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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4'-Tetrabromodiphenyl ether (BDE 66) 2.5'-Tetrachlorobiphenyl (PCB 44) 2.2’.6'-Hexabromodiphenyl ether (BDE 154) 2.1-Trichloroethane (Methyl chloroform) 1.2'.What’s New in this Report What’s New in this Report In this Fourth Report.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 (2.1. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.4.4'.1.2'.1-Dichloroethane 1.3’. Table 1.2'.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .4'-Tribromodiphenyl ether (BDE 28) 2.2.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.2'.4’.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.2-Dichloroethene trans-1. Paradichlorobenzene) 1.4-Tribromodiphenyl ether (BDE 17) 2.3.5'-Hexabromodiphenyl ether (BDE 153) 2. The process for selection is described at http://www.3.5.4'.4'-Pentabromodiphenyl ether (BDE 85) 2.html.gov/exposurereport/chemical_selection.2-Dichloroethene Dichloromethane (Methylene chloride) 1.2'.5.3-Dichlorobenzene (m-Dichlorobenzene) 1.4.2'.2'3.3.4'.4.4'.2'4.2-Trichloroethane Trichloroethene (Trichloroethylene) m.4.4'.1.5-Pentabromodiphenyl ether (BDE 99) 2. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4.4.6.6-Pentabromodiphenyl ether (BDE 100) 2.4.1-Dichloroethene (Vinylidene chloride) cis-1.3'.5'.2-Dichlorobenzene (o-Dichlorobenzene) 1.4-Dichlorobenzene (p-Dichlorobenzene.4.3-Tetramethylbutyl] phenol) Triclosan (2.cdc.5'-Tetrachlorobiphenyl (PCB 49) 2.2-Dichloroethane (Ethylene dichloride) 1.2'.5.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.3.2'.4.4.4.4’.5.2-Dichloropropane 2.6-Heptabromodiphenyl ether (BDE 183) 2.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.4'-Tetrabromodiphenyl ether (BDE 47) 2.2'. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.5’.

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

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

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

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

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

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

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

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

2) 57. EPA.5) 58. are heated at temperatures used for frying and baking.1 (52.6-61.6 (51.9) 58. Since acrylamide has limited volatility and high water solubility. In humans.6 (56. People may be exposed to acrylamide from foods.7-64.S. 2006. Elimination occurs mainly in the urine as mercapturic acid conjugates. in some sealing grouts. 217 million pounds of acrylamide were produced commercially in the U.9 (60.0) 57. population from the National Health and Nutrition Examination Survey.1) 46.4-83. and is either metabolized to the reactive epoxide.6) 71.0 (69.5 (74.4-76.1-64.7 (65. 2006). widely distributed in tissues. Animal studies indicate that acrylamide is well absorbed. EPA.5-80. and in some cosmetics. the main source of exposure is from the diet. 2005).9-52.2-59. Tareke et al. and binding agents. Acrylamide is not thought to accumulate in the body at environmental doses.1) 53.2-118) 98. and from dermal contact with products that contain residual acrylamide.3-2. or to glutathione conjugates (Calleman et al. 1990.4-89.6-108) 61.3) 63.S.7) 54. mineral processing.4) 100 (89. and an average daily intake is estimated as 0..S.2-70.9) 63. Fennell et al.0 (53.5) 66. but can covalently bind to form adducts with proteins.4 (51. in permanent press fabrics.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. FDA. interval) 61. FAO/WHO.1-64.5 (44.1 (83.7) 58.0) 85. but are generally above the U.2-93.3 (53.9 (69. In the general population. Estimated intakes in children are about twice that of adults (DiNovi and Howard.2-77.S.7) 75th 79. and well below doses known to cause nerve damage or carcinogenicity in animals.8-57. gels.0-58. acrylamide is synthesized and used in the production of polyacrylamide polymer.6-65.4) 57. 2004).6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.1-57.4 (54.4-60. In 1997. pulp and paper production.2 μg/kg/day (U.8-55.1 (47.. 2002).4 (59. soil conditioners.0-49. 2005). acrylamide has produced upper airway irritation following inhalation of high levels.7) 73.7 (63. smoking.7-64. 2004. 2005).3) 86. and cosmetics (NTP-CERHR.2-67. ocular and dermal irritation from direct contact with acrylamide containing materials.8 (91..1-61.1 (88. 2005). Natural substances in the food are converted to acrylamide.7) 96.0-108) 152 (139-175) 126 (111-142) 108 (86. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U. Foods such as french fries and potato chips can contain acrylamide at levels up to 100 times greater than levels found in cooked fish or poultry (DiNovi and Howard.6-104) 82. glycidamide.9 (54.6) 73. as an absorbent in disposable diapers.2 (62. These estimated intakes are hundreds of times lower than occupational exposures.3 (55.1) 55. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.0 μg/kg for adults (FAO/ WHO.2) 57. Fourth National Report on Human Exposure to Environmental Chemicals 11 .6) 50.1) 62.4) 57.Acrylamide Acrylamide CAS No.5 (52.4) Selected percentiles ( 95% confidence interval) Sample 95th 192 (168-217) size 7101 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 54. 1994). although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. EPA reference dose of 0.8 (81.6-75. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. Survey Geometric mean (95% conf. Polyacrylamides are useful water-compatible polymers used in water treatment.1 (73.2 (58.2-114) 163 (147-191) 96.5 (79.0-66. and in the synthesis or compounding of dye materials. 2005).9-61.3-71.7 (58.1) 101 (95. such as potatoes and some grains.4 (53.8 (52.9) 75.6 (81.7-60. it was discovered that acrylamide is formed when starch-rich foods.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 61.0.5-85.8 (57.0 (57.4-60.7 (55.2-91.9-105) 86.4 (54.3) 70.S.6) 90. 2005.2 (75.9) 57. see Data Analysis section) for Survey year 03-04 is 3. drinking water.0 (67. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. (NTP-CERHR. Commercially. Recently.6-66.

4-98. interval) 59.. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.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.0 (75.6-64.1-56. 2001).5 (59. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. altered gene expression in testicular tissues (Yang et al. and neuronal DNA reactivity (Doerge et al.4 (51.9 (81.3 (56. male germinal cell injury. In addition.2) 65. 2002.8) 60. thyroid.9) 87. 2005.9-76.5 (56. 12 Fourth National Report on Human Exposure to Environmental Chemicals .9) 59... IARC classifies acrylamide as probably carcinogenic to humans.1 (70..6 (66.5) 75th 85. 2006).2 (72. 2005). The degree of formation of the more toxic glycidamide and levels of GHA can be influenced by polymorphisms in several of the enzymes that metabolize acrylamide (Duale et al.1 (66.S. 2004. 2005)..1) 60.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.0 (70. population from the National Health and Nutrition Examination Survey. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.9-62. 1997. Rice. probably through its epoxide metabolite.7-86. 2005.0. EPA at: http://www.9 (58.5) 71.3) 59. 2005) have been demonstrated in animals.. 1997.2 (56.7-62.4 (81.9-77. Maniere et al. respectively) are markers of integrated acrylamide exposure over the preceding few months.4 (56.. reproductive effects (reduced litter size.2) 55.8-61.. Schettgen et al. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. most non-smokers had levels less than about 100 pmol/gram hemoglobin. fetal death. Puppel et al. Hagmar et al. 2006.5-92.4 (61. After exposure ceases..8-49.0 (52. Mucci et al.0-62.9-64.S.8 (44.4-103) 79.4) 83. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.7-64.7) 90.. 2005. EPA.1 (82. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.S.1 (56.1-70.5-94. 2003. dominant lethality). Survey Geometric mean (95% conf. Vesper et al. 2005. 2005. 2005.8 (51.Acrylamide occupational exposures.int/ ipcs/food/jecfa/summaries/summary_report_64_final.. scrotal. Vesper 2005) and smoking (Bergmark.0) 118 (103-126) 121 (112-134) 113 (94. Glycidamide has been shown to react with DNA (Doerge et al.6 (90.7 (84. U.4) 46.9-78. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).2-68. 2006). Schettgen et al.2) 87.. 2005.3-78.7 (87.5-66.2 (63.7 (57. 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.5) 87.1) 62.9 (57. 2004).0-93.who.9) 75. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.. 2005. 2008). presynaptic nerve terminal binding (LoPachin.5 (42. Klaunig et al.4-65.3) 85. and cancer (mammary..7) 74.1) 56. Acrylamide is clastogenic and can produce dominant lethal mutations. see Data Analysis section) for Survey year 03-04 is 4.6-90. 2009)..3-101) 95. 2005).. adrenal.7 (61..0) 94. U. although different analytic methods can affect results..epa.1-62. AHA levels have been shown to increase with dietary intake (Hagmar et al. 2006) have been demonstrated after acrylamide dosing. 2005. glycidamide (NTP-CERHR. 2005.9) 65.1) 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. Additional information is available from U.S.3) 59. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. uterine.0 (80. 2008).4) 53. 2005). NTP-CERHR.7) 60.4-59.5 (83. 2005.4 (57. 2005) and sperm DNA adducts (Xie et al.1 (57.pdf.8) 45. Axonal degeneration. and other sites) (FAO/WHO.3) 59.5-64. Puppel et al.2-90.2-91. 2002..6-62.9-138) 143 (130-159) 96..1-60. EPA.4 (90.0-103) 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 64.7) 61. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.8-48.

Bjellaas T.niehs. Doerge DR. Bridson WE. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Hagmar L.. 2/3/09 Klaunig JE. Summer SCJ. Andersen M. February. Wilson KM.580(1-2):131-141. 2009 Jan 8. Nordander C. Hagmar et al. CFSAN/Office of Plant and Dairy Foods. 6013-6019.gov/chemicals/ acrylamide/Acrylamide_Monograph. April 13-15. Aprea P. Available at URL: http://cerhr.pdf. 64th Meeting: Summary and Conclusions (FAO/WHO). Guffroy M. Tian G. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. He F. Joint FAO/WHO Expert Committee on Food Additives. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. et al. Chicago. Mutat Res 2005.Toxicol Appl Pharmacol 1994.10(1):78-84. Churchwell MI. Survey data on acrylamide in food: individual food products. Godard T.43:365–410. Costa LG. 1993. Toxicol Appl Pharmacol 1993. National Toxicology Program.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Toxicol 2005.561:21-37. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation.580(1-2):119-129. Rosen I. et al. Paulsson B. Illinois. 2005. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Calleman CJ. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Perez et al. Tornqvist M. Food and Drug Administration (FDA). Calleman CJ. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Bruze M. 1994).pdf. He F. Kautiainen A.html#u1004. Chem Res Toxicol 1990. Metabolism and hemoglobin adduct formation of acrylamide in humans. Snyder RW.580(1-2):157-165. Axmon A. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide.27(4):219-226.3:406-412. Scand J Work Environ Health 2001. Twaddle NC. The Updated Exposure Assessment for Acrylamide. Zhang S. J Agric Food Chem 2008. Human exposure and internal dose assessments of acrylamide in food.fda. Alexander J.. Available at URL: http://www. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Magnusson AL. 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. and Research Strategies. smoking habits and gender. Wu Y. Paulsen JE. gov/~dms/acrydata. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Mutat Res 2005. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Available at URL: http://www. Kamendulis LM. Mechanisms of acrylamide induced rodent carcinogenesis.nih. Acrylamide neurotoxicity: neurological. Malmberg B. Calleman CJ. 054472. Spicer R. Granath F. Adv Exp Med Biol 2005. Bergmark E. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats.56. Cheong HK. July. Duale N. Italy.85:447-459. Beland FA. 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. Costa LG. Bergmark E. morphological and molecular endpoints in animal models. Maniere I. et al. 2001).. 2001. McDaniel LP. Rome. Tornqvist M. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. 2006.Acrylamide In occupational settings. References Bergmark E.cfsan. 2/3/09 Perez HL. Farmer PB. Toxicol Sci. Osterman-Golkar S. Bergmark E. Doerge DR. Acrylamide intake through diet and human cancer risk. Chem Res Toxicol 1997 Jan. 2004. Yang JS. 1999). da Costa GG. smokers and nonsmokers. Haugen M. 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. NIH Publication No.who. Churchwell MI. LoPachin RM.120(1):45-54. Mutat Res 2005. 2/3/09 Hagmar L. et al. Food Chem. et al. [Epub ahead of print] Dybing E. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. 8-17 February 2005.. Adv Exp Med Biol 2005. Fennell TR. DiNovi M and Howard D.. Mucci LA.561:49-62. Fennell TR. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Laurentie M. In another study. Burgess J. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Uncertainties. Wirfalt E. Becher G. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Toxicol Sci 2005.126(2):361-371.

Drexler H.epa. Toxicol Lett 2002. Hallmans G. Eriksson S. Drexler H.S. Fueller F. Rossbach B.19(4):527-34. Office of Pollution Prevention and Toxics. Kutting B.Acrylamide glycidamide by gas chromatography-mass spectrometry. Fu D. EPA). Benetou V. Meyers T.gov/chemfact/s_acryla. Smith A.20(6):959-64. Integrated Risk Information System (IRIS).580(1-2):3-20. Reprod Toxicol 2005.S. Jin Y. Weiss T.580(1-2):71-80. Rapid Commun Mass Spectrom 2006. Anal Biochem 1999. Vesper HW. Lee MH. U. a carcinogen formed in heated foodstuffs. Yang HJ.htm. et al. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Washington (DC). J Agric Food Chem 2008. Angerer J. Slimani N. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Tornqvist M. Tjønneland A. Ospina M.epa.56(15):6046-53. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Han CH. Mutat Res 2005 Feb 7. Schettgen T. et al. Liu Y. Mutat Res 2005. Choi JH. Tjaden Z. Meyers T. Drexler H. J Agric Food Chem 2002. Schettgen T. Hemoglobin adducts of ethylene oxide. Agudo A. Angerer J. Rice JM. 2/3/09. Sun H. The carcinogenicity of acrylamide. Xie Q. Toxicological effects of acrylamide on rat testicular gene expression profile.txt. Angerer J. Rydberg P. Han DU. Gray JG. Chemical Summary for Acrylamide. 1994. Adv Exp Med Biol 2005. Karlsson P. Liu K. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Analysis of acrylamide.206(1):9-14. Myers GL. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Broding HC. Marko D. Toxicol Lett 2006.207(6):531-9.561:89-96. Chae C. Environmental Protection Agency (U. propylene oxide.50(17):4998-5006. September. Ingham L. Available at URL: http://www. Ding X. EPA). Vesper HW.S.274(1):59-68.134(1-3):65-70. Available at URL: http://www. Puppel N. 14 Fourth National Report on Human Exposure to Environmental Chemicals .163(2):101-8. Tareke E. Ospina M. Letzel S. Schettgen T.gov/iris/subst/0286. Environmental Protection Agency (U. Licea-Perez H. Int J Hyg Environ Health 2004.S. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. U. revised 1/3/06. Acrylamide. Lee SH. 2/3/09 Vesper HW. Int J Hyg Environ Health 2003.

068) .44 (2.370-.470-.09-3.42-4.052 (<LOD-.400-.63-2.770) . and 0.77 (1.580-1.050-.057-.167 (.800 (.48-3.690 (.308 (.213) .050) .066) .111-.302) .059-.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.30) * .28) .310) 90th 1.087-.160) .89) 1.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .063) .124 (.66-3.040 (.071 (.180) .21 (.061) < LOD .12 (1.164 (.052 (<LOD-.130 (.043-.95) 1.080-.350-. stroke.230 (.140-.240 (.20 (1.075 (.62 (2.625) .990 (.540-.190-.060 (.16) .144 (.500 (.840) 3. ear problems.450-.310-1.154-.23 (1. 486-56-6 Metabolite of nicotine (a component of tobacco smoke) General Information Tobacco use is the most important preventable cause of premature morbidity and mortality in the United States.015 ng/mL.110 (.730 (.160 (.620 (.059-.920 (.15) 2.077) .43 (1.96 (1.120 (.910-1.260) 1.30) 2.30) 2.02) 1.234) .070) .050-. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.145) .990) .83-2.600-1.12-4.120 (.00) .180) .12 (2.094) . 2004).44) 2.110) .68) 2.201) .01) 3.23 (.050 (<LOD-.188) .130) .93) .180) .18-3.087) < LOD < LOD .080) < LOD .110) .580 (.20 (. acute respiratory infections.020-.05 ng/mL.570 (.950-1.110 (.050 (<LOD-.312) .50) 3.070) .153-.120-.05) 1.148-.040 (.630 (.19) 1.17 (.089) Age group 3-11 years 99-00 01-02** 03-04 .740-1.14) . which may vary for some chemicals by year and by individual sample.710 (.054 (.99) 2.49) 1.510 (.670) .94) 1.14) .950 (.770) .99) 2.17 (1. see Data Analysis section) for Survey years 99-00.210 (.310-1.84-3.160 (.19-2.220-.88 (1.070) 75th . 83% of measurements had an LOD of 0. Survey Geometric mean (95% conf.040 (.20) 1.38-2.09-2.160) .01 (1.120-.506 (.090-.726) .073) < LOD .175 (.220) .030-.058 (.77 (2.65 (1.068) .85 (1.164 (.071) .066-.480-1.17) .49) 1.216 (.580) .850 (.533-.080-.540 (.131 (.62) 2.120) .997-3.110-.21-1.63 (2.280 (.047-.050) .160-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.57) 2.060 (.32-2.53-4.28-1.00) 1.55 (1.23 (2.060-.39 (1.630 (.077) .Cotinine Cotinine CAS No.34 (1.19) .104-..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 . and 03-04 are 0.180) .137 (.09-3.505 (.68 (1. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.68) .050 (. 2006). The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.76 (1.02) 1.140-.96-4.820) .160 (.066 (.320) .190-.79) 3. acute respiratory illness.180 (. respectively.110-.40) .660) .04 (1.198) * . 2004).50 (1.570-1.15 (2.54 (1.110-.350-.088-.110 (.621-1.120 (.142-.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .115-. emphysema.900-1.070 (<LOD-.11) . Fourth National Report on Human Exposure to Environmental Chemicals 15 . Cigarettes contain about 1.108) * .180 (.090-.230) .040-. DHHS. and various other disorders (U.047-.77 (1.410) .740-1.32-2.187) .S.20) .090-.030-.05.076-.930 (.53 (1. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.053 (<LOD-.630 (.50-4. and exacerbated asthma (U.060-.137-.70-2.360) .81-2.S.22) 2.66) 1.70) 2.75) 1.42 (1.02 (.080-.126) .015.S.96) 2.087 (.080-.47-3.060-.140 (.190-.163 (.860 (. cardiovascular disease.106-.54) 1.120 (.070-.200) 1.080 (.100-.20-2. 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.26-1.139) * .520 (.062 (.50-1.030-.480-.45) 1.78) 2.23-2.14-1.54 (1.32) 1.193) .430-1. 1998). and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.140 (.180) .310) .428-.060) .163) .790) .44) 2.030 (.620-1. DHHS.960-1.084) .770-1.55-2.197) .120 (.080) < LOD < LOD . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.88 (.260-1.60-2.220) . and 17% had an LOD of 0. ** In the 2001-2002 survey period.040-.39) 3. maternal exposure during pregnancy can result in lower birth weight.086 (.35 (2.050 (<LOD-.060 (<LOD-.21-1.080 (. Children exposed to ETS are at increased risk for sudden infant death syndrome.87-3.92 (1.060 (<LOD-.300) .33-2.050 (<LOD-.150) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.48-2.12) 1.110 (.44 (1.150) .110 (.66 (1.350 (.5% nicotine by weight (Kozlowski et al.

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

Racial/ethnic differences in serum cotinine levels among adult U.S. Mowery PD. Exposure of the U. Turner DM.57(1):79115. Caraballo R.280:152-156. et al. JAMA 1998. Bernert JT. June. and the United States. Vol 83. Caudill SP. Available at URL: http://monographs. References Armitage AK. Department of Heath and Human Services. Nicotine metabolism and intake in black and white smokers. Schwartz SS. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency.63:139-43. Pollack HA.4:313-316. National Institute for Occupational Safety and Hygiene (NIOSH). Jacob III P. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace.280:135-140.pdf.iarc. Absorption and metabolism of nicotine from cigarettes. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Schober SE.275:1233-1240. Tob Control 2006.291(3):1196-1203. 1999.S. Maurer KR.nih.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Trends in the exposure of nonsmokers in the U. Jacob P. Centers for Disease Control and Prevention.gov/ntp/roc/eleventh/profiles/ s176toba. Ethnic differences in N-glucuronidation of nicotine and cotinine.7:369-375. JAMA 1998. Etzel RA.56:483-493.94(2):314-320. iarc. Sosnoff CS. Filter ventilation and nicotine content of tobacco in cigarettes from Canada.S. Office on Smoking and Health [online] 2006. Sweeney CT. Richter PA.gov/eid/rmca/critdocs/ criteriadoc/33. U. U. 1988-1991. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects.php. Department of Heath and Human Services.18:188-204. Tobacco Smoke. Flegal KM. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Kozlowski LT.pdf. Available at URL: http://ntp. 4/13/09 International Agency for Research on Cancer. JAMA 1996. Houseman TH. Tob Control 1998. 2004. et al.fr/ENG/Monographs/allmonos90. Brody DJ.S. Modin G.niehs.S. Perez-Stable EJ. cigarette smokers: the Third National Health and Nutrition Examination Survey. National Toxicology Program (NTP). Soliman S. Fong I. George CF. 1991. Kira S.S Department of Health and Human Services (U. Warner K. Metabolism and disposition kinetics of nicotine.cdc.cancer. 4/13/09 Centers for Disease Control and Prevention (CDC). Available at URL: http:// cancercontrol. Pirkle JL. Benowitz NL. Dollery CT. Summary of Data Reported and Evaluation [online] 2004. 11th ed. available at URL: http://mtn. In Report on Carcinogens. Jarvis MJ. DHHS).114(6):853-858. Pickett MA. Tobacco Smoke and Involuntary Smoking.php. Cotinine as a biomarker of environmental tobacco smoke exposure. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Giovino GA. Benowitz NL.surgeongeneral.S Department of Health and Human Services (U. Clin Pharmacol Ther 1994. 4/13/09 Perez-Stable EJ. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Summary of Data Reported and Evaluation [online] 1986.S. Herrera B. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. 4/13/09 National Cancer Institute (NCI). Epidemiol Rev 1996. Aiba M.gov/library/ secondhandsmoke/. Jacob P III. IARC Monogr Eval Carcinog Risks Hum.15:302-307. Pechacek TF.gov/tcrb/monographs/10/. Centers for Disease Control.niosh. Lewis PJ. [online]. BMJ 1975. Vol 38. Herrera B. IARC Monogr Eval Carcinog Risks Hum. Bernert JT. Benowitz NL. Atlanta (GA): 2005. the United Kingdom. Int Arch Occup Environ Health 1991. Am J Public Health 2004. Jacob P III. Strauss WJ. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. International Agency for Research on Cancer. Coordinating Center for Health Promotion. Pirkle JL. population to secondhand smoke: 1988-2002. U. Vogler GP. Brody DJ. Respiratory nicotine absorption in non-smoking females during passive smoking. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Environ Health Perspect 2006. Pharmacol Rev 2005. Giovino G. Mehta NY. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . 1988-1991. DHHS). Available at URL: http://monographs. Smoking and Tobacco Control Monograph 10 [online]. Coordinating Center for Health Promotion. National Center for Chronic Disease Prevention and Health Promotion.fr/ENG/Monographs/ allmonos90. Available at URL: http://www. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Tobacco related exposures. Centers for Disease Control and Prevention. Curtin LR. Third National Report on Human Exposure to Environmental Chemicals. 4/13/09 Iwase A. Benowitz NL.S. Hukkanen J. Benowitz NL. 4/13/09 U. 1999-2002. J Pharmacol Exp Ther 1999. Pechacek TF.

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

DEET is not a developmental or reproductive toxicant in animals (U.130-.130 (. have been reported as result of self-poisoning by ingestion or excessive dermal application.449 and 0.130-.1.140) < LOD .S.. and it has not been rated by IARC or NTP with respect to human carcinogenicity.N-Diethyl-meta-toluamide (DEET) N.. (Kolpin et al.100-. Neurological effects in humans.100-.160) < LOD ..250) < LOD . Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.130) < LOD .S.560) < LOD .140-. (U.130-. 2003).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 . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . and they range in concentration from 4% to 100%.100-. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.100-.270) 688 678 518 700 598 956 Limit of detection (LOD.110 (<LOD-.110 (<LOD-.EPA at: http://www.170 (. 134-62-3 General Information N.110 (. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. 2005).140) < LOD . 2002).520) < LOD .180 (.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 .N. 1995. 1998).100-.100 (<LOD-.N-Diethyl-meta-toluamide (DEET) CAS No.140 (. which may vary for some chemicals by year and by individual sample. DEET can be applied to clothing and the skin to repel biting insects.S.110 (. One survey detected DEET in 74% of sampled streams in the U.170 (. 2003). 1998).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 .S.100-. DEET is not genotoxic.140) < LOD . After absorption. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.130) < LOD .210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.gov/pesticides/. < LOD means less than the limit of detection. Sudakin and Trevathan. DEET has low acute toxicity. DEET is not registered for use on agricultural commodities. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.EPA. Fourth National Report on Human Exposure to Environmental Chemicals 19 .110 (.130 (.180 (. Its use is recommended for prevention of several vector-borne diseases.240) < LOD . EPA.210 (. There are over 225 insect repellents brands containing DEET. Survey Geometric mean (95% conf. 2002).120-.EPA.180 (. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. About 3-8% of dermally applied DEET is absorbed.110-.150) < LOD .130 (.220 (.110-.110 (.epa.130-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.120-.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.180) < LOD . DEET is also used in combination with dermal sun screens (U. Additional information is available from U. Urinary N.190) < LOD .S. including seizures and encephalopathy.

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .370-. 2007).240-.230-.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 .150) < LOD .480 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U..190 (<LOD-. 20 Fourth National Report on Human Exposure to Environmental Chemicals .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.150-. 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.350-.270 (<LOD-.370) < LOD . DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.630) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.230-. Urinary DEET levels as high as 5. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.190 (.320) < LOD .130 (<LOD-. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.S.270 (.640 (. representative subsamples from NHANES 2001-2002.500 (.250 (.410 (.300 (.190 (.410-.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 . population from the National Health and Nutrition Examination Survey.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.270-.280 (.S.440) < LOD .230) < LOD .140-.490) < LOD . 1992).250-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .320 (.190-.250) < LOD .550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.240) < LOD .330 (.170-. In this survey period.350) < LOD ..270) < LOD . 2005).280-1.330 (.410 (.350) < LOD .200 (.390-.290-.N.93) < LOD . Urinary N. Survey Geometric mean (95% conf.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 .

Environ Sci Technol 2002.gov/teach/chem_summ/ DEET_summary. Environmental Protection Agency (U.2:341352. Osimitz TG. Schoenig GP. Barr DB. metabolism. Selim S.S. September 1998.EPA).36(6):1202-1211.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. DEET: a review and update of safety and risk in the general population.pdf. EPA 738-R98-010.N-diethyl-mtoluamide following dermal application to human volunteers. Page BC. Grzywacz JG. 4/9/09 U.EPA. DeBord KE. 2005 Kolpin DW. Barber LB. streams. and excretion of N. Hartnagel RE Jr. 1-118. J Anal Toxicol 1992.115(8):1254-1260. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Quandt SA. U.16(1):10-13. Veltri JC. Trevathan WR. Available at URL: http://www. 2005. Furlong ET.S. pdf. Environmental Protection Agency (U. Washington (DC): U. Meyer MT.S. Zaugg SD. Gabriel KL.S. EPA. Third National Report on Human Exposure to Environmental Chemicals. Human exposures to N.gov/oppsrrd1/REDs/0002red. N. Diethyltoluamide (DEET). et al. Toxicity and Exposure Assessment in Children’s Health.S. 1999-2000: a national reconnaissance.EPA). Available at URL: http://www.S. Lowry LK. 1993-1997.25:95-100. Chen H.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. Fundam Appl Toxicol 1995. Centers for Disease Control and Prevention (CDC). Bell JW. Sudakin DL. Int J Toxicol 2002. Tapia J. Reregistration Eligibility Decision (RED): DEET. Thurman EM. Atlanta (GA).N-Diethyl-meta-toluamide (DEET) References Arcury TA.N. hormones.epa. Smallwood AW. Chemical Summary.S.epa. pp. U. J Toxicol Clin Toxicol 2003. Absorption. Pharmaceuticals.41(6):831-839. Environ Health Perspect 2007. and other organic wastewater contaminants in U.

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

Occup Environ Med 2002. Belgium. In vitro and in vivo interactions of bisphenol A and its metabolite. Pharmaceuticals. Needham LL. Environ Health Perspect 2008.116(1):39-44.59(4):403-408.35(2 Pt 1):238-254.S. Wong LY. Gender differences in the levels of bisphenol A metabolites in urine. Cha SW. 2/4/09 European Commission. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. 2007. Biochem Biophys Res Commun 2003. Available at URL: http://ec. Haighton LA. 2/4/09 Ouchi K.nih. et al. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. National Institute of Environmental Health Sciences. Rat two-generation reproductive toxicity study of bisphenol A. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats.pdf.S. T. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Barton L. Myers CB. Furukawa M. Needham LL. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.pdf . 2/4/09 Fujimaki K. hormones.14(2):149-157. Bradley S.europa.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Arakawa C. Pyo MY. Timms BG. Kuklenyik Z. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Munro IC.pdf .59(9):625-628. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Han SY. Klinefelter GR. Brussels. Environ Sci Technol 2002.nih. Available at URL: http://cerhr. Endocrinology 2008. Ispra. May 22. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. C. Kawamura N. and other organic wastewater contaminants in U. Kiguchi M. Richter CA. Barr JR. and Hajszan. Watanabe C. Ye X.nih. Department of Health and Human Services.niehs. 4. Kim YH. Kim JC. Park S. Marr MC. Caudill SP. Hara K. Brine DR. Available at URL: http://ecb.gov/chemicals/bisphenol/BPAFinalEPVF112607. 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.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. NC. Thurman EM. Yang M. Furlong ET.. Serizawa S. An evaluation of the possible carcinogenicity of bisphenol A to humans. bisphenol A glucuronide. Ecotoxicity and the Environment (CSTEE). Available at URL: http://ntp. Chem Res Toxicol 2001. Joskow R.. Howdeshell KL. Szigeti-Buck. Proc Natl Acad Sci USA 2005. Zaugg SD. Toxicol Sci 2002. National Institutes of Health. Fujii S. Bisphenol A. August 2001. DirectorateGeneral Health and Consumer Protection.pdf. K. September.145:592-603. Meyer MT. Watanabe S. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Reidy JA.149:988-994. Cohen JT. Chung MK. Joint Research Centre Institute of Health and Consumer Protection. November 26.Environmental Phenols References Akingbemi BT. niehs.Scientific Committee on Toxicity. Ikka T. Sottas CM. Calafat AM. Zacharewski TR. Needham LL. Rhomberg et al. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Calafat AM. Hum Ecol Risk Assess 2004. Lynch BS.69(22):2611-2625. Barber LB. 2003. Exposure of the U.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325.pdf. Matthews JB. Human Health. Ema M. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Calafat AM.eu/ health/ph_risk/committees/sct/documents/out156_en. MacLusky.137(3):353-362. 2008. 5: 505-523. 2002. Nippon Eiseigaku Zasshi 2004. vom Saal FS. N. Cunha G. Research Triangle Park. Doull J.J. Italy. with estrogen receptors alpha and beta. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Yoshinaga J. Barr DB.S. J Am Dent Assoc 2006. Hanaoka T.780(2):365-370.jrc. Life Sci 2001. Keimowitz AR. 1999-2000: a national reconnaissance. McConnell EE. Ekong J.113(4):391-395. Rubin C.36(6):1202-1211. Kroes R. Thomas BF.102(19):7014-7019.312(2):441-448. Leranth. Imai H.gov/chemicals/bisphenol/bisphenol.. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Tyl RW. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. National Toxicology Program. Available at URL: http://cerhr. Kolpin DW. Endocrinology 2004. Koulova AI. Regul Toxicol Pharmacol 2002. streams. et al.68(1):121-146. Harazono A. Hlywka JJ. Hughes C. Gray GM. European Commission. Tsugane S. Shin HC. and Hardy MP. Kim CS. Koh WS. U. Twomey K. niehs. Reidy JA. Reprod Toxicol 2001.10:875-921. Han SS. et al. Environ Health Perspect 2005.

Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Csanady GA. Filser JG. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration.103(1):9-20.Environmental Phenols Volkel W. Hughes C. bisphenol-A. Lee SM. Sheldon LS. Lordo RA. and nonylphenol at home and daycare. Wilson NK. An observational study of the potential exposures of preschool children to pentachlorophenol. et al. Biological monitoring of bisphenol a in a Korean population.40(7):905-12. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Morgan MK. Jang JY.147(6 Suppl):S56-69. Environ Health Perspect 2005. Large effects from small exposures. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Chang SS.113(8):926-33.15:12811287. Vom Saal FS.44(4):546-51. Colnot T. Chuang JC. Dekant W. Kawamoto T. Endocrinology 2006. Witorsch RJ. Yang M. vom Saal FS. Food Chem Toxicol 2002. Kim SY. Welshons WV. Nagel SC. Chem Res Toxicol 2002. III. Environ Res 2007. Arch Environ Contam Toxicol 2003.

.60) 1.60-3..g. and some personal care products.00 (.00 (. Bian et al. 2002). They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). 34 Fourth National Report on Human Exposure to Environmental Chemicals . Blake and Boockfor..50 (1.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30 (1.10) 2.80 (1. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. In the 1990s.20) 2. orally administered 4-tert-octylphenol was well absorbed.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.600-1.40) 1. which are anionic surfactants used in detergents.500) .50-2.50) 1.. 140-66-9 General Information 4-tert-Octyphenol. Survey Geometric mean (95% conf.300-. 2006.20-2.600) 1.400 (. and was quickly eliminated from the blood (Certa et al. In 1999-2000.60-3.50-3. altered estrus cycles and reproductive outcomes.300 (<LOD-. 2000.30) 90th 1.300-.900 (.20-2. the various alkylphenols have also been used as emulsifiers and modifiers in paints.S. leading to inhalation as another potential exposure route (Rudel et al.500) . In rats.497) * .900 (. The alkylphenol ethoxylates enter the environment through human use of products containing them. During the 1980s and 1990s.70 (1. fish) and drinking water. and emulsifiers. and the polyethoxy chain may consist of up to 50 ethoxy units. Saito et al. 2000. including 4-tert-octylphenol.200-. Ying et al. and from contact with some personal care products and detergents.00 (1.10-2. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.500-1.60) .20) 1.60-3.000 tons of alkylphenol ethoxylates were produced annually worldwide. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.300 (<LOD-. and through manufacturing waste streams (Warhurst.50) 1.50) .. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.30 (. Indoor and to a lesser extent.30 (1. and some of their degradation products are toxic to aquatic life. industrial cleaners.60-3.600-1.30-2.00) 1229 1288 03-04 03-04 03-04 * . which may vary for some chemicals by year and by individual sample.40) 2.20-2.500-1.5% of 139 U.40) * 03-04 03-04 03-04 .20) 314 715 1488 03-04 03-04 * * .507) * < LOD . The alkylphenols can bioaccumulate in some fish. Urinary 4-tert-Octylphenol (4-[1. 1995. did not bioaccumulate.90) 2.20-2. and to alkylphenoxycarboxylates.477) . Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.600-1.3.50) 1.30) 1. testicular atrophy.70 (1.30 (1.20-2. and impaired spermatogenesis (e.600) .S. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. 2004).70 (1. see Data Analysis section) for Survey year 03-04 is 0.30 (1. Less frequently.50) .2.40 (1.700-1.10 (. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.10) 1. Several alkylphenols. is used to manufacture alkylphenol ethoxylates.900 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.357 (. over 500. streams in 30 states (Kolpin et al. an alkylphenol.200-.20) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .500) .299-.20 (1.900 (.300 (<LOD-.268-.80 (1.600-1. Disposition in humans has not been studied sufficiently. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. impaired steroidogenesis.400) 1.60-3.20-2.g. 4-octylphenol monoethoxylate was detected in 43.400 (.900 (.500) 75th . population from the National Health and Nutrition Examination Survey. 2003. textiles.600-1.. altered neonatal sexual development. 1997. < LOD means less than the limit of detection. pesticides.40) 2.300 (<LOD-.600) . Katsuda et al.300 (<LOD-. 2002).369 (.. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.60-3..600-1.90) 2. have demonstrated estrogenic effects particularly when injected at high doses in animals.80) 2.800-1.400 (.10 (1.274-.600) .40) 1.80 (1.70 (1.30) 2.389 (.60) 613 652 1092 Limit of detection (LOD. to shorter chain alkylphenol ethoxylates.1.. Laws et al. through sewage.10 (.Environmental Phenols 4-tert-Octylphenol CAS No. 1996).500 (.

420) .64 (.740 (.78) 3.62) .20 (1.435 (.68-2.03-6.43) 1.. 2003. representative subsample of NHANES 2003-2004.280-. Yoshida et al.410 (.40-4.1.Environmental Phenols Myllymaki et al. 2001.06 (2.560) . It is unclear if estrogenic or other effects occur in animals through oral dosing.S. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.380 (<LOD-.18-4..550-1. 2004.00 (. In a small number of adult Japanese volunteers. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.850 (.78) 1228 1286 03-04 03-04 03-04 * .54) * 03-04 03-04 03-04 .17 (.11-2.. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure. nonylphenol. 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.36-3.25) 2.25-2. Sweeney et al.3.02-4.470-1.610) .3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.450) .60 (1.890-2. or their corresponding ethoxylates with respect to human carcinogenicity.00 (.199-.260 (<LOD-.. Biomonitoring studies on levels of 4-tert-octylphenol provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 4-tert-octylphenol than are found in the general population.570) .31-2.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.160-.270 (.65-3.22) .85 (1.S.384) * . IARC and NTP have not rated octylphenol.03 (1.620) .269 (.08) 1.81 (1. Survey Geometric mean (95% conf.270-.00) 1.71) 2.540-1.470) 75th .05-2.10-2.78 (1. Kawaguchi et al..770 (.530) .62 (1.76 (2. Fourth National Report on Human Exposure to Environmental Chemicals 35 .170-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .59 (1.630-1.400) .337-.96-4.500-1.00) 2.620-1. 1999).31 (1. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.910 (.730-1.15) 1.68) 2.73) 2.276 (. Urinary 4-tert-Octylphenol (4-[1. 2001).00) 2.41) .11) 1. Tyl et al. Nagao et al.33 (2.67-2.53-3.03 (1.320 (<LOD-. 2000.640-1. 2004).43-3. 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.33) 3.460 (.29) 2.270 (.25) 90th 1.59) 1.62 (1.470-1.40 (1. Calafat et al.14) 314 713 1487 03-04 03-04 * * . population from the National Health and Nutrition Examination Survey. 4-tert-Octylphenol is not considered directly genotoxic.370 (<LOD-.740 (.450) 1. at lower or environmentally relevant doses (Blake et al..50 (2.300 (<LOD-.207-.11) 2.349) * < LOD .43) 1.860 (.

et al. Environ Sci Technol 2003.30(2 Pt 1):81-95.116(1):39-44. Reidy JA. Blake CA. Toppari J.799(1):119-125. Cooper RL. polybrominated diphenyl ethers. Ito R. prolactin. 1999-2000: a national reconnaissance. Toxicol Appl Pharmacol 2000. Sakui N. Watanabe G.28(3):215-226. bisphenol A and methoxychlor in rats. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.uk/resource/reports/ethoxylates_alkylphenols.18(1):43-51. Meyer MT.71(1-2):112-122. Laws SC. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Paranko J. Reprod Toxicol 2001. Haavisto TE. Myllymaki SA. Camann DE. Nagao T. Environ Health Perspect 2008. Kookana R. Regul Toxicol Pharmacol 1999. Brine DR. Pharmaceuticals. Ferrell JM. 2003.121(1):21-33. Williams B. pesticides. Izumi S. Saito I.54(1):154-167. Katsuda S.S. Usumi K. Reprod Toxicol 2004. Kolpin DW. Certa H. Yoshida M. Onuki A. Maekawa A. Seely JC. Spengler JD. Horie M.44(8):1355-1361. Kawaguchi M. McCoy GL. Maekawa A. Karjalainen M. Furlong ET. Watanabe G.15(6):683-692. Xu L. Nakagomi M. and testosterone. Yoshimura S.36(6):1202-1211. Zaugg SD. Inoue K. Nair-Menon JU. Barber LB. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Ono H. Estrogenic activity of octylphenol. Endocrinology 2000.165(3):217-226. Calafat AM. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Food Chem Toxicol 2006. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Saito Y.207(1):59-68. Anal Chim Acta 486:41-50. 1995.co.foe. Biol Reprod 1997. Bodman GJ. Sweeney T. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone.57(2):255-266. Wong LY. nonylphenol. Inoue K.pdf. Qian J. Chen J. Bolt HM. 2/4/09 Ying GG. Ye X. Roche JF. Takai N. Indoor Air 2004. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Boockfor FR. Brody JG. Yoshida M. Toxicokinetics of p-tert-octylphenol in male Wistar rats.141(7):2667-2673. Takenaka A. Yoshimura Y. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Needham LL. and other organic wastewater contaminants in U. 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. Okada F.Environmental Phenols References Bian Q. et al.folliclestimulating hormone.S. Nicol L. Environ Int 2002. Marr MC. Rudel RA. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Tyl RW. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Millette CF. Korn LR. Toxicol Appl Pharmacol 2005. Taya K.37(20):4543-53. Myers CB. hormones. Thurman EM. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Toxicol Lett 2001. Fedtke N. Toxicol Sci 2000. Environ Sci Technol 2002. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. and other endocrine-disrupting compounds in indoor air and dust. Boockfor FR. Arch Toxicol 1996. Seto H. Indoor air pollution by alkylphenols in Tokyo. Raychoudhury SS. testis size. Brooks AN. Taya K. et al. Muller AM. Katsuda S. Kawaguchi M. alkylphenols. Exposure of the U.14(5):325-332. Wiegand HJ. Two-generation reproduction study with para-tert-octylphenol in rats. Song L. Warhurst AM. Phthalates. streams. Wang X. Carey SA. Available at URL: http:// www. Makino T. Blake CA. and sertoli cell number. et al. Fail PA.

Calafat et al. 1969). Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al.. 2004). 2005.. and medical devices.8-dichlorodibenzo-p-dioxin (Aranami et al. 2007. Mezcua et al. the median urinary triclosan level of 7. streams sampled in 30 states (Kolpin et al. Triclosan has a low bioaccumulation potential in fish.. 2006). Veldhoen et al. 2008 has shown higher levels during the third decade of life and among people with the highest household income. 1996. In animal studies.. but not by race/ethnicity and sex. Moss et al. Biomonitoring studies on levels of triclosan provide physicians and public health officials with a reference values so that they can determine whether people have been exposed to higher levels of triclosan than are found in the general population. Calafat et al. Some reports show endocrine effects are observed in amphibians and fish (Foran et al. (Sandborgh-Englund et al. triclosan was found in 57.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. deodorants. 1987). it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. 2002). Matsumura et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent.. 2008).. a process that can result in the formation of small amounts of 2.6% of 139 U. it has low acute toxicity....Environmental Phenols Triclosan CAS No. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. 2000). acne medications. Triclosan can be absorbed across skin into the blood stream. Biomonitoring Information Urinary triclosan levels reflect recent exposure.. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. General population exposure results from dermal and oral use of products containing triclosan. IARC and NTP do not have ratings with respect to human carcinogenicity... 2007)... In a U. mouthwashes. Fourth National Report on Human Exposure to Environmental Chemicals 37 . and wound disinfection solutions. In animal and human studies. Triclosan formulations may rarely cause skin irritation. toothpastes.S. young girls. 2007. Triclosan has been added to soaps. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2007).2 µg/L was comparable to the median level (8. Lyman and Furia. 1976. In the body it is conjugated to glucuronides and sulfates (Bodey et al.S. It acts by inhibiting bacterial fatty acid synthesis. toys. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. Triclosan is not considered teratogenic at maternally toxic doses. In 1999-2000. and has also been impregnated into some kitchen utensils. In a study of 90 U. Triclosan enters the aquatic environment mainly through residential wastewaters. 1988. representative subsample of NHANES 2003-2004.S. It can be photochemically and biologically degraded. 2000..

9 (8.4 (38.9) 32.80 (5. population from the National Health and Nutrition Examination Survey.18 (5.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4) 75th 43.29-12.70-16.8) 7.50) 10.8-112) 30.5-14.2 (13.7 (9.9-61. interval) 12.30-14. Urinary Triclosan (2.20-13.93 (7.21 (6.00-8.45-13.4-18.3 (11.20 (7.40-17.4) 357 (225-456) 203 (87.1-39.38-18.2 (37.4) 73.1) 9.6-65.2 (25.1) Selected percentiles ( 95% confidence interval) Sample 95th 368 (294-463) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9. interval) 13.8-63.1) 7.0) 9.0-15.3) 47.1 (15.7 (28.4 (32.90-10.5 (11.1 (8.1) 9.16 (6.6) 39.82 (8.40-11.45-10.S.5) 13.6-14. Survey Geometric mean (95% conf.5-86.2) 12.8) 116 (39.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.1) 9.3-15. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.50-10.2 (11.6 (10.6-14.20-10.89-11.3) 10.3-31.11-11.2 (10.4.S.2-14.1) 13.9-236) 193 (90.4) 90th 249 (188-304) 03-04 03-04 03-04 8.3) 6.0 (11.0) 49.3-67.6) 12.6-111) 33.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.94 (7.8-85. see Data Analysis section) for Survey year 03-04 is 2.3-35.54 (8.7 (14.5) 20.6) 90th 212 (172-241) 03-04 03-04 03-04 9.0) 65.48 (8.22-10.8) 9.2-58.0 (36.8 (21.00 (4.6-15.4) 7.10-9.7) 123 (36.8) 14.8-60.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.6) 31.0-15.9 (11.Environmental Phenols Urinary Triclosan (2.72-13.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.1) 50.3 (26.92-12.43-13.9) 7.9) 8.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.7 (39.32-14.20-11.4 (12.1) 11.4) 317 (231-433) 144 (96.60 (8.2 (27.0 (26.8-127) 37.2-58.86-12.2) 9.2-46.0-73.5) 11.55 (4.3.7) 292 (151-432) 132 (78.4 (11.1) 9.5) 66.7) 10.10) 84.6-37.9 (33.60 (6.6-20.9) 75th 47.4) 51.7 (11.48-10.3 (8.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.4-19.9 (50.3 (9.4) 25.0-19.1) 14.6 (9.0 (34.6 (12.0 (8.6) 10.6 (30.45 (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 .1 (45.74 (5.20 (7.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.2) 13.4.

Bhargava HN. Kaneshima H. Ekstrand J. Wolff MS. Anal Chim Acta 1004.67(4):532-537. Moss T. Photolytic degradation of triclosan in freshwater and seawater. population: 2003-2004.45 Suppl 2:S137-S147.80(3):217-227. Watanabe N. Needham LL. Hirano M. Sandborgh-Englund G.38(4):361370. et al. Pharmacokinetics of triclosan following oral ingestion in humans. Calafat AM. Nagao Y. and phenols in girls. Howes D. Williams FM. Levy SB. Percutaneous penetration and dermal metabolism of triclosan (2.S. 1999-2000: a national reconnaissance. et al. Am J Infect Control 1996.66:1052-1056. Adolfsson-Erici M.50(1-5):153-156. Pharmaceuticals. Triclosan: applications and safety. et al.Environmental Phenols References Aiello AE.28(9):1748-1751. Britton JA. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Clapson DJ. Lyman FL. IMS Ind Med Surg 1969.115:116-121. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Benson WH. Okui T.69(20):1861-1873.4’-trichloro-2’hydroxydiphenyl ether). Thurman EM. Ebersole R. Environ Health Perspect 2008. Pilot study of urinary biomarkers of phytoestrogens. Pinney SM. Ye X. Ishibashi H. Environ Health Perspect 2007. Kanetoshi A. Environ Sci Technol 2002. J Toxicol Environ Health A 2006. Zaugg SD. Larson EL.4.7/2. J Invest Dermatol 1976. and other organic wastewater contaminants in U. Chelimo C. Gilbert RJ. Furlong ET.36(6):1202-1211. Toxicology of 2.524:241-247. streams. Windham G.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Bennett ER. Leonard PA. Osachoff H. 4. Bodey GP. Food Chem Toxicol 2000. Evidence of 2. Aranami K. Veldhoen N. Foran CM.17(5):637-644. Shiratsuchi H. Wigmore H.83(1):84. et al. The oral retention and antiplaque efficacy of triclosan in human volunteers. Arch Environ Contam Toxicol 1988. Br J Clin Pharmacol 1987. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Aguera A. Hernando MD. Skirrow RC. Ferrer I. 4’-trichloro-2’-hydroxydiphenyl ether.116(3):303-307. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice.23(5):579-583. Matsumura N. phthalates. Mar Environ Res 2000. Ogawa H. Erratum in: Aquat Toxicol 2007. Gomez MJ. Readman JW. Chemosphere 2007. Fernandez-Alba AR. Reidy JA. Hong HC. Mezcua M. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Kolpin DW.24(3):209-218. Wong LY. Teitelbaum SL.S. hormones. Katsura E. Fourth National Report on Human Exposure to Environmental Chemicals 39 .38(2):64-71. Gunderson MP. Biol Pharm Bull 2005.. Meyer MT. Aquat Toxicol 2006. Odham G. Urinary concentrations of triclosan in the U. Williams PE. Barber LB. Furia T.

interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. Since 1984. has been restricted.350 (.350-.590-1.350 (. < LOD means less than the limit of detection.76) .65 (.54-2.75) 2.62 (. The parent compound and conjugates. and possibly of lindane (IPCS. are eliminated in the urine.S.350) < LOD < LOD 75th . hypertension.30 (. with repeated or chronic exposure. Human exposure to PCP has become less common.660 (.350-. air.350 (.70) 2.350-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.98 (1. the elimination half-life may be a week or more (Uhl et al.94 (1.350-2. so it is relatively non-persistent.. 1979).47-3.510-3.30) 1.350 (. bactericide. ingestion of contaminated food or water.01 (<LOD-1. population from the National Health and Nutrition Examination Survey.76) 1.350-.350) < LOD .850-2.10 (.350 (.37 (.350-2..10 (<LOD-1.10) 1.890 (.350) < LOD . and animals. PCP cannot be used on wood in residential or agricultural buildings.350-.350-.350 (.350) < LOD .00) 1.390 (.990-2. Acute.48 (.S.350-.58-2.350-1. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.00 (.350) < LOD .890-1. mollusicide. PCP is absorbed rapidly and well by all exposure routes. along with small amounts of tetrachlorohydroquinone and conjugates. General population exposure to PCP may occur by inhalation of contaminated air.350-. PCP use in the U.10) 1.70) .08-3.530) 1. PCP is degraded by sunlight and metabolized rapidly by microorganisms. plants.650 (.350-. which may vary for some chemicals by year and by individual sample.350 (.350-. 1997).350-1.350-1. herbicide.33-2.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .350) . high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation. utility poles and fence posts).10 (1.350) < LOD .350-.350) < LOD .350-.350 (.350 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . After absorption.45-2.350-2.350-.350-.00) 1. PCP is eliminated over a few days (Braun et al.350-2.350 (.350) 90th .58-2.47-5.350-.67) 1.350 (.350) < LOD .350) < LOD .23 (.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. 1976.32 (.350 (.25 and 0.48-2.500-2.350-.64) 1.78) 1.91 (1.40 (. water and sediments because of the large amounts that were produced and used historically.350) < LOD .350-.80) .42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350 (.60) 1.980 (.650) 1.350) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.04) 1.33) . other polychlorinated benzenes. and dermal contact with PCP-treated products.350-2.390 (.350 (.53) size 1994 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .37) .350-.00) 2.30 (.30 (1.09) .480-2.30) 1.990 (<LOD-2.94 (1.90 (1.350) < LOD .350) < LOD .350) < LOD .630 (.350) < LOD .5. and it is used primarily as a preservative for wood to be used outdoors (e.50) 1.350) < LOD .350 (.350 (. After a single dose.30) . To-Figueras et al. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Effects including hyperthermia.350 (.680-1.350 (.18 (<LOD-1. Survey Geometric mean (95% conf..42) 696 680 521 696 603 951 Limit of detection (LOD.73 (1. 1986).350 (. 40 Fourth National Report on Human Exposure to Environmental Chemicals .90) 2.g. In the environment.770 (.90) 1. and metabolic acidosis were observed in CAS No. 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) < LOD . 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.65 (.350-.510-5.350 (..83 (2.60) 1. 2002. PCP is distributed to most tissues and is not extensively metabolized. PCP has been detected in soils. algaecide and insecticide.350-.860-2.51) 1.350-. Kohli et al.350-.960) 1..350-1.350 (.

atsdr.320) < LOD ..S.610 (.18) .cdc.570 (.830) < LOD .57 (1.290) < LOD .21 (.420) < LOD .S. chronically administered high doses of PCP were hepatotoxic.40) 1.300 (.67 (1.75) 1.590-1.430-. 1991).250 (. In animals.10 (1. 1989). More information about external exposure (i.30-2.epa.94 (1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .40-2.25-2. In a small sample of U. or skin absorption.10-2.280) < LOD .40) 1.94 (1. the 95th percentile of urinary PCP levels was about fiftyfold higher than that for 6-11 year olds in NHANES 2001-2002 (Hill et al.06 (.06) 1.730) < LOD . and the FDA has established a standard for bottled water. In NHANES 2001-2002 subsamples. 2003).36) .13 (. Fourth National Report on Human Exposure to Environmental Chemicals 41 . 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.950-1.950-1.67 (1.25 (1.490) < LOD ...51) 1. respectively) (Becker et al.18 (1.500-.650 (.95) 3.650 (. 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.780-1..52 (1.19 (1.35-2. 2004..900-1.67-3. population from the National Health and Nutrition Examination Survey.EPA.html. EPA has developed standards for PCP in drinking water and the environment.00-1.780) < LOD . respectively) (Seifert et al.380-. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.S.650) 90th 1.57 (.84 (1.320 (.48-2.370 (.320) < LOD .500-1.40) 1. OSHA has established an occupational standard.78) 1.470 (. van Raaij et al.75 (<LOD-2.55) 1.94-3.220-.290-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.52 (<LOD-1.Fungicides adults and children severely exposed to PCP through ingestion.00-1. 2000).08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 1995).S.19) 2. Death can result from seizures and cardiovascular collapse.83 (1.250 (.35) 1.21-2.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 1989).270-.330-.950-1.29-3.500 (. environmental levels) and health effects is available from the U.67 (1.00) 1.430) < LOD .580-.67-2.290-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.73 (1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .300 (.710-1. 2003).35-2.09-1.30 (.9 mg/L. 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.25) 1.270-.30) 1.310) < LOD .gov/ toxpro2.30) 1.510-.25-1.360-.990 (.11) 2. EPA at: http://www. children in the 1980’s.26 (1.19) 2.06-3..440 (.560-.52 (<LOD-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 (4.16-1. inhalation. Pentachlorophenol is not mutagenic or teratogenic. 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. and adversely affected thyroid function (U.78) 1.26 (1.67-3.90) 1.910-1.52) 1.09) 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 .gov/ pesticides/ and from ATSDR at: http://www.40) 1.400 (.340-.19) 2.300 (.e.25 (1.310-.760 (.16 (.560) < LOD . carcinogenic.800) < LOD 1.84) 1.82 (1.82) 1.0 mg/L.09 (<LOD-2.240-.79) 1.560) < LOD .590) < LOD .08 and 5.56) 1. The U..630 (.92) 1.220-.40) 1.360 (.67 (1.800-1.34 (.67 (1.S. Among adults in the NHANES 1999-2000 subsample.320) < LOD < LOD 75th .6 and 14.700-2.84-4.. Survey Geometric mean (95% conf.69 (1.510-.920 (.25-2.350) < LOD .260 (.35) 1.850 (.

Cline RE. Environmental Protection Agency (U. Available at URL: h t t p : / / w w w. Hill RH. 4/21/09 Kohli J. Otero R. 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. Seiwert M.10:552-65. Schmid P. Engel R. drinking water and indoor air.58:182-186. 42 Fourth National Report on Human Exposure to Environmental Chemicals . htm. Shealy DB.54(3):203-208. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Chenoweth MB.S. r e g u l a t i o n s . 2002. Holler JS. EPA). Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Uhl S. 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. Barrot C. Notten WR. Arch Environ Contam Toxicol 1989. Needham LL. Rodamilans M. Schulz C. available at URL: http://www. house dust. Lindane. 4/21/09 van Raaij JA. Arch Environ Contam Toxicol 1989.71:99108. urine. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Blau GE. et al. Schulz C.105(1):78-83. Jones D. Bailey SL. Kaus S. 11/30/2004. Head SL. Arch Toxicol 1986. hair. Pharmacokinetics of pentachlorophenol in man.18:475-481. To-Figueras J.inchem. Hill RH Jr.S. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Bragt PC.4:289296. Baker S. Needham LL. van den Berg KJ. Becker K. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.org/documents/jmpr/jmpmono/2002pr08. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Helm D. Seifert B. Int J Hyg Environ Health 2003. Braun WH. Gregg M. References Becker K. To T. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Krause C. Schlatter C. Dev Toxicol Environ Sci 1979. Environ Res 1995. Environ Health Perspect 1997. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Seiwert M. J Expo Anal Environ Epidemiol 2000. Safe A. Phillips DL. PCP: Human Risk Characterization [online]. The metabolism of higher chlorinated benzene isomers. Toxicology 1991: 67(1):107-16. Smith SJ. Pesticide residues in urine of adults living in the United States: reference range concentrations. U. Seifert B. Sala M. et al. Hill RH Jr. Can J Biochem 1976. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. International Programme on Chemical Safety (IPCS).Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Fast DM.18(4):469-474. 206:15-24. Santiago-Silva M.

