1.278-. interval) .313-.703-.738 (.324-.314 (. and to a lesser extent.378-. respectively.895-1.757-1.16) .349) .273 (.294-.36) 1.363) .455 (.16 (1.353-.44 (.362-.515 (.781-1.29) 1.361-.10) Total .343-.355) . in the feces.15 (. Exposure in the workplace may come from electroplating.647) .337) .707) . or using diamond-polishing wheels that contain cobalt metal.581) .753) 1. 1994.30 (1.10-1.733-1.543) .49) 1.313-.29 (1.360) .554 (.844 (.500-.976 (.542 (.343 (.554 (.975 (.12-1.463-.949) ..324) .361-.16 (.388 (.471-..00 (.346 (. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.704-.352 (.271 (.323) .522) .609) .333-.417 (.638-1.479-.838 (.293 (. refining or processing alloys.302-.282 (.28) 1.391) Selected percentiles ( 95% confidence interval) 50th .334) .

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

406:282-296. et al. Pisati G. Bozec C. Epidemiological survey of workers exposed to cobalt oxides. Absorption and retention of cobalt in man by whole-body counting. Schaller KH. Romazini S. Cobalt cardiomyopathy. Health Phys 1972.533:135-152. Ichikawa Y. oxides. The release of metals from metal-onmetal surface arthroplasty of the hip. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Edmonds CJ.” Contact Dermatitis 2001. Lasfargues G.87(5):628-631.69(3):193-200. cobalt salts. Schramel P. and cobalt metals. Am J Epidemiol 1998. et al.216:253-270.88(4):443448. et al. Iavicoli I. Blunn G. Unwin P. Steffan I. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Science 1988. Cobalt and antimony: genotoxicity and carcinogenicity.22:359367. Laippala P.204:147-160. Int Arch Occup Environ Health 1997. salt. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Shirakawa T. Cleland D. Molders J. A report of two cases from mineral assay laboratories and a review of the literature.150. Jarvis JQ. Bacis M. Sci Total Environ 1998. Lison D. et al. Fujimura N. X. Zedda S. 3rd ed. Meyer zum Buschenfelde K-H. Lung cancer risk in hard-metal workers. Outcome of occupational asthma due to cobalt hypersensitivity.58(10):631-634. Rorabeck CH. Ziaee H. Lhotka C. Thakker DM. Mosconi G. Industrial Chemical Exposure: Guidelines for Biological Monitoring.242:1412-1415. Ghat IS. Cannon SR. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Am J Ind Med 2003. Roto P. Zhuber K. Salama A. Gross RT.55(4):269-276. Occup Environ Med 2001. Kato M.28(5):1121-1128. Daniel J. 2001. McMinn DJ.21(2):189-195. J Bone Joint Surg Br 2006. Weber A. J Occup Med 1992. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. a study of 13 elements in blood and urine of a United Kingdom population. DeSantis V. Biological monitoring of workers exposed to cobalt metal. Carnes WH. Hoet P.48:172-173. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Sci Total Environ 1994. Buchet JP. Contact Dermatitis 2003. Kriss JP. Zobelein P.36:732-734. Co-sensitivity between cobalt and other transition metals. 1985. Kraus T. Kristiansen J. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Christensen JM.148:241-248.50(9):835-842. Dickel H. Hoher T. Moulin JJ. Thomassen H. Lauwerys R. Swennen B. J Bone Joint Surg Br 2005. Falcone G. Uitti J. Respiratory health of cobalt production workers. Wild P. Hedge AG. Barnaby CF. Cresti R. Tilley S. Chest 1989. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Sanghrajka AP. Goto S. and hard metal dust. Radulescu M. Salvatori S. Bunn HF. Mutat Res 2003.Metals effects of cobalt. Sci Total Environ 1997.95:29-37. Leghissa P. Smith T.150(1-3):167-171. Iversen BS. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Br J Ind Med 1993. Swennen B. et al. J Orthop Res 2003. Dunstan E. Stanescu D. Kirsch-Volders M. Weyher I. Lisi P. Trace element reference values in tissues from inhabitants of the European Union. Sabbioni E. Linna A. Lison D. Occup Environ Med 1994.45:246-247. Kiilunen M.34:620-626. Chess DG. Goto S. Linnainmaa M. Long-term clearance of inhaled 60Co. Buchet JP. Sabbioni E. Sabbioni E. Alessandrelli M. Zweymuller K. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Boca Raton (FL): Lewis Publishers. J Trace Elem Med Biol 2006. Pradhan C. Lison D. Schank M.44:124-132. Kusaka Y. J Rheumatol 2001. Hammon E.51(7):447450. Palmroos P. Arch Intern Med 1990. MacDonald SJ.20(1):25-31. Vitali MT. Dunning SP. Occupationallyinduced “isolated cobalt sensitization. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Peltier A. De Boeck M. Meier R.157:117121.150:177-183. Sci Total Environ 1994. Angerer J. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Oksa P. Kuska Y. Lauwerys RB. Bourne RB. et al. Thabe H. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Health Phys 1979. Heki S. HoffmannB. Diepgen TL. Lauwerys R.(1-3):133-139. Robinson C. Szekeres T. Goldberg MA. McCalden RW. Int Arch Occup Environ Health. Clin Orthop Relat Res 2003. White MA.

32-1.62) 1.30 (1.55-1.50 (1.60-6.30 (2.00) 2.09) 1.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.90) 2.40) 1.80 (5.00 (2.30) 95th 5.10-4.50-2.25 (1.50 (3.60) 2.80-4.20 (3.90 (3.14-1.10) 1.40-6.80) 1.80) 2.00) 2.90-2.43 (1. leaded glass.20) 4. bronze).50) 2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10-3.20) 1.30-5.86) 1.50) 3.80) 3.70 (2.40-5.20 (4.80-2. Before the 1980’s.60 (1.90) 2.40) 1.30 (4.49-1.50-1.10-1.10) 5.80 (1. 0.80 (1.60 (2.60 (3.10-2.20-3.40 (5.31) 1.70) 4.60) 1.70 (2.50-1.40 (1.87 (1.90 (2.20-3.80 (4.70-6.878-1.80-5.60-1.90 (3. lead was added to gasoline and residential paints and used in soldering the seams of food cans.66 (1.62 (1.50) 1.60 (1. plastics.60) 3. and 03-04 are 0.20 (3.00 (4.52-1.43) 1.60-2.20-3.71-1.50 (2.00-4.60-1.10 (3.60-3. population from the National Health and Nutrition Examination Survey.60) 2.78 (1.50) 2.10-3.60 (2.70-2.87) 1.50 (2.80-3.14-1.50-5.80-4.30 (1.70-5.37 (1.70) 3.70) 2.50 (1.80) 1.90) 1.40) 1.986) .10) 1.12-1.50) 5.68-1.60 (3.10-4.60 (1.20 (1.30 (1. such as lead phosphate and tetraethyl lead.70) 3.40-1.70) 4.80 (2.00) 5.10-3.10-2.20) 4.10-6.90) 2.10-2.60) 4.46 (1.00 (5.50) 4. ceramic glazes.90) 2.60) 1.90-3.30 (2.53) 1.55 (1.00) 2.20 (1.70) 1.10 (2. Lead was used in plumbing for centuries and may still be present.70) 4.20-1.40) 2. the main source of lead exposure for the general U.70 (1.10-2.70) 1.70) 1.30-1.83 (1.70-1.90 (3.80-4.20) 5.50-4.20 (2.00-5.00-6. antique-molded or cast ornaments.g. and 0.10-1.946 (.70-1.40-4.60) 5.32-1.70) 3.20) 3.70-2.70) 1.60 (2.00-4.S.70-2.28.20) 90th 3.39) 1.36) 1.50-6.40-2.900 (.70 (2.75-2.20 (3.900-1.00-2.40 (1.10) 3.75 (1.40-1.00) 1.60) 3.25 (1.40 (1.60) 3.36-1.50-3.50-1.00 (4.50 (4.80) 1.50-4.40) 2.30) 1.90) 1.10) 2.20 (3.80) 2.60 (1.39-1.30) 2.10) 1.40 (2.20 (1.00) 1.80) 1.20-2.20 (3.60) 1.30) 5.80 (1.60 (3.40 (3.40) 4.50 (2.69) 1.70 (5.90-2.50 (2. blue-gray metal that occurs naturally in soils and rocks.90) 5.50) 5.50) 1.00) 6.3.69) 1.80 (1.20 (1.19 (1.20) 3.37-1.Metals Lead CAS No.70-4.60) 5.80-3.90-4.10 (1.00) 3.900 (.80 (2.20-3.30-1.70 (3.51 (1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.60-1.20-1.50) 4.52-1.50-2.20 (2.30-4.20-2. 7439-92-1 General Information Elemental lead is a soft.30) 2.70-1.90) 3.00) 1.40) 5.50-3.30 (3.60) 2.52 (1.3.69 (1.40-3.40-1.20-4.60-1.75) 1.50 (3.80-3. 01-02.90 (1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.30 (2.60 (4.91) 1.60 (1.50) 75th 2.90) 2.37 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. malleable.60) 2.10-2.40-1. solders.90 (4.30-1.75-1.60) 4.30 (2.90 (3. respectively.90 (1. Lead has a variety of uses in manufacturing: storage batteries.S.60-2.90) 3.81) 1. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.50) 1.20 (3.30-2.80 (4.65 (1.40-2.60) 4.60 (3. ammunition.60-4.40) Total 1.90-4.10 (2.25) 1.40-1.80) 2.30-2.90) 1.10-3.60) 2.50-2.10-2.30-2.30 (2.00) .23 (1.30-1.30-6.80 (1.80-3.50 (1.50-1.02) 1.10-6.30 (4.96-2.00) 4.30 (2.70 (1.60-4.00 (1.45 (1.30-1.72) Selected percentiles ( 95% confidence interval) 50th 1.90-6.60 (2. Since lead has been eliminated from gasoline.01 (1.51) 1.20-6.90-4.00-4.00 (1.80) 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. and for radiation shielding.00 (6. brass.40 (2.00-1.70 (1.40-6.04-1.20) 3.40-1.34-1.10 (4.20 (1.50 (2.70) 1.17) .40-2.00 (3.69 (1.00) 1.20) 3. 212 Fourth National Report on Human Exposure to Environmental Chemicals .40-3.10) 3.90 (2.80 (2.43-1.80 (1.80) 1.00) 2.40-3.50) 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 2.70-3. Elemental lead can be combined with other elements to form inorganic and organic compounds.70 (1.90-2.00) 4.80 (3.60) 4.800-1.50-1.50-2.90-2.55-1.89) 1.10 (2.899-.36-1. metal alloys (e.50-5.00-1. interval) 1.20) 2.20) .66) 1.93-2.30 (4.60) 3.40) 3.00) 3.30-2.48) 1.43) 1.90-4.60 (1.20 (3.62-1.10-8. dense.80 (5.10-1.30-1.00) 1.40 (1.10) 2.30) 2.60) 1.50) 7. Lead is most often mined from ores or recycled from scrap metal or batteries.30 (1.50 (4.43 (1.56 (1.50) 1.95) 1. see Data Analysis section) for Survey years 99-00.30 (2.942 (.60 (2.90 (3.60 (2.70 (3.50 (1.10) 3.40 (4.40) 2.70) 4.45-1.10 (1.77 (1.60) 1. In the past.10 (1.22 (1.60 (1.14-1.10) 4.40) 2.

97) 4.589-.21 (2.30-3.700 (.1.70 (2.70-2.800 (.749) .80) 2.600-.03 (1.13-3.900-1. battery and radiator manufacturing) and recreational sources.660) .560-.600) .40) 1.600-. and 03-04 are 0.90-2.800-.70 (2.40 (2.g.30) 2.570-.32 (1.20 (1.60 (1.52 (1.920 (. 2007.11 (1.10) .50 (2.00-2.20 (2.40) 1.923 (.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 1.30) 2.50-2.600 (.90-3.09) 1.00) 1.620 (.90 (1.564 (.12) 90th 2.86 (1.20) .900 (.986) .680-.671-.540-. and contact with soil.700-.40 (1.20-2.630 (.700-.20) 1.30) 1.91) 2.04 (.90 (2.535-.642 (.60-2.540 (.640 (.00) .00 (1.50-2.14 (1.10-1.33.556-. CDC.10-3.828) Selected percentiles ( 95% confidence interval) 50th .50) 2.600-. or after soluble lead compounds are ingested.80-2.80 (2.940 (.800) . which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.19 (1.700 (.90-2. 1991).Metals occupational (e.840 (. 01-02.70) 1.30-1.960-1.60-3.24-1.06) .729-.23-4. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.731 (.03-2.80-2.480-.800 (.650) 1.690) 75th 1.50 (2.625 (.800-1.900) .10) . However.70 (1.10 (. lead-contaminated dust in indoor firing ranges.S.50) 1.935) 1.10 (.773) .700-.20-1.600) .30 (2.591 (.10) 1.80) 2.900-1.810-1.59) 1.752 (.1.850 (.20) 1.900-1.70) 1. Fourth National Report on Human Exposure to Environmental Chemicals 213 .757-.900) .90) 2.40 (1.11) 2.604 (.07-1.50) 3.00 (2.960-1.815 (.60-3.62) Total .82 (1.506-. imported children’s trinkets and toys.00-2.27) 1.90) 2.50) 1.600 (.10-1.710-1.20 (1.02) 1.833-1.636 (.00 (1.50 (1.800) .20) .23) .738) .900) .30) 1.29) 2.10-5.641-.30-2.49 (1.10) 2.941) .02 (.80) 3.600-.808 (. Approximately half of the absorbed lead may be incorporated into bone. interval) .75) 3. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.78-2.70-3.40) 2. bullet fragments retained in human tissue.20) .27 (1. In the blood.30-1.40) 2.680-.10 (1.80) 1.40 (1.90-3. see Data Analysis section) for Survey years 99-00.40-1.60 (1.30) 1.90) 1. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient.29 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.90 (2.59-2.64) 2.86) 95th 2.40-1.50) 1.637-.661-.526-.800-1.745-.862) .86-2.10-1.50) 2.00) .80 (1.790 (.13) .640-.800-.700 (.70) 3.708-.580-.910-.605) .70 (2.78-2.90 (1.78-2.52-1.40) 1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.86) 1.35 (.50 (1.616) .00-2.800 (.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 1.90 (2.785) .20 (1.00 (1.66 (2.700) .822-1. stained glass framing.20) 1.700) 1.20-1.40-1.04-2.40 (2.900-1. pewter utensils and drinking vessels.620) 1.80) 2.90 (1.820-1.558 (.00-1.33 (2. respectively.595-.573 (.900) .795 (.70 (2.30) 1.579-.72) 1.80) 3.40-1.613) .990) 2.40) 1.66 (2.10 (.10-3.80) 1.753 (.628) 1.677 (.22) 1.579-.00) 2.600-.80-3.700 (.80) 1.700-1.920 (.20) .955-1.90) 2.62-4.30 (1.674) 1.70) 1.50 (2.40 (1.20 (2.40-2.33-2.89) 2.30) 2.710-.20 (2. population from the National Health and Nutrition Examination Survey.41) 2. 0.60-1.00) 2.900) .31-3.60 (1.800) .00) .30) .00-1.90-2.80) 2.40) 2.00 (1.900 (.00) . lead-containing folk remedies and cosmetics.40) 1.700 (.20 (1. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.40 (1.75) 4.00 (.651) .20-1.800) .30) 1.40) 3.49) 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 .60 (2.17 (1.695 (.680) .659 (.80) 2.10-3.30-1.572-.970-1.90-4.31 (1. or water contaminated by mining or smelting operations.10 (1.14 (1.800) .50-1.500-.60-2.990) 1.700 (. 2000).931) .14-1.30 (3.553-.30-5. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.40-5.590 (.18-1.688 (.80 (1.10-1.900 (.04) .700-.718) .800 (.730 (.20 (1.20 (1.07 (.60) 2.10 (1.40) 2.70) 3. dust.82 (2.960 (.60 (1.04 (.701) .40 (2.857) .818) . lead-based painted surfaces undergoing renovation or demolition.04) 2.40 (2.915-1.50-3.44-2.700-.20-2.10 (1.833 (. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR. and 0.10-1.70) 2.90-2.900) .20 (3.30-1.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.40-3.766 (.10) 2..691-..610 (. older plumbing systems with leaded pipes or lead soldered connections.50-2.52-1.00-1.848 (.625-.73 (1.

75 (2.79) 1. Staessen et al.10 (.607-.74 (1.51 (1.708 (.56) 3.686) .00) .460-.862-.342-.657) 1.601-.15) 1.38 (2.04-3.89-5.700-.41 (1.926 (. In 1991.812-1.682) .988-1. The skeleton acts as a storage depot.853-1.17 (.588-.739) .615 (.746) .404 (.633 (.900 (.992-1.37-1.712 (.940 (. 1996).04) 2.720 (.688) .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 .17-1. CDC.51) 1.962 (.50-2.03) 1. seizures.03) 2.07) .670) 1.07 (.508) .S.957-1.43-1.62) 2.677-. 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. encephalopathy.69 (1.73-2.61) 1.41) .09-1.914-1.00 (1.592-.18) 1. kidney injury.571-.15-2.551-.608-.85-2.01 (.Metals 90% of the body lead burden in most adults. 2004.887 (.781-1.03 (1.734) . zinc.667) .432 (.593 (.31 (1.53-1.569 (.62-1.79) 2.08) . with lesser amounts eliminated via the feces.18) 2.28) 2.810 (.88 (1.03) 2.655-.15) 1.623 (.707 (.33) 1.19) 1.654) .693 (.639) .559-.62-2.898) . Lead can cross the placenta and enter the developing fetal brain.997-1.683-.11 (1. and paralysis.41-1.731-.71-2.97) 1.22) .710) .97-18.00 (1.52) 1.97 (1.98-2.698) .47) 1.979 (. 2003.612-.625 (. scant amounts are lost through sweat.838) .535) .43) 1.870 (.03) 90th 1.618 (.639 (.59-3.72-2.383-.14) 1.45 (1.. and nails (Leggett.796-1.83) 1.975-1.658 (.49 (1.679-.33) 2.43 (2.793-1. interval) .89-2.933-1. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.26) 2.02-1.82) 1. hair. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.623 (.22) 1.681-.00 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.19-5.603-.25-1.11-1.29 (1.541-.428) . 1995).579-.720 (.35) 2.03 (..18 (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 . O’Flaherty.18) .66 (1.24 (1.98 (1.380-.26) Total .529-.655) .404-.639 (.15-2.725) .617-.561-. For instance.20-3.31) 1.594-.841-1.648 (.64-2.25-1.09) 1.758) .78-4.400) .510-.800-.38 (2.742) .88) 2.09-1.92) 2.609 (.66) 2.681-.15-3.659-. Large amounts of lead in the body can cause anemia.05-1. through the inhibition of certain enzymes.55 (1.22-2.608 (.701) .55 (1.938 (. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.88) 2. BLLs and associated toxic effects differ in children and adults..918-1.06) .649 (.05 (.645-.72-2.721 (.725) .587-.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 .655) 75th 1.94 (1.718) .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 1.977) 1.639 (.50) 1.78 (2.621 (.469 (.990 (. population from the National Health and Nutrition Examination Survey. 1991.44 (1.18) 1.31) 1.492-.981-1.61) 1.677) .47 (1.828) .56-3. 1993).06 (.31 (1.64 (1.56-2.50-2.755 (.28-1.58) 1.94-2.22-1.606-.03) .914 (.27 (1.48 (1.11) .63) 4.08-2. 1995.594-.33 (1.0) 3.05-1.11 (.08) .622 (.774 (.70 (1.64) 2.938-1.676) .87) 1.917-1.03) .61) 1.375 (. 2007).709 (.718) 1.673) .436) .66 (1.61) 3.20) .98) 2.645-.77) 2.03 (.722 (.79 (1. The toxic effects of lead result from its interference with the physiologic actions of calcium.36-2.742) Selected percentiles ( 95% confidence interval) 50th .828-1.408-.920-1.722 (.01) .679) 1.698) .65-2.44 (1.605-.988 (.644 (.68 (1.61) 1.703) .586-.31 (2.668-.404 (. Approximately 70% of lead excretion occurs via the urine.37-1.06) 1.00 (1.75-2.918 (.11 (.97) 1.02) 1.946-1.03-2.644) .44) 1.56 (1.702) .765) .677 (.46 (2.03) 1.992-1.96 (1.882-1.33-1.671 (.23 (1.83 (2. and through binding to ion channels and regulatory proteins.667-.635 (.43 (1.62-3.73) 2.701 (.702) .50-1. Schwartz. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.696 (. based on prospective population studies.638 (. with a half-life of years to decades.88) 1.64) 95th 2.28) .603 (.63) 1. abdominal pain.667-.461) .876-1.641 (.963-1.46 (1.86 (1.39-1.933) .03 (.632 (.50-2.583-.893) .914 (. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.604-.38 (2.571-.615 (. and iron.588-.67-4.971 (.65 (1. 1993.05 (1.52 (1.71 (1.88-2.14 (1.603-.851) .11 (1.753) .496 (.09-1.20) .50 (1.10 (1.85-2.22) 1.652 (.790) .85) 1.11) 1.12-1.43) 2.702-.07-1.763) . Nash et al.53) 1.85 (1.730) 1.47 (2.06 (1.72) .40-1.10) 1.34-1.

. 1999). Borja-Aburto et al. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U.21% of approximately 3.cdc... However. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. 1984. the geometric mean BLL was 3..6% in NHANES 1988-1991 to 1. particularly in the skeleton. and low family income (CDC. Staessen et al.. 1996. adult residents. urban residence. respectively.. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. Schwartz et al.07 µg/dL (Becker et al. both the geometric mean (1.. residing in housing built before the 1950’s.75 µg/dL in U.. 1995. Bellinger 2005.4% in NHANES 1999-2004.S. though there is greater individual variation in urine lead than in blood and greater potential for contamination.e. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. 1996. BLLs reflect both recent intake and equilibration with stored lead in other tissues.Metals µg/dL or higher as the level of concern in children.. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. seizures. EPA.. and decrease fertility (Alexander et al. 2003. 2002a). 2003). High dose occupational lead exposure. approximately 11. 2006). Muntner et al. The U. The Adult Blood Lead Epidemiology and Surveillance program has tracked BLLs reported by states for mostly for occupational but also for non-occupational exposure in U.S.S. 1998). 1991. 2003. 2000).. 2000). environmental levels) and health effects is available from ATSDR at: http://www. Schwartz. with overt encephalopathy..gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. 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.. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. Telisman et al. reduce sperm count. Information about external exposure (i. 1987. More recently. Data submitted through state public health programs from 2006 showed that 1. lead in women may be associated with hypertension during pregnancy. IARC considers inorganic lead compounds probable human carcinogens. 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.. almost double the geometric mean of 1. usually with BLLs greater than 40 mg/dL. premature delivery.. In NHANES 1999-2002 in children 1-5 years old. Overall.S. and spontaneous abortion (Baghurst et al.. CDC. 2002. 2005b). In occupationally exposed adults. Urine levels may reflect recently absorbed lead. Surveillance data reported by U. and organic lead compounds not classifiable with respect to human carcinogenicity.5 per 100. 2006). Jones et al. 2003.0 µg/dL in females (Soldin et al. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH.. may alter sperm morphology.gov/toxpro2.g.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. 1996. and peripheral neuropathy generally occurring at much higher levels (e. 2009). 1994). Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.xls)..000 adults. 1999).9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1.html. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. which is an 84% decline.S. At low environmental exposures.2 µg/dL in males and 3.. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. 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..3 million children tested had BLLs of 10 mg/dL or higher (http://www. Both drinking water and ambient air standards for lead have been established by the U. 2005a). when the geometric mean BLL was 2. Payton et al. Pirkle et al. adults in the 19992000 NHANES sample (Apostoli et al. the prevalence rate has declined annually since 1994 (CDC. 2001). including minority race or ethnicity. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. 2007). Many animal studies have established the multiple neurotoxic effects of lead (ATSDR..6%) were lower than those from NHANES 1991-1994.S.. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. 2005b. Lanphear et al. For example. adults in the 1999-2000 NHANES sample.4% of children had BLLs of 10µg/dL or higher (CDC. Korrick et al.7 µg/dL and 4.atsdr..cdc. 2002). Fourth National Report on Human Exposure to Environmental Chemicals 215 . higher than 100-200 µg/dL).

Hänninen H. Vimpani FB. Baj A. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention.cdc. Lead. Bellinger D. Brody DJ. Mantere P. Pirkle JL. et al. 2002 [online]. References Agency for Toxic Substances and Disease Registry (ATSDR).55(32):876-879. 2005b. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Cox C. Hertz-Picciotto I. Environ Health Perspect 1993. Ewers TG. Ronchi L.atsdr. Adult blood lead epidemiology and surveillance—United States. et al. Int J Hyg Environ Health 2002. 4/14/09 Alexander BH. Ga. 4/14/09 Centers for Disease Control and Prevention (CDC). Acquisition and retention of lead by young children. Chiodo LM.89:330-335. Atlanta.113(4):1016-1022. Blood lead reference values: the results of an Italian polycentric study. Blood lead levels measured prospectively and risk of spontaneous abortion. Available at URL: http://www.53:411-416. MMWR Morb Mortal Wkly Rep 2006. Kaus S. Blood lead levels—United States. Jones RL.htm.gov/toxprofiles/tp13. Hu H. Lanphear BP. Hu H. Coresh J. Cox C. doi:10. Robertson EF. MMWR Morb Mortal Wkly Rep 2005a. Weiss ST. Checkoway H. JAMA 1996. Third National Report on Human Exposure to Environmental Chemicals. Managing Elevated Blood Lead Levels Among Young Children.275:1177-1181. The relationship of bone and blood lead to hypertension. Leggett RW. Henderson CR. Jacobson SW.82:60-80. Public Health Rep 2000. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. 4/14/09 Centers for Disease Control and Prevention (CDC). Preventing Lead Poisoning in Young Children. Weiss ST. Semen quality of men employed at a lead smelter. Bavazzano P.275(15):1171-1176.54(20):513-516. IARC Monogr Eval Carcinog Risks Hum 2006. Roberts RR. Muntner P. Birth Defects Research (Part A). Apostoli P. Krause C. Auinger P.gov/nceh/lead/ CaseManagement/caseManage_main. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Available at URL: http://www. Kuehnemann TJ. Batuman V.73:409-420. Rojas LM.287:1-11. Occup Environ Med 1996. et al.348:15171526.cdc. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. gov/mmwr/preview/mmwrhtml/mm5420a5. et al. Centers for Disease Control and Prevention (CDC). Wager C. Baghurst PA. Toxicological profile for lead.87:1-471. Teratogen update: lead and pregnancy. 1988-2004. Sparrow D. Rios C. Neri A. McMichael AJ. Farias P. Cory-Slechta DA.cdc.115:521-529. Lead and hypertension in a sample of middle-aged women. Angle CR.26:359-371.123:e376-e385. CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Payton M.cdc. Stanek KL.gov/mmwr/preview/mmwrhtml/ mm5532a2. Neurodevelopmental effects of postnatal lead exposure at very low levels. JAMA 1996. 2003-2004. Bellinger D. 4/14/09 Centers for Disease Control and Prevention (CDC). Sparrow D. et al. Vupputyuri S. Available at URL: http://www. Atlanta (GA). Dietrich K. Speizer FE. 4/14/09 Centers for Disease Control and Prevention (CDC). Hunter DJ. Blanco J. Seiwert M. Homa DM. Available at URL: http://www. Rotnitzky A. Am J Public Health 1999. Borja-Aburto VH. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.cdc.htm. Available from URL: http://www. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.150(6):590-597.htm. Meyer PA. Age-specific kinetic model of lead metal in humans. Becker K. 1991 [online]. Pediatrics 2004. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study.10:43-50. van Netten C. Muller CH. Reese YR. Aro A. Neurotoxicol Teratol 2004. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development.htm.8(3):395-401. Rotnitzky A. Wigg NR. Jusko TA. Canfield RL. Hu H.html. Sci Total Environ 2002. Korrick SA. Am J Epidemiol 1999. Jacobson JL. Environ Res 2000. Neurotoxicol 1987. Manton WI.1542/peds:2007-3608. Luukkonen R. Caldwell KL. 1999-2002.Metals Biomonitoring studies on levels of lead provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of lead than are found in the general population.gov/nceh/lead/publications/ books/plpyc/contents. N Engl J Med 2003. Intellectual impairment in children with blood lead concentrations below 10 µg/dL.205:297-308. 2005. Kim R. Lepom P.101(7):598-616. Aug 2007 [online]. Pediatrics 2009. Inorganic and Organic Lead Compounds. Atlanta (GA). Ganzi A. Hernberg S. Korrick S. Kaufman JD. Schulz C. Lanphear BP. Scand J Work Environ Health 1984.

Lauwerys RR. Am J Epidemiol 2001. stable lead isotopes to determine release of lead from the skeleton. blood pressure and cardiovascular disease in men. Int J Hyg Environ Health 2006. 50:31-37.140:821-829. Hickman T. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Nash D.106:745-750. Rocic B.327:109-113. Flegal AR. Lee BK. Kidney Int 2003. Schwartz J. Blood lead. Use of endogenous. Osterloh JD.108(1):45-53. Smith DR. cadmium. Lead. Soldin OP.9:303-327. Toxicol Appl Pharmacol 1993. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Weiss ST. Schwartz BS.S.289(12):1523-1531. Am J Epidemiol 1994. Blood lead concentrations in children: new ranges. and tibia lead with neurobehavioral test scores in South Korean lead workers. lead. and copper in men.63:1044-1050. Schulz D.209:301305. zinc. Hanak B.Metals results from NHANES III. Pirkle JL.153(5):453464. Wilhelm M. Telisman S.118:16-29. Roels H. Kaufmann R. Soldin SJ. Amery A. Lee GS. Association of blood lead. Schwenk M. Arch Environ Health 1995. Rubin R. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Hwang KY. Kinetics of lead disposition in humans. et al. Gavella M. Sherwin R. JAMA 2003. et al. Environ Health Perspect 2000. Revised and new reference values for arsenic. J Hum Hypertens 1995. cadmium. Pizent A. Low-level lead exposure and blood pressure. IV. and hypertension in perimenopausal and postmenopausal women. Stewar WF. population to lead: 1991-1994. Clin Chim Acta 2003. Hu H. Lustberg M. Lee SS. Brody DJ. O’Flaherty EJ. Gunter EW. dimercaptosuccinic acidchelatable lead. Environ Health Perspect 1996. Low-level lead exposure and renal function in the Normative Aging Study. blood pressure. Environ Health Perspect 1998. Cvitkovic P. Exposure of the U. Payton M. Sparrow D.104(1):60-66. Kaufmann RB. Jurasovic J. Physiologically based models for bone-seeking elements. Paschal DC. Magder L. Staessen JA.

70 (1.80 (1.900) 1.326 (. 1993). 2002).30) 4132 4241 03-04 03-04 03-04 .40-1. 1980. an organic form of mercury.40) 1.860-1. mercuric chloride).90) 3. The ingestion of methyl mercury.300) .00-1. interval) .02) .10-3.00 (2.50-2. and is distributed to most tissues.900) 75th 1. Also.60 (2.80 (1.00 (.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 . solid-waste incineration.776 (.800-1..Metals Mercury CAS No.500-.90 (1.900) .703-. Woods et al.00) 1.40 (3.700) .700 (.372) . Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury. constitutes the main source of dietary mercury exposure in the general population.70 (3.00 (.30) 3. Kingman et al. Other major uses include electrical equipment (e.700-.500 (. and mining and smelting. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.800-1.753-1.70 (4.30-6.60-3. and organic forms.919) .903) Selected percentiles ( 95% confidence interval) 50th .419 (.800 (. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach. and dental amalgam.70-2.40-3.672) . IARC..814 (.40-2. predominantly from fish and other seafood. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.60-2. electrical lamps.S.80 (3.886) .g.80) 4.285-.300 (.20-4.80 (1. inorganic.655-.g.30) 3. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).00) 4.400-.80) 3.50-3.700-. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.877 (.40) 3.50-1. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.50) 2.40 (4.30 (1. 1998.2.40 (3. 2007).500) ..900) 1. merbromin).20 (2.574) .60) 1.800-1.927) . which can bioaccumulate in aquatic and terrestrial food chains.400 (.60) 1..800-1. Elemental mercury is a shiny.30) 5.800 (. Accidental spills of elemental mercury.800 (.90) 90th 3. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).700) .60 (1. population from the National Health and Nutrition Examination Survey.30 (2.20-3.50) 1.90 (4.700-.563 (.484) .50) 4. After elemental mercury is absorbed.40-2.00) 1. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.90-3.800-1. with the highest concentrations occurring in the kidneys (Barregard et al.400-.800 (.g. synthetic organomercury compounds were once used in pharmaceutical applications. Some cosmetic skin creams from countries other than the U.600) 1. thimerosal. 218 Fourth National Report on Human Exposure to Environmental Chemicals .20) 2.. phenylmercuric acetate) or topical antiseptics (e.. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.30) 1. elemental mercury is absorbed mainly by inhaling volatilized vapor.30) 1.500 (.40-1. Survey years 03-04 Geometric mean (95% conf.70 (1. sphygmomanometers and barometers.90) 95th 4.80) 1.20-4.30-4.00 (2. see Data Analysis section) for Survey year 03-04 is 0.60-5.500-.40 (4.00) .472-.60-6.700-. sulfur. 1994.60) 2085 2293 3478 Limit of detection (LOD. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.30-5. The kinetics of the different forms of mercury vary considerably.00 (..50) 5.600 (. have often required public health intervention (Zeitz et al. Poorly absorbed from the gastrointestinal tract. Hursh et al. such as chlorine (e.70) 911 856 2081 4525 03-04 03-04 . to form inorganic mercury compounds or salts. Apart from methyl mercury.10) .363-.00 (2.781 (. In addition.g. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. thermostats and switches). Atmospheric elemental mercury can be deposited on land and water.00-5.979 (.900) 1.90 (1. which create an episodic potential for volatization and inhalation of mercury vapor. or oxygen.00 (..S.418-.700-..300-.60-6.00 (1.30-2. may contain inorganic mercury.60 (1.797 (. and mercury compounds are still used as preservatives (e.12) .714-.490 (. 1999 .00) 3. thermometers.689-.900 (.

200-.00) 4.256-.700) 2.800) . The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.800-1.06-1. 1993). Vimy et al.14 and 0.377 (.60) 3.200-. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury. and a useful marker of exposure in epidemiologic studies (Grandjean et al.820 (. Smith et al. 1994.377) .90 (1.500-.40-1.200 (.23) .20) .70 (1.10) .50) 1.800 (.374) .268-.20-3..50 (1.00 (2.500 (. with most elimination occurring through in the feces (Sherlock et al.10 (.200-.20-2. 1992.90) 5.70) 4.02 (.20-11.50-12.30 (1.700-1. Geometric mean Survey years (95% conf..00) 7.697-.60 (2. 1999-2002.30-2.50-3.0) 4. population.80) 579 527 370 436 588 806 Limit of detection (LOD.10 (3.300) . Methyl mercury enters the brain and other tissues (Vahter et al.664-1.30-5.900 (.600) .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 ..00) . 1973).700 (.30-4. Methyl mercury is incorporated into growing hair.318 (.200-. 1996.30-6.70-6.70 (1.30 (.00-2. 1994) and then undergoes slow dealkylation to inorganic mercury.297-. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.00) 6.329 (..00-2. Suzuki et al.50) 1..871-1. 1971). excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al. McDowell et al. for both acute and chronic exposures.307 (.600) . thereafter. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.833 (.50) 2.300) ..300 (. Jonsson et al..30-3.299-.90 (4.500-1.00 (1. Myers et al..10) .60 (1.10) 1.700-.90 (4.300 (.800 (.500-.300 (.29) .30 (1.200 (.60) 1.395) . 1999). Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.944 (.800 (.. 1992).800-1. 2004. Miettinen et al.10-1.20) 1. 1984..825-1. a measure of accumulated dose (Cernichiari et al..90) 90th 1..80-3.60 (3.919) .40-2. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.317 (.70) 4.00-2..40) 1. National Health and Nutrition Examination Survey.06 (. 2003). Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.00 (2.10 (5.824) 1.00 (3.900 (.738-. 2003).27) .70) 1. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.800) 75th .20 (..700 (.900 (.667 (..10 (1.60 (1.30) 1. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.20-3...30 (1.30-6.60 (1.200-.01) . 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.200-.50) 3.90) 2.S. 1998).800) 1.73) 1.50 (2.10 (1.00-1.300 (.50) 95th 2.00-6.70-5.80 (1.70-5.80) 1.70 (1.800-1.60) 1. interval) Selected percentiles (95% confidence interval) 50th .265-..60) 2.700-.300) .3) 4.500 (.00) 1. 1975.30) 3.500-. Blood concentrations decline initially with a rapid halflife of approximately 1-3 days followed by a slower half-life of approximately 1-3 weeks (Barregard et al.600 (..300) .30-6. Sandborgh-Englund et al. 1996).Metals the tissues to mercurous and mercuric inorganic forms.14.20 (2.40) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.400-.40) 5.10 (1... 1995. 1992 and 1999.00 (2.30) 1. Vahter et al..900-1.700 (.40 (1. 2005).500-.7) 4.940) Race/ethnicity (females.475) .00) 1.343 (. 1969.00) 2.90) 2.80 (3.407) . 1994).800) 1. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.90 (1.10 (.30-11. Smith and Farris.20-3. After exposure to elemental mercury.90) 3.700 (.369) 1.60 (3. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .40-2.00-3.541-. Fourth National Report on Human Exposure to Environmental Chemicals 219 . 1990).20) .30-4.500-. 1993).726-1.90 (3. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al. Excretion occurs by renal and fecal routes.70-3.10-3.300) .900-1.35 (1. 1998).800) .700-1.70-3.40 (1. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.50-2.300) .269-. 1991.

500 (. Smith et al..600-.700-.600) . Inorganic mercury exposure usually occurs by ingestion. limb deformities.700-..500) .600) . At levels below those that cause acute lung injury.. Once absorbed. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 2005).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 . Smith et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 1987). 1996). < LOD means less than the limit of detection. and progressive constriction of the visual fields.600 (. fatigue. 2000.700 (. Bellinger et al. hearing impairment.500-. Sakamoto et al. 2004. 2006.600 (.700) ..600) .500-. Survey Geometric mean (95% conf. short-term memory loss.800) . particularly irritability.500-. and neurocognitive and behavioral disturbances. 220 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. overt signs and symptoms of chronic inhalation may include tremor.500-.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . 2003). cerebellar ataxia. causing parasthesias. Rissanen et al. insomnia. Drexler and Schaller...500-.600) .600-. and cerebral palsy (NRC. Stern 2005. Acute... 2000). 1995.600 (..600) .700) 2007 2240 3406 Limit of detection (LOD. typically after a latent period of weeks to months. see Data Analysis section) for Survey year 03-04 is 0. ataxia. anorexia. Vupputuri et al. In recent epidemiologic studies.600 (. population from the National Health and Nutrition Examination Survey. DeRouen et al. hypertension. altered physical growth.600 (. 1995.600) .. gingivitis.500-. Sakamoto et al. sensory impairments. 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. dysarthria..600-. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.600) . Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al.700 (.42.600 (.600-. pain in the extremities. which may vary for some chemicals by year and by individual sample. The constellation of findings may include anorexia. Factor-Litvak et al.600) . Overt poisoning from methyl mercury primarily affects the central nervous system.500-.700 (.800) .800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .. the existence of a causal relation is unresolved (Chan and Egeland. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. high-dose exposure to elemental mercury vapor may cause severe pneumonitis.500 (. 2004.600 (. irritability. and sleep disturbance (Bidstrup et al. 2004).700-. 1951. 2002..S.500-. 2000.600) . 1970.500-.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1998.700 (. 2004). 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. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. 2006.500 (<LOD-. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. dysarthria. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. maculopapular rash.Metals may be more efficient for inorganic mercury (Grandjean et al.600 (..500 (<LOD-. 1963). 1993). and pinkish discoloration of the hands and feet (Tunnessen et al.. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. Salonen et al. Rice.. depression. Oskarsson et al.700 (. 1983).700 (.