34) 1.490 (<LOD-.30-2.930 (.580-1.80 (2. OPP is still used as a disinfectant fungicide for industrial applications.600) < LOD .00) . SOPP is applied topically to the crop and then rinsed off.520 (.50 (1.90 (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.20-3.00-2.S.20) 2. Survey Geometric mean (95% conf.645) * .570 (.27 (. < LOD means less than the limit of detection. 1998).10-2. OPP is volatile.508 (.830 (.60 (1.60-3.560-8. are antimicrobial agents used as bacteriostats.570 (.61) 2.780) < LOD . 2006).490 (<LOD-.88) 1.22) 2.410-.790) 2.389-.00 (1.30) < LOD 90th 1.10) 2.20-2.742) * .22 (.370-. 1989).624) * .750-2.710-2.02) 1.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 . Both chemicals degrade within hours to weeks in the environment (U. fungicides.50-2. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.670) 2. or 2-phenylphenol) and its water-soluble salt.696) * .30 (1. interval) .350-1. 2002.450 (<LOD-.20) < LOD 2.890) 1.770 (. it was used in home sanitizers for surfaces. and as a wood preservative.50-4. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.370-.40-2.420 (<LOD-.40-7. however.10) 1.00) .600-1.470 (<LOD-.3.552 (.540-2.760-2.76) 1. whereas SOPP is not volatile and is more water soluble.570-1.50 (1.90) 2.349-.30) < LOD .90) .50 (1.50) < LOD . 2006). on ornamental plants and turfs.600) < LOD .389-.970 (.03) 1.860) * 99-00 01-02 99-00 01-02 99-00 01-02 . or apply these chemicals may be more highly exposed than the general population.466 (.EPA.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 . but OPP and SOPP are still used on pears and citrus (U.80-3.450 (<LOD-.50) ..09) 2. and sanitizers. 90-43-7 General Information Ortho-phenylphenol (OPP.20 (1.28-3.60 (1. Estimated human intakes have been below recommended intake limits (U.S.92 (.836) * .493 (. and it has limited water solubility.10-1.Fungicides ortho-Phenylphenol CAS No.3 and 0.490 (<LOD-.10) .770 (.90) .600-1.80) 1.710) 3.00 (1. Both have been used in agriculture to control fungal and bacterial growth on stored crops. Workers who manufacture.40 (...498 (.10) . Fourth National Report on Human Exposure to Environmental Chemicals 43 .364-.820 (. sodium ortho-phenylphenate (SOPP). population from the National Health and Nutrition Examination Survey.EPA. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al. Most agricultural food applications have been revoked.890 (.890 (.10) 1.638) * .17 (.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.85) 2. inhalational.600-1.690-1.402-.90) 1. OPP is considered to be moderately toxic after acute oral doses in animal studies. leaving the chemical residue OPP.509 (.S.10 (1.50) < LOD .610-1.600) < LOD 1.14 (<LOD-3.800-3. 2006).00) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) < LOD 1.610 (.480-1.570-2.490 (<LOD-.S.390-.40-5.80) 1.370-. which may vary for some chemicals by year and by individual sample.570-.590-2. 1998. 2006). EPA.950) < LOD . such as fruits and vegetables.10) .386-.567 (. Timchalk et al. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. in paints.50) 1.00 (1.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 . In the past.640) < LOD .00 (1.860 (.450 (<LOD-.490 (<LOD-. Available evidence suggests that OPP does not accumulate in the body.497 (.10 (1.690) < LOD . OPP is efficiently absorbed from the gastrointestinal tract and through the skin.20 (.23) 695 680 520 695 603 953 Limit of detection (LOD.90 (1.630) < LOD . small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.60 (1.28 (. Cnubben et al. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment. General population exposure can occur via dermal.840-1.30-7.496 (.50-3.50) < LOD .07 (.850 (.20 (1.880-2.500-2.33 (.433-.19 (.621) * .30) 1.20) < LOD 1.600) < LOD 75th .636) * .60-2.40-5. formulate.740 (.550-1.

97 (2.420 (<LOD-.31) < LOD .0) 1.02 (. Additional information is available from U. 1993.11) 4. Murata et al.S. 1984.96-4.11-1.88-4.810) < LOD .470) < LOD .11 (.480-. leading to production of two metabolites.09 (1..980 (. U.32) 1. or. or developmental toxicity was observed (Bomhard et al. Ito et al.S.270-.550 (. Brusick. Survey Geometric mean (95% conf.666) * . 2002).508) * . 44 Fourth National Report on Human Exposure to Environmental Chemicals .40-13.84 (1.980 (<LOD-1.670 (. Volunteers exposed to 0.361-.656) * .900-1.64 (2. 1999.33-2.791) * .96 (1.810-1. Biomonitoring studies on levels of OPP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of OPP than are found in the general population.78 (2.410 (<LOD-.568) * .570) < LOD 1..780-14.620-1.93 (1.800-1.gov/pesticides/. Detectable levels were seen in over half the U.470 (<LOD-.13) 1.510-.590) * .560) < LOD 75th .329-.610) < LOD 1.900) < LOD .770-2.600-1.311-.61 (.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .59) 1.248-.52 (.460-.epa. 1997.96 (1.06-4.24-2.670) < LOD .21) 1.93) 1.12-2.550) < LOD .61 (2.86 (1.28 (<LOD-4.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Kwok et al. 2000.444 (.93) .. by possible genotoxic mechanisms (Hagiwara et al. 2005.07) 2.500) < LOD .62) .970) 1.860 (.320 (<LOD-. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.08-1. IARC has classified SOPP as a possible human carcinogen.496 (.27) < LOD .38) 2.43 (1. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.750 (. 1986). and it has classified OPP as not classifiable with respect to human carcinogenicity. Biomonitoring Information Urinary OPP levels reflect recent exposure..00 (1.291-. In high dose animal studies.96) 1..880-1.01) 1.18) 2. CDC.990) < LOD .93) . population from the National Health and Nutrition Examination Survey.473) * .S.24-2.17) 2.43-2.08) 1.580-1. less likely.690 (. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.380 (.69 (1. 1998. 2002. reproductive.43-2.11) < LOD 90th 1. 2002.EPA at: http:// www.47) .20) < LOD 3.29) 1.750-2.301-.25-6.910-1. OPP was not found to be mutagenic.580) < LOD .06 (1. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.17 (.04-4.840 (.53) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.420 (<LOD-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.484) * ...650-1.38) 1.S. 2005).51-3.750 (.00 (.560-2.455-.EPA 2006).620-1..910 (<LOD-1.44 (1.950) < LOD . 2005).780 (. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.28 (2.EPA 2006).33) size 1991 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .38-3.410 (<LOD-. Pathak and Roy.S.860 (.75 (1. Zhao et al.29) 1.46) < LOD 1. 1984.11 (.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.403-.360 (<LOD-.08-2.21-2. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. U.514 (.343 (.Fungicides anemia.81) 1.940-2.21 (. interval) .353-.06-5.26) 1.17 (.58) 2.670 (. Bomhard et al.385 (. but no neurologic.550-.05-2.89 (1..33) ..382 (.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .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.91 (1. Smith et al.09-6.74 (1.43) 3.12) < LOD 1.453 (. Nakagawa et al.640-1.510 (<LOD-.59) . 1992.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .910 (.4) 3. 1999.09-3.32) 3.75 (1. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.440 (.61 (1.

Gierthy J.74(2):61-71.Fungicides References Appel KE. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Toxicol Appl Pharmacol 1998. March 1986. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Fukushima S. J Agric Food Chem 2006.gov/ntp/htdocs/LT_ rpts/tr301.286(2):309-319. Ito N.43(7):14311437.22(10):809-814.54(16):5731-5735. Centers for Disease Control and Prevention (CDC).S. Carcinogenesis 1999. 1989. Xenobiotica 1998. Bomhard EM. Mutat Res 1993. Bromig KH.gov/oppsrrd1/REDs/ phenylphenol_red. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Arch Toxicol 2000. Hum Exp Toxicol 1998. Elliott GR. Vogel JS. Bartels MJ. Narang A. EPA-560/5-89-003. J Agric Food Chem 2002. IARC Sci Publ 1984.nih. Moriya K. Hakkert BC.28(6):579594. Buchholz BA.pdf.159(1):18-24. Available at URL: http://ntp. Biochem Pharmacol 1992. Christenson WR. rat and man. Fourth National Report on Human Exposure to Environmental Chemicals 45 .S. Murata M. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries.20(5):851-857. Roberts AL. Nakagawa Y.45(5):460-481. Freyberger A. Christenson WR. Available at URL: http://www. U. O-phenylphenol and its sodium and potassium salts: a toxicological assessment.150(2):402-413. Meuling WJ.32(6):551-625. Turteltaub KW. Hirose M. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Selim S. National Toxicology Program (NTP). July 28.S. EPA 739 R-06004. Imaida K. 4/9/09. Regul Toxicol Pharmacol 2002.niehs. Moore GA. Crit Rev Toxicol 2002. Eastmond DA.pdf. Hagiwara A. Coelhan M. Eadon G. The carcinogenicity of the biocide ortho-phenylphenol. Environ Mol Mutagen 2005. Leser KH. Drugs. food additives and natural products as promoters in rat urinary bladder carcinogenesis.703(12):97-104. Bartels MJ.17(8):411-417. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Arnold LL. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Ito N.35(2 Pt 1):198-208. Roy D.50(11):3351-3358. Pathak DN. Tayama S. Comparative metabolism of orthophenylphenol in mouse. Shirai T. Bartels MJ. Bormett GA. Food Chem Toxicol 1984. Environmental Protection Agency (U. Stanley JS.EPA). Cano M. Environmental Protection Agency (U. Kwok ES. Inoue S. 2005. Brendler-Schwaab SY. 4/13/09 Onstot JD. Timchalk C. Identification of SARA compounds in adipose tissue. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Kawanishi S. Fukushima S. EPA). et al. Richter M. 2006. J Chromatogr B Biomed Sci Appl 1997. Toxicol Appl Pharmacol 1999.epa. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). et al. Shibata M. Zhao S. Cnubben NH. Office of Toxic Substances. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Glas K..S. Hagiwara A. St John MK. Sangha GK. U. Brzak KA. Herbold BA. 90-43-7) in Swiss CD-1 mice (dermal studies). Mendrala AL. van de Sandt JJ. Smith RA. Sangha G. Third National Report on Human Exposure to Environmental Chemicals. Bartels MJ. McNett DA. Atlanta (GA). Timchalk C. Moldeus P. Brusick D.(56):399-407.

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

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

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

Camann DE.39(17):6561-6574. EPA). Burkhardt MR.Herbicides References Ashby J. Bravo R. Casida JE. J Expo Sci Environ Epidemiol 2007. 2000. Acetochlor (Harness) Pesticide Petition Filing 1/00. Third National Report on Human Exposure to Environmental Chemicals. Available at URL(non U. Environmental Protection Agency (U. Deddens JA. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor.248(2-3):123-133.S. Hein MJ. Coleman S. Environ Sci Technol 2005.pdf. Rose RL. Alavanja MC. EPA 738-R-00-009.S. Reynolds SJ. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.cce. Larsen GL. Linderman R. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Linhart SM. Tinwell H. March 2006.108(12):1151-1157. J Expo Anal Environ Epidemiol 2005. et al. acetochlor.15(6):500-508.S. J Agri Food Chem 1989. Battaglin WA.cornell. 5/30/06.EPA): http://pmep. 2005. Barr DB. imidazolinone. Hladik ML. et al. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Lefevre PA. Kinney PL. Environ Health Perspect 2003. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Xenobiotica 1994. Olsson AO. Available at URL: http://www.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Ward EM. 5/30/06 U. Sanderson WT. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Occurrence of sulfonylurea. Kolpin DW. Peter CJ. EPA). Feng PCC. epa. and metolachlor herbicides in rats. Feil VJ. Hines CJ. Atlanta (GA). Heederik D. Barr DB. Chem Res Toxicol 1998. Thurman EM. and other herbicides in rivers. Andrews HF. Davison KL.S. Dialkylquinonimines validated as in vivo metabolites of alachlor. Curwin BD.24(10):1003-1012. Jefferies PR. sulfonamide. pages 3682-3690. Striley CA.248(2-3):115-122. Quistad GB. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Number 15. Wilson AG. Sci Total Environ 2000.37(4):10881093. Environ Health Perspect 2000. Hum Exp Toxicol 1996. Whyatt RM. Roberts AL. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Barr DB.S. Furlong ET. U. Environmental Protection Agency (U. Kier L. Comparative metabolism and elimination of acetanilide compounds by rat. Hsiao JJ. Wratten SJ. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. reservoirs and ground water in the Midwestern United States. Sci Total Environ 2000. Centers for Disease Control and Prevention (CDC). Barr JR. Green T.15(9):702-735.17(6):559-566.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Federal Register: January 24. 1998. Volume 65. Hodgson E.html.11(4):353359.111(5):749-756. Fourth National Report on Human Exposure to Environmental Chemicals 49 . et al.

1996. 2000. U. 2003).1 to 1. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. the dermal exposure route is potentially significant for applicators. 1998). U. In animals.S. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. USGS.. 1996).. 1988. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates.EPA. the latter may account for some observed effects (Davison et al. 1999. 1998). mean values of urinary concentrations of alachlor metabolites.. 2003). and on non-crop land for general weed control. U. 1998.Herbicides Alachlor CAS No. but another metabolic pathway can produce 2.epa.EPA. 1998. mercapturate conjugates were predominant metabolites. Hill et al. 2003). Because it can be absorbed through skin. WHO.. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. U. stomach. 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. Hines et al.S.EPA. alachlor has demonstrated hepatotoxicity. but has not shown developmental or reproductive toxicity in mammalian systems (U. Alachlor itself is not considered mutagenic.. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al.. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell 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. ranged from 0.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. corn cropland was treated with alachlor. 1996. Kolpin et al.gov/pesticides/.. Hladik et al. 2005. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and field workers. as measured through conversion to deethylamine. WHO. 1995). In a study of applicators and workers exposed to alachlor. including corn. Feng and Wratten. WHO. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. General population exposure to alachlor may occur through consumption of contaminated food or drinking water.S.. soybeans. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. about 20-25% of the U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Jefferies et al. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect.EPA. Additional information about is available from U. 1995. NTP and IARC do not have ratings regarding human carcinogenicity. In animal studies. IPCS.S. 1998).. In 1993-1995. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. In chronic animal testing. 15972-60-8 General Information Alachlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural cropland. but shows little bioaccumulation. 1999 and 2007. 1994. Alachlor has a soil half-life of a few weeks.S.S.1 mg/L at various collection times (Sanderson et al. and uveal degeneration. 2000..EPA considers alachlor to be a probable human carcinogen at high doses. Alachlor has low potential for acute toxicity. It is absorbed by plants and inhibits plant protein synthesis. Since the late 1980s alachlor use has been declining. 1998. 2005). 1989. 50 Fourth National Report on Human Exposure to Environmental Chemicals . Estimated human intakes have been below recommended limits (U. formulators. 2003). and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. but not likely at low doses.6-diethylaniline and its reactive metabolite. EPA at: http://www. peanuts and other crops.S.EPA. 1997. Tessier and Clark.S. WHO. whereas 60% of applicators had detectable amounts. hemosiderosis. (2003) showed that 2.

population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 99-00 is 1.18.S. 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. * 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.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. 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1942 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 463 662 817 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 992 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 679 507 586 Limit of detection (LOD.S.

Dialkylquinonimines validated as in vivo metabolites of alachlor. Geological Survey (USGS). reservoirs and ground water in the Midwestern United States. Kinney PL. Biagini RE. Gilliom RJ).org/documents/pds/pds/pest86_e. Linhart SM. Feng PCC.44(18):1325. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. U. et al. Circular 1291. Wratten SJ. Environmental Protection Agency (U. Wilson AG. Hull RD. et al. Erratum in: Life Sci 1989. Reregistration Eligibility Decision (RED) Alachlor. EPA 738R-98-020. Available at URL: http:// www. 98-4245 (by Barbash JE. 2003. Camann DE.111(5):749-756. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. 2/27/09 Jefferies PR. Larsen GL.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. World Health Organization (WHO). Sacramento. imidazolinone. Sanderson WT. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Hines CJ. December 1998. acetochlor. Hladik ML. Xenobiotica 1994.47(6):503-517. Brown KK. Kolpin DW. California. Casida JE. Clark JM. Hill RH Jr. Geneva. 1998. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Davison KL. J Agri Food Chem 1989. Occurrence of sulfonylurea. Supplemental Technical Information (available on-line only). March 2006. Henningsen G. Bull Environ Contam Toxicol 1996. 1996. Hines CJ. Geological Survey (USGS). Biagini R.S.S.htm.24(10):1003-1012.pdf. Comparative metabolism and elimination of acetanilide compounds by rat.gov/oppsrrd1/ REDs/0063. Life Sci 1988.11(4):353359.39(17):6561-6574. Lau H. MacKenzie B.int/water_sanitation_health/dwq/chemicals/en/alachlor. Roberts AL.S. revised February 15. Barr JR. Quistad GB. Tolos W.inchem. Shoemaker DA. Mutat Res. WHO/ FAO Data Sheets on Pesticides. Casida JE. Shealy DB. Hum Exp Toxicol. 2005. Centers for Disease Control and Prevention (CDC). Brown MA. 1999. Driskell WJ. An evaluation of the carcinogenic potential of the herbicide alachlor to man.Herbicides References Battaglin WA. Burkhardt MR.37(4):10881093. Ann Occup Hyg 2003.43(25):2087-94. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Casida JE. 4/2/09 U. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Kier LD. Hill AB. Quistad GB. Background document for development of WHO Guidelines for Drinking-water Quality. Atlanta (GA). and other herbicides in rivers. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.pdf. Barr DB. Whyatt RM. Tessier DM. 1999. Deddens JA. Kolpin DW. EPA). Thurman EM. World Health Organization. No. Striley CA. Environ Health Perspect 2003. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. 2/27/09 U. Sci Total Environ 2000. Feil VJ. Andrews HF.S. Martens MA. J Ag Food Chem 1995. International Programme on Chemical Safety (IPCS). Available at URL: http://www.56(9):883-889.56(6):853-859.248(2-3):115-122. who. 1992-2001. Thake DC. Chem Res Toxicol 1998.usgs.php. 86. Am Ind Hyg Assoc J 1995. Sci Total Environ 2000. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. 1997.395(2-3):159-171. Available at URL: http://water. 2007. ALACHLOR. Peter CJ.18(6):363-391. Available at URL: http://www. Alachlor in Drinking-water. Furlong ET. sulfonamide. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Jefferies PR. Third National Report on Human Exposure to Environmental Chemicals. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. DNA adduct formation by alachlor metabolites. Environ Sci Technol 2005. Hsiao JJ.248(2-3):123-133.epa. Kimmel EC. Thelin GP. and metolachlor herbicides in rats. Heydens WF.43(9):2504-2512.

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

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

Seiber JN. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Moseman RF. et al. Chen H. Maroni M. Gammon DW. Hein MJ. J Toxicol Environ Health 1994. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Geneva. In small studies of Maryland residents in 19951996 (MacIntosh et al. Cooper RL. Wetzel LT. Saiz SG. Proc Natl Acad Sci USA 2002. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. 2005). Eldridge JC. Shoemaker DA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. ATRAZINE. Environ Health Perspect 2001. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate).61(4):331-355. Noriega N. 3/11/09 Laws SC.gov/toxprofiles/tp153. atrazine was detected in only four children (Arcury et al. Toxicological profile for atrazine. 1996.org/documents/pds/pds/pest82_e. Freeman NC. Reynolds SJ. Barr DB. Blewett C. Schmid J..47(6):503-517. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. McElroy WK. Laws SC. 82. 1993). Fleenor-Heyser DG. Carr WC Jr.76(1):190-200. Brown KK. 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. Goodrow MH. Cooper RL. Pfeifer KF.inchem. Barbieri F. 2007). Ferrell JM. Toxicol Sci 2000. Sanborn JR. Bradway DE. J Expo Anal Environ Epidemiol 2005. In a study of 60 farm worker children. Toxicol Lett 1993.atsdr. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Jones AD. Barr DB. Hines CJ.109(6):583-590. Stoker TE.53(2):297-307.. WHO/ FAO Data Sheets on Pesticides. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. World Health Organization. Catenacci G.115(8):1254-1260. Simpkins JW. Steroids 1999. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Grzywacz JG. Stuart AA. Bersani M. Cottica D.htm.69(2):217-222. 2000). 2001 [online].. Pest Manag Sci 2005.. Aldous CN. Collins A. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Centers for Disease Control and Prevention (CDC). et al. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. A risk assessment of atrazine use in California: human health and ecological aspects. Biagini RE. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . 2005). Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Mendoza M. Tyrey L.64(9):672-678. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. J Toxicol Environ Health 1994. 2001). Cooper RL. Barr DB. et al.58(2):366-376. Lee M. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L.30(2):244-247. 3/11/09 Arcury TA. Atlanta (GA). Hermaphroditic.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. In the NHANES 2001-2002 subsample. Environ Health Perspect 2007. Deddens JA. Extrom PC. et al. diamino-S-chlorotriazine and hydroxyatrazine. Gillis JH. International Programme on Chemical Safety (IPCS). levels of atrazine mercapturate were generally not detectable (CDC. 2005. Stoker TE. Toxicol Sci 2000.cdc. Gillis JH. Goldman JM. Tapia J. Ann Occup Hyg 2003.43(2):155-167. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Available at URL: http://www. Vonk A. Stevens JT.99(8):5476-5480. et al. Third National Report on Human Exposure to Environmental Chemicals. Stoker TE. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al.html. Eberly LE. 2003. The geometric mean of urinary atrazine mercapturate was 1. Wetzel LT. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Perry et al. Agency for Toxic Substances and Disease Registry (ATSDR).. No. Hayes TB. Ferrell JM. Ferioli A. Striley CA. Lucas AD. Heederik D. In a small number of field workers. Eldridge JC. Biological monitoring of human exposure to atrazine. References Adgate JL.. Clayton CA.43(2):155-167. Curwin BD. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Breckenridge CB. et al. J Agric Food Chem 1982. Lioy PJ. Sanderson WT. Toxicol Sci 2003.. Available at URL: http:// www. Quandt SA.15(6):500-508.

6/1/09 U. Delzell E. Office of Prevention. March 2006. Pesticides and Toxic Substances.S.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Environmental Protection Agency (U. Stoker TE. revised February 15. Dagenhart D. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Sathiakumar N.27(6):599612. Timchalk C. EPA). Environmental Protection Agency (U. Pesticides in the Nation’s Streams and Ground Water. Stoker TE.S.58(1):50-59. Chem Res Toxicol 1993. Interim Reregistration Eligibility Decision For Atrazine. U. Circular 1291. Toxicol Sci 2002. Wood C. Cooper RL.56(2):69-109. Ryan PB. 1992-2001. Rayner JL.epa.9(5):494-501. A review of epidemiologic studies of triazine herbicides and cancer. Osborne DW. Available at URL: http://water. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine.195(1):23-34. Crit Rev Toxicol 1997.182(1):44-54. Christiani D.pdf.S. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. EPA Office of Pesticide Programs. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Needham LL. Guidici DL.epa. Lansbergen GW. van den Berg M. Laws SC. May 2003a. Singzoni B. Langvardt PW. Perry M.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Toxicol Appl Pharmacol 2002. Stevens JT. EPA). 3/11/09 U. Case No. Hammerstrom KA.gov/oppsrrd1/REDs/ atrazine_ired. A longitudinal investigation of selected pesticide metabolites in urine. Boerma J. Dryzga MD. 2003b. Cooper RL. Environmental Fate and Effects Division.61(1):27-40. Toxicol Sci 2000. Toxicology 1990. 0062. Supplemental Technical Information (available on-line only).usgs. Fenton SE.S.php.6(1):107-116.10(7):479. MacIntosh DL. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . White paper on potential developmental effects of atrazine on amphibians. J Expo Anal Environ Epidemiol 1999. 2007. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Tortorelli J. Sanderson JT.pdf. Geological Survey (USGS). The Quality of Our Nation’s Waters.Herbicides development of a biomarker of exposure. Available at URL: http://www. Breckenridge CB. Toxicol Appl Pharmacol 2004. Ann Epidemiol 2000.67(2):198-206. Laws SC. Wetzel L. A risk characterization for atrazine: oncogenicity profile. Guidici DL.S. Kastl PE. J Toxicol Environ Health A 1999. Washington (DC). Available at URL: http://www.

EPA.60) 1. 1977). Similar to other chlorophenoxy herbicides..230 (<LOD-. 1989. 94-75-7 General Information Widely used throughout the United States.27-2.51 (1.66) < LOD 1.07 (.740 (.690 (.. with a half-life of several days to several weeks. 4-D.610-.4-dichlorophenoxyacetic acid (2.210-.760 (.960-1.32 (1..690 (.10 (<LOD-1.420) < LOD .02-1.210 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 57 .540-. these herbicides can enhance plant growth. the chlorophenoxy herbicide 2.4-D is rapidly absorbed via oral and inhalation routes. 2.4-D may occur during residential applications. and mecoprop).2.27 (.S.310) < LOD . Kohli et al. and by consuming food or drinking water contaminated with 2.250 (<LOD-. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.30 (<LOD-2.490 (. 2.80) 1.440-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.680-1.230-.310 (.EPA. It is not well absorbed through the skin.420-. nausea.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .890) < LOD .250 (<LOD-.Herbicides 2. and delayed Urinary 2.43) 1. but at higher levels they are herbicidal.350) < LOD < LOD < LOD .22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .4-D has low acute toxicity.410) < LOD .21) 1.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Human health effects from 2. General population exposure to 2.330 (. by direct contact with agricultural and residential areas after applications. Sauerhoff et al. renal and hepatic injury. myotonia. 1974.610 (.260 (<LOD-.670-1.00-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.690-1. MCPA.16) < LOD .S.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 . 2004). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.22) < LOD .4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.560-1.810-1. It is rarely detected in ground waters (USGS. in 2001 (U. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.4-D have been below recommended intake limits (U.320) 90th .S.930 (.55 (1. which may vary for some chemicals by year and by individual sample.48) < LOD 1.660) 1.S.10) < LOD 1.S. 2.370-. It was first registered with U.20 (. It is poorly bound in soils.4-Dichlorophenoxyacetic Acid CAS No. abdominal pain.EPA in 1948. population from the National Health and Nutrition Examination Survey.03) 695 659 520 668 589 892 Limit of detection (LOD. hypotension. 2.910) < LOD . agricultural. it acts as a plant growth hormone.40) 1. headache.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.70) 1.910) 1. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.08) < LOD .400) < LOD .890 (.952 and 0.490) < LOD < LOD < LOD .930-1.27 (1.20 (<LOD-1. Once absorbed. 2005).10 (<LOD-1.4-D can be applied either as an aqueous salt or as oil-soluble esters.13) < LOD . 2007).550-1. As much as 62 million pounds of 2.690 (.4-D or exposed for prolonged periods. < LOD means less than the limit of detection.4-D were used in the U.4-D) controls broadleaf weeds in residential. Recent estimates of chronic intakes of 2.730 (. dizziness. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. At low levels.24 (. Survey Geometric mean (95% conf. and aquatic environments.05-2.560-.

2001. Additional information is available from U.390) < LOD < LOD < LOD .4-D reflect recent exposure. liver.270-. Epidemiological studies have reported associations of several types of cancer..4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.27-1.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . or to contaminants in the herbicide formulations (specifically 2. 2005. Kutz et al.930-1.05) .56) .24) 1.810-1. IOM.410) < LOD < LOD < LOD .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 . 1996. and evidence of histological injury to the kidneys. Hill et al.S..780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .EPA. 2005). U. 2002.330-.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. or teratogenic effects in chronic rodent studies (Charles et al.gov/pesticides/.340-.790) < LOD .380) < LOD .8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.740 (.560-.700 (.32 (<LOD-2.Herbicides neuropathy (Bradberry et al. 2000)..810-1.670 (<LOD-1. U.410 (<LOD-. 1989).S.340 (.890) < LOD 1. U.4-D are eye irritants. Biomonitoring Information Urinary levels of 2.73) .410) < LOD 1.S.. 2005).26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.EPA.550-.380-. 2.270 (<LOD-. Knopp et al.590 (<LOD-1. 1985.890-1.610-. IPCS.13 (.780 (. 1980. CDC. U. developmental.470) < LOD . such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 1996.440 (.920) < LOD 1.980) < LOD 1. In previous samples of the U.560-.660) < LOD . other exposures.3.epa.670 (.350 (<LOD-. 2005).EPA at: http://www. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. The acid and salt forms of 2.820-1. eyes. Kolmodin-Hedman and Erne. 2006. Pearce and McLean. Acute high doses administered to laboratory animals produced ataxia. 2005). adrenals and gonads (NTP.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.35) < LOD .380 (<LOD-. It is unclear whether these associations are related to the chlorophenoxy herbicides. Average post-application urinary levels of 2.680) < LOD . IPCS.S.660 (.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. thyroid..410) 90th .790) 1. 1994).. 2004). with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.08 (.380 (<LOD-.4-D production plant workers and a few forestry workers spraying 2.. 2005.780) ..19) . 1992)..S.480 (.13 (.41 (1.780-1. population (Hill et al. in small samples of children (Hill et al. urinary 2.. 2005.16) 1.4-D does not have significant reproductive. 2003. 2. 1996. 1995.670 (. and of adults and children (Baker et al. 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.620-.EPA 2005). 2005. 2002.490 (.08 (.590 (<LOD-1.580-.14 (.EPA.17 (. Post-application levels in farmers and home gardeners were dependent on Urinary 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08 (.S.990-1. 1995). 2.640 (.4-D levels were detectable in less than a quarter of the individuals studied. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.7. myotonia. Survey Geometric mean (95% conf.850) < LOD .570) < LOD . Frank et al.S.720 (. 58 Fourth National Report on Human Exposure to Environmental Chemicals .520-. IPCS.39) < LOD 1.610-.

Hill RH Jr.org/documents/jmpr/jmpmono/v96pr04. et al. Arch Environ Contam Toxicol 1989. Sirons G J. J Expo Anal Environ Epidemiol 2005 Nov. Biomonitoring studies of 2.60(1):121-131.gov/index. Arnold EK. Garabrant DH. Heederik D. 2006. Baker BA. Estimation of occupational exposure to phenoxy acids (2. Hein MJ. Murphy RS. Exposure of homeowners and bystanders to 2. Bailey SL. Arch Toxicol Suppl 1980.4-dichlorophenoxyacetic acid (2. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Khanna RN.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Selected pesticide residues and metabolites in urine from a survey of the U. Pesticides residues in food: 1996 evaluations Part II Toxicology.51(3):152-159. 2005 Charles JM. Reynolds SJ. 914. Sanderson WT. Dhar MM. 2005).4..edu/catalog. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Barr DB. Washington (DC): National Academies Press.4:318-321. Environ Res 1995. References Arbuckle TE. Kutz FW. Erne K. Occup Environ Med 1994. TOX-63 Peroxisone Project (2. Crit Rev Toxicol 2002.4-D) epidemiology and toxicology. Toxicol Sci 2001.4-D and 2. Wilson RD. Atlanta (GA). Hill RH Jr. Absorption and excretion of 2. et al. 2005).15(6):500-508. van Ravenzwaay B. Hanley TR Jr. Ritter L. Philbert MA.htm. National Toxicology Program (NTP). Biomonitoring of herbicides in Ontario farm applicators. Scand J Work Environ Health 2005.4-D.php?record_id=10603. To T..4-D than levels found in the general population. In farm families. Harris SA. Beasley VR. Vet Hum Toxicol 1989.5-T). Assessment of exposure to 2. Campbell RA. Fast DM. et al. Centers for Disease Control and Prevention (CDC).31 Suppl 1:98-104. Tandon JS.4-D in urine does not mean that the level of the 2.4-dichlorophenoxyacetic acid and its forms. Kolmodin-Hedman B. Mandel JS. TOX-63: TOXICITY REPORT CURVES. and the use of protective clothing or equipment (Arbuckle et al.nih. J Toxicol Environ Health 1992.4-dichlorophenoxyacetic acid in man. Tables. Updated March 7. Baker SE.4-D were highest in the farmers who applied the 2.inchem. Acquavella JF. 2005.31 Suppl 1:90-97. Arch Environ Contam Toxicol 1985.nap. Holler JS. 3/17/09 Knopp D. Baker S. Head SL. Biomonitoring for farm families in the farm family exposure study. the amount of pesticide applied. Barr DB. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Mandel et al.4-D will result in an adverse health effect. Carter-Pokras OD. Forestry workers involved in aerial application of 2.4-.32(4):233-257. Beeson MD. J Environ Sci Health B 1992. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. the number of acres to which it was applied (Curwin et al. 2. Honeycutt R. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Frank R. Developmental toxicity studies in rats and rabbits on 2. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Available at URL: http://ntp. Veterans and Agent Orange: update 2002. Survival and Growth Curves from NTP Toxicity Studies.18(4):469-474. Alexander BH. Sircar KP.71(2):99-108. 2005.S. general population. Ripley BD.4:97-100. 3/17/09 Institute of Medicine (IOM). Cook BT. Needham LL. Chapman P. Gregg M. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . International Programme on Chemical Safety-INCHEM (IPCS). Available at URL: http:// www. Cole DC. Review of 2.27(1):23-38. Board on Health Promotion and Disease Prevention.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 2.4-D).niehs. Gupta BN.37(2):277-291. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.4-Dichlorophenoxyacetic Acid).Herbicides the time since application. 1992). Finding a measurable amount of 2.4:427-435. Shealy DB. Bus JS. Harris et al. Stephenson GR.4 dichlorophenoxyacetic acid (2. Curwin BD. Dichlorophenoxyacetic acid. J Expo Anal Environ Epidemiol 2000. Scand J Work Environ Health 2005. Driskell WJ.10(6 Pt 2):789-798. Smith SJ.31(2):121-125. Solomon KR.. 2003. Third National Report on Human Exposure to Environmental Chemicals. geometric mean urinary levels of 2. Xenobiotica 1974. Brody D. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Available at URL: http:// www. Needham LL. Kohli JD.4-D): exposure and urinary excretion..4-dichlorophenoxyacetic acid (2. Pesticide residues in urine of adults living in the United States: reference range concentrations.

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

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

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

In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. et al. and metolachlor herbicides in rats. Thelin GP. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. April 1995. Environ Health Perspect 2000. Barr DB.S.ESTfeature_gilliom. and other herbicides in rivers.php.S. 6/1/09 Whyatt RM. usgs. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.html. Barr DB. Environmental Protection Agency (U.pdf. Available at URL: http://water. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Curwin BD. imidazolinone. Deddens JA. World Health Organization (WHO). 1999. 1998. EPA). Supplemental Technical Information (available on-line only). Thurman EM. Atlanta (GA). California.epa. Centers for Disease Control and Prevention (CDC). streams and groundwater. Burkhardt MR. Comparative metabolism and elimination of acetanilide compounds by rat. Third National Report on Human Exposure to Environmental Chemicals. Geological Survey (USGS).gov/nawqa/pnsp/pubs/circ1291/ supporting_info.pdf.111(5):749-756. 4/2/09 U. Feng PCC. Striley CA. Environ Sci Technol 2005. J Expo Anal Environ Epidemiol 2005. reservoirs and ground water in the Midwestern United States.248(2-3):115-122.S. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.gov/nawqa/ pnsp/pubs/wrir984245/text. Reregistration Eligibility Decision (RED) Metolachlor. Chem Res Toxicol 1998. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. EPA 738R-95-006. 2007.248(2-3):123-133. Davison KL. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Camann DE. Hladik ML.int/water_sanitation_health/dwq/chemicals/ metolachlor. Coleman S. R. Xenobiotica 1994. Barr JR. March 2006. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Sci Total Environ 2000. Feil VJ. Geological Survey (USGS). 3/26/09 U. Hsiao JJ.gov/nawqa/pnsp/pubs/files/051507. Reynolds SJ. acetochlor. 98-4245 (by Barbash JE. Biagini RE. Sacramento. Occurrence of sulfonylurea.usgs. revised February 15.S. Casida JE.who. Wratten SJ. Sanderson WT.pdf 3/30/09 Hines CJ. Metolachlor in Drinkingwater.gov/oppsrrd1/ REDs/0001. Shoemaker DA. Larsen GL. U.39(17):6561-6574. Available at URL: http://water. Kinney PL.37(4):10881093. Kolpin DW.usgs.S.108(12):1151-1157. Heederik D. Available at URL: http://water. 2005. Circular 1291. Available at URL: http://www. Hein MJ. sulfonamide. Ward EM. Quistad GB. 2003. et al. Ann Occup Hyg 2003. Dialkylquinonimines validated as in vivo metabolites of alachlor.24(10):1003-1012. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Brown KK. Linhart SM. Background document for development of WHO Guidelines for Drinking-water Quality.11(4):353359. Environ Health Perspect 2003. Furlong ET. Andrews HF. Available at URL: http://www. Peter CJ. Hodgson E. Gilliom RJ).47(6):503-517.15(6):500-508. Linderman R.Herbicides References Battaglin WA.41:3409-3414. Roberts AL. Sci Total Environ 2000. Rose RL. Gillion. Pesticides in U. Kolpin DW. Jefferies PR. Alavanja MC. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Environ Sci Technol 2007. 1992-2001. J Agri Food Chem 1989.

5-Trichlorophenoxyacetic Acid CAS No.5-T and 2. Ester forms of 2. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. 2007). hypotension.5T is rapidly absorbed via oral and inhalation routes. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness...4.4. 1986.5-T has been rarely detected in ground waters (USGS. The half-life of 2. 2004). dizziness. 2.4. 1974). At low levels. 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.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4-D were used as defoliants in the Vietnam War (e.5-T was once applied as either an aqueous salt or as an oil-soluble ester.5-T degrades to 2.4. which may vary for some chemicals by year and by individual sample..4.5-T is eliminated mostly unchanged in the urine. Chlorophenoxy herbicides act as plant growth hormones.5-trichlorophenol and other degradates.4. 2. myotonia. 2.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Nelson et al.4. population from the National Health and Nutrition Examination Survey. 1989. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. these herbicides can enhance plant growth.5-Trichlorophenoxyacetic acid (2.1.5-T.4.g. headache. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD.Herbicides 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1992. 1992). Kohli et al. 93-76-5 General Information 2. and concern about contamination with 2..4. 2.4.4. ranging from several weeks to many months. Mohammad and St. it is not well absorbed through the skin. Agent Orange).S. < LOD means less than the limit of detection.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. Omer.5-T in soil varies with conditions. but higher levels are herbicidal.. renal and hepatic injury.. the general population is unlikely to be exposed to it.7.2 and 0.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.5-T (Holson et al.4. Epidemiological studies have reported associations of several types of cancer. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2.5-T use as a herbicide in 1985. Given the commercial unavailability of 2. 64 Fourth National Report on Human Exposure to Environmental Chemicals .4.4. Although 2.4. Human health effects from 2.4.3. abdominal pain. nausea. and delayed neuropathy (Bradberry et al. Once absorbed into the body. Survey Geometric mean (95% conf.

4.4. 1980).5-T reflect recent exposure.epa.4. IOM. IPCS.S.4. Biomonitoring Information Urinary levels of 2.5-T than levels found in the general population.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2005).4.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.S.7. Fourth National Report on Human Exposure to Environmental Chemicals 65 . 2004). 1992).5-T were generally below the limit of detection. 2003.5-T also were below the limit of detection (Kutz et al.S. urinary levels of 2. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 1996. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. It is unclear whether these associations are related to the chlorophenoxy herbicides.4. Urinary 2. similar to results of NHANES II (19761980).8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.EPA at: http://www. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2005.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2.5-T does not mean that the level will result in an adverse health effect. Biomonitoring studies on 2. Mean urinary levels of 2.EPA.4.5-T itself is not mutagenic. Pearce and McLean. Survey Geometric mean (95% conf. or to contaminants in the herbicide formulations (specifically 2.Herbicides or contaminated herbicides. Additional information is available from U. 2. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.4.4. 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. in which urinary levels of 2.3. population from the National Health and Nutrition Examination Survey. U.. Finding a measurable amount of 2. other exposures.gov/pesticides/. 2002.

4. gov/oppbead1/pestsales/01pestsales/market_estimates2001.php?record_id=10603. 2004. Environmental Protection Agency (U. Toxicol Rev 2004.4. Multireplicated dose-response studies with technical and analytical grades of 2. Nelson CJ. Vet Hum Toxicol 1989.htm.4.4. Erne K.5-T). Carter-Pokras OD. Developmental toxicity of 2. Gaines TB. Cook BT.EPA). May. International Programme on Chemical Safety-INCHEM (IPCS). Dichlorophenoxyacetic acid. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.4. Wolff GL.4. McCallum WF. Veterans and Agent Orange: update 2002. U. Gaines TB. Garabrant DH. Proudfoot AT.31 Suppl 1:1825. LaBorde JB.epa.5-trichlorophenoxyacetic acid (2. et al.5-t mixture. Dhar MM. II.4:318-21. Mohammad FK. Khanna RN.EPA. Brody D.4.31(2):121-125. Sheehan DM. Poisoning due to chlorophenoxy herbicides. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Nelson CJ.8(5):551-60. Holson JF.org/documents/jmpr/jmpmono/v96pr04. Fundam Appl Toxicol 1992.S. Kutz FW.4-D/2.5-T).4-D) epidemiology and toxicology.pdf. Scand J Work Environ Health 2005. Holson JF. Washington (DC): U. 3/17/09 Institute of Medicine (IOM). Third National Report on Human Exposure to Environmental Chemicals. Tandon JS. Agricultural exposures and non-Hodgkin’s lymphoma. Behavioral and developmental effects in rats following in utero exposure to 2. Neurobehav Toxicol Teratol 1986.4-dichlorophenoxyacetic acid (2. Gaylor DW. St Omer VE. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Arch Toxicol Suppl 1980. Gupta BN. Crit Rev Toxicol 2002. Kolmodin-Hedman B. general population.5-trichlorophenoxy acetic acid in man. 914. Pesticide industry sales and usage . I. Estimation of occupational exposure to phenoxy acids (2. Available at URL: http:// www. McLean D.inchem. Pearce N. Review of 2. Philbert MA. 210:250-255.32(4):233-257.S.4. J Toxicol Environ Health 1992.19(2):286-297. Absorption and excretion of 2. discussion 5-7. Selected pesticide residues and metabolites in urine from a survey of the U.5-T in four-way outcross mice. Washington (DC): National Academies Press. LaBorde JB. Bradberry SM. 3/17/09 Kohli JD.4-.37(2):277-91. S.nap.2000 and 2001 market estimates. Available at URL: http:// www. 2003. Vale JA. Arch Int Pharmacodyn Ther 1974. Atlanta (GA). 2005.23(2):65-73. Fundam Appl Toxicol 1992. Sircar KP. 2. Available at URL: http://www. Murphy RS. Board on Health Promotion and Disease Prevention. Office of Prevention Pesticides and Toxic Substances.Herbicides References Arnold EK. Pesticides residues in food: 1996 evaluations Part II Toxicology. Centers for Disease Control and Prevention (CDC). Developmental toxicity of 2.5-T).5-trichlorophenoxyacetic acid (2. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .19(2):298-306.S. Beasley VR.4-D and 2. et al.edu/catalog.

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

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

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

4-18.077-.1) 15.1) 20.140) .9 (12.130-.063-.086-.8-25.110-.130) .117) < LOD .120 (.6) 16.5-17.100-.1 (13.S. 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 9.138) .4) < LOD < LOD 16.190) .058) < LOD .5 and 7.103 (. which may vary for some chemicals by year and by individual sample.093) .062-.4 (12.8 (18.0 (11.7 (<LOD-15.4) 19.8.8-24.242) .3-21.1-19.1 (18.102 (.5) 15.110 (.075) < LOD .9-23.30 (8.8-17.8) < LOD 8.00 (8.60-10.1-16.90) 90th 15.0 (15.9-22.130) .100-.160 (.090-.056-.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .3 (18.7 (14.7 (15.064 (.4) 14.060) .9 (13.073-.064) 90th .090 (<LOD-.8) 15.147 (.109 (.084-.109-.6-24.139 (.40-9.8-19.8-17.062 (.109-.6) 19.5-17.2-15.139 (.089 (.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 8.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.100) .190) .9-38.138 (.158) .2) 12.100-.4) 20.0 (10.090 (.7-19.6-24.180) .160 (.00-14. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD .0) 19.110) .1-18.120 (.055 (.0) < LOD 9.9 (12.2) 11.062 (.0) 21.112) 95th .4-17.103 (.80-9.50) 15.048 (<LOD-.120) .3 (13.108-.2) 14.70 (7.160) .0-25.5) 21.098 (.50 (8.9 (14. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.4) 539 456 484 487 980 885 Limits of detection (LOD.5-15.1) 13. see Data Analysis section) for survey years 01-02 and 03-04 are 10.40-10.110 (.8 (9.090-.7) 15.150 (.130) .1-24.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.077 (.4 (12.130-.5 (<LOD-11.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.054-.30 (8.100) .054-.110) .049-.7-22.140 (.090-.10 (<LOD-16.1) 14.070 (<LOD-.059 (. population from the National Health and Nutrition Examination Survey.101) .3 (18.6 (15.069) < LOD < LOD .9 (13.2) 15. Fourth National Report on Human Exposure to Environmental Chemicals 79 .120 (.3 (19.130 (.080 (.180) .80 (<LOD-10.3 (14. population from the National Health and Nutrition Examination Survey.1) 10.5 (16.080) .113 (.1) 15.096-.4) 95th 20.8 (11.149) .120-.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.6 (14.6-33. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110 (.100 (.80-10.116) .170) .112-.6) 9.054-.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .080-.088-.147) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .6 (15.083-. Survey years 01-02 03-04 Geometric mean (95% conf.140-.070) .070-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.150 (.0 (10.8) 14.1) < LOD 9. Survey years 01-02 03-04 Geometric mean (95% conf.S.5) 19.053 (<LOD-.124) .4) 21.130-.0-21. Serum Dieldrin (whole weight) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.

html. Hartvig HB. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. et al.html.150:263-271. Ginsburg KS.atsdr. J Toxicol Environ Health 1989. Schulte P.gov/toxprofiles/ tp1. Olea N. Soto AM. Aldrin and Dieldrin [online]. Int Arch Occup Environ Health 1994. Priestly BG. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Serrano FO. Demographic and seasonal influences on human serum pesticide residue levels. Sanchez-Ramos J. Reprod Toxicol 2000.352:1816-1820. Tully DB. 2007 [online]. Corrigan FM. No:429-436. are nonestrogenic in transfected HeLa cells. Li AA. Grajewski B. Brock JW.59:229-234. 1992-2001. Chung KL.26:701-719. Academic Press. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.54:1431-1443. Jr. Jorgensen T.org/documents/ehc/ ehc/ehc91. Smith AG.64-65 Spec. PA. Basit A.cdc. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Toxicol Lett 1992. Pesticides in the Nation’s Stream and Ground Water. Turner W.cfsan. Eds. Environ Health Perspect 1995. Kanthasamy AG. Six high-priority organochlorine pesticides. Toxicological profile for aldrin/dieldrin [online]. Vol. Chemosphere 2004. Grandjean P. Chlorinated Hydrocarbon Insecticides. toxicology. Wienburg CL. Carlson JN. New York. September 2002. 2 Classes of Pesticides. Teta MJ.103(Suppl 7):113-122. References Agency for Toxic Substances and Disease Registry (ATSDR).inchem. David VL. either singly or in combination. Daniel SE. Kitzazwa M. and lymphocyte sister chromatid exchange. Mumtaz MM. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. 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.gov/ circ/2005/1291/. Ellis H.htm. Facca A. J Occup Environ Med 2005. bioaccumulation. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. International Programme on Chemical Safety (IPCS). August 2008. Environ Health Perspect 2001. Lancet 1998. Kanthasamy A. Available at URL: http://www. Cox. 15. Song S. Anantharam V. 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. Cancer Epidemiol Biomarkers Prev 2000. Frey JM. Environmental Health Criteria 91. United States Geological Survey (USGS). Available at URL: http://www.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994).14:95-102. Patterson DG Jr. Rosellini RA. Edwards JW. Available at URL: http://pubs. Available at URL: http://www. 4/21/09 Hoyer AP. Roy ML. Needham LL.66(4):229-234. 4/21/09 Bates MN. Buckland SJ. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Shore RF. Finley B. plasma dieldrin. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Stehr-Green. J Toxicol Environ Health. Sonnenschein C. 731-915. et al. Fernandez MG. Inc. 1989. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Mann D.47:1059-1087. Revised Feb.fda. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Neurotoxicol 2005. Exp Neurol 1998. Andersen A. Mink PJ. VT. and epidemiology in the United States. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Chapin RE. 4/21/09 Jorgenson JL. Psychopharmacology (Berl) 1987. Organochlorine exposure and risk of breast cancer. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. 80 Fourth National Report on Human Exposure to Environmental Chemicals . 6/1/09 Ward EM. McIntosh LJ. Part A 2000.91(1):122-126. Narahashi T. In Hayes WJ.usgs. Patterson DG Jr.109(Supp1):113-139.27:405-421. Organochlorine insecticides in substantia nigra in Parkinson’s disease.9:1357-1367. Garrett N. pp. 1991. Handbook of Pesticide Toxicology. Food and Drug Administration (FDA). Jr and Laws ER.gov/~dms/ pesrpts.

see Data Analysis section) for Survey years 99-00.5) < LOD < LOD 9.6) 8. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.20 (<LOD-11.7 (<LOD-13.4) < LOD 11.1) 30.6 (25.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.4-40. Since 1992. and in soil.5) 38.10-11. and 7.1 (<LOD-12.0 (32.0) 27.5) 10.7-12.70 (<LOD-10.5-47.2-21.9) 47.9 (15.5) 37.6) 39.4) < LOD < LOD < LOD 23.6-12.7-39.1-51. Until 1988.7 (10.3) 18.2) 46. < LOD means less than the limit of detection.6) < LOD 11.3 (25.36-11.8-20.0-12.1-25.4) 22.0) 37.8) 27.8-43.8-42.2) 34.3) 10.7) 19.3 (11.9 (21.9) 10.1 (44.5 (<LOD-12.1) < LOD < LOD < LOD < LOD < LOD 8.7-56.0 (20.9) 11.7-70.9) 37.8 (17.8) 52. Fourth National Report on Human Exposure to Environmental Chemicals 81 .4) 12.8 (40.8 (17.37 (8. 2007).63 (8.8-73. Consequently.8) 18.3 (28.9 (36.6) 49.1) * 11.9 (11.8) 44.2) 22. 01-02.9) 13.8) 52.4-45.0) 31.8) 53.4 (30.5) 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. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.4 (10. which may vary for some chemicals by year and by individual sample. chlordane was used to kill termites and other insects on agricultural crops.5-41.4 (<LOD-12.0) 21.5) 44.7 (34.3 (27.8.1) 16.2-26.4-14.7 (42.5 (33.82-11.9-38. 1994).5. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.8-31.3) 18.. from the early 1950’s until the mid-1980’s.3-45.5-40.1 (11.2-56.0 (<LOD-12. Survey Geometric mean (95% conf. and 03-04 are 14.6) 36.4-51.S.7) 31. fish. the technical grade product of each chemical contains 10%-20% of the other chemical.2 (36.9-40.9 (26.1-65.0-18.5) < LOD < LOD < LOD < LOD 13.1 (16.6-53.4) 37. buildings.9 (29.0) 20.6 (16.3 (26.9) 23.9 (26.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.8-23.0 (26.0-13.69-10.7-25.2-49. 10.9) 31.6-45.1) 90th 34.6 (43.4 (30.5-65. 2007).7 (19.2 (39.5) 56. 57-74-9 Heptachlor CAS No.6-24. respectively.6) 23. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 41.9 (31.1 (<LOD-12.3 (21.3-43. 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.5-43.1 (27.2-28.3-32.2 (28.5 (31.6) 48.9 (18. lawns. Chlordane is not currently produced or used in the U.6-18.6-24.2) < LOD 11.7 (34.7 (17.8 (10.5 (34.4 (35.S.8 (42.9) 17.1-50.3 (20.7) 42.1) 22.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.7) 35.1 (20. 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. and dairy products are the usual sources of exposure to these chemicals in the general population.0-61.7) 19.8-61.2) * 12.0-33.8-33.2) < LOD 11.9-42.10-18.9) 23.20-10.2) 33.4) 39.7) 28.5 (8.0 (16.7-14.6 (9.5. foods high in fat such as meat.2) 37.7 (<LOD-32.0 (37. 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.90 (8.1 (17.9-21. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.6) 11.6) 9.S.2 (37.1-25.4) 29.1-15.7 (32. heptachlor use has been limited to treatment of fire ants near power transformers.1 (15. Technical grade chlordane had contained 7% trans-nonachlor.5-32.9-21.89-10.5-42.6) 9.9) 11.2-49.3 (9.3) 10.9 (17. As a result of the manufacturing process.1 (25.1) * 11.1-19.6) 20.74 (<LOD-10.Organochlorine Pesticides Chlordane CAS No.8-32.30-11.3) 41.20-11. in addition to trace amounts of numerous other related compounds (ATSDR.7) 9.8-33.1 (40.7 (43.3-45.4-21.0-67.5-44.2 (9.6 (9.9 (11.9) 39.3 (<LOD-19.5-13.3) 37.9) 36.2 (10.3-24.1) 30.6) 48.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2 (41.1 (<LOD-12.4) 18. 1994. population from the National Health and Nutrition Examination Survey.9 (15.5) 9.3-49. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.8 (10.4 (22.2 (21.0) 75th 20.8 (18.0-25.5-38.5 (41.4 (31.2) 36.5) 21.10 (8.

063) * .280-.120 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.246-.300) .373) .062) < LOD .250 (.074-.057 (.S.320 (.140-. and alterations in immune function of offspring. 2007.126 (. and breast milk is a major excretion route in lactating women.130-.220-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans. heptachlor.070-.199-.320) .058-.253-.370 (.146) .189 (.140 (.290-.240-.271 (.320) .430) . 1996.170-.210 (.061-.080) .100-.055-.260 (. 1986).053-. dermal.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 * * * * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.056 (.200-.128 (. 82 Fourth National Report on Human Exposure to Environmental Chemicals .063) .080) .126) .060 (<LOD-.057-.050-.133) 90th .049 (<LOD-.130 (.203-.230-.083) .302) .170) .370 (. 1977b.140 (. FDA established allowable residues of chlordane.450) .310-.510) .245-. The major metabolite of heptachlor is heptachlor epoxide. 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.150 (.068) 75th .104-.240-. Shindell and Ulrich.066-.300-.287) .083 (. Rogan. 2002. Elimination of all these chemicals from the body occurs over months to years.230-.280 (.080) .250 (. Survey Geometric mean (95% conf. Takahashi et al.220-.087-. Acute.070-.079) .170) .140-.310) . In laboratory animal studies.280-.069 (<LOD-.290) . 2006). chronic doses of heptachlor have produced liver enlargement and injury.320 (.170) .250-.560) .068) .070 (<LOD-..242-.258 (. Chlordane and heptachlor are absorbed after oral..269 (.380) .112 (.058-. The U.290) .290-.208 (.258-.310) .066 (.073) < LOD < LOD < LOD < LOD .130-..140) . and heptachlor epoxide in foods and bottled water.350 (.189-.130-. neonatal mortality.348) .073 (.160) .140 (.180-.100 (.300) .077) .170) .079) < LOD < LOD < LOD .065-.165-.350) .120-.410) .148-.310) .057) * .120-.440) .136) . 2001.077) .320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .280) . which may vary for some chemicals by year and by individual sample.207) .320 (.300 (.210-. OSHA has established occupational exposure criteria..200 (.130) .070 (<LOD-.146) < LOD < LOD .168-.260 (. 1991.070) .180) .230) .200-.230 (.240) .071 (.370 (.160 (.300) .047 (<LOD-.240 (. Smith.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.090) .290 (.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .070 (.106-.115-.180-.225 (. IARC.130-.130 (.130-.270 (.063 (.190-.066 (<LOD-.150-.220 (.340) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD . EPA has established environmental criteria for chlordane and heptachlor. 1991).048-.115 (.100-.090) .330 (.080 (.216-. 1981).104) . Le Marchand et al.090-.053-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide. to heptachlor.068-.070) < LOD < LOD < LOD < LOD < LOD .110-.160) . and inhalation exposure.310 (.070 (<LOD-.230-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.150 (.400) . characterized by seizures and paralysis.058 (.149 (.075 (.092) .070-.231) .063 (.070 (<LOD-.286 (.180) .140 (.063-.S.150 (.430) .280 (.082 (. 1977a.110 (<LOD-.064) < LOD .210 (.260-.320 (.160) .300) .190-.100 (<LOD-.286 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.223) . which is also persistent in the body (ATSDR.280-.170) .350 (.315 (. 2007).063 (. and the U.260 (.091) . Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.340) .130 (.108-.204 (.213) * .450) . population from the National Health and Nutrition Examination Survey.400) .148) .150) .207 (.S.270 (.230 (.270 (.190-.Organochlorine Pesticides (Dallaire et al.200-.050 (<LOD-.119 (.290-.066-. 1986). Chlordane is metabolized primarily to oxychlordane and to a lesser extent.077) .076) < LOD .120-.227) < LOD .063 (.130) .067 (. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.077) .360) .080 (.

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

9-29.2 (<LOD-25.2 (<LOD-62.8-24.3) 23.6.6) < LOD < LOD < LOD 27.0-17. see Data Analysis section) for Survey years 99-00.8) 14.8-24. < LOD means less than the limit of detection.1 (16. 01-02.3) 22.5 (18.8) 19. and 7.S. which may vary for some chemicals by year and by individual sample.2-27.7-25. and 03-04 are 14.1-16.4 (<LOD-54.1) 20.6 (11.6) 14.2-17.7 (16. population from the National Health and Nutrition Examination Survey.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9-29.8-23.3-18.2) 15.6 (12.3) 10.6-21.8) 13.8) 21.1-29.8 (13.8) 20.8 (18.1-15.0-17.8 (<LOD-23.10-13.0 (15.6 (8.9) 15.20 (<LOD-9.9-16.4 (15.2-27.5) 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.8 (13.6) 13.6 (13.8) 16.7 (10.4) 18.8) 15.1) 13.40) 15.5.90 (<LOD-9.4 (<LOD-19.9 (12.5 (10. respectively.0-54.0) 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 13.3) 18.50) < LOD < LOD < LOD 17.7-19.5 (<LOD-32.7 (13.0) 13.2 (<LOD-16.1) 23.1-38.8.8 (15.8-46.0 (11.3 (<LOD-25.8-24. 84 Fourth National Report on Human Exposure to Environmental Chemicals .2) 13. 10.5 (<LOD-21.2-16.2) 26.9) * * * 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 8.4) 21.5) 19.9-25.4 (11.3 (13. Survey Geometric mean (95% conf.6 (16.6 (16.3) 16.4 (11.0-16.6 (<LOD-27.5) < LOD 14.5 (11.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.7-18.8) 19.2 (18.8) 14.9-23.9 (15.0-19.6-17.1 (19.3) 18.5 (11.2) 20.3) 27.6) 22.8 (18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (14.8) 13.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.3) 18.