93 (1.52) 2.400 (.55 µg/L.85-2.350-.01 (.330-. 2009).530) . range 40 years to 78 years) had an average total blood mercury concentration of 2.492) Selected percentiles ( 95% confidence interval) 50th . Sanzo et al.930-1.870-1.atsdr.54 (2.09 (2.442-..58 µg/L for 4645 adults. population from the National Health and Nutrition Examination Survey.S.89) 3. From 1996 through 1998. environmental levels) and health effects is available from the U.360 (.05) 1.e. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.23) . Among the three racial/ethnic groups. During the same survey periods.330-.19 (2.42) 95th 3.60) 619 713 1066 Limit of detection (LOD.870-1.88-3. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women. 1995.16 (..31) 1266 1272 03-04 03-04 03-04 ..549) .31) 2.396-.03-4. However. who participated in a 1998 representative population survey (Becker et al. Biomonitoring Information In the general population.416 (. EPA..8 years. 2004. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. see Data Analysis section) for Survey year 03-04 is 0..88 (1.24) 1.700 (. aged 18 to 69 years.840-1.28) 1. Fourth National Report on Human Exposure to Environmental Chemicals 221 .30) 3.39-3.. Kingman et al. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.495 (.480 (.68 (2.430 (. Information about external exposure (i.250) . et al.99-6.gov/toxprofiles.413-.gov/mercury and from ATSDR at: http:// www.88) 287 722 1529 03-04 03-04 . 1997.340-.200 (.78-2. A cord blood mercury level of 85 µg/L (lower 95% confidence bound = 58 µg/L) is associated with a 5% increase in the prevalence of an abnormal Boston Naming Test (NRC. 2001.406-. Grandjean et al.24 (2.14-2. 2003).13-2.360-.76-4. interval) .476 (. Mahaffey et al.S.420 (.Metals standard for inorganic mercury has been established by U. Survey years 03-04 Geometric mean (95% conf. 2003)...60-2.610-1. Benes et al.304) .520) .63-2..770-1.76-3.534) . 1998).20 (1.55) 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 . Total blood mercury levels increase with greater fish consumption (Dewailly et al.78 µg/L for adults and 0. Schober et al. 2006). slightly higher total blood mercury levels were found in U.05) 3.33 (2. These distinctions can help interpret mercury blood levels in people.67-2.08 (1.46 µg/L for children.90) 2. 758 children. 2009).07 (.430 (. 2000)..463) .epa. the median concentration of blood mercury was 0. 2001.26 (1.530) .358 (.. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al. In NHANES 19992002.08 (1.555) .960 (.430) .65) 1.480) 75th 1. the total blood mercury concentration is due mostly to the dietary intake of organic forms.433 (. average age 33 years.46) 3. A cohort of 1127 U.29) 1.580) .00 (.S. adult women in several ethnic subgroups (Hightower et al.313-.cdc.280-. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.408) .254 (.405-..410-.420 (.23) 2.330 (.530-.840-1.570) .940 (. EPA at: http://www.96 (1. and the age-related changes differed across the groups (Caldwell et al. 2002).. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.440 (. total blood mercury increased with age. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females..840) 1.890 (.382-. Over the NHANES 1999-2006 survey periods.34-3. and increased slightly in non-Hispanic white children (Caldwell.77-2.213-.18) 2.66) 3.441 (.00) 1.S.290-. 1998).447 (. particularly methyl mercury. In Germany the geometric mean for blood mercury was 0.12 (.S.460) .60 (1. total blood mercury geometric mean levels in females aged 16-49 years did not change.509) . IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.14.509) .460 (.67-3. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.16 (1.700-1. average age 9.9 years).160-.61) 1. military veterans (mean age 52.330-.97) 2.370) .360-.76-3.19 (1.14) 90th 2.96 (1.

11) 1.289) .30) 1.588) .498) 75th .463 (.970 (.365 (. 2002) adult population surveys were similar to those in a U.447-. and on average.65 (1.07) 1. mean urinary mercury was 3.25 (.280-.04-3. 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.S.01) 2.400) ..217 (.376-.384 (. 2003).67 (1.343 (. 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. et al. Information about the biological exposure indices is provided here for comparison.417) . women of childbearing age have generally been much lower than these levels (CDC.368) .307-. population from the National Health and Nutrition Examination Survey.532 (.265-.1 µg/L for each surface with a dental amalgam (Kingman et al. Langworth et al.362 (.86) 95th 2.225-.485 (. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.909 (. and Italian (Apostoli et al.32-2.78-4. DeRouen et al.31 (1. Czech (Benes et al. In the study of U.S.652) ..276 (.32 (1.77 (2. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.S.447 (.62 (1.00) 286 722 1529 03-04 03-04 .455-.67 (1.12-3. not to imply a safety level for general population exposure.56) 1266 1271 03-04 03-04 03-04 . 2005).54 (2.306 (.06 (.667-1.00 (.297 (. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.87) 2..768 (.476 (.784) 1.88 (1.39) 1.616) . interval) .61) 1.566) .13 (1. 2009).630) . Urinary mercury levels in recent German (Becker et al.00) 90th 1.Metals 2000).03) 2.620-.46-2.16) 1.443 (. 1988. 1992).358) .64-2.508 (.385-.275) .480) ...714-1.875-1..87 (1.06 (.28 (. reversible increase in urinary N-acetyl-glucosaminidase.40-1.525 (..391) .365 (. Urine mercury and the number of dental amalgams were correlated.392-.404-.537) .400-.800-1. 1998). 2006).88-2. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.88-2.969-1.545 (.464 (.347) .30) 2.S.391-.35 (1.79) 1.63) 1.18-1.785-1.1 µg/L.21) 1.11-2.85) 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 .. military veterans with dental amalgams. 2002).76 (1.40 (1. Department of Health and Human Services noted that several studies have observed a modest.522-.23-2.486) Selected percentiles ( 95% confidence interval) 50th .246-.208-.13-2.619-.990) . Levels in U.11) 2.41-2.472-.587 (.455) .599) ..S.301-. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey years 03-04 Geometric mean (95% conf. et al. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.255 (. 2006. 2009).333-.964-1.79 (1.687) . the urine mercury increased by approximately 0.535) 1. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.455-. a biomarker of perturbation in renal tubular function.309-.51-2.696 (.. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.196-.44) 1.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .09) 1. An expert-panel report recently prepared for the U.

84 (2.21 (1.30-2.97) 2.47) 1.790) .37) 1.41 (1.79) 1.582-. National Health and Nutrition Examination Survey.83-3.57-4.00 (2.565 (.721 (.14-2.21-3.84 (2.04-1.45) 2.742-1.639 (.91 (2.560-.657 (.522 (.615 (. Geometric mean (95% conf.32) 2.92) 4.553-.68-3.16-5.508-.72) 1.39-3.04-10.27 (1. Geometric mean Survey years (95% conf.892) .S.30 (2. 1999-2002.45-2.76 (1.18) 3.24-1.596 (.35) .41 (1.14.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.592 (.03-2.56 (1.30 (2.77) 1.560 (.79) 3.55-3.41-6.21 (2.691) .670) 75th 1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.500-.13 (2.44) 3.23-1.85-3. 16-49 years) 99-00 01-02 .03) 1.95 (2.3) 5.45) 2.55) 90th 3.32 (1.56) 4.76-5.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .10-4.14) 3.833) .99 (2.686) .06 (.420-. interval) Selected percentiles (95% confidence interval) 50th .42-3.99-2.03 (.69-3.97) 2.831) .62 (3.53-3.719 (.92) 3.92) 2.966) .605-.18 (3.09-1.665) .610-.15-1.68) 3.07) 1.46 (1.606 (.650) 1.61) 1.799) .665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .14-1.69 (1.810) .850-1.35 (1.70 (2.656-.709) .22 (. 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.520-.68 (3.450-.616-.52) 3.30 (1.23-1.43-1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.710 (.76) 2.710) 1.10-2.806) .00 (3.38) 4.85) 4.45 (1.42) 90th 2.48 (2.637) .579-.22-3.07-2.410-.578-.650 (.709) 75th 1.45-3.846) .502-.27-1.50 (1.50-4.475-.710 (.580-.658 (.870) .09-1.46-4.81 (3.501-. 16-49 years) 99-00 01-02 . National Health and Nutrition Examination Survey.15 (2.600 (.65-4.831) .526-.706 (.94) 1.910) .540-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.41 (2.47) 1.46) 3.61-6.07-5.97) 2.724 (.387-.930) .772 (.65) 1.03 (.45) 95th 3.16) 5.28 (1.632 (. population.51) .99) 1.05 (3.744) 1.91-7.685 (.631-.624-.32-3. interval) Selected percentiles (95% confidence interval) Survey years 50th .557-.27 (2.Metals Urinary Mercury−Females Aged 16-49 Years Old.77) 2.426-.89 (2.17) 95th 5.809) .14 and 0.699) 1.540 (.24) 6.516 (.98 (5.81-6.824) .622-.54) 595 531 381 442 594 826 Limit of detection (LOD.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.909-1.620 (.774) . population.50 (2.37 (1.760 (.31 (1.97 (1.636-.62 (1.13-4.723 (.62 (4.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .42) 2.650 (.87-4.580 (.S.51 (3.832-1. 1999-2002.569-.664) .25) 2.56) 3.00) 2.740 (.520-.05 (2.59-5.99 (3.655 (.31-1.

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9-82.6-42.7 (36.5) 85.5) 60.6) 93. 7439-98-7 General Information Elemental molybdenum is a silver-white.3 (53.8) 48.0) 60. interval) 45.3) 37.7 (45.5 (81.5-41.4-52.1) 57.2-91.4 (72.3) 41.0 (48.1) 46.8) 39.2) 48.9) 62.0-110) 90.3) 65.0-53. and in pigments for ceramics.2-59.7-68.1-63.2-37. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.3) 83.2) 41.9 (52.7 (51.8.2 (49.5-124) 108 (92.8) 46.5 (74.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52. urinary excretion over six days CAS No. aldehyde dehydrogenase.2-79. hydrogenation catalysts.3 (38.7-105) 69.2) 53.3 (47.2 (49. respectively. molybdenum is a cofactor for three enzyme classes— sulfite oxidase. 1997). population from the National Health and Nutrition Examination survey. and xanthine oxidase (Kisker et al.9 (44.5 (37.9-83.1) 59.9 (73.7-39.5-46. and 03-04 are 0.3) 47. Fourth National Report on Human Exposure to Environmental Chemicals 227 .9-55. 2001.5. 1996).4-75.9 (34.6 (40.8-106) 88.6-46.2) 52.5-66.0 (42.2-70.9 (78.2 (40.6 (52.2 (55.S.1-88.3-108) 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 47.6) 51.6 (43.8-49. semiconductor and battery industries have begun to use molybdenum.7-51.1-52.6-96.2-42.8 (42.3) 85.9 (33.2-53.7) 46.3-75.1-48.3 (73.9 (32.1 (34.2 (38.7-60.1-44. At a daily oral molybdenum dose of 24 µg.4) 42.4) 76.7-84.2 (56.2) 37.3-115) 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.5-91.3-91.4) 49.3 (84.7-50.7 (58..4) 52.1 (38.7 (50.5-52.4 (48.3 (64.3-44.5) 44.9-56.4-61.8-90.4 (79.7) 77.3 (71.4) 56.1 (71.8 (67.0-65.7 (71.0 (46. 0.7) 51. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.4) 41.5 (48.7) 57.1) 82.6-55. 2001).7) 78.0) 62.2 (61.3-47.2 (63.1) 35.3 (46.6 (55.5-68. More recently.7 (37.9-55.4-82.2) 178 (147-259) 169 (138-197) 138 (127-152) 146 (112-171) 145 (129-159) 118 (105-125) 126 (114-134) 114 (103-124) 105 (98.1) 126 (106-147) 109 (94.3 (79.7-96.2 (69.4 (34.3 (37.5 (41.6-72.0 (81. 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 (41. chemical reagents in hospital laboratories.3 (55.6-62. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.4 (80.9) 34. In humans.0 (41.6) 53.7-73.9 (40.5) 80.6 (73.0) 55.9) 67.0 (42.6 (40.Metals Molybdenum or ore deposits.8.9-109) 97.1) 60.8) 44.8-46.9 (37.6 (55.8) 75.7-91. see Data Analysis section) for survey years 99-00.0-62. Compounds of molybdenum are also used as corrosion inhibitors.5 (43.0-77. Excretion occurs predominantly via the kidneys.7) 86.8) 40.7-47.3 (55. lubricants.5 (49.0-56.5) 80.0-38.0) 97.6-58.2-59.6) 71.9-85.7) 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 78.0) 39.3) 54. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.8 (82.2 (83.5 (67.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.6) 71.7 (73.0 (43. and paints. which exert homeostatic regulation over molybdenum balance.1-52.2) 40. and 1.8-94.0) 45. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5) 47.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.5-65.6) Selected percentiles ( 95% confidence interval) 50th 50.0) 84.8 (85.4 (48.7-122) 93.6-82.7) 78.6) 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 (99.1-55. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.4) 45.7) 45.0-101) 82.1 (91. 01-02.0) 54.8-108) 87.0 (76.7-41.0-71. WHO.1-51.2) 79.0-85.7) 75th 84.7-92. inks.7 (44.5-52.0-100) 63.1-59.

7-43.1 (40.7) 115 (93. In industry.4) 89.0) 39. interval) 43.S.S.3-52.6) 48.2 (43.1-112) 78.6 (38.3 (71.5 (39.5 (65.2) 58.2-40.8-47.1-67.4 (55.5-62.8-42.6 (36. and clinical or epidemiologic evidence of adverse effects is limited.8-52.9-61.3 (37. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.0 (35.5 (54.2) 39.0-133) 119 (88.8) 37. Biomonitoring Information Molybdenum is an essential element for health.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 40.6-88.4) 47.2-121) 107 (92.3 (83.1-100) 86.0-103) 103 (90. at daily oral doses of 95 µg and 428 µg. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2) 42.1-127) 90.9) 92.5-44.1-41.6-63.5) 60.1 (38.5-119) 90. 1995).6-45.9-87.9 (40.0) 88. U.5) 72.5-70.1 (38.3 (55. 1961.8) 39.3) 43.5-48.8 (36. 1993).0 (58.2 (50. Based on studies finding adverse reproductive effects in rats and mice.3-68.8-46.5-69.1 (54.1-81.1) 43.8) 62.1) 65.3) 56.0-56.5 (41.9) 41.3-56.2 (57.3) 41.8) 71.5 (40.Metals was 18% of the ingested dose.0 (74.9-41.9 (64.3 (51.8 (37.8) 61.6 (59.7) 45.4-41.1) 101 (83.2) 42.5 (38.6-61.8) 45.5 (59.7) 57.4) 44.9-40..1 (82.1) 37.6) 39. 1999).0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.1-43.8 (75.5-46.2 (40.2 (69.0) 33.4-42.3 (36.3-43.4) 77.7-40.4 (44.5 (35.5) 73.1-79.7) 41.6-61.6 (42.8-65.7-93.4-107) 85.1 (39. urinary excretion over six days rose to 50% and 67%.2 (37.0) 39.4) 40.5-60.1-39.0) 72.2) 55.2-96.9 mg/kg/day and established a tolerable upper intake level of 0.7 (77.5) 90th 108 (97.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.6) 39.4 (67.4-106) 85.3) 57.4 (53. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6 (57.4) 61.2 (33.5 (39.9-45.1 (30.3-45. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.0-120) 85.3-59.5) 63.2 (36. but available epidemiologic data are scant.1-38.8-84.3) 44.3-44.4) 48.6-41.1-40.7 (75.2-96.5 (35.2) 39.6 (36.4 (40. and urinary levels reflect intake from all sources.6-78.9 (73.4-118) 172 (131-195) 138 (120-163) 118 (106-134) 780 682 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites 228 Fourth National Report on Human Exposure to Environmental Chemicals .9) 40.4) 122 (107-133) 109 (99.4 (78.4-120) 101 (84.1) 37.5-97.0) 62.2) 37.0-38.0) 36.1-109) 89.9-96.0 (80.6) Selected percentiles ( 95% confidence interval) 50th 41.5-45.8-47.4 (59.1 (49.5 (40.2-49.1 (37.9 (49.5 (80.9 (39..8-118) 81.5-99.5 (37.5-35.0) 53. Molybdenum is generally considered to be of low human toxicity.1-43.4) 60.6) 36.7 (30.9) 44.3-141) 109 (81.5 (79.9 (39. EPA.2 (40.1-45.3 (36.7-38.4-185) 106 (94.5-50.7) 112 (95.5 (34.2-41.0-46.8-66.9-117) 57.4) 58.8) 38. 2001).2-65.2 (40.03 mg/kg/day in humans (IOM.5 (65.9 (36.3) 40.7-120) 87.3 (71.7-62.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.5 (36. of the ingested dose (Turnlund et al.2 (73.9-71.0-41.2-47.0) 38. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.7-44.9 (64.5 (37.5) 71.9) 31.5 (41.3 (53.4 (56.1-34.7 (66.4 (37.0-46.7-52.3-46.1) 56.0) 44..2) 37.8) 38. 1997).5 (50.9) 79.1) 40.2) 43.4-76.7) 62.5-92.7) 42.3-115) 98.8-67.9 (79.4) 116 (101-126) 104 (88.6 (71.9-42. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.6) 43.3) 61.6-76.1 (42.4-39.3) 64.3 (37.1-39.3) 37. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.2 (52.5 (83.4-66.7) 53.3 (58.2-80.2-46.5 (78.9-118) 91.9 (35.7) 75th 63. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.8 (57.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.9-45.1 (44.7-100) 77. respectively.8 (56.9-68.2) 38.6-63.7-137) 129 (109-155) 112 (97.8 (90.8) 79. population from the National Health and Nutrition Examination survey.1 (33.

. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Christensen JM. manganese. Vermeire PA.nih. Sciarra G. World Health Organization (WHO). Kristiansen J. 4/14/09 Sievers E. 2005). Zhurnal Obshchey Biologii 1961. Molybdenum. 420-441. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Washington. Available at URL: http://www. 2001. Yarovaya GA. Available at URL: http://books.15(2-3):149-154. National Toxicology Program (NTP). Ann Rev Biochem 1997.niehs. pp. X. Analyst 1998. TR-462. iron. Molybdenum absorption.epa. Ronchi A. Dietary reference intakes for vitamin A. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. 1998. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. Schleyerbach U. nickel. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Sabbioni E. Environmental Protection Agency (U. White and Sabbioni.22(3):179-191.htm. Am J Clin Nutr 1995. U. vanadium. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. 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. et al. Turci R. Turnlund JR. edu/openbook. Koval’skiy GA.nap. van Sprundel MP. Aprea C. and zinc: a report of the Panel on Micronutrients. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. 4/14/09 White MA. 16:1313-1319. A study of 13 elements in blood and urine of a United Kingdom population. Schindelin H. iodine. copper. Kisker C. Rees DC. Rapid Comm Mass Spectrom 2002. Food and Nutrition Board.123(1):81-85. (DC): National Academy Press. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. Available at URL: http://ntp. In: Trace elements in human nutrition and health. 2005. Geneva: WHO.php?record_id=10026&page=420. silicon. 56:322-327. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Weyler JJ. References Centers for Disease Control and Prevention (CDC).gov/iris/ subst/0425. Occupational risk factors of lung cancer: a hospital based case-control study.S. 2001). 1996. vitamin K.. Occup Environ Med 1999. 1998). Trace element reference values in tissues from inhabitants of the European Union. excretion. Sci Total Environ 1998. Van Meerbeeck JP.Metals in urine for the U. 2002. Molybdenum in infancy: methodical investigation of urinary excretion. Keyes WR. 144-154. pp. Gatti A. Sabbioni E..62(4):790-796. arsenic. 4/14/09 Iversen BS. Institute of Medicine (IOM). Droste JHJ. Minoia C. chromium. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Peiffer GL.216:253-270. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Shmavonyan DM. boron. Menne C. molybdenum. White MA.gov/index. Schaub J. Atlanta (GA). Molybdenum 1993 [online]. Minoia et al. EPA).S. J Trace Elem Med Biol 2001.66:233-267. Third National Report on Human Exposure to Environmental Chemicals. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces.

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

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

Jankofsky M.70(3):205-208. 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. ruthenium. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine.. 2001). Schierl et al. van de Weyer C. Saindelle A. Ewers U. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect.htm. Kavanagh P.35:313-321. Pethran A. Alimonti A. Neuendorf J. Int J Hyg Environ Health 2004. Angerer J.Metals the International Programme on Chemical Safety at http:// www. Pethran et al. Br J Pharmacol 1969. Rommelt H. Grimm CH. International Journal of Hygiene and Environmental Health 2003. 2004). Campbell K. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Ensslin AS. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Petrucci F. Schierl R. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Environmental Health Criteria 125.04 µg/L) in this Report.005 µg/L (Iavicoli et al. et al. Bocca B. 289-380. Allergy and histamine release due to some platinum salts.76(1):5-10.. Environ Health Perspect 1975b. Int Arch Occup Environ Health 1997.. International Programme on Chemical Safety (IPCS).10:63-71. Parrot JL. Blanks R. and platinum. Hebert R. Biomarkers 1999. 2004. Schulz C. Schierl. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Urinary excretion of platinum from platinum-industry workers. Wilhelm M. Levels of platinum in urine for the U. 2003. Platinum.56(3):283-286.org/documents/ehc/ehc/ehc125. References Becker K. Analyst 1998. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Iavicoli I. et al. Turfeld M.01 µg/L (Becker et al. Kuster W. Moore W Jr. Nowak D.. 2003. Czerczak S. eds. 1998).S. Kazantzis G.inchem. 1998). Raab W. palladium. Pethran A. Ruff F: Histamine release by sodium cholorplatinate. Hauff K. Kaus S. Part 1: monitoring of urinary concentrations. Hall L. Wilhelm et al. Uptake of antineoplastic agents in pharmacy and hospital personnel. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. 3/31/08 Moore W Jr. Arch Environ Health:1969. 5th ed. Patty’s Toxicology.207(1):69-73..htm.4(1):27-36. New York: John Wiley & Sons. 1999. Int Arch Occup Environ Health 2003. rhodium. 2004) or less than 0. Seiwert M. Begerow J. Gromiec JP. Available at URL: http://www. Ruff F: Platinum and platinosis. Farago ME. 1991 [online]. 2003). Biomonitoring Information Urinary platinum levels reflect recent exposure. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Stilianakis NI. osmium. Hysell D.55(2):138-140. palladium.. 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.. Kulka U. Fruhmann G. and in blood and urine in the United Kingdom.. population were below the limit of detection (0. Herr CE. Schierl R. Cohrssen B. Schierl R. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2000. 206:15-24. Herr et al. Thornton I. Occup Environ Med 2004. pp. Environ Res 1975a.org/documents/ehc/ehc/ ehc125.. Influences on human internal exposure to environmental platinum. Carelli G. In: Bingham E. Hysell D. Seifert B. Arch Environ Health 2001. Several studies have shown that background concentrations in general populations were usually less than 0. 1997. Biomonitoring of traffic police officers exposed to airborne platinum. 2003. Urinary platinum levels associated with dental gold alloys. Boos KS. Crocker W.19:685-691.inchem.61(7):636-9. Kelly J. Senofonte O. Powell CH. Occup Environ Med 1998. and gold excretion of patients after insertion of noble-metal dental alloys. Schulz C. Saindelle A... Herr et al.9:152-158. which elevate urinary platinum by five to twelve-fold (Begerow et al. Huber R. et al.13(1):24-30. Duneman L:Long-term urinary platinum. Fries HG.123(3):451-454. Nickel. Schierl R. Gieler U. Platinum concentrations in urban road dust and soil. J Expo Anal Environ Epidemiol 2003.

450 (.410 (.370 (.145-.280) .410 (.148-.170-. 0. In the past.320 (.177) .430 (.400) 95th .172 (.290) .290 (.330-. From these and other sources.400 (.200) .410 (.330) .350-.260-.330-.290 (.230 (.220 (.420) .160-.250-.Metals Thallium depilatory cosmetics.400) .320) .220 (.190-.520) .290 (.200-.210 (.250-.230) .640) .400-.280-.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 .520) .270 (.160 (.290 (.450 (.200-.182-.370) .162-.290 (.420) .202 (.170 (.147-.200) .400-.470) .250-.250 (.370 (.300 (.480) .310 (.133-.220-.280 (.170-.450) .270 (.330-.400 (.185 (.360-.140-.02.160-.250-.270) .430) .156) .270-.440) .320-.320) .220) .145-.250-.390-.340-.200-.160-.460 (.202) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .400-.155 (.410-.420) .380) .150-.370) .410 (. 01-02.370-.290) .201 (.149 (.550 (.300) .218) .350) .410 (.196) .230-.270-.184 (.220) .390) .450 (.171 (.440-.370 (.410-.430-.340-.420 (.167 (.440 (.480) .400 (.200 (.400-.200 (.230) .440) .390) .370 (.170) .350-.480) .360 (.196) .S.280 (.350-.159 (.410) .560) .490 (.450 (.185-.390) .135-.260-. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing. thallium readily crosses the placenta and also distributes into breast milk.02.370-. In the United States.170-.430 (.460) .144 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.197 (.340-.350-. population from the National Health and Nutrition Examination Survey.160 (.158) .340) .153-.260-.510 (.500 (.170-.218) . and 03-04 are 0.430 (.190 (.173-.178) .370 (.420) .260-.150-.200) .180) .156) .280) .197-.400 (.187-.340-.410-.480) .430-.320) .150-.160 (.250-.500) .02.350 (.163) .290-.420) .200 (.500) .360-.190 (.460-.183) .220) . Thallium disappears from the blood with a half-life of several days. representing distribution into other tissues.179-.390 (.180-.490) Total .300) .450 (.230-.590) .176 (.400-. however.350-.400 (.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 .310 (.210) .150-.260-.220 (.440 (.290) 90th .200 (.370 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.230-.410-.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 .260 (.440) .200 (.240) .220) .180 (..225) .300) .170 (.200 (.330-.350-.217) .380-. thallium was obtained as a by-product of smelting other metals.190 (.310-.450 (.165 (.167-.217 (.170-.147-.290) .310) .380-.330) .180 (.440 (.157-.330) .188) .172 (.160 (.370-. respectively.156-.450 (.500) .230) .150-.280-.390-. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.154-.400) .175) .390-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.510) . see Data Analysis section) for Survey years 99-00.183) .170) .146 (.470 (.420-. the latter being the current major industrial consumer of thallium in this country.470 (.200) .290) .239) .134-.330) .360 (.360) .470) .180-.180-.270 (.160-.170-. In addition.280 (.410-.300 (. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.173) .690) .180-.420) .420-.172) .390 (.220 (.250 (.145 (.360-.170 (. it has not been specifically mined or refined in the United States since 1984.420-.167-.240) .300 (.340 (.220 (.220) .450 (.243) .200) .190 (.350 (.420) .410-.260) .290 (.159 (. Human health effects from thallium at low environmental CAS No.210-.390) .390-.330-.180) 75th .240-.250) .370-.430 (.490) . 2005).240-.380 (.160 (.400) .201 (.400) .202 (.170) .190 (.280) .340) .173) .260 (.300) .300-.270) .240-.159 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.590) .440 (.480) .137-.520) .330-.240) .270 (.450 (.170-.520 (.210 (.180 (.192) Selected percentiles ( 95% confidence interval) 50th .360 (.310 (.470) .250-.430-.630) .360-.350) .200-.260 (.420-.380 (.490) .290-.490) .147-.200) .181-.230) .220) .270-.430) .410 (.190 (.360 (.270 (.206) .330-.370 (.160-. and 0.191 (. interval) .215) . 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.250-.360-.150-.

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

Pirkle JL. Ewers U. Dolger R. 1992 [online]. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. and serum of Italian subjects. Boisson P. 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. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Ting BG.1 mg/m3 (Marcus. et al.35(1):4-9. Schmidt M. Raithel HJ. Available at URL: http://www. Brockhaus A. 1985). Minoia et al. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Pozzoli L. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Pietra R.atsdr. Kramer U. Trace metals in urine of United States residents: reference range concentrations. Third National Report on Human Exposure to Environmental Chemicals. Martin J-C. Fourth National Report on Human Exposure to Environmental Chemicals 235 .216:253-270. Marcus RL. Morrow JC.76(1):53-59.48(4):375-389. White and Sabbioni. A study of 46 elements in urine. Jackson RJ. Manke G. 2005. Trace element reference values in tissues from inhabitants of the European Union. Sabbioni E. Gallorini M. Trace element reference values in tissues from inhabitants of the European community I. Toxicological profile for thallium. Wiegand H. 2005. Brockhaus et al. et al.cdc. Sabbioni E. with concentrations ranging up to 76.. Cassot G.265 people living near a thallium-emitting cement plant in Germany. Paschal DC.html. X. Valentin H. 1998). References Agency for Toxic Substances and Disease Registry (ATSDR).5 μg/L.. Sci Total Environ 1998. 2005) and are shown with results from NHANES 2003-2004 in this Report. Int Arch Occup Environ Health 1980. (1981) studied 1. 1990.. Apostoli P. Celier D. 1980. Sampson EJ. 1998. A study of 13 elements in blood and urine of a United Kingdom population. Challeton-de Vathaire C. Investigations of thallium-exposed workers in cement factories. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Centers for Disease Control and Prevention. Minoia C. Radiat Prot Dosim. Int Arch Occup Environ Health 1981. J Soc Occup Med 1985. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U.95:89-105. White MA. 1981. Schaller et al.47(3):223-231. Buhlmeyer G. Paschal et al.S. 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. Soddemann H.Metals (CDC. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Sci Total Environ 1990.gov/toxprofiles/tp54. Investigation of a working population exposed to thallium..113(1):47-53. Environ Res 1998. Schaller KH. blood. Atlanta (GA). 7/15/09 Blanchardon E. et al.

101-.170) .090 (.080-.350) .092) .380-.100) .068) .470 (.050-.270-.560) .400 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.460) .158 (.550 (.090-.084-.160) .110) .090-.080 (.070-.120) .190 (.058-.140-.190-.300-.360-.120) .140 (.230-.093) .070 (.100-.630) .210 (.180) .200 (.330 (.530 (.069-.470 (.360 (. which is used in the steel industry.101 (. 01-02.270 (.230) . population from the National Health and Nutrition Examination Survey.500 (.060-.250) .830) .210 (.520) .060 (.490) .092 (.04.290) .230-.460 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.120 (.430) .080) .123-.116) .070-.320) .250) .500 (.132) .370 (.180 (.480) Total .082-.810) .090) .210 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.430-.080 (.110 (.133) .060-.073) .135) .510-.113 (.170) .060-.360 (.070) .190 (.290-.350) .070-.370 (.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 .320-.290-.097-.340-.790) .110) .300 (.560) . which are used in rock drills and metal-cutting tools.113 (.160-.110 (.380-.065 (. see Data Analysis section) for Survey years 99-00.670) .620) . their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.550) .087) .111-.690) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).050-.400 (.160 (.420-.220) .340-.240 (.330-.080) 75th .120) .093-.260-.370-.070-.120-.070 (.160-.070) .53) .370-.100) .100-.190-.520) .100) .620 (.137 (.073-.090-. and 0.104) .082 (.190-.460 (.450 (. Evidence is lacking for the carcinogenicity of tungsten.160 (.220) .450-.390 (.095-. Tungsten compounds are used as lubricating agents. and as catalysts in the petroleum industry.120-.113 (.160 (.340-.520) .100) .170) .062 (.140 (.110 (.105 (. mainly as scheelite (CaWO4).090-.065-.210) .230) .150 (.560) .077-.100 (.050-.00) .090 (.078-.060-.080) .260 (.270 (.090-.300) .510 (.290) .080) .090-.140 (.087-.370) .300) 95th .270-.950) .230-.150 (.130-.220) .320 (.080-.230 (.130) .400) .260-.380-.380-.082) .064-.180-.110-.400-. filaments for incandescent lamps.130) .060-.073 (.230-.050-.04. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.340) .100-.580) .430 (.370 (.110-.350 (.170) .190) .060-.086 (.056-.310-.073-.084) .081 (.110 (.400 (.126) .140) 90th .180-. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.210 (.170 (.100) Selected percentiles ( 95% confidence interval) 50th .090-.310-.310-.088 (.250) .120-.090) .390) . Tungsten is used mainly for producing hard metals.130-.300 (.170-.130-.069) .070) .280 (.066-.090) .105) .410-.380) .150-.500) .310 (.04.350-1. and 03-04 are 0.330) .310-.076 (.160 (.130) .180) .120-.360-.120) .060 (.320-.430-.090-.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 .590) .270-.120-.530 (.100 (.800) .250-.250-.100 (.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 .120) .180-.060 (.092 (.070) .093 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .080 (.770 (.530 (. interval) .160 (.070 (.240-.200) .160-.204) .160-.130-.100) . Occupational exposure is from dusts released during grinding or drilling of hard metals.250) .210 (.550) .260) .310) .070-.640 (.074-.110-.560) .430 (.110 (.160) .290-.400 (.076 (.510-1.250) .084 (.280-.360) .080 (.800) .056-.170 (.109) .620) .062 (.410 (.490 (. Little information is available on the toxicity of tungsten.107 (.280 (.180-.140-.090) .330-.650) .420-.151) .550) .096-.270 (.096 (.360 (.570 (.220 (. 0.380 (.090 (.310-.560 (.290 (.060 (.210-.470) .460 (.330) . and for producing ferrotungsten. bronzes in pigments.088) .080-.130 (.130) .270-.060 (.071 (.300 (.350) .Metals Tungsten CAS No.250) .082 (.180) .470) . respectively.091) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.130) .060 (.570 (.200-.122) .190-.150 (.150) .113 (.460) .130 (.180) .470-.071-.180 (.220-.260 (.380 (.080 (.120) .S.430 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.140 (.260-.440) .320 (.095-.100 (.120-.

197-.068-.084) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report. (1987) found possibly due to methodologic.253 (.138 (.S.168 (.245-.197 (.059-.215) .278-.083-.279 (.095) Selected percentiles ( 95% confidence interval) 50th .341 (.386) .091) .364 (.667) .158) .084) .158 (.116-.078) .065-.148 (.082 (.216-.154) .209-.555 (.167-.138 (.179-.072 (.326) .214) .117 (.148) .054-.133) .061-.075 (.439 (.078-..250-.354) .436-1.065 (. Using neutron activation analysis to 2000.060-.392) .083 (.231 (.077-.161) .431) .077) .287) .379 (.079) . 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.231-.582) .096) .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 .071 (.217-.727) .199 (.331-.329-.086) .057-.302-.071-.054-.462) .098-.131-.208-.275 (.105 (.116) .086) .360 (.482 (.286-.080-.150-. similar to those in this Report (Schramel et al.074-.283) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.28) .099-.062 (.203-.119-.122-.205-.150 (.267) .300) .436) .667 (.165) .086) .211 (.124-.145 (.426) .198-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.459) .085 (.093-. population from the National Health and Nutrition Examination Survey.333) .087) .119 (.301) .075) . Nicolaou et al.078 (. interval) .083 (.333) ..084 (.158) .222) .125 (.333 (.174) .059-.308) .144 (.465) . 2003.410-.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 .255 (.070 (.237) .169 (.138) .080 (.146 (..120) .200-. measure urinary tungsten.063-.126-.063-.299 (.070 (.240-.091 (. population (CDC.216 (.353 (.068 (.167) .170-.090-.293 (.074) .107-.079) .215 (.(Kraus et al.197) .067 (.075-.098-.081 (.329 (.084 (.073 (.431) .358) .333 (.253-.100 (.218 (.136-.063 (.082) .079) .261-.169) .090-.091) .181 (.071) .383 (.267-.200-.216 (.302-.091) .333-.069 (.344-.216-. and 2003-2004 (Paschal et al.058-.125) .431) .184 (.074 (.412 (.353 (.255-.060-.198) .136-.139) .091 (.359 (.150-.063-.088) .233-.081-. Patients with medically-inserted tungsten found at increased levels in drinking water.059 (.222-.079 (.214-.497 (.081) .258-.130-.083) .067-.077-.075) .315-.279 (.S.086-.105 (.136-.453) .224) .164 (. 2005).187) .063 (.300-.059-.158) .452-.108-.151 (.049-.106 (.500) . 1997).130 (.056-.116 (.136-.237-.060 (.078) .088) .139-.265 (.167-.109-.S.284) .250 (.217-.484) .359 (. 1998).117) .121-.089) .063-.255 (.093) .072-.120) .133) 90th .317) .301) .069-.124 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.053-.333 (.074) 75th . 2001).073 (.067 (.111 (.143 (.103-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.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 .167) .340 (.092) .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 .237) .146) .083) .087 (.071 (.333-.121 (.465) .098-.285) .538) .065-.073 (.133) .098) .074-.199 (.065-.154) .080-.279 (. population.100) . population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.155-.091) .100) .095-.605) .439) Total .153-.176-.317 (.065) .201) .333 (.300-.122-.201 (.300 (.109 (.272-.094) .176-.079) .823) .094-.186 (.075-.085) .066 (.055-.108) .072-.136 (.065 (.085-.073 (.250 (.104-.554) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.301) .082) .152-.071) .179-.180-.634 (.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.308) .075 (.197) .056-.347 (.061-.375) .146 (.216-.484 (.797) .061-.153) .081 (.157) . 2001-2002.294 (.057-.174 (.089 (.317-.339 (.739) .071 (.188-. or exposure that a control group of non-metal workers had mean levels differences.414) .064-.122 (.880) .079 (.094) .354-.066 (.080 (.439 (.143-.077) .098 (.144-.078 (.339 (.253) 95th .385 (.064-.071) .069 (.306) .426) .139 (.381) .190) .258 (.270 (.206-.

Schaller KH.htm. [online] 2003. 2004). Wendler I. The determination of metals (antimony. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. mercury. Zobelein P. Nevada Exposure Asssessment. National Center for Environmental Health. Trace metals in urine of United States residents: reference range concentrations. Sampson EJ. Atlanta (GA).58(10):631-634.76(1):53-59. bismuth. Schramel P. Seghizzi P. thallium. Weber A. 238 Fourth National Report on Human Exposure to Environmental Chemicals .Metals blood. J Trace Elem Electrolytes Health Dis 1987. References Bachthaler M. Paetzel C. Link J. Kraus T.. 2005. cadmium. Paschal DC. lead. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Schramel P. Jackson RJ. palladium. Cassina G. Available at URL: http://www. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Lenhart M. Catheter Cardiovasc Interv 2004. Occup Environ Med 2001.(2):73-77. 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.cdc. Cancer Clusters. Feuerbach S. platinum. Pirkle JL. et al. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect.62:380-384. and hair (Bachthaler et al. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Mosconi G. Nicolaou G.gov/nceh/clusters/Fallon/study.69(3):219-223. Environ Res 1998. tellurium. Morrow JC. urine. Churchill County (Fallon). Pietra R. 4/15/09 Centers for Disease Control and Prevention. Angerer J. Int Arch Occup Environ Health 1997. Centers for Disease Control and Prevention. Angerer J. Manke C. Ting BG. Third National Report on Human Exposure to Environmental Chemicals. Sabioni E.

036 (.010) * .016) .004.006-.018) .007) .013-.036) .024-.023 (.021 (.008-. interval) .010) * .067) .010) .022 (.020) .037) Total .158) .006-.008-.030 (. see Data Analysis section) for Survey years 99-00.009 (.037-.027 (.046 (.027) .030-.010) . Since the 1990’s.014 (.008 (.007-.014 (.033 (.060 (.005-.007 (.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.007-.007-.008 (.006 (. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.012-.023-.018 (.036-.007 (.043) .088) .012-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).011 (.009) . human exposure occurs primarily by inhaling dust and other small particles.007 (.007-.014 (.024-.046) .010) .035) .010) .011) .007-.028-.011) .007-.012-.007-.042) .009) .019-. 01-02.007-.008) Sample size 2464 2690 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .017-.018) .005-.009-.007-.012) .054) .009) .038 (.017) .043 (.019-.039-.033) .015 (.011) .008) .007) . population from the National Health and Nutrition Examination Survey.007 (.030) .012-.007-.056) .021) .028-.006-.009) .031 (.007 (.026) .017) .026 (. or processing.013 (.007) 75th .012 (.006-.034-.008) .010 (.015-.029 (.017 (.010-. including nuclear weapons.015 (.027-.008 (.014 (.007 (.009) * .006 (.030 (.010 (.015 (.056) .062) .017) .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 .012) .042 (.021 (.023-.007-.063) .007) .009-.020-.007-.026-.019-.012) .006-. in some ceramics.033-.040) .114 (.040-.026-.005-.017-.048 (.011-.016-.053 (.020) .008 (. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.026 (.064 (.022-.018) .011-.005-.013 (.040 (.008-.009-.051) .009) . nuclear fuel.013 (.021) .006-.028 (.009 (. respectively.008 (.017) .009 (.029-.027 (.049) .010-.023) .016 (.009 (.026) 95th .009-.007-.033 (.066) .028 (.052 (.009-.013-.008 (.009 (.007 (.023 (.011-.037 (.038) . 235U (about 0.012) .012 (.016) .027) .010) .026) .011-.053) .045) .008) .007 (.012 (.008 (.007-.008) .054-.015) .011-.025-.016-.017-.067) .041 (.024 (.036 (.022-.041 (.013 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.055 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.017-.021-.032 (.021-.013 (.012-.065) .279) .011) .017-.065) . 0.009 (.020-.Metals Uranium CAS No.039) .020-.006-. In workplaces that involve uranium mining.006 (.016) .069) .010) .015) .011-. and 0.005.027) .022-.009-.046 (.010-.010 (.008) .009) . Thus.006-.050) .005-.016) .013) .031 (.009-.008-.023-.020-.007 (.006-.011) .034) .009) .009 (.008 (.029-.010 (.017 (.008 (.034-.030 (.020-.023) .008 (. Variable concentrations of uranium occur naturally in drinking water sources.040) .007) .023 (.008 (.006 (.006-.048) .046-.013 (.011) .072) .012 (.023) .022) .018 (.039) .016-.009 (.015 (.026 (.009) .027 (.011) .014 (.012 (.047 (.031 (.040 (.004. milling.013) 90th .021 (.007) .008 (.050) . 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.009) .006-.017-.044 (.009 (.012 (.035) . Uranium has many commercial uses.127) . 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.007 (.013-.009) .010 (.009) .019-.037) .016) .019 (.006-.028 (.008-.008 (.049) . Fourth National Report on Human Exposure to Environmental Chemicals 239 .009) .010) .045) . and 03-04 are 0.046 (.008 (.009 (.008 (.018) .036) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.008-.007 (.010-.073) .010) .72%).009-.031-.009) Selected percentiles ( 95% confidence interval) 50th .017) . Depleted uranium (DU) refers to uranium in which the proportions of 235U and 234U isotopes have been reduced compared with the proportion in natural uranium.008 (.040-.014 (.037) .011 (.009-.027-.011-.027-.035-.013 (.031 (.023-.007-.007-.006-.008-.008-.027) .037) .020 (.016) .021) . and as an aid in electron microscopy and photography.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 . and 234U.007-.010-.046 (.027 (.007-.031 (.S.008 (.009) .009-.012-.018-.036-.010-.024-.054) .