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

7-160) 86.5) 14.1) 32.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.3-74.9) 51.9 (36.2) 39. see Data Analysis section) for Survey years 99-00.4 (11.7-17.3-58.1) 17.2-18.9-58.3) 19.8-110) 59.1) 18.7-32.4) 107 (84.1) 17.1) 30.2 (26.0-113) 68.8.9-35.6) 10.5) 77.1) 17.6) 13.6 (<LOD-14.10 (<LOD-11. and 03-04 are 14.1) 31.5-36.8-19.2) 19.8) 80.2 (36.4) 59.2 (14.9 (15.2) 59.6-54.5-20.7 (59.8 (26.7-38.7) 15.8 (19.7) 35.0) 49.7-29. < LOD means less than the limit of detection.8) 47.0 (15.6 (56.5 (25.6 (12.3) 16.3 (56.1 (41.1 (47.2) 20.9-20.7 (28.7-22.0-93.0) 33.5 (15.7) 56.1-16.4 (16.9-36.9-40.8-16.8 (<LOD-20. interval) 18.1-20.5) 22.1 (17.2 (7.8 (28.5 (44.5) 9.3-86.0-23.3 (14.1-22.7 (74.2) < LOD 10.0 (29.5) 30.8 (30.2-16. respectively.0-37.0) < LOD < LOD 8.2 (25.3) 32.5-87.2) 30.5-69.9 (28.9) < LOD < LOD < LOD 20.9-45.6) 56.5) 78.6) 54.0-68.1) 16.3) 30.2) 34.8 (17.5-17.3) 32.8-129) 74.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.4) 19.2 (15.4-62.3-32.0) 13.0-20.1-18.8-19.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.7) 28.1) 17.0 (48.4-23.7 (11.0 (42.6-22.0-22.8-77.7) 78.1 (22.7) 73.5) 26.2-37.0 (16.3) 18.0) 19.5) 90th 55.7-21.9 (15.0-38.7 (35.3 (14.6) 82.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. which may vary for some chemicals by year and by individual sample.0) 18.7) 14.0 (16.2-18.5 (15.1-16.0-23.3-21.2 (14.1-34.5) 19.6 (50.8 (26.4-36.2 (19.3) 25.8 (26.1-51.2 (27.8-21.3-50. Survey Geometric mean (95% conf.1-34.4 (12.S.1) 14.5) 20.8 (12.6 (57.1-126) 67.9 (16.5-95.1-55. and 7.7-20.9-22.7) 59.7 (16.5 (45.6-66.9 (51.6-19.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.4-18.6 (15.3) 30.3 (45.8 (49.9-65.1) 17.0) 75th 31.6 (16.0) 40.3) 15.1) 78.9-64.2-23.4-22.4 (45.8 (11.86-13.1) 78.8 (13.3) 36.8-16.2-21.3-39.3) 18.7-34.3 (58.6 (56.9) 51.1) 18.9) 14.2 (60.9 (29.7) 52.5-111) 68.1) 17.6 (52.8 (13.9-89.6-20.3 (16.3) 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.0 (14.0 (62.0 (19.4-35.8 (16.8 (15.9) 14.7-113) 68.8-41.9 (<LOD-14.3-57.9-69.6) 25.7-35.5-19.8 (71.5) 35.3-30.8) 51.4) 16.7 (13.7-23.1) 62.0 (13.6) 56.4) 55.5) 14.8) 19.7) 78.0-93.1 (65.8 (28. population from the National Health and Nutrition Examination Survey.5 (13.4-67.5) 48.6 (32.4) 20.3 (17.9 (19.9-65.4) 48.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.3 (49.0 (15.4 (30.8 (45.7-18.70 (<LOD-12.0 (13.0-123) 74.4 (67.6-82.7 (18.6) 84.8 (28.2-88.6-88.2) 17.8-90. 86 Fourth National Report on Human Exposure to Environmental Chemicals .9 (51.1 (10.5.0-59. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 01-02.1 (48.7 (30.5.8-90.7-77.1) 17.2 (64.5) 36.4 (28.9 (66.8-79.8 (42.8-67.7 (59. 10.0-24.6) 34.7) 17.0-143) 112 (68.4-52.2-17.9 (47.0 (60.6) 60.0 (42.1-28.2 (59.

630) .565) .510-.105 (.190-.320-.100-.430-.690) .173-.220 (.409-.461 (.171-.360-.098-.131) .202 (.320-.093-.078-.430-.090 (<LOD-.127) < LOD < LOD .089 (.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.288-.310) .161-.220 (.103 (.559) .240) .340-.096-.093) .490-.090-.190-.096) .047-.080) .069-.100-.120) .410-1.343 (.400-.160-.071 (<LOD-.470 (.095-.150) .100-.108 (.060-.116) .098 (.590 (.210-.055 (<LOD-.081 (.840) .600) .109 (.090-.130) .330-.084-.232) .420) .100 (.120) .390-.120-.830) .272-.081-.098) .400) .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.414 (.960) .430-.090) .460) .205 (.220 (.124) .080-.091) .288 (.458 (.211) 90th .470-.260) .190-.210 (.110) .090-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .062 (.158-.125 (.085-.090-.114) .440-.370 (.112 (.550 (.130) .068-.120 (.106 (.417 (.370 (.270-.220 (.191 (.161) .240-.210) .440) .190-.490 (.234) .085-.390 (.220 (. which may vary for some chemicals by year and by individual sample.111 (.630) .367) .097) .397-.470 (.130) .186 (.080-.145-.087 (.122) .079-.140) .340) .190-.082) .470 (.110-.520) .069) .330-.210) .590) .286-.460) .109 (.680) .410-.104-. interval) . Survey Geometric mean (95% conf.120) .150) .098 (.350 (.590 (.300-.061-.300) .110 (.220 (.210 (.080 (.160 (.580 (.395) .096-.395-.490 (.390 (.110 (.135 (.112 (.120-.500) .310-.041 (<LOD-.119) < LOD < LOD < LOD .120-.250) .930) .085-.090 (.380 (.301-.117) .110 (.390 (.106 (.128 (.100 (.126) .651) .120 (.450) .120) .640 (.285-.594) .240) .129) .110 (.510 (.183 (.630) .134) .106 (.20) .260) .099-.113) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.054-.110 (.186-.405) .130) .130 (.103 (.350-.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .684) .108) 75th .520 (.092 (.340-.220) .S.111-.093-.470-.580 (.800) .091-.220 (.092 (.130) .580 (.324 (.180-.400 (.355 (.460-.130) .094 (.104 (.230 (.060 (<LOD-.130) .130 (.141) .070 (.080-.079-.250) .400-.108) .480) .310 (.242) . population from the National Health and Nutrition Examination Survey.240) .116 (.400 (.680 (.170 (.141) .210 (.830) .237) .390) .240 (.600 (.180-.190-.290-.490) .122) .520 (.310-.573 (.250) .100-.177-.119) Selected percentiles ( 95% confidence interval) Sample 95th .330 (.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 .210-.317 (.090-.220 (.093-.116-.310-.113) < LOD .760 (.090-.099-.310-.540) .390 (. Fourth National Report on Human Exposure to Environmental Chemicals 87 .279-.120 (.078 (.080-.390) .327 (.690) .565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .280) .060) .360-.125) .420 (.110 (.237) .180-.371) .497-.210) .

Head SL. Takei G. Dewailly E.org/documents/iarc/ vol79/79-12. Wong L. Saidein D. Wolff MS. New York. Bull Environ Contam Toxicol 1981:27:506-511. International Agency for Research on Cancer (IARC). Available at URL: http://www. August 2007.html. 6/1/09 National Toxicology Program (NTP). gov/toxprofiles/tp12.nih. 2 Classes of Pesticides. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Shindell S and Ulrich S. Circumpolar maternal blood contaminant survey. Dendle WH. Jaraczewska K. Bioassay of heptachlor for possible carcinogenicity. Aune M.niehs. Bioassay of chlordane for possible carcinogenicity. Inc. 4/21/09 Dallaire F. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii.org/site/foundation/ research/projects2. Mortality of workers employed in the manufacture of chlordane: an update. 6/1/09 Rogan WJ.150:981-990. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Atuma S. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum.9:1-109. 731-915. Available at URL: http://www.pdf.inchem. Lawrence River (Quebec. Siegel BZ. Arch Pediatr Adolesc Med 1996. 2006. 79. et al.nih. Available at URL: http://ntp.html. 4/21/09 Baker DB.gov/ntp/ htdocs/LT_rpts/tr009. 1994-1997 organochlorine compounds. Available at URL: http://www. LeMarchand L. Barker J. Covaci A. Loo S. 88 Fourth National Report on Human Exposure to Environmental Chemicals . 1963-1967. et al. Environ Health Perspect 2003. Handbook of Pesticide Toxicology.cdc. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Lulek J.html.84:151-161. Chashchin V. 9/25/07 International Programme in Chemical Safety (IPCS). Environ Health Perspect 2002.259(3):374-377. Chlorinated Hydrocarbon Insecticides. Vol.atsdr.heptachlor. Charles MJ. National Toxicology Program (NTP). Available at URL: http://ntp. Bleiweiss IJ. Vol.110(8):835-838.htm. Hertz-Picciotto I. Gilman A. Willman E. Environ Res 2000.gov/ntp/ htdocs/LT_rpts/tr008. Keller JA. Organochlorines in Swedish women: determinants of serum concentrations. Smith AG. 2001. Jr and Laws ER.pdf. 1986. Concise International Chemical Assessment Document 70 Heptachlor [online]. KalubaSkotarczak A. Kolonel LN. Takahashi W.111:349355. A Report to the Hawaii Heptachlor Research and Education Foundation.28:497501. Dewailly E. Available at URL: http://www. Stehr-Green P. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. maternal serum and milk from Wielkopolska region.inchem.Summaries & Evaluations. Muckle G. Toxicological profile for heptachlor and heptachlor epoxide [online]. Ayotte P. Canada).41:145–148. Hawaii Med J 1991. International Agency for Research on Cancer (IARC) . Distribution of polychlorinated biphenyls. et al. Senie R. Chlordane and heptachlor [online]. Glynn AW. In Hayes WJ. 1979-1980.gov/toxprofiles/tp31. JAMA 1988. Odland JO. Bjerselius R. Drews K. Hansen JC. Royce W. Poland. J Occup Med 1986. Arch Environ Health.htm. Organochlorine exposures and breast cancer risk in New York City women. Organochloride pesticide residues in human milk in Hawaii. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).372:20-31.50(3):108-118. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Academic Press.org/ documents/cicads/cicads/cicad70. et al. Granath F. Jr. Sci Total Environ 2004.niehs.atsdr. Van Oostdam JC.8:1-123. Pollutants in breast milk.cdc. Available at URL: http://www. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Laliberte C. Environ Health Perspect 2002. Voorspoels S. May 1994. 1991 pp. 4/21/09 James RA. Tartter P.330:55-70. Baker DB. Toxicological profile for chlordane [online].110:617-624. 1993. Sci Tot Environ 2006. Wohlleb JC. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Brower S. Eds. Darnerud PO. Berkowitz GS.

DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.6 (9.0-53. 1988). particularly meat.0) 40. or dermal exposure. Fourth National Report on Human Exposure to Environmental Chemicals 89 .5) 25. p.7) 677 756 595 1002 1549 1370 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 10.2) 155 (59.2) < LOD < LOD 9. fish.1’-dichloro-(2.9-34. 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.0 (18.0 (10.5) 23.1) 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 12.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3 (<LOD-31. DDT is converted in the environment to other more stable chemical forms.3 (<LOD-21.3-590) 293 (104-541) 48.0-15. o.6-33. and 7.1 (<LOD-39.5) < LOD < LOD 9.S.7-16.90 (<LOD-12.5 (23.9 (10. It was produced and used in the U.6 (25. particularly for endemic vector and malaria control.S. continues to be the primary source of DDT exposure.0-35. DDT and DDE can cross the placenta. 01-02. Both Serum p. as well as in plant and animal tissues.7.0-27.6 (<LOD-25. < LOD means less than the limit of detection. resulting in fetal exposure. Only a small proportion of DDT is metabolized and excreted (Smith. inhalation.5 (23. see Data Analysis section) for Survey years 99-00.1-71.2-65. DDT was used at one time as a treatment for head and body lice. and water.2-bis(p-chlorophenyl) ethane (DDD). when virtually all use of it was banned. These chemicals are highly persistent in soil.7) 12.3) 21.8. Smith.1) 31. and 03-04 are 20. including 1.4 (23.8-23.2 (<LOD-40.8-39. Survey Geometric mean (95% conf.9) 29.0) 19.9 (21.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. and trace amounts of several related compounds.7 (19.3-16.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. In the body. DDT usually refers to the technical product.0-37.9-28.9 (<LOD-20. and dairy products.8-26.S. population from the National Health and Nutrition Examination Survey.8) 30.6 (31. which is a mixture containing p.1 (23.9) < LOD < LOD 9.p’-DDT (65%-80%).4) < LOD < LOD < LOD 61.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.7) < LOD 18.8) 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. respectively.2) 30.0) 26.5-54.10 (<LOD-12. DDT is converted to DDE and several other metabolites.1 (33. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9) 17.5 (15. The biodegradation half-life of DDT in soil varies from 2 to 15 years. 2008. which may vary for some chemicals by year and by individual sample.p’-DDD (4% or less). food.3-236) 24.1’-(2.3) 28.3) 21. 1991).10-13.9 (10. 1991). It is still used in some countries. after World War II until 1972.5 (14. 2002.6 (22.0 (21.4) < LOD 17. although DDT and DDE intakes have decreased over time (FDA. air. population. DDT can be absorbed after ingestion. sediments.9 (10.2 (11. In the general U.2-95.0) 20.50-11.70 (8.5-36.0-155) 83.p’-DDT (15%-21%).9) 14.7 (15. depending on conditions.4.0 (18.8-17.00 (<LOD-10. Gunderson. 17.8) 15. Food imported from countries that still use DDT may contain the chemical or its residues.3 (27.8) 36.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. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.1-27.3) 22.

population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Calle et al.063 (<LOD-. which may vary for some chemicals by year and by individual sample.074-.180-.108 (. Hayes et al.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 .250-1. accidental exposures.071 (. and seizures. 90 Fourth National Report on Human Exposure to Environmental Chemicals .160-. and altered behavior after neonatal exposure (Eriksson and Talts.150 (<LOD-. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.095) < LOD .200 (.051 (<LOD-. Longnecker et al.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. and duration of lactation. resulting in exposure to nursing infants (Rogan.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 . 2002. 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. In high dose.107) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. fertility.330-4.142 (. 2004. 2006.400) .190 (.201 (.069) .. A workplace standard for DDT has been established by Serum p.530) ..140-. Beard.061) < LOD < LOD < LOD . and o. In laboratory animals. 1956).250 (.150 (<LOD-.180) .343) < LOD .130 (<LOD-.00 (.. 2006). 1997).106) < LOD < LOD . and leukemia have also been inconclusive (ADSDR. 2001). Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. dioxins and furans).120 (<LOD-.627) .. Jusko et al. Mariussen and Fonnum.132-.084 (.146 (.140) .260) .170-.62 (.048 (<LOD-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.130 (<LOD-. lung cancer.054-.Organochlorine Pesticides chemicals are excreted in breast milk.313 (. Survey Geometric mean (95% conf.106-. Jusko et al.065-.230) .S.143) < LOD < LOD ..150-. 2006).180) .087 (. 2006.p’-DDE can produce anti-androgenic effects (Gray et al. 2001). 2001). Gray et al.078-. Snedeker.p’-DDD and p. 1995.240) .00) .106) .01) .079) < LOD < LOD . Studies of DDT exposure and pancreatic cancer.086 (. 2001).180 (.075) 1.071-.170) . overt signs of acute human toxicity include vomiting.150-.059-. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2006).105-. 2000.203) .130-. reproductive organ abnormalities. tremor.114-.g.098-.130 (<LOD-.400 (.290) .420) . 1996).112 (.064 (.. Animal studies reported reduced fertility.150) .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 .34) .146 (.078 (.230) . 1998). other organochlorines.180 (. 2002.220) . Gladen and Rogan... Reproductive effects in humans affecting birth weight. 2002. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al...570-4.068-. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.170 (.220) . DDT may bind to estrogen receptors (Chen et al.080-.128 (. 2002.26) 1.530 (. 2006.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .120-.190-1.240 (.. polychlorinated biphenyls.190 (. have not been consistently demonstrated (Beard..189-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. premature delivery.

In general.Organochlorine Pesticides OSHA and a guidance established by ACGIH. and 03-04 are 18. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.S.. mean serum levels of DDT and DDE in the U. NTP considers DDT as being reasonably anticipated to be a human carcinogen..epa.6. population from the National Health and Nutrition Examination Survey.atsdr. Since the 1970’s.. Survey Geometric mean (95% conf. Heudorf et al. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. Link et al. EPA at: http://www. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al.S. population declined by about fivefold to tenfold.gov/ toxpro2. Smith. 8. respectively.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. Biomonitoring Information DDE persists in the body longer than DDT.S. 1991). respectively. 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. 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.. 2004). In a population-based sample of men and women from eastern Slovakia. 1998. Compared to females in the NHANES 1999-2000 subsample.p’-DDT) as a possible human carcinogen. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. for males and females in the NHANES 19992000 subsample (Pavuk et al. A study of New Zealand adults sampled in 1996-1997 reported median DDE levels that were about threefold higher than the median for adults in the NHANES 1999-2000 subsample (Bates et al. Fourth National Report on Human Exposure to Environmental Chemicals 91 . 2002.gov/ pestcides/ and from ATSDR at: http://www.cdc.8. IARC classifies DDT (p. see Data Analysis section) for Survey years 99-00. compared to levels observed in this Report (Anderson et al. interval) 260 (226-298) Selected percentiles ( 95% confidence interval) Sample 95th 1830 (1410-2300) 2320 (1830-2780) 1860 (1400-2380) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 226 (184-278) 251 (228-278) 203 (163-275) 75th 537 (476-631) 598 (521-699) 509 (376-655) 90th 1150 (976-1350) 1410 (1210-1500) 1170 (836-1570) 295 (267-327) 238 (195-292) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 118 (102-135) 124 (106-146) 105 (84.6 (81.p'-Dichlorodiphenyldichloroethene (DDE) (lipid adjusted) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. 2003).html. Stehr-Green. Declining DDE levels over time have also been observed in the German population. 01-02.... More information about external exposure (i. 2002. and 7.3.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. 2005). 2004). 1989). environmental levels) and health effects is available from the U. 2003.e..

1) 12.10-1.26-10.71) 12.51) 1.05) 1.56-2.57 (1.25 (1.75) 6.54-7.534-.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.66) 3.38 (1.13) 4.796 (.4-19. In the NHANES 1999-2000.61-2.10-5.680-1.820-1.37 (1.23 (7.27-1.00 (6.88 (2.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.456 (.55-9.3 (8.71) 32.18) 1.p’-DDT were below the limits of detection. 1991).02 (2.54 (1.13 (1.9) 5.6) 9.75) 2.30-1.8 (14.91 (6.32-1.59) 6.51) 3.36 (3.430-.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.76) 1. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.50 (2.48 (6.0) 2.92) 1.890-1.56-6.00) 7. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.75 (4. population from the National Health and Nutrition Examination Survey.5) 7..6) 12.520 (. interval) 1.1) 40.22-1.66-4.01-1.57-3.635) 1.6) 9.91) 3.66) 4.34-3.87-16.69 (2.25-16.2 (9.7-20.32-9.88-35.92 (3.59 (1.57-13.55 (2. or p.18-1.57) 2.8 (9.65 (1.40-4.31 (1.385-.6) 11.0 (12.49 (1.63 (6.84-3.66) 1.75 (8.860 ng/L) and DDE (about 14.53) 7.14-9.01-1.01-15. 1971).76-3.68 (2.71 (6.83 (1.02-8.59) 3. less than one percent had detectable serum levels of o.90-8.66) 1.11-1.0 (9.33-1.19) 4.25 (.65) 1.03-1.34) 2.31-12.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.Organochlorine Pesticides nearby agriculture (Botella et al.06) 1.58) 1.63 (1.92 (3.01) 1.12-1.82 (1.26 (1.590 (. Survey Geometric mean (95% conf. Serum p.06) 3.84 (3.18-3.61 (1.6) 8.85-4.43-4.870 (.50-17.14-1.43-8.4 (8..2) 26.18-4.8 (13.5) 16.34-11. 2001-2002 and 2003-2004 subsamples.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.49 (1.6) 13.4) 14.69) 8.557) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.3) 16.34) 6.p'-Dichlorodiphenyldichloroethene (DDE) (whole weight) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.37-1.36-1.97 (3.51-8.2) 19.56) 2.6 (17.63 (1.78 (4.31-2.S.51 (1.p’-DDT.05 (3.16 (2.43 (5.64-2.9 (15. o.32-1.49) 8.21) 90th 7.646) .30-1.5) 5.03-4.75) 1.6 (8.611-1.5) 10.09-1..40-8.40 (3.6 (9.24) 1.6 (7.57 (3.07 (5.58) 75th 3.79) 4.32 (1.70) 1.7-48.p’-DDT (Stehr-Green.39-2.26-2.34 (7.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .99) 1.70-3.01) 1.7) 16.22) .25-14.62-6.0) 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 .39 (3.80 (2.07) 1.01-11.6) 9.64) 3.68-4..85 (1.15-4.41 (1.39) 1.4) 9. serum levels of o.24-17.14 (1.76 (2.2 (9.3 (9.7-19.963-1.10) 2. 2004).53-15.18-1. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.45 (1.623 (.32 (1.19-14.965-1.9-38.01-11.7) 13.488-.77 (1. Finding a measurable amount of p.29 (1.60-13.30 (1.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.10) .9-17.12 (.8 (13.46-2.3) 13.90) 22. 309 versus 268 ng/g lipid.37-16.32) 1.35) 1.69 (1. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE than are found in the general population.66-17.28) 1.68) 2.43-4.53) 1.8-90.46 (1.96) .80) 1.5) 22.54) 8.49 (6.72) 1.02) 1.14) 2.p’-DDT.16-1.66-2.36-2.17-3.7 (8.82) 1.39-1. High mean levels of whole blood DDT (about 3.93 (7.87 (5.17 (3.96) 1. In a subsample of NHANES II (19761980) participants.419-.51-15.516 (.7) 9.37-4.9) 7.27) 3.600) .6) 9.25) 8.8) 15.37-10.63-15.69 (.57 (1.80) 1.40-4.47) 3.45 (1.69) 4.52-6.91-2. 2004).01-5.76) 1.47 (1.18 (6.04 (6.97-4.1) 7. 1989). considerably higher than levels in this Report (Smith.77 (1.52 (3.21) 3.56-3.26) 3.3) 10.59 (1.53 (2.2 (19. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.1 (8.81 (1.04-1.1 (9.14) 2.13-2.48-4.4 (12.25) 1.44) 1.91-3.51-49.00-1.80) 3.81-18.57-2. 2005).59 (4.46 (1.41-12.726) .38 (1.2 (6.00 (.3-43.85-10.24 (1.500-.20 (.11 (2.58) 1.81) 11.12 (6.561 (.30 (1.72) 1.22 (7.36) 3.07) 1.2-32.36-11.81 (7.730) .994-2.9 (26.71 (5.52 (1.81-5.4) 13.

S.4. 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. and 7. which may vary for some chemicals by year and by individual sample. 01-02. 17. Fourth National Report on Human Exposure to Environmental Chemicals 93 .7. respectively.8.Organochlorine Pesticides Serum o. < 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. see Data Analysis section) for Survey years 99-00.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. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. and 03-04 are 20.

Organochlorine Pesticides Serum o. 94 Fourth National Report on Human Exposure to Environmental Chemicals . 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. Survey Geometric mean (95% conf.p'-Dichlorodiphenyltrichloroethane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.S. 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. which may vary for some chemicals by year and by individual sample.

gov/~dms/ pesrpts. Angerer J. Food and Drug Administration (FDA). Neurotoxicol 2000. Patterson DG Jr. Koepsell TD. Henley SJ. Zaidi SS. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Atuma S. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Hanrahan L. Arnold SF. Longnecker MP. Botella B. Gabrio T. Zoellner I.atsdr.53(8):1161-1172. Maternal DDT exposures in relation to fetal and 5-year growth. et al. Zhou H.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Bloom MS.358:110-114. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Calle EE. and polythelia among male offspring. HCH.112(17):1761-1767. Lepom P. Herrman T. 4/21/09 Anderson HA. Kulkarni PK.1-dichloro2. J Assoc Off Anal Chem 1988. Environ Res 2005. Bjerselius R. Rivas A. Biochem Pharmacol 1997. DDT and human health. Longnecker MP. India. Int J Hyg Environ Health 2002. Crespo J. 4/21/09 Gladen BC. Cueto C.fda.7(3):248-264. Darnerud PO. Durham WF.58:1185-1201. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Moysich KB. FDA total diet study. Rogan WJ. DDE and shortened duration of lactation in a northern Mexican town. Levels of DDT. FDA Pesticide Program Residue Monitoring 1993-2006 [online].cfsan. Jr. Granath F. Burse VW. Gladen BC. dietary intakes of pesticides. The Great Lakes Consortium. Ostby J. Krause C. Seiwert M. Int J Hyg Environ Health 2003. Beard J. Piechotowski I. Environ Health Perspect 1998. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.97(2):178192. selected elements. Bates MN. Willman EJ. Schulz C. JAMA 1956. hexachlorobenzene. Garrett N. Chemosphere 2005. Olea N. Sci Tot Environ 2006. Baker RJ. Cerrillo I. April 1982 to 1984. and dichloro(diphenyl)ethylene (DDE). Hum Reprod Updat 2001. CA Cancer J Clin 2002. Bhatnagar VK. Am J Epidemiol 2002. Bull Environ Contam Toxicol 2004. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. and DDD [online]. Chemosphere 2004. Brock JW. et al. Gray LE Jr. Aune M. Wolf CJ. Olson J.72:261265.gov/ toxprofiles/tp35. et al. Zhou H. Am J Public Health 1995. Klebanoff MA. Toxicological profile for DDT. Eriksson P. Buckland SJ. Olea-Serrano MF. et al. Exposure of women to organochlorine pesticides in Southern Spain. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Olson JR.155(4):313-322. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Environ Health Perspect 2004. Davis MD.17(6):692-700. Klebanoff MA. Needham LL. Needham LL. et al. DDE. Vena JE.21(1-2)37-48. Frumkin H. August 2008. Hediger ML. Barr DB. Maternal serum level of 1. Drexler H. Notides AC. Becker K.206:485-491. Kaus S. hypospadias. Biomonitoring of persistent organochlorine pesticides. Effects of environmental antiandrogens on reproductive development in experimental animals. and other chemicals. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Ellis H. Thun MJ. Falk C. Parks L.355:7889. Organochlorines and breast cancer risk. Profiles of ortho-polychlorinated biphenyl congeners. Kashyap R.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT).. Charles MJ. Fourth National Report on Human Exposure to Environmental Chemicals 95 .96:34-40. Organochlorines in Swedish women: determinants of serum concentrations. Vorojeikina DP. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.cdc. September 2002. Environ Res 2004. et al.205:297-308. Brock JW. Hayes WJ. Greenfield TA. et al. Chen CW. Lambright C. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Furr J. Katz SH. Available at URL: http://www. Paepke O. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. lindane (g-HCH).54:1431-1443. Talts U. Jr. Hurd C. Jusko TA. Available at URL: http://www. Glynn AW. Lancet 2001. et al. Swanson MK. Epidemiology 2006. Link B.111:349355. Heudorf U. et al.85:504508.52:301-309.162:890-897. dichlorodiphenyldichloroethylene.71(6):1200-1209. and HCB residues in human blood in Ahmedabad. Saiyed HN.html. Klebanoff MA. Environ Health Perspect 2003. Savitz DA.106(5):279-289. Needham LL. Gray KA.html. Gunderson EL.

150:981-990. Radomski JL.54:1509-520.109:35-47. Rogan WJ. Vol. Rey AA. Chovancova J. Crit Rev Toxicol 2006.36:253-589. Jones CR. Petrik J. Nims R. Pavuk M. Cerhan JR. Comparative pharmacodynamics of CYP2B induction by DDT. Lynch CF. Pollutants in breast milk. PA. Snedeker SM. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Toxicol Appl Pharmacol 1971.20(2):186-193.53:455-477. Deichmann WB. Jr.Organochlorine Pesticides Mariussen E. In Hayes WJ. Academic Press. Reddy AB. J Toxicol Environ Health Part A 1998. J Toxicol Environ Health 1989. New York. Neurochemical targets and behavioral effects of organohalogen compounds: an update. et al. 1991 pp. 731-915. Fonnum F. Chemosphere 2004. Eds. Handbook of Pesticide Toxicology. et al. Pesticides and breast cancer risk: a review of DDT. Demographic and seasonal influences on human serum pesticide residue levels. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. and dieldrin. Astolfi E. children and newborn infants. Smith AG. Fox S. Lubet R. DDE. Environ Health Perspect 2001. and DDD in male rat liver and cultured rat hepatocytes. Stehr-Green. Arch Pediatr Adolesc Med 1996. Schecter A.27:405-421. DDE. Chlorinated Hydrocarbon Insecticides. Jr and Laws ER. 2 Classes of Pesticides. Thomas PE. Inc. 96 Fourth National Report on Human Exposure to Environmental Chemicals .

40 (<LOD-6.09 and 7.S.. Hepatic effects of endrin exposure have included necrosis. endrin usually is not detected in serum of exposed individuals.S.50) < LOD 5. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.. Survey Geometric mean (95% conf. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. Because it is metabolized so rapidly. endrin has been detected with declining frequency in U. Endrin has been detected in soils. total diet surveys (FDA.. Endrin was not widely used as a termiticide. 1992). Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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. Ketoendrin is a major photodegradation product (IPCS. 72-20-8 General Information Endrin. At high doses. In the body. inhalation or dermal exposure routes.20 (<LOD-5.8.S. Smith.60 (5. population from the National Health and Nutrition Examination Survey.30 (<LOD-6. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. unless the dose is high and the exposure is very recent. and occasionally at low levels in sediment and surface waters. and inflammation (Smith. 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. endrin can persist for years. 1996. 1979. Kavlock et al. Endrin is absorbed rapidly after ingestion. Endrin was used as an insecticide. is no longer manufactured in the U. 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. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. rodenticide and avicide. have been cancelled by the U. An epidemic of acute endrin poisoning.Organochlorine Pesticides Endrin CAS No. Over time. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al.20 (<LOD-5. or from contact with contaminated soils and sediments in areas where endrin was applied. largely the result of historical agricultural application or run off from contaminated soils (ATSDR.10 (<LOD-5. Endrin does not accumulate in body tissues (IPCS. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. < LOD means less than the limit of detection. unlike aldrin and dieldrin. IPCS. manufactured. All uses of the pesticide in the U. Depending on soil conditions. which may vary for some chemicals by year and by individual sample.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 5.50) < LOD < LOD < LOD 5. or discarded. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. 1987).40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. 1981). 1992.S.. anti-12hydroxyendrin. 2008). a stereoisomer of dieldrin. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. EPA.10 (<LOD-5. Fourth National Report on Human Exposure to Environmental Chemicals 97 . 1991). 1991).S.30) < LOD 5. 1992).40-5. endrin is converted rapidly to its major metabolite. fatty infiltration.

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

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

particularly by consuming fish.3 (22. primarily as a fungicide and seed treatment until the U. < LOD means less than the limit of detection. distributes widely throughout the body.7 (27.3-20.0) < LOD < LOD 15.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. respectively.4-15. Urinary metabolites include pentachlorophenol (PCP).0-25. 1976).2 (17..7 (19. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.5-33.4) < LOD < LOD 19.S.0 (18.4. 2005).1) * * 15.6) < LOD < LOD 25.3) < LOD < LOD 20.3 (14. 31. population from the National Health and Nutrition Examination Survey. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. HCB is well absorbed after oral administration.6 (21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-15. and 03-04 are 118.9 (14.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.1) < LOD < LOD 15.5 (13.4 (11.7-30.9) < LOD < LOD 15.6-33.4) < LOD < LOD 22.2) < LOD < LOD 29.9-17.6) < LOD < LOD 24. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides. 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.5) < LOD < LOD 18. and foods with a high fat content.3 (20.Organochlorine Pesticides Hexachlorobenzene CAS No.4-16. The FDA dietary surveys have shown that over time.7) < LOD < LOD 24.7-16. Therefore.5-14.6-TCP) (To-Figueras et al.7-26. and sediment (Barber et al.0) * * 15.5-18.0-19.7-21. wildfowl.9-30.4) < LOD < LOD 23.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13. EPA cancelled its use in 1984.4) < LOD < LOD 14. HCB has been detected in fewer foods since the 1980s (FDA.1 (14.3-26.1-20.0) < LOD < LOD 24. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.3) * * 15.9) < LOD < LOD 20. and 7.5-15.4) < LOD < LOD 33.1 (17.6) < LOD < LOD 26.8.5 (14. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.6-trichlorophenol (2.9) < LOD < LOD 19.9-24.5 (13. breast milk is an additional route of elimination in nursing women. HCB is slowly metabolized.6-44.3-22. see Data Analysis section) for Survey years 99-00.1 (13.7-15. 100 Fourth National Report on Human Exposure to Environmental Chemicals .0-28.8 (15.2-15. The general population may be exposed to HCB through diet..2 (14.3) 24.6 (24.5-15. and accumulates in fatty tissues where it persists for years.5-trichlorophenol (2.5-TCP) and 2. 2002).6) < LOD < LOD 26.1 (14.0.9 (25..8) < LOD < LOD 27. 2008.0 (25.9 (23.S.9) < LOD < LOD 20.6-26.9-20. or game taken from areas with HCB contamination.4 (18.7) * * 14.6-32.4) < LOD < LOD 18.2 (24.3) < LOD < LOD 29. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications. Although it is not manufactured as an end-product in the U. Gunderson.3 (16. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.0) < LOD < LOD 15.3 (12.0 (14.2 (13.0 (18.S.8 (22.8-15.1-16. which may vary for some chemicals by year and by individual sample.7 (15.7 (15.0-16.S.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 * * 14.4.9) < LOD < LOD 16. air.7-29. and elimination occurs by renal and fecal routes.3 (22.4 (18.6 (23.7-16.9 (25.6-19.8 (26. 1988). 2.2 (14. and has been detected in soil.9-32. 1997).4.5-14.9) < LOD < LOD 28.2) < LOD < LOD 13.. Survey Geometric mean (95% conf.2-31.4. 01-02.7-22.4 (22.4.6) < LOD < LOD 14.9-15. water.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.9) 19.

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

Schulz C. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. 2002) and among children (Link et al. Sweetman AJ.349:144. Schwartz JM.html.. Holland NT. Darnerud PO... Eskenazi B. Bjerselius R. Barr DB..71(6):1200-1209. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.111:349355. Hexachlorobenzene in the global environment: emissions. Environ Health Perspect 2002. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Ozalla D. Link B. Santiago-Silva M. Dallaire F. 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. Aune M. Available at URL: http://www. Dewailly E. Muckle G. Cripps DJ. Bradman et al.54(3):203-208. Food and Drug Administration (FDA). 2002. Kohli J. et al. Reference values updated. distribution.gov/~dms/ pesrpts.58:1185-1201. Kemper FH. Kaus S. In the 1976-1980 NHANES subsample. 1999). Lackmann GM. et al. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al.. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. HCB detection in serum also was proportional to age. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Lawrence River (Quebec.44 mg/L. August 2008. Gunderson EL. 2002). Lepom P. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Lecha M. and the geometric mean concentration of HCB in whole blood was 0. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. respectively. Paepke O. Atuma S.cfsan. Peters HA. Glynn et al. Biol Neonate 2002. Jones D. 2005). Safe A. The metabolism of higher chlorinated benzene isomers.gov/ toxprofiles/tp90. References Agency for Toxic Substances and Disease Registry (ATSDR). April 1982 to 1984.81(2):82-85.110(8):835-838. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. As a result of the lower limit of detection in NHANES 2003-2004. Chemosphere 2005. Bertram et al. Available at URL: http://www. In a representative sample of the 1998 German adult population. 1986.17:388–399. but overall. 1989). September 2002. 4/21/09 Barber JL. Bradman A. however.cdc. FDA total diet study. Fenster L. 2005). 2002.. Organochlorines in Swedish women: determinants of serum concentrations.. Int J Hyg Environ Health 2002. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Gocmen A. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Over the past two decades. IARC Sci Publ 1986. 2006). PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.205:297-308. Arch Neurol 1982. 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. Becker K. Lackmann.9% of participants had quantifiable levels (Stehr-Green. Bertram HP. trends and processes. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Muller C.html. 2002. Zoellner I. Arch Dermatol 1999. J Assoc Off Anal Chem 1988. and other chemicals. et al. Sala M. Laliberte C. van Wijk D. Herrero C.39(12):744-749.. 4/21/09 Glynn AW.. Lackman. only 4. levels. In Spain. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. 2002.. Herrman T. Granath F.fda. Gabrio T.. Environ Health Perspect 2003. HCB levels were directly related to age. Otero R. selected elements. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 2003). Sci Tot Environ 2005. Biomonitoring of persistent organochlorine pesticides. Can J Biochem 1976. Seiwert M. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. 2005. Toxicological profile for hexachlorobenzene update [online].77:173182. Jones KC. Dogramaci I. Krause C. more HCB levels were quantified.atsdr. Link et al. dietary intakes of pesticides. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Bryan GT.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Canada).135(4):400404. J Exp Sci Environ Epidemiol 2007. Piechotowski I. Ayotte P.

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

6-89. and have been used either as fungicides or to synthesize other chemicals.2 (50. 2005).3-85.9) 15. Technical grade HCH is a mixture of all four isomers.7-96.9-14.6-37.7 (<LOD-16.7) 32.0-23.5-29.5528.7 (30. soil. exists in several isomeric forms.5 (24. and sediment as a result of historic production and use.6-42.9-24.70 (8. see Data Analysis section) for survey years 99-00.1-27.36.4) < LOD < LOD < LOD 46. containing about 64% alpha and 10%-15% gamma isomers.0-21.6 (22.8) < LOD 10.5) 22.9 (40.7 (35.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.2-52.7 (29.1-32.6 (40.2 (48.8-19.4 (50.6) 653 758 589 1240 1533 1370 20 years and older 10.5) 40.5 (14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. so they can accumulate in fatty tissues of animals. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.43 (<LOD-9.8 (23.3) 25.0) 7.5) 67. 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.1) 12.8 (32.6) 35.2) 13.9 (32.70 (6. Lindane has a half-life of about two weeks in soils and water.6-14. It is no longer produced or sold in the U.1 (21.7-26.1 (27. water.4-111) 84. the U.2 (31.8) 12.7 (62. which may vary for some chemicals by year and by individual sample.5-123) 49.70-19.3) 34.2-55. HCH isomers.2) 142 (99.1-32.8 (21.9 (62.2-42. and 7. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.1-49.4) 44.2-20.50) 8. each result has been multiplied by 1.0 (35. beta.80 (6.8 (17. However.4) 901 1067 952 992 1224 1007 Females 11. 58-89-9 General Information Hexachlorocyclohexane (HCH).S.3 (42.8) 7.1 (30.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.1) 12.7) 18.6-18.0 (8.6-62.4 (12. particularly alpha and gamma have been detected widely in air.56-12.8) 39.7-20.7) 10.7 (53.6-135) 69.4 (52.6) 16.90-8.9 (9.9-51.1) 13.6 (17.9-56.89 (<LOD-9.6-47.Organochlorine Pesticides Hexachlorocyclohexane CAS No.5 (16.S.7 (13.9-178) 48.2-67.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.90) 7.9 (11.6-20.2 (29.5) 90th 42.3) 37.6) 36.9) 81.3 (26. interval) 9.7) 56.3-38.8 (9. 104 Fourth National Report on Human Exposure to Environmental Chemicals .1-15.2) 9.6) 18.0) 35. < LOD means less than the limit of detection. 01-02.8) 52.4) 11.7-69. In 2006.4) 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 21.7) 27.8) 95th 68.8) 27.1) 31.0 (33.0) 41.4) 21.90-8.2) 62.1 (9.60-13.76.7-96. population from the National Health and Nutrition Examination Survey.8-54.2-17.0-34.5 (43.6 (10.8-199) 134 (85. The other isomers can be formed during the synthesis of lindane.9 (26.2-87.4) 10.70-12.8.9-81.5) 29. environmental levels declined.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.8 (64.87 (9.0-70.3 (62.7) 10. The gamma isomer.0 (<LOD-12.2 (9.9) 45.9 (30.3) 14.68 (<LOD-10.2) 36. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.7-166) 70.4) < LOD 9. gamma.2-98.20-16. As pesticide applications of HCH were increasingly restricted or eliminated.6) 47. including alpha.6) 50. HCH isomers are lipophilic. and delta.1) 71.1-36. 319-85-7 gamma-Hexachlorocyclohexane CAS No.5) 16.5 (8. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.2 (34.6 (33.4 (16.S.1 (16.7) 23.30-11.4) 51.1 (9.9) 17.4-73.8-68.0-20.0-111) 70. See the section “What’s New” at the beginning of this Report for details.2-46.4 (11.0 (14.7) 97.2-22.5) 11.1 (11. and 03-04 are 9. commonly known as lindane.3-56.8) * * * * * * 15.4-50. **In survey period 2001-2002.7-69.8 (33.0) 8.0 (37.66-12.3 (13.0-70. EPA cancelled agricultural uses of lindane (ATSDR.04-10. formerly referred to as benzene hexachloride.6 (16.4) 27.9-21. 608-73-1 beta-Hexachlorocyclohexane CAS No.8-16.2 (18.4-45.8-87.46-11.4 (8.3) 51.61-12.1 (12. 2005).9 (50.1-37.0) 17. 6.8 (10.7) 73.5 (11.0 (19.1-16.3 (42. respectively.7 (25.80 (<LOD-14.0) 71.5) 14.1 (18.5 (37.

ataxia.110) .221-. 2008.260-.290) .048 (<LOD-.060) .214) .501) .300-.450) .190-1.287 (.250 (.410) .254) 95th .160-.330 (.080) * * * * * * .270 (.220-.710) .140) ..290 (.120-.100-.420-.210) .240-.050-. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.480 (.210-.160) .100) . Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways. 1986).078 (.32) .058 (<LOD-. and seizures. EPA has established a drinking water standard.370-.460 (.098 (.090 (.410) . 1971.180-.S.382-. resulting in a half-life of about seven years.442 (.240 (.120 (.170-. 2002).280-.330-.062 (.070-.5528.080-. population from the National Health and Nutrition Examination Survey.103-.191-.110) .. OSHA and ACGIH have established workplace standards and guidelines.120-.190) .118 (.290 (.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.200-. HCH crosses the placenta and is also excreted in breast milk (Radomski et al. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.320 (.120) .090-.092 (.412 (.470) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD . Gunderson 1988).050-.480) .190) .700) . Fourth National Report on Human Exposure to Environmental Chemicals 105 .360 (.620-1.090 (.380 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.340) .210 (.910 (.260) .570 (.S.083) ..222 (.250 (.080-. 1981).100) .310) .390 (.125) < LOD < LOD < LOD .144 (. respectively.051 (<LOD-. tremors.139 (. 1977).360) .080 (. Saxena et al.250-.260) .05) .S.600) .680) .130 (.050-.200-. Distribution is mainly to fatty tissues.070 (.297-.064) .250-.404) . each result has been multiplied by 1.331 (.410-.140 (.450-.100 (.319) .37) 1.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .131-.140) .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 .460) .281 (.560) .120-.103 (.070-.040-.216 (.150-..400) .305) .175 (.510) . for lindane.077) < LOD .310) .470 (.350) .308-.290 (. enlarged livers.089) .310 (. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.110) . 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.124-.244-.230-.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .191-. The beta isomer accumulates in fatty tissues and is metabolized more slowly.620) .01 (.120) .103) 90th .083 (.. paresthesias. 1983).051-.130) . **In survey period 2001-2002.480 (.050) .086) < LOD < LOD < LOD < LOD < LOD < LOD .146-.250) .070-.119) .580-1. The U.150) . which may vary for some chemicals by year and by individual sample.521 (. and FDA has established a bottled water standard and food residue tolerances for lindane.410 (.174) .080 (.050 (.390-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1996.340-.587) 653 758 589 1240 1533 1370 20 years and older . ingestion.100-.065 (.067 (.073-. the serum half-life was about 20 hours among children (Ginsburg et al. Rogan.110-.065 (.250 (.150) . probably by blocking inhibitory neurotransmitters in the central nervous system.057 (<LOD-.067) .089-.068-.220-.096) .190-.360-. When animals were chronically fed lindane at high doses.070) .100-.220 (.090 (.840) .130-.220) .580 (. and memory loss (Nigam et al.280-. hepatic enzyme induction.234 (.050 (.661) 901 1067 952 992 1224 1007 Females .173-.081-. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.057-.200 (.294-.560 (.077) < LOD . or dermal exposure.450 (.210 (.050-.120 (.056-.118-. and nephropathy developed (IPCS.690) .400) .150 (.091) .814) .167 (.062 (.290) .050 (<LOD-.050 (<LOD-.Organochlorine Pesticides exposure to HCH is through the diet.160 (.372 (.047-.064 (.100 (.070 (.059-.140) .080) .057-.350 (.056-. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity. U. After dermal application of lindane 1% lotion. See the section “What’s New” at the beginning of this Report for details. Workers who directly handled HCH have complained of headache. interval) .080-.069) .170-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. HCH isomers are absorbed after inhalation.120 (.072 (.

. More information about external exposure (i.. and 2003-2004.gov/toxpro2..gov/pesticides/ and from ATSDR at: http:// www. 2005. Stehr-Green. which may vary for some chemicals by year and by individual sample. Kutz et al. 1998). 1991.html. population from the National Health and Nutrition Examination Survey. Becker et al. male sex. EPA at: http://www. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 2002. 01-02.5. Bates et al.. older age. 106 Fourth National Report on Human Exposure to Environmental Chemicals .. Link et al. In an earlier (1996-1997) sample of German children. 2001-2002. and 7. Kutz et al..e. 2002).5. Stehr-Green. 1991.S. environmental levels) and health effects is available from the U. In recent years. and 03-04 are 14. aged 9-11 years. In populationbased studies of New Zealand adults and German adults and children. the maximum and 95th percentile beta-HCH values.. 10.8..S. Additional factors associated with higher beta-HCH levels include rural residence. < LOD means less than the limit of detection. Survey Geometric mean (95% conf...cdc. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. were similar to the 95th percentiles in this Report. respectively.. In NHANES 1999-2000. serum levels of lindane were generally below the limits of detection.. Sturgeon et al. 2005.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens.atsdr. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. 1989.epa. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. see Data Analysis section) for Survey years 99-00. Radomski et al. 1989). and a diet that includes meat (Becker et al. 1971. 1998. Biomonitoring Information Because of its longer half-life. 2004) and India (Bhatnagar et al. 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. respectively. 2004. 2004).

1971).. 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. respectively.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. Fourth National Report on Human Exposure to Environmental Chemicals 107 . Radomski et al. in this Report (Nigam et al. 2005). 1986. 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. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson 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..Organochlorine Pesticides 2001-2002 survey period (Link et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1998).. Survey Geometric mean (95% conf. 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. 2003). In a small study of adults who consumed sport fish from the Great Lakes.. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.

Bjerselius R. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Pollutants in breast milk. Absorption of lindane (g benzene hexachloride) in infants and children. selected elements. 4/21/09 Anderson HA. Botella B. FDA total diet study. Ellis H.72:261265. et al.205:297-308.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). children and newborn infants. Zoellner I. Demographic and seasonal influences on human serum pesticide residue levels. J Toxicol Environ Health 1989. Siddiqui MKJ. et al. Olea-Serrano MF. Environ Health Perspect 2003. Burse VW.atsdr. Karnik AB. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Majumder SK. Lindane.htm.71(6):1200-1209. et al.cfsan.57(4):315-320. J Pediatr 1977. Toxicol Appl Pharmacol 1971. Rogan WJ. Reisch JS. HCH. Arch Pediatr Adolesc Med 1996. Kulkarni PK. Buckland SJ. 4/21/09 Kutz FW. J Assoc Off Anal Chem 1988. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. gov/toxprofiles/tp43.91:998-1000. Int J Hyg Environ Health 2002.20(2):186-193. PA. Bates MN. Seiwert M.96:34-4Food and Drug Administration (FDA). Crespo J. Lepom P. Cerrillo I. Brinton LA. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Saxena MC. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). 2002. The Great Lakes Consortium. Krause C.54:1431-1443. et al. Environ Res 2004. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. April 1982 to 1984.gov/~dms/pesrpts. Bull Environ Contam Toxicol 2004. Arch Toxicol 1981. August 2008. Int Arch Occup Environ Health 1983. et al. Krishna Murti CR. Stehr-Green. Rey AA. Available at URL: http://www. Metabolism of gammahexachlorocyclohexane in man.150:981-990.html. available at URL: http://www. Olea N. Aune M. Atuma S. August 2005. Bai KM. Biomonitoring of persistent organochlorine pesticides. and HCB residues in human blood in Ahmedabad. Int Arch Occup Environ Health 1986. Glynn AW. Falk C. et al.fda. Hanrahan L. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Needham LL. org/documents/jmpr/jmpmono/2002pr08. Gunderson EL. Garrett N.120:1-82. Bhatnagar VK.html. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Astolfi E. Deichmann WB. Nigam SK. Kaus S. International Programme on Chemical Safety (IPCS). Darnerud PO.52(1):59-67. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Rivas A. Toxicological profile for hexachlorocyclohexanes update [online]. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Rev Environ Contam Toxicol 1991.27:405-421. Cancer Causes and Control 1998. Needham LL.48:127-134. Becker K. Brock JW. et al. Raju GS. Levels of DDT. Gabrio T. Rothman N. Herrman T. Piechotowski I.cdc. Granath F. Schulz C. Sturgeon SR. Chemosphere 2004. India. Angerer J. and other chemicals. Needham LL. Bhargava AK. Radomski JL. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Olson J. 4/21/09 Ginsburg CM. Zaidi SS. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. dietary intakes of pesticides. Lowry W. Organochlorines in Swedish women: determinants of serum concentrations. Chemosphere 2005. Exposure of women to organochlorine pesticides in Southern Spain. Heinrich R.111:349355.106(5):279-289. Kashyap R. Paepke O. Potischman N. Saiyed HN. Kutty D. Bottimore DP. Patterson DG Jr. Available at URL: http://www.9(4):417-424. Wood PH. Visweswariah K.inchem. Maass R.58:1185-1201. Environ Health Perspect 1998. Occupational exposure to hexachlorocyclohexane. VI. Placental transfer of pesticides in humans. Link B.

its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.10-37.. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.4 (8.8 (12. which may vary for some chemicals by year and by individual sample.3-225) 15.8) < LOD 15.6 (<LOD-31. 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. sediments.5 (<LOD-115) 153 (30.6) 9. especially those from persons living in the southeastern U. population from the National Health and Nutrition Examination Survey.0 (14. soil. 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.4) < LOD 15. Mirex is absorbed through the skin and from the gastrointestinal tract.5 (9.1 (8. (Kutz et al. see Data Analysis section) for Survey years 99-00.70-24.40 (<LOD-13. where it has a half-life of 12 years. aquatic organisms.6) < LOD < LOD < LOD < LOD 71.S. water. disposal. Occupational exposure is limited to workers at sites where mirex contamination is present.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.S.10 (<LOD-15.2 (7.5-82.1) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 16. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.7) < LOD 66. it is a highly persistent chemical in the environment.0 (<LOD-108) < LOD < LOD 50. Mirex binds strongly to soil.6 (<LOD-108) 9.5-425) 40.4) < LOD 63. 1991). 2385-85-5 General Information Mirex has not been produced or used in the U. < LOD means less than the limit of detection.S.6-305) 15.2) 51.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. Formerly.70-40.3) 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. and foods.6.8 (<LOD-73.S. resulting in exposure to newborns and nursing infants.4-230) 18. Survey Geometric mean (95% conf. since 1977.70 (<LOD-15. and 03-04 are 14. 01-02.1 (<LOD-65. Fourth National Report on Human Exposure to Environmental Chemicals 109 .7 (<LOD-47. where it was applied directly to soil and by aerial spraying. after which it is widely distributed in the body and stored in fat. Mirex can cross the placenta and be excreted in breast milk.0 (12.0) * * * 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. Mirex has been detected in air. Some states and the U. 10..4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6 (<LOD-23. 1985. In studies conducted in the 1970’s and 1980’s.3 (15. animals.8.90-29. mirex was detected in human adipose samples. 1995).3 (15.5. and 7. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.0-374) 11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 (13.7) 8.2-230) 13.5-291) 11. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.S. or pesticide application. respectively. Mirex is not metabolized in the body.Organochlorine Pesticides Mirex CAS No.5 (<LOD-42.7 (12.

.100 (<LOD-. IARC classifies mirex as possibly carcinogenic to humans.73) .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.100 (<LOD-.635) < LOD .110 (<LOD-.256 (. 110 Fourth National Report on Human Exposure to Environmental Chemicals . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.080-1.450 (.090 (<LOD-.470) .41) .106 (. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. and 4.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .690) .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 .Organochlorine Pesticides exposures are unknown. 1995.610) < LOD < LOD < LOD < LOD . as well as in a subsample of NHANES II (1976-1980) participants.79) . which may vary for some chemicals by year and by individual sample.054 (<LOD-.070-1.S.077 (<LOD-.8.470) . 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.140 (<LOD-. EPA has established environmental standards for mirex. 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.090-1. 1989).055-.052-.310 (.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 . More information about external exposure (i.e.089-.079 (<LOD-.gov/toxpro2.090-1.170) < LOD .093 (.79) .. serum mirex levels were generally below the limits of detection (Stehr-Green. 2005).cdc.02) .062-.370 (. 2001-2002. population from the National Health and Nutrition Examination Survey.090 (<LOD-.053-..220 (<LOD-. In addition. reproductive toxicity included decreased fertility and testicular damage.510) < LOD < LOD .37) . 7.html.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 . 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.059 (<LOD-. The U. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.410 (.470 (.090 (<LOD-. 1991).430 (.080-1.268) < LOD .106) < LOD . environmental levels) and health effects is available from the ATSDR at: http://www.S. Biomonitoring Information In the NHANES 1999-2000. Laboratory animals fed high doses developed liver enlargement and liver tumors.220) . 2004).090-1. 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.112 (.7 ng/g of lipid.92) . and 2003-2004 subsamples.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 .064 (<LOD-.102) < LOD < LOD < LOD < LOD . Smith. In samples obtained between 1994 and 1997.450) 1. Survey Geometric mean (95% conf. and NTP classifies mirex as reasonably anticipated to be a human carcinogen. The geometric mean mirex levels of the Inuit mothers were 8.atsdr.08 (.108 (.

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

hexachlorobenzene.71 (<LOD-8.40-11. public drinking water systems did not detect 2. population from the National Health and Nutrition Examination Survey.20) < LOD 90th 5. including hexachlorobenzene and hexachlorocyclohexanes.40 (2..5TCP and 2. Historically.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.3. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.40 (2.40 (2. may occur by inhalation or dermal routes.4. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.0) < LOD 21. Exposure to trichlorophenols also may result from metabolism of lindane.0 (4. 1999).0) < LOD 11. 2.30) < LOD 4.4. surface water.50-25.20-36.30-11. EPA.40 (2.4.60-8.5-trichlorophenol (2.5-Trichlorophenol CAS No.19 (<LOD-6.30-40.0 (3.20) < LOD 1.20) < LOD 5.0 (8.50) < LOD 1.20 (4.9.0) 2.80-41.S.60) < LOD 8.4. soils.57 (<LOD-15.50 (1. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.4.90-33.40) < LOD 1.40) < LOD 6.50 (2.40 (.4. Survey Geometric mean (95% conf.Organochlorine Pesticides 2.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.6-TCP).7) 24.900-2.950 (<LOD-1.0) 2.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .980-3.40-18. Both chemicals have been detected in air. Occupational exposures.5-TCP) and 2.00 (3.0 (3.0) < LOD 5. 95-95-4 2. recent sampling of U.0) 2.30-27.71 (<LOD-8.4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.0 (4.6-Trichlorophenol CAS No.80) < LOD 1.0) 2.6-TCP in any of the samples (U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. however.31 (<LOD-9.7. 2.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.30-27. 2006).60 (. Trichlorophenols are no longer manufactured commercially.30-27.30 (.0 (4.80 (2.30-3.0) < LOD 5.5-trichlorophenol.0) 14.00-3.0) < LOD 11.S. 1999).30) < LOD < LOD < LOD < LOD < LOD 1. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.4.42 (<LOD-12.00-3. Formation of 2. and sediments. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR. 2.4.40 (1.80 (1.940-3. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.980-3. Such workers would probably Urinary 2.8) 21. other organochlorines.27) size 1994 2497 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1.4.10-3.60 (2.4. 112 Fourth National Report on Human Exposure to Environmental Chemicals .0) 2.40 (.42 (<LOD-8. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.9 and 0.30-44.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.40) < LOD 4.6-trichlorophenol (2.60-18.20-71.0) < LOD 5. and polychlorinated benzenes (Kohil et al.4.S.00 (2.0) 2.0 (5. usually at herbicide production or waste incineration facilities.40 (1. 1976).50-63.50-16.00-8.27) 696 661 521 696 603 939 Limit of detection (LOD.72) < LOD 1.63) 18.60 (4.6-TCP were used as intermediates in the production of certain pesticides.9 (<LOD-121) 9.0) 5. are metabolites of several organochlorine chemicals.50 (.920-3.03) 9.

00) < LOD 4.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.0 mg/L.64 (4. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.820-2..19-12.16 (.Organochlorine Pesticides be exposed to mixtures of chlorophenols... 1995) and up to 19 times higher than the 95th percentile value of 1. the 95th percentile urinary 2..5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4.9 (5.. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.4.3 mg/L reported in German adults aged 18-69 years (Becker et al. 1989).8) 4.05-17.37) 16.980 (<LOD-1. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.88-16.6) 4.15) < LOD 2. 7.32) < LOD 4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11. in addition to dioxins.36 (1.2) 2.1) 2.6-TCP.24) < LOD 5.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al. Laboratory animals chronically fed high doses of 2.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .5-TCP and limited for 2.95 (3.S.62-20.24-11.27-17.68-4.4.6-TCP had increased rates of hepatic tumors.02-3.24 (3.16) < LOD 90th 5.00-19.47-8.19-4. as being possibly carcinogenic to humans.57 (<LOD-7..6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).2) < LOD 5. More information about external exposure (i.4.80 (1. Human health effects from 2.13-13.31) < LOD 2.4. population from the National Health and Nutrition Examination Survey.17) 9.81 (<LOD-9. leukemias.82 (<LOD-32.67 (1.7 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003.37-11.43 (2. urinary 2.24) < LOD 1.78 (3.24) < LOD 6.60-3.68 (<LOD-8.57 (<LOD-7. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.53-3.44 (1. IARC classifies combined exposures to polychlorophenols. At lower doses.75 (<LOD-6.86 (3.8 (5.75 (3.6) 4.44 (.90 (4.6-TCP as reasonably anticipated to be a human carcinogen. Neither 2.9) 12.4) < LOD 3. However.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.29 (1.05-8.6-TCP level was approximately eight times higher than the corresponding percentile in a small group of 2-6 year old children living near an herbicide manufacturing facility: 33 versus 4 mg/L (Hill et al.4.4.5-TCP or 2..02) < LOD 7.79-4.73 (<LOD-8.4. 1995) were similar..5) < LOD 12. The 95th percentiles for 2. 1989). recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.4) < LOD 3.46 (1.69 (2. and lymphomas.78-19.0) 7. Survey Geometric mean (95% conf. which includes trichlorophenols. Radon et al. In the same 2-6 year old children. animals showed hepatocellular abnormalities.cdc. and other chlorinated compounds.920-2.4.3 (5.11) 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 2.4) 5.33) < LOD < LOD < LOD < LOD < LOD 2. furans.4.83-12.67 (1. 2003). NTP classifies 2.4.74) 11.5-TCP.55 (4.6) 4.5) 11.8) < LOD 9.1 (<LOD-58.20-6. Among 6-11 year old children in NHANES 1999-2000.6-TCP levels at the 95th percentile were up to eight times higher than 3.4 (6.5-TCP nor 2.78) < LOD 1. Urinary 2.4.28-25. the 95th percentile urinary 2.50) < LOD 2.93-11. environmental levels) and health effects is available from ATSDR at: http://www. 2003).69-18. Fourth National Report on Human Exposure to Environmental Chemicals 113 .gov/toxpro2.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.53-3.4.html. 2004).49 (1.43) < LOD 12.atsdr.e.57 (3.2 (2.00-29..11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.

90 (3.40) 2.70-6.7 (13.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.09-7.2-0.0 (14.25-11.0) 19.70) 5.4.06) * 2.1 (8.67-12.80 (2.79 (5.4.0) 9.56 (3.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.57 (<LOD-2.7 mg/L.00 (4.10-3.4.0) 7.60-37.63) 90th 15.89-6.10) 6.0) 13.98-7.80 (2.23) 2. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.70) 5.3) 23.6-TCP exposure and health effects. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.5-TCP and to the median 2.85) * 3.0) 17. Biomonitoring data will also help scientists plan and conduct research about 2.0-18.60-3.40) 4.40-2.1 (10.4.0) 13.40-2.70-3.5-TCP or 2.72-10.7) 33.4.1-25..0-38. Urinary 2.6-TCP level.4.20-23.10-2.69 (3.50 (2.8-24.5-TCP (0.60 (3.5-46. the median urinary 2.30-2.2) 25. 0.9) 13.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.0) 6.6) 26.6 (11.95) 3.60 (3.78 (2.3 (11.20 (3.02) 2.5 mg/g creatinine) were similar to the limit of detection for 2.23-2.40-7.0) 14.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.0-44.45 (5.S.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 2.4.10 (5.0 (14.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.0) 14.32) 3.76) 3.0-54.20 (3.70) 3. 1991).0 (4.6) 21.5-TCP or 2.60 (2.0-37.84) 2. 2003).00 (2.09) 15.8) 32.0) 12.0 (6.78 (2.14 (2.0 (8.0 (13.54) 6. which may vary for some chemicals by year and by individual sample.0) 19. Finding a measurable amount of 2.3 (11.0) 13. was about six times lower than the median urinary levels for males in this Report (Radon et al.4 (10.0-68.30-11.53) 2.92 (2.60-21.55-3. Urinary 2.49 (6. Survey Geometric mean (95% conf.23) 3.9 (13.0) 13.70 (2.4.87-14.3.90) 2.26 (2.59) 4.0 (8.40) 2.90-8.4.53) 4.40-14.40-4.9) size 1989 2503 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.35-3.0 (15..0 (20.04) 2.89 (3.60) 6.80-7.2) 12.08 (2.10) 2.52-3.0 (15.66 (8.95-6.6-22.9 (11. < LOD means less than the limit of detection.98-11.90 (4.0-43.6-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.8-15.48-26.4 (9.0 (9. interval) 2.50-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.75 (8.36-5.28) * 2.6-17.31) * 2..0 (16.01-6.65 (5.4. respectively.0 (20.59-6.30-2.0 (6.47 (3.0) 7.74 (2.7-3.07 (<LOD-3.95 (4.0) 10. In harbor workers exposed to chlorophenol-contaminated river silt.20-6.0 (6.73-9.6-TCP than are found in the general population.45) < LOD 11.5-TCP and 2.32-4.32) * 3.4.36 mg/g creatinine.40 (2.74-3.4 (17.4.68 (<LOD-2.0 (14.6TCP causes an adverse health effect.0) 9.58-3.4 (8.70-6.91-4.45-9.33-4.4.6-19.40 (2.30) 4.80-25.20-3.4.00 (1.8) 18.9) 694 677 519 696 602 931 Limit of detection (LOD.30-33.0-38.18) Selected percentiles ( 95% confidence interval) Sample 95th 25. Biomonitoring studies on levels of 2.0) 11.51-12.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.5-TCP or 2.4.80-6.52 (2.45 (2.3-26.0 (7.0) 10.4-17.6TCP values.85 (2.00-4.0 and 1.40) 3.18-3.5-TCP and 2.5-TCP or 2.1) 16.28) 24.7-16.70 (2.80) 1.4.0-50. Mean values of 2.6 mg/g creatinine) and 2.0) 11.58 (1.46-3.3-17.4.0-41.80-20.4.2 (14.8 (9.24 (2.8-13. population from the National Health and Nutrition Examination Survey.60) < LOD 5.99) 6.10-3.0 (11.4.44) 75th 4.4. for males in NHANES 19992002 (Agramunt et al.67) 4. 2004).36 (1.31 (3.0 (12.0) 17.5-TCP level of 0.7 (9.20) 4.65) 15.7) 21. 1998).80 (3.6-TCP in urine does not mean that the level of 2.3) 37.12) 2.6 (12.0) 15.3) 20.70) 1. 114 Fourth National Report on Human Exposure to Environmental Chemicals ..6-TCP (0. similar to the limit of detection for this Report (Anderson et al.00-21.40-32.

population from the National Health and Nutrition Examination Survey.9 (9.5) 9.4 (11.91-2.42) 2.50-8.28-4.7) 6.42 (2.25-17.87-6.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.22-9.17) 13.00) 4.04-16.41-6.1 (13.5 (10.6 (22.6) 12.68) 2.8) 11.02 (1.9) 7.3 (9.63) 4.63 (<LOD-2.3-23.25-15.27-9.35 (3.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.22 (<LOD-2.30-2.83 (3.29-4.88 (2.26-13.4) 4.87) * 2.08-2.77) 2.73-22. Survey Geometric mean (95% conf.6) 13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.49) 4.5) 11.Organochlorine Pesticides Urinary 2.25-2.65) 2.4) 8.2 (12.04-2.70-9.21-11.82 (8.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.65-21.2 (8.11) 10. Fourth National Report on Human Exposure to Environmental Chemicals 115 .14-13.91 (3.40 (7.72-16.67-17.9-29.46-14.17-4.78) 90th 12.55-2.56-5.33 (1.20-2.13 (1.53 (3.6 (10.56) < LOD 11.81-9.6 (6.98 (1.0 (11.88) 4.00) 4.6 (5.79-17.52) 2.9) 8.53) * 2.50 (2.8 (8.7 (14.77-4.06) 11.76-8.40 (2.9 (9.09-3.33-2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.83-6.23 (1.96) < LOD 4.3-37.51 (2.7) 25.94-13.5 (8.18-4.88) 1.5) 12.9-32.65-2.60-2.58 (4.72) 32.2 (13.17) 2.8) 21.63) * 4.87-7.99-2.89) 10.4) 9.62-15.8) 12.92) 4.88) * 2.0) 8.9) 19.63-13.52 (5.38 (2.82 (3.44 (3.29 (6.26 (6.6 (9.38 (4.9-64.0 (6.51) 18.76) 4.38) 22.5-28.32-19.01 (3.88) 4.6 (9.2) 19.1-32.8) 19.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.16-10.76) 1.56 (7.82) 2.73) 5.6) 8.S. interval) 2.76) 2.22-2.23) 4.33) * 2.49-3.33 (7.5) 8.1) 11.47-5.24 (1.4 (12.22 (3.54 (2.52 (3.78 (2.98) 10.0) 10.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.38-5.18-2.15 (6.66-4.59 (2.5 (7.63 (2.63-15.89-2.4.1-21.88) 5.19-5.71 (3.05 (6.83-6.48-2.9-34.52) 2.00 (3.6 (12.0 (9.75) 75th 4.22 (1.29-4.06-2.25 (3.65) 18.13-6.14-2.10 (6.91 (7.95-2.90 (1.88-7.87) 2.10) 4.43 (2.53-11.7-36.43-7.9) 8.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.53) 4.3) 8.02) 3.43 (<LOD-2.68) 2.60 (4.1 (8.81) 2.2 (7.51-21.00 (2.05 (3.1) 14.41 (3.78) 2.83-5.15 (1.82-2.90) 2.87 (3.32 (2.25 (3.10-9.6-31.5) 11.8 (7.06) 4.

Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Arch Environ Contam Toxicol 1989. Domingo JL. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Olson J. Luotamo M. Becker K. Hill RH Jr.71:99108. Radon K. Int Arch Occup Environ Health 1991. Environ Health Perspect 1998. Pekari K. 4/21/09 Agramunt MC. Wegner R. Baur X. Safe A.gov/toxprofiles/tp107. Holler JS. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Shealy DB. Lindroos L. html. December 2006 Draft.EPA). Szadkowski D.S. The metabolism of higher chlorinated benzene isomers. 206:15-24. et al. Available at URL: http://www. Gregg M. The analysis of occurrence data from the first unregulated contaminant monitoring regulation (UCMR 1) in support of regulatory determinations for the second drinking water contaminant candidate list [online].146:83-91. Falk C. Hanrahan L. Environmental Protection Agency (U. S. Seifert B. Available at URL: http://www. Domingo A.epa. Aitio A. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Hill RH Jr. Heinrich-Ramm R. et al. Urinary excretion of chlorinated phenols in saw-mill workers. Toxicol Lett 2003. Am J Ind Med 2004. Seiwert M. Needham LL. Corbella J. Anderson HA. Poschadel B.106(5):279-289. Can J Biochem 1976. Toxicological profile for chlorophenols [online]. Burse VW. Kohli J. The Great Lakes Consortium. Bailey SL. To T. Fast DM. Pesticide residues in urine of adults living in the United States: reference range concentrations.cdc.63:57-62.45:440-445. Needham LL. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Head SL. Jones D. Baker S. U. et al.54(3):203-208. Smith SJ. Jarvisalo J.18(4):469-474.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Int J Hyg Environ Health 2003. July 1999. Environ Res 1995.atsdr. Schulz C.pdf. Chlorophenol exposure in harbor workers exposed to river silt aerosols.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Kaus S.

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

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

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

10) < LOD .94) * * .8 (12.81) 11.00 (4.80 (4.2-20.7) 11.61) 4.70) .80) .61 (3.73) * * .86-15.30 (4.970-2.290 (<LOD-1.50 (.10 (.0 (7.26-6.50 (2. < LOD means less than the limit of detection. 0.50 (4.70) < LOD < LOD 1.48-7.90) 3.89) 9.1) 95th 13.490-2.0 (8.90) 2.2 (9.71 (2.08-15.2 (7.56-13.8 (8.670-1.55-8.80) .4 (9.1 (10.82) 10.35-12.14) * * .2.0) 20.17-3.43-12.599-1.30-6.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.0 (8.S.0 (6.27-15.8) 7.0 (9. which may vary for some chemicals by year and by individual sample.47) * * 1.01) * * 1.40-19.0-28.70-14.860-2.60 (1.2) 16.40-16.0 (12.955 (.33-18.93 (4.79 (5.16 (2.02-5.00) 3.52) 6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7 (12.58 (5.46) 10.2.0) 5.0) 10.0) 10.40-14.34-3.0 (7.30 (2.60-25.11 (.10 (2.60 (5.74 (8.80) 3.2) 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 1.42-3.8) 7.38-5.21 (.12-19.700-1.60) < LOD < LOD 4.830 (<LOD-3.32) 1.2) 14.1-23.00) 3.47) 5.13 (2.0) 9.12) 4.4) 20.00-7.810-1.44 (2.579-1.58 (3.37 (3.15-12.890 (<LOD-2.80) 2.95) 5.5 (8.58 (2.71-9.57-7.1) 13.97) 90th 7.54 (3.00-12.0) 12.98-5.00-19.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 11.52-11.90-5.13 (2.34-7.44-3.3) 17.15) 14.600 (<LOD-1.0) 15.93-24.29) * * 1.27-3.9-18.56 (6.79-7.6) 7.8 (14.8 (9.2 (14.20 (.60) .0 (6.23-5.00 (1.60-18.82-12.21) 9.4) 17.13-2.08-2.3) 14.80) 2.0) 11.39 (3.0) 10.10) < LOD < LOD 4.70-11.530 (<LOD-2.40-1.1) 10.0 (5.623-1.2) 16. 120 Fourth National Report on Human Exposure to Environmental Chemicals .4) 18.2 (9.80) 4.08 (<LOD-2.83 (5.60-11.74 (8.780) < LOD 3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0-27.35-11.0) 11.9) 14.8) 11.1 (9.98-12.2) 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 1.96-3.03 (.2 (14.00-12.02) 4.6) 18.750-1.717-1.32 (.51) 2.70) < LOD < LOD 75th 3.0 (8.50-36.68-7.67) 3.3-15.5-17.0) 6.19) 9.7 (14.0) 10.1.290 (<LOD-.00-27.30 (2.26 (5.80 (2.39 (8. respectively.40-11.70 (2. and 0.28) 1.30-4.35-16.0 (4.2 (11.0) 5.20-4.0 (9.2 (7.10-7.5) 15.9) 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 1.20-30.2 (7.50-5.0) 5.85 (3.07-10.80) 11.70-19.90 (1.8) 19. and 03-04 are 0.53) 4.757-2.0) 11.0 (7. interval) 1.70 (4.56 (4.840-1.45 (2. 01-02.5 (11.758-1.0) 6.56 (1.91) 4.72) 5.16) 4.55-6.20 (2.4 (9.42) .20 (.0) 7.0 (7.20 (.90-4.5-16.20 (.70-23.76 (2.00 (5.63) 1.99 (5.80) 2.5) 20.10 (2.80-22.04) < LOD 1.620-1.1-17.94) 3.33 (5.10 (.00-27.05-7.36-4.80-4.4 (7.740-2.9 (8.20-7.86 (1.80-24.3) 16. see Data Analysis section) for Survey years 99-00.52) * * 1.97) 8.50) 2. population from the National Health and Nutrition Examination Survey.0) 10.44-38.8-32.22 (.9) 8.40-5.66) * * 1.81) 11.4 (7.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.981 (.0) 6.40 (.26-8.81) 1.954 (.

72) 11.29 (2.34) * * .66-15.35 (1.31 (3.3) 12.64-5.87 (3.40) 4.03 (7.09 (.09-11.69 (4.94-23.533-1.3) 5.960 (.47 (3.1) Sample size 1949 2519 1928 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.10 (3.75) 14.3) 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 1.7) 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.00 (4.7) 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 .03) 2.2 (8.4 (9.04-6.89-3.7) 5.8 (10.35) < LOD < LOD 3.28) 10.2) 9.0 (8.773-1.41) Selected percentiles ( 95% confidence interval) Total * * 50th .1) 4.94-22.93) 9.0) 6.900 (.30) 2.7 (8.04 (1.05 (1.38 (1.61-13.94 (4.40-5.633-1.45-5.53-11.5) 7.37) 9.9) 16.43 (.20-8.11-6.61-29.5) 12.28 (4.90-8.87 (1.00-13.8) 16.60) 2.94 (2.61 (1.1 (11.01-2.500-1.80) 9.5) 11.41) .883 (.750 (<LOD-1.85) 2.4) 4.40) < LOD < LOD 75th 2.82-14.549-1.5 (4.75 (7.89) * * 1.6) 11.66-34.40-3.960 (<LOD-2.574-1.87-5.98-5.54-4.95) 2.13) 4.62) .2) 5.95 (3.09) 2.54) .5-20.1 (8.932 (.7 (10.42) 12.54-11.890 (<LOD-1.790 (.47) 2.5-16.76-4.98-22.38) .07 (.23) 4.4) 13.8) 12.37-5. population from the National Health and Nutrition Examination Survey.47 (3.98) 9.53) 9.68-4.32-12.69) 4.608-1.34 (6.0) 7.710 (<LOD-1.37 (5.2) 5.98) .79-3.43 (3.68) < LOD < LOD 3.93-5.870-2.90-5.25) < LOD .1 (10.855 (.45-5.82-6.44 (2.2 (10.2) 7.56) 4.02 (7.28 (5.28-9.75 (3.3) 15.00-17.18 (.71-2.2) 13.890 (<LOD-1.1-15.00) 8.9 (9.818 (.21-23.830-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.81 (1.10-13.57-10.57 (6.55-20.54-2.66 (2.40-14.69) 2.2 (6.43) 2.430-1.560-1.996 (.05) .03-6.15-10.540-1.37-3.5-32.50) 7.52) 4.02-14.60) * * .820 (.1 (9.77 (6.8) 7.780 (<LOD-1.40-12.81-5.82-14.41-12.98) . interval) .6) 9.71) 10.94-10.25) 6.2) 8.75) 2.23 (4.75-7.56) 7.7 (9.5) 7.47) * * .03 (2.5-13.5) 8.860 (.2) 95th 12. Fourth National Report on Human Exposure to Environmental Chemicals 121 .34) < LOD < LOD .650-1.02 (2.02-2.620-1.84) 7.57) 4.37 (4.78 (2.8) 6.66 (5.14 (3.84 (5.42 (3.1) 4.73 (1.920 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.19 (4.29) * * .34 (6.03) 2.9) 11.40-28.9-28.83 (7.47 (1.88 (5.570-1.7) 18.66 (1.39 (2.74) 4.4 (4.57 (4.6) 8.6 (9.67-19.1 (6.28 (2.30 (1.440 (<LOD-2.51-5.60-9.9 (5.85 (6.9 (9.6) 13.56-13.80 (7.6 (10.06-2.8) 8.510-1.69-10.9) 12.67) 1.98 (3.79-9.92-2.00 (4.82-26.31-14.40 (3.93-9.00-19.83) 8.24-3.S.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.61 (1.80 (6.76) < LOD .88) 2.36) * * 1.45-11.80 (2.53 (6.46) 2.7) 12.3) 16.46-5.1 (7.74) 90th 7.88-10.94-9.566-1.58) * * 1.88-15.924 (.54-15.27) < LOD 2.4) 4.92-5.05 (.67) 4.56) .26) * * .62-5.

30) < LOD < LOD 4.0-19.28 (7. which may vary for some chemicals by year and by individual sample.6-19.0) 23.5.53 (3.3 (11.00-9.50) .16-1.2 (7.4) 11.15-2.15-6.90 (2.670 (<LOD-1.90-9.80 (2.70-9.10-10. and 03-04 are 0.650-1.8) 8.25 (2.0-29.34-10.90 (2.0-24.75 (3.0) 9. 01-02.66-13.3 (12.00 (.70-5.34-5.39-13.18) * * * * * * * * 1.82) 8.8 (12.00-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.61 (3.7 (11.35 (6.970 (<LOD-2.8-21.0) 12.3 (7.27 (3.9 (12.9-17.14 (6.90 (5.0 (9.6) 18.4-17.80-8.50-5.90 (6.41-5.0) 14.22 (6.4 (14.31) 1.89 (2.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20 (<LOD-2.12 (4.1-23.6) 11.90 (2.90-31.33-11.95 (5.80-14.0 (10.0 (7.0) 6.3 (9.20-18.670 (<LOD-1.80-12.40 (2.0-33.6 (10.8 (12.80) 5.7 (10.00) 8.5) 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 * * * * * * .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 * * * 1.98-9.740 (<LOD-1.10-4.4 (10.37 (3.62-17.17 (7.70 (8.2) 14.50) 3.2 (9.10) 6.27 (7.45 (3.1 (10.5 (8.4 (10.37) 2. 0.3 (6.81-6.0) 12.7) 14.35) 4.1) 11.24 (2.52 (6.67) 3.0) 7.74) * * * * * 1.670 (<LOD-1.70) 2.77-14.0) 9.20) 3.35-3.3) 20.9) 95th 14.73) 7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 22.90) 4.61-32.4) 7.99 (3. population from the National Health and Nutrition Examination Survey.46-28.50-4.7) 22.20-4.5) 21. and 0.40 (2.00) 7.6) 14.70-8.8-20.60 (2.67) 4.92-17.84-4.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.20) .70-9.0-24.34 (6.580-2.7-19.7) 16.20-8.80) .60) < LOD < LOD 2.8) 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 1.0) 12.60 (5.67-10.46-4.10-15.0 (8.22-12.66) 4.80-4.64) 10.88) 3.96) 3.39 (5.10 (<LOD-1.80 (5.40) < LOD < LOD 75th 2.6 (10.90 (1.S.680 (<LOD-1.30) < LOD < LOD .3) 8.47-6.0) 13.75 (2.6) 14.0 (13.80 (2.58.7) 10.90-15.00) < LOD .9-15. 122 Fourth National Report on Human Exposure to Environmental Chemicals .20) 3.95 (2.96) 90th 7.89) 2.0) 19. respectively.00-4.27) 4.49-4.34-3.0 (14. < LOD means less than the limit of detection.30) 3.0) 13.0 (10.0) 14.88) 10.63-14.50) 5.70 (1.60 (6.24-5.01 (2.0) 11.90) 8.06 (2.95-9.0) 11. see Data Analysis section) for Survey years 99-00.00) 3.92) 9.30) 3.59-3.58 (1.5 (9.27) .670 (<LOD-1.80) .00-18.77-3.42 (1.910 (<LOD-2.29-4.90 (6.9) 9.5 (8.11-6.27) 9.0 (9.51) < LOD 1.9) 16.31-7.80-21.0 (15.00-16.86-10.6-41.41) 3.9) 10.22 (6.5.00-18.29) < LOD < LOD < LOD < LOD 3.3) 14.31-12.00) 3.5-26.90 (6.7) 15.30) 8.10 (.9 (7.8-17.22) 8.80-3.8-20.3 (9.72) 2.90 (6. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .04 (3.78) 5.8) 9.0 (5.90-15.18 (3.80-6.3) 10.0) 18.790 (<LOD-1.97-4.9-14.7-21.1 (10.

07 (5.620 (<LOD-.6 (10.28) 6.S.2 (9.00 (<LOD-1.7 (8.96-11.68-19.68-10.4) 6.6-19.6 (12.72) 4.92) 3.63 (2.00 (<LOD-1.30) 2.01-5.5 (11.89-3.7) 12.20-3.95) 3.1 (19.77 (2.8) 16.9) 19.4-15.4) 7.4) 9.82-11.3-17.86) 9.00 (3.55) 16.4-16.850 (<LOD-1.38 (2.0 (10.71 (1.5 (8.82-8.02-4.25-9.19) 3.29 (5.4-18.8 (10.6) 6.07) 2.69-11.54) 9.83 (6.94 (5.97-4. population from the National Health and Nutrition Examination Survey.86 (3.88 (1.7 (10.4) 7.89 (3.41 (7.89-10.06) .530-1.51-10.73 (5.5) 13.89 (2.15 (1.95 (2.52-3.9-25.85-8.96-10.18) 2.11-3.1 (8.590 (<LOD-.27-13. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7) 15.45) 6.5-17.29) 3.04) 9.9 (9.4-16.5 (9.9-17.21) * * * * * 1.2) 12.43 (2.5) 22.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.99) 2.6) 95th 16.4) 15.9) 16.6) 7.89) 5.30-5.89-3.0 (13.4 (11.7-23.80) 3.30) 7.81 (7.7) 14.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .27) * * * * * * * * 1.7) 9.6 (11.890-2.2 (9.3-21.87 (3.21-21.16-14.6) 12.6) 14.42) 7.920 (<LOD-1.3 (7.54-5.61 (2.28 (1.7 (11.29 (2.63 (6.7 (10.950) .16 (3.7) 14.32-8.77 (2.03 (6.2) 10.74-19.0-21.38 (.4) 7.44-6.810 (<LOD-1.91-9.50-17.8 (8.54 (7.36 (2.8) 11.0) 14.99 (4.78) 4.78-10.6 (13.5 (10.71) < LOD < LOD 2.38-13.6 (11.3) 6.03 (2.06 (<LOD-1.12 (7.95) 90th 8.0-19.64-11.85-17.33-10.00) 8.5) 8.55 (2.25 (4.910 (<LOD-1.0 (11.39-17.89-13.34-18.2-30.53-8.94-14.27) 1.7-19.14 (2.2) 16.67 (7.75-3.37-5.74-4.70-35.2) 12.5) 10.3) 9.72-4.48 (2.940) < LOD < LOD 1.83 (7.70-2.45) 3.09-11.00 (5.86-3.93 (2.12) < LOD < LOD 4.30) 8.00 (2.00 (7.93 (<LOD-2.78 (6.50 (6.1) 20.67 (1.42-19.5 (15.78 (4. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .38) 1.07) 2.75-3.23-3.38 (1.2) 19.27) < LOD .3-17.760 (<LOD-1.47-9.93-10.973 (.2) 8.92 (5.07-3. * 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 123 .4) 16.27) 5.6 (13.6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.91) 3.29-2.1) 10.3-15.15) < LOD < LOD 75th 2.28-12.3) 8.55) .690 (.93 (6.8) 14.03) 3.2) 672 678 497 509 694 578 595 948 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.79-9.780-1.9 (9.79-6.37) 3.0 (8.1 (13.97) < LOD .33) 3.05-3.11 (5.00) 2.1) 13.2) 12.51-7.3) 12.68) .88-7.9 (9.59-3.2) 15.3-34.32) 2.34) < LOD < LOD < LOD < LOD 3.68-4.6) 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 * * * .2-15.09-11.58 (4.42) 8.77) 3.6) 13.

17) 1.10) 3.30) 2.05-3.96-5.78) 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 * .30 (1.1.10-1.10-1.20 (1.10) 1.15) 2.74) 3.970) .90 (1.89) 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 * .29) 1.390-.63 (1.90) 3.48 (1.20) 1. and 0.30) 1.690-.09 (.25-1.30-1.359-.780 (.70-2.90) 2.50 (1.65 (2.680-1.76 (1.34) 2.353-.00) 1.950) 90th 1.11-3.70 (1.27 (3.50 (1.70 (1.88) 1.510 (.618) * .650-.467 (.17) 1.80) 5.240 (<LOD-.750) 1.570 (<LOD-.47) 2.91) 2.20 (2.54 (2.80) 3.620-1.83) .580-1.760 (.46-3.990-1.98-3.22-3.810) .49) 2.03) 1.590-.453 (.54) . 0.73 (2.440-.700) .20) 2.46 (1.400) .50 (1.70 (1.80) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.960) 1.37-2.95-5.449 (.95 (2.00 (1.45-4.780) .840 (.64 (1.16) 2.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.460-.23-3.70-7.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.584) .80 (1.20 (1.700) .30) 4.592) * .32 (1.15) 2. respectively.450 (<LOD-.970) 1.31-3.910) 1.58 (1.68-5.46) 1.17-4.00) 2.14-1.60-4.22 (1.20-2.910-1.90-4.510 (<LOD-.18 (1.2.31-3.00-2.10) 1.600-1.597) * .398-.30-3.22-2.740-1.60) 2.930) < LOD .78) Sample size 1949 2519 1905 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .47 (1.16-3.50-2.570-1.78) .27 (2.340-.87-3.585) * * .960) .04) 1.505 (.60 (2.600-.45 (2.749 (.20-3.710 (.720-1.30-3.74-5.41-5.960 (.73 (1.01) .80) 3.98) .79) .S.48 (2.45 (1.20) 1.350-.380-. and 03-04 are 0.570 (.740-.790 (.86) 3.830 (.540 (.560-.500 (<LOD-.20) 3.94 (2.69-4.750-1.20) 2.657) * * .490 (<LOD-.880) < LOD .960) .710 (.592-.75 (2.580-.690 (.459 (.35) 1.41 (2.59-6.86 (1.690-1. which may vary for some chemicals by year and by individual sample.54-2.720-1.670) .08 (2.83) 2. 124 Fourth National Report on Human Exposure to Environmental Chemicals .29-2.83) 1.30 (.77 (1.95) 2. interval) Selected percentiles ( 95% confidence interval) Total * .550 (.31) 95th 2.80 (2.13) .710) .820 (.55 (3.57 (1.20) 3.30) 4.20 (1.50) 1.759) * . < LOD means less than the limit of detection.94 (3.32-1.880 (.33-2.04) .587) * * .76-6.83 (2.260 (<LOD-.800 (.201-.49) .720 (.94) .77-2.61 (1.380-.570 (.16) 1.30 (.303-.930) 1.90) 2.850) < LOD .388-.343 (.39) 2.690) .13) 2.57 (2.50-2.14 (1.96-3.336-.34) 2.457 (.79) .350-.60) 3.592) * 50th .10) 1.860) < LOD < LOD .820 (.50 (1.910 (.570) * .930 (.26) . see Data Analysis section) for Survey years 99-00.740 (.32) 3.730) .940) < LOD .380) .455 (.89) .09.21) 3.11-3.600 (<LOD-.00-4.740 (.05-2.73-5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.89-6.45 (1.80) 2.26 (2.40 (1.390-.30 (.549 (.89) 1.59-2.42-2.97 (2.949) .46 (2.930-1.19-1.680-1.50 (1.550 (.20-1.570 (<LOD-.960-1.01-1.80) 2.40 (1. 01-02.780 (.20-2.98 (2.880) < LOD 75th .382-.980) 1.31) 2.75-2.210 (<LOD-.83 (2.08 (2.18 (.425 (.22-8.22-3.01-3.160 (<LOD-.280-.38) 1.36-4.

00 (3.69 (3.670 (.67-3.552 (.270-.43) 2.320-.630) * .05) < LOD .52) 3.16-2.79 (1.72) Sample size 1949 2518 1903 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .61) 2.390-1.330-.08-3.591 (.42 (.25-3.830 (.250 (<LOD-.11 (.92 (1.380-.70 (3.97 (1.440-1.460-1.63 (1.34 (1.05-4.540-.62 (2.58-6.88) .23) 2.33 (1.08) 2.71) .590 (.67 (1.77 (3.22-3.17-2.820) .320-.07-2.87 (2.20-7.84-6. interval) Selected percentiles ( 95% confidence interval) Total * .50 (1.08 (2.760) < LOD 75th .82) 2.350) .75-3.400) .330 (<LOD-.55 (1.18-2.16) 1.61-3.800-1.485) * * .07) 1.52 (1.335-.870) .180 (<LOD-.22-3.910) < LOD .47 (1.04-1.940-1.S.08-2.76) 1.38 (2.09) .60 (1.97) 1.400-1.950-2.920) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60) 1.13 (1.739) * .393 (.830) 90th 1.453 (.580-.234 (.700 (.710 (.99) 2.16-1. Fourth National Report on Human Exposure to Environmental Chemicals 125 .04) 95th 2.60) .310 (<LOD-.700 (.17) 2.22) 1.75) 6.580 (.28 (1.760) .348-.77-3.05 (1.412-.372 (.84 (2.700 (.02-3.660-.480) .06-2.08 (.790) .49 (1.680 (.230 (<LOD-.510 (.44) 2.253-.850) 1.20-2.75 (1.520 (.32) 1.75 (2.640 (.03-1.58) 3.08-2.57-2.72 (2.390) .32) 5.800) < LOD .990-1.930-1.550-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.730) .742) * * .70 (2.50) 1.24) 4.480-1.136-.72 (1.05) 1.460) .550-1.49-4.750 (.310-.73 (2.98) 1.91 (1.490 (.31-1.08-3.42-6.72) 1.590-1.448 (.43) 2.22) .90) 2.22-2.403) .Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.62 (1.300 (<LOD-.99) 1.64 (2.23) 1.08-3.520-.510 (.77-4.97) 2.07) 5.97) 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.89-3.08-3.640 (.00-3.60 (2.69 (1.530 (.32) 2.750 (.22) 4.81) 2.94) .57 (3.47 (1.45 (1.39 (1.05-2.79) 1.710 (.515) * * .88 (1.78) 3.45 (2.57 (1.535 (.720 (.38-3.02-3.89 (1.590) * 50th .30) 3.310 (<LOD-.08) 1.23) 3.840) .740) < LOD 1.92) 3.368) * .07 (.92-8.39) 2.33) .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 * .270-.61 (3.710 (.07) 1.67 (1.305 (.22 (2.11-2.61-3.42-8.510-.900) 1. population from the National Health and Nutrition Examination Survey.66 (2.32 (.270 (<LOD-.02-6.471-.41 (.82 (2.580) .250 (<LOD-.500-.380) .370-.55-3.72-4.43 (1.285-.66) .690) < LOD < LOD .07) 1.377-.550-.597) * .10) 2.560 (.470) .04-5.32-1.17) 2.444-.38 (1.00-1.460 (.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 * .30-2.509 (.550) .470 (<LOD-.71 (1.20) 1.43) 1.08-2.300-.870 (.58 (1.65) 2.560-.23 (.318-.14 (2.880) 1.380-1.19 (1.280 (<LOD-.42) .820) 1.29-4.97 (1.980-1.11) 1.688) * .67) .71) 2.720-1.740) .560-.95) 1.03-2.44-2.57-4.47-4.73-3.645) .840) 1.67) 1.23) 2.07-3.447 (.840) 1.36) 3.80) 2.790 (.64 (2.06) 4.640 (.53) .

74-2.85) * 2.70 (1.7 (12.30) 4.0) 45.41-4.70 (7.31-6.0-31.1) 38.48-2.30 (.1 (22.45) 2.0 (40.0) 28.95 (5.2 (19.6-22.1-20.91 (4.26 (.14) 5.77 (1.5-20.830-4.85 (1.70) 1.5) 69.36-2.67 (1.610 (<LOD-1.3) 33.0-49.13 (1.0-62.2-33.2-47.6-45.1) 18.9) 38.0-110) 42.8 (12.29-4.70-6.0) 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 2.0-69.80) .79 (1.21 (3.18.70 (. and 03-04 are 0. population from the National Health and Nutrition Examination Survey.00 (.32 (2.59 (1.52 (4.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.41) 5.1 (25.0-41.41) 1.30) 11.70-17.2-80.3 (23.9) 48.61-2.8) 41.3) 38.0 (8.83 (1.53 (1.60 (2.05) 1. interval) 1.58) 16.54 (3.9) 17. see Data Analysis section) for Survey years 99-00.71) 5.50-2.7 (12.0) 3.3) 26.50-7.8) 39.3 (10.2-26.7-22.0 (25.97) 6.80) < LOD 1.50-17.7-41.53) 1.70) 1.6 (26.0-29.0) 42.16) * 1.1) 140 (46.71-2.0) 3.88) 1.77) 38.0) 5.0) 3.0 (7.2-27. which may vary for some chemicals by year and by individual sample.46-6.92) * 2.0-52.0 (17.83-2.76 (2.0 (32.10 (1.06 (1.0 (37.0) 4.0) 30.53) * 2.13) 12.41 (1.80-18.0 (38.0) 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 2.1-47.6) 52.0-41.1 (26.1 (11.10-4.9-51.0) 31.75-14.41) 1.80) 90th 38.0) 32.0) 4.53) 40.7) 20.8 (22.46 (.94 (1.86 (1.40) < LOD 1.0) 20.0-43.1-19.21 (1.0) 4.6 (9.66-5.19) 2.6-27.64-3.72 (1.54 (1.3 (12.0 (20.06) * 2.7) 47.2-39.12) 1.78) 9.86-3.0-47.5) 30.0-50.8) 62.80) 1.40-4.50-20.63-6.27-6.2) 31.10-13.82 (1.0 (8.83-2.42) 1.79-2.10 (1.46-2.05) * 2. 126 Fourth National Report on Human Exposure to Environmental Chemicals . 01-02.59 (1.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.3 (12.0) 8.2) 16.1 (10.05-3.9) 18.18) 20.23) 9.00 (.4-76.0 (26.92-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-58.10 (7.0-92.26) 75th 11.02 (2.48) 5.0 (38.0) 33. respectively.0) 19.50-5.78 (1.830-3. < LOD means less than the limit of detection.5-74.9 (27.4-22.4) 19.20-4.8 (26.4 (10.93-3.13 (1.530-4.2-62.19-2.25-3.S.60) < LOD 1.71 (4.0 (33.87-7.0 (38.04-8.0-41.0 (24.0) 3.0-53.90 (1.6 (15.0) 13.3 (24.45) 2.79 (2.3) 28.8) 32.58-2.0) 18.57-2.65 (4.600-2.80-2.81-2.00-24.0 (8.07-5.44) Selected percentiles ( 95% confidence interval) Total * 2.2-27.8) 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 1.98 (1.4 (19.9 (19.4 (15.690-3.12 (3.0 (6.0 (20.57-2.470 (<LOD-1.50 (2.04) 3.11 (4.30-14.18) 6.40) < LOD 2.0 (38.69) 2.40-16.0-110) 34.20 (2.44-7.90-8.6 (11.70 (1.1) 95th 48.1-46.11) 2.7 (28.5 (24.660-2.9 (23.10 (1.10 (1.10) .4) 38.1) 38.43-7.18) 14.0 (38.9 (10.0) 20.0) 6.0 (19.0-39.0-58.70) 5.29-9.2 (12.10) 39.64-8.0) 16.98) * 2.0-62.6-54.17-2.9-21.48-2.0 (21.4.33 (5.1 (25.5-45.90) 11.76 (2. and 0.0-260) 34.0) 16.44) 2.0) 15.81-3.0) 15.88) 3.8-21.44) 3.8-24.3) 31.0-39.0 (38.29) 2.35-6.20) 1.49-2.0 (11.5-40.61 (1.0 (13.23-2.99 (2.0) 28.8 (12.0-230) 35.0-53.40) 50th 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (38.5.5-27.83 (3.1-40.04 (<LOD-2.16) 2.3 (14.21 (4. 0.9 (19.1-25.0) 17.96) 5.23-2.0) 17.90 (1.09 (4.

08 (1.71) 8.47-17.5 (17.8-43.50 (2.0-71.75-6.56) 1.94) 1.90 (.2) 36.0) 30.6-51.43-12.2 (21.5 (15.6 (24.3-19.2 (15.2 (22.2) 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.2-34.9-95.8) 11.70-4.02) 1.2 (16.69-5.23) 37.64 (1.5-190) 30.67-3.0) 13.00 (4.51) < LOD 1.37 (1.6) 11.1) 36.88 (1.0) 25.02 (.11-2.5 (6.0 (23.8-37.0 (14.16 (1.36-13.5-36.88 (4.4) 12.9 (19.860 (<LOD-1.00) 1.9) 3.2) 41.27) 50th 2.48 (4.0-40.9 (7.33) 1.68 (1.28 (1.57 (6.24 (1.51) . interval) 1.5 (13.7-37.22-2.96) 2.4) 12.0) 47.5 (15.40 (2.91 (6.9-37.45 (1.8) 15.75) * 1.670-1.48) 1.43-2.7 (24.6 (11.0-70.33-5.7) 95th 51.6) 3.35 (2.67 (1.47 (3.9) 24.14 (.94-20.8) 32.3 (8.3-42.67-16.1-60.19 (1.11) < LOD 1.76-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4-34.8) 3.27-3.9-36.0 (39.69-18.9) 12.52 (1.23) < LOD 2.06) 75th 9.58-2.4 (5.5) 70.03) 1.88 (4.22 (2.7-47.4 (12.35) 1.29-5.83) .95 (2.35) .46) 1.6) 7.14-8.27) 10.54-2.899-2.1 (12.8) 31.46-5.3 (10.30) 28.17-3.6) 112 (40.94) 19.2) 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 2.7) 15.6-32.68) 47.9 (13.1) 17.7-109) 22.7-43.52-4.1) 27.1) 13.1-63.19) 5.6) 23.60 (.888-1.680-4.7-20.63-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.22-3.2) 13.19) 5.70 (1.4-71.890-4.7 (10.82) 1.0) 3.06) 1.59-2.1 (39.7-19.40-4.7 (11.9) 54.6 (7.6 (27.0) 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 1.4 (25.4 (19.46-22.870-3.5) 27.3 (20.71 (1.83 (.88 (1.00) 6.8) 23.66) 8.75 (1.870-3.66 (1.56 (2.19-14.20-5.7) 30.79-17.96-16.2) 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 1.7-38.79 (2.3) 13.4-21.2-70.7) 66.36 (4.750 (<LOD-1.5 (8.3-22.8-26.0 (23.31) 2.37-2.0 (19.97 (1.07) 9.2-38.06-1.38 (3.5-97.S.930 (<LOD-1.95-16.4) 3.0 (17.2-47.0 (25.62 (2.91-2.82 (2.66 (1.27 (6.20) Selected percentiles ( 95% confidence interval) Total * 1.36) 10.26-2.5 (34.7) 61.47 (1.41 (2.5-43.17) 2.28) 1.1-22.38-1.00-16.9-41.16 (1.0-118) 29.21 (4.4 (21.75 (1.43) * 2.4 (11.22 (.62) 4.01 (.86) * 3.50-5.2) 33.99-4.07-2.18) 3.6) 19.61-22. population from the National Health and Nutrition Examination Survey.9-18.2 (8.06) 1.23-1.07-2.6) 3.67 (1.26-4.55 (2.16-2.7) 26.34) * 1.2) 4.15 (.61 (1.38-5.9) 24.12) 3.59-15.95-16.40 (5.7) 23.9-52.1 (33.9) 3.93) 5.1 (50.7 (18.8-45.95) 90th 32.58-17.0 (6.7 (18.45-1.4-67.32 (3.6-38.71-2.1) 25.3) 28.44) 9.7) 34.02) * 1.72) 2.4 (25.57) 4.4 (9.2) 13.9 (26.4) 14.1) 13.6-49.0) 48.19-6.9 (39.1 (25.09 (5.2-28.16 (1.60) 4.4-39.18-1.1 (34.59-2.40-7.80-8.54-15.61-2.3 (9.86) * 2.12 (1.80 (1.2 (9.1) 25.1) 52.3 (10.39 (1.33) 2.33) < LOD 1.0 (32.9 (10.38) 5.870-3.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.8 (7.1) 15.1) 27.3-27.03-2.84-13.46-6.5 (41.08) 1.53) 1.25-3.18) * 2.32-3. Fourth National Report on Human Exposure to Environmental Chemicals 127 .0) 10.8-34.

850) < LOD .870 (.350) < LOD < LOD < LOD < LOD .720-1.450 (.050-.720) . and 03-04 are 0.430-.32) .640) . 0.990) .200) < LOD < LOD .770 (.430 (.090 (<LOD-.640 (.680-1.390) < LOD < LOD .820 (.120-.680) .400-.650-1. see Data Analysis section) for Survey years 99-00.30) . < LOD means less than the limit of detection.15) .540) .820 (.870 (.780) < LOD 1.640) .830 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .130) .860) .840) .150 (<LOD-.1.36) .870) < LOD .540 (<LOD-.490 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .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 .850 (.58) .1.180) .120 (<LOD-.60) 1.10) .370-.42) .850 (.610-.100 (.380-.130) .700-1.12 (.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.940 (.280) < LOD < LOD < LOD < LOD .330-.320-.930 (.600 (.990 (.080 (<LOD-.380-.720 (.650) .560 (.190 (.120-.190 (.360-.630 (.680-1.450 (. 01-02.240 (<LOD-.230-.660 (.470 (.140-.300-.760) < LOD .170-.290 (<LOD-.05.860-1.090 (<LOD-.310-.700-1.360-.S.084-.870 (.20) .460 (. population from the National Health and Nutrition Examination Survey.130-.220 (<LOD-.110-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) .150) .080 (<LOD-.10) .370-.870 (.990) .460-.10 (.540) .450 (.230) .700-1.130-.03) .162) * * * * * .090 (<LOD-.099-.830) < LOD .650 (.160) .680 (.900 (.310) < LOD < LOD < LOD < LOD .30) . and 0.290) < LOD < LOD < LOD < LOD 90th .700-1.840) .140-.00) .160-.290) < LOD < LOD < LOD < LOD .830) .210 (.550) .410-.140) .620 (.510-1.10) .130-.42) .830 (.410-1.870 (.300-1.730-.320 (.630 (.530-.090 (<LOD-.310 (.090 (<LOD-.090 (<LOD-.410-.610 (.650) .640-1.260 (.117 (.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 * * * * * * .160) .740) < LOD .220 (.310 (.30) .140-.13) .470-1.570) .610-1.770) < LOD 95th .390 (.270 (.380-.650-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130 (.560 (.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 * * * * * * * * * .190 (.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.210 (. which may vary for some chemicals by year and by individual sample.420-.310) < LOD < LOD < LOD < LOD .730) .440-1. 128 Fourth National Report on Human Exposure to Environmental Chemicals .610 (.171) * * .690-1.350) . respectively.410) < LOD < LOD < LOD < LOD .

570-1.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.330 (.520-.250-.58) 1.400 (<LOD-.540) 471 576 310 664 821 715 814 1118 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .660-1.360-.410) .110) .720 (.140-.410 (.090 (.780 (.300-.180-.700) .12) < LOD .550 (.810 (.170) < LOD < LOD .084-. population from the National Health and Nutrition Examination Survey.170 (.500 (<LOD-.260) .111) * * * * * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.710-1.670 (.490-1.38) 1.230) < LOD < LOD < LOD < LOD .S.370 (<LOD-.570-.67) .970) .580 (.300 (.110-.730) .860-2.600-1.700 (.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .03 (.880 (.330-.60) .700 (.060-.24 (.24) .760) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.116 (.860 (.270 (.260-.450) .990) .380 (.510) Sample size 1949 2515 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .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 .850 (.120) .730) .750) < LOD 95th .670 (.190 (.880-1.740) < LOD 1.110) .360 (.190-.140-.110) .02) .400) .940) .86) .580-1.100 (<LOD-.500) .070 (<LOD-.070 (<LOD-.870) .14) 1.600) .02-1.610-1.03 (.390-.450 (.19 (.170 (.320 (<LOD-.36 (1.110) .080 (<LOD-.120) .360-.100-.01 (.330-.410) < LOD < LOD .09) .29 (.290) < LOD < LOD < LOD < LOD 90th .090 (<LOD-.580) < LOD .390-.730) .86) .62) 1.280) < LOD < LOD < LOD < LOD .990) .200 (.070 (<LOD-.440-1.140-.360) < LOD < LOD < LOD < LOD .540) .230-.580) .380-.140) .410-.560 (.960) .057-.460 (.210 (.050 (<LOD-.380-.080 (.410-.540 (.500-1.340-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .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.800-1.330-.890 (.740 (.470 (<LOD-.00) < LOD .161) * * .700-1.650-1.190 (.440 (.140-.220) < LOD < LOD < LOD < LOD .570 (.080) .720 (.230 (<LOD-.550 (.070 (<LOD-.670-1.150-.330 (.220 (.300-.580 (.860 (.20) 1.380-1.140-.640-1.03) .410 (.270) < LOD < LOD < LOD < LOD .66) 1.200 (.03 (.540 (.43) .780) < LOD 1.310) < LOD < LOD < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 129 .78) .380-.940) .240-.650) < LOD .730 (.510-.

0-38. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.68) 2.770) 2.0) 4.35-10.0 (16.0 (6.425-1.620-1.07 (3.37) .21) 3.85-3.600 (.00) .51-8.00 (1.30) 95th 19.840 (.00-17. and 03-04 are 0.0-40.30 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 2.40-8.63 (3.0) 3.96 (1.42) 2.0 (3.0) 2.170-1.55-8.94-3.50) 2.94 (1.0 (17.20-4.70-7. 130 Fourth National Report on Human Exposure to Environmental Chemicals .910) 2.890 (.610 (.20-17.01) 5.90 (1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.260-.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.0) 4. respectively.690 (.28) 1.55-4.800) 90th 13.35) 5.960 (.49 (1.0 (4.0 (17.0) 5.30 (1.14) .18) 1.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.12) * * * * * * * * . population from the National Health and Nutrition Examination Survey.0) 2.32-9.0-39.36-3.38-3.23-6.380-.07-3. see Data Analysis section) for Survey years 99-00.62-8.30-6.30) .53) 20.94-8.0) 4.0) 2.51 (2.36-3.0) 2.0-40.90) .0 (5.840 (<LOD-1.07 (3.08.210-1.46 (1.750-1.0) 7.640 (.11 (1.330 (<LOD-1.30-3.10-9.840-3.66) 4.43-4. < LOD means less than the limit of detection.13 (3.87) 12.10-3.26 (2.0 (4.1.30-7.70-30.52 (1.350-.20 (1.48 (2.870) < LOD < LOD .99) 19.74 (3.400-1.35) 11.0 (13.70-3.28-9.880) 5.720) 2.580 (.74) 5.0 (17.97) 20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30 (2.0) 5.40) 1.05 (2.190-1.90) .0) 2.590 (.6) 5.640 (.370-.0 (7.67) .62) 471 575 306 664 821 699 814 1122 925 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .00) 1.90-28.90 (2.15) 19.29-10.97) 20.10 (.850) 16. which may vary for some chemicals by year and by individual sample.45 (2.24-7.33 (4.S. 0.40-4.03 (.40 (1.31) .1.610) < LOD < LOD < LOD < LOD < LOD 2.0-44.360-1.14-5.0 (17.30 (.00 (.20-4.61 (1.90-9.42) .830 (.47 (3.960 (<LOD-1.88-3.80 (4.52) 5.53 (2.10 (3.0-38.0 (17.800-4.49 (1.250 (<LOD-.70-17.110 (<LOD-.080-1.05 (3.10 (3.30 (1.750-2.480-.20 (1.50) .32 (1.60) 1.0 (5.730 (.0 (5.0-38.83) 2.691 (.99) 11.99 (1.86) 4.65) 1.48) 13. and 0.67 (1.40) 2.40-7.11) .14) 2.0) 2.90-37.05-3.49) 17.16) 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 (5.40 (1.510-.00-17.60) .40-20.20) < LOD < LOD < LOD < LOD < LOD 1.11) 13.770 (<LOD-1.28) .0) 5. 01-02.63) 32.83-3.15) 14.67 (2.90) .82-4.70-50.07-3.90-20.39 (2.21-3.0 (5.07 (1.07) 1.0) 4.59-5.3) 952 1187 935 997 1331 995 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .53-7.00) .31-10.87) 5.52 (1.350-.10-3.0) 5.740 (.800) 17.76 (1.39) .12-1.83-3.900 (.70) 2.

44-11.41 (4.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.83 (4.650) 90th 10.840-3.30 (4.47-10.91) 2.250 (<LOD-.660) < LOD < LOD .22) 2.11-5.5) 7.970-3.690-5.430 (<LOD-.8) 7.86 (3.370-1.820) .47-10.1) 672 678 497 509 694 551 595 947 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.5 (8.79 (.7) 3.67) 2.18) 95th 21.8) 7.740-1.4) 2.260-.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 (1.25 (1.790) 11.3) 3.71 (2.92 (2.700) < LOD < LOD < LOD < LOD < LOD 1.47) .340-.1 (5.04-16.190-1.8) 2.580) 16.S.51-44.580 (.67) 1.56 (1.67 (2.09-3.860-2.780-4.29 (4.24) 3.50) . population from the National Health and Nutrition Examination Survey.64-4.8) 2.330-1.25-9. Fourth National Report on Human Exposure to Environmental Chemicals 131 .67-6.85 (1.43) .04 (1.474-1.36 (.5) 2.1 (7.2 (8.02-4.18) * * * * * * * * .540 (.21-3.9 (11.77 (.960 (.40-12.38 (2.7) 5.9) 5.88 (.10) 2.05) .74 (2.65 (2.41) 18.770) .320-1.7) 4.730-3.85-3.850-3.0 (9.7 (12.5-40.1) 2.44) .370) < LOD < LOD < LOD < LOD < LOD 1.59 (1.31) .40 (.33-4.8) 4.83-11.62 (1.240-.96-8.37) 4.57) 8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07-21.56) 2.12-4.97) .15) 9.1) 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 * * * * * * .07 (2.48-42.31-7.23-7.7 (6.55) 21.03) 16.260-.540-1.12 (4.390-.22-27.930) .370 (.31) .52 (.08) .340-.830-3.5 (11.73 (4.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.64) 30.270-.33-5.35 (.790 (.33 (3.03) 2.69) 2.48-7.88) 17.10-3.32) 9. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.17 (1.630-1.830 (.500 (.80 (.55) 21.18) 1.9) 6.470 (.57-40.80) 3.800-2.13 (2.88-3.29-4.0 (4.02 (1.25-38.890 (.28-6.4-34.90-6.4 (4.50) 11.590) 2.89 (2.00-19.8 (20.96-25.56) .57) 1.820 (.31-18.02) .14 (1.7) 6.450 (.27 (2.06 (.5 (9.88 (2.51-4.11) .150 (<LOD-.84) 9.33-3.45 (1.00) .10 (2.8-33.49-2.02 (.620-3.650 (.50 (4.32-6.310-.560 (.5) 2.55 (3.81-17.748 (.98 (4.360 (.17) 5.580-1.69-7.86) .940-4.82-11.40-2.3) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) 1.61) Sample size 1949 2517 1927 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .53) .53) 27.75) 5.39) 20.580) 1.670 (.340-.91-4.47) 5.430) 1.96) 2.340 (.8) 1.50 (2.0) 4.01 (1.48 (4.710 (<LOD-1.57 (.60 (1.62-17.600 (<LOD-1.66-47.2-38.14-6.270 (<LOD-.700) 6.71 (.

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5.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. malathion is metabolized to malathion dicarboxylic acid. parathion and methyl parathion are metabolized to para-nitrophenol. For example. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides.” Organophosphorus insecticide (CAS number) Chlorpyrifos (2921-88-2) Chlorpyrifos-methyl (5598-13-0) Coumaphos (56-72-4) Diazinon (333-41-5) Malathion (121-75-5) Ethyl parathion (56-38-2) Methyl parathion (298-00-0) Pirimiphos-methyl (29232-93-7) Primary urinary metabolite (CAS number) 3.6-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 . The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. For general information about the organophosphorus class of insecticides. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. the level may reflect exposure to the environmental degradation products of these pesticides. In addition to reflecting exposure to the parent insecticide.

and sprayed to kill mosquitoes.4 and 0.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.67 (2.19-3.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.20) 4.20-14.71 (1.63 (1.00-8. 1999.98-15.10 (5.0) 12.70 (1.22 (1.90 (2.0 (7.90) 7.0-28.90) 3.15 (1.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.20) 2.36 (4.77 (1.5 (8.97) 2.3 (11.70-16.70-17.05-5.61-7. Survey Geometric mean (95% conf.74-9.66-15.10-17. but can be detected in streams receiving runoff from application sites.71 (6.50-2.0 (9.3 (10.0) 10.0) 12.13 (1.63 (2.9 (7.8) 10.70 (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.59-2.5) 7.40 (5.80) 4.04-10.61 (1.S.9) 697 660 521 701 602 947 Limit of detection (LOD.51-2.25) 1. 2921-88-2 Chlorpyrifos-methyl CAS No. interval) 1.57 (2.55-5.43-2. Exposure can also result from contact with contaminated surfaces. applied to structures to kill termites.60-4.00-24.40 (5.50 (1.3) 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 1.0 (13.90 (3. It also has been applied directly on animals to kill mites.9 (10.30-2.89 (2.00) 2.28-3. and on plants for days to several weeks.79-2. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.95) 7.89-2.22) 2.EPA.83) 1.60 (2.and post-construction structural applications for termite control were to be phased out by 2005 (U.60-3. 2007).9-18. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.25) 3. Approximately 21-24 million pounds per year were used domestically from 1987-1998.63 (8.31-2. 5598-13-0 General Information The chemical 3.68-2.10 (1.20-16.50-4.60-3.35) 2.20-2.20 (4.97-7.02 (7.80-8.50-14.70-11.26) 7.67 (1.76 (1.46-2.32-1.74 (1.10 (4.70-5.0) 7.31-2. For instance.27 (7.0 (7. and inhalation routes.04-10.97) 7.61) 75th 3.30-1.91) 16. air.40-13.30-9.0) 15.50-8.30 (2.80 (7. Fourth National Report on Human Exposure to Environmental Chemicals 135 . Approximately 80.2 (10.09 (2.40-26.40 (6. pre.9 (9.10) 2.02) 1. dermal.90 (1.30 (4.92 (1.3) 8.44-5.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.88 (1. After 2001.0) 6.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.03) 1.5-24.81-2.7) 8.38 (3.70-15.5.77) 1. 2002).90 (6. and dust.1-16.29-1.30) 4.09 (3.35) 1.87-6.80) 1.72-4.51) 1.59) 2.47) 1.8) 9.50 (2.90-4.17 (1.30-5.47-13.20-3.97) 2.60 (4.0) 11.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.52-12.45 (1. Chlorpyrifos is Urinary 3.90-2.20-11.47-11. 2005).84) 1.20) 2.10 (3.02 (1.47-9.94 (4.77-6.67 (2.0) 9.16) 2.40-10. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.29) 90th 7.5.40) 9.34) 1.05) 1.30-11. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.8-15.4 (10.50 (2.0) 12.40-2.10) 6.44-2.7-23.50 (2.97) 4.0) 8.0 (7.0 (7.0) 10.66-4.S.4 (9.30 (2.90 (1.9) 11.60) 5.37) 5.19 (1.4-15.20) 10. population from the National Health and Nutrition Examination Survey.21) 3. It has low leachability..30) 5.30-12.000 pounds are used per year.44 (3.50-2.4 (8.39-2.0) 12.43-2.24-1.50-5.96) 3.68 (7.13-3.0 (7.72) 2.76 (1.28) 2.77-15. USGS.78 (7.70) 1.20-4.01) 1.39) 4.20 (2.0 (10.80) 2.60 (5.37 (4.60-2.00) 3.32) 2.0) 10. staying bound to soil particles.0) 8.52-2.7) 9.50 (1.24-3.80) 12.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.30) 4.3 (8. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.00) 1. chlorpyrifos was no longer registered for indoor residential uses in the United States. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.40) 2.62-2. The general population may be exposed to chlorpyrifos via oral. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.91 (1.EPA. 2002).4.71 (2.86) 4.37 (1.90-8.1) 5.0) 18. Estimated intakes from diet and water have not exceeded recommended intake limits.7) 13.95 (4.99-4.80 (1. in 142 urban homes and preschools in North Carolina.0) 14.53 (1.0) 12.90-7.6) 7. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.64) 3.S.50-4.47 (4. and is infrequently detected in ground water (IPCS.51 (1.80-10.