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.058) .034) .021) .007 (.005-.008) .006-.009) .010-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.024 (.010) .039) .017-.007 (.021 (.020-.010-.063) .074) .015) .027 (.035 (.007-.050) .027) .019-.006-.008 (.007-.025-.011) .011-.029) .007) .011-. the initial half-life of uranium is about 15 days (Bhattacharyya et al.025) 95th .025 (.050 (.030 (. liver.034 (.006) .030-.047) .015-.010-.050) .012) .009) .007 (.007-.016-.026 (.021 (.010) .007 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.009) .013) .030) .025-.017 (.009) * .030 (. 2005).019-.011 (. low level exposure.010-.030 (.007-.018-.026) . After exposure to soluble uranium salts.007 (.016-.014) .008) .019) .014-. Health effects from uranium exposure result from chemical toxicity to the kidney.020 (.021 (.019) .029) .006 (.024) .019-.009) .016-.028) .014-.007 (.013 (.011-. Inhaled uranium-containing particles are retained in the lungs.006-.007-.1%-6% of an ingested dose may be absorbed.028) .045 (.018) .018-.014 (.007 (.028 (.034-.013 (.029) .012 (.005-.024-.006-.005-.008 (.007-.015-. 2003).022-.024) .035 (.006) .008 (.030-.021-.010-.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 . which can occur occasionally from high occupational exposure.004-.020 (.033 (.006 (.027-.031 (.006-.011-..013 (.022 (.010 (.009-.017) .007 (.005-.008 (.006-.028) .006) .034 (.010-.009 (.039) .010) .010-.022-.024 (.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.051 (.016) .024-.024-.006 (.007-.016) .006 (.008) . about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.027 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. After long term or repeated exposure.022 (.007 (.100 (.007 (.010) .017-.080) . kidneys.041) .006) . with much slower elimination from bone.027) .006 (.019 (.009) Selected percentiles ( 95% confidence interval) 50th .006-. the shrapnel acts as a source of chronic. Uranium is eliminated in feces and urine.033 (.004-.018-.005-.016) .039) .014) 90th .006-.019 (.008) .032) .042) .020-.009 (.042-.012-. 240 Fourth National Report on Human Exposure to Environmental Chemicals .009-.026-.013) .008-.026 (.012 (..008 (.015 (.025 (.048) .013 (.011-.011) * .034-.025-.017-.030) .026 (.007 (.031-.037 (.010-.Metals impact.011) .013 (.010) .009-.010-.007-.005 (.024) .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 .027-.029) .014 (.009-.008 (.010 (.009 (. After inhalation.006-.032) .018-.024) . Depending upon the specific compound and solubility.006-.008) .015-.008-.028) .005 (.043 (.020-.017) .051) .009) .007 (.010 (.007 (.012) .010 (.019-.009) .017) .016) .008) .015 (.027-.007 (.008-.051) .006-.010-.006-.007 (.005 (.015 (. population from the National Health and Nutrition Examination Survey.033) .008) .008-.007) .012 (.012 (.006-.010) * .061) . interval) .018-.016) .006-.016 (.027 (.017 (.008 (.029 (.025-.007 (.009 (.009-.015 (.008) .024) .027-.077) .008) .006) .033 (.019-.022) .007 (.053) .029 (.011 (.007 (.009) .006-.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 .007-..006-.010) .007 (.007) .016) .040 (.042) .006-.013 (.018 (.058) .009) .010 (.011-.034 (. where limited absorption occurs (less than 5%).015) .013 (.048) .017-.067) .034 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al. 0.011-.009) .011-.008) .008-.011) .006-.012-.016-.006 (.016) .007 (.014) .007 (.009) .009 (.006-.015) .059 (.015-.013) .056) .028-.008 (.039) Total .006-.024 (.007-.006-.021 (.008 (.010-.044) .012 (.022 (.013 (.005-.028 (.012 (.012 (.034 (.012) .053) .009-.054) .S. which represents distribution and excretion.011-.029 (. In cases of retained DU shrapnel.033 (.014) .270) . Radiation risks from exposure to natural uranium are very low.008-. 1992).013 (.005-.020 (.008) 75th .005 (.023-.013 (.015-.015) .006-.009) .019 (.016) .006-.146) .022-.014-.008) .006-.008 (.013-.020-.020) .

. Kent (England): Nuclear Technology Publishing. McDiarmid et al. Stradling GN.. Benedik L. 2000). 2004). 1992. Six workers in a depleted uranium program showed concentrations of 0.62:562-566. Third National Report on Human Exposure to Environmental Chemicals. 2006).. 2005.066 μg/g creatinine (Gwiazda et al. urinary levels of uranium were as high as 9. A cohort of 46 U.html. during.. Sci Total Environ 1991. Hamilton MM... In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. but in whom no shrapnel was embedded.S. Breitenstein BD. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. (Kurttio et al. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure.. 1978). In two studies of a Finnish population with high natural uranium concentrations in their drinking water. environmental levels) and health effects is available from ATSDR at: http://www. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. population..55 μg/L (median 0. the median urinary concentration was 0.S. NRC. 2003. Radiation protection dosimetry.65 μg/L). Boyd P. Hamilton et al. Determining the normal concentration of uranium in urine and application of the data to its biokinetics.61 μg/g creatinine. the median urinary uranium concentration was 2. or wound contamination.78:143-146.1996.168(8):600-605. 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. Drinking water and other environmental standards have been established by U. Karpas et al.. In 17 U. Volf V. Durakovic A. Dang HS. IARC and NTP have no ratings for uranium human carcinogenicity. Zimmerman I. 28 soldiers who may have been exposed to DU by inhalation. eds. 2002.atsdr. respectively. 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. Ejnik JW. and no consistent effects on multiple endpoints of kidney function were found. 2002). Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.S. McDiarmid M.1992. Byrne AR.S. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Centers for Disease Control and Prevention (CDC). Horan P. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Pillai KC...... Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Squibb K. Vol.gov/ toxpro2. 1-49.S.Metals injury associated with elevated urinary uranium levels (Kurttio et al. Atlanta (GA). in that the levels were below their respective detection limits (Byrne et al. 2004). Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U.cdc. Guidebook for the treatment of accidental internal radionuclide contamination of workers.110 to 45 μg/L (Ejnik et al. Galletti. although slightly increased during and after deployment. Information about external exposure (i. References Bhattacharyya MH. Komaromy-Hiller et al. Metivier H. 2006).. In the same study.S. pp. Dietz LA. 1994. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al.. Carmichael AJ. Uranium content of blood. 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. (May et al. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. 2006). The U. 2006). 2001-2002.162 μg/L) (Orloff et al.e.078 μg/L (ranging up to 5. Mil Med 2003. et al. 2004). Fourth National Report on Human Exposure to Environmental Chemicals 241 . had a mean urinary uranium concentration of 0. and 2003-2004 (Dang et al. 2004). 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000.107:143-157. Health Phys 2000. soldiers evaluated before. 2006. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. 2000).. EPA. 1991. In a study of 105 persons exposed to natural uranium in well water. Thomas RG. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. the geometric mean urinary uranium concentration was 0. ingestion. Pullat VR. 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. Muggenburg BA.. with emphasis on quality control. 41 (1). Health Phys 1992. Tolmachev et al. In: Gerber GB.011 μg/L (McDiarmid et al.

Smith D. rapid. Washington (DC): NRC.87:51-56. Health Phys 2006. Gwiazda RH. Biokinetic modeling of uranium in man after injection and ingestion.110(4):337-342. Roth P.91(2):144-153. Gucer P. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Ough EA. Paretzke HG. Charp P. Kalinsky V.67(8-10):697-714. Halicz L. Englehardt SA. Ting BG.22–Bioassay at uranium mills. Nuclear Regulatory Commission (U.Metals Galletti M. Uranium and thorium in urine of United States residents: reference range concentrations. Cordero S. Environ Health Perspect 2002. Howerton K. Karpas Z. et al. Scott K. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Engelhardt SM. Kidney toxicity of ingested uranium from drinking water. McDiarmid MA. Am J Kidney Dis 2006. Uranium daily intake and urinary excretion: a preliminary study in Italy. Costa R.S. Human exposure to uranium in groundwater.94:319-326. U. Metcalf S. Bennett LG. Lewis BM. Kurttio P. et al. Andrews WS. Shelly T.86:12-18. Salonen L. Kuwabara J. Ejnik J. Health Phys 2003.82(4): 527-532. Saha H. Cremisini C. plasma and urine and a critical evaluation of reference values for the United Kingdom population. D’Annibale L. Hollriegl V. et al. Squibb K. Oeh U. Makelainen I. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. July 1978.S. Squibb K. Karpas Z. Mistry K. Inductively coupled plasma mass spectrometry as a simple. Orloff KG. U. Pekkanen J.S. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. McDiarmid M. Health Phys 2004. Jarrett JM. Element reference values in tissues from inhabitants of the European community. Pinto V. Wilson PD. Heller J. Environ Res 2004.S. Lorber A. Paschal DC. Salonen L.85:228-235. Sci Total Environ 1994. Auvinen A.296(1-2):71-90. Marino R. Saha H. Komaromy-Hiller G. Int Arch Occup Environ Health 2006. Environ Res 1999. Comparison of representative ranges based on U. Oberbroekling KJ. Komulainen H. Health Phys 2004. Kurttio P. Ash KO. Review of elements in blood. Radiat Environ Biophys 2005. Marko R. Health Phys 1996. Tolmachev S. Katorza E. Clin Chim Acta 2000. Van der Venne MT. NRC). Health Phys 2002. Sampson EJ. May LM. concentration and daily excretion of uranium in urine of Japanese. J Toxicol Environ Health A 2004. patient population and literature reference intervals for urinary trace elements.71(6):879-85. VI. Noguchi H.47(6):972-982. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Pirkle JL. Hamilton EI. Roiz J. McDiarmid MA.79(1):11-21. Nuclear Regulatory Commission (NRC) Guide 8.158:165-190. et al. Sabbioni E. Li WB. Jackson RJ. Wahl W. et al. Auvinen A. Kane R.81:45-51. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. et al. Renal effects of uranium in drinking water. Biologic monitoring for urinary uranium in Gulf War I veterans. Harmionen A. Oliver M. Hancock RG.44:29-40.

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 3.00) 7.60 (4. Perchlorate was added to the U.00-6.70 (3.90-11. and electroplating.10 (7.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.90 (5.80 (3.49-3.20-11.0 (8.70-7.0) 13.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.80 (6.80-4.0 (9.00) 3.0) 13. or ammonium salt.0) 13.70-11.40 (5.76 (3.5 hours and has a small estimated volume of distribution (Crump and Gibbs.40-13.0-29.90-12.81) Selected percentiles ( 95% confidence interval) 50th 3.50 (3. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.0 (11.0 (12.05 (2.67-5.10-7.40) 90th 10.0) 19.0) 9.30-6.29-3. milk.18-3.90 (4.60-7.0 (9.40 (5.40-11.05 and 0.93 (4.38) 5. and reducing agents.47-4.0) 15.80 (3. 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.40-4.40 (8. In addition.0 (9.40) 2.01 (2.30-17.0 (12.30 (2.20 (7.0-17.50) 6.0 (9.80-6.0 (12.60) 8. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.90-9.0-23.30) 6. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS. 2005).10-11.0) 9.19-4.40 (3.10) 3.0 (11.60 (7.30 (5.g. and certain plants with high water content (e.60) 3.80) 12.19 (3.02 (3.0) 16.90-9.0 (8.88) 3.40) 3.0 (11.70-9.50-4.79 (2.20 (4.50-7.0) 13.30 (2.60) 5.0 (10.12) 3.10) 12.80-15.0 (11.70-3.90) 5.10 (6.0 (11.89-3.0) 95th 14.46) 3.30 (5.08-3.35 (3.50) 5.0 (11.0) 9... 2002).05.00) 3.0 (12. 1998).20) 4.90-10.40 (5.0) 9.0) 13.0 (8.40-6.0) 11.90 (5.0) 9.10-11. 2007).30) 6.40 (3.70-3. leather tanning.75-3.50-11.EPA.0) 14.0) 8. interval) 3.51 (3.60-6.80-4.10-12.0 (9.0) 10.0 (13.50-3. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.11) 4. potassium. It is normally found and produced as the anion of a sodium.70-12.90 (5.0) 13.11) 3.93-3.00) 5.40-5.0) 8.56) 3. fabric dyeing.70) 3.20 (8. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.10) 5. but has strong oxidant properties in the presence of concentrated acids.00) 4.00-5.0) 11.31) 2.10-4.20 (6.68) 4.0) 10.20-4.62 (3.0) 9.22-5.30-7.70-5.96 (3.45-4.84) 14. laboratory analysis.90-3.80-12.90 (3.26 (2.09) 3.0) 10.80) 75th 6. lettuce) can be the main sources of intake for humans (FDA.10 (5.00-6.30-7.0) 11.0 (8. Other manufactured uses include fireworks.0-14.16) 3.0 (9.0-17.0 (8.0-15.66) 3.0) 13.22 (2.51 (3.50) 11. 2005). small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.0-18.40 (4.0 (11.0-18.S. matches.0) 14.50) 5.07-4.93-4.S.0-17. 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.0 (11.60 (4.50) 3.0 (11.0-15.10 (6. certain catalytic metals.0-18. Perchlorate is stable under most environmental and physiological conditions.40) 6.20 (5.0-17.40-4.65) 3.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.03) 3.40 (4.44-4.0 (11.80) 3.40) 3. population from the National Health and Nutrition Examination Survey.75 (3.32 (3.70 (3.0) 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.0-17.90-3.70 (3.0-19.74-3.40) 3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .87-3.90-6.10 (2.0-20.Perchlorate Perchlorate (Urbansky.40-7.30-19. Survey years 01-02 03-04 Geometric mean (95% conf.90) 6.80-8.81-16.0 (9.0) 708 617 681 652 1228 1092 Limit of detection (LOD.70-6.20-3.76) 4. Drinking water.50 (5.39-4.S.0) 12.20-4.20) 3.20 (4.10) 5.54 (3.0) 13.20-12.80 (7.20 (2.20) 7. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.80) 7. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.50-4.50 (8.90 (2.0) 15. and limited applications in pharmaceutics.0-17.10) 3.40) 4.90-11.21 (2.20 (2.

98) 3.39 (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.43) 6.0 (9.22-4. and the presence of other substances known to affect thyroid function (e.30-5.30-5. Li et al.22 (2.07 (2. Greer et al. 2007).45-2.03 (2.30 (6.70) 10.4-16.1-22. In these small short-term experimental studies on males and studies of male perchlorate workers with doses or estimated exposures thousands-fold higher than known environmental exposures.90 (2.50) 5.00) 3..10-7.61-5.2) 8.50-3..90 (7.80 (4. population from the National Health and Nutrition Examination Survey.70-3.72 (3.1-14.40 (4. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al. perchlorate is negative in most genotoxic assays (U.44-6.50) 9.30 (3. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.1-16.35 (4. 2003.50-5.50) 95th 12.56-3.50 (6.0) 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 .97-5.02-4.70 (2.80) Selected percentiles ( 95% confidence interval) 50th 3.50) 6.46 (3.00 (4.12-2.90 (4...1 (11. Lamm and Doemland. Also.10 (6.0) 12.0) 7.10) 13.93-5.30) 5.10 (2.90-2.61-10.84) 2.0-19.70-4.00-3.36 (8.1-13.44) 3.7 (11.59) 3.60-15.52 (8.76-3.37-13.0) 12. Survey years 01-02 03-04 Geometric mean (95% conf.81-3.22-4.30) 90th 9.0) 13.10) 6.60-6.74) 7.40-10.10 (4.47) 2. menopausal status.0 (8.00 (6.93-8.0 (8.40 (7.10 (4.56 (3..0) 11.20 (4.60-8.20-3. 2005). 2005).39) 2.87) 7.20 (6.20 (2.60-5.. up to 68% RUI has been demonstrated.34-3.2) 8.60-8.60) 8. medications).60) 10.77 (3.21 (2.35 (2.60) 3.33 (7.87-3.4) 8.46-4. 2006. thiocyanate.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5..10) 4.0 (9.51 (3.S. 2002)..20) 8. 2005).87) 2.0) 14.40) 3.86) 4.80-3.89-3.61 (5.64-3.60-11.25) 5.00-11.70 (2. During gestation and infancy.3 (10.26 (3.19-6.45) 3.70) 2.20-9.S.24 (4.54 (2.Perchlorate inhibition (RUI).20 (3.60-5.82 (5.4 (10.40) 17.15-12. 2000).05 (4.EPA.3) 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 3.3) 11.99-3.60 (3.02) 3. In the U.22-6.51-4.0) 6.0 (10.0-44.40) 5.12 (6.09 (7. interval) 3. 2001.0) 10. women with urinary levels of iodine less than 100 micrograms per day. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability. age.30-10. 2005.08) 3.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.99 (5.90-3.08 (3.6) 20.0 (11.20-10.58) 2.95 (2.42 (3. 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.6) 12.10-3. levels and sufficient in most participants (Tellez et al..00) 4.30) 75th 5. levels.37 (4.26) 4.0-14.16-3.41-9.0) 9.EPA.20) 3.4 (8.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.91) 4.40 (3.0) 9.29) 2. gender. 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.1) 8.73) 3.0) 12.0-14. Many factors may be important in consideration of perchlorate action on the thyroid: dose.54 (3.93-5.66) 3. in a representative sample of U. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al. NAS.18-3.93) 3.0) 13.80 (7.50 (3. chronicity of exposure.30 (5.46-13.0) 4.0 (11.30) 3.19-10.3) 12.90-15. 2002. although iodine intake was higher than U.25) 5.1 (8.. Lawrence et al.20-4. nitrate.90) 5.25 (3. 2002.90-11.76 (3.80 (7.04-3.5) 8.35) 3. dietary iodine intake.4 (11. 2005.25) 5.60-11.50) 2.S.70-15.6-17. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.70 (4.96) 2. U.24-2.32) 5.67) 5.4) 13.0) 12.33-6.87 (5.04-3.4 (11.70-5. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.71 (5.87 (7.83 (5.40 (3.8 (11.00) 9.39-4.g.00-2.52-9. 1999.29-6.80-3.20 (7. However.S.00 (2.50-9.89 (2.S.3-14.0 (9.90-20.14 (2.5 (13. Steinmaus et al.90-9.50) 2.75) 3.53 (2.S.S.60-3.09) 3.33-12.0 (11.10) 3.90 (2.10 (1.93-7.0-17.64) 5.20-3. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.

11(3):295.html and from ATSDR at: http://www. Greer SE. Mauldin JP. Pleus RC. J Expo Sci Environ Epidemiol 2007. Lamm SH. Buffler PA. Lamm SH.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis.10(8):659-663. Washington (DC): National Academy Press. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Goodman G. Low dose perchlorate (3 mg daily) and thyroid function. thiocyanate. Food and Drug Administration (FDA). Blount BC.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Daaboul JJ. Lawrence JE. Pirkle JL. 6/2/09 Greer MA. Jackson WA. Braverman LE. et al. (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.S.90(2):700-706. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Perchlorate Exposure of the US Population. Benchmark calculations for perchlorate from three human cohorts. Skeels MR. Primary congenital hypothyroidism. 2005. J Occup Environ Med 2003. most of the population is considered to be below the U. Blount et al.EPA at: http://www. Erratum in: J Occup Environ Med 2004. Environ Health Perspect 2005. Environ Sci Technol 2006. Environ Health Perspect 2002.115(9):1333-1338. Health Implications of Perchlorate Ingestion.html. Pirkle JL. Thyroid 2001. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Blount BC.46(5):509. References Blount BC. Analysis of relative source contributions to the food chain. Lawrence J. Tellez RT. Thyroid 2000. et al. and nitrate on thyroid function in workers exposed to perchlorate long-term. Pino S. Magnani B. population.113(11):A732.17(4):400-407. Braverman LE. Kelsh MA.fda. Environ Health Perspect 2006. epa.45(10):1116-1127. Pino S.113(8):10011008. Valentin-Blasini L. 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. Landingham CB.atsdr. Li Z. Byrd D. 2005). Osterloh JD. 2005). Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. 2001-2002. Dasgupta PK. et al.110(9):927-937.114(12):1865-1871. 2007). Dyke JV. 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. J Clin Endocrinol Metab 2005.gov/toxpro2.42(2):200-205.gov/safewater/ccl/perchlorate/perchlorate. Miller MD. Available at URL: http://www. Page Last Updated: 05/28/2009. newborn thyroid function. Caldwell KL.cdc. Crump KS. Braverman LE. May 2007. Deyhle GM. National Research Council of the National Academies.. Abarca CR. Kirk AB. Valentin-Blasini L. 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.. Crump KS.S. Lamm SH. Gibbs JP. Neonatal thyroxine level and perchlorate in drinking water. Lau EC. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U.. Lamm S. Chacon PM. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . National Academy of Sciences (NAS). Steinmaus C. Li FX. Osterloh JD. J Occup Environ Med 2000. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. CFSAN/Office of Plant & Dairy Foods. EPA reference dose (Blount et al. Environ Health Perspect 2007. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Richman K. The effect of perchlorate. Barnard JC. Sesser DE. Erratum in: Environ Health Perspect 2005. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data.41(5):409-411. Perchlorate in the United States. Cross M. Also. and environmental perchlorate exposure among residents of a Southern California community. Howd R. Doemland M. Rutherford GW. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans.40(21):6608-6614. He X.htm. Additional information about exposure and health effects is available from the U. et al.S.