94-14.63 (4.27-7.99) 1.EPA. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.71 (1.88-9.2) 6.59-2. Slotkin et al.00 (7..91) 1. 2005.80-11.91) 2.9 (12.35) 2. Roy et al.87-3.28) 2. 1984). weakness.42-2.45-1.81) 2.30-1.01) 3.3) 9.22 (6.75) 6.1-38.44-6.12-3.1 (7.S.69 (1.940-1.29 (3.07) 5.93) 2. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals . 2005.47 (1.58 (1.39) 6.7) 7.25-11.3) 8.62) 90th 5.65-11..0) 16.25-12.91-13.06-4.57) 9.96) 3.95 (3.00) 1.48 (2.58 (4.05-4.56) 2.42 (5..51 (1.19-2.33-7. and other metabolites.74) 1.19) 3.65-15.6-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.40) 1.16) 6. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.88-10.52 (5.44 (5.39 (2.43 (4.2 (7. 2002).44 (5.98 (7. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.31-1.22) 1.49-2.5 (6.66-11..09 (1.01) 3.58) 1. TCPy is more persistent in the environment than chlorpyrifos itself (U.00-13.56-2.09-1. 2005.1-21.85) 4.91) 1. Ricceri et al.32) 1.93 (1.55) 1.56) 5.76 (2.33 (.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1. TCPy can also occur in the environment from the breakdown of the parent compounds.46 (2.50 (4.58-5..33 (5.41 (1.83-2.3) 8.53-5.97 (2.6) 10.22-6. Urinary 3. 2006.68) 6.49 (1.93 (2.63-2.3) size 1994 2508 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.35) 1. Based on animal data and human cholinesterase monitoring during occupational exposure.39 (4.07) 1.91) 10.82-4. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.97 (3.54 (2.80-6.47 (5..23) 14.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.27-1.99-8.06 (5.85 (2.94-12..81 (3.6) 9.05-3.86 (1.S..17-4.55 (1. Betancourt et al. interval) 1.15 (4.14-8.21-1.20 (2.26-14.12) 1.11 (2. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.97) 3.66 (1.62) 1.83) 1. cholinergic effects.92 (1.57-2.95 (1.55 (4.84-6.02 (5.16 (4.80-4.57-2.49-2. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.53 (2.31) 1.44 (1.36) 1.28) 2.71) 3.91 (4. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).31-4.24) 75th 2.82) 8. 2000). Survey Geometric mean (95% conf.93) 5.68) 1.73 (1.64-7.24-24.05-1.5) 5.4) 4.80) 3. 2006b).64 (1.54) 5.37 (1. Thus.76 (3.24-4.60 (1.58 (1.88-8.85-4. Metabolic hydrolysis leads to the formation of TCPy. 2006a.06 (1.43-10.39-1.56 (4.20-1..01) 1.82 (3.85 (3.72-2.89) 4.46 (1.35-1.82 (2. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.88 (1.23-1.83-11.88 (1.02) 7.11 (2.75 (1.92-2. and seizures. vomiting.24-5.91-4.09-2.85) 1.1 (10.38) 3.30-4.0) 6.60-3.42 (6. neurotransmission.12-1. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.47-2.91 (3.59) 3.24 (1.33 (1. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.92) 3. Once absorbed.24) 5.19) 6. Two observational studies of pregnant women and their offspring exposed to chlorpyrifos at environmental levels have found inconsistent relationships with birth outcomes of weight and length (Eskenazi et al.64-2.21-6.86 (3.09-3.5.00-8.08) 6. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.33) 2.05-8.03) 1. resulting in excess acetylcholine at nerve terminals.88) 6.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.11-9.45 (1.78 (1.97) 3. and producing acute symptoms such as nausea.62-7. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.24-1. population from the National Health and Nutrition Examination Survey.17-4.88-8.97-3.0) 12.22 (4. paralysis.98 (6.0) 10.49-2.47 (1.11) 7.93 (4.66) 1.86 (1.90-9.58) 5. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.77) 1.63 (5.44 (6.70-4.48 (1. In pesticide applicators.8) 9.25-1.72) 1.05) 3.56 (1. 2006.79-13.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.3 (7.57) 2.34-1. Howard et al.72) 2.19-1.14) 1.44 (1.

113(8):1027-1031. Berent S.. 2005. but not chlorpyrifos. urinary TCPy levels in children were reported not to have increased (Hore et al. In Minnesota and South Carolina farmers who used chlorpyrifos. 1999).Organophosphorus Insecticides: Specific Metabolites 2004.S.gov/pesticides/. Environ Health Perspect 2005. Fourth National Report on Human Exposure to Environmental Chemicals 137 .. 2006). urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Barr DB. population (CDC. Additional information about external exposure (i.. 2007). 2005). Betancourt AM.atsdr. environmental levels) and health effects is available from ATSDR at: http://www. but levels were roughly four to six times higher than the geometric means in the U. Seidler FJ. 2005). 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. Haidar S.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. 2001) and Italy (Aprea et al.epa..gov/toxpro2. 2005).6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. the geometric mean urinary TCPy levels were similar in parents and children. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. Occup Environ Med 2006.82(2):305-312.EPA. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos.. 2005. Clayton CA. 2005). 2004). subsamples of NHANES 1999-2000 and 2001-2002 (CDC.. Environ Health Perspect 2001.. et al. Albers JW.S. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Barisano A. In a probability-based sample of 102 Minnesota children aged 3-13 years. Catenacci G. CDC.html and from U. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy.92(2):500-506. 2001). Chlorpyrifos exposure and biological monitoring among manufacturing workers.S. References Adgate JL. J AOAC Int 1999. EPA at: http://www. 2005). Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. Whyatt et al. 2002). Lotti A.S. Giordani B. Eberly LE.Reference values of urinary 3. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al.cdc. Lioy PJ. Carr RL. 2003. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect.. Aldridge JE. Magnaghi S.. et al. Koch et al. 1992. et al. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. Levels of TCPy in the U. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. MacIntosh 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.. Slotkin TA. Toxicol Sci 2006. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC.. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure... Betta A. U. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. Following crack-and-crevice application of chlorpyrifos in their homes. Burns CJ. Meyer A. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP.5.e. Perera et al. Aprea C. In Iowa farm families using several different pesticides. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S.. 2000).. Garabrant D. 2005. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. Burgess SC. 2004). Curwin et al. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns 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. Of 482 pregnant women living in an agricultural community. 2005).63(3):218220. representative subsample of NHANES 19992000 (CDC. the weighted population mean of TCPy measurements was approximately three times higher (Adgate.. Freeman NC.

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Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Camann D. Chlorpyrifos. Chrislip DW. Chlorpyrifos: pharmacokinetics in human volunteers. Lein PJ.S. et al. Gurunathan S. Chapman P.204(2-3):175-180. Environ Health Perspect 2006. Environ Health Perspect 2006b. 4/7/09 Koch HM. EPA). et al.114(10):1542-1546. Gregg M. Seidler FJ. Toxicol Appl Pharmacol 1984. J Expo Anal Environ Epidemiol 2000. Environ Health Perspect 2006a. Cometa MF. Hore P. Ryde IT. Brain Res Dev Brain Res 2005. Barr DB. Eskenazi B. Jones PA. Environmental Protection Agency (U. Robertson GL. Int J Hyg Environ Health 2001.6-trichloro-2-pyridinol. Croghan CW. chlorpyrifos.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Head SL.111(2):201-205. Reid TM. Third National Report on Human Exposure to Environmental Chemicals. Shealy DB. Ryan PB. Edwards RD. Freeman N. 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Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice.5. Sharma V. Freshour NL.108(4):293-300.113(2):211-219.htm.org/documents/jmpr/jmpmono/ v99pr03.nih. Executive summary of safety and toxicity information. Weltzien E. mothers and fathers living in farm and non-farm households in Iowa. Meeker JD. J Expo Anal Environ Epidemiol 2005. MacIntosh DL. Bailey SL.15(4):297-309. Neurologic function among termiticide applicators exposed to chlorpyrifos. Bruun D. Needham LL. Hines CJ. Urinary pesticide concentrations among children. International Programme on Chemical Safety-INCHEM (IPCS). EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . 4/7/09 Perera FP. Rauh V. National Toxicology Program (NTP).15(3):271-281. et al. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Steenland K.6-trichloro 2-pyridinol in their everyday environments. Pellizzari E. Lu C. Alexander BH.9(5):494-501. gov/ntpweb/index. Harley K. Slotkin TA. Fenske RA. Howell RJ. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures.10(4):327-340. Bennett DH.

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

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

population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.2. 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.670 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 141 .S. 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 . which may vary for some chemicals by year and by individual sample.S. see Data Analysis section) for Survey year 01-02 is 0.270) < LOD 659 701 920 Limit of detection (LOD. Survey Geometric mean (95% conf.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380 (<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.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 .560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

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

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

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

Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. May 2004. The Quality of Our Nation’s Waters. 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. EPA 738-R-04-006.. Diazinon. Pesticides in the Nation’s Streams and Ground Water. Semen quality in relation to biomarkers of pesticide exposure. Oloffs PC. Bravo R. Carrier G. Nguyen JV. Sadowski MA. Bull Environ Contam Toxicol 1986. Interim reregistration eligibility decision (IRED. Dumas P. Banister EW. Centers for Disease Control and Prevention (CDC). 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. Seifert J. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kruse RL. et al. References Anthony J. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. 2005. Available at URL: http://www. Pewnim T. Diazinon. Beeson MD.gov/circ/2005/1291/. Swan et al. Ann Occup Hyg 2006. 2006). Barr DB. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 .44(11):2243-2250.epa. Banister E. Rajendra W. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Brunet RC. Effect of sublethal levels of diazinon: histopathology of liver. Redmon JB.114(2):260-263. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. U. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. In 54 Canadian greenhouse workers. Garfitt SJ. Jones K.inchem. 2006). Barr DB. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Drug Chem Toxicol 1986. Olsson AO. Environmental Health Criteria 198. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Barr DB. Drobnis EZ. Study for Future Families Research Group. 4/7/09 Lu C. Barr DB. 1/14/09 U. Atlanta (GA).37(4):501-507. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids.111(12):1478-1484.usgs. In 23 children. Toxicol Lett 2002. Third National Report on Human Exposure to Environmental Chemicals.gov/ oppsrrd1/REDs/diazinon_ired. In a small number of men visiting fertility clinics in Missouri and Minnesota. Toepel K. Available at URL: http://pubs..htm. Swan SH. Geological Survey (USGS). Fenske RA. March 2006. EPA). International Programme on Chemical Safety-INCHEM (IPCS).S. Driskell WJ. Oloffs PC.376(6):808-815. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Noisel N. Cocker J.org/documents/ehc/ehc/ehc198. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. revised February 15. 2007 [online]. Biochem Pharmacol 1992. Needham LL. 1992-2001. Available at URL: http://www. Environmental Protection Agency (U. J Expo Anal Environ Epidemiol 2000.S.pdf.Organophosphorus Insecticides: Specific Metabolites 2005). Irish R. Liu F. Bouchard M.50(5):505-515. 1998.134(1-3):105-113.S. Environ Health Perspect 2006. Mason HJ.10(6 Pt 2):789-798.9(2):117-131. Environ Health Perspect 2003. Anal Bioanal Chem 2003. Baker SE.

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

Fourth National Report on Human Exposure to Environmental Chemicals 147 . Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. EPA at: http://www.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. and it is not considered an animal teratogen or a reproductive toxicant. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.74 (<LOD-5.S. Urinary Malathion dicarboxylic acid (creatinine corrected) Metabolite of Malathion Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.e. Flessel et al. 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. Pluth et al. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. Thomas et al.gov/toxpro2. 1993. Malathion itself has not been considered genotoxic (U..S. Toxicity from unprotected bystander exposure during applications is rare (U.. 30% had detectable levels of malathion dicarboxylic acid at a detection limit about tenfold lower than the detection limit in the NHANES 1999-2000 analyses (Eskenazi et al. Survey Geometric mean (95% conf. 2005). Human studies of single oral doses between 0.. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. Lu et al.5 and 5. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. population from the National Health and Nutrition Examination Survey. 2006). 2005). 2005. 2006)... 1987. 2006)...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. but isomalathion. 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.epa. 1990). 2003). IARC considers malathion not classifiable as a human carcinogen.. Of 382 pregnant women living in an agricultural community.gov/pesticides/. 2001.S.. Additional information about external exposure (i. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid.. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. 2000). 1996. Giri et al. but cholinesterase activity was not affected. 1999). CDC.cdc. 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.EPA.EPA.html and from U. environmental levels) and health effects is available from ATSDR at: http://www. representative subsample from NHANES 19992000 (Adgate.S.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. 2004). 2002. 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. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC.atsdr. 1999.. 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.

S. Pesticides in the Nation’s Streams and Ground Water. A longitudinal investigation of selected pesticide metabolites in urine. Environ Health Perspect 2001.15(2):164-171. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers.514(1-2):223231. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Brunet RC.org/documents/jmpr/jmpmono/v2003pr06. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Curl CL. 4/7/09 Kissel JC. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues.usgs.109(6):583-590. 2007 [online]. Grether JK.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Malathion (addendum). Blasiak J.S. Lioy PJ.22(1):7-17. Mutat Res 2002. htm. Environmental Protection Agency (U. Swan SH. Erratum in: Toxicol Sci 2003 Aug. Harley K. Petitti D. Pluth JM. Irish R. 1992-2001.74(2):following table of contents. J Expo Anal Environ Epidemiol 1999. Szyfter K.445(2):275-283. Barr DB. revised February 15. J Expo Anal Environ Epidemiol 2005. March 2006. Nicklas JA. Toepel K. et al. Giri S. Hammerstrom KA. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Available at URL: http://www. Goldhaber M.gov/circ/2005/1291/. Barr DB. Third National Report on Human Exposure to Environmental Chemicals. 2005. Reregistration eligibility decision (RED) Malathion. Carrier G. Weltzien E. Lu C. Am J Epidemiol 1990. metabolite clearance.73(1):182-94. Prasad SB. Gosselin NH. Malathion deposition. Fenske RA. Kedan G. Mutat Res 1999. Ryan PB. Needham LL. Griffith W. Cancer Res 1996. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Sharma GD. Centers for Disease Control and Prevention (CDC).56(10):2393-2399.112(10):1116-1124. et al. Environ Health Perspect 2006. Genetic toxicity of malathion: a review. O’Neill JP. et al. Available at URL: http://www.77:1009-1010. Available at URL: http://pubs. Environ Mol Mutagen 1993. Thomas D. The Quality of Our Nation’s Waters. International Programme on Chemical Safety-INCHEM (IPCS). Neutra R. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Atlanta (GA). Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. EPA). Hooper K. Environ Health Perspect 2004. Bradman A. Harris JA. 6/1/09 U. Giri A. Eskenazi B.114(2):260-263. MacIntosh DL. Jaloszynski P. Jewell NP.9(5):494-501. Arch Environ Contam Toxicol 2000.pdf.132(4):794-795. Dinoff TM. and cholinesterase status of date dusters and harvesters in California. July 2006. Barr DB. Geological Survey (USGS). Eberly LE. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Clayton CA. Hertz-Picciotto I. Reproductive outcome in women exposed to malathion. Rappaport E. EPA 738-R06-030. Albertini RJ. Bravo R. Trzeciak A.S. Quintana PJ. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Barr DB. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Samuel O. Dumoulin MJ. U. Flessel P. Am J Public Health 1987.epa. Toxicol Sci 2003 May. Freeman NC.gov/oppsrrd1/REDs/ malathion_red. Lu C. Krieger RI. Bouchard M.38(4):546-553.inchem.

20) 5.33 (1. ethyl parathion.37-2.00) size 1989 2477 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1.34 (3.50 (2. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.40) 2.57-4.10 (3.30 (2. 2002. It had been applied to cotton. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.20 (<LOD-2.70) 2.49 (1.0) 3.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .S.37) 2.EPA. fish. and to a lesser extent. Estimated intakes from diet and drinking water have been below recommended limits.05) 4. methyl parathion was rapidly absorbed after ingestion.71 (3.40) 1.32-1.0) 3..01-4.48) 90th 2.60-24.66 (2.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.50 (1.860 (<LOD-1. more slowly absorbed through the skin.44) 2.40) 4. Increased risk of exposure via dermal. and oral routes can occur in pesticide and agricultural workers (Muttray et al.69) 4.32-3.69 (2. and eliminated rapidly from the body after absorption (Kramer et al.91-3.298-00-0 Ethyl Parathion CAS No.11-4.40-3.10) 22. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.01) 4.45) 5.S. Both are toxic to birds.85 (2.0) 4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.60-5.10) 4.72 (3. Given its limited use.40 (1.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70-6.18-3. which may vary for some chemicals by year and by individual sample. Morgan et al. Many previous registered agricultural uses of methyl parathion have been cancelled (U.50 (1.26 (1.15-3.910) < LOD < LOD < LOD 1.0) 3.37-4.89 (2.10 (3. and of the chemical nitrobenzene.57) 1.S.0) 3.50) 3.30-3.92) 5.70 (2. 1977).50) 2. was once a restricted-use insecticide with limited applications on certain agricultural crops.12) < LOD < LOD 1. < LOD means less than the limit of detection.50-14.940 (<LOD-2. binds tightly to soils resulting in low leachability.37-4.70 (<LOD-3.70 (3.50 (1.45 (1.70) 2. all registered uses were voluntarily cancelled (U.730 (<LOD-.36-1.70 (2.300-.30-16.01) 695 660 518 679 603 941 Limit of detection (LOD.61) < LOD 1..50 (1.790 (<LOD-.20-5.70) 2.50-9. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.28 (1. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.30-5.60 (4. and aquatic invertebrates.90-11. first registered in 1948.19 (.02-6.58) 3.00) 3.70-6.21-1. pulmonary.28-4.0 (3.70-3. 2007). Ethyl parathion.80) 2. Methyl parathion use is highly restricted.50) 1.70-3.80 (2.27) 2.770 (.EPA.21 (2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.67 (1.700 (<LOD-.13-1. Methyl parathion is not registered for residential use in the United States.60-19.20 (2.50) 3. Fourth National Report on Human Exposure to Environmental Chemicals 149 ..33) 2.09-1.11) 2.10-11.80 (2.74) 5.71 (2.28 (1.50 (2.60) 1.62 (1.67) < LOD 1.32-1.47) 2.90 (1. population from the National Health and Nutrition Examination Survey. on cereal grains.00 (2.00 (2.40-4. Methyl Parathion.92-2. Survey Geometric mean (95% conf.70 (2.80 (1.70-6.1.30 (1.16) < LOD 1.46 (3.0) 3. Methyl parathion has low water solubility.32 (1. In the 1990s. and has a short half-life in soils and on plants.8 and 0. In animal studies.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . but by 2003.90-9.40-4. 2000).910) < LOD .10 (<LOD-6.990-1. with limited applications in agriculture.10-1.79) 4.41-4.910) < LOD < LOD . 2003). Once absorbed.22-3. 2006).60-36.850) < LOD . peak domestic use was as high as 5-6 million pounds per year.61) < LOD 1.0) 2.

67 (3.79 (1. In large doses.37-1. and seizures.17) . 1995. Additional information about external exposure (i.850-1.82 (2.01-3.20) . Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.11-4.00) 2.23) 1.44-3.97-10. 150 Fourth National Report on Human Exposure to Environmental Chemicals .61) 4. 1991)..26 (1.S..94-47.70) 3.25) 1.82) < LOD . population from the National Health and Nutrition Examination Survey.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .530) < LOD < LOD < LOD .60 (1. and producing acute symptoms such as nausea.cdc.97 (<LOD-4. Survey Geometric mean (95% conf.7) 3.84) 3.09) 2.00 (1.31-3.10) 90th 2.440 (<LOD-.html and from U. 2006. weakness. 1990. but lists ethyl parathion as a possible human carcinogen.720-1. vomiting.35-3.91 (1.96 (1. Slotkin et al.29) 2.01 (.79) 1.80 (1. resulting in excess acetylcholine at nerve terminals.71) 1.35-3. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS. Parathion and methyl parathion have high acute toxicity in animal testing. In addition to being a metabolite of methyl and ethyl parathion.13) 4.25 (2.60) 2.08-3. Lores et al.80 (1.04 (2.98-7. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.83 (1.33-3.17-4.86 (2.33-6.97 (2.07) 2.39 (1.39) 1.77-7.01 (2.73 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.800-1.690-1.2) 2.57-2.940 (<LOD-1.atsdr.38-3.930 (.00 (1.500) < LOD < LOD .830-1.30-1.41-2. gov/toxpro2.76-14. Karanth and Pope et al. 1978. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS. does not inhibit acetylcholinesterase enzymes.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . and unintentional acute or chronic high-level occupational exposure (Hill et al. gov/pesticides/. Jaga and Dharmani. Orsorio et al.87 (1. 2004). and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.29 (2.3) 2. environmental levels) and health effects is available from ATSDR at: http://www.95) 1.89 (2.72-2.78 (2. 2005.430 (.15) 3. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.2) 2.970 (.540) < LOD . teratogenic.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.790-1.96 (1.20 (3.71 (1. paralysis..880 (. At high animal doses of methyl parathion. methyl parathion.88) 1.980 (.04) 1.Organophosphorus Insecticides: Specific Metabolites Metabolites”).13-12.56-2.10 (1.400 (<LOD-.48-4..20) 3.59 (1.720 (<LOD-.15-10.78) 2.78-2.67-2.790-.640) < LOD < LOD 1. Thus. ethyl parathion.11) 1.78-2. Methyl parathion is not considered genotoxic.epa.30) 3.94-4.88 (1.930 (.08) < LOD .1) 2.310-.970 (.55) 2..93 (2. and other metabolites. The metabolite.57) 6.9) 1.EPA considers methyl parathion unlikely to be carcinogenic to humans. WHO.14-3.60-2. 2004).S.730-1. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.55 (<LOD-3..89 (2. U.S. Methyl Parathion.26) 17.950) < LOD .21) 1.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .21-21.31) < LOD . 1995).840 (. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2003.16-4.370 (<LOD-.4 (3.07 (1. cholinergic effects.92 (2. Zurich et al.680 (<LOD-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 .29) 1..57-7. 2006. paranitrophenol..e. accidental exposure.33-3.90 (1. 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.91) 1. EPA at: http://www.44-3.08 (1.43) 4.05) 4.870) < LOD .

Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect.33(5):270-276. Jewell NP. 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..56(7):449553. 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. J Biomed Sci 2002.110 Suppl 6:1085-1091. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.inchem.htm.25(5):599-606.. Rubin et al. Morgan DP. Neurotoxicol Teratol 2003.15(2):164-171. population (Olsson et al. 2005). 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al.215(3):182-190. Environ Health Perspect 2004. Runkle KD. Baker S. Hill RH Jr. References Barr DB. Needham LL. ACGIH recommends a BEI of 0. J Expo Anal Environ Epidemiol 2005..6(2-3):159-173. et al. Ashley DL. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Leng G. Harley K. 2005). J Anal Toxicol 1990. Griffith W. Barr JR. Occup Environ Med 1999. et al. Alley CC. 2002. Arch Environ Health 1978. Rev Environ Health 2006. Lu C. DiPietro E. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Giordano G. Shealy DB. Hryhorczuk DO. et al. Lin LI. Costa LG. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Available at URL: http:// www. Kramer RE. Laboratory investigation of a poisoning epidemic in Sierra Leone. Lewalter J. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Environ Health Perspect 2002. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine.. Moomey CM. Wellman SE.14(4):213-216. Parathion-Methyl (addendum). Bailey SL. and levels were similar or slightly lower that those in a small convenience sample of the U. Turner WE. Arch Environ Contam Toxicol 1977. Bradway DE.9:311-320. Barr DB. Bradman A. 1995. 2005. Curl CL.71:99108.. Kissel JC. Eskenazi B. 2004). 4/7/09 Jaga K. Cline RE. Environ Res 1995. et al. Rockhold RW. Hill RH Jr. McClure PC.S.21(1):5767. Moseman RF.112(10):1116-1124. Lores EM. and many residents were symptomatic (Barr et al.. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Role of individual susceptibility in risk assessment of pesticides.org/documents/jmpr/jmpmono/v95pr14. Atlanta (GA). Pesticide workers may have much higher levels following pesticide applications. Third National Report on Human Exposure to Environmental Chemicals. International Programme on Chemical Safety-INCHEM (IPCS).Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Toxicology 2005. Gregg M. CDC. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects.5 mg (500 µg)/g creatinine for workers at the end of shift. 2002. Hetzler HL. Baker RC. a range of values several hundred times higher than levels found in the U.110 Suppl 6:1075-1078. Dharmani C. Clark JM. Kedan G. Methyl parathion: an organophosphate insecticide not quite forgotten. Barr DB. 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.. Pathak S. Slach EF. Baker SE. 1995). 2002). Hill et al. McCann et al. Biomonitoring studies of para-nitrophenol can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of parathion than are found in the general population. Pope C. et al. In a study of workers who handle parathion. Karanth S. Pesticide residues in urine of adults living in the United States: reference range concentrations. McCann KG. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. 1999). 2005. oral or dermal administration. Centers for Disease Control and Prevention (CDC). end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. 2005. general population (CDC. Head SL. Guizzetti M. Environ Health Perspect 2002. Chicago area methyl parathion response. Head SL. Barr DB.S. Weltzien E.

revised February 15. Seidler FJ. Hill RH Jr. 1995-1996. 1/12/07 U. 5/19/09 Zurich MG. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Environmental Protection Agency (U. Kieszak S. 2007 [online]. gov/oppsrrd1/REDs/methylparathion_ired. Osorio AM. Schilter B. Environmental Protection Agency (U.who. WHO/SDE/WSH/03. Am J Ind Med 1991. Ames RG. Tate CA. Available at URL: http://www. The Quality of Our Nation’s Waters.S. Environ Health Perspect 2002. Monnet-Tschudi F. Hill G.int/water_sanitation_health/dwq/chemicals/ methylparathion. Costa LG. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.201(2):97-104.gov/circ/2005/1291/. Ohio. 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. pdf. Case No. EPA). Anal Bioanal Chem 2003. Available at URL: http://www. Rosenberg J. 152 Fourth National Report on Human Exposure to Environmental Chemicals .20(4):533-546.pdf. Honegger P.376(6):808-815. et al.S. Esteban E. May 2003.S.S. EPA-738-FOO-009. U. 1/14/09 U. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Available at URL: http://pubs. Backer G. 6/1/09 World Health Organization (WHO). Yacovac R. Letzel S. Toxicol Lett 2006.110 Suppl 6:1047-1051.usgs. Dunlop B. Environ Health Perspect 2006. Levin ED. Rubin C.E. Slotkin TA. Ryde IT. Nguyen JV. EPA). Olsson AO. Jung D. Pesticides in the Nation’s Streams and Ground Water. Toxicol Appl Pharmacol 2004. Geological Survey (USGS).04/106. External and internal exposure of wine growers spraying methyl parathion. Sadowski MA. Facts. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos.epa.gov/oppsrrd1/REDs/factsheets/0155fct.162(2-3):219-224.pdf. March 2006. Barr DB. Available at URL: http://www.D.epa.S. R. Methyl parathion in drinking water. Mengle DC. 0153. Investigation of a fatality among parathion applicators in California. 2004.114(10):1542-1546.Organophosphorus Insecticides: Specific Metabolites Muttray A. September 2000. Ethyl parathion. 1992-2001.

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

31) .S.850 (.700-1.27) . population from the National Health and Nutrition Examination Survey.780 (<LOD-1.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .430 (<LOD-.950) < LOD < LOD 1.Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.700-.94) .740-1.680 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .250 (<LOD-.840) 669 687 929 Limit of detection (LOD.610 (<LOD-1.410 (<LOD-1.780 (. 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.210-1.780 (<LOD-1. which may vary for some chemicals by year and by individual sample.210-.670 (<LOD-1.760 (<LOD-. 154 Fourth National Report on Human Exposure to Environmental Chemicals .200-.2.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .07) .470 (. 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.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 .820) < LOD < LOD .00) 669 687 929 < 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.840 (.500 (.21) < LOD . Survey Geometric mean (95% conf.780 (.64) .210 (<LOD-. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.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 .17 (. < LOD means less than the limit of detection.55) .08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .740 (.300-1. see Data Analysis section) for Survey year 01-02 is 0.15) < LOD .580-1.S.

Available at URL: http://www. July 2006.pdf.pdf.Organophosphorus Insecticides: Specific Metabolites References Centers for Disease Control and Prevention (CDC). Pesticides residues in food: 1992 evaluations Part II Toxicology. Finalization of interim registration eligibility decision for pirimiphos-methyl. Environmental Protection Agency (U. 4/7/09 Olsson AO. Pirimiphos-methyl. Food and Drug Administration (FDA). Case No. EPA). Nguyen JV.epa. Sadowski MA. 2535. Market Baskets 91-3-01-4. Barr DB. 4/7/09 International Programme on Chemical Safety-INCHEM (IPCS).gov/~acrobat/tds1byps. Total Diet Study: Summary of Residues Found Ordered by Pesticide.htm. June 2003.S. gov/oppsrrd1/REDs/pirimiphos-methyl_ired. Available at URL: http://www. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Available at URL: http://www. Anal Bioanal Chem 2003.S. Atlanta (GA). 2005. 850.376(6):808-815. 1/14/09 Fourth National Report on Human Exposure to Environmental Chemicals 155 . cfsan.fda.inchem. org/documents/jmpr/jmpmono/v92pr16. Third National Report on Human Exposure to Environmental Chemicals. U.

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

et al. EPA at: http://www. Xenobiotica 1997.23(6):665-673. Ose K. et al. hypersensitivity.107(3):173-177.8(1):197-202. cdc.1/15/09 Aziz MH. J Reprod Dev 2004. Chen JH.. McCarthy et al. Kamita Y. Fredriksson A. Kuhn KH. 2003. McCarthy AR. Garey J. Lemonica IP. Leng A. Abell AD. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Song L. Lee SJ. Int J Hyg Environ Health 2002. Kim HS. Go et al. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays.atsdr. Yang J. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. WHO. 2006. Shukla Y. 2005). Bull Environ Contam Toxicol 1999. Additional information about pesticides is available from U.27(12):1273-1283. Moniz AC. Salzgeber SA. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Spinosa HS. salivation. and permethrin) in the Hershberger and uterotrophic assays. on immature and adult mice: changes in behavioral and muscarinic receptor variables. 2000.. Estrogenicity of pyrethroid insecticide metabolites. epa.. 2003. Kim et al. Kunimatsu et al.. Ray et al.gov/toxprofiles/ tp155. Neurosci Lett 2001. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Generally. 2005). Adhami VM. 1991. Pyrethroid pesticide-induced alterations in dopamine transporter function. Kim TS. 1998. Caudle WM. 2003. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Shin JH. Lazarini et al. 2006. Eriksson P.. 2005). Idel H.108(1):78-85. 2006). though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Kuhn K. bioallethrin and deltamethrin. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Toxicol Appl Pharmacol 1991. Sugiri D. Eriksson and Fredriksson. Go V. choreoathetosis. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Miller GW. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation.html.html. dopaminergic. Sunami O.cdc. J Environ Monit 2006. Wolff MS. fenvalerate. Kunimatsu T.gov/toxpro2. Wieseler B. Toxicological profile for pyrethrins and pyrethroids. 2003.S. Levsen K. Agrawal AK.. Shafer. Varoli FM. et al. 2005). The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Leng G. 2001. Ranft U. and striatal dopamine levels in male and female rats.. motor activity. Hu et al. Shaw IC. Yamada T.251(3):855-859. Seth PK. 2002). Wolff MS.62:101-108. Neurotoxicol Teratol 2005.50(2):245-255. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. tremor. Regul Toxicol Pharmacol 2002. Kang IH. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Lewalter J. Neurotoxic effects of two different pyrethroids. Neurotoxicol Teratol 2001. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. et al. Wang SL.205(6):459-472. Garey J.. Garey and Wolff.atsdr. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. No relationship of indoor air or housedust concentrations of permethrin and irritant symptoms was found in a study of urban residents in 80 private homes (Berger-Preiss et al. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate.300(3):161-165. Elwan et al. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. 2001. September 2003. Leng G. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects.. 1999. Kim IY. Available from URL: http://www. Pogo BG. 2002.. Thomson BM. References Agency for Toxic Substances and Disease Registry (ATSDR). Toxicol Appl Pharmacol 2006. Environ Health Perspect 1999.. Zhao RC. Soderlund et al. Okuno Y. In developing rodents. Guillot TS.27(4):609-614. Bernardi MM. 2004. Moniz et al.gov/pesticides/ and from ATSDR at: http://www.35(2 Pt 1):227-237..211(3):188-197. In California. Richardson JR. neurochemical changes in cholinergic. Lazarini CA. Cruz-Casallas PE.8(1):18-21.. Indoor pyrethroid exposure in homes with woollen textile floor coverings. and seizures (ATSDR. Elwan MA. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Bernardi MM. Pauluhn J. Florio JC. Berger-Preiss E. Idel H. 2002).Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Leng G. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Biochem Biophys Res Commun 1998. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Hu JY.

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

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..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. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. 2005. Cyfluthrin is rapidly metabolized and eliminated from the body. 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. Studies in Germany of 396 children and adolescents (Becker et al. representative 2001-2002 NHANES subsample (CDC. 2006) and 1177 urban adults and children (Heudorf et al. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. 2001.95 µg/L. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate..Pyrethroid Pesticides Cyfluthrin CAS No.. 2005). 2003). the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0. Following an indoor application exposure.. but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment. 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. representative subsample in NHANES 2001-2002 (CDC. Baker et al. Leng et al. 2004). In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). Thus.. 2003).S. 2006). Biomonitoring studies of 4-fluoro3-phenoxybenzoic acid in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of cyfluthrin than levels found in the general population.. most of which were dermal and respiratory irritations (Spencer and O’Malley. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. Fourth National Report on Human Exposure to Environmental Chemicals 159 . Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002. Urinary levels for adults and children in these studies were similar (Heudorf et al.S. 2005).

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

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

Ball M.109(3):213-217. Environ Health Perspect 2001. O’Malley M.Pyrethroid Pesticides References Baker SE. Seiwert M. Spencer J. Third National Report on Human Exposure to Environmental Chemicals.46(3):281-288. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Heudorf U. Leng G. et al. Hadnagy W.209(3):221-233. Becker K. Arch Environ Contam Toxicol 2004. Rev Environ Contam Toxicol 2006. Atlanta (GA). Int J Hyg Environ Health 2006. Int J Hyg Environ Health 2003. Butte W.209(3):293-299. Pyrethroid illnesses in California. Idel H.186:57-72. J Expo Anal Environ Epidemiol 2003. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Angerer J. Olsson AO.206(2):85-92.13(2):112-119. Krieger RI. Hoppe HW. Bernard CE. Angerer J. Ranft U. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Drexler H. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Heudorf U. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Int Arch Occup Environ Health 2004. Angerer J. Barr DB. Heudorf U. Kolossa-Gehring M. 19962002. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Angerer J. Schulz C. Berger-Preiss E. Int J Hyg Environ Health 2006. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Williams RL. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Sugiri D. 2005.77(1):67-72. Centers for Disease Control and Prevention (CDC).

2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.350) .880 (.13 (.200-.200) .2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.310) .200) .2-Dichlorovinyl)-2.600) .210) .35) 1.220-.280-.120-.430-.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .240) .380-.300 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.770-1.or trans-3-(2.820 (.110-.580-1.2-dichlorovinyl)- CAS No.340) .460-1. The chemical trans-3(2.300-.160 (..150 (.710) .570-.270-.155-.170 (.28) 671 680 518 701 591 957 Limit of detection (LOD.110-.120-.680-3.11) .12 (.700) .2dichlorovinyl)-2.300-.490-.47 (.202 (.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .68 (.340-..35) . 1999).270 (.1.670-2.08) .250 (.400-.890 (. In the body.330) .580) 1.68359-37-5 Cypermethrin Permethrin CAS No.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.470-1.50) .210-.2-dichlorovinyl)-2.210) 90th .920) 1.240) .330 (.54) .490-1. cis-permethrin. cis-3-(2.230) .08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .780) .370-.262) * * * < LOD < LOD .470 (.520) . 52315-07-8 CAS No.43) .790 (.380-.77 (.220-.380 (. Survey Geometric mean (95% conf.730 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin. Cyfluthrin.960 (.630 (.120-.270 (.500 (. Fourth National Report on Human Exposure to Environmental Chemicals 163 .370 (.24) 1.140 (<LOD-.650-1.710-1.53) .1 and 0.490-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. the presence of trans-3-(2.2-dichlorovinyl)2.220-. but can also reflect exposure to trans-3(2.740-1.890 (.900 (.680 (.68) .200) < LOD < LOD < LOD .110 (<LOD-.200-. 1999).740 (.32) .300 (.140 (.80) .770) .44 (.530 (.200 (.740) 1.460-. more of the trans-metabolite than Urinary cis-3-(2.610) . and trans-cyfluthrin.S.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis. population from the National Health and Nutrition Examination Survey.460 (. 1985. and ciscyfluthrin.670-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (.340) . which may vary for some chemicals by year and by individual sample. transcypermethrin and trans-cyfluthrin.740-2.550) . trans-cypermethrin.420-.180 (.and trans-isomers.120-. ciscypermethrin and cis-cyfluthrin.510 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.220-.280 (.200-.160 (.790-1.870) 1. 1985. The presence of cis-3-(2.68) .630-. Kuhn et al.2-dichlorovinyl)-2.730 (.490-.15) .510 (.510 (.790-1.440 (.21) .180) .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 . Biomonitoring Information Urinary levels of cis. but it can also reflect exposure to cis-3-(2.220) .600 (.790) . < LOD means less than the limit of detection. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.670 (.07 (.380) . trans-permethrin.250-.850 (.570 (.690) .630) .160 (<LOD-.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.110-.950-2.910-5. Kuhn et al. Generally.270 (.410) .670-1.610) .2-dichlorovinyl)-2.410) .640 (.260 (.2dichlorovinyl)-2. cis-cypermethrin.730 (.600-1. Similarly.380-.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.630) .

300 (.400 (.840 (.410) .. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. In the same residents. Schettgen et al.400-1. Studies in Germany of 396 children and adolescents (Becker et al.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.540 (. 2005) In a small group of indoor pest-control operators.250-.11 (. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.220 (.320-. 2005).780 (.190) .680-1.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.130-. 164 Fourth National Report on Human Exposure to Environmental Chemicals .200 (..450-.640-1.190) .580-1. Lu et al.182) * * * < LOD < LOD . 2005).2dichlorovinyl)-2.340) .140-. the median and 95th percentile of urinary levels of cis-3-(2..300 (.840 (. In these volunteers.260 (.540) .230-. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.320) .540 (.350) . 2002).470-1.290) .14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.250-.67 (.11) .890 (.and trans-3(2..190 (. representative NHANES 2001-2002 subsample (CDC.11) 1.150-.170 (.430-.300-.690-1.. 2006).59) . Other studies have provided evidence that urinary levels of cis.570) . 2006.590 (.920 (.220 (.290-.. post- Urinary cis-3-(2. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.80) .300) .2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U. 2006) and 1177 urban adults and children (Heudorf et al.430-1.200) . 2001) showed urinary levels of cis.360-1.550 (. urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.120 (. Cyfluthrin.440-. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al. median urinary levels of trans-3-(2.550) . In a study of urban residents in Germany (Berger-Preiss et al.230-.2-dimethylcyclopropane carboxylic acid did not increase.200-.31) .380) .250-.S.640) 1.230 (.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.260 (.640-1.550-1.430 (.350 (.260 (.640-.880) .2-dichlorovinyl)-2.270) .33 (.300) .550-1.750 (.230-.37) .560) 1.270 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC. In a study of volunteers.600 (.370-.710 (.Pyrethroid Pesticides 2.59 (1..550) . 2004). population from the National Health and Nutrition Examination Survey.270-.780) 1.700) .710-3.160 (<LOD-.280-. 2006).33) .530 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.180 (.810 (.080-.2-dichlorovinyl)-2.700) .270) . 2003).380-.390-.24) .390 (.440-.250) 90th .12-2.260-.750-1.and trans-3-(2.290 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.138 (.450-1. 2001.250 (<LOD-.250) .290) .170 (. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.59) .900 (.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .680-1.510-1.2-Dichlorovinyl)-2. 2005). urinary trans-3-(2.180-.280 (.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .830) . 2004. 2005).340) .150-.640 (..2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al..380 (. 2002).2-dichlorovinyl)-2.150-.560) .340-.220) .03) 1.49) .240 (<LOD-.250) .440 (.370-.67) . 2003).580) .500 (. Survey Geometric mean (95% conf.2-dichlorovinyl)-2.800 (.890) .590) .21) .104-.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.440 (.680 (.530 (.450 (.29 (.2dichlorovinyl)-2.420 (.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 .200-.260) .11) ..210-.700-2.12 (.390-. 2006.370-..170) < LOD < LOD < LOD .S.

55-4.490-1.85) 4.01 (1.50 (1.77 (1.70) size 1976 2525 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .08-6.400-.28 (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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.500-.7) 2.530) .42 (2.440 (<LOD-. however.560 (.56) 2.94 (1.26 (.660) 1.820) .20 (.and trans-3-(2.25-3.64-4.60) .910-1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.37 (1.68) 1.570) 90th 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.68) 2. population from the National Health and Nutrition Examination Survey.95) 3.670) .670) .920-1.10) 2.400 (<LOD-. trans-Cypermethrin. 2005).11-1.63) 1.54 (1.19) 1.970 (.49-3.500 (.39 (1.42) 1.76-4.40 (1.68-3.48) 4.20 (.410 (<LOD-.940 (.43) 2.68) 1.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.62 (1.76-3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.49-5. < LOD means less than the limit of detection.460-.14) 1.63) 1.580 (.560 (.2-dichlorovinyl)-2.480-.490 (<LOD-.730) .520-.700-1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.460-.55-3.95) 2.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .550 (.07 (1.2-dichlorovinyl)-2.03-1.49-3.81) 2.Pyrethroid Pesticides application median urinary levels of summed cis.17 (.2-Dichlorovinyl)-2.910-1.2dichlorovinyl)-2.5) 2.410 (<LOD-.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .19 (3.41 (1.90) 1.610) 1.S. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.860) .560 (.69) 1.14-2.850-1.87 (1. 2005).800-1.08) 1.07-3.84 (1.4.780 (.23 (.56 (1.or trans-3-(2.420 (<LOD-.89 (2.17 (.27 (1.470 (.500) . Survey Geometric mean (95% conf.35) 1.17-1.14-6.760) .60-4.54) 4.08-4.680-1.520) .09 (.700) .2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.4 and 0.39-5.410-. Finding a measurable amount of cis.710 (.810-1.03-1.66) .55-5. Urinary trans-3-(2.620) < LOD 2.12-6.77) 2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.01) 4.68-2.830-1. Fourth National Report on Human Exposure to Environmental Chemicals 165 .97-11.77) 1.56) 2.59 (1.23) 2.20 (. The maximum post-application urinary levels. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.840-1.41-14.91 (1. Biomonitoring studies on urinary levels of cisor trans-3-(2.69 (1.25 (1.16) 1.56 (1.470 (<LOD-.60) 1.750) .77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .11-2.66) 691 680 518 690 595 954 Limit of detection (LOD.28 (2.410-.22 (1.19 (2. which may vary for some chemicals by year and by individual sample.13) .

16 (1. Survey Geometric mean (95% conf.800-1.91-11.880-1.60 (1.60) 2.27-2.67 (2.87-8.19) .730) .11) .00-5.15-3.15) 3.410-.720-1.64 (1.15-3. 166 Fourth National Report on Human Exposure to Environmental Chemicals .20-2.08 (.13) 1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .Pyrethroid Pesticides Urinary trans-3-(2.35 (1.700 (.29) 1.610-.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .33-1.91) 1.08 (.39 (1.42 (.61) 1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.87) 1.720 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.26 (1.470-.780) .22-2.07-1.65 (2.15) 2.39) 1.500-.28) 2.45 (1.13) .880 (<LOD-1.45-2.07-3.47 (1.57) 3.570 (<LOD-. trans-Cypermethrin.12 (.850) .48 (1.850) 1.530 (<LOD-.47-2.570-.47-2.31 (2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.470 (.2-Dichlorovinyl)-2.800-1.00 (1.56-5.57 (1.850-3.56-2.80) 1.880 (.560 (.580 (.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 .37 (1.89) 2.40-2.74) .88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.570 (.760 (.68) 3.86 (2.33 (1.660) .720-1.55 (2.750) .56 (1.74) 2.31 (.00) 5.700 (.34-3.15-3.55 (2.42) 1.480-.87-3.81 (2.22) 1.33-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.930-1.440-.700-.530 (.48-2.00) 1.35) 1.820-2.00) 1.580) .640) .770) < LOD 2.02-1.07) 2.44) 2. population from the National Health and Nutrition Examination Survey.55 (2.98 (1.19 (1.22-1.740) .87 (1.30-6.31) 1.520 (<LOD-.70 (.670) .07-2.07) 2.780) 90th 1.30-3.20 (1.780 (<LOD-.970 (.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.65) 1.41) 1.27-2.75 (1.900 (<LOD-1.36 (1.60) 2.36) 2.540) .87) 1.3) 2.34-4.15 (1.12-1.S.91 (1.

Bravo R. Int Arch Occup Environ Health 2004. Levsen K. Idel H. Drexler H.62:101-108. Butte W.114(9):14191423. Berger-Preiss E. Angerer J. Indoor pyrethroid exposure in homes with woollen textile floor coverings.68(6):1160-1163. Kuhn K. Fourth National Report on Human Exposure to Environmental Chemicals 167 .209(3):293-299. Bartell S. Idel H. Seiwert M. Permethrin and its two metabolite residues in seven agricultural crops. Ranft U. Biological monitoring of workers after the application of insecticidal pyrethroids. Leng G. Wieseler B. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Environ Health Perspect 2001. Barr DB. Pearson M. Drexler H. Leng G.209(3):221-233.205(6):459-472. et al. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Kolossa-Gehring M. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Sugiri D. Heudorf U. Hoppe HW. Heudorf U. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Schettgen T. Angerer J.206(2):85-92.Pyrethroid Pesticides References Becker K. Bull Environ Contam Toxicol 1999. Berger-Preiss E. Centers for Disease Control and Prevention (CDC). GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.76(7):492-498. Sugiri D. Int J Hyg Environ Health 2003. Int J Hyg Environ Health 2006. Int Arch Occup Environ Health 2003. Idel H.134(1-3):141-145.109(3):213-217. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Angerer J. Leng G. Hadnagy W. J AOAC 1985. Ball M. Schulz C. Int J Hyg Environ Health 2006.77(1):67-72. Third National Report on Human Exposure to Environmental Chemicals. George DA. Int J Hyg Environ Health 2002. Angerer J. Angerer J. Hardt J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Lu C. Atlanta (GA). Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Heudorf U. Environ Health Perspect 2006. Ranft U. 2005. Angerer J. Heudorf U.

39 µg/L.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.. 1990). 2006) and 1177 urban adults and children (Heudorf et al. Following residential spraying with deltamethrin for malaria protection in Mexico..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. Baker et al. 52918-63-5 General Information Cis-3-(2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.2-dimethylcyclopropane carboxylic acid of 0. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.3-0.5 μg/L) than the detection limit (0. In the NHANES 2001-2002 subsample. urinary levels of cis-3-(2..2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2-dibromovinyl)-2.1 μg/L) for the NHANES 2001-2002 subsample (CDC. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.2-dibromovinyl)-2. Biomonitoring Information Urinary levels of cis-3-(2... mean peak urinary levels of cis-3-(2. 2005). Deltamethrin can degrade to cis-3(2.2-dibromovinyl)-2.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. Thus. 2004). 2005).2-dibromovinyl)-2.Pyrethroid Pesticides Deltamethrin CAS No. (2004) reported a geometric mean concentration of cis-3(2. 2001. 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. Urinary levels for adults and children in these studies were similar (Heudorf et al.S. in detection of cis-3-(2.2-dibromovinyl)-2. in some situations replacing the use of DDT. 168 Fourth National Report on Human Exposure to Environmental Chemicals .. 2001) showed that urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. Finding a measurable amount of cis-3-(2.2-dibromovinyl)-2.2-dibromovinyl)-2.2-dibromovinyl)-2.2dimethylcyclopropane carboxylic acid formed in the environment.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.2-dibromovinyl)2.2-dibromovinyl)-2. Outside the U. deltamethrin has been used against mosquitoes that carry malaria. Studies in Germany of 396 children and adolescents (Becker et al.

< LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 169 .Pyrethroid Pesticides Urinary cis-3-(2.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin 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. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 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.S. which may vary for some chemicals by year and by individual sample.1.2-Dibromovinyl)-2.1 and 0.

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

Third National Report on Human Exposure to Environmental Chemicals. 5/26/09 Ortiz-Perez MD. Schulz C. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.77(1):67-72. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Heudorf U. Environmental Health Criteria 97.htm.209(3):221-233.Pyrethroid Pesticides References Becker K.inchem. toxicokinetics. Batres LE. Atlanta (GA).org/documents/ehc/ehc/ ehc97. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Heudorf U. Angerer J. Environ Health Perspect 2005. Heudorf U. [online] 1990. and genotoxicity in exposed children. Grimaldo M.113(6):782-786. Torres-Dosal A. Ball M. Hoppe HW. Butte W. Drexler H. et al. Lopez-Guzman OD. Carranza C. et al. Available at URL: http://www. Int J Hyg Environ Health 2006. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Int J Hyg Environ Health 2006. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Environ Health Perspect 2001. Int Arch Occup Environ Health 2004. Deltamethrin. 2005. Kolossa-Gehring M. Seiwert M. Angerer J.209(3):293-299.109(3):213-217. Angerer J. Centers for Disease Control and Prevention (CDC). Angerer J. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. International Programme On Chemical Safety (IPCS).

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

750) .238-.990) .230-.430-.330) .1 and 0.27-11.18 (2.32-21.560-.260 (.35) 2.78 (1.34) 8.320) .49-2.73) 1.25-4.62) 5.406) .352-.710 (.297 (.65-2.220-.290 (.250-.29-1.586) .640 (.36) 1.23 (2.260 (.30) 3.230-.48-2.520 (.265-.S.390) . Survey Geometric mean (95% conf.340) .340) 1.360) .83-11.1) 3.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.35) 2.270) .300 (.369) .440) .630) .210-.03 (3.1) 3. Fourth National Report on Human Exposure to Environmental Chemicals 173 .33 (1.210-.56-5.320) .26) 2.300) .60) .190-.69 (1.590 (.530-.32 (1.250 (.650 (.72 (1.05) .160-.507 (.52-4.470-.315 (.190-. Deltamethrin. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.46) .277-.271-.41-2.12) . population from the National Health and Nutrition Examination Survey.740 (.49-2.01 (1.38 (2.850) .26) 2.620-1.04) .190-.79) 3.510-.78) 6.50 (2.51-6.230 (.69) 3.92-3.417 (.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .340) 75th .200-.700-1.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.292 (.760 (.90) 1.247-.44) 5.45-5.1) 3.64) 697 680 524 701 603 957 Limit of detection (LOD.49 (1.25) size 1998 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .590-.53-3.250 (.288 (.320) .53) 1.830) 90th 1.300 (.35) 1.490-.314) .260 (.253-.52-5.26-2.600 (.610) .510-.63-3.355) .370) .54) 1. interval) .800) 1.12) 4.30 (1.830-2.490) .387) .266-.311 (.160-.200-.02-6.320) .190-.850) .227-.27-2.233-.18 (1.428-.601) .450 (.870 (.800 (.180-.550-.34 (2.28) 1.33) .820) .560-.325 (.740 (.78) 1.384) .240 (.750) .434) .570-.314 (.330) .750-1.93 (1.336 (.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .940) 1.35 (2.295) .730 (.276-.430-.230 (.51-3.700 (.595) .820) .250 (.49 (1.25 (2.41) 3.1.200-.55 (1.34-6.62-6.71 (1.298 (.38 (2.350-.328 (.530-.710 (.560-1.454 (.76 (1.14-6.43) 3.670 (.86 (1.246-.364) .05) 1.78) 1.39) 2.273 (.230-.04-5.41 (1.960 (.260-.16-1.270 (.35 (1.226-.65 (1.21 (2.362) .353 (.46) 2.570-1.12 (.75 (1.780) 4.25-1.63 (3.13 (.30 (.16) 1.280 (.427) .8) 3.240 (.32 (2.48-2.25 (2.33 (2.27-2.81 (1.25-7.45 (2.89-71.42-2.840-1.62-8.292-.373) .321 (.13) .41-3.810) 1.680 (.374) 99-00 01-02 99-00 01-02 99-00 01-02 .300 (.267 (.288-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.320 (.420) .

840-1.11 (.80) 4.160-.460-.350) .19-6.274 (.67 (1.210 (.740) .261-.240-.09) 3.95) 1.330 (.41-4.323 (.550 (.200-.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .440-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.510 (.750-1.730) .63) 1.49 (1.06-3.240 (.216-.230) .225-.410-.53 (1.720) 90th 1.49) 3.580 (.300-.43 (1.510 (.16-4.274-.21 (1.178-.03 (.230-.328) .330) 75th .640 (.43-64.530-.400-.423 (.44) 2.370 (.860 (.63-3.91 (2.27) 1.91) .730) .316 (.67) 1.550 (.410) .17 (.270) .88-5.36 (1.530-.271-.670) .460-.19 (2.54 (1.02 (2.670) 3.440-.330) .240-. Deltamethrin.480 (.677) .270 (.490 (.35) .330) 1.13-1.91-4.246 (.40 (1.312 (.04 (.250 (.25) 2.370-.227 (.240 (.00) 1.760) .357) .446) .226-.43 (2.73) 1.560 (.09 (.372) .230-.72 (1.200-.15-2.224-.86 (1.329) .51-7.62) .335-.590-1.264 (.238-.580) .48 (1.S.220-.320) .280) .75-8.400-.32 (2.272) .37 (1.62) 1.83 (1.378 (.229-.25-2.534) .860-1.330) .35-3.94 (1.52 (1.190-.590) .500) .67 (1.35 (1.309) .150-.19) 2.930) .387) .00) 1.400) .390-.240 (.321-.173-.60-4.290) .930) 1.650) .25-5.202-.590) .11 (.17-1.44 (1.610 (.420-.270 (.510 (.13-1.81 (1.91) 9.200-.270-.401) .309 (.234 (.365) 99-00 01-02 99-00 01-02 99-00 01-02 .329) .250 (.630) .35) 1.590) .07-5.440-.290) .640 (.253) .64-5.39) 1.96 (1.200-.540 (.09-2.480-.280 (.49) 1.450 (.240-.210-.07) 2.88) 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 .275 (.74) 3.550 (. population from the National Health and Nutrition Examination Survey.10 (2.700-1.960-1.83) 1.190 (.437) .860-1.362 (.810) 1.350 (.210 (.36-6. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.280 (.09-2.250) .41) 1.240 (.280-.55) 3.60) 1.90) 3.61-2.299-.0) 3.43) 1.270) .92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .311 (.290-.278) .49-2.190-.261 (.730-1.55 (1.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .280) .272 (.300-.21-4.280 (.570) .04 (3.380-. Survey Geometric mean (95% conf.05-3.37) 1.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.73-4.13 (.40) 2.310) .52) 2.00) 5. interval) .490 (.22 (1.240-.03-1.490-.720 (.380 (.220 (.02-1.84 (1.

Environ Health Perspect 2005. et al. Obel J.111(1):79-84.114(9):14191423. et al. Hadnagy W. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Sugiri D. Grimaldo M. Ortiz-Perez MD. Fourth National Report on Human Exposure to Environmental Chemicals 175 .205(6):459-472.206(2):85-92. Seiwert M. Sugiri D. Int Arch Occup Environ Health 2003. Centers for Disease Control and Prevention (CDC). A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Becker K. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Carranza C. Int J Hyg Environ Health 2003. Bartell S. Idel H. Ball M. Lapinski R.76(7):492-498. Berger-Preiss E. Hoppe HW. toxicokinetics. Batres LE. Exposure to indoor pesticides during pregnancy in a multiethnic. Bravo R. Ranft U. urban cohort. Barr DB. Godbold J. Angerer J. Int J Hyg Environ Health 2006. Olsson AO. Hardt J. Liu Z. Torres-Dosal A. Berkowitz GS. Leng G. Atlanta (GA).46(3):281-288. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Environ Health Perspect 2003. Pearson M. Kolossa-Gehring M. Deych E. et al. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Environ Health Perspect 2006. Lopez-Guzman OD. Leng G.209(3):221-233. Arch Environ Contam Toxicol 2004. Lu C. Ranft U. Barr DB.Pyrethroid Pesticides References Baker SE. Biological monitoring of workers after the application of insecticidal pyrethroids. Levsen K. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. 2005. Angerer J. Idel H. Third National Report on Human Exposure to Environmental Chemicals.113(6):782-786. Int J Hyg Environ Health 2002. and genotoxicity in exposed children. Berger-Preiss E.

170-.350) . It is used in metal alloys. and +5. +3.130 (.130 (.280) .160-.140) .120-.160-.120 (.130) < LOD .126 (.130) .280-.130-.330) . distribution.114) .200 (.110-.180 (.190 (.136-.132 (.170-.099 (.410) . 176 Fourth National Report on Human Exposure to Environmental Chemicals .210 (.390) .130 (.170) .170 (. 01-02.230-.132 (.210) . ammunition.390-.150-.190-. or other substances containing antimony is another means of exposure.156-.230 (.340 (.250 (.350-.130-.390-.200) .490 (.133) * .130) .144) .080) .207) . and pewter.350 (.146 (.090-.150 (.135) * .130) .079-.070-.470 (.270) .390) .330 (.350 (.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 .350-.260-.300) .440 (. 0.120-.220-. 0.160 (.136) * .280) .090-.120 (.095 (.320 (.180) .600) .280-.430 (.320-.140 (. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.300 (.142 (.330-.137) .220 (.410) .390 (. ceramics.190) . Antimony enters the environment from natural sources and from its use in industry. see Data Analysis section) for Survey years 99-00. 7440-36-0 General Information Antimony is found in ores or other minerals.140 (. and glass.190 (.120-.200 (.180 (.430 (.300-.500) .330 (.320-.128 (.134-.460 (.280) .390) .154) .180-.110-.117-.330-.190) .300) .190) .460 (.240 (. and refuse incinerators that process or release antimony.400-.270 (.150 (.470) .180) .280 (.360) .098-. People are exposed to antimony primarily through food and.04.250-.200) .160 (.210-.130 (.160) .154) . from air and drinking water.180-. It is also used in paints.340 (.170-.230) .070 (<LOD-.230-.160) .240 (.080 (<LOD-.210-.220-.120 (.470) .120) .150) .230 (.400) .340) .100) .360 (.200-.Metals Antimony CAS No.280-.200 (. The absorption.220) . 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. and as a fire-retardant in textiles and plastics. respectively.100-.180-.120 (.300-.210) .130 (.200-. Stibine is a metal hydride form of antimony used in the semiconductor industry.180 (.270 (.260 (.350-.143 (.320 (.120) .160 (.100-.160) .120-.130-.500) . to a lesser extent.115-.330) .095-.310-.170-.220 (.710) .250-.160-.400 (.270 (.150-.200 (.S.100 (.230-. enamels.370) . castings.440) .330 (.390-.260-.090) 75th .260) .090 (.230-.119-.120-. storage batteries.350) .180 (.290-.530) .300 (.134 (.370-.510) .080) .240) .240-.190-.130 (.103) .260 (.150) .197) .180-.330) . and 0.400) . and 03-04 are 0.160) .200) .178) .270) .320-.154-.070 (<LOD-.460) .158 (.130-.350) .160) .570) .240-.170-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.119) .120-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.164-.161) .490) . interval) .190-.190-.230) .190 (.117-.200-.210) .190-.150-.04.260) .310) .200 (.148-.200 (.140) .220) .150 (.310 (.250-.120) .210 (.112-.126-.100 (.180 (. metal bearings.310 (.120) . sheet and pipe metal.270 (.250-.130-.350) .170 (.560) .230 (.360 (.090 (<LOD-.105 (.280-.140 (. Workplace exposures can occur at smelters.240 (.130-.290-.220-.120 (.320) Total .145) Selected percentiles ( 95% confidence interval) 50th .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400 (.169 (.260 (.400) .093 (.122 (.310 (.220-.290 (.310) .180-.350 (. and excretion of antimony vary depending on its oxidation state.125 (. solder.220) 95th .110-. Dermal contact with soil.130 (.280 (.230-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.360-.270-.430 (.140) .320) .200) .330) .130-.120-.440) .230) .140-.300) . water.088-.310-.280) .350 (.460 (.07.240 (.190 (.420) .300-.110 (.141-.110-.130 (.120-.180 (.108 (.210) .250 (.140) .220) .280-.320-.190) .140 (.220-.140) .080-. population from the National Health and Nutrition Examination Survey.250 (.220-.150-.210) .160-.115) .400 (.176 (.123 (.160) .120-.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 .410-.109-.087-.150) 90th .240 (.128 (. < LOD means less than the limit of detection.350 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3. coal-fired plants.200-.175 (.131-.260) .250) .190) .190 (.150) .137) .390) .110) .310 (.184) .140) .108-. which may vary for some chemicals by year and by individual sample.150-.360) .145 (.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 . fireworks.157) .

266 (.167-.447 (.485) .135 (.741) .228 (.098) .085) .250-.114 (.235-.117-.128-.205-.317) .193) .122 (.208-.209-.228 (.276 (.130) .113-.127) .185 (.136) .164 (.294) Total .163 (.727) .148-.242-.200) .438) .238) .084) .259 (.153-.125 (.320-.179-. abdominal pain.115 (.135) .318-.116 (. and kidney have been demonstrated in high dose animal studies depending on the dose.120 (.280-.185-.167 (.267 (.217 (.278 (.267-.078 (.124 (. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.126 (. 1962).224 (.138-.121 (.150-.106-.163 (.195-.132 (.138) * .343 (.147) .147-.238) . Acute antimony poisoning may cause a metallic taste.148-.250) .074 (.140) .200-.082 (<LOD-.213 (.135 (.405) .121) .123) .159-.126) .267) .181) .238 (.113-.115-.298 (. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.112 (.206-.471) .225) .154-.195 (. 1954).268) . diarrhea.278) .333-1.119-.203) .400 (.317) .300) .086 (.199-.193 (.061-.444) .352) .233) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.092) ..146) .151) .105-.185 (. Ming-Hsin et al. and gastrointestinal symptoms such as vomiting.144-.113) .148) * .114 (.371 (.188-.286 (. 1995).115) .156 (.S.228-.149-.192 (.236 (.152) .108 (.173-.320) .099-.214) .480) .143 (.152) .119-.146-.313-.183) .225 (.100 (.131-. resulting in hemolysis with abdominal and back pain (Dernehl et al.425) .233 (.207) . liver.200-.333-.241-.121 (.153 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.167 (.079 (<LOD-.124-.109 (.429) .195-.226 (.133) .263 (.109 (. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.129 (.117-.104-.108-.111-.209) . 1944).118 (.139 (.140) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 177 .250-.068 (.204-.173 (. Workplace standards and recommendations for air exposure Urinary Antimony (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.176-.127) .250 (.189 (.099-.080 (<LOD-.092-.229-.135) .198) .176 (.178-.176 (.244-. species.178 (.122 (.444) .256 (.421) .164) .253-.080 (.082) .315) .102-.320 (.300 (.192-.175 (.146-.098-.143) .102-. Histopathologic inflammatory and degenerative changes in the lung.253 (.300) . 1988.143) 90th .417) .417) .118 (.135) .119 (.261) .272) .089) ..145) .081) . 1986).310) .265-.239-.106-.338 (.318-.112 (.230-.162-.129) * .320-.130) .269 (.200-.112-.255) .196 (.208 (.076-.081 (<LOD-.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 .132) .137 (.430) . and ulcers (Werrin.156-. 1953).220) .187) .338) .076-.108-.097-.146-.308) . and route of exposure (Elinder and Friberg..250-.115 (.103-.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.173) .125-.104-.170 (.385 (.333 (.139 (.149) .471 (.164-. skin.186) .308-.082) .209 (.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 .271-.194-.117-. 1973).248) .131 (.115-.245) .333-.107-.068-.380 (.429 (. and eyes.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 .192) .143) .086) 75th .172-.167 (.127) .096-.500) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.130) .257) .321) .181) .069-.317) .333 (. interval) .391) .138 (.30) .182 (.265 (.188) .069-.333-. myocardium.126-.159-.227-.357-.143) Selected percentiles ( 95% confidence interval) 50th .115 (.203) .171) .071-.320 (.310) .255-.333) .173 (.127 (. 1958) and occupational exposures (Briegner et al.414) .138-.107-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.247) . Inorganic antimony salts irritate the mucous membranes.295 (.103-.095-.108-.281-..161) .124-.263-.150-.120 (.250-.391) .230) 95th .075 (.127) .087) .310 (.160 (.075 (.338 (. population from the National Health and Nutrition Examination Survey.098-.123 (.241-..134) .107-.233-.222 (.116-.248-.130 (.131) .095-.277 (.114 (.109-.111 (.209) .333 (.352 (.357) .120 (.250 (.364 (.161) .191 (.280 (.077) .211) .364 (.741 (. 1986).159-. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.181) .129) .124) .373) .129 (.Metals than for trivalent compounds (Elinder and Friberg.120 (.288 (.

Stead FM. Iavicoli et al.. Environ Health Perspect 1998.64(2):182-185.521-523.16: 33-39. Chest 1973. Suchenwirth R. which may be due to methodologic. Liao Y-H et al. 1998) or compiled reference ranges (Hamilton et al. Bolten C. External and internal antimony exposure in starter battery production. Element reference values in tissues from inhabitants of the European community. Kentner M.. Cordasco EM.51:238-240. Mayne P. and a drinking water standard has been established by the U. 2004. Yang C-Y. and 2003-2004. Schacke G. Costeloe K. Hamilton EI. et al.atsdr. Stone FD. 26-42. Ho C-K. Leinemann M. Dernehl CU. pp. Elinder CG. Cheng-Wei L.. In: Friberg L. Ju-Sun P. Pilgrim L. 2nd ed.Metals to antimony have been established by OSHA and ACGIH. stibine. Arsine. Alimonti A.10(3):560-586. Atlanta (GA). Information about external exposure (i. Urinary antimony in infancy.)1954. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. 1997). population. Biological assessment of exposure to antimony and lead in the glass-producing industry. Mayer P. Weltle D. Kiberd B. gov/toxpro2. Biological monitoring of exposures to aluminum. Delves HT. Antimony trioxide is rated by IARC as a possible human carcinogen. 1998).. 2005. Konings J. Bailly R. Dunkelberg. Int Arch Occup Environ Health 1995. Buchet JP.. Wu M-T. Mahieu P. Industrial Medicine and Surgery (Dec. 1991. and future strategies. gallium. Stasney J. 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. Industrial Medicine 1944. Br J Ind Med 1991. et al. Chia-Yu H. Earlier measurements in general populations (Minoia et al. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Nau CA. Antimony. clinical efficacy. J Occup Environ Med 2004. Friberg L. Fuchs A. Dezateux et al. Dezateux C. J Clin Pathol 1998. arsenic. Paschal et al. Sabbioni E. Gebel TW.. Skulsukai G.. environmental levels) and health effects is available from ATSDR at: http://www. Apostoli P. Pozzoli L. Delves HT. Industrial antimony poisoning.. 1994) have reported values slightly higher than those in this Report.48:93-97. Matthews T. Roland H. Third National Report on Human Exposure to Environmental Chemicals.76:432436..106:33-39. 1986. eds. Lenert G. Kuo-Juie Y. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1987). Lauwerys R. Ludersdorf et al. HH. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al.. Int Arch Occup Environ Health 1987. or exposure differences. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Antimony in blood and urine of infants. 1990. respectively. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. and hydrogen sulfide. Stocks J. Sabbioni E. Trace element reference values in tissues from inhabitants of the European community I. EPA. Yu H-S. and antimony in optoelectronic industry workers. Caroli S. Pulmonary edema of environmental origin. 2002.cdc. Arch Dis Child 1997. 1995. Chin Med J 1958.76(2):103-115. Nordberg GF. Kentner et al.158:165-190. Piatnek DA. Schaller KH. Vouk VB. References Berman JD. indium. Biomonitoring of a worker population exposed to low antimony trioxide levels. Wade A. 20012002. even when exposure levels were below workplace air standards (Bailly et al. Minoia C. New York: Elsevier. Semisch CW. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication.html. Rev Infect Dis 1988. Gallorini M. Briegner H. et al. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Review of elements in blood. Carelli G. Iavicoli I. Chen J-R. VI.S.. Centers for Disease Control and Prevention (CDC).46:931-936.59:469-474. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Ming-Hsin H. Sci Total Environ 1994. Shao-Chi C. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Van der Venne MT. Handbook on the toxicology of metals.e. 1998. Pietra R. Chemotherapy for leishmaniasis: Biochemical mechanisms.67:119-123. plasma and urine and a critical evaluation of reference values for the United Kingdom population.. Cullen A. O’Regan M. J Trace Elem Med Biol 2002. Petrucci F. Liao Y-H. Luedersdorf R.13:361-362.

Environ Res 1998. 27:38-45. Pirkle JL. Morrow JC. Antimony poisoning in industry.99-108.95:89-105.76(1):53-59. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Werrin M. blood. Sci Total Environ 1990.Metals in urine. et al. Renes LE. Sampson EJ. Industrial Hygiene and Occupational Medicine 1953. Trace metals in urine of United States residents: reference range concentrations. Paschal DC. Ting BG. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Chemical food poisoning. Jackson RJ. and serum of Italian subjects.

7-95.80 (5.90-14. ocean and fresh waters. and as a cosmetic to lighten complexion.8) 29. from coal burning. lead hydrogen arsenate.90) 75th 16. Various arsenic compounds were used in paint pigments and for tanning animal hides. arsenites. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.30 (6.5-52.90-7. In the last century. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. or rarely as elemental metalloids (yellow. as alloy in metal bearings. mental disorders.1 (32. and indium arsenides are used in the semiconductor industry. alloys.29 (8. and gray forms).30 (7.1) 7.4 (31. Arsenic trioxide (As2O3.2 (12. 180 Fourth National Report on Human Exposure to Environmental Chemicals .84) 8.77) 6. and arsenosugars.34-10.50 (8.0 (22. Arsenic is measurable in most soils.9 (8. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.6 (13. interval) 8. arsenocholine. Survey years 03-04 Geometric mean (95% conf.30) 17.1) 290 725 1542 03-04 03-04 9.5) 66.0 (15.10-10. black.S.40) 7.0-60.Metals Arsenic CAS No.9-46. solders.2) 15. meats.4 (24. Before the 20th century.7 (11. to a lesser extent.70 (6. and as homicidal poisons.10-7. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.9-34. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.9) 21.90 (5.8) 30.02-8.3-15. sodium arsenite.4 (48.0-19.0 (11. referred to as inorganic arsenic compounds.3-19.000 metric tons annually.57) Selected percentiles ( 95% confidence interval) 50th 7.8) 34. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and. pesticides.90 (7. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. aluminum. Also.5 (23. copper arsenates.2) 46.5-19. cancers.6-141) 53. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. 2001).5-178) 46. cacodylic acid. were used as treatments for syphilis. Arsenic trioxide is approved to treat acute promyelocytic leukemia.8-61.1-40.90-8. and play sets.25-9.90) 16.7) 24.6) 11. retaining walls.10) 10. psoriasis.4 (7. gaseous hydride manufactured in small quantities for use in the semiconductor industry.2 (13.6 (9.8) 7.12 (6.5) 41.3-111) 78.00-9.5) 95th 65.0 (14.41 (7. see Data Analysis section) for Survey year 03-04 is 0.3) 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. In nature.2 (41.3) 10.8) 33. The United States no longer produces arsenic from mining but imports about 22.2-17.90-8.6) 618 722 1074 Limit of detection (LOD.90 (7. Although it is still widely used in the United States.4 (26.2 (51.80-9.13-8.9-62.4-65. the smelting of copper.7) 65.2-93.55 (7.80) 6.1) 1281 1276 03-04 03-04 03-04 9.0 (43.8-77. grain.66-8. and arsenates (oxidation states of -3.00 (6. mostly for use in wood preservation (ATSDR.2-20.12-10. arsenic as elemental metalloids may be used in some ammunition.7) 90th 37.5 (40.6-43.6-35.8 (48. population from the National Health and Nutrition Examination Survey. such as arsenopyrite (FeAsS) and realgar (As4S4).70-9.08 (5. Arsenic and its compounds have had many uses in the past and present as medicines.8) 17. lead.97) 8.1-18.2-61. and in lead-acid storage battery grids.74. 2005). a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.4) 40. Since the 1940s.1) 15. General population exposure to inorganic arsenic can occur through consumption of drinking water and.9) 68. Gallium.5) 43. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.5 (14.70) 8.5 (34.90-11. and produce.6 (15.5 (36. though in some locations arsenite may be prevalent (WHO. arsenic compounds. to a lesser extent.7-83. Water sources contain mostly inorganic arsenate. particularly arsenic trioxide.20 (8. Arsine (AsH3) is a reactive.6 (32.19-9. it is found in over 200 crystalline or mineral forms.27) 9.9 (17.4) 60. and foods. and other metals.10 (6.34-9.4) 13.8) 7. trimethylarsine oxide.50-14.5-41. +3 and +5). semiconductors.1 (38.84) 8.

cacodylic acid and monosodium methyl arsenate.66-8. 2001.9) 53.01) 7.0 (31.3-41.8-75.0) 42.8 (11.93-8.86-17.6 (17. trimethylarsine oxide (TMAO).1) 7. 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.0) 12.2) 90th 30.24 (7.8) 27.61 (7.30-9.4) 32.4-64. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.3-53.1) 8.10-8.76 (6..8) 22..50 (6. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. so exposure to the general population is extremely limited. and some other seafood can contain organic forms of arsenic including arsenobetaine. The semiconductor dopants. and folate status (Chen et al.38-10.25 (6.20-9. mine tailings).2 (12. 2001. Smoking tobacco is also a source of inorganic arsenic. kelp.7-18.8-32. population from the National Health and Nutrition Examination Survey. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.12-10. NRC. 2007. Survey years 03-04 Geometric mean (95% conf. dust.41) 6.5-120) 40.2-15..1 (11.9) 13.0-26. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. 2001).6-17.0-18.47 (7.S.2) 40.3-62.0) 33.0) 26.1) 24. inorganic arsenic is widely distributed within the body.3-64. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al. and arsenosugars. but is poorly absorbed dermally (WHO. 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. Direct exposure to DMA and MMA may result from use of the two pesticides. Inorganic forms of arsenic demonstrate high acute toxicity.32 (5.11 (5.07-9.7 (11. Gamble et al. 2001).4 (24. organic arsenic can be converted back to methylated and inorganic arsenic.7-35.3) 9. Children may have additional exposures from ingestion of contaminated soils (e.59) Selected percentiles ( 95% confidence interval) 50th 7. 2001).33-10. arsenocholine.88 (5. 2003.2-46.99-9. though some reduction may occur in the gut prior to absorption.3 (24. Fish. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.64 (7. arsenic does not show biomagnification in the food chain (WHO. In aquatic organisms.66-8.1) 6.8 (27.45) 5.58-10. 2007. gallium arsenide and indium arsenide.18 (5.7) 95th 50.0-69. 2006.S.5-17.7-188) 27.10-16.35) 7. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.6) 45.3 (27.04 (5. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC. WHO.7 (9. In aquatic sediments.4 (11. are used in enclosed ultraclean operations within the semiconductor industry. After absorption.88) 7.0-38.75 (5.3) 6.4 (26.8 (21.. Tseng. have caused clinical arsenic poisoning.1) 58.8 (12.00 (6. 2001).04) 7.51) 75th 14. Extremely high groundwater arsenic levels.44) 6.7 (25.33 (6. 2007. Arsenate is reduced in the body to arsenite (oxidation state +3). interval) 8. 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.5) 290 725 1542 03-04 03-04 8.66 (7.7-34. EPA’s maximum contaminant level (Hughes. dose level.6 (10.93-9. as observed in Bangladesh where millions of people have been exposed.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. WHO.75) 13.25-9. 2001).. Though modest bioconcentration occurs in some aquatic life.6 (35.9 (45.5 (9. age.4 (12.01) 11.0) 1281 1276 03-04 03-04 03-04 8.g.8-62..8 (20.7) 28.4) 54. U.81-9.28-7.9-56. 1988). and contact with CCA-preserved wood structures.S.44-11.4 (42. 2001). shellfish.40) 8.5) 17.4 (40. 2001).0) 14.96) 12.1-36.06 (4. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.47 (6.31 (6. selenium.1 (14. EPA.0 (17.2) 15.47-6.23-7. 2001). 2006. Chowdhury et al.7-17.13) 8.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .

Arsenic has many actions demonstrated in cellular studies. interference in signal transduction pathways.. leading to a decrease in adenosine triphosphate energy production. and production of glutathione may be affected as well. substitution in phosphate metabolism. Bredfeldt et al. including inhibition of numerous enzymes. Although arsenate is reduced in the body to arsenite. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. hyperkeratosis.20 (<LOD-1.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. food residue. can cause peripheral sensorimotor neuropathies.60) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.g.. With chronic exposure. and DNA repair inhibition (Cohen et al. Cellular glucose uptake. vomiting. peripheral vascular disease. 2001.. see Data Analysis section) for Survey year 03-04 is 1. which can lead to dehydration and shock. Chile). 2007. 182 Fourth National Report on Human Exposure to Environmental Chemicals . Such actions may lead to decreased energy production. 2001). 2001). 2006) or when exposure occurs in smokers (Chen et al. Raml et al. Taiwan.10 (<LOD-1. 2000. WHO. and it also will inhibit succinate dehydrogenase. and hyperpigmentation of the skin (NRC. hypertension. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. 2006. U.10 (<LOD-1. < LOD means less than the limit of detection. 2004. respectively. which may vary for some chemicals by year and by individual sample. renal failure..Metals +3) shows greater toxicity than arsenite itself (Aposhian et al.S. Chronic arsenic exposure in humans is considered to be a cause of skin.0.EPA. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. and altered gene expression. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e..20 (<LOD-1. cell transformations. WHO.50) 1.10 (<LOD-1. fatty acid oxidation. Cardiac arrhythmias. Chronic elevated arsenic intakes have been associated with diabetes. hematocytopenias. and childhood neurodevelopmental effects in observational human studies. increased oxidative stress. and endothelial injury (Kumagai and Sumi. 2001). WHO. 2001. including drinking water sources with elevated arsenic levels (e. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells.. but additional or confirmatory research is needed (Kapaj et al. apoptosis. Survey years 03-04 Geometric mean (95% conf.10 (<LOD-1. some of these effects may take years to develop. WHO. population from the National Health and Nutrition Examination Survey. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. Acutely. Bangladesh. cytotoxicity.EPA has established drinking water.S. and bladder cancer (IARC. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al.50) 621 725 1078 Limit of detection (LOD. 2001). 2007. NRC.S. 2001). 2004).20 (<LOD-1.. lung. and by uncoupling oxidative phosphorylation (NRC. The U.60) 1. Chronic human intake of arsenic at less than acutely toxic doses. arsenic trioxide) includes hemorrhagic gastritis with nausea. noncirrhotic portal hypertension..80) 1. 2006. 2004). Cohen et al. hepatotoxicity. 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..50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.10 (<LOD-1.30) 1. and diarrhea. 2006.. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose.g. 1998. The organic forms of arsenic occurring in seafood have little known toxicity. 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.20 (<LOD-1. NRC. Studies of arsenic at levels typical of U. drinking water have not been associated with increased cancer rates (Schoen et al.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. 2001).. gluconeogenesis. 2007)..S.

Caldwell et al. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. population from the National Health and Nutrition Examination Survey. 2007.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.41) 3. Consequently. population in the National Health and Nutrition Examination Survey (NHANES) 2003–2004 were similar to levels reported in the National Human Exposure Assessment Survey (NHEXAS) 1995–1996 for about 80 children residing in the Great Lakes region (Caldwell et al.html.atsdr. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. Compared with this Report..18) 3. 1999. Josyula et al. Valenzuela et al.S.S. 2003.. 2006. 2008).. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. Pellizzari and Clayton.. 2004. 2008. 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.18 (<LOD-3. arsenic has been fetotoxic and teratogenic. environmental levels) and health effects is available from ATSDR at: http://www.00) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Vahter et al. 2001)..S.61 (<LOD-3. Shalat et al.19) 3. 1992. 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. gov/toxpro2.. In a Nevada town where groundwater levels were naturally elevated.. population in NHANES 2003–2004 (Schulz et al.. although urinary arsenic levels were not associated with CCA contact (Shalat et al. Offergelt et al...50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.. 2006). 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey years 03-04 Geometric mean (95% conf.cdc.. 2000. 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.75 (<LOD-2. In animal studies.69 (<LOD-3. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. 2006. 2006).. 2001).. Pellizzari and Clayton 2006). 2004. but generally only at maternally toxic doses (WHO.. 2001).04 (<LOD-3..... and were about two-fold lower than those for the U.e.. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 1998.33 (<LOD-3. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. had decreased since the prior 1990– 1992 survey. 2000). 1999). median urinary total arsenic levels in 4052 adults varied with seafood intake. DMA produced bladder cancer in some chronic rat studies (Cohen et al. Levels of total urinary arsenic in the U.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. 1986). Pellizzari and Clayton.50) 1.Metals compounds. Caldwell et al.33 (<LOD-3. 1999. In the German Environmental Survey III of 1998.S. 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. and the FDA has established a bottled drinking water standard. Shalat et al.80 (<LOD-4. 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. Additional information about external exposure (i. population (Rubin et al. 2008).. 2007. 2006). Meza et al. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. 2006.. Calderon et al.75 (<LOD-2. WHO. 2006).

871-1.2-38. 1996. Also.50) .6 (11. In the residents of a Chilean town who consumed water with high levels of arsenic. Caldwell et al.80 (3. arsenite.05) < LOD .37 (1.10) 8.4 (16.3% of a representative sample of the U. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.500-1. MMA. 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. 2000.g. arsenocholine.1-51. and TMAO.20) 7. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.S. 2008). Survey years 03-04 Geometric mean (95% conf.700-1.70-21.20-25.9-23.. arsenobetaine.90-29. 2001).800-4. Caldwell et al..800) 1. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.. which may vary for some chemicals by year and by individual sample..10) 4. 2007). Caldwell et al. see Data Analysis section) for Survey year 03-04 is 0..700-1.3) 35.55 (1.1-25.4) 31.70-21. 1.0 (27. population in the NHANES 2003–2004 subsample. when seafood organic arsenic is subtracted). Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic. Chowdhury et al.8 (17.60-3.. arsenite.17-1.1) 18.8-40. with DMA. Blom et al. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1. DMA and MMA.45 (1. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.70 (5..3) 1284 1284 03-04 03-04 03-04 1. 2001.40) 5.11-1. After recent seafood ingestion. 2005. Aposhian et al.00-1.7 (13. Caceres et al.3) 95th 35.900 (. 2000.50) .0) 29. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. 2005.48-2. and other factors such as nutrition.20 (2.400-.50-6. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine. population from the National Health and Nutrition Examination Survey. and two methylated metabolic products. Some noncancer effects of arsenic (e. 1985. population (Sun et al.7-22..9) 13.30 (1. WHO.20 (.2 (6.800 (.7) 15. 2007) with higher levels of arsenic in the drinking water. 184 Fourth National Report on Human Exposure to Environmental Chemicals .93) 1. In the late 1980s.30 (2. Measurable organic arsenic species in this Report are three biologically generated environmental forms. 2008).9 (7..6 (25.20-190) 31..1) 45.0 (26.29 (1.5 (26.00-4.3 (9..43-1. arsenocholine.. For residents of Inner Mongolia.68) .. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.0-23.S. 2006).40) 75th 5.1-94. When seafood intake is avoided. Tseng et al. Pellizzari and Clayton.8 (12. < LOD means less than the limit of detection.600 (.6. population showed a higher contribution of arsenobetaine (Caldwell et al.5) 292 728 1548 03-04 03-04 1. Sun et al. 2008). 2008). Valenzuela et al.. and TMAO were detected in only 7.30) 2.30) 10.. 1990. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. dermal keratosis.90-7.. population (Ahsan et al. interval) 1.20 (1. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.60) 1.20) 3.4-35.4) 23.5) 29.9 (6. The higher percentiles of total urinary arsenic levels in the U.20 (4.83) Selected percentiles ( 95% confidence interval) 50th 1.00 (. Arsenate.00-6.6-44. 2000. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.19 (.3-39.80-5.S.31-1..6.50) 90th 16.4.8. Individually measurable species resulting from inorganic arsenic exposure are arsenate.5 (14. 2008. 2003).900-1. and duration of exposure are also considered important.2-35.8) 35.7) 13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80 (4. methylation capacity.3 (21.00-12.0) 4.S. respectively.80 (.70) 6.7 (21. These associations are stronger at higher urinary levels.6 (13. in NHEXAS 1995–1996. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.70 (3. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. 2005.20) 18.S.00) 3. geometric mean levels were about 70-fold higher than for the U.40-7.20-3. China. and 0.Metals other areas of the world (Ahsan et al.5) 32.e.10 (4. 2008..74 (1.66 (1.5) 621 725 1078 Limit of detection (LOD.8-50.62) 2.28) 1.800 (.80) 1.. 4. In most human studies. vasospasm.40-6.00 (1.800-1..

00 (1.88 (5.4) 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 * * 1.72) 12. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Biomonitoring studies of urinary arsenic can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of arsenic than are found in the general population.9 (25.7) 17.Metals as with DMA.833-1.6 (6..400-.43) 75th 5.55) 1.81 (4.5 (18.2 (4. Caldwell et al.0-36. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5-20.16 (.3) 95th 29.15-4.13-39.39-3.4-82. population for the sum of inorganic related species was 18.5) 26.45) 1.9 (13.43) 14. 2008).76-27. 2001).00 (3. Sun et al.909-1.9) 14.67) 4.29 (4.4 (24.05 (.7) 30.79 (1.53 (. Survey years 03-04 Geometric mean (95% conf. 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..6-29.37-2.83) 2.1) 26.S.. 2003. In recent years.1 (26.15-1.19-2.91) 90th 16.21) 5.93 (1.. 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. not to imply a safety level for general population exposure.6 (9.28) 1.91 (4..47 (1.32-7. population from the National Health and Nutrition Examination Survey.612-1.901-2.05) 1.70) 5.786-1. 1986.73-6.61-6. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.3 (10.36) 2.51-2. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. Vahter et al.2 (12.82) 4. interval) 1.67) 1.40 (1.6-46.938-1.9 μg/L.25 (.4 (11.6-32.7) 9.50-15.4) 292 728 1548 03-04 03-04 1..51) 5. The 95th percentile of the U.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2 (12.78 (3. Fourth National Report on Human Exposure to Environmental Chemicals 185 . 2006.50-7.9) 32.30) 1.2 (13.29-14.80-153) 17.88) 2.30-1.15-1.0 (9.58 (3.25-7.4) 13.3) 1284 1284 03-04 03-04 03-04 1.64-29. 2001).6) 19.4) 32. 2008).9-18.12) < LOD .83) 8.1-18.40) 1.54 (1.68 (1.18-1. Information about the biological exposure indices is provided here for comparison.44 (1.10 (.4-21.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5) 17.531 (.877 (.4-28.65 (1.80) . which is below the ACGIH BEI (Caldwell et al.14 (1.5 (18.47 (2.3-24.78-5. 1998..638) 1. 2007). WHO. 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.82) Selected percentiles ( 95% confidence interval) 50th 1. Offergelt et al.62-6.1-36. 1992.11 (.3 (10.959-1.8) 29. 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.

Urinary Arsenocholine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6.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 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey years 03-04 Geometric mean (95% conf.S. 186 Fourth National Report on Human Exposure to Environmental Chemicals .S. population from the National Health and Nutrition Examination Survey. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 621 725 1078 Limit of detection (LOD. Survey years 03-04 Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 0. < 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.20 (<LOD-1.00) 1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Survey years 03-04 Geometric mean (95% conf.95 (<LOD-2.08 (<LOD-4. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey years 03-04 Geometric mean (95% conf.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < LOD means less than the limit of detection.00 (<LOD-3.S.2.80) < LOD 621 725 1078 Limit of detection (LOD.S.44) 2.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. see Data Analysis section) for Survey year 03-04 is 1. population from the National Health and Nutrition Examination Survey.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. Fourth National Report on Human Exposure to Environmental Chemicals 187 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. 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 1.70) < 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 2.00 (<LOD-2.40 (<LOD-1.

08 (2.70 (3.9) 13.48 (3.71) 3.0 (10.50 (4.00-11.27-2.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.72 (4.74 (2.0) 9.7-16.42) 3.9) 5.00-5.6 (9.00) 6.5) 95th 13.16 (2.2) 10.8) 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 3.80 (4.9) 11.0) 16.60-7.00-4.06) 5.97-3.50-5.6) 1284 1284 03-04 03-04 03-04 4.90 (3.78 (4.7) 12.00-4.17-4.79 (3.8) 7.0-18.67) 9.00-11.03 (3.00 (5.3 (7.00-7.0) 621 725 1078 Limit of detection (LOD.20-12.45) 8.00 (7.80) 7.14) 3.48 (2.00-12.0 (9.67) 8.0 (14.00) 3.38 (3.S.00 (3.34 (3.0-25.12 (3.73) 6.46 (4.00) 9.00) 5.14) Selected percentiles ( 95% confidence interval) 50th 3.00-15.77 (3.65-6.57-5.00-22.1-18.25 (4.00 (3.00-4.11 (3.69 (3.5) 12.00-7.16 (4.15) 4. population from the National Health and Nutrition Examination Survey.32 (8.0 (10.24) 3.91) 75th 5.71 (4.1-15.62) 4. Survey years 03-04 Geometric mean (95% conf.17-6.00-13.1 (8.6-18.60-4.00-4.95-4.80-3.55 (2.S.22) 4.39-3.00-8.0-17.45) 3.0) 13.19) Selected percentiles ( 95% confidence interval) 50th 3.0 (9.0-17.37 (2.82-9.6) 292 728 1548 03-04 03-04 3.49) 10.00-7.29-4.57 (3.00) 6.30 (7.20) 11.0 (10.00 (6.12-4.27-5.0-16.00-3.00 (6.74) 90th 9.86-21.0 (13.80-6.7 (10.45 (8.03-6.00 (5.3 (8.95-6.86-7.00 (3.05) 3.0) 12.4 (7.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (8.00-9.00 (5.00) 6.9 (7.0 (8.9 (11.0) 292 728 1548 03-04 03-04 4.00 (3.0 (12.7.0) 13.0) 17.33) 3.00 (7.0) 17. population from the National Health and Nutrition Examination Survey.00-3.52) 3.85 (3.05) 10.13-4.32 (4.69-6.49-4.00 (3.95-3.16-11.00 (3.00-7.71-4.0) 9. see Data Analysis section) for Survey year 03-04 is 1.78) 4. interval) 3.05) 5.92) 3.0-12.00 (6.60-6.34 (3.73 (3.00) 90th 11.89 (3.98) 4.00) 3.3 (8.88 (4.94-3.0-16.90) 2.00-4.0) 14.31) 4.27 (2.44 (2.61-11.00 (4.0 (10.59 (6.82-5.94) 3.80-5.0 (9.27 (3.34-4.33-4.00) 4.0 (11. interval) 3.90) 5.70-3.70-12.00-15.00) 7.7) 1284 1284 03-04 03-04 03-04 4.5 (11.86 (2.00 (5.00) 6.30) 3.37 (3.70) 5.28) 2.84-8.1-22.9) 12.0) 11.0) 9.34-4.60-3.18 (6.32-10.34) 3.71 (3.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .80) 2.70-4.8) 7.0 (12.7) 13.0 (13.84-18.00-11.10) 3.20-4.11) 4.0) 11.44) 5.0) 95th 16.17 (2.31-4.10) 6.00-4.0-19.69-3.95 (4.00) 12.0) 10.50-15.81 (5.00) 75th 6.61-16.92-12.00-10.24-4.82) 3.00) 4. Survey years 03-04 Geometric mean (95% conf.00 (5.0) 16.09 (7.00-15.65-8.00-12.69 (3. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

70-3.20 (1.85) 1.50 (1.20 (1.80 (1.46-2.90 (2.60-2.50 (1.10) 95th 2.70) 2.20 (1.62) 2.86 (2.80 (1.70-2.40-2.30 (1.20 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00) 1.50) 621 725 1077 Limit of detection (LOD.77) 1.53-2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.82-2.10 (. population from the National Health and Nutrition Examination Survey.40-3.985) 1.30-2.S.11-1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1. which may vary for some chemicals by year and by individual sample.86) 3.53 (1.82-2.40-2.80-2.50-2.85) 2.86 (2.36 (1.20-3.86) 2.816 (<LOD-.00) 2.80-2.30) 1.73-2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.61-3.90) 1.33 (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 1.61) 2.00-1.37 (1.60) 1.40) 2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.07) 2.07 (1.80 (1.30 (1.18-1.00-2. < LOD means less than the limit of detection.50 (2.33 (1.31 (1.10-3.50) 1. Survey years 03-04 Geometric mean (95% conf.10-1.40-3.10) 2.20 (1. population from the National Health and Nutrition Examination Survey.00 (<LOD-1.28 (1. see Data Analysis section) for Survey year 03-04 is 0.853-1.30 (1.70-2.88-2.30) 90th 1.07-3.40) 1.57) 95th 2.80 (1.23) 1.00) 1.00 (2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.40 (2.S.70-2.00 (2.34) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.18-1.00 (1.96-2.63 (<LOD-1.16 (2.81) 1.14-1.30) 2.90) 2.10 (.60 (1.46 (1.15-1.05-1.80 (2.30) 1.52 (2.22 (1.79) 2.60) 2.40) 1.88 (1.10 (1.40 (1.9. Survey years 03-04 Geometric mean (95% conf.45) 3.00-2.900-1.43-3.22) 3.93) .Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60) 2.35-3.17) 2.20-1.10 (1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.88 (1.10-1.30 (2.30-1.20) 2.00) 1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.28 (1.58) 2.90 (1.50 (<LOD-1.10 (<LOD-1.00-1.00) 2.90) 2.84-3.70-2.54) 90th 2.30-1.80) 1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .60 (2.20 (1.31-3.00-4.71-2.36) 1.

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

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24 (4. 2001).70-6.50 (5.76-3.11 (3.91) 6.10 (3.50-6.46) 1. interval) 1.26-7.90 (6.27) 2.31 (2.15 (1. respectively.87-3.71) 2.80-2.36-1.35-1.15) 5. water. The general population can be exposed to low amounts of barium in air.60 (1.30-1.10) 3.37-8.30-1.00) 1.65 (5.02 (7.86) 6.90-2.90) 4.94-6.64-3.51) 7.90-9. bricks.35 (2.50) 2.00-8.61-8.70) 4.18 (6.43 (5.70 (5.45 (1.30-2. Barium salts have also been available as rodenticides.76) 1. population from the National Health and Nutrition Examination Survey.37 (4.80 (2.34 (2.39 (1.20-8.28) 90th 5.73) 3.92) 2.49) 8.62) 1.06-1.39) 1.20-5.70) 3.25 (1.90 (4.30 (1. and food.51) 1.66) Selected percentiles ( 95% confidence interval) 50th 1.20-1.52 (1.56 (2.56) 1.70) 5. and 03-04 are 0. see Data Analysis section) for Survey years 99-00.38 (1.11-1. soluble forms of barium.50 (4.20) 2.77-3.12.70-2.61 (1.8) 9.40) 7.27 (1.69 (1.99-5.24-1.65) 3.09 (1.71 (2.50) 4. whereas others are practically insoluble (e.88 (5.30) 4.60) 1.51) 2.40-13.36-1.17-1.70) 7.21-8. 7440-39-3 Medically. Workers employed by industries that make or use barium compounds can be exposed to barium dust.81-2.14-6.11 (2.29-5. barium sulfate and barium carbonate).63 (1. and ceramics.4) 7.57 (5.61 (1.30) 5.60) 1.56) 4. In single dose animal studies.12-1.70) 1. rubber.54-1.48-4.48) 1.50 (1.44-2.70-5.82-6.04-6.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.11 (3.15 (2.55-7. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.77 (3.53) 1.00-76.15-11.52 (4.30) 8. and 0.76-7.78) 1.70-3.86-5.03 (1.63) 1.05-2.49 (1. depilatories.01 (4.62) 1.84) 5.50 (2.06-2.56 (1.21 (1.65) 1.40 (1.10-5.15-1.60-10.10) 5.49-9.71) 95th 6.21-2.87-9.76-2.8) 5.48) 1.80 (1.73) 1.00) 6.35-4.55-3.36) 5.93-8.08 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00 (2.49) 4.90) 2.43 (1.68 (1.87 (6.64 (1. In nature.99 (4.41-3.78-2.38 (1.80 (1.30) 3.54 (2.54-8.80-5.50 (1.74-3.29-1.59-11.80-7.50 (4.47-1. such as brazil nuts.34) 2.g.60) 3.86 (4.85) 1.29) 5.30-3.88) 7.43) 6.86 (4.61 (5.18-1.70 (1.40 (1.60-6.28-1.40 (5.80 (5.49) 11.50 (4.50 (6.35-1.43 (1.56 (6. Barium compounds are used by the oil and gas industries to make drilling muds.33 (1.07 (2.82) 2. Barium compounds are also used commercially in paint.1) 9.25-11.30 (5.19-1.20 (1.10) 1083 1335 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.48-4.57) 3.98) 1.61 (2.15-1. Small amounts of barium can be released into the air during mining and other industrial processes. such as barium chloride.78) 1.12.65) 1. Certain foods.10 (2.9) 5.26) 2. 01-02. glass.54) 2.50 (1.60) 4.74) 3.42 (1.8 (6.70-2.16) 5.96-2. tiles.60-6.19) 2.30-2.45) 7.91 (2.14-1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.31. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.32-1.73 (6.82) 1.63 (8.18) 3.50-6.47) 4.80) 6.34 (1.54) 1.70) 1.50-1.38) 2.65-1.37) 1.67) 6.80-3.44 (1.37-1.31-2.78-3.12) 6.87-14.30 (3.49-1.93-2.63 (5.86-4.35 (3.65-5.60-3.20 (4. are high in barium (Genter.30 (5.64) 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 2.12 (2.36 (1. it combines with other chemicals such as sulfur or carbon and oxygen.40) 3.04-2.85 (2.39-1..40) 7.63) 1.20-1.01-7.87-7.60 (2.40 (4.72) 1. Some barium salts are freely soluble in water.08-8. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).88) 1.30-5.87) 7.4) 9.36 (4.50-1.63) Total 1.20 (3.80 (2.34 (1.48 (6.62 (1.Metals Barium CAS No.54 (6.30 (2.57-7.60-2.20-8.70-8.10 (4.90) 1.12) 7.40 (1.54-1.22) 6.05% of the earth’s crust. Fourth National Report on Human Exposure to Environmental Chemicals 193 .74-2.71) 1.50) 1.14 (6.20-1.00) 1.00-3.38) 8.53-5.87 (5.51 (1.49) 2.30) 5.47-1.61 (3.32-7.88) 4.41-1.00 (1.80) 7.90) 2.90 (1.00) 4.80 (1.20-8.40 (5.72) 4.65-8.22-1.30) 5.25-1.95-6.43) 2.59) 3.81-3.73 (5.63 (2.53) 2.21 (1.91) 2.81-2.50 (1.50) 2. fireworks.26) 5.32) 8.20-1.35) 5.90-13.50 (1.75-3.50 (3.41) 1.12 (2.4) 6.54) 1.46) 1. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.15 (6.85) 1.71-9.76 (3.27 (1.77) 1. 0.40 (5.80) 1.09 (2.46-1.95 (4.16 (1.24-1.39) 4.26-1.56 (1.97 (1.20-6.S.22-1.37) 5.10-4.30) 2.73-5.75) 2.44-5.62 (1.72) 75th 3.2) 6.93 (4.66 (4.35 (1.39 (1.

10 (6.35-3.32 (2.45-1.50) 1.34-3.19-2.31) 5.49-1.65 (2.73) 2. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.62 (4.832-1.0) 5.69 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.29-1.35-1.49-1.49 (1.48 (1. 1986).33-1.76) 2.62 (1.99 (2.88 (6.72) 4.91 (3.10) 3.48-5.36 (3.46 (2.48) 2.74) 1.38) 1.00 (3.75-3.19-1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.24-6.53-21.35-1.56) Selected percentiles ( 95% confidence interval) 50th 1.96-6.12) 2..32) 2. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.29) 1.54) 2.02) 4.0) 6.97-4.68 (2.963 (.47 (5.921 (.710-1.60) Sample size 2180 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.36-1.29-4.71 (5.64) 7.59) 1.26-1.81-7.49-1.00) 1.54 (2.16-1.45) 95th 6.36-1.66 (1.30 (1.24-1.20-1.68) 3.68-3.19-1.23-2.41) 4.16) 11.8) 4.69-9.00) 4.37 (1.S. and cardiac dysrhythmias.00) 4.26-1.84-5.87) 1.37) 2.97 (5.61 (4. 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.64) 7.51) 4.84-2.53) .10) 6. paralysis.51) 6.56 (1.39) 4.27-3.59-7.37-1.45-1.75) 1.38) 1.77) 5.08-1.25) 4.39 (3.36 (1.60 (5.52 (3. and route of exposure.58) 75th 2..29-3.03-1.881 (.30) 2.58 (4.50) 1.34-5.28-1.98 (2.48 (1.19-1.76 (2.48-3.52-10.76-3.59 (1.92) 2.41 (1.03) 1.39-1.25 (1. interval) 1.68) 1.48-1.80) 4.56 (1.51 (3.59) 2.58) 1.44-2.65 (5. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.42) 1.76) 1.29 (1.77) 1.55-6. in urine.55 (4.38 (1.91 (3.63) 1. 2001).38) 4.01) 1.23-5.85-5.55) .31-1.51-3.14-2.28 (1.33 (1.75-22.24 (5.00) 6.33 (1. 1990).22-1.75) 2.47) 4.83) 2.15-4.10-1.58) 4.54 (1.92 (4. 1984.40 (1.38-1.88 (2.60 (2.52-4.60 (1.31 (1.31-1.76) 2.56) 4.33 (5.32 (1.49 (1. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.09) 6. hypertension.58 (2.44 (1.77) 1.62 (2.11) .45-8.70) 1.59 (1.16 (1.73-2.47) 1.22-2.905 (.02 (3.83) 3.52) 1.73-4.28-7.75) 1.39-5.29-7.32 (1.64 (1.72) 6. The health effects of exposure to barium compounds depend on the dose.52) 2.90-2. Wones et al.75) 2. Symptoms following acute high dose include perioral paresthesias.00-1. Toxicity from soluble barium salts is rare.76 (4. 1985.99) 1.26-1.40 (1.22-1.96 (4. population from the National Health and Nutrition Examination Survey. diarrhea..59) 1.25-11.06) 2.99 (4.57 (6.81-6.04) 1.11) .80) 3.915 (.24-11.40-1. a benign condition that may occur among barite ore miners.20-2.11-2.47) 10.31 (4.46) 2.24) 3.97-3.78 (2. weakness.96) 4.70) 10.39 (2.72 (2.26-1.31-1.50) 2.58-6.20) 4.00 (5.77) 1.86 (2.03) 3.81-6.4 (5.47 (2.82) 1.42 (4.97 (4.46) 3.33-4.3) 6.79-5.86-7.43-6.29-4.77-5.03-1. Chronic high doses in animals resulted in kidney damage (McCauley et al.0) 7.63-4.24-6. such as those used in medical radiographic procedures. Following intravenous injection in animals.13-3.10-2.33) 1.24 (3.21 (1.38 (4.34 (1.41) 5.06) .26-4.74) 1.36 (5.55 (1.57-5.01 (5.43) 1.57-7.55 (1.24-1.91) 2. 1994.36 (1.89 (2.97) 1.42) 1.18 (1.52) 7. vomiting.4) 5. Perry et al.39-10.60 (2.96) 4.91-2.28-11.77) Total 1.30 (1.02-5.08-2.45 (3.45) 1.55 (5.64 (1.2 (3.48 (1.51 (1.13-2.56-3.33) 6.40 (1.38-7.62) 2.22-4.64 (1.96 (4.46) 1.44-2.32) 2.34-1.36 (3.39 (2.53 (2.04 (2.61) 2.37 (1.24-3.96) 4.18 (1.68 (3.01 (4.89) 90th 4.50 (4.96) 7.27) 7.3 (6.82) 1.80-6.68-3.26) 4.00 (3.51) 4.703-1.20 (1.57-10.55-5. Insoluble barium salts.880-1.20-8.34) 1.46-22.05-1.67-6.02) .37-2.38-5.2) 6.70) 4.27-1. water solubility.27 (2.45-6. 1989).57) 2.51 (1.38 (1.86) 5.84 (3.84) 2.891 (.28-6.74 (5.68 (3. are not absorbed when administered.38 (4.29 (3.777-1.39-1.79) 1.2) 5.28) 5.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .45 (1. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.41 (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 1.03) 2.60 (1.39 (2. NTP.Metals was eliminated primarily in feces and to a lesser extent.76 (3.754-1.47) 1.23-1.36-2.00 (2.54) 1.47-8. chemical form. Barium is not rated for human carcinogenicity.04) 5.50) 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 1.64 (1.00-7.41 (2.

gov:8080/cs. 1989. Schaller KH. New York: Elsevier. Vol 2: Specific Metals. New York: John Wiley & Sons. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. 84-94. eds. Atlanta (GA). 1992). and serum of Italian subjects. 2005. 1985. Minoia C. 2000) to levels in NHANES 1999-2000 and 2001-2002.85:355-359. Environ Health Perspect 1990.95:89-105. Pirkle JL.28(3):373-388. 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.html?charset=iso-88591&url=http%3A//ntp. Investigations into the effect of drinking water barium on rats. Vouk VB. eds.cdc. 1998).gov/toxpro2.... Magnesium. p. Laurie RD. 4/8/09 Paschal DC. et al. Biomonitoring Information Levels of urinary barium reflect recent exposure. Wones RG. J Toxicol Environ Health. EPA. et al. calcium. Princeton NJ: Princeton Scientific Publications. Int Arch Occup Environ Health 1992.atsdr. ed.296(1-2):71-90. Perry EF. Pozzoli L. Levy. Reeves AL. In: Calabrese EJ. 1986. 1990. 2001-2002. Calabrese EJ. Inc. 5th ed. Ash KO.niehs. p. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://ntp.64(1):13-23.gov/ntp/htdocs/LT_rpts/tr432. ed. 2nd Ed. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies).. Epidemiological study of barium in Illinois drinking water supplies. Genter MB. McCauley PT.S. the welders had no obvious adverse clinical effects (Zschiesche et al. References Brenniman GR. Princeton (NJ): Princeton Scientific Publications.nih. Handbook on the Toxicology of Metals. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. 1984.76(1):53-59. Jr. Exposure to soluble barium compounds: an interventional study in arc welders. environmental levels) and health effects is available from ATSDR at: http://www. Centers for Disease Control and Prevention (CDC). Jackson RJ. Gallorini M. Stadler BL. Advances in modern toxicology. Sci Total Environ 1990. National Toxicology Program (NTP). blood. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Information about external exposure (i. PS. Ting BG.niehs. LA. Howerton K.. Sampson EJ.S. and 2003-2004 (CDC. Patty’s toxicology. 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. pp. In: Inorganics in drinking water and cardiovascular disease. and a drinking water standard has been established by U. Comparison of representative ranges based on U. barium. Barium. 221-252 Komaromy-Hiller G.197210. Fourth National Report on Human Exposure to Environmental Chemicals 195 . Apostoli P. Douglas BH. Powell C. Clin Chim Acta 2000.html. Trace metals in urine of United States residents: reference range concentrations. [online]..pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en.. et al. p.. Nordberg GF. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Lack of effect of drinking water barium on cardiovascular risk factor. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. 1994. Sabbioni E.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. Pietra R. Perry HM. Morrow JC. In Friberg L. patient population and literature reference intervals for urinary trace elements.nih. 2001. Weltle D. Environ Res 1998. Minoia et al. strontium. Paschal et al. et al. A study of 46 elements in urine. Frohman. Cohressen B. Zschiesche W.. 231-249. Kopp SJ. Trace element reference values in tissues from inhabitants of the European community I. NTP.e. Costa R. and radium In: Bingham A.

and 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. In studies of laboratory animals.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 . x-ray machines. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. are mined for commercial recovery of beryllium. and machine-parts industries. Exposure to beryllium occurs mostly in the workplace. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. nuclear. or drinking water containing the metal. < LOD means less than the limit of detection.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 . In medicine.130 (<LOD-. soil. and refined beryllium is used in mirrors and special metal alloys for the automobile. 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 . bertrandite and beryl. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. Beryllium compounds are commercially mined. and from breathing tobacco smoke.13. see Data Analysis section) for Survey years 99-00. respectively. 196 Fourth National Report on Human Exposure to Environmental Chemicals . less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. aircraft. coal. the lightest of all metals. eating food. 7440-41-7 General Information Pure beryllium is a hard gray metal. 0.140 (<LOD-. near some hazardous waste sites. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 01-02. Two types of minerals.130 (<LOD-. and volcanic dust.13. Low-level beryllium exposure in the general population can occur through breathing air. and 03-04 are 0. electrical.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. computer.13.Metals Beryllium CAS No. beryllium is used in instruments. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. and can be found in mineral rocks. and dental bridges.

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

Apostoli P.. VI.S.157:388-398. Hamilton EI. Sci Total Environ 1994.inchem. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2000.. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure.. International Programme on Chemical Safety (IPCS). In other studies. Sci Total Environ 1990. Andrew M.org/documents/ehc/ehc/ ehc106. 3/27/08 Komaromy-Hiller G. 1990. less than 0. Beryllium [online]. Trace metals in urine of United States residents: reference range concentrations.gov/toxpro2. Hamilton et al.cdc. 1990. blood. patient population and literature reference intervals for urinary trace elements.. population are lower than levels in workers. 2001).html.Metals (i.e.95:89-105. Paschal et al. Sabbioni E.296(1-2):71-90.atsdr. et al. A study of 46 elements in urine. Int Arch Occup Environ Health 2001. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Centers for Disease Control and Prevention (CDC). Gallorini M. it is likely that urinary beryllium levels in the U. Ash KO. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Environmental Health Criteria. Morrow JC.htm. population were generally undetectable in NHANES 1999-2000. Pietra R. Available at URL: http://www. Biomonitoring studies on levels of beryllium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of beryllium than are found in the general population. Pozzoli L. 1998). Ting BG. They reported urinary beryllium levels ranging from 0. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Jackson RJ. Howerton K. Kriess K. Sabbioni E.S. References Apostoli P. Van der Venne MT.74:162-166. Atlanta (GA) 2005. environmental levels) and health effects is available from ATSDR at: http://www. HLA-DPB1 and chronic beryllium disease: a HuGE review.23:827-839. Third National Report on Human Exposure to Environmental Chemicals. and serum of Italian subjects. Costa R. et al.S. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Pirkle JL. Schaller KH.e. Genetic and exposure risks for chronic beryllium disease. and the fact that most NHANES participant levels were undetectable. Am J Epidemiol 2003.. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al.13 μg/L. and 2003-2004. Element reference values in tissues from inhabitants of the European community. Levels of beryllium in urine for the U. Sampson EJ. Clin Chest Med 2002. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Minoia C.158:165-190. McCanlies EC. Given these results.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. 20012002. Environ Res 1998.12 to 0.1 μg/L). Paschal DC. Weston A. 106. and the 95th percentile for males in NHANES 2001-2002. Trace element reference values in tissues from inhabitants of the European community I. Comparison of representative ranges based on U. Maier L. which approximate this Report’s limit of detection. Review of elements in blood. 0.76(1):53-59. Minoia et al. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Clin Chim Acta 2000.

20-1.80) 1.300 (.400 (.500 (.10 (1. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.300-.900-1.700) 1.400 (.300-.20-1.700) . or copper smelters (U.500 (.10) 1.20-1. and 03-04 are 0. lead.500-.600 (.400-.70) 1.600 (.600-.30) . Fourth National Report on Human Exposure to Environmental Chemicals 199 .382 (.900-1.700-1.200-.300-.10) 1.700 (.00 (.10 (1.600 (.700) .00-1.300-.14.304 (.300) .400) < LOD .600 (.600) .600) 1.300) .3.300-.40) 1.10 (1.235 (.400) .800) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (.300) .10) 1.300) .300) .300 (.900 (.60 (1.800-1.20) 1.500) .900-1.468 (.300 (.300 (.300-.289-.40 (1.400) < LOD .900-1.00 (1.600 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .400) .200-.300) .700-1.400) .10 (1.300 (.398) < LOD < LOD < LOD < LOD < LOD < LOD .300 (<LOD-.00-1.50 (1.70) 1.500-.300 (.20-1.70) 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 . cadmium use has declined in response to environmental concerns (http:// minerals.400) .449) Selected percentiles ( 95% confidence interval) 50th .700) .200-. The predominant commercial use of cadmium is in battery manufacturing.40 (1. and nonferrous alloys. 7440-43-9 General Information Cadmium is a soft.600-1.378-. interval) .90) 1.3.300-.30) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.500-.421 (.usgs.300 (<LOD-.10 (1.400 (.400) .20-1.300) 75th .80) 1.30 (1.10) 1.50) 1.300-.600 (.300) . and incineration of municipal waste materials.600 (.304-.00-1. Cadmium also may be emitted into the air from zinc.700) .500 (.386-.600-.300-.00) .600 (.10 (1. 0.500) .300 (.300 (.400 (.337) .300) 1.300 (.500 (.331) .50-1.300-.20) 1.60) 1.395 (.60 (1.366) * * .gov/minerals/pubs/commodity/cadmium). malleable.400-. see Data Analysis section) for Survey years 99-00.378 (.300 (<LOD-.300) .00 (.20) 1.500) .400-.200 (<LOD-.362-.500) .400) .400-.20) 1.00 (.500-.500-.361-.500-.300-.900-1.600 (.30-1.400) . < LOD means less than the limit of detection.60 (1.275-.400 (.300 (.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 * * * * * * .200 (.600) 90th 1. during refining of lead and copper from sulfide ore.00 (.20) 95th 1.900-1.00 (.20 (.600 (.425 (. population from the National Health and Nutrition Examination Survey. plastic stabilizers.400 (.368-.500-.40 (1.50-1.300) .40 (1.500) .500-.700) .00-1.400) < LOD < LOD < LOD .600) .400-.700) .500 (.400) .900-1.200-.50-1.400-.426-.00-1.20) .600 (.40-1.900-1.376-.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.470) * .20) 1.500-.500 (.400 (.393 (.300-.300-.500) .304 (.500-.900-1.50-1. and 0.900 (.00 (.500-.S.300 (.255) .20-1.300) .500 (.200 (.00) .300) .500 (.400) .60-1.800 (.500-. 01-02.441) * .200) .600-.300-.333 (.600) .400 (.300 (<LOD-.400 (.283 (.70) 1.60) 1.344) .Metals Cadmium CAS No. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.500-.700) .900-1.600 (.80 (1.500-.10) 1.400-.30) 1.00 (.400 (.412 (.420 (.30) 1.30-1.30-1.427) * .452) .400 (.400-. Other uses include pigment production. Since 2001.359-.200-.10 (.800-1.300 (.300-.460) .00-1.00-1.400) < LOD .300-.400 (.400 (.700-1.00 (.60 (1.20 (1. respectively.20) 1.400 (.300 (.400-.400) .20) .300) .800 (.10) 1.313 (.30-1.309-.296-.400) . EPA.500-.400 (.600) .300-.326 (.200 (<LOD-.600 (.10) 1.00 (.600 (.300) .00-1.367-. as zinc sulfide) and to a lesser extent.60 (1.600) .403) .600) . coatings and plating.500-.403 (.266-.200) .700) .300-.S.50) 1.424) * .00-1.40 (1.40-1.40 (1.40 (1.50 (1. U.10) 1.600) .50 (1.70) 1.513) .50) 1.30-1.600) .00 (1.300 (.60) 1.20) 1.300-.800) 1.400) .10 (1.300-.S.20-1.500 (.50 (1.20) 1.60) Total * .300-.500) . which may vary for some chemicals by year and by individual sample.400 (.400) .500-.400-.40) 1.600) .200 (.00 (.300-.400) .216-.500-.400-.800) .