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

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

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

Lau et al.800) 1.600-2. U. U. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.600 (. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. EPA.400-...500 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .600 (. In such studies. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.900 (..50) .400 (<LOD-. 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) .700 (. Serum PFOS levels associated with toxicity in test animals were 310-1550 fold higher than 95 percent of the levels found in a study of adults (Olsen et al. and changes in thyroid hormone concentrations (Grasty et al.S. 2003). At high but non-toxic maternal doses of PFOS. or increased cancer rates (Alexander et al. However. developmental and teratogenic effects were demonstrated in offspring. 2003.10) . Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.500-1.300 (<LOD-. 2003a).00) . possibly related to lung immaturity (Lau et al.500-..80) 485 538 962 Limit of detection (LOD. PFOA. monkeys. see Data Analysis section) for Survey year 03-04 is 0. population. 2004).400 (<LOD-.500-3. thyroidal).00 (.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al.400-1.400-. 2005)...600 (. 2003). perfluorohexanesulfonate (PFHxS). 2003a.10) . 2004). Fourth National Report on Human Exposure to Environmental Chemicals 249 . In comparing three separate reports on adults. 2007a. Survey Geometric mean (95% conf. 1999..300-1. the median PFCs values tend to be roughly similar in these age categories (Olsen et al.900 (. Animal studies of PFOS have demonstrated weight loss. Thibodeaux et al. population from the National Health and Nutrition Examination Survey.. PFOS.400) . 2003a).500-1. 2007.700) . 2003. EPA. development in offspring was stunted and hypothyroxinemia was observed.S. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. 2004.300 (<LOD-.3.00) . reproductive. 2003a. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. 2007). the potential to estimate risks to humans from animal doses is uncertain. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.500 (. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal...00) .500) .800 (. 2003). Olsen et al.S.800 (.. 2007a.. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. and humans. PFOA.400-1. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. 1992. Harada et al.. 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. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.80) 640 1454 03-04 03-04 * * < LOD < LOD .S.. Olsen et al.108 times higher than background serum levels in humans (Butenoff et al. Fei et al.400-1. Cook et al. 2003. and there was no clear evidence of excess all-cause or diseasespecific mortality..500) . 2004b). PFOS.10) * 03-04 03-04 * * < LOD < LOD < LOD ..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 . 2007b. Olsen et al.800) 1.800 (.800 (.20) ..500) .300 (<LOD-.40) . Kennedy et al. elderly and children.400 (<LOD-. 2004.500-1.500) 90th .400-1. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. 2005). 2001. 2007b).900 (.10 (.. which may vary for some chemicals by year and by individual sample. hepatotoxicity..400-1.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection. 2003a. 2004a. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (<LOD-1. At doses causing maternal toxicity.500-1..

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

400 (<LOD-.500 (<LOD-.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD .400 (<LOD-.900) < LOD . Survey Geometric mean (95% conf. Survey Geometric mean (95% conf. 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300-. Fourth National Report on Human Exposure to Environmental Chemicals 251 . see Data Analysis section) for Survey year 03-04 is 0.400) .600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S. which may vary for some chemicals by year and by individual sample.300 (<LOD-.3.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600 (.500-.S.400 (.0. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.600) < LOD . Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. < LOD means less than the limit of detection.500) 485 538 962 Limit of detection (LOD.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (<LOD-. population from the National Health and Nutrition Examination Survey.

900-1.90) 1.00 (.40 (1.10-5.80-6.700 (.20) 485 538 962 Limit of detection (LOD.30 (1.26) 2.00 (1.S. Survey Geometric mean (95% conf.30) 3.30 (1.60-8.20 (6.42 (1.809) 1.912-1.80) 3.10) 6.30) 03-04 03-04 .90 (1.20-1.30-6.50 (1.50-6.03) 1.00) 1.60 (1.586-.80-8.00-7.30) 3.20) .S. interval) .40) 1.10-9.70) 13.40 (1. interval) 1.05-2.10) 6.14 (.62-2.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.80-7.3.44 (2.60 (6.10 (.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.900 (.30 (1.800 (.721-1.10) 4.40 (1.90) 90th 5.04) .90 (4. population from the National Health and Nutrition Examination Survey.20-1.50 (1.01 (1.80) 5.20 (1.5) 8.10 (4.80) 90th 2.92 (1.20-3.835-1.70-10.1) 485 538 962 Limit of detection (LOD.51) 1.600-.0) 8.70-2.700-1.70-2.50-10.90-19.91) 2.80-7.00 (1.10) 1053 1041 03-04 03-04 03-04 .30 (2.60-4.70) 3.20 (6.08) 2.80-4.20-1.80-12.90) 1.60-3.90 (1.27) 1.20) 1.00 (1.60) 3.40) 1.60-4.40 (1.30-9.20) 1.30 (7.30) 3.60) 9.90-2.50 (1.70) 1.3 (9.73-2.70 (2.00) 2.80-3.10) 1.30-2.80) 1.72) 1.816-1.90) 8. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.70) 2.10 (4.80-4.90 (2.70-5.70 (1.50 (4.93 (1.00-1.87-2.40-1.1.00 (.20-1.00-1.90-10.50) 6.861 (.10) 1.10) 4.50 (4. population from the National Health and Nutrition Examination Survey.70-7.00) 1.0) 1053 1041 03-04 03-04 03-04 1.60 (1.20 (1.80-8.50 (2.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.80-3.80-4.20) 2.00-8. 252 Fourth National Report on Human Exposure to Environmental Chemicals .6) 7. see Data Analysis section) for Survey year 03-04 is 0.80-2.834-1.40) 2.900-1.900 (.56-1.60) 1.00-6.50-6.17 (1.40) 640 1454 03-04 03-04 1.50) 2.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.900) 1.60-2.16) .54) .30 (3.50 (6.20 (1.80 (1.900-1.10) 5.900-1.80 (1.90 (1.00 (2.984 (.10 (.50 (6.60-3.72 (1.30) .40) 640 1454 03-04 03-04 2.10) 75th 1.90) 3.70-6.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.5) 5.80) 4.50 (1.50) 2.77-2.90 (4.10 (.40) .40 (2.80 (4.900-1.20 (1.966 (.12) .50-3.70) 2.10 (1. see Data Analysis section) for Survey year 03-04 is 0.86 (1.00) 3.67-2.852 (.30 (2. Survey Geometric mean (95% conf.30 (1.60) 2.40) 4.60-2.40-3.60-7.17-1.09 (.00 (5.10) 8.40-1.30-12.800-1.689 (.900-1.20-2.60 (1.00 (1.90 (1.90) 1.826-1.10) 75th 3.697-1.70) 1.10-9.20) 03-04 03-04 2.60-2.30 (6.963 (.

3) 485 538 962 Limit of detection (LOD.2-57.9) 22.3 (35.S.4-25.30-11.2-22.5-23.60 (5.1.50) 4.2 (16.4-42.5 (28.30-6.11 (2.47-4.0) 03-04 03-04 19.5-62.4) 56.1 (23.6 (44.3 (28.79) 4.60-9.9 (22.70-7. interval) 3.35) 3.18 (3.30-5.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.80-12.0) 36.1-35. Survey Geometric mean (95% conf.20-9.1) 57.70 (3.40-6.8) 46. Survey Geometric mean (95% conf.6 (35.70) 4.8-22.60 (3.4 (19.40) 90th 7.6) 1053 1041 03-04 03-04 03-04 3.9) 9.70-7. interval) 20.10-3.2 (28.90) 6.40-6.60 (6.8-81.10 (6.1) 15.60 (7.50-13. population from the National Health and Nutrition Examination Survey.6) 21.3-61.0-20.0) 485 538 962 Limit of detection (LOD.1-24.40 (4.6 (19.8-22.40) 75th 5.0-66.8-35.50-4.7 (13.20-5.5) 9.90 (7.3) 28.60 (6.8-30. see Data Analysis section) for Survey year 03-04 is 0.70-10.6) 9.6-50.0) 90th 41.80-9.90 (5.10 (3.5) 1053 1041 03-04 03-04 03-04 14.95 (3.70-5.6-45.8-22.2) 640 1454 03-04 03-04 4.7 (35.8 (34.00) 3.89 (3.40) 5.80) 8.20 (4.1 (19.40 (6.00 (5.4 (23.50-6.50) 7.37 (2.3-22.7) 39. see Data Analysis section) for Survey year 03-04 is 0.90-4.1 (24.5-33.0) 23.40-10.7-69.3 (44.6) 42.1-25.1-33.1-52.21-3.60) 8.5) 8.80 (6.6-24.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80-4.S.4 (19.4.4) 75th 30.0 (20.4) 21.30) 6.80 (6.5) 32.90-4.96 (3.20) 7.5) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 21.2) 30.47 (4.40) 3.2 (21.7 (19.70-9.20) 7.30 (3.2 (27.9) 22.60-14.8) 27.0 (27.7-30.7-53.70) 6.80 (7.90 (7.1) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 4.30-3.30 (5.10) 5.65-4.7 (7.00 (5.8-78.4 (28.20) 5.6) 35.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.70 (5.60-6.7 (35.0-16.8) 32.5) 19.9-23.91) 3.82) 4.2) 30.99-3.30) 7.20 (4.0) 21. Fourth National Report on Human Exposure to Environmental Chemicals 253 .60) 03-04 03-04 3.70) 3.9) 27.60-13.7 (43.4-17.2 (19.30-8.9 (19.70 (5.3 (35.27) 4.5-21.07-4.3 (17.8 (37.40-17.9 (13.6) 18.40-14.84-3.53) 3.50 (3.2) 45.0) 43.90 (7.67-4.5) 18.4 (17.7 (43.9 (17.7-49.50 (4.0) 21.20) 5.0-70.6) 62.1-36. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20) 4.4) 640 1454 03-04 03-04 23.5 (28.6) 7. population from the National Health and Nutrition Examination Survey.10 (3.4) 20.00 (3.2 (18.90-12.60 (4.85-4.3) 41.3) 42.9-38.30 (3.20) 10.8 (45.6 (42.7-23.7-33.5) 7.80 (5.20-4.5) 57.9-19.

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

10-1.10) 1.10) * 03-04 03-04 * * < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.900) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .600 (<LOD-1.10-1.700 (<LOD-. population from the National Health and Nutrition Examination Survey.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .6.700 (<LOD-.800) .50 (1.30) .10 (.900-1.400 (<LOD-1.800 (<LOD-.00 (.40) 1.700) 1.80) 1.30 (1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 0.700 (<LOD-2.900-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .10-1.900-1.50 (1.600 (<LOD-1.900-1.700 (<LOD-.900 (.40) < LOD < LOD .900) 485 538 962 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.30 (1. which may vary for some chemicals by year and by individual sample.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.600 (<LOD-.10-1.00 (.700 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.S.700) 1.900) . population from the National Health and Nutrition Examination Survey.20) 1.20-1.30) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900 (<LOD-1.10 (.10) 1.700 (<LOD-.800) .80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.90) .30) 1.00) < LOD .900-1. Survey Geometric mean (95% conf.00 (.00 (.600 (<LOD-1.300 (<LOD-1.10) . < LOD means less than the limit of detection.30 (1.900-1.10 (.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 .80) 1.10-1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .700 (<LOD-.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (<LOD-.3.10 (1.700) 90th 1.10) .00-1.500 (<LOD-.300 (<LOD-.70) 1.700) .60) 485 538 962 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60) 640 1454 03-04 03-04 * * < LOD < LOD .S.900-1.20 (1.300-2.600) .

Toxicol Appl Pharmacol 1992. Kannan K. and ex vivo studies. Butenhoff JL. Watanabe T. Caudill SP. Kennedy GL Jr. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Kuklenyik Z. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Edwards EA.34(4):351-384. Environ Sci Technol 2007a. Environ Sci Technol 2005. Mandel JS. Environ Sci Technol 2006a. Fei C. Reidy JA.115(11):1677-1682. Yoshinaga T. Polyfluoroalkyl chemicals in the U. et al. Hekster FM. et al. Taniyasu S. J Occup Health 2004. Peterson RE. Witter FR. Wong LY. Kamiyama S. Calafat AM. Suzuki E. Moore JA. Calafat AM. 2007b. Fluorotelomer alcohol biodegradation yields poly. O’Connor JC.Koizumi A. Environ Sci Technol 2004. Harada K. Environ Sci Technol 2005. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Yamashita N. Yun SH. Olsen J. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Regul Toxicol Pharmacol 2004. Katakura M. Environ Sci Technol 2004. Hurtt ME. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Toxicol Appl Pharmacol 1995. Needham LL. McLaughlin JK.39(23):9057-9063. Toxicol Sci 2001. Laane RW.63:490496. Characterization of risk for general population exposure to perfluorooctanoate. Koizumi A. Perkins RG. Kuklenyik Z. Cook JC.38(17):4489-4495. Cook JC. Grasty RC. Birth Defects Res B Dev Reprod Toxicol 2003. The influence of time.134(1):18-25. et al.40:21282134.60(1):44-55. Falandysz J. Fillmann G. Mabury SA. Occup Environ Med 2003.39(3):363-380. J Environ Monit 2005. Environ Health Perspect 2007. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Dinglasan MJ. Olsen GW. Frame SR. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Rodricks J. Mohotti KM.S.113(2):209-217. Aguilar-Villalobos M. Inoue K. Hurtt ME. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort.179:99-121. Guruge KS. brominated. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Burris JM. Hurtt ME.46(2):141-147. et al. Sasaki S. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Reidy JA. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Environ Res 2005. Harada K. Gaylor DW. Frame SR. Environmental and toxicity effects of perfluoroalkylated substances. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Wijeratna S. Tully JS. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion.and perfluorinated acids. Morikawa A. Environ Sci Technol 2005. Taniyasu S. Chemosphere 2006b.39(23):9101-9108. Seneviratne HR. Perfluorinated chemicals in selected residents of the American continent. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Murray SM. Tarone RE. Yamashita N. Ye Y. Chem Biol Interact 2000. Corsolini S. Saito N. The toxicology of perfluorooctanoate. Reidy JA. Rogers JM. Bandai N. Crit Rev Toxicol 2004. Evans TJ. Day RD. Reidy JA. Cook JC. Seacat AM. O’Connor JC. et al. Saito N. Needham LL.7(4):371-377. et al. Calafat AM. Rev Environ Contam Toxicol 2003.115(11):1670-1676.60(10):722729. Needham LL.124(2):119-132. Caudill SP.104(2):322-333. Kudo N. Mandel JH. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Calafat AM. Jarnberg U. Yoshinaga T. Grey BE.39(1):80-84. Biegel LB.38(10):2857-2864. Keller JM. Loganathan BG.99(2):253-261. Biegel LB. Kannan K. Halden RU. Kumar KS. Mandel JH. Arendt MD. Ingall GB. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Toxicol Appl Pharmacol 1990. Calafat AM. Lau CS. Liu RC. and perfluorinated contaminants in livers of polar bears from Alaska. Moore RW.1968--2003. et al. Kawashima Y. Herbstman JB. Tully JS. Olsen GW. Chlorinated. Butenhoff JL. Bookstaff RC. Inoue K.41:2237-2242. Serum concentrations of 11 polyfluoroalkyl compounds in the U.Perfluorochemicals References Alexander BH. Olsen GW. Needham LL.68(6):465-471. Bignert A. Environ Health Perspect 2007. de Voogt P. Holmstrom KE.115(11):1596-1602. Kannan K. Kuklenyik Z. Kuklenyik Z. in vivo. Environ Health Perspect.S. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Apelberg BJ.

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

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

McKee RH.22(3):688-695. Skakkebaek NE.nih. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Hartle RW. Milligan SR. Albro PW. Richthoff J. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate.gov/chemicals/ phthalates/dbp/dbp-eval. Gans G. Available at URL: http://cerhr. Jacobsen H.26(8):1219-24.html.110(5):515-518. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Harris CA. Kessler W. 2000a [online]. Ryan L. Hauser R. 2000c [online]. Tsukino H. et al.18(1):122. et al. Fromme H. gov/chemicals/dehp/dehp-eval. Calafat AM.gov/ chemicals/phthalates/bb-phthalate/bbp-eval.niehs. and infant formula by tandem mass spectrometry (LC-MS-MS). The estrogenic activity of phthalate esters in vitro. Duty SM.niehs. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004.html. Nielsen J. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP).112(17):1734-1740.195:142-153. Hauser R. Sumpter JP. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. NTP-CERHR.111(2):139-145.106(1):23-26. Environ Health Perspect 2002. Dalgaard M.46(11):643-647. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Reprod Toxicol 2004. J Androl 2004. Chahoud I. Yoshimura M. Jonsson BAG. Hum Reprod 2007. Research Triangle Park (NC). Drexler H. Yokoyama Y. Numtip W. Calafat AM. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Silva MJ. Liss GM.105:802-811. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. 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Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Environ Health Perspect 1997. Kano K. Scand J Work Environ Health 1985. Brock JW. Zhang S. Mortensen GK. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Hagmar L. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic.16(4):487-493. Int J Hyg Environ Health 2007. Determination of phthalate monoesters in human milk. Epidemiol 2005.niehs. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Andersson A-M. Environ Health Perspect 2004. David RM. Kalita JC. Environ Health Perspect 1998. 6/2/09 NTP-CERHR. Jarfelt K. Jobling S. Hoppin JA.html. Lovekamp-Swan T. 2000b [online]. Mechanisms of phthalate ester toxicity in the female reproductive system. Meeker JD. Boehmer S. Main KM. Hass U. Toxicol Appl Pharmacol 2004. et al. Giwercman A. Henttu P. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Baird DD.112(17):1740]. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.382:10841092.19(4):505-515. Am Ind Hyg Assoc J 1985. White R. Available at URL: http://cerhr. Biol Pharm Bull 2003.nih.nih. Parker MG. Ladefoged O. Koch HM. Csanády G. Sumpter JP. Park S. Balasubramanian AV. Skerfving S. Chen Z. Borch J. 6/2/09 NTP-CERHR. Reprod Toxicol 2005. Int Arch Occup Environ Health 1993. Meeker JD. Angerer J.25(2):293-302. Duty S.gov/chemicals/dehp/dehp-eval. Leffers H. Reynolds T. Davis BJ.nih.103:582-587. Reproducibility of urinary phthalate metabolites in first morning urine samples. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Available at URL: http://cerhr. Ryan L. Silva MJ. 6/2/09 Okubo T.210:21-33. Kano I. Silva MJ. Brock JW.

Cunningham ML. Klinefelter GR.Phthalates phthalate (DEHP): a cross-sectional study in China. Toxicol Sci 2000.58:339349. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Caudill SP.36:459-479. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Reidy JA. Orton TC. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Barlow NJ. Meek MD. Albro PW. Pratt IA. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. 112(5):A270]. Urinary levels of seven phthalate metabolites in the U. Fielden MR. Matthews JB. Batten PL. et al. Wu ZF. Bratt H. Environ Health Perspect 1982.114(11):1643-1648. Barr DB. Environ Health Perspect 2004. Peck CC. Environ Health Perspect 1986. Lambright CR. Silva MJ. Fourth National Report on Human Exposure to Environmental Chemicals 261 .65:299-308. Environ Health Perspect 2006. Rhodes C. Parks LG. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver.45:11-17. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat.S. Zacharewski TR. Malek NA. Peters JM.46:282-293. Abbott BD. Rusyn I. et al. Clemons JH. Jackson SJ. Toxicol Sci 1998. Hodge CC. et al.112(3):331-338. Crit Rev Toxicol 2006. Ostby JS.