440 (.101) .233) .354) .221 (. copper) and protein.253-.229) .281 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.596) .680 (.200-.061-.388-.210 (.633 (.800-.510-.257) .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 .41 (.381-.07-1.141 (.498-.990) .539) .705-. Inhalation of cigarette smoke is a predominant source of exposure in smokers.204 (..387) .480) .500) . 2003.22 (1.551) .790 (.433-.260-. Horiguchi et al.82) 1.447 (. whose body burdens of cadmium can be approximately twice that of nonsmokers.17 (.090) .220-.545 (.400-.790 (.200 (.262) .640) .34) 1.209 (.30-1. 2003).741-1.199 (.52 (1.157-.972 (.255) .200 (.265 (.240) .38) 1.210) .412) .195-.299) .189) .165-.800 (.848 (.13) . and 03-04 are 0. With chronic exposure.187 (.06) .230) .32 (1.519) .220) .246) .128 (. ingestion through food is the largest source of exposure. interval) .450 (.170 (.855-1.257-.200-.393-.980-1. 1994).100-.300 (.918-1.700-.20 (1.061 (<LOD-.633-1. however.280 (.227 (.980-1. calcium.184-..080 (. 2001).219 (.507) .190-. Renal tubular and glomerular damage.** Survey Geometric mean (95% conf.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 .308) . The kidney is a critical target and shows the earliest sign of cadmium toxicity.57) 1.589 (.210 (.700-.748-1.121 (.211-.177-. 2003).S.207-.610) .470-.092 (.173) .892-1.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .220-.476-.220 (.202 (.36) 1.237-.540) .28-1.160) .458 (.092) .390 (.175 (.15) 1. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.890-1.210 (.249) .310) . and 0.24) 1.717-.28) 1.114-.202-.550 (.436-.963-1. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.886) .83) 1. see Data Analysis section) for Survey years 99-00.169-.13-1.135-.989-1.818 (.339) .430-.445 (.115-.180 (.327 (. Cadmium in soil is absorbed by plants. rice.20 (1.06-1.206) .285-.490) .126) .238) .135 (.51 (1.836-1.255) .260-. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.279 (. population from the National Health and Nutrition Examination Survey.423-.233) .130 (.192-.148-.01-1.623) .265) .980) .810-1.216 (. including many food crops such as cereal grains.820) 1.15) .081) .295) .316 (.520-.190-.886-1.260 (.700-.960 (.329 (.210 (.249-.247) .272-.763-.806) .223 (.231) .733-.48 (1.20 (1.067-.753-.482) .607) . 01-02.322 (.492 (.302 (.72) 1.450 (.175 (.25 (1.251) .559 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.. potatoes.232 (.Metals 2000).110-.839 (.210) .310 (.817 (.157) .01 (.12 (.211 (.270 (.372) .462 (.06.880) .160-. wheat.820 (.255) .977) .087-.445 (.277 (.580) .38) .273 (.400-.219 (.179-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.366) .20) 1.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .206 (.226) .06-1.134) .17) .220) Selected percentiles ( 95% confidence interval) Sample 95th 1.390-.858 (.239 (..38) 1.060-.241) .090) .263) .196-.09-1. For nonsmokers who are not exposed to cadmium in the workplace.875 (.22 (.19) 1.456-.282 (.733) .150) .551 (.219 (. To a lesser extent.04 (.481) .350 (.490) 1.351-.112-.13 (.493-. 200 Fourth National Report on Human Exposure to Environmental Chemicals .230) 75th .766 (.686-.208-.366-.189-.235) .153-.326) .730-.875) .150-.183-.320) .240-. drinking water is a source for cadmium intake.160) .870) .243-.510) .230 (.43) 1.222) .290-.430) .192-.06. **All results are corrected for molybdenum oxide interference in the ICP-MS method. an inducible metal binding protein.078 (.261-.136) .440-.940-1.193-.313) .466 (.530) .20-1.74) 1..191 (.120 (.17 (.843-1.077 (.232) .813 (.17 (.892 (.306 (.191-.04 (.261-.203) .210 (.860) 1.229-.15 (.191-.140 (.160 (.193 (.229) .47) 1.107-.181 (.189-.390-.02-1. Diamond et al. 1999.330-.067-.01) . 2003).148) .960) 1.167-.10 (1.25) 1. Cadmium is absorbed via inhalation and ingestion.38) . a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.28 (1. Cadmium absorption may be increased with iron deficiency (Berglund et al.178-.519) .890 (.479) .475 (.170-. respectively.12-1.201 (..109 (.289-.980 (. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al. 0.820-1.283 (.238-.151-. zinc.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. 2004a.366-.214-.234 (.426 (.362) .203 (.194-.06.221) .360) .065-.077 (.980) .713) .109-.03) .394-.171-.190-.714-1.817 (.530 (.270 (.440 (.919) .336) .198) .500) 90th .300) .170-. Kikuchi et al.455 (.284) . and various seeds.452 (.

433-. 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.234) .147-.13) .280 (..197-.364) .14) 310 368 287 648 762 724 1299 1559 1532 12-19 years 20 years and older 99-00 01-02 03-04 Gender Males 99-00 01-02 03-04 ..104) .06 (.107) . a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.084 (. Staessen et al.827) .472) .929) .223) .906) .170 (.884) .985 (.614) .690-.281) . 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.208-.962) .398-.783) .795) 1.175 (.10) 1.666-.779 (.00 (.343-.083-.240) .171-.250) . most often a result of occupational exposure (Roels et al.126 (.267 (.826-1. 2004).234 (.12) 1.826-1.678-.263-.220 (.227-.S.533) ..431) .806-1.085-.917) .236-.719 (. Horiguchi et al.238-.950) .391-.979 (.210) .297) .199-. 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.205 (.381-.157-.182) ..382-.156) .219 (.507-.484 (.136-.288 (..224 (. However.708-1. 1996.144-.263 (.215 (.418-.449) .833-1.210 (.168-.096) . can result from high dose chronic exposure.688-.154-.176 (.178) .140-.219 (.289) . population from the National Health and Nutrition Examination Survey.240) .219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * . 2002.168-.190 (.238) .696-.591 (.438) 90th .740 (.148 (.813-1.147-.196 (.647-.321) .839) .404) .318 (.909-1.387 (.086 (.185) .653) .630-.300-.415) .783 (..38) .137 (.135) .181 (.335 (.08) .274) 1.941 (.687 (.518) .718 (.340) .136-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.446) .607) .674-1.338 (. 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.678 (.077-.412 (.423 (.551) ..211 (.123-.229) .154 (.331 (.146-.404 (.113-..304-.162 (.830-1.722-.288) . 1999).245 (.828) .256-.091 (.147 (.350) .189-.686 (.173 (.729 (.873 (.490 (.241) .998) .100 (.156-.316) .202 (.101) .388-. Noonan et al.470) .181-.150-.247-.308) .232) .261 (.05) 1.161-.159 (.940-1.487 (.538) .182) .175 (.191-.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 .303) .191) .769 (.479 (.336-.177) .187-.075 (<LOD-.207-.232) .850) .700) .545) .622 (.700 (.267 (.650-.316 (.067-.122 (.444-. During the 1950’s and 1960’s.281) . 1999).687-.131-.476) .182) .174-.130-.667) .198) .158-.645-.166 (.500-. 2003.210 (. At lower environmental exposures. Olsson et al.143) .184-.098) .304) .802 (.176 (.716-.191 (.434 (.16) 1.481 (.111-.757) .04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .239-. 1999).516-.226) 75th .289) .754) .181) .225) .225) .074-.668-.063-. 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.200 (.17) .663 (.856) .716) .235) .233 (.075-.725-1.201-.690 (.818) .** Survey Geometric mean (95% conf.690-.387-.218) .501 (.329 (.856 (.206-.190 (.097) .183 (.212 (.830) .216-.07 (.194-.473 (.02 (.123-.438-.253) .308 (.221 (.00 (.874-1.261) .184-.927-1.789 (. interval) .352) .261-.441-.382) .157-.085 (.173-.266-.432 (.423-.421 (.09 (.792 (.07) .426-.106) .876-1.531 (.268 (.185 (.140-.537-.767 (.159 (.168 (.156 (.414-..143-.850) . 2004b).491-.255-.288-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.940 (.222-.051-.208 (.470) .325 (.917 (.137-.691-.192) .209) Selected percentiles ( 95% confidence interval) Sample 95th .104) .283 (.784) ..163) .278) .617 (.273 (.931 (.293-.631) .693 (.209) .094) .187) .252 (. 2000.767) . 2002.175-.414 (.727-.813-.084-.440) .757 (.090 (.143-.536 (.181 (.078 (.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate. Jarup et al.865 (.112) .311) .919 (.071 (.266) . 2002.270 (.170-.292) .282 (.541) .559-.093 (.440) .16) .078-.712 (.091) .253 (. Fourth National Report on Human Exposure to Environmental Chemicals 201 .418) .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.377-.562-.178-.163 (.184) .228-.818) .247-.560-.234-.207) .247-.242) .183) .221-.204-.296 (.091 (.199 (.

e. Wilhelm et al. 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..S. Further research is needed to address the public health consequences of such exposure in the United States.. 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). 2006). 1999). 2003. 2003.. Horiguchi et al.. Staessen et al. 2005. 2003. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . has resulted in severe. 2004b. not to imply a safety level for general population exposure. Several studies of populations residing in areas with higher cadmium soil concentrations or with frank cadmium pollution have reported mean blood and urine cadmium levels considerably higher (as much as 10 times higher) than control groups or representative U. Staessen et al... respectively.. 2003. 2003. Jarup et al. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. In postmenopausal women... 2002). pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Wennberg et al. Ezaki et al. 2002. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. Women had higher blood and urine cadmium levels compared to men of similar ages. 1996. potentially fatal pneumonitis (Fernandez et al. 2004. Olsson et al. 1988). Zhang et al. 2000. Friedman et al.. Moriguchi et al. 2006). Occupational standards are provided here for comparison only..cdc.S. maternal blood or maternal urine and birth weight (Nishijo et al. with peak values observed in the fifth to sixth decades (CDC. Jarup et al. 2002) and length at birth (Nishijo et al. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. 2002.html. 2005. Jin et al. 2004.. Staessen et al. 2000. EPA. 2005. In adults aged 60 years and older. 2002). 2002. approached these values associated with subclinical changes in renal function and bone mineral density.. 2002. 2002. Wennberg et al.1 mg/L (Alfven et al. In the typical environmental exposure. Mannino et al.. and drinking water and environmental standards have been established by U...atsdr. 2004b). urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney..S. 2005. intermediate in former smokers and lower in never-smokers (Becker et al. Salpietro et al. 2003.. 2002. Cadmium can produce lung. Becker et al. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. 2006.gov/ toxpro2. 2002).. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. 1999). as may occur from welding cadmium-alloyed metals. 1996). 2003). Noonan et al.. For NHANES 19992000. Ezaki et al.... 2006. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC.. 2005). Komaromy-Hiller et al. 2002). Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. 2004. respectively. 2004... 2002). Becker et al. 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. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. 2000. Olsson et al. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population.. Olsson et al..Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. CDC.. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH.46 mg/gram of creatinine) (Ezaki et al. Acute and heavy exposure to airborne dusts and fumes. 1999. Both IARC and NTP consider cadmium a human carcinogen. Creatinine-corrected urine cadmium values in U. However. 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..... Horiguchi et al.. Becker et al..26 and 3. data (CDC. Blood and urine cadmium levels are typically higher 202 in cigarette smokers.. 2004).. Animal studies have demonstrated reproductive and teratogenic effects.... Suwazono et al. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. environmental levels) and health effects is available from ATSDR at: http://www. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. Information about external exposure (i...

Buchet JP. Elinder CG.cdc. Seiwert M. patient population and literature reference intervals for urinary trace elements. et al. Vahter M. 206:15-24. Fourth National Report on Human Exposure to Environmental Chemicals 203 . et al.1(8587):663-667. diabetes mellitus. Horiguchi H.46:372-374. Thorax 2004.110:699-702. Alfven T. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Occup Med 1996. Miyamoto K.S. Comparison of representative ranges based on U. Palomar M. Darbyshire J. Bo M. Costa R. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria.76:186-196. Machida M. Environ Res 2006. Toffoletto F. Nermell B. Environ Health Perspect 2005. Agency for Toxic Substances and Disease Registry (ATSDR). 196:114-123. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers.296(1-2):71-90. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Lepom P. Hellstrom L. Consonni D. Ikeda Y. Nerbrand C. Sasaki S. Savage-Brown A. Ikeda Y. Okamoto S. Toxicol Lett 2004. Tsukahara T. Zhu G. Nordberg G.atsdr. Mascagni P. Ukai H. Int Arch Occup Environ Health 2003. Uemura T. Ye T. Environ Health Perspect 1994. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Oguma E. Ezaki T.html.57:668-672. Fernandez MA. Seifert B. Lancet 1988. Environ Res 2004b. Furuki K. Lukyanova EM.205:297-308. Chislovska NV. Moriguchi J. Anthropometric. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. et al. Machida M. Venables KM. ShkiryakNizhnyk AZ.148(1-2):11-20. et al. Carlsson MD. Miyamoto K. Sanz P. Lison D. 1999 [online]. Becker K. Friedman LS. Dekio F. Bernard A. Fatal chemical pneumonitis due to cadmium fumes. Tsukahara T. possibly better than b2microglobulin. Sasaki S. Becker K. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Holguin F. Serra J. Takebayashi T. Kundiev YT. Environ Health Perspect 2002. Gadea E. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Choudhury H. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Occup Environ Med 2000. Seiwert M. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Fukui Y.96:353-359. Nomiyama T. Oguma E. 4/8/09 Alfven T. Kumagai N. Kaus S. Vahter M. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Mucha A. Kaus S. Centers for Disease Control and Prevention (CDC). Greves HM. Olfactory function in workers exposed to moderate airborne cadmium levels. Lauwerys R. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers.S. Jarup L. Ezaki T. Howerton K. References Akesson A. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Jones RL. 2005. et al.59:497]. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Davison AG. Taylor AJ. Schulz C. Krause C. Atlanta (GA). Stock AL. Jin T. iron deficiency. Bregante G. Bellerup P. Komaromy-Hiller G.13(11):1627-1631. Third National Report on Human Exposure to Environmental Chemicals. Neurotoxicology 2003. Chiappino G. Comprehensive study of the effects of age. Fayers PM. 102:10581066. Lidfeldt J.354:1508– 1513.000 women in the Japanese general population: a nationwide large-scale survey. et al. Toxicological profile for cadmium update. et al. J Occup Health 2003. Schulz C. Fukui Y. Akesson A. Int J Hyg Environ Health 2002. Clin Chim Acta 2000. et al. Jarup L. Toxicol Appl Pharmacol 2004a. et al. Lundh T.59:194-8. J Toxicol Environ Health 2003.Metals with reference values so they can determine whether people have been exposed to higher levels of cadmium than are found in the general population.gov/toxprofiles/tp5. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Horiguchi H.24:717-724. Wang H. population. Mannino DM. environmental. Available at URL: http://www.66(Pt A):2141-2164. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Ash KO. Moriguchi J. Furuki K. Berglund M. Thayer WC.95:20–31. et al. Diamond GL. Grubb A. Environ Res 2004. Hotz P. Cadmium fume inhalation and emphysema. Lancet 1999. Persson B.45:43-52. Pickering CA. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Int J Hyg Environ Health 2003. Kikuchi Y.102:83-89. et al.

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59-5.38) 5.72-7.64) 4.00) 7.6) 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 4.09) 5.4 (9.70) 5.3 (8.49 (4.34 (4. For absorbed cesium salts.50-7.05) 5.22 (4.9) 8.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.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 4.43-8.2-12.8 (10.90 (6.05) 5.0) 10.81 (4.1) 9.3) 10.49) 75th 7.7 (10.0) 11.34) 9.62 (5.40) 7.30) 5.5 (10.8) 11.40-5.88 (8.40-5.8) 11.7 (10. see Data Analysis section) for Survey years 99-00.92-13.0 (9.35 (4.70 (5.03 (4.00) 6.23) 9.1) 10.6) 10.23-4.17-6.9) Total 4.40-11.90-12. and clay.20-8.10 (8.12) 5.60) 5. Little is known about the health effects of this metal. although cesium was generally of low toxicity when given to animals.6 (11.33 (5.25 (3.71-8.84) 5.80-10.0-15.81) 4.55 (7.8) 12.01) 7.87 (4.2 (9.3-15.63-4.9 (11.70) 7.14.24) 4.40-7. Radioactive 137Cs has been used medically to treat cancer.50 (7.05-5.77 (4.86 (7.70 (8.79 (4.50 (4.27 (7.8-13.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4.9 (11.2-13.8) 12.16-6.00-8.05-5.07) 4.99-11.15-8.37) 5.80-11.40) 5.07-11.66 (7.4) 10.14 (4.30-5.40-5.00 (7.5-14.1-12.37) 7.81) 4.99) 7.70 (8.5-13.4 (10. infrared lamps.83-4.42-7.94 (4.20-7. the body half-life is estimated to be 70-109 days based on 137Cs exposures.12 (4.63) 6.29 (4.61) 7.13 (8.35-5. However.70 (6.02 (4.9 (10.80 (8.53 (6.90) 4.64) 5. nausea.3) 12.84) 8. and as polymerization catalysts.80 (4.10-5.03 (4.55 (4.4 (9.32 (3.50 (4.64-10.32-5.98 (7. 2004).0) 12.4) 10.60-12.70) 5.2 (9.7) 11.00-4.10-9. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.54-11.5) 9.0) 12.71-9.1) 11. interval) 4.70 (4.80 (4.3) 10.1) 9. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.20 (6.13 (7.20) 7.64 (4. cesium hydroxide is corrosive and irritating at high concentrations.2-13.36 (3.70-8.9) 11.97 (7.00-10.87) 5.86-12.60-7.61-6.31-8. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.42) 6.1 (11.59-5.67 (4.49) 4.10-8.04 (4.7 (10. Most human exposure to cesium occurs through the diet.89) 4.3) 10.90-12. respectively.77-8.60-5.7 (9.33-5. semiconductors.70 (9.7) 11.5) 12.0 (10.1-13.8) 9.57-5.3-13.2) 12.4) 95th 11.08-5.44 (8. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.60-6.40-11.1-12.30) 7.5-16.47-8.70-5.80) 7.20) 5.73-5.45-5.90-8.69-6.81) 9.45-8.4) 9.56 (4.84 (4.93 (4. diarrhea. 01-02.7 (9.7 (9.12-5.22-4.56) 5.59 (5.40 (4.90-10.71) 4.21) 90th 9.35 (4.8) 12.68) 9.25-5.17) 4.3) 10.63 (4.20-5.09-5.6 (9.2-14.56-11. and high-power gas-ion devices.16-6.77 (9.83) 6.76-6.32) 4.01-8.96 (6.60) 7. soil.52-9. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.1 (9.73-11.7 (8.7-14.36 (6.2.26 (3.80 (4.50) 9.14.39-4.Metals Cesium CAS No.04) 7.81-14.97-7.00) 4.9) 12.95) 5.4) 12.20-4.90-10.60 (7.25) 4.62 (5.6 (11.26) 7.2) 11. and cardiac arrhythmia (ATSDR.7 (11.71 (8.60) 7.8 (11.64-5.94 (4.08-5.4-13.84-5.74) Selected percentiles ( 95% confidence interval) 50th 4. and 03-04 are 0.80-13.59-5.71-5.50 (6.2-13.30-10. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.60-7.0) 12.00-8.7) 10.6 (9.36) 3.90 (4.68 (7.91-8.08 (6.12-11. scintillation counters. Whether cesium compounds are carcinogenic is unknown.90) 5.87 (4.91 (7.6 (9.7) 10.53-11.27) 4.43 (5.94-4.08) 7.3 (8.3) 9.9 (11.90) 7.56 (4.5-14.5) 10.40) 5.4) 11. photographic emulsions.80-10.80 (8.1) 11.21 (4.6 (9.99-6.8) 9.10-7.82-4.98 (7.80 (8.70 (6.00-9.60-6. and 0.77 (9.47-4.29) 4.82) 5.30 (6.01-6.08 (7.90) 9.89-5.6) 11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.99-11.26-11.13 (5.52) 7.4) 12.8 (10. Fourth National Report on Human Exposure to Environmental Chemicals 205 .60 (8.86-11.10 (6.0) 9.S.9 (11.72) 4.55-11.90) 5.50) 5.17 (6.74 (4.95 (3.26) 4.87 (4.84-9.62) 4.97) 4.50 (4.3-13.71 (4.80-6.74-5.46) 7.95-4.10 (6.49 (5.20 (4.54) 4.80-10.94) 4.5 (8.27-5.39) 7.90-10.0) 11.99) 9.1 (10.03-4.87-7.0-13.33 (6.20) 4. population from the National Health and Nutrition Examination Survey.40-5.13-8.42) 7.10 (8.30 (6. 0.89) 5.64) 5.59) 7.9 (10.20) 8.

50) 4.26 (4. 2005.S.53 (4.71) 6.43) 8.0) 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 .5) 7.44) 3.29-3. population results shown in this Report (Alimonti et al.96) 4.15) 95th 8.61-3.65-4.99-9.50 (7.79) 9.31-6.9 (9.3) 11.38-12.14) 4.66 (6.56-10.20-4.19-3.40) 6.00-5.41) 9.8) 10.65-3.56) 4.50-5.08) 4.20) 5.98) 5.91-9.10 (5.44-5.18-6.94 (5.04) 5.59-8.36-6.28 (5.08 (6.86 (4.78 (3.35 (3.73-4.04-11.06) 4.56) 3.09) 8.87) 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 5.95-12.20-8.38) 10.45-6.16) 5.31 (4.28) 8.87) 5.30 (3.00-5.3) 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 3.77 (4.3-15.98) 5.55) 4.47 (4.15-11. Using clinically submitted specimens.17-4.30-4.20-4.67 (6.85-4.82) 7.50 (5.12) 3.47) 6.05-4.22-11.20-4.33-3.56 (4.15-4.99) 4.41-7.11 (5.47 (7.55 (3.50) 8.06 (5.03-6.54 (4.47) 4.7) 10.58-5.60-10.96-4.83-6.64-6. interval) 4.03-5.02 (5.43-11.00) 6.05) 6.S.8 (9.65 (6.79-5..13 (3.83) 8.0) 7.64) 4.78) 4.33 (5.7-12.90 (7.60) 3.30) 10.58) 8.48) 90th 7.14 (6.64) 9. and were also roughly similar to those in this Report.30-4.47) 7.31 (4.56) 4.42 (4.2 (8.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.51) 4.63 (7.2 (8.48-6.43 (8.72-5.06) 5.41 (8.55-5.39) 8.78 (3.13) 7.75 (7.68-11.58) 3.59) 4.58 (4.08 (3.67) 5.34 (5.95-6.46) 6.9 (10.24-4.70 (7.60 (3.58 (6.41 (4.90-3.14) 4.91 (5.46 (7.00-4.93-9.92 (5.95) 10.77 (6.09 (4.14-7.40) 7.18-7.66 (5.5 (9.10) 7..41 (5.17) 9.88-10.24 (3.10 (3.63 (4. Biomonitoring studies on levels of cesium can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cesium than are found in the general population.51 (3.45 (4.05) 3.3 (10.07) 8.29) 5.71 (7.84-9.37-3. Komaromy-Hiller et al.11 (5.38 (3.21-4.6 (9.95) 4.09) 4.50 (6.00-9.51 (3.51 (7.6) 6.74 (4.44 (8.64 (4.3 (8.42-4.05 (4.23 (7.79 (5.21 (2.29) 4. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.28) 7.76-6.98 (6.33 (5.80) 6.07-4.52-5.77) 4.47) 6.07 (5. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.51 (4.08-3.43-6.27 (6.96-4.70) 6.25) 4.02-4.10-4.72 (4.46 (8.26 (3.18 (7.18) 8. population.90-8.54 (4.26-6.8) 5.95 (5.87-4.84-7.43 (4.54 (3.98 (7.67 (5.15 (7.14-4.35) 3.22) 6.50) 4.3) 9.95) 8.44-9.16-5.38 (3.00-8.30 (4. Minoia et al.91) 4.43 (3.41) 4.84-7.88-4.21-3.37) 4. population from the National Health and Nutrition Examination Survey.03) 6.27 (8.31-4.17) 4.2) 11.3 (9.30) 10.27-6.63-6.99-9.1) 11.44 (4.66 (5.0 (7.53) 6.63-6.64) 5.63 (6.75-11.53) 3.53 (6.07) 8.2) 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 3.35-11.75 (6.64 (8.49) 3.01-8.27) 4. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.74 (5.91-7.91) 5.48) 7.78) 4.25) Selected percentiles ( 95% confidence interval) 50th 4.40-5.9) 10.93-7.68) 3.74) 75th 5.S.08-7.79) 6.00 (8.8) 6.84-11. (2000) found urinary cesium levels that were slightly lower than those reported for the U.24-10. Two small studies of European populations reported urinary cesium levels similar to U.19-6.06 (3.66-6.16-8.50) 4.92) 3.17 (6.43 (4.7) 10.79) 4.46-8.96) 4.5) 9.0) Total 4.29-3.91) 5.63) 6.91 (5.39 (5.29) 4.21-5.27 (6.97-4.36-10.16-8.14-6.68) 4.42-4.35-7.10 (3.83-7.27-4.41-4.6 (9..61 (7.05-3.28 (4.90-8.60 (5.68) 6.96 (4.99-4.42 (5.87 (5.42-6.85) 5.72) 4.12 (3.89-4.57) 3.05-3.81 (4.35 (4.08) 3.74-11.60-20.08 (5.03) 5.73 (3. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.62-8.99 (3.97-5.77 (7.68 (4.00-10.04-5.13-9.4) 10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.77-5.46-4.85) 4.62) 5.38-7.51 (4.12-6.30 (7.39) 5.95 (3.97) 8.5) 9.33-8.36-3.76-9. 1990).94) 7. 2004).54 (5.74) 3.13-9.84-9.22 (3.70) 7.08) 4.04) 6.91-6.82-4.81 (4.

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

12) 1.330-.900-1.369 (.502) .26-2.371 (.33 (1.450) .390 (.523) .650 (.21) 1.32 (1.530 (.340 (.380 (.327-.308-.270-.420 (.540-.460-. diamond-polishing wheels.469-.840) .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 .450-. and kitchenware.750 (.394) .310 (.390 (.940-1.630 (.01 (.540-.290-.550 (.316-.431) .379 (.47 (1.313) . hard metal (alloys of cobalt and tungsten carbide).05 (.540) 1.05 (.367 (.410) .630-.340) .420) .680 (.01 (.25-1.32) 1.620-.790) .770) .520-.487) .01-2.75 (1.530) .50 (1.418 (.890) 95th 1.583) .338-. interval) .16-1.410-.520) .45 (1.900-1.580 (.330 (. The cobalt used in U.333-.350-.388-.580 (.47) 1.301 (.48) 1.15-1.08) . and inks.333-.620-.640) .47 (1.285 (.16 (1.03) .17 (1.640) .480 (.373-. and soil.26) Total .28 (1.410 (.670-.570-.06-1.398) . and in synthesizing polyester and other materials.660) .900) .430 (.405-.343 (.330) .460) .680) .710) .452 (.419) Selected percentiles ( 95% confidence interval) 50th .600) .24 (.410 (.339 (.490-.900) .740-. It is also a component of porcelain enamel applied to steel bathroom fixtures.890-1.07-1.28-2.430) .470 (.515 (.364-.640) .28 (1.60 (1.420) .64) 1.373) .520-.499 (.17 (1.496) .09 (.29 (1.670-.32) 1.294 (.520 (.20 (1.375 (.32-2.870 (.510) 1.543) . steel-belted radial tires.435 (.760) .23-2.680 (.320 (.300 (.710 (.16 (.06 (.550-.370-.81) 1.830-1.564) .319) .14) .52 (1.259-.390) .310-.360-.581) .09) .461 (.360-.550) 90th .880 (.540-.410 (.590) .07 (.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.47) 1. 208 Fourth National Report on Human Exposure to Environmental Chemicals .08.65) 1.850) . Cobalt compounds are used as catalysts in producing oil and gas.380 (.372) .850-1.13) 1. respectively.390 (.03-1.02-1.398 (.480-.50) 1.380-.16-1.340-.590 (.610 (.454 (.520 (.920-1.560 (.440-.33-1.07.39) 1.410 (.410-.280-.28 (1.434 (.690-.430-.620) .820 (. and fertilizers.37-1.950 (.670 (.750 (.22) 1.660) . Usual human exposure is from food sources.17 (.540-.350-.01-1. Cobalt compounds are also used in manufacturing battery electrodes.04) 1.370 (.580 (.270-.59 (1.36) 1.340) .950) .430 (.740 (.352 (.850) 1.26) 1.800) . Cobalt is used as a drying agent in paints.370-.750-.430 (.940 (.500) .890-1.500 (.16) 1.910-1.428-.404) .650 (.09 (. varnishes. and magnetic recording media.67) 1.790-.379 (.463-.870 (.340-.68 (1.410-.05) 1.410 (.336-.610) .03) 1.520 (.950-1.360-.470) . blue-colored pigments.424) .460) .460 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.46 (1.81) 1.417) .44) 1.56) 1.S.890) . 0. see Data Analysis section) for Survey years 99-00.16) 1.680) .350-.04 (.760 (.17-1.650-.06 (. shiny.305-.399) .350 (.630 (.670 (.690-.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 .920) 1.520-.19) .850-1.316 (.930 (.416) .730) 1.570-.700) .48) 1.460 (.73) 1. It is emitted into the environment from burning coal and oil and car and truck exhaust.374 (.427-.750 (.377-. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.15 (1.520) . 01-02.980-1.465) .23) . Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.670 (.860 (.359 (.790 (.04-1.519 (.04-1. population from the National Health and Nutrition Examination Survey.810) .450) .16 (1.22 (1.610) .900) .410) .570) . automobile airbags.431) .380-.348-.42) 1.820 (.334) .590-.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 .590-.370-. and 0.820 (.22-1. 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.07-1.690 (.610-.810-.800-.570) .490-.450) .430) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.710) 1.03 (.950-1.600-.870-1.07.450-.386) .370) .99) 1.S.460) .348-.00) . hard metal or in combination with other elements.393-. industry is imported or obtained by recycling scrap metal that contains cobalt. large appliances.530-.660-.53) 1.890-1.300-.350) 75th .03 (.12) 1.800-. seawater.570 (.32 (1.520 (.331-.930) .24 (1.940-1.620-.960-1.740-.450) .980) .08-1. Cobalt occurs naturally in airborne dust.930-1.600 (.400-.92) 1.03) 1.380 (.950 (.26-1.520-.414) .270-.14-1.291-.880-1.355-.810) .Metals Cobalt CAS No.390-. and 03-04 are 0.04-1.480 (.700) .

457-.425) .279) .337) .781-1.461) .329-.829) .500-.215-.293 (.257 (.239-.468) .844 (.487-.421) .12 (.50) 1.842) .438) .990-1. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.402 (.700 (.500-.396) .487-.06 (.247 (.700 (.384) .29) 1.937 (.298 (.286) .929) .310) .11-1.975 (.369 (.388 (.911-1.824 (. in the feces.562) . cobalt is excreted predominantly in the urine.740-1.313-.281) .280-.386 (.500 (.349) .362-.952 (.353-.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 .756 (.328 (.429) 1.259) .444 (. 1994. Exposure in the workplace may come from electroplating.376 (.24) .495 (.271 (.Metals fabricated from cobalt alloys (Lhotka et al.667-1.595) .976 (.363) .346 (.316 (.851 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.29 (1.319-.279 (.600-.259-.462) .387) .857-1.33) .606 (.55) .393 (.534 (.515 (.638-1.550-.306 (.561) .960 (.10 (.662) .14 (.529 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.792-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.598 (.29 (1.344-.09) 1.785) .537 (.554 (.689 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.737 (.335 (.479) .339-.964 (.337 (.290 (.23 (1.428-.388 (.362 (.333-.00 (. A portion of cobalt retained for long periods is concentrated in the liver.861 (.392 (.679-.17) .408 (.248-.365-.804) 1.829-1.417 (.505) .938-1.333 (.409) .361-.290 (.16) .10) .850-1.278-.328 (.435-.274-.348) .329 (.452-.750-.872 (.00 (.503-.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 .562) .290 (.630-.644 (.313-. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.361 (.331-.268 (.327 (.294-.313 (.15 (.365) .895-1.28) 1. using hard metal cutting tools.593) .273 (.608 (.826-1.582-.25 (.753-.368) .27) 1.469-. Smith et al.19) .393-.426 (.50 (1.11-1. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.547 (.16 (.296-. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.324-.439) . Once absorbed and distributed in the body.02 (.33) 1.342-.534-.278 (.616-.457 (.792 (.630-.895-1.296) . Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).352 (.750) .574-.660-.04-1.306) 75th .694) .259 (.786-.753) 1.635 (.250) ..03-1.955) .378 (.455 (.36) 1.949) .669) .433) .513 (.272-.361-.60) 1.334) .234 (.691 (..419) .917) ..275-.44 (.50) 1.00) .736-.391 (.634-.522) .355) .523 (.382-.963-1.850 (.353 (.983-1.963) .381) .313-.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 . respectively.15) 1. 2003).404-. 1994).449) .333-.905) .301-.289) .727 (.683-.256-.523 (.554 (.543) .323) .282 (.434-.313-.435 (.60) 1.848 (.585) . population from the National Health and Nutrition Examination Survey.611) .391) Selected percentiles ( 95% confidence interval) 50th .333-.581) . an essential human nutrient.314 (.632-.703-.938) .16 (1.733-1.774 (.277-.243-.963-1. refining or processing alloys.352) .442-.898 (.838 (.760-1.560-.471-.04 (.707) .488) .425-.248-.417) .879-1. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.708) .10-1.542 (.407) .563-.25 (.297-.304) .667-1.471-.626-.380-.343-.03 (.599) .291 (.83) 1.821 (.932-1.343 (.647) .73) 1..738 (.821-3.S.35) 1.300) .303-. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.378-. 1972).237-.309) .463-.327-.368 (.29) .830 (.457) .407 (.673-.378-.594) .728 (.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 . Cobalt is absorbed by oral and pulmonary routes.352 (.00 (.361 (.257-.744) 1.372) .757-1.16 (.36) 1. 1972).533 (.833-1.30 (1.326-.00 (. or using diamond-polishing wheels that contain cobalt metal.591 (.57) 1.27) 1.317 (.29 (1.282-.360) .777-. interval) .900-1..396) .297) .983) .400 (.513) .861-1.781) 95th 1.955) .481) 90th .449-.49) 1.362) .738 (.35) .990) .640) .475 (. and to a lesser extent.476-.963) .324) ..467-.378-.611) .508-.301) .358 (.304-. 1979).313-.00-1.704-.615) .847) .328) .275-.302-.609) .723 (.471 (.12-1.54) 1.00) .548 (.513-.368) .552 (.479-.394) .728) .10) Total .251-.

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

Goto S. Thabe H.406:282-296. Contact Dermatitis 2003. Oksa P. Sci Total Environ 1997. Bacis M. HoffmannB. Salvatori S. A report of two cases from mineral assay laboratories and a review of the literature.87(5):628-631.55(4):269-276. Sci Total Environ 1994. Schaller KH.51(7):447450. Science 1988. Lasfargues G. Dunning SP.157:117121. Co-sensitivity between cobalt and other transition metals. J Bone Joint Surg Br 2006. Kraus T. Unwin P. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. J Occup Med 1992. J Rheumatol 2001. Thomassen H. Carnes WH. 1985. Kato M. Dickel H. Szekeres T. Lison D.36:732-734.150(1-3):167-171. Goto S.45:246-247. Absorption and retention of cobalt in man by whole-body counting. McMinn DJ.34:620-626. Goldberg MA. et al. Br J Ind Med 1993.150. Swennen B.(1-3):133-139. et al. Dunstan E. Blunn G. et al. and hard metal dust. Cannon SR.69(3):193-200. Shirakawa T. MacDonald SJ. J Orthop Res 2003. Lhotka C. Roto P.88(4):443448. Iversen BS.148:241-248. Peltier A.20(1):25-31. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Tilley S. Chest 1989. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Edmonds CJ. Am J Ind Med 2003. Cleland D. Romazini S. Linnainmaa M. Arch Intern Med 1990. Leghissa P. The release of metals from metal-onmetal surface arthroplasty of the hip. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Pisati G. oxides. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Gross RT. et al. Hammon E. Diepgen TL. 3rd ed. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Lauwerys RB. Occup Environ Med 2001. Sabbioni E. Weyher I. Schank M.48:172-173. Sabbioni E. Uitti J. McCalden RW. Swennen B. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Respiratory health of cobalt production workers. Moulin JJ. Palmroos P. Mosconi G. Hedge AG. Health Phys 1972.21(2):189-195. salt. Boca Raton (FL): Lewis Publishers.150:177-183.Metals effects of cobalt. Jarvis JQ. Int Arch Occup Environ Health 1997. Wild P. Pradhan C. Falcone G.58(10):631-634. Long-term clearance of inhaled 60Co. Kriss JP. Linna A. Robinson C. Cresti R. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Lauwerys R. Schramel P. Occup Environ Med 1994. X. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Alessandrelli M. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Hoher T. Sci Total Environ 1994. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Kristiansen J. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis.” Contact Dermatitis 2001. Epidemiological survey of workers exposed to cobalt oxides. Laippala P. White MA. Zweymuller K. J Trace Elem Med Biol 2006. Sanghrajka AP. et al. Buchet JP. De Boeck M. Zobelein P. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Angerer J.44:124-132. Christensen JM. Cobalt and antimony: genotoxicity and carcinogenicity. Ghat IS. cobalt salts. Heki S. et al. Lison D. Ichikawa Y. Trace element reference values in tissues from inhabitants of the European Union. Outcome of occupational asthma due to cobalt hypersensitivity. Kiilunen M.50(9):835-842.533:135-152. Zhuber K.95:29-37. Bunn HF. Daniel J. Sci Total Environ 1998. DeSantis V. Kuska Y. Clin Orthop Relat Res 2003. Salama A. 2001. Radulescu M. Int Arch Occup Environ Health. Chess DG. Health Phys 1979. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Steffan I. Zedda S. Bozec C. Molders J. Weber A. Occupationallyinduced “isolated cobalt sensitization. Kirsch-Volders M.28(5):1121-1128. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Iavicoli I. a study of 13 elements in blood and urine of a United Kingdom population. Thakker DM. Meyer zum Buschenfelde K-H. Lauwerys R. Cobalt cardiomyopathy. and cobalt metals. Rorabeck CH. Hoet P.22:359367. Lison D. Sabbioni E. Lisi P. Vitali MT. Bourne RB. Fujimura N. Buchet JP. Meier R. Biological monitoring of workers exposed to cobalt metal. Smith T. Stanescu D. Mutat Res 2003. J Bone Joint Surg Br 2005. Kusaka Y. Barnaby CF. Lung cancer risk in hard-metal workers.242:1412-1415. Ziaee H. Am J Epidemiol 1998.216:253-270.204:147-160.

80) 3.70-1.10) 2.50 (3.00) 2.60 (2.40) 4.60) 4.986) .10 (1.70-6.46 (1.10-6.70) 3.00-5.00-4.40-1.50-1.20-2.80-4.3.60) 2. lead was added to gasoline and residential paints and used in soldering the seams of food cans.90 (3.20-3.60) 4.00) 4.S.20 (1.60-1.00) 2.50) 7.00) 2.20-1.70-5.50) 1.43-1.900-1. antique-molded or cast ornaments.50-3.30-1.50-4.30-4.25) 1.50-3.50-1.91) 1.30) 1.40 (1.70-1.56 (1.90-2.899-.51) 1.60 (2. ceramic glazes.40) 2.30-1. Since lead has been eliminated from gasoline.10-6.69) 1.36-1.20-3.80 (4.10-3.96-2.00 (1.90) 2.43) 1.80) 1.80) 1.00) 3.70 (2.00) 3.45-1.80 (1.90 (3.43) 1.17) .20 (1.60 (1.37 (1.40-3.30-2.20) 90th 3.80 (2.50 (4.60) 4.40 (1.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.90) 2.40-3.60 (1.20 (2.10) 3.00) 1.20 (3.45 (1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.40) 1.70-2.90 (1.30) 5.20) 3.80) 1.20) 5.90 (4.S.50-6.72) Selected percentiles ( 95% confidence interval) 50th 1.00) 2.25 (1.20 (1. plastics.30 (3.50-1.Metals Lead CAS No.50 (1.30-2.81) 1.10 (2.10) 5.10-4. In the past.60 (1.30 (2.40-4.90-2.75) 1.60 (3.10-3.02) 1.10 (4.00 (2.20-3.50) 5.50-2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.77 (1.30-5.90 (2.00 (6.800-1.80) 2. 212 Fourth National Report on Human Exposure to Environmental Chemicals .60 (1.30 (2.60) 3.90 (3.37-1.90-2.20) 4. blue-gray metal that occurs naturally in soils and rocks.70) 4.55-1.60-1.80 (1.40) 2.40 (4.946 (.69 (1.60-3.20) 3.00-6.66) 1.20) 1.70) 1.87 (1.40-6.10-2.70) 2.50-2.50) 75th 2.80 (1.80 (2.10 (2.10) 4.80 (5.80) 2.90-4.12-1.80 (1.48) 1.00) 1.31) 1.40-2. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.50-4.50) 4.60 (3. ammunition.10-1.10 (1.90) 3.30 (1.62 (1.60) 2.60 (1.78 (1.20 (3.30) 95th 5.90) 1.50 (1. bronze).66 (1.04-1.20 (3.30 (2.10) 1. Elemental lead can be combined with other elements to form inorganic and organic compounds.90) 2.50) 2.00) 4.90-6. Lead was used in plumbing for centuries and may still be present.40-6.30 (2.00 (3.55 (1. solders. Lead has a variety of uses in manufacturing: storage batteries.70-2.80-3. 01-02.20) 3.70) 3.20 (3.50 (1.60 (2.69 (1.80 (5.70 (2.3.93-2.83 (1.00-2.14-1.10-2.70 (5.10-1.10) 1.50-2.90-2.80 (2.40-5.80 (4.50) 3.90) 2.50-1. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.60) 1.60 (1.10 (2.49-1.70) 1. brass.70 (3.75-2.60) 3.20-3.90) 1.43 (1.40-1.43 (1. population from the National Health and Nutrition Examination Survey. interval) 1.39-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80-4.60) 2. see Data Analysis section) for Survey years 99-00.90 (2.90-4.30-1.40 (1.40 (2.80) 2.10) 2.90) 5. 7439-92-1 General Information Elemental lead is a soft. leaded glass.50 (2.30-2.30 (4.40-2.52-1.68-1.80) 2.00-1.70) 1.50 (2.70 (1.60 (2.75-1.70-4.30-1.10-3. and for radiation shielding.40) 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 2.30-1.60-2.00) 1.60 (2.00) 6.55-1.50 (2.60) 5.00) 5.50-1.40-1.10-1.62) 1.80-2. 0.30 (1.20) 2.40) 2.878-1.40-1.40 (3.80 (1.50-5.60) 1.20 (4.90) 1.70) 4.942 (.19 (1.80) 1.40 (1.22 (1.00-4.30 (2.90) 2.50) 4.30 (2.60-1.10-2.40-1.70) 1.60) 2.60-1.10-3.60) 1.10 (1.30) 2.60) 1.50) 5.50) 1.10-8.39) 1.89) 1.80-4. such as lead phosphate and tetraethyl lead.00 (4.70 (1.90 (3.80-5.80-3. metal alloys (e.30 (1.20 (3.60) 3.20-1.20-4.70 (3.09) 1.70) 4.90-4.00 (1.70 (1.60) 2.50 (4.34-1.40) 1.20 (1.g.60-4.30-6.70 (2.50 (2.60) 3.70) 4.20) .60 (3.70-3.60) 1.10) 3.50-2.60) 5.00-4.40-2.30 (4.10-2.60 (4.14-1.65 (1.40-1. and 03-04 are 0.80-3.30-1.28.20 (3.20-2. and 0.10) 1.80 (1.90-4.20) 4.36-1.50) 1. Lead is most often mined from ores or recycled from scrap metal or batteries.40) 3.10-2.70-1.30) 2.90 (1.10-2.90) 3.14-1.60-4. dense.87) 1.50 (3.30 (1.10) 3.71-1.20-6.01 (1.25 (1. respectively.80) 1.60 (2.60-2.20 (3.95) 1.00) 1.80 (3.900 (.50) 2. Before the 1980’s.10 (3.30 (2.30 (4.60 (1.60 (3.50 (1.40) 1.00) 1.30-2. malleable.50) 1.90 (3.51 (1.30) 2.37 (1.90-3.36) 1.50 (2.900 (.40) Total 1.70) 3.00) .86) 1.80-3.10-4.52-1.00 (5.80) 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 1.53) 1.32-1.20 (2.20 (1.40 (2.40 (5.70) 1.40) 5.00-1.00 (4.75 (1.32-1.70 (1.60) 4.69) 1.23 (1.20) 3.52 (1.60-6.50-5.62-1. the main source of lead exposure for the general U.70-2.40-3.

respectively.40-1.24-1.600-.59-2.50) 1.688 (..06) .90) 2.800-1.641-.40) 2.628) 1.661-.752 (.570-.33.70) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10 (1.900 (.800-1.30) 1.900-1.40 (1.11) 2.14 (1.86) 95th 2.40 (2.757-.710-1. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.20-1.90 (1.33-2.04-2.674) 1.579-.30-5.10 (.00) 2.749) .1.22) 1. stained glass framing.10) .591 (.50) 2.10-1.60-3.700 (.990) 2.625 (. 01-02.10-3.86-2.40-2.13-3.850 (.700 (.70 (2.40) 1.19 (1. or water contaminated by mining or smelting operations.82 (2.753 (.31-3.80 (1.17 (1.600 (.32 (1.30 (3.642 (. bullet fragments retained in human tissue. Approximately half of the absorbed lead may be incorporated into bone.862) .60 (1.941) .700-1.700 (.10-1.605) .729-.560-.90 (1.70-3.30) 1.40 (1.40 (1.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.50 (2.90-2. CDC.730 (. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.828) Selected percentiles ( 95% confidence interval) 50th .80-3.62-4.02 (.20-1.910-. older plumbing systems with leaded pipes or lead soldered connections.00-1.604 (.651) .701) .72) 1.00-2.27) 1.00 (.40) 2.900) .12) 90th 2.990) 1.900 (.78-2.70 (2.10) 2.590 (.20 (3.66 (2.600) . 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.595-.70 (2. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.600-.30-3.50 (2.10-3.30-1.659 (.10-5.49 (1.700-.677 (.718) .800 (. lead-based painted surfaces undergoing renovation or demolition.710-.691-.00-2. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.700-.506-.73 (1.815 (.13) .90-2.960-1. imported children’s trinkets and toys.708-.80 (1.66 (2.790 (.900-1. pewter utensils and drinking vessels.10-1.700) .30) 1.785) .800-.60-2.857) .50) 2.840 (. 2000). battery and radiator manufacturing) and recreational sources.78-2.900-1.30-2.50-3.795 (.700 (.90-4.90-2.62) Total .90 (2.900) .70 (1.00) .86 (1.30) 1.935) 1.70) 2.80) 2.20 (2.650) 1.60 (2.60-1.20) 1.23) . Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead. However. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.700 (.80) 2.90 (2.00-2.600 (.808 (.10 (. population from the National Health and Nutrition Examination Survey.52-1. 2007. and contact with soil.21 (2.04) 2.64) 2.03-2.30-1. In the blood.70) 3.700-.35 (.30) 1.50) 1.923 (.540 (.00) .g.640 (.20 (1.600) .10-1.20) .900) .40-1.90-3.766 (. 0.50) 3.970-1.810-1.800 (.20) 1.50-2.30) 2.818) .90 (2.18-1.773) . or after soluble lead compounds are ingested.Metals occupational (e.960-1.00 (1.40 (1.833 (.800) .80) 2.986) .11 (1.636 (.20 (2.59) 1.40) 1.20) .97) 4.900) .86) 1.20 (1.690) 75th 1.80-2.30-1.80) 2.630 (. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.572-.900-1.700) 1.556-.20-2.700-.20 (1.848 (.00 (1.31 (1.900) .80-2.S.526-.573 (.00 (2.40-5.731 (.70-2.00) . lead-containing folk remedies and cosmetics.50) 1.50-2.30 (1.00 (1.80) 3.00-1.89) 2.40) 1.955-1.738) .10 (.40) 1.60-2.00 (1.900 (.800-.40) 2.40) 2.04) .50 (1.90) 2.33 (2.14 (1.90) 2.40 (2.680-.800) .75) 3.80) 2.40) 1.60) 2.610 (. interval) . Fourth National Report on Human Exposure to Environmental Chemicals 213 .820-1.20) .20 (1. 1991).29) 2.1. dust.480-.30-1.30 (2.580-.00) 1.20 (2.82 (1.553-.671-.40-1.540-.680) .613) .00-1.40 (2.80) 3.70) 1.75) 4.07-1.10-3.620) 1.625-.931) .40-1.10-1.660) . lead-contaminated dust in indoor firing ranges.60 (1.00) 2.70) 1.20-2.41) 2.800 (.40) 3.80) 1.50-2.564 (.940 (.822-1.10 (1.800) .500-.27 (1.10 (1.600-.03 (1.20 (1.680-.745-..52-1.20 (1.14-1.558 (.44-2.90-3.23-4.616) .20) .10) 1.10) 2.50 (1.10 (1.90 (1.600-.833-1.20) 1.900) .30) 2.60-3.30) 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 1.637-.80) 1.07 (.920 (.90-2.78-2.29 (2.90) 1.30) 2.70 (2.52 (1.620 (.04 (.09) 1.40 (2.40 (1.700-.579-.640-.600-.80 (2.04 (.960 (.60 (1.30) . see Data Analysis section) for Survey years 99-00.70) 3.20-1.800 (.00) .920 (. and 03-04 are 0.535-.60 (1.800) .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 .915-1.695 (.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 1.700 (.91) 2.589-.800) .40-3.80) 1.50-1.10) .02) 1. and 0.50 (2.

62-3.404 (.03) 1.810 (.781-1.914 (. encephalopathy.68 (1. 2003.62-1.88 (1.720 (.731-.66 (1. 1991.625 (.793-1.41-1.876-1.43) 1.50-2. kidney injury.639 (.679) 1.22-2.469 (. For instance.693 (.46 (2.05-1.70 (1.380-. 1993).47) 1.06 (1.606-.15) 1.71-2.25-1.655) .18) .622 (.800-. with a half-life of years to decades.89-2.461) .22) 1.662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.721 (.645-.11 (.725) .44) 1.655) 75th 1.742) Selected percentiles ( 95% confidence interval) 50th ..97) 1.35) 2.07-1.85 (1.700-. 1995.02) 1.31 (2.603 (.56 (1.900 (.841-1.65 (1.812-1. and through binding to ion channels and regulatory proteins.594-.18 (1.85) 1.893) .89-5.56-2.492-.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 .623 (.64) 95th 2.671 (.61) 1. abdominal pain.887 (.52 (1.58) 1.02-1.673) .31 (1. through the inhibition of certain enzymes.50-2. CDC.588-.22) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.88-2.862-.67-4.742) .605-.03) 1.31) 1..588-.45 (1.20) .64-2.763) .82) 1.710) .88) 1.88) 2.654) .638 (.508) .607-. BLLs and associated toxic effects differ in children and adults.63) 4.06) .37-1.07 (.541-.11) .15) 1.09-1.918-1.09-1.47 (2.652 (.08) .72-2.828) .87) 1.29 (1.551-.698) .17 (.64 (1. In 1991.38 (2.708 (.774 (.18) 1.03) .43 (1. interval) .37-1.677) .98) 2.644 (.639 (.61) 1.01) .20-3.617-.725) .94-2.79) 2.97) 1.720 (.702) . Staessen et al.698) .75-2.04-3. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.03) 2.383-.09-1.46 (1.657) 1.882-1.28) 2.408-.43 (2.975-1.98-2.707 (.97-18.61) 1. O’Flaherty.38 (2.88) 2.22-1.940 (.730) 1.33) 1.587-.53) 1.79 (1.48 (1.962 (.11 (.56) 3.50) 1.05 (.44 (1.44 (1.594-.914-1.618 (.712 (. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.604-.74 (1.72) .41 (1.667-. Lead can cross the placenta and enter the developing fetal brain. and iron.755 (.56-3. 1996).50 (1.08-2.603-.649 (.78 (2.94 (1.33) 2. and nails (Leggett.633 (.03) 2.55 (1.06 (.746) .404 (.15-2.20) .718) 1.957-1.50-1.59-3.375 (.51 (1. population from the National Health and Nutrition Examination Survey.603-.753) .938 (.22) 1.06) 1.609 (.18) 1.992-1.342-.677 (.709 (.593 (.03 (.43-1. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al. hair.670) 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 . with lesser amounts eliminated via the feces.739) .682) .639 (.615 (.73-2.33-1.400) .31) 1.0) 3.655-.571-. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.78-4.85-2.15-3.79) 1.681-. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.436) .40-1.03 (1.28-1.10 (1.703) .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 .61) 3.03 (.926 (.404-.38 (2.73) 2.97 (1.639) .14 (1.04) 2.979 (.24 (1.72-2.796-1.00 (1.702) . 2004.26) 2.432 (.01 (.933-1.00 (1.85-2.11 (1.990 (.26) Total .898) .Metals 90% of the body lead burden in most adults. The skeleton acts as a storage depot.62) 2.31 (1.12-1.977) 1.765) .11 (1.679-.571-.676) .561-.658 (. The toxic effects of lead result from its interference with the physiologic actions of calcium.28) .851) .66) 2.790) . 1993.529-.43) 2.988 (.52) 1.722 (.S.00 (1.03-2.683-.39-1.702-.688) .77) 2.677-.03 (.853-1. the Centers for Disease Control and Prevention (CDC) established a BLL of 10 Urinary Lead (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.917-1.918 (.963-1.47 (1.645-.25-1.63) 1.722 (. Schwartz.586-.460-.592-.870 (.65-2.03) .07) .667) .53-1.933) .535) .62-2.61) 1.09) 1.981-1.27 (1.17-1.838) .686) .988-1. scant amounts are lost through sweat.681-. Nash et al.696 (.10) 1.971 (.632 (.51) 1. 2007).635 (.10 (.496 (.946-1.00) .34-1.66 (1.559-.938-1. and paralysis.55 (1.19-5.49 (1.75 (2.644) . Approximately 70% of lead excretion occurs via the urine.36-2.758) .33 (1.41) .23 (1.641 (.03) 90th 1.98 (1.668-.667-.05-1.648 (.18) 2.96 (1.583-. Large amounts of lead in the body can cause anemia.00 (.623 (.83) 1.601-.701) .15-2. based on prospective population studies.14) 1.579-.992-1. seizures.50-2. zinc.510-.569 (.83 (2.612-.701 (.11-1.86 (1.621 (.92) 2.718) .64) 2.920-1.828-1.05 (1.19) 1.71 (1..69 (1.608-. 1995).734) .608 (.997-1.428) .615 (.11) 1.914 (.659-.08) .

subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al.S.g. Fourth National Report on Human Exposure to Environmental Chemicals 215 . particularly in the skeleton. In NHANES 1999-2002 in children 1-5 years old. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. Jones et al. when the geometric mean BLL was 2.. 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... premature delivery.xls).html. 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.. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. and organic lead compounds not classifiable with respect to human carcinogenicity. 2003. adults in the 19992000 NHANES sample (Apostoli et al. 1984. 2002). Both drinking water and ambient air standards for lead have been established by the U. Overall. the prevalence rate has declined annually since 1994 (CDC. may alter sperm morphology. urban residence. higher than 100-200 µg/dL). Staessen et al.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. residing in housing built before the 1950’s.. Bellinger 2005. Payton et al. 2005a).75 µg/dL in U. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. 1996. 1996. 1991. Muntner et al.6%) were lower than those from NHANES 1991-1994.4% in NHANES 1999-2004.6% in NHANES 1988-1991 to 1. CDC. and peripheral neuropathy generally occurring at much higher levels (e. Schwartz et al..000 adults. 2006). 2003. Schwartz. Pirkle et al.Metals µg/dL or higher as the level of concern in children. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. 2005b.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. 2003. including minority race or ethnicity. 2006). At low environmental exposures.. respectively... and low family income (CDC.. 1999). the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. In occupationally exposed adults. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. 2000). 2000). Lanphear et al. Surveillance data reported by U.. Urine levels may reflect recently absorbed lead. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. 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.S. with overt encephalopathy. 2007). and spontaneous abortion (Baghurst et al. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. which is an 84% decline.gov/toxpro2. reduce sperm count.21% of approximately 3.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample.07 µg/dL (Becker et al..5 per 100. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. 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. adult residents.. BLLs reflect both recent intake and equilibration with stored lead in other tissues. usually with BLLs greater than 40 mg/dL. environmental levels) and health effects is available from ATSDR at: http://www.7 µg/dL and 4..e. 2009).S. Telisman et al.. and decrease fertility (Alexander et al. 1994). Korrick et al. seizures...4% of children had BLLs of 10µg/dL or higher (CDC. 2002. High dose occupational lead exposure. though there is greater individual variation in urine lead than in blood and greater potential for contamination. Borja-Aburto et al. 2005b). For example. both the geometric mean (1.cdc. 2002a). Information about external exposure (i.. the geometric mean BLL was 3..2 µg/dL in males and 3. NTP considers lead and its compounds reasonably anticipated to be human carcinogens.S. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. lead in women may be associated with hypertension during pregnancy. The U.cdc. Data submitted through state public health programs from 2006 showed that 1.S. 1999).3 million children tested had BLLs of 10 mg/dL or higher (http://www. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. approximately 11. More recently.. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. almost double the geometric mean of 1.0 µg/dL in females (Soldin et al. 1987... IARC considers inorganic lead compounds probable human carcinogens. EPA. 2001). BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors.S.. adults in the 1999-2000 NHANES sample. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. 2003).atsdr. 1998). 1995. However. 1996.

gov/nceh/lead/publications/ books/plpyc/contents. Cory-Slechta DA. Available at URL: http://www. Checkoway H. JAMA 1996.275(15):1171-1176. Schulz C. Kim R.115:521-529. Jacobson SW. Teratogen update: lead and pregnancy.87:1-471.113(4):1016-1022. Jusko TA. Age-specific kinetic model of lead metal in humans. Meyer PA.26:359-371. Leggett RW.atsdr.htm. Lead and hypertension in a sample of middle-aged women. Cox C. 4/14/09 Alexander BH. Pediatrics 2009. Atlanta (GA). Seiwert M.cdc. Hernberg S. McMichael AJ. Bellinger D.348:15171526. Manton WI. Becker K. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Baghurst PA.55(32):876-879.89:330-335.275:1177-1181. Coresh J. IARC Monogr Eval Carcinog Risks Hum 2006. Brody DJ. Hertz-Picciotto I. Neri A. Korrick S. Inorganic and Organic Lead Compounds. et al.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. MMWR Morb Mortal Wkly Rep 2006. Preventing Lead Poisoning in Young Children. Weiss ST. Kaufman JD.gov/mmwr/preview/mmwrhtml/ mm5532a2. Lanphear BP. et al. Reese YR. Baj A. Neurotoxicol Teratol 2004. doi:10. Public Health Rep 2000. 1999-2002. Lead. Hunter DJ. Chiodo LM. A prospective follow-up study on psychological effects in workers exposed to low levels of lead.101(7):598-616.1542/peds:2007-3608. Aro A. 2005b. Birth Defects Research (Part A). Third National Report on Human Exposure to Environmental Chemicals. Sparrow D. Kuehnemann TJ. Available at URL: http://www. Kaus S. Bellinger D. CDC. 4/14/09 Centers for Disease Control and Prevention (CDC).html. Aug 2007 [online]. Available at URL: http://www.73:409-420. JAMA 1996. Centers for Disease Control and Prevention (CDC). et al. Rios C. Cox C. Angle CR.10:43-50. Environ Res 2000. Environ Health Perspect 1993. Available from URL: http://www. Hu H.82:60-80. MMWR Morb Mortal Wkly Rep 2005a. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. 4/14/09 Centers for Disease Control and Prevention (CDC). Jacobson JL. Blanco J. Blood lead levels—United States. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Krause C. Muntner P. Ronchi L. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Pediatrics 2004. Vimpani FB. Homa DM. Ga.htm. Rotnitzky A. Payton M.53:411-416. Roberts RR. Batuman V.cdc. References Agency for Toxic Substances and Disease Registry (ATSDR). Wigg NR. Blood lead reference values: the results of an Italian polycentric study. van Netten C. Occup Environ Med 1996. Am J Public Health 1999. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Sci Total Environ 2002. Dietrich K. Muller CH. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Canfield RL. 4/14/09 Centers for Disease Control and Prevention (CDC).54(20):513-516. Am J Epidemiol 1999. 4/14/09 Centers for Disease Control and Prevention (CDC).gov/toxprofiles/tp13. Neurotoxicol 1987. Wager C. 2003-2004. Hu H. Speizer FE. Rojas LM.205:297-308. Scand J Work Environ Health 1984. Caldwell KL.cdc. N Engl J Med 2003. 1988-2004. Lepom P. Bavazzano P.cdc. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Borja-Aburto VH. Int J Hyg Environ Health 2002. Neurodevelopmental effects of postnatal lead exposure at very low levels. Atlanta (GA). Sparrow D. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Blood lead levels measured prospectively and risk of spontaneous abortion.htm. Acquisition and retention of lead by young children. Auinger P. 1991 [online].150(6):590-597. Ewers TG. The relationship of bone and blood lead to hypertension. 2005. Managing Elevated Blood Lead Levels Among Young Children. Weiss ST.cdc. Luukkonen R. Semen quality of men employed at a lead smelter. Available at URL: http://www. Adult blood lead epidemiology and surveillance—United States. Jones RL. Pirkle JL. Farias P. Stanek KL. et al. et al. Ganzi A. Vupputyuri S. Mantere P. Hänninen H.gov/nceh/lead/ CaseManagement/caseManage_main.287:1-11. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Lanphear BP.8(3):395-401. gov/mmwr/preview/mmwrhtml/mm5420a5. Korrick SA. Atlanta. 2002 [online].123:e376-e385.htm. Apostoli P. Rotnitzky A. Toxicological profile for lead. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Henderson CR. Hu H. Robertson EF.