6) 25.2) 14.9-27.3 (12. residents (Blount et al.6) 13.2) 66.1 (58.7 (12.8.0 (33.3) 37.5-84.0 (15.9 (16.4 (53.5) 82.3) 23.6 (13.6-29.4 (32.4) 71.7 (82.7-14.3-74.5-97.4) 12.6-18.8-13.0) 16.3-130) 122 (88.5-40.8-17.7-172) 103 (74.4 (10.3 (22.8 (80.0) 20.7 (80.6) 50.8 (28. NTPCERHR.4 (10. interval) 15.5 (27.1) 12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9) 14.3 (12.8 (14.2-38.7 (51.5-35.7 (53.3 (54.6) 37.7-16.9-30.4 (13.2 (11.7 (70.4) 49.2) 22.3) 13.2) 12.2) 15.1 (13.3-82.0) 24.9) 15.8) 24.1-90.4 (68..9 (22.6) 63.1) 31.2 (19.1-43.5-94.9) 13.9) 11.7-17.0 (12. High dose BzBP and its monoester metabolites.5-62.4) 129 (98.4) 75th 35.9 (70.6-17.2) 14.0) 70.0) 34.3-34.2) 33.2-16.7-58.0-85.9 (12.3) 63.7-25.3) 54.4 (29.8-14.6-92.7) 38.6 (12.1.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16.6-150) 94.8 (12. because it is not bound to products in which it is incorporated.2) 32.0) 90th 67.0 (30.6) 13.8-98. and 2003-2004 were generally similar those reported in U.2) 17.9-49.5) 30.5 (55.6) 67.1 (20.9-87.2-115) 113 (91.1-16. see Data Analysis section) for Survey years 99-00.8 (21.1 (55.8) 14. 262 Fourth National Report on Human Exposure to Environmental Chemicals .3) 15.4) 38.5 (61.2 (19.5-41.5 (67.9) 49.2-17.0 (20.4 (31.1) 67.0 (34.0 (14.4 (27.9-28.7-119) 99.3-18.3-75.4 (53.0 (30.4-127) 80.8) 63.2-31. and diet is the major source for general population exposure.9 (21.7-35.8-76.8 (10.2-40.9-47.9 (28.0 (23.1-15.8-64.3 (44.3 (29.6 (13.2 (47.8-14.1-214) 166 (116-191) 145 (110-213) 88.1-15.5-25.4 (48.0 (43.3 (13. sealants.6) 95th 103 (94.3-88.3-12.3-21.4) 65.8 (30. 01-02.6) 16.5 (13.5-18.6-39.4-92.0-106) 58.1) 76.4) 35.5) 27. particularly male animals (McKee et al. 2000).6-79.0) 33.3) 13.9 (13.5) 16.6) 14.4 (63.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.0 (55.3 (33. and 03-04 are 0.Phthalates Benzylbutyl Phthalate CAS No.2 (10.1-35.7-16. 2004.6-92.8-48.9) 12.4-24.7) 23. IARC considers BzBP not classifiable with respect to human carcinogenicity.5 (76.5 (26.8-35.2 (25.6 (13.4) 51. respectively.9 (11.6-38. Food crops take up BzBP.9) 43.9-14.6) 35.1 (19.4) 98.3 (30.6 (13.4) 81.7-82.1 (32.6-43.4 (32.0 (27.8-17.7) 40.2-183) 101 (78.8 (53.5 (57.6-116) 122 (102-142) 101 (85.6-72.4-16.4-62.2) 69.1-116) 122 (93.6) 29.5-145) 138 (106-241) 143 (127-179) 120 (99.8-18.8 (38.3-18..2) 13.9-190) 86.4) 14.3-27.0 (11.6) 24.1) 68.5) 65.6 (21.0) 32. it can be released into the ambient air during use or disposal of the products.1) 29.6) 35.7-15.5 (66.2-155) 91.4-25.7-13.4-15.5-36.4) 35.5) 15.8-72.2 (14.0-55. 2001-2002.5 (47.4-120) 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 13.7 (11.8-16.0-26.6-132) 103 (84.6 (32.0-130) 101 (86.9 (39.9) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 39.1-61. some personal care products.3. population from the National Health and Nutrition Examination Survey.5) 23. 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.2-19.5-36.1) 32.0) 23.9-16. 2000).1-120) 52.3-125) Total 15.1) 14.3) 94.1 (14.8-121) 79.8 (71.8-41.0 (26.1 (10.7-170) 169 (134-198) 152 (99.8 (50.2 (43. can produce developmental and reproductive toxicity in rodents.6 (53.8) 33. and 0.5) 15. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.2-16.8 (71.1-16.3-43.8 (86.S.9-62.4) 108 (96.7-16.2-39.4) 33.3-161) 99.2) 78.5-33.6) 14.9) 14.2-20.6 (41.1 (14.4 (59.2-116) 122 (102-143) 101 (84.1) Selected percentiles ( 95% confidence interval) 50th 17.6) 15.3 (12.1-18.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7 (13.2-33.1) 13.5-14.3-91.9) 18.5) 55.1 (13.1-39. vinyl tile.9 (12.8) 28. car care products. and to a lesser extent.7 (15.4) 80.3 (29.S.1-38.0 (15.8-133) 89. 0. including MBzP.8-16.6 (66. BzBP can be released into the environment during its production and.

2) 12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.73-12. and in a small sample of German residents (Koch et al.7 (14.8) 26.9-13.4 (21.7-15.1-120) 77.6) 13.7-90.8) 54.6-20.7-56.9-16.2) 11.5-58.9 (10.4-79.1) 80. 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.5 (35. population from the National Health and Nutrition Examination Survey.5-58.8 (69.7-61.8) 56.6-81.4 (34.6-13.9 (10. interval) 14.6 (30.1 (21.3 (15.3) 89.8 (12.6) 12.9-13. adolescents compared with adults.3) 55.4) 28.7-14.7) 56.9-83.8 (50.8 (30.3-38.0-53. In NHANES 1999-2000.1 (11.3) 14.7) 38.4) 60.8 (46.8-48.6-47.9-14.3 (39.9) 11. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults. 2003)..2-12.4 (13.2 (69.2-117) 95.5 (10.1 (41.7) 11.4-18.4 (11.4-99.7 (11.1) 24.5) 10.2-15.5) 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 .0-26.1 (21.6) 25.7-397) 70.4) 13.0 (11.8) 53.2 (27.3 (35.1-12.4 (11. Hauser et al.8-16.4 (33.0 (41.4-14.8) 24.5) 13.2 (41.0 (67.4-17.6) 73.9) 24.3 (13.5 (10..3 (24.3) 16.4 (26.1 (21..8-34.8) 15.9 (15.9-28.5-79.4 (10.5 (42.9 (51.2 (40.7 (13.9 (55. in young Swedish men (Jonsson et al.2) 15.7 (54.9-104) 62.4 (46.9-115) 57.1) 24.8) 13.8 (13.5-13.5-26.9 (43.5 (48. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.9 (9.Phthalates York City (Adibi et al.6 (11.7-69.6-26.9) 100 (80.4-142) 134 (116-176) 136 (85. 2006).8-39.3) 67.3) 73.5 (49.8 (64.4-14.9 (24.1-27.1-79.9) 52.7 (18.6) 30.5-26.6) 75th 25.4) 90th 50.2) 67.5) 95th 77.0 (12.6-40.5-16.2) 11.9 (12..3) 21.0 (49.5) 14.1) 35.8-13. 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. 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.5-31.9) 12.6 (34.1-125) 86.6 (51.4 (12.1 (14.0 (12.0 (33.4 (11.9 (24.6 (11.3-64.1 (34.2-26.7-14. Hoppin et al..8-60.4) 21.7-19. 2007). in men attending a Boston infertility clinic (Duty et al.5) 23.6-116) 74.8 (57.0) 60.3) 18.0 (38.9-62. 2002).0 (10.6 (24.5-76.2 (56.6 (22.3) 13.1-12.8-14.8) 46.8-13. 2004.1) 142 (99..0-27.9 (22.S.6) 38.3) 36.7-20.8) 80.5) 78.1 (13. A small study of African-American women in Washington.0 (13.6 (11.0) 24.5) 17.6 (57. 2002.7 (12.7-12.2-21. 2003).4-102) 70.4-15.3 (12.3) 12.4-42.4) 12.8 (49.3 (38.8-173) 195 (121-305) 229 (99. 2004).8) 68.0-109) 65.3) 37. and females compared to males (Silva et al.8) 33.6-99.8) 34.6) 53.7-19.8) 53.7 (11.4-19.7) 19.0-48.5 (9.0) 49.4) 50.5) 16.5) 20.3) 90.1 (19.2-57.3) 29.4) 104 (89.2-17. Limited studies in children younger than 2 years old have found median and geometric mean urine MBzP that were similar to children aged 6-11 years in the NHANES subsamples (Brock et al.9) Total 14.9) 64.4) 25.6 (14.9-23.3 (23.4-90.0) 24.6) 58.9) 42.8-80.8 (10.5-99.3-73.2) 11.4 (60.0) 15.0-90.7-29.7-20.4) 44.6 (36.1 (13.9) 12..1 (15.5-61.8-15.4-23.7 (11..8) 108 (75.5 (11.3-34.5-23.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.0 (62.4) 14.1) 27.8-27.9 (12.9 (15.2-49. 2005).9 (39.4-116) 73.1 (43.4 (25.2-15.69-11.7 (55.1) 39. Weuve et al.1 (21.8-64.2) 32.9-69.6-12. 2007).5-57. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.7-31.3) 13.6 (30.9) 12.4-60.7 (38.1) 12.8-14.2) 26.5-213) 49.7 (23.0) 13.7 (13.3) 13.1 (9.7-15.5) 41.9-40.6 (19.0-15.8-42.4) 13.3-11.2-13.1) 23.0-51.7-123) 77.95-14.3-16.4) 51.5 (12.0) 11.1) 17.9 (29..8-13. 2005.5 (56.5-38.8-15.8-85. In an annual sample of German university students.4 (69.9) 11.1 (46.7 (59.7) 25.8) 16.3) 14. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.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 40.5-42.4) 17.5) 46.8 (11.6 (15.8) 71.4-93.3 (60.4-27.4 (74.1-29.7) 46.5-29.7 (21.2-78.4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.6-86.9 (54.7 (19.1 (18.4) 15.1-14.6) 12.6-15.8) 11.8-69.0 (41.1-58.4 (63.0) Selected percentiles ( 95% confidence interval) 50th 13.2-51.2-13..1 (25.1 (23.8) 33.1-35.1 (53.0) 12.

et al. Bull Environ Contam Toxicol 2002. Reidy JA.111(14):1719-1722. J Androl 2004.nih. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Needham LL. Sampson EJ. 112(5):A270]. Giwercman A. Environ Health Perspect 2006. Environ Health Perspect 2004. Environ Res 2003. et al. Poland. Barr D. Meeker JD. et al. Silva MJ. Schettler T. Silva MJ. Research Triangle Park (NC). Camann DE. Perera FP. Duty SM. Hilborn ED. Hum Reprod 2007. Environ Health Perspect 2000. Hagmar L. Butala JH. Blount BC. David RM. Caudill SP. Brock JW. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.112(3):331-338. Caudill SP. Rylander L. Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 2002. Weuve J. Richthoff J. Dobler L. Prenatal exposures to phthalates among women in New York City and Krakow. Brock JW.22(3):688-695. Eckard R.114(9):1424-1431. Baird DD. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Reprod Toxicol 2004. Calafat AM. Ryan L. Jonsson BAG. Green RA. et al. Drexler H. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Davis BJ. et al. Singh NP. Available at URL: http://cerhr. Hauser R. Hodge CC. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Calafat AM. Atlanta (GA). Centers for Disease Control and Prevention (CDC). McKee RH. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. 4/20/09 Silva MJ. Wittassek M. Koch HM. Hu H. Epidemiol 2005.S. Jacek R. Gans G.110(5):515-518. Brock JW.108(10):979-982. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Barr DB. et al. Koch HM. Angerer J. 2000 [online].gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Urinary phthalate metabolites and biomarkers of reproductive function in young men. 2005. Silva MJ. NTP-CERHR. Ryan L.25(2):293-302. Jedrychowski W.Phthalates References Adibi JJ. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Phthalate monoesters levels in the urine of young children. Hoppin JA. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.18(1):122. Int J Hyg Environ Health 2007. Chen Z. Environ Health Perspect 2003. Needham LL. Helm D. Malek NA. Duty S. Caudill SP.niehs. Pirkle JL.210(3-4):319-333. Silva MJ.html.93:177-185. Urinary levels of seven phthalate metabolites in the U. Rossbach B. et al.68:309-314. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Wiesmuller GA. Sanchez GN. Levels of seven urinary phthalate metabolites in a human reference population.16(4):487-493. Reproducibility of urinary phthalate metabolites in first morning urine samples.

7 (17.6) 12. they have been referred to as monobutyl phthalate (MBP).0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.0-25.30-2.56 (5.1 (13.4-27. 2003).6) 26. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.0-14.56) 3.3.6-26.9 (16.63) 3.40 (2.3-30.9-23.10) 11. OSHA has established a workplace air standard for external exposure to DBP.2 (11.10-9.9) 10.0 (19.8 (9.0-38.1 (8.20-9.10) 2.40 (6.10) 3.30-13. Koch et al.24-8.2-22.7) 4.33 (2.48 (2. When total DBP metabolites have been measured.3 (18. population from the National Health and Nutrition Examination Survey.40 (3.20-12.6) 17.7-18.82-3.6) 16. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates. interval) 2.00 (5.00-6.7-31.11-3.2 (12..30-3. in a small sample of pregnant women in New York City (Adibi et al.6) 17.73 (2.17 (2.5) 18.5-16.0) 9.50-6.40-17.30-7.40-3.55) 2.4 (20.97) 2.22) 3.26 (2.20 (3.30-6.80) 75th 5.6-20.10-9.9 (16.10 (4.5) 19.46 (2. and also in some printing inks.81 (3.02) 4.67 (5.84) 4. 2005). see Data Analysis section) for Survey years 01-02 and 03-04 are 1.3-48.3 (16.30-6. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.6 (13. and insecticides.6 (14.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.60 (5.70 (5.90) 12.5-16.0) 20.00) 7.60) 3.5) 23.80 (5. 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.72-3. residents (Blount et al.8) 21.40-9. 84-74-2 Di-isobutyl Phthalate CAS No.30-11. mostly as MnBP (Anderson et al.3 (19. Studies of children found age-related differences in urine MBP levels.00) 6.30) 10.30) 2.3-43.00-9.60 (4..2-14.20 (7.60 (2.5) 18.46 (3.70-4.S.5-24.1-20.00-6.5 (11.30) 6.5 (20.50 (6.0-18.2-33.70) 5.1-17.80 (2.7 (9. 2007).90-7.10 (3.50-4. and in a small sample of Japanese adults (Itoh et al. 2005.1-12.6) 16.0 (13.7 (16.20 (6. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.00) 10.5) 25.5 (27.0) 12..0 and 0.4-12.91) 4.44-2.6 (13.70) 3.20-6.7 (7.6 (10.6 (14. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.Phthalates Di-n-butyl Phthalate CAS No. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.6-34.97-7.5 (17.46-5.30) 5.40-4.10) 9.3-18.73-5.66) 2.43) 6.7-31.80-5.00) 4.0 (11.50) 2.5-29.40) 5.50-2.5 (10.1) 22.90 (3.50) 18. In addition.6 (11.96) 3.00-4.90 (6.17) 4..70-8. Biomonitoring Information Median concentrations reported in the NHANES 19992000.9) 15.00-11.30 (1.70 (2.4 (14.3 (11.2 (8.50) 8.40 (7.3-24.10) 8.3 (16.90-4.6-14. Following oral administration of DBP to humans.6 (9.80-5.7) 15.1) 25. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.30) 10.4) 22.7 (18.07 (3. in men attending a Boston infertility clinic (Duty et al.7) 14.40-3.6) 10..90-4.6 (10.50-10.7 (17. 2004.40 (2.50 (3.49-2.4) 5. NTP-CERHR.22 (3.20) 4.3) 3.30 (3.20) 7.00) 4.6-18.80 (5.59) 3.97) 4.0 (13.0) 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. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.60 (8.80 (2.50) 90th 12.40-12.3 (13.71 (2.40-4.50) 7.3-19. 2000.3) 18.7-20.10 (4. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.80 (3.19-3.37) 6.3-20.70-4.90 (4.56-4.1-25.7) 7.3) 33.55 (3..6 (29. pharmaceutical coatings. CDC.4) 12.50) 5.28-5.8) 677 652 703 699 1216 1088 Limit of detection (LOD.60-6.5) 14.3 (13.7) 18. Fourth National Report on Human Exposure to Environmental Chemicals 265 . 2003). 2000). 2001).10-2.30 (4. Survey Geometric mean (95% conf. 2005).20-2.40-5. 2005).. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.1) 16.2) 5..5) 12. about 65% to 80% of a dose is eliminated in urine within 24 hours.90 (4. Hauser et al.8) 40.85-6.68 (2.46) 2.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.0) 13.90-2..20-12.S.0) 24.9-14.00 (7.5) 22. DBP can produce reproductive toxicity in male rodents (McKee et al. 2004.56 (3.

65 (4.32 (3.6 (15.and gender.26-2.14 (4.19 (2. 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.76-3.20-3. while MnBP declined (Wittassek et al.9-26.62-12.1-24.15) 3.6 (12.57-4.44 (3.18-10.1-12. Survey Geometric mean (95% conf.6 (10. 2007).8-13.7 (11.1) 4.52-20.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.0 (12.31 (2.0) 11.0) 15.34 (3.9 (9. An analysis of NHANES 2001-2002 showed similar age.2) 24.3) 16.81) 4.2-13.74-3.22 (2.08) 75th 4.95) 2.29-3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.0) 7.69 (2.64-10.25) 5. 2004).75 (6.6-19.56-4.92 (7.3) 13.17 (2.17-12.47-5.0 (10. 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.84 (8.54) 2.1) 15.36-7. 2005).1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals . Weuve et al.18 (4. 2002.11 (5.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.2-15.4-16.46) 3. to about two to fourfold higher (Fromme et al.8-18. interval) 2.8-18.86-4.30) 2.7) 11.1-15.29-8.5 (9.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.2) 9.66) 10.31 (7.1) 7.86) 6.21 (5.82 (4.0-18.02-10.81 (6.98 (2.85 (2.3 (13.81) 9.79-6.66) 4.00-7.20-4.20 (2.76-3. ranging from more than one-tenth the NHANES median (Itoh et al.36-2.04) 7. Over this time. 2006).69-7. 2007).51) 5.96 (3.88 (2.67-5.08-2.03-11.7) 10.95) 10. 2004).33-9.04) 3.56) 2.4) 15.8 (10.5-19.89 (3..00-3.83 (2.28-13.43) 3. Between 1998 and 2003.37) 3.5) 13.3 (17.80) 7.13 (2.28 (4.52) 3.04-5.94) 6.13-6.64-7.03-7.58-4.6) 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 2.81 (3.54 (2.7 (13.2 (10.64-7.97-2. the students’ median values for MiBP levels remained relatively unchanged.6-19.27-12.26 (2.10-5.38-10.30 (6.79-8.18) 3.18 (1.4) 7.55-6.53-5.9 (11. Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 (11.35) 3.69) 6. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.52-3.62 (6.20-2.09-2.74 (4.8 (8.6 (8.9-40.31) 2.58-3.54 (4..00 (3..84 (4.0 (8. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples. than adults in NHANES subsamples during the same time period.53-4.1 (10.51) 2.39-3. respectively.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.69) 4. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.51) 15.7) 19. In an analysis of NHANES 1999-2000.72) 5.68) 5.99-4.07 (2.2) 8.57 (3.53-3.31) 2.65-4.1) 13.0) 3.3) 13.52 (2.66) 2.66 (8.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.33 (2.01-2. 2005).4 (12.33 (3.33) 3.9 (15.57 (3.20 (2.3) 28. 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.32 (7.9-16.1) 10.68 (2.65-11..76-15.5 (11.17) 90th 8.07-5.94-12. samples from German university students had consistently higher median urine levels of MnBP and MiBP.1-25.79 (4.46-11.43) 3..32) 7.56) 5.78-8. population from the National Health and Nutrition Examination Survey.20 (7.7-28.76 (3.93-6.78) 9.95-3.75 (4.89) 6.18) 4.61-3.82) 4.73 (5.6) 13.11-2.99) 7.5) 15.59 (4.41 (2.02 (7.47 (3.2 (11. up to four and 13 fold.7 (21..7) 3.1) 11.05) 2.21) 10.00-3.11) 5.56-15.47-12.4) 23.6) 11.89-5.39) 5.18-4.8) 10.6 (9.8-36.3) 18.78) 8.68) 3.8 (9.03 (5.6 (8.S.43) 3.38 (6.91-6..42) 2.80 (3.46 (2.80-3.94 (5.45) 3.7 (9.24) 3.72-7.15-4.9) 12.

4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.1) 20.0) 27. interval) 24.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.6-48.1) 30.4-26.4.2 (21.2-24.4) 20.1-92.7-92.2-63.3-24.6-69.6-29.3-145) 85.0-24.7-53.7 (64.7 (18.4 (72.6) 20.2) 68. Survey Geometric mean (95% conf.4 (71.2 (78.5-27.6-33.2-93.1) 46.8) 43.1 (17. *In the 1999-2000 survey period.5) 40.0-21.1-80. 01-02.1) 25.6 (65.8-29.2) 90th 98.7 (16.3 (30.7 (22.8-123) 101 (90.4-25.6) 38.8-22.1 (54. see Data Analysis section) for survey years 99-00.3 (30.4-31.4) 52.2-21.1) 23.0) 31.9 (17.5 (30.8) 19.2) 20. and 0.9-92.0 (30.7 (70.S.8) 48.4 (35.3) 24.1 (19.0) 117 (104-131) 112 (84.9 (79.1-20.5-43.1) 47.1) 31.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.5) 47.0) 120 (98.9) 26.6) 80.2) 32.5) 36.4 (25.6-20.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.9-114) 116 (97.5-42.0 (23.1 (16.6 (61.7 (33.0 (72.9 (79.0 (15.7 (24.7-42.2 (25.6 (90.8) 62.2-56.7 (19.1 (36.4 (35.5) 24.6 (16. and 03-04 are 0.5) 95.9) 46.6-29.6-31.0 (36.4-20.2-159) 92.5) 34.2-114) 73.0) 20.6 (26.4-60.3-60. referred to as monobutyl phthalate (MBP).6 (44.7) 52.1) 36.9-101) 77.1) 23.7-127) 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 22.1 (19.5) 31.1-27.9.2 (59.7-121) 97.3) 19.1 (58.3 (56.5-47.7-26.8-42.0 (45.0 (31.3-79.1 (18.9-28.3 (60.8) 23. 1.2 (74.4 (23.0 (78.1 (28.2 (79.4) 22.3 (17.6 (22.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.0 (18.7 (43.4-44.9-22.0 (20.6-143) 127 (99.5) 85. population from the National Health and Nutrition Examination Survey.7-91.7 (28.5) 36.0) 38.7-111) 64.0) 30.8-132) 95.9 (20.7-34.0-19.0-73.1-22.5-47.5) 21.4 (21.3) 36.7-20.1-29.6) 71.7) 74.3 (42.1 (21.3) 40.5) 26.6-36.4 (36.0) 21. respectively.6-24.6 (55.1 (19.2-87.3 (51.9 (17.1-51.5-53.9) 36.3 (23.6) 17.7) 124 (98.2 (19. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.2) 26.5 (74.9-42.1 (41.9) 29.2) 38.7-124) 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.3) 26.7-34.1-24.3 (37.9-33.6-40.4 (35.0-51.9) 75.6-113) 108 (90.7-42.4 (19.4 (38.6-49.5) 20.5) 17.8 (19.1 (51.3) 18.6) 21.4-18.5-44.0) 84.7 (38.2 (21.5) 65.5) 19.2 (58.3-96.5 (28.7) 28.0-24.5 (29.9-87.0 (17.3) 21.1) 17.0-32.7) 42.6 (48.9-53.7-116) 95.8-25. Fourth National Report on Human Exposure to Environmental Chemicals 267 .5 (59.7-24.5-60.4) 64.8 (57.2) 42.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 (17.0-26.1 (26.2) 62.2-33.1) 19.2 (18.7 (18.6) 46.3-85.3-40.6) 39.4-42.1 (19.4) 59.8-119) 90.3-21.7 (51.9-22.6) 35.7-117) 118 (108-143) 93.6 (32.8) 75th 51.7-106) 69.1 (31.1 (34.6 (19.2 (20.2-22.4-159) 107 (84.8-111) 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 (36.2 (75.0-19.9-79.0 (25.9) 21.5) 78.1.2-49.5) 37.3 (23.3) 23.5-121) 106 (94.4 (35.1 (62.4 (84.5 (59.1-82.3-76.6-37.1-75.9) 18.5-117) 95.2-32.2-23.9) 71.3-67.3-136) 137 (107-162) 119 (90.8) 58.6-44.0-58.7) 92.1) 23.

7) 19.7-51.6-92.4) 19.4 (53.9 (30.2-18.1-21.3-23.1) 20. interval) 22.7) 20.6 (29.7 (19.6 (27.5-142) 89.3-49.0 (70.3-78.8) 17.0 (20.3 (46.0-92.9 (16.4 (33.4-24.3) 33.6) 18.9 (35.1-99.9) 19.5 (15.7-19.0 (71.0 (18.6 (74.2) 31.9 (39.4 (45.2 (19.9-105) 85.9) 24.3) 67.5 (18.5-16.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.6-128) 96.6) 25.8-235) 137 (108-198) 88.3 (16.5 (64.8-24.3) 18.2-86.9) 28.1) 50.9 (30.3) 52.9-26.3 (24.4) 51.8-32.6-16.6-26.3) 21.7 (60.6) 14.1 (61.0) 29.1 (29.4 (31.3-39.9 (64.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9-68.6) 38.2) 65.9-49.8) 34.4) 16.6) 83.7 (27.0 (61.8) 34.5-76.3 (19.7 (28.6-74.3 (42.3) 19.2 (83.2-22.8 (17.6) 39.3) 33.0-47.9 (56.6-155) 91.7-19. 268 Fourth National Report on Human Exposure to Environmental Chemicals .5 (30.7 (54.4-135) 71.9) 14.4) 21.5) 60.7 (57.7 (20.4 (31.3-26.5 (18.6) 31.4 (18.4-72.1 (34.S.4-61.9-34.0-17.3 (28.1) 21.1-62.3 (17.3) 17.0-113) 104 (83.0) 41.9-14.4 (16.6-43.8) 20.6 (31.2-21.4 (17.8 (65.6-23.0-41.8-43.5-23.0) 81.9 (20.6) 65.0) 28.8) 30.5-41.3-18.7 (14.6 (25.6) 64.1 (15. Survey Geometric mean (95% conf.7 (43.0-90.6 (72.8 (25.6-44.3 (55.4 (50.8) 28.5) 90th 68.6) 23.1-128) 97.2) 59.3 (52.0 (26.0) 19.8) 63.4 (47.4) 15.4 (13.9-70.2-16.2-48.3-114) 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 17.6 (57.4-164) 96.2-179) 84.9 (30.1 (56.6-19.5-37.4-65.1-83.9) 62.1 (32.6-32.4) 53.3-38.9 (37.4-131) 81.6-23.4-76.6-44.8) 75th 38.0 (52.7-80.2-106) 64.2) 159 (102-263) 147 (93.4 (68.1) 35.8) 13.9-84.8-24.0 (34.3-71.8 (16.3) 59.2-22.3 (21.0-19.0) 70.0 (19.3 (69.3-21.1-32.0) 94.8) 20.0) 53.0 (15.4) 20.0 (50.3) 20.4 (19.8) 40.0) 55.1) 20.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.2-28.9 (21.5 (81.1) 44.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.7-39.6 (61.5) 39.0) 108 (71.3-32.8 (50.5-15.2 (16.6-53.7 (16.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.3 (17.3 (76.0) 25.6 (25.7 (73.6-24.3-40.2 (35.6) 24.7-78.9) 91.5) 134 (93.4 (16.8) 19.8 (18.1) 37.0) 75.0 (16.8) 23.9 (58.0 (27.3-106) 74. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.9-56.6-119) 63.5-30.4-34.7-28.4 (20.1) 61.9) 30.2) 16.8) 22.0) 59.1) 22.5-22.3 (17.7-21.5) 84.3 (48.7) 42.1) 42.6-27.3) 35.5-142) 81.8 (18.3-17.6) 34.9-36.4 (31.6 (41.2) 74.2-73.6 (19.6 (17.9 (73.2 (38.3 (52.5) 82.8 (13.4-103) 117 (83.9-38.8) 35.7-26.3-81.7-23.5-18.2 (19.6) 37.0-60.1-18.8 (33.9 (19.4) 15.9-68.8) 17.7 (12.9-100) 86.9) 39.1-23.1-99.2-61.0) 26.9) 20.1) 17.7-37.0 (69.4-47.2) 21.9) 52.4 (23.1) 53.4) 62.7 (60.4 (56.7-20. population from the National Health and Nutrition Examination Survey.8 (22.1 (21.8) 17.3 (60.6-22.5-70.3 (71.8-23.7) 36.0 (18.5-64.5) 91.5-21.4 (17.5 (14.3) 19.6) 24.0-38.0-75.2-27.4 (50.7-42.3-21.0 (43.4 (37.3-20.7 (81.6-24.6-28.6-50.5) 21.8 (18.1 (46.6-42.9 (35.9) 49.2-85.0) 35.2-108) 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.5) 17.2-22.

Weuve J. Drexler H.68:309-314. Green RA. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Massey RC. Needham LL. et al. Koch HM. Richthoff J. Boehmer S. McKee RH. Calafat AM. Pirkle JL. Duty S. 2005. Hagmar L. et al. Silva MJ. 2000 [online]. Int J Hyg Environ Health 2005. Environ Health Perspect 2003. Scotter MJ. Atlanta (GA). Rylander L. Hu H. David RM. Silva MJ. Epidemiol 2005. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Barr D. Bolte G. Hodge CC.Phthalates References Adibi JJ. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Caudill SP. NTP-CERHR. Int J Hyg Environ Health 2007. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Castle L. Hum Reprod 2007. Jonsson BAG.208:237-245. Schettler T. Sampson EJ.210:21-33. Brock JW. 112(5):A270]. Brock JW. Research Triangle Park (NC). Anderson WA. Masunaga S. Prenatal exposures to phthalates among women in New York City and Krakow. Environ Health Perspect 2000. Jacek R. Rossbach B. Hilborn ED. Available at URL: http://cerhr. Springall C.22(3):688-695. Fromme H. Poland.nih. Third National Report on Human Exposure to Environmental Chemicals. Angerer J. et al. et al. Wittassek M. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Singh NP. Barr DB. Phthalate monoesters levels in the urine of young children. Itoh H. Sanchez GN. et al. Caudill SP. et al. Drexler H. Environ Health Perspect 2004. Koch HM. Blount BC. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.html. Wiesmuller GA. Angerer J. et al. Food Addit Contam 2001.114(9):1424-1431. Camann DE. Reidy JA. Eckard R.25(2):293-302. Jedrychowski W. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Ryan L.16(4):487-493. Reprod Toxicol 2004. Malek NA. Levels of seven urinary phthalate metabolites in a human reference population.18(1):122. Butala JH. Calafat AM.111(14):1719-1722.niehs. Centers for Disease Control and Prevention (CDC). Environ Health Perspect 2006. Environ Res 2003. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Koch HM.112(3):331-338. Giwercman A. J Androl 2004. et al.210(3-4):319-33.108(10)979-982. Chen Z.gov/chemicals/ phthalates/dbp/dbp-eval. Dobler L. Duty SM. Int J Hyg Environ Health 2007. Hauser R. Urinary levels of seven phthalate metabolites in the U. Needham LL. 4/20/09 Silva MJ. Yoshida K.93:177-185. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Gans G. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Bull Environ Contam Toxicol 2002. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Silva MJ.18(12):10681074. Meeker JD. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Ryan L. Helm D. Caudill SP. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Silva MJ. Perera FP.S.

500) 1.600) .20) .900-1. < LOD means less than the limit of detection. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.400) < LOD < LOD .300 (.400) 1.300-. and 03-04 are 0.70 (1.70 (1.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400-. see Data Analysis section) for Survey years 99-00.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .80) .00-3. population from the National Health and Nutrition Examination Survey. 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. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers. polyvinyl acetate.70) .400 (.500 (.00 (<LOD-1.3. only levels at or above the 90th percentile could be characterized.700) .500) .300 (.200-.400 (<LOD-.400 (.400) 1.600) < LOD .400 (.300) < LOD .500 (.300-.10 (.200-.200-. resins.500 (. and polyvinyl chloride.400 (.200 (<LOD-.300-.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 1.700) .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-.600) .50) .300-.70) .400-.300-.500) .500) .300 (.500 (.500 (.300 (<LOD-.500 (.300 (.400-. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.90) .400 (<LOD-. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.300-. 0. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.300 (.Phthalates Dicyclohexyl Phthalate CAS No. and 0.500) < LOD < LOD . which may vary for some chemicals by year and by individual sample. 270 Fourth National Report on Human Exposure to Environmental Chemicals .400 (. In this Report.9.10) .200-.200-.50) .600 (.500 (.500) < LOD 1.400 (.200-.600) .400 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) < LOD .00 (<LOD-1.700) .500) < LOD < LOD .00 (<LOD-1.500-.500) 1.00-2.500) .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 .600) . Survey Geometric mean (95% conf.300-. including nitrocellulose.400) < LOD 1.500 (.400 (<LOD-.300 (.400-.400-.400-.00) .500 (.600) . and polymers.300-.S. respectively.10 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.2.300 (.400 (.10 (<LOD-1. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.500) 1. 01-02.300-. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10 (<LOD-2.400-.

710) . population from the National Health and Nutrition Examination Survey.660) < LOD < LOD .82) .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.690 (.390 (.510 (.940 (. Survey Geometric mean (95% conf.910 (.470) 3.44) .05) .500) 3.400-.910 (.14 (<LOD-3.06) .800-1.770-1.470 (.510-.54 (<LOD-2.530 (.500-.290-.67 (1.36-1.950 (.590 (.310-.22 (<LOD-1.610 (.480 (.410 (.11) .380-.450 (.34) .690-1. Fourth National Report on Human Exposure to Environmental Chemicals 271 .910 (.240-.910 (.10) .06) .82 (1.670 (<LOD-.170-.00) .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.630 (<LOD-.380 (.620) < LOD .690) < LOD < LOD .54) .12-1.740) .00 (<LOD-3.670-1.740) < LOD < LOD .54-6.500) 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 .880 (.310) < LOD .270) < LOD .33) .490) .530) 1.17) .350-.770 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.220 (<LOD-.420-.53) .830) 1.250 (.74) .420-.420-.770) < LOD 2.S.18) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.33 (<LOD-3.770-1.330 (.560) 1.590) 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 .450 (.690) < LOD 2.16) .630 (<LOD-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .43 (1.370 (<LOD-.660) .590 (<LOD-.400-.330 (.530-1.690) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.360-.530-.770-1.500 (.16 (<LOD-3.53) .260-.790-1.

272 Fourth National Report on Human Exposure to Environmental Chemicals . and 03-04 are 1. 2007). 2002). Biomonitoring Information MEP levels in the NHANES 1999-2000. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. see Data Analysis section) for Survey years 99-00. 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. particularly those containing fragrances. 01-02. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.3 (74. and 0.. 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7) 71.5) 81.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. and hand lotions. 2001-2002. respectively. population from the National Health and Nutrition Examination Survey.3 (82. 0.3-103) 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. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.S. soaps.1 (71. DC (Hoppin et al.7 (70.Phthalates Diethyl Phthalate CAS No.2-102) 95.2..8-111) 85. Products that may contain DEP include perfumes.9 (61.9-92. 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. In contrast. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.4.4 (62.1-93.9.. 2003) and African-American women in Washington. deodorants. shampoos. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. colognes. and also in men attending a Boston infertility clinic (Hauser et al.

. 2003) were slightly lower than levels found in NHANES 2001-2002.3-105) 87. Other population estimates also differed by sex and race ethnicity (Silva et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.S.6 (77.0 (66. Median MEP levels found in a small sample of German residents (Koch et al.9-110) 96.. 2004). with adjusted geometric mean levels of urinary MEP that increased with age (CDC. 2002). 2005).9 (82.0-156) 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 .Phthalates 2002 (Brock et al.5-114) 101 (87.2 (66. Urinary Mono-ethyl phthalate (MEP) (creatinine corrected) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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.5-113) 122 (93.7-110) 81. Analysis of NHANES 2001-2002 showed similar findings. This age-related trend is opposite the direction seen for other phthalates. In an analysis of NHANES 1999-2000. Finding a measurable amount of MEP in urine does not mean that the levels of MEP or the parent compound cause an adverse health effect. population from the National Health and Nutrition Examination Survey. interval) 163 (149-178) Selected percentiles ( 95% confidence interval) 50th 141 (129-157) 148 (133-162) 153 (137-177) 75th 360 (307-422) 388 (330-435) 452 (386-504) 90th 905 (753-1180) 969 (805-1180) 1110 (889-1290) Total 167 (150-185) 181 (163-202) Sample size 1950 (1670-2310) 2536 1840 (1450-2200) 2782 2040 (1640-2540) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 92. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.6 (65..

et al. Silva MJ. Singh NP.110(5):515-518. Ryan L. Urinary levels of seven phthalate metabolites in the U. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). Phthalate monoesters levels in the urine of young children. Hauser R. Angerer J. 2005. Silva MJ. Caudill SP.S. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Baird DD. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Environ Health Perspect 2002.93:177-185. Prenatal exposures to phthalates among women in New York City and Krakow. Duty S. Hodge CC.68:309-314. Malek NA. Bull Environ Contam Toxicol 2002. 112(5):A270]. Brock JW. et al. Reproducibility of urinary phthalate metabolites in first morning urine samples. Hilborn ED.22(3):688-695. et al. Centers for Disease Control and Prevention (CDC). population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Drexler H. Environ Health Perspect 2004. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Barr D. Camann DE. Needham LL. Meeker JD. Barr DB.112(3):331-338. Davis BJ. Brock JW.111(14):1719-1722. Poland. Silva MJ. Hoppin JA. Jacek R. Caudill SP.Phthalates References Adibi JJ. Reidy JA. Rossbach B. Jedrychowski W. Environ Res 2003. Koch HM. Hum Reprod 2007. Environ Health Perspect 2003. Perera FP.

5-40.10-2.87-2.70 (1.7) 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 3.85) 4.4-53.0 (18.6) 5.9) 13.40) 1.20 (3.30) 2.70-8.61 (3.1 (8.50 (3. 1.6-25.77 (2.0 (16.40) 4.7) 22.0 (9.50-6. 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.1) 29.3) 52.9 (29.70-2.40) 11.6) 15.10) 4.4 (21. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).4-20.80 (8.2 (31.2 (10.96) 4.8) 15.6-38.6 (20.9 (29.5) 37.5 (18.4) 6.10-11.42-5.10-4.1 (11.6 (11.70 (3.80 (8.80 (2..50-3.9 (17.4 (16.30 (4. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP). respectively. see Data Analysis section) for Survey years 99-00.2) 4.84 (2.4 (13.31 (3.86) 2.6) 14. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.9-57.0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.10-5. packaging film.4-20.7) 18.70 (7.70-4.10 (4.44) 4.00) 2.03-2.5) 23.90-5.41 (3.57-7.4-27.82 (3.00) 1. Fourth National Report on Human Exposure to Environmental Chemicals 275 .40) 2.8-36.92-2.3-26.98) 2.30 (3.2) 23.50-8.10) 2.50-2.34 (2.2) 42. 01-02.0 (21.10 (6. DEHP has been removed from or replaced in most toys and food packaging in the United States.9.70 (8.6 (10. 1982.43 (3.70-3. and in humans.85 (3.9-29.3 (24.1-17.4) 7.7) 37.5 (31.90) 4.70-5.6-60.90) 4.50-14.6) 95th 23.68 (3.7) 8. Peck and Albro.90-8.0) 23.92) 4.4-40.93) 6.3 (15.50-3.27) 2.70-6.1 (10.60-7.07-4.6-23.80) 6.6) 39. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.2) 29.90 (4.60 (6.37-4.10) 8.40-11.54) 4.31-4.5 (11.4) 13.30-8.9 (15.70 (1.5) 31.50 (2.90-11.4) 15.27 (3.9-55.2) 6.9) 27.84-4.14 (1.1) 25.60) 10.7) 19.51) 4.92-2.5) 19.80) 9.9-19.15 (1.69) Selected percentiles ( 95% confidence interval) 50th 3.50) 4. population from the National Health and Nutrition Examination Survey.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 5.7) 6.9 (16.90) 4.9) 5.00) 11.90) 3.60 (5.0) 23.2-35.00 (7.40-8.50 (7.0 (19.25-3.23 (2.10 (3.21 (2.0) 31.00) 1.2-28.9 (26.90-3.4) 33.50-5.21 (2.57 (3.9 (7.5) 32.20 (3.7) 27.0