Kaufmann RB. O’Flaherty EJ. Weiss ST. Lee GS. Jurasovic J. Telisman S. Exposure of the U. Fourth National Report on Human Exposure to Environmental Chemicals 217 . stable lead isotopes to determine release of lead from the skeleton. Hanak B. Environ Health Perspect 2000. cadmium. Cvitkovic P. Hickman T. and hypertension in perimenopausal and postmenopausal women.9:303-327. Rocic B. Use of endogenous. Payton M. dimercaptosuccinic acidchelatable lead. Toxicol Appl Pharmacol 1993.S. Pirkle JL.63:1044-1050. Kidney Int 2003.327:109-113. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Pizent A. and copper in men. zinc. Blood lead concentrations in children: new ranges. Staessen JA. Low-level lead exposure and blood pressure. et al. Schwartz J. Lee SS. Sparrow D. Arch Environ Health 1995. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Paschal DC.118:16-29. Lee BK. Clin Chim Acta 2003. Association of blood lead. Sherwin R.108(1):45-53.209:301305.Metals results from NHANES III. cadmium. Schulz D. JAMA 2003. Lustberg M. Hu H. Osterloh JD. Magder L.289(12):1523-1531. Soldin SJ. Blood lead. Flegal AR. 50:31-37. Hwang KY. Gunter EW. Schwenk M. Environ Health Perspect 1996. Revised and new reference values for arsenic. Roels H. Schwartz BS. Int J Hyg Environ Health 2006. Smith DR. Rubin R.153(5):453464. Brody DJ. Am J Epidemiol 1994. Environ Health Perspect 1998. Nash D. et al. Kaufmann R. and tibia lead with neurobehavioral test scores in South Korean lead workers. blood pressure. Gavella M.140:821-829. J Hum Hypertens 1995. Lauwerys RR. Physiologically based models for bone-seeking elements. blood pressure and cardiovascular disease in men. Amery A.104(1):60-66. population to lead: 1991-1994. Soldin OP. lead. IV.106:745-750. Lead. Kinetics of lead disposition in humans. Am J Epidemiol 2001. Low-level lead exposure and renal function in the Normative Aging Study. Wilhelm M. Stewar WF.

30) 5.40-1.797 (.484) .40 (3. thimerosal.490 (.70 (1.70-2.g.700-.500-.800-1. Some cosmetic skin creams from countries other than the U.30 (2.700-.372) .672) . Survey years 03-04 Geometric mean (95% conf.30) 1.800 (. an organic form of mercury.40 (4.20-4. and mining and smelting.60) 1.80) 4.800 (.30) 1.900) .00-1. constitutes the main source of dietary mercury exposure in the general population...500) .860-1.979 (.800 (.50) 4. sulfur.60-6. mercuric chloride). Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. or oxygen.900) 1.563 (. interval) .30) 3.700-.90 (1. solid-waste incineration. Accidental spills of elemental mercury.326 (.00 (2.30) 4132 4241 03-04 03-04 03-04 .60 (1.00 (. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach. IARC.800-1.90 (1.776 (.00) 1. with the highest concentrations occurring in the kidneys (Barregard et al.80 (1.. 2007). and organic forms.40-2. may contain inorganic mercury.50-2. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).90-3.00 (. 1994.877 (.753-1. In addition.30 (1..472-. Apart from methyl mercury.800-1.g.90) 90th 3.50) 5. which can bioaccumulate in aquatic and terrestrial food chains. and dental amalgam. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.00 (1. thermostats and switches).40) 3. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.781 (.655-.30-6. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).30-5. Kingman et al. such as chlorine (e.70 (1. to form inorganic mercury compounds or salts.60) 1.500-.80 (1.900) 1.00-5.20 (2.50) 1. electrical lamps.60 (2.800-1.30-4.500 (.00 (2.30) 3.363-.90) 95th 4.30-2.2.800-1. have often required public health intervention (Zeitz et al.400 (.40-2.00) 1..90 (4. synthetic organomercury compounds were once used in pharmaceutical applications.80) 1. which create an episodic potential for volatization and inhalation of mercury vapor.903) Selected percentiles ( 95% confidence interval) 50th .90) 3.S.900) 1. 1980.00 (.00) 3.700-.886) .80 (1. Hursh et al. and mercury compounds are still used as preservatives (e. 2002).419 (.20) 2.714-.400-.574) . Atmospheric elemental mercury can be deposited on land and water. sphygmomanometers and barometers.10-3.50-1.60-5.418-.70 (3.60) 2085 2293 3478 Limit of detection (LOD. and is distributed to most tissues. After elemental mercury is absorbed.10) . The ingestion of methyl mercury.20-3.700-.40 (3.40 (4. elemental mercury is absorbed mainly by inhaling volatilized vapor.80 (3.60-2. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.800 (. predominantly from fish and other seafood.40) 1. thermometers.70) 911 856 2081 4525 03-04 03-04 .700 (.703-.689-..Metals Mercury CAS No.80) 3.50-3. inorganic.20-4.700) . Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements..60 (1. Poorly absorbed from the gastrointestinal tract.g. merbromin).919) ..40-1.500 (.900 (. 1998.300) ..g.285-.12) . The kinetics of the different forms of mercury vary considerably.900) 75th 1.00) 4.S. Woods et al.300-.00 (2.300 (.60-6.600) 1. phenylmercuric acetate) or topical antiseptics (e. 1993).400-.60-3. Other major uses include electrical equipment (e. see Data Analysis section) for Survey year 03-04 is 0.00) . Also.00 (. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.600 (. 1999 .40-3.927) . silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.02) .814 (. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. 218 Fourth National Report on Human Exposure to Environmental Chemicals .700) . water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.70 (4.50) 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 .50) 2. population from the National Health and Nutrition Examination Survey. Elemental mercury is a shiny.

for both acute and chronic exposures.700-.664-1.S.10 (.30 (1.40) 2.10 (5.600) .300 (. and the newborn’s levels decline gradually over several weeks (Bjornberg et al. 2003).500 (.30) 1. Methyl mercury enters the brain and other tissues (Vahter et al.667 (.70) 4.10-3.60 (2. 1990).377) . 1975.70-5...00-2..10 (3.06-1.395) .. Vimy et al.60 (1.30 (1.800-1.500-.256-. Excretion occurs by renal and fecal routes.50) 1.800) 75th .900 (.20) 1.800) 1. 1998).73) 1. 1992).90) 2.800) .00) 7.900 (..800) 1.00-2. 1999-2002.825-1. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.10 (.90 (1.300) .50 (1.30 (.40-1.60 (3. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.40-2. and a useful marker of exposure in epidemiologic studies (Grandjean et al. 1992.20-11. Jonsson et al.00) 1. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.30-6.700-1.10) .300 (.30-4. population. 1971).697-. a measure of accumulated dose (Cernichiari et al..500 (. 2005).919) .00-3.500-1.30-3. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . 1969.500-.70 (1.833 (.700 (.0) 4.20-2.30-11.. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.318 (.200-. Geometric mean Survey years (95% conf.297-.40-2.700 (.400-. Sandborgh-Englund et al. Fourth National Report on Human Exposure to Environmental Chemicals 219 .500-.80) 579 527 370 436 588 806 Limit of detection (LOD. Smith et al.23) .800) . 1996.700-.90) 90th 1.40 (1.800 (.800 (.90) 5. 1973).00) .407) . Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations..600 (.377 (.60 (1.90 (4. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.90) 2.00 (3.50 (2. Methyl mercury is incorporated into growing hair.50) 95th 2.824) 1.900-1.30-6.80 (3.268-.50) 2.Metals the tissues to mercurous and mercuric inorganic forms.40) 1.500-.90 (4. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.70 (1. 1984. Miettinen et al.01) ..00 (2.30 (1.90) 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) 4.30-5. 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.. 1991.300 (.00-1.944 (.30) 3.900-1.70-3.10) . Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.7) 4.200-. 1993).70-5.20 (2. interval) Selected percentiles (95% confidence interval) 50th . Vahter et al. 2004.269-.500-. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.20) . 1994) and then undergoes slow dealkylation to inorganic mercury.10 (1.800-1.200 (.00 (2.10 (1.60 (3.29) .50) 1.820 (.200-. 1998)..343 (..10 (1.300) .70) 4.40) 5.317 (.60 (1. 1994.50-3.50) 3..300) .80) 1. 1999).20-3.70-6.265-.70-3. 1994).200-.600) .900 (.738-. 1992 and 1999.30) 1.50-2.871-1. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.200-..800-1. with most elimination occurring through in the feces (Sherlock et al.307 (.541-.20) .50-12.00-6.35 (1.60) 3.30-4.3) 4. 2003).30-2. National Health and Nutrition Examination Survey.00) 2. 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 (. Smith and Farris.00) 1.00 (1.299-. Myers et al..800 (. Suzuki et al..00-2.70) 1. After exposure to elemental mercury.60) 2.700 (..90) 3.700-1.14 and 0.374) .300 (.30-6.60) 1.90 (3.10-1.329 (. 1995.726-1..00 (2.02 (.10) 1.80-3.200-...70 (1. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.300) .20-3.60) 1.20-3.369) 1.14. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al...300) . thereafter.27) . McDowell et al.300) .940) Race/ethnicity (females.06 (.40 (1. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.700) 2.00) 6.475) .80 (1.20 (.700 (. 1996).90 (1. 1993).

800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . dysarthria.600 (. typically after a latent period of weeks to months. 2000.500-. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.S. irritability. Sakamoto et al. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.600 (. Salonen et al.. Smith et al. 1987). Inorganic mercury exposure usually occurs by ingestion. and sleep disturbance (Bidstrup et al.500 (<LOD-.. 2004). 1998. particularly irritability. The constellation of findings may include anorexia. insomnia.600 (. depression. 220 Fourth National Report on Human Exposure to Environmental Chemicals . 1963). hearing impairment. In recent epidemiologic studies.500-.500 (.600-..42.. 1993)..500) .600 (.500-.500 (.700) 2007 2240 3406 Limit of detection (LOD.700 (. population from the National Health and Nutrition Examination Survey. overt signs and symptoms of chronic inhalation may include tremor.600-. 2000.600-. limb deformities.600) . Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.800) . 2004..500 (<LOD-. 1983).800) .. dysarthria.. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. 1995.600 (.700 (. short-term memory loss. Drexler and Schaller. see Data Analysis section) for Survey year 03-04 is 0.700 (. Bellinger et al.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . 2002. Rissanen et al. At levels below those that cause acute lung injury.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 . 2006. Stern 2005. Vupputuri et al.700) .500-. the existence of a causal relation is unresolved (Chan and Egeland.600 (.. The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. 2005).500-.600) .500-. Once absorbed.600) . Smith et al. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. maculopapular rash.600-. 2003)... and pinkish discoloration of the hands and feet (Tunnessen et al.600) . which may vary for some chemicals by year and by individual sample. hypertension.. Sakamoto et al. gingivitis. 2000). Oskarsson et al.. < LOD means less than the limit of detection.. sensory impairments. Factor-Litvak et al. 2004.. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.600) . Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. cerebellar ataxia. anorexia.. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. DeRouen et al.600) .600 (. fatigue.700-.700 (.. and progressive constriction of the visual fields. 1995. 1996).500-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Overt poisoning from methyl mercury primarily affects the central nervous system. 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. 1970. causing parasthesias. and neurocognitive and behavioral disturbances. 2005. Rice.600) .600) . altered physical growth. 1951. Acute.700 (. Survey Geometric mean (95% conf.600 (.600) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.700-. 2006. pain in the extremities. and cerebral palsy (NRC.Metals may be more efficient for inorganic mercury (Grandjean et al. ataxia. 2004).500-.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500-.700-..700 (.

Survey years 03-04 Geometric mean (95% conf..63-2.08 (1. In NHANES 19992002..530) . IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.396-.18) 2.495 (.430) .840) 1.509) .370) .09 (2.420 (.42) 95th 3.61) 1. 2003).34-3.19 (2. total blood mercury increased with age.580) . Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.330-.160-.304) .476 (..24 (2.480) 75th 1. Benes et al. In Germany the geometric mean for blood mercury was 0..420 (.610-1.28) 1. EPA. the total blood mercury concentration is due mostly to the dietary intake of organic forms.930-1.24) 1.447 (.. aged 18 to 69 years.700 (.Metals standard for inorganic mercury has been established by U.400 (.31) 1266 1272 03-04 03-04 03-04 .330-.290-.413-. During the same survey periods.52) 2.890 (. et al. Grandjean et al.65) 1.33 (2.96 (1. 1997. population from the National Health and Nutrition Examination Survey. 2004. range 40 years to 78 years) had an average total blood mercury concentration of 2.16 (.330-.570) .509) .460 (..8 years.250) .492) Selected percentiles ( 95% confidence interval) 50th .68 (2.55 µg/L..340-.. adult women in several ethnic subgroups (Hightower et al.85-2.360 (.16 (1.26 (1.460) .358 (.19 (1. Sanzo et al.430 (.67-3.00 (.88 (1. 2000). A cohort of 1127 U.05) 1.S.23) 2.254 (.440 (. 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.76-3.60) 619 713 1066 Limit of detection (LOD.840-1.463) . average age 33 years.93 (1.67-2. Kingman et al.530) .870-1.382-. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC..S.96 (1.408) . interval) .97) 2.14-2.770-1. the median concentration of blood mercury was 0.480 (.23) . 2006). 2002). These distinctions can help interpret mercury blood levels in people.07 (.840-1. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.S.00) 1.405-.9 years). EPA at: http://www. Total blood mercury levels increase with greater fish consumption (Dewailly et al. Biomonitoring Information In the general population.433 (.78 µg/L for adults and 0.360-.01 (.03-4.410-.416 (. From 1996 through 1998. Among the three racial/ethnic groups.520) .39-3.31) 2. 2001.. Fourth National Report on Human Exposure to Environmental Chemicals 221 .14) 90th 2.46) 3. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning. Schober et al. and increased slightly in non-Hispanic white children (Caldwell.88) 287 722 1529 03-04 03-04 . 2003).360-.e. However. average age 9.200 (. 758 children.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 .549) .555) .29) 1.330 (.05) 3..76-3.90) 2. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children..60-2.12 (.870-1. 2009). total blood mercury geometric mean levels in females aged 16-49 years did not change.gov/toxprofiles. Information about external exposure (i. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.54 (2.S.30) 3. environmental levels) and health effects is available from the U.406-.530-.960 (.280-.313-..46 µg/L for children. see Data Analysis section) for Survey year 03-04 is 0.78-2. military veterans (mean age 52.14.700-1. particularly methyl mercury.89) 3.76-4.13-2. 1998).88-3.534) .442-.08 (1.20 (1. 2009). and the age-related changes differed across the groups (Caldwell et al. 1998). slightly higher total blood mercury levels were found in U.gov/mercury and from ATSDR at: http:// www. who participated in a 1998 representative population survey (Becker et al. 1995. Over the NHANES 1999-2006 survey periods.441 (. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. Mahaffey et al.atsdr.350-.940 (.cdc.60 (1.epa. 2001.99-6.58 µg/L for 4645 adults.430 (.213-.77-2.66) 3.. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.

306 (. women of childbearing age have generally been much lower than these levels (CDC.385-.63) 1.301-. reversible increase in urinary N-acetyl-glucosaminidase.1 µg/L.S.04-3.404-.535) 1.545 (. 2003).217 (. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.768 (.909 (. 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. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects. Information about the biological exposure indices is provided here for comparison.64-2.56) 1266 1271 03-04 03-04 03-04 .537) .S. Czech (Benes et al. 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.18-1.525 (.30) 2. 2009). among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.11) 2.51-2.54 (2.32 (1.455-.333-.67 (1..343 (.255 (.09) 1.65 (1.472-.Metals 2000).620-.508 (. a biomarker of perturbation in renal tubular function.67 (1.280-.62 (1.79) 1.969-1.696 (. An expert-panel report recently prepared for the U.25 (.35 (1.486) Selected percentiles ( 95% confidence interval) 50th .687) .309-.417) . Department of Health and Human Services noted that several studies have observed a modest.785-1.88 (1. Urinary mercury levels in recent German (Becker et al.208-.77 (2.476 (.12-3.S.11) 1. military veterans with dental amalgams. 1998). Urine mercury and the number of dental amalgams were correlated.13 (1. In the study of U.88-2. interval) .875-1.522-.. the urine mercury increased by approximately 0. et al...384 (..07) 1.246-..365 (.652) .86) 95th 2.532 (.392-.275) .13-2.498) 75th .46-2.587 (.44) 1.800-1..79 (1.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .32-2.23-2. 2002). 1992).365 (. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.01) 2.391-.970 (.31 (1.S.276 (.599) .30) 1.368) .76 (1. 2006).78-4.485 (.00) 90th 1.28 (.1 µg/L for each surface with a dental amalgam (Kingman et al..447 (.61) 1.667-1. population from the National Health and Nutrition Examination Survey.40 (1.41-2.225-. 2002) adult population surveys were similar to those in a U.88-2.347) .464 (.964-1.990) .40-1.297 (.06 (.358) .21) 1.455-.376-..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 .S. 2005). mean urinary mercury was 3.307-. and Italian (Apostoli et al.87 (1.11-2. 2006. DeRouen et al.619-.784) 1.289) . Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.480) . 2009).39) 1. Langworth et al. et al.87) 2.455) .630) .00 (.06 (. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.714-1. not to imply a safety level for general population exposure.16) 1.443 (.391) .196-. Survey years 03-04 Geometric mean (95% conf. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.265-..03) 2.362 (.400) . Levels in U. and on average.616) .566) .447-.00) 286 722 1529 03-04 03-04 . 1988.463 (.588) .400-.

622-.62 (1.48 (2.744) 1.24-1.721 (.30 (2.501-.14.13 (2.502-.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.30 (2.579-.637) .870) .45-3.580-.910) .710 (.94) 1.87-4.966) .23-1.578-.43-1.42) 90th 2.00 (2.475-.07) 1.81-6.656-. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.23-1.560-. 16-49 years) 99-00 01-02 .14-1.21-3.831) .32 (1.55) 90th 3.97 (1.76) 2.30-2. National Health and Nutrition Examination Survey.17) 95th 5.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .650 (.65-4.45) 95th 3. interval) Selected percentiles (95% confidence interval) 50th .14) 3.81 (3. 16-49 years) 99-00 01-02 .632 (. Geometric mean Survey years (95% conf.56 (1.685 (.592 (.50-4.850-1.605-.831) .85) 4.710) 1.97) 2.52) 3.420-.32) 2.91 (2.655 (.54) 595 531 381 442 594 826 Limit of detection (LOD. interval) Selected percentiles (95% confidence interval) Survey years 50th .508-.S.99 (2.31 (1.930) .50 (2.95 (2.97) 2.32-3.526-. National Health and Nutrition Examination Survey.846) .03 (.27 (2.387-.540-.582-.41 (2.03) 1. Geometric mean (95% conf.89 (2.45 (1.84 (2.14-2.520-.38) 4.99) 1.557-.657 (.S.810) .15-1.710 (.61-6.516 (.09-1.500-.14 and 0.68-3.658 (.46) 3.699) 1.06 (.565 (.41 (1.664) .91-7.44) 3.560 (.740 (.03 (.92) 4.723 (.706 (.639 (.3) 5.522 (.55-3.45) 2.51 (3.70 (2.27-1.809) .760 (.68 (3.46-4.624-.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .92) 2.631-.99-2.610-.05 (2.615 (. 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.30 (1.580 (.616-.650) 1.61) 1.76 (1.15 (2.540 (.Metals Urinary Mercury−Females Aged 16-49 Years Old. population.50 (1.31-1.37) 1.69 (1.35 (1.35) .85-3.833) .83-3.37 (1.42) 2.10-2.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.709) .59-5.28 (1.56) 4.25) 2.10-4. 1999-2002.824) .520-.742-1.99 (3.27 (1.553-.04-1.13-4.806) .410-.606 (.46 (1.72) 1.97) 2.16) 5.45-2.450-.42-3.620 (.03-2.16-5.62 (3.719 (.77) 1.596 (.691) .00 (3.09-1.04-10.709) 75th 1.665) .05 (3.600 (.832-1.56) 3.18) 3.47) 1.79) 3.774) .92) 3.47) 1.909-1.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .45) 2.41 (1.18 (3.79) 1.07-5.76-5.799) . population.21 (1.69-3. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.62 (4.41-6.57-4.21 (2.00) 2.650 (.68) 3.24) 6.22-3.22 (.724 (.84 (2.98 (5.07-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.77) 2. 1999-2002.892) .569-.686) .790) .426-.53-3.670) 75th 1.65) 1.39-3.636-.772 (.51) .

Persson G.113(10):1381-1385. I. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. JAMA 2006. Atlanta (GA). Kaus S. Barregard L. Woods JS. Schulz C.149:301-305. Budtz-Jorgensen E. Hg. Hultberg B. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo).289:1324. Lancet 1951. Lepom P. Ayotte P. Kinetics of mercury in blood and urine after brief occupational exposure. Subrt P. Osterloh JD. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Bjornberg KA. Bonnell JA. Bernard AM. Conradi N. Int J Hyg Environ Health 2009. and lead. Chronic mercury poisoning in men repairing direct-current meters. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits.16(4):705-710. Becker K. Marsh DO. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. Skerfving S. Egeland FM. Locket S. Jorgensen PJ. Cutress T. Jacobs D. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Geier J. Mangili A. 206:15-24. J Toxicol Environ Health 1997. Buchet JP. Bellinger DC. Elia G. Bidstrup PL. Markers of early renal changes induced by industrial pollutants. Ekman L. et al. Arch Environ Health 2001.111:719-723. Echeverria D. Barregard L.7(3):176-184. ACGIH. Caudill SP. Cincinnati (OH): Signature Publications. Cox C. Leitão J. et al. Third National Report on Human Exposure to Environmental Chemicals. Seifert B. Mortensen ME. population: 19992006. Townes BD. Roels H. et al. Garrett N. Drexler H. et al. et al. Rosenbaum G. Total blood mercury concentrations in the U. Cortesi I. Videro T. Int JHyg Environ Health 2002. Metabolism of methyl mercury (203Hg) compounds in man. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. Aposian HV. mercury exposure. Cu. Krause C.8(2):117-119. Cernichiari E. Health effects of dental amalgam exposure: a retrospective cohort study. Niklasson B. Schuzt A. Weihe P. JAMA 2006. Am J Epidemiol 1999. Arch Environ Health 1969. The concentration levels of Cd. Kline J.50:17-27. Weber JP. Environ Health Perspect 2003. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Lauwerys RR. Greitz U. Barregard L. Apostoli P. Fish consumption. Jarvholm B. Int Arch Occup Environ Health 1988. Begg M. and heart diseases. Trachtenberg F. Grandjean P. Harvey DG. Martins IP.212:588-598. Seiwert M. Chan JM. Int Arch Occup Environ Health 1999. Schulz C. Grandjean P. Int J Epidemiol 2004. Myers GJ. Impact of maternal seafood diet on fetal exposure to mercury. McKinlay S. 2005. Sallsten G. Debes F. Tavares M. Jones RL. Bruneau S. Brewer R. Lebel G. Centers for Disease Control and Prevention (CDC). Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial.61:65-69. Cernichiari E. Berglund B. Vahter M. Assessment of reference values for mercury in urine: the results of an Italian polycentric study.62(2):68-72. Weihe P. Cejchanova M. Pb. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.. Lapham LW.72:169-173. Kaus S. et al. Hasselgren G. Mercury derived from dental amalgams and neuropsychologic function. Enzymuria in workers exposed to inorganic mercury. Luis H. et al. Snihs JO. Arch Environ Health 1992. Biennow M.47(3):185-195. Leroux BG. Arch Environ Health 1992. Fawcett J.Metals References Aberg B.295(15):1775-1783. Cianciola ME.56(4):350-357. Clarkson T. Spevackova V. Cent Eur J Public Health 2000. Cardenas A. Barbon R. Martin MD.2:856-861. Benes B. Schaller KH. DeRouen TA. Sandborgh-englund B. Tissue levels of mercury determined in a deceased worker after occupational exposure. Attewell R. Barregard L. Daniel D. Environ Res 1998. Nutr Rev 2004. Zn. Falk R. White RF. Dewailly E. Cernichiari E. Drago I. Br J Ind Med 1993. Caldwell KL. Becker K. Neurotoxicology 1995. Schutz A. Bernardo M. Sallsten G. Sallsten G.19:478-484.295(15):17841792. Gagliardi T. 52:19-33. Jorgensen PJ. 2007 TLVs and BEIs. selenium. Bates MN. Cerna M. Int J Hyg Environ Health 2003.S. Sci Total Environ 2002. Martin MD. Application to workers exposed to mercury vapour. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure. 224 Fourth National Report on Human Exposure to Environmental Chemicals . Woods JS. Factor-Litvak P.205:297-308. Kjellstrom T.77(2):124-129.33:1-9. Smid J. Castro-Caldas A. Seiwert M. Levallois P. and Se in blood of the population in the Czech Republic. Environ Health Perspect 2005.

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Hongo T.124:221-229. Lorscheider FL.4(5):981-988. Baser M. Hall LL. Dorronsoro M. Suzuki T. McMahon KJ. Leroux BG.2:117-131. 1993-1998. Jones RL. JAMA 2003. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Mooney TF. Environ Health Perspect 2002. Toxicol Appl Pharmacol 1994. Effects of exposure to mercury in the manufacture of chlorine. Martin MD. Kaye WE. Sherlock J. Stern AH.110:129-132. 1999-2000. Osterloh J. Environ Res 2005. Sinks TH. Toxicol Appl Pharmacol 1996. Effects of occupational exposure to elemental mercury on short term memory. Am Ind Hyg Assoc J 1970. Patil LS.111(12):1465-1470. Langolf GD. Nakazawa M. Takahashi Y. Allen PV. Yoshinaga J.79:786789. Topping G. Vimy MJ. Daniels JL. Leitao JG. Friberg L. Smith PJ. Bolger PM. Woods JS. Longnecker MP. Goldberg J. Stern AH. Amurrio A. et al. Am J Physiol 1990. Aguinagalde FX.97(2):195-200. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Public Health Nutr 2001. Environ Res 2005. Amiano P. Vahter M. Toxicol Appl Pharmacol 1994. The kinetics of intravenously administered methyl mercury in man. et al.31:687-700. Imai H. Zeitz P.37:245-252. Smith RG. Most B. Hum Toxicol 1984. Methyl mercury pharmacokinetics in man: a reevaluation.258(4 Pt 2):R939-945. Blood mercury levels in US children and women of childbearing age. Sandler DP. The hair-organ relationship in mercury concentration in contemporary Japanese. Br J Ind Med 1983. Whittle K. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Tunnessen WW. DeRouen TA. Schober SE. Bernardo MF. Mottet NK.98(1):133-142. Shen DD. The contribution of dental amalgam to urinary mercury excretion in children. Acrodynia: exposure to mercury from fluorescent light bulbs. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury.289(13):1667-1674.128(2):25125-25126. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Vorwald AJ. Smith JC. Smith JC. Newton G. Matsuo N.48(4):221229. et al. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Fisher HL. Azpiri MA.40:413-419. Farris FF. Smith AE.Metals Sanzo JM. Burbacher T. Arch Environ Health 1993.115(10):1527-1531. Environ Health Perspect 2003. McDowell M. Lind B. Turner MD. Vupputuri S. Guo S. Hislop D. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Environ Health Perspect 2007. Orr MF. Pediatrics 1987.

2-53.5-68.9-85.2-79.2) 79. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.5-66. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.2) 52.6) 93.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.2 (55.6-82.9-82.0-101) 82. 2001).4 (72. In humans.8 (85.7-73. 01-02. population from the National Health and Nutrition Examination survey.0 (48.S.3 (53.9) 62.8) 44. and paints.5 (41.4) 52.2-91.6) 53. inks.7 (71.3-47.7 (50.0) 39.4-82.7) 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. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.7) 75th 84.3) 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.2) 40.6-58.8-108) 87.7) 57.0-71.1-51.0-62.5) 47.5-52.0 (43.0) 45.2 (49.9 (52.2-70.5-46.6 (40.4 (48. and in pigments for ceramics.7 (44.0 (81.3-44.7 (51.5) 80. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5 (43. semiconductor and battery industries have begun to use molybdenum.1) 46.9) 34.7 (45.6-96.2) 41.8) 39.3 (38.3-108) 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 47.2) 37.7-122) 93.3) 47.3) 65.7 (36.2 (61.0-77.9 (37. and 1. WHO.Metals Molybdenum or ore deposits.1-52.0) 62.6) 51.7-92.2 (49.4-75.5 (37.5) 80.0) 97. Fourth National Report on Human Exposure to Environmental Chemicals 227 .8-46.7 (58.2 (40. Compounds of molybdenum are also used as corrosion inhibitors.5-41.2-37.5) 60. and xanthine oxidase (Kisker et al.3 (84.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.0) 54.0 (41.3) 85.6 (40.4 (34. 2001.9-83. lubricants.1-55.7-41.7) 78.1-88.3 (55.3 (71.0) 84.1) 35.. chemical reagents in hospital laboratories.9 (40.6 (43.1 (34.7) 46.5 (74.1 (91.8) 75. 0.1) 60.0 (76.8-106) 88.9-109) 97.8.8 (67. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-59.7-51.6-42.0-38. urinary excretion over six days CAS No.7-91.3) 41.6 (55.0 (46.8) 48.5 (67.4 (79.8) 40.5 (49.8-90.5 (48.4-61.2 (38.6-62.1-44.0) 60.8 (42.2 (83.8) 46.7 (73.7-96.0-85.7-84.2 (56.7-68.1 (38.7) 77.2 (69. respectively. interval) 45.3 (47.6 (52.3 (79.9 (34.6) 121 (103-139) 133 (113-155) 121 (106-143) 153 (126-188) 132 (121-147) 117 (109-129) 135 (119-154) 117 (108-129) 107 (99.5-91.4) 41.8.9-55.5-65.5-124) 108 (92.2-59.7) 86. 1997).6) 71.2) 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 (98.4) 45.0-53.0-100) 63.7 (37.8 (82.0 (42.5 (41.5-52.1 (71.7) 78.3) 83.6 (73.4) 56.9 (32. aldehyde dehydrogenase.1-59.7-60. More recently.1-48.3 (46.9 (73.0-56. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.2 (63.7-105) 69.6-55.7) 45.4 (48. see Data Analysis section) for survey years 99-00.2-42. At a daily oral molybdenum dose of 24 µg.2) 53.4-52.4) 49.9-55. Excretion occurs predominantly via the kidneys.5.4 (80.3) 54. 7439-98-7 General Information Elemental molybdenum is a silver-white.1) 126 (106-147) 109 (94.0) 55.3 (64.6-111) 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 52.1) 59.6-46.3 (55.7) 51.0-65.0-110) 90.0 (42.4) 76.5) 44.3-75.2) 48.3 (37.7-50.5 (81.6) Selected percentiles ( 95% confidence interval) 50th 50.9) 67. which exert homeostatic regulation over molybdenum balance.5) 85.3-91.1-63.8-49.1) 82.1) 57.3 (73.4) 42.8-94. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.1-52.9 (44. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.9 (78. hydrogenation catalysts. and 03-04 are 0.6) 71.7-47.7-39.6-72.9 (33.9-56. 1996).6 (55.

2-49.9 (39.2 (40.4-120) 101 (84.1 (38.0 (80.8) 38.1) 37.7) 75th 63.9-42.2 (52.3) 61.3 (36.2 (37.8) 37.5 (35.2-41.4-76.1-81. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.4 (56. 1995).1 (38.3-46.5) 73.8 (36.4 (67.5-92.9 (64.6-45.5 (38.0 (74.1-43.6 (42.7) 53.1) 65.1 (44.0-38.2) 39. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.9-61.1 (82.4) 61.0-46.5 (50..2 (40.9) 79.7-137) 129 (109-155) 112 (97.3-141) 109 (81.4-106) 85.Metals was 18% of the ingested dose.9 (39.0) 39.6-88.1 (39.0) 39.1-100) 86.5 (65.2-96.4) 44.9) 40.3) 64.8) 71.3-115) 98.6 (36.3-43.2 (36.5) 60.0) 33.5-69.5 (39.6 (71.3 (53. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0-133) 119 (88.8-47.3) 43.3 (37. EPA.0) 72.1 (49.6 (36.2) 37. In industry.8 (75.2 (43.2) 43.4-66.1-45.8 (57.8) 38.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.1-109) 89.5 (41.7-62.8-52.7-40.4) 60. of the ingested dose (Turnlund et al.7-100) 77.6-61.0-46.9 (35.0-56.0 (58.0) 44.3-52.1) 37.4-118) 172 (131-195) 138 (120-163) 118 (106-134) 780 682 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites 228 Fourth National Report on Human Exposure to Environmental Chemicals .4) 116 (101-126) 104 (88.2 (40. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.9-40.5 (40.9-45.5-119) 90.6-63.9) 92.8-47. and urinary levels reflect intake from all sources.3-56.8) 45.5 (37.2-80..7-93.7 (75.3) 56. interval) 43.0) 88.7) 57.7-120) 87.5-50.8-84.7) 42.1 (54.9-71.3 (83.5 (59.2 (69.4-185) 106 (94.2) 38.9 (73.7) 45.5) 90th 108 (97.5-70.6 (57.5 (54.4-107) 85.5) 72. 2001).2-40.1 (33.4 (37.7) 41.5 (36.4) 89.3-68.8-66.5-46.6 (59.8 (37. but available epidemiologic data are scant.6) 48.1) 40.S.8 (56. Based on studies finding adverse reproductive effects in rats and mice.5 (83.1-39.3) 44.3 (58. at daily oral doses of 95 µg and 428 µg.9-118) 91.5-44.2 (33.1-127) 90.0) 62. population from the National Health and Nutrition Examination survey.4 (78.7 (77.6-78.9) 31.2-65.4) 48.1-112) 78.5 (78.8) 62.6) Selected percentiles ( 95% confidence interval) 50th 41.4) 58.5) 63.0-103) 103 (90.4) 40.3) 37.9 (79.9 (40.5 (35.S.1 (37.5 (79. U.3 (55. Biomonitoring Information Molybdenum is an essential element for health.6) 43.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.1 (42.2 (73.3-59.2) 55.5 (65.9-117) 57.3) 57.5 (41.3 (37.0-120) 85.8-67.0) 38.6) 39.1-43. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5 (39.7 (30.5-60.5-45.0-41.2 (50.9 (49.4-41.5 (80.1-41.5 (40. 1997).3 (51.3-45.8 (90.4 (40.3 (36. 1999).2-46.2) 42.2 (57.2) 39.1-39.1) 56.7 (66.2) 37.6-41.5-99.4 (53.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78..7) 62.4-42.3) 40.4-39.2) 42.8-46.3-102) 122 (116-147) 123 (109-139) 118 (101-134) 310 368 290 648 762 725 1299 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 40.0 (35.7) 115 (93.3) 41.3 (71.03 mg/kg/day in humans (IOM.1) 101 (83.8-118) 81.2-121) 107 (92. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.7-43.1-67.5 (34. respectively. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.6 (38.4 (44.1-38.9-96.7-38.5-62.3-44.9) 41. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.8) 79.9-45.4) 77. and clinical or epidemiologic evidence of adverse effects is limited.5 (37.4 (59.1 (30.8-42.7) 112 (95. 1961.9) 44. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.7-44.9 mg/kg/day and established a tolerable upper intake level of 0.2-96.9-41.4) 122 (107-133) 109 (99.9 (64.8) 39.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.5-48.1 (40. urinary excretion over six days rose to 50% and 67%.4 (55.0) 53. 1993).0) 36.9-87.1) 43. Molybdenum is generally considered to be of low human toxicity.4) 47.1-34.6-76.5) 71.2) 58.8-65.1-79.6) 36.5-97.9-68.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.6-61.3 (71.5-35.6) 39.6-63.7-52.9 (36.8) 61.1-40.2-47.

A study of 13 elements in blood and urine of a United Kingdom population. Molybdenum in infancy: methodical investigation of urinary excretion.. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Van Meerbeeck JP. Sabbioni E. Keyes WR. Turnlund JR. Shmavonyan DM. boron. 2005). 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. 16:1313-1319. Third National Report on Human Exposure to Environmental Chemicals. Minoia C. Schaub J. 56:322-327. Rapid Comm Mass Spectrom 2002.S. World Health Organization (WHO). References Centers for Disease Control and Prevention (CDC). Trace element reference values in tissues from inhabitants of the European Union.S.niehs. pp. Schindelin H. silicon. molybdenum. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. pp.216:253-270. chromium. and zinc: a report of the Panel on Micronutrients. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Molybdenum 1993 [online]. Occup Environ Med 1999. iron. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. arsenic. et al. Food and Nutrition Board. 2001.nap. Vermeire PA.php?record_id=10026&page=420. Zhurnal Obshchey Biologii 1961.epa. TR-462. Kisker C. Turci R. White MA. 4/14/09 Iversen BS. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. Sci Total Environ 1998.66:233-267. iodine. 1996.Metals in urine for the U. Sabbioni E. Geneva: WHO. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. 2002. Gatti A. In: Trace elements in human nutrition and health. Available at URL: http://ntp. van Sprundel MP.htm. National Toxicology Program (NTP). vitamin K. Sciarra G. Analyst 1998.15(2-3):149-154.. 1998. Atlanta (GA). Dietary reference intakes for vitamin A. Ann Rev Biochem 1997. Institute of Medicine (IOM). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 4/14/09 White MA. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. Weyler JJ. Occupational risk factors of lung cancer: a hospital based case-control study. Available at URL: http://books. Fourth National Report on Human Exposure to Environmental Chemicals 229 . 2005.. Washington. Ronchi A. White and Sabbioni. Yarovaya GA. 420-441.gov/index. Kristiansen J. EPA). Minoia et al. Available at URL: http://www. Rees DC. Menne C. vanadium. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Am J Clin Nutr 1995.62(4):790-796. 1998). copper. X. Koval’skiy GA. edu/openbook. Schleyerbach U. manganese. 4/14/09 Sievers E. Droste JHJ. nickel.gov/iris/ subst/0425. 144-154.S. J Trace Elem Med Biol 2001. Christensen JM. Peiffer GL.22(3):179-191.123(1):81-85. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces.nih. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. 2001). Environmental Protection Agency (U. excretion. U. Molybdenum absorption. (DC): National Academy Press. Molybdenum. Aprea C.

230 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey years 99-00. copper. 1998).g.Metals Platinum CAS No. cisplatin.04.07. Important properties of platinum are resistance to corrosion. as oxidation catalysts in chemical manufacturing. respectively. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. jewelry. dental alloys. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. and iron. 7440-06-4 General Information Platinum is a silver-gray. which may vary for some chemicals by year and by individual sample. and 0. < LOD means less than the limit of detection.. Platinum compounds are used in electrodes.. and 03-04 are 0.04. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. however. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. and as drugs (e. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. 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. thick-film circuits printed on ceramic substrates. carboplatin) in the treatment of cancer.S. 0. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. and high catalytic activity. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. strength at high temperatures. 01-02.

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

Herr et al. et al. Schierl R. Environ Health Perspect 1975b. Arch Environ Health 2001. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Urinary excretion of platinum from platinum-industry workers. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure.9:152-158.htm. Influences on human internal exposure to environmental platinum. Gieler U. Environ Res 1975a. Schierl et al.04 µg/L) in this Report. Stilianakis NI. Czerczak S. Campbell K.35:313-321. Schierl R.. and platinum. J Expo Anal Environ Epidemiol 2003. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 2000. Grimm CH. Fries HG. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. 2003. Iavicoli I. Schierl R. Biomonitoring Information Urinary platinum levels reflect recent exposure. et al. Herr CE.. Alimonti A. Arch Environ Health:1969. Several studies have shown that background concentrations in general populations were usually less than 0. Moore W Jr. Ensslin AS. Hysell D.10:63-71.. Senofonte O.56(3):283-286. Schulz C. International Journal of Hygiene and Environmental Health 2003. et al. eds. Thornton I. Urinary platinum levels associated with dental gold alloys. Fruhmann G. Patty’s Toxicology. Ruff F: Platinum and platinosis. 232 Fourth National Report on Human Exposure to Environmental Chemicals .org/documents/ehc/ehc/ ehc125. Schierl R.org/documents/ehc/ehc/ehc125. Angerer J. Schulz C. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al.55(2):138-140. 289-380. Biomarkers 1999.123(3):451-454. 1999.inchem. Biomonitoring of traffic police officers exposed to airborne platinum. Hauff K. Farago ME.Metals the International Programme on Chemical Safety at http:// www. Powell CH. Herr et al. Kaus S. Levels of platinum in urine for the U..4(1):27-36. population were below the limit of detection (0.. Kavanagh P. Int Arch Occup Environ Health 2003. 1991 [online]. Seifert B. 2003). 2004). et al. Huber R. 1998). Hysell D. Parrot JL. Wilhelm M. 2004. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine.htm. Int J Hyg Environ Health 2004. Kuster W. 3/31/08 Moore W Jr.. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Boos KS. Analyst 1998. Cohrssen B.. palladium. Hebert R. Saindelle A. Wilhelm et al. In: Bingham E. 2001). Crocker W. Bocca B. Platinum. 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. 1997. 2003. Rommelt H. Carelli G.inchem. Ewers U. Jankofsky M. Petrucci F.76(1):5-10..207(1):69-73. Hall L. pp. Pethran A. Kelly J. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Environmental Health Criteria 125. and in blood and urine in the United Kingdom. and gold excretion of patients after insertion of noble-metal dental alloys. 206:15-24. New York: John Wiley & Sons. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. 1998). Begerow J. Pethran et al.005 µg/L (Iavicoli et al.19:685-691. which elevate urinary platinum by five to twelve-fold (Begerow et al.. Pethran A. Seiwert M. Available at URL: http://www. Turfeld M. Occup Environ Med 2004. 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. Platinum concentrations in urban road dust and soil.13(1):24-30.61(7):636-9. rhodium. Gromiec JP. Ruff F: Histamine release by sodium cholorplatinate. 2004) or less than 0. 5th ed. palladium. Br J Pharmacol 1969. Kulka U. van de Weyer C. Saindelle A. ruthenium. Occup Environ Med 1998. Kazantzis G..S. Part 1: monitoring of urinary concentrations. 2003. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Raab W.01 µg/L (Becker et al. Blanks R. Duneman L:Long-term urinary platinum. Allergy and histamine release due to some platinum salts. International Programme on Chemical Safety (IPCS). Schierl.70(3):205-208. References Becker K. Nickel. Uptake of antineoplastic agents in pharmacy and hospital personnel. Nowak D. Neuendorf J. osmium. Int Arch Occup Environ Health 1997.

135-.330-.200 (.400-.171 (.270 (.165 (.290) .243) .150-.. and 03-04 are 0.300) .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 .350-.340) .420) .470) .420) .160 (.170) .320) .170 (.290 (.310 (.400) .180-.390) .330) .500 (.167 (.310 (.172 (.250) .140-.200) .360 (.220) .230) .220) .410-.149 (.260-.330-. interval) .440 (.300 (.280 (.154-.340-.330-.190 (.180-.188) .250-.240) .330-.350-.480) .290) .146 (.330-.260 (.290) 90th .430-.430 (.430-.190 (.182-.240-.390-.270-.480) .160-.230-.290 (.300) .159 (.270) .190 (.430 (.400 (.180 (.160-. In the United States. 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. From these and other sources.270 (.340) .218) .172 (.156-.430 (.310) .410-.330-.480) .230-.450) . 2005).420-.133-.220 (.290 (.440) .410 (.400 (.145-.217 (.420) .200-.170-.450 (.490) Total . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.160 (.300) .200-.450 (.430 (.290 (.280 (.178) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.410) .420-.153-.390) .510) .191 (.201 (.520) .350-.179-.170 (.170-.320) .420) .190 (.176 (.400) .270 (.183) .250 (. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.210) .196) .159 (.200 (.270-.460) .370-.196) .400-.160-.340-.206) .202 (.240-.440 (.380 (.440) .183) .480) .185 (.420 (.360-.Metals Thallium depilatory cosmetics.330) .350 (.400 (.175) .500) .260-.197-.420) .220) .410-.172) .230-.440 (.370) .410 (.201 (.170-.390-.190-.160 (.150-.240) .400 (.220) . see Data Analysis section) for Survey years 99-00.320-.430) .160-.158) .220) .137-.02.390 (.200 (.370-.162-.173) .170) .192) Selected percentiles ( 95% confidence interval) 50th .480) .147-.410 (.280) .420) .300-. population from the National Health and Nutrition Examination Survey.180-.157-.240-.330) .02.200) .185-. Fourth National Report on Human Exposure to Environmental Chemicals 233 .167-.200) .250 (.290 (.200) .270) .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 .410-.470) .450 (.300) .200-.155 (.230 (.450 (.290-.200-. representing distribution into other tissues.490) .290 (.230) .430) .239) .360) .180 (.150-.270-.220 (.370 (.590) .500) .220 (.173) .330) .147-.330-. 0.280 (.370) .350 (.170) .380-.380 (. In the past. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.400-.370 (.420-.250-.470) .202 (.410-.230) .450 (.150-.163) . thallium readily crosses the placenta and also distributes into breast milk.250-.280) .156) .215) .150-.250-. the latter being the current major industrial consumer of thallium in this country.390-.210 (.370 (.260-.200 (.350-.400 (.225) .134-.218) .180-.400) 95th .420-.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 .184 (.270 (.260-.370-.360 (.147-.400) .310 (. respectively. In addition.520) .220-.250-.280-.390) .450 (.180 (.360-.170-.173-.156) .450 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.180) .400) .160 (.360 (.340-.470 (.290-.180) 75th .420) .145 (.250-.490 (.340-.210 (.220) .510 (.450 (.460 (.320) .177) .360 (.370 (.410 (.560) .590) .390) .350-.148-.217) .210-.160-.460-.230) .260 (.430-.440 (.220 (.410-. and 0.202) .280) .290) .360-.144 (. Human health effects from thallium at low environmental CAS No.490) . 01-02.360-.340 (.450 (.370 (. it has not been specifically mined or refined in the United States since 1984.197 (.170-.160 (.350-.360-.240) .300 (.170-.690) .290) .550 (.190 (.145-.S.470 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.159 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.200 (.310-.400-.370-.170 (.380-.520 (.200 (. thallium was obtained as a by-product of smelting other metals.320 (.410 (.190 (.260) .02.280-.170-.300 (.640) .181-.490) .520) .260-.250-.220 (.380) .167-.390-.400-.187-.270 (.350) .350) .370 (.370 (.150-.260 (. however.200) .440) .390 (.200) .410 (.500) .630) .250-. Thallium disappears from the blood with a half-life of several days.440-.

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

Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect.5 μg/L. 1992 [online]. et al. Available at URL: http://www. Valentin H.atsdr. Sci Total Environ 1990. with concentrations ranging up to 76. 1998). 7/15/09 Blanchardon E. and serum of Italian subjects.. Int Arch Occup Environ Health 1981. Sci Total Environ 1998. blood.Metals (CDC. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. 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.216:253-270. Schmidt M. Radiat Prot Dosim. 2005. 1990. Pirkle JL. Paschal DC.48(4):375-389. Schaller et al. Kramer U. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Fourth National Report on Human Exposure to Environmental Chemicals 235 .gov/toxprofiles/tp54. Atlanta (GA). Schaller KH. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium.265 people living near a thallium-emitting cement plant in Germany. Celier D.76(1):53-59. Centers for Disease Control and Prevention. et al. Pozzoli L. Third National Report on Human Exposure to Environmental Chemicals. 1980. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Minoia et al. Investigation of a working population exposed to thallium. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust.. References Agency for Toxic Substances and Disease Registry (ATSDR). White and Sabbioni. X. Brockhaus A.113(1):47-53. 2005) and are shown with results from NHANES 2003-2004 in this Report. Investigations of thallium-exposed workers in cement factories. A study of 46 elements in urine. Challeton-de Vathaire C. 1998. Minoia C. Ewers U. White MA. Manke G. Boisson P. Cassot G. Marcus RL. 2005. Buhlmeyer G. Trace element reference values in tissues from inhabitants of the European Union. Sampson EJ. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Trace element reference values in tissues from inhabitants of the European community I. Sabbioni E. Soddemann H. Jackson RJ.35(1):4-9. Dolger R.cdc. Gallorini M. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. A study of 13 elements in blood and urine of a United Kingdom population. Sabbioni E. Pietra R.html.. Trace metals in urine of United States residents: reference range concentrations. Brockhaus et al. Ting BG. Environ Res 1998. et al. Apostoli P. Martin J-C. Morrow JC. 1985).1 mg/m3 (Marcus.S. Biomonitoring studies on levels of thallium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of thallium than are found in the general population. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Wiegand H. 1981..47(3):223-231. Paschal et al. Int Arch Occup Environ Health 1980.95:89-105. (1981) studied 1. Toxicological profile for thallium. J Soc Occup Med 1985. Raithel HJ.

190 (.350) .230) .400-.130-.430-.151) .490 (.120) .073 (.190 (.330) .100) .070-.520) .210 (.160) .056-.084 (.082) .170) . 0.170) .060 (.050-.120-.093) .290-.116) .140 (.510-1.090-.133) .076 (.430 (.250) .300) 95th .060-.380-. Occupational exposure is from dusts released during grinding or drilling of hard metals.086 (.135) . bronzes in pigments.360 (. interval) .470) .078-.160 (.250) .092 (.105) .310-.090-.097-.160 (.430-.140) 90th .490) .113 (.093 (.300 (.400 (.420-.310 (.080 (. and as catalysts in the petroleum industry.060-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.120-.180) .400 (.220) .640 (.120-.110 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.130-.060-.53) .060-.090-.111-.460) .460 (.250) . and for producing ferrotungsten.062 (.110) .410-.Metals Tungsten CAS No.260-.200 (.530 (.120) .360 (.105 (.260-.190-.123-.150) .430 (.110 (.360 (.580) .270-.120) .440) .410 (.380-.230-.120-.084) .510-.650) .180) .320 (.200) .050-.070 (.170-.280-.400 (.064-.340-.370) .380) .180-.095-.190) .093-.290-.500) .062 (.310-.290-.160 (.110 (.060-.088 (.070) .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 . see Data Analysis section) for Survey years 99-00.090 (.100-.090-. 236 Fourth National Report on Human Exposure to Environmental Chemicals .050-.180 (.500 (.170 (.080-.280 (.113 (.310-.510 (.560) .320 (.120 (.101 (.090 (.070) .260) .113 (.090) .380-.110) .310-.360) .080) .330) .190-.070 (.100) Selected percentiles ( 95% confidence interval) 50th .100 (.470 (.450 (.180-.400 (.073-.170 (.130) .101-.180 (.140 (.126) .690) .087-.530 (.092) .470 (.065 (.250-.060 (.520) .130) .140 (.060 (.071 (.074-.122) .260-.800) .00) .140 (.430) .310) .170) .260 (.300-.340-.150 (.080 (.130) .460) .084-.160-.100-.470) .380-.210-.070 (.150 (.140-.109) .400) .080 (.070-.070) .082-.076 (.230 (.120) . which are used in rock drills and metal-cutting tools.056-.550 (.180-.360-.800) .091) .320-.670) .060 (. respectively.310-.090-.370 (.073-.100 (.190-. 01-02.158 (.110 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).210) .100) . and it has not been classified with respect to its carcinogenicity by either IARC or NTP.550) .160-.150 (.240-.520) .270-.090 (.830) .068) .066-.220 (.220) .230-.300 (.210 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.132) .130-.170) .390 (.620 (.530 (.300 (.180) .370-. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.370 (.104) .204) .080 (.110-. Little information is available on the toxicity of tungsten.04.230-.100) .080 (.100-.073) .460 (.770 (.080) 75th .350) .095-.071-. mainly as scheelite (CaWO4).090-.370 (.570 (.096-.220) .160 (.210 (.280 (.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 .137 (.160-.100 (.480) Total .04.230) .350) .065-.230-.140-.350 (.810) .360-.340-.550) .270-.160 (.120-.560 (.060 (.130 (.240 (.160-.090) .060-.110 (.080-.090-.350-1. which is used in the steel industry.130 (.620) .290) . and 0. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.200-.330-.380 (. filaments for incandescent lamps.080) .320-.630) .04.390) .560) .130) .069) .100) .120) .180) .250) .290 (.090) .560) .950) .370-.070-.420-.340) .092 (.082 (.260 (.113 (.087) .130) .290) .270-.080-.430 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.S. Tungsten compounds are used as lubricating agents.100 (.190-.130-.180-.330 (.077-.270 (.090) .096 (.450-.120-.460 (.380 (.590) .110-.270 (.470-.300) .270 (.790) .570 (.250) .250-.081 (. Evidence is lacking for the carcinogenicity of tungsten.100) .210 (.500 (. population from the National Health and Nutrition Examination Survey.110-.069-.120) .070-. and 03-04 are 0.460) 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 .560) .050-.150-.070) . Tungsten is used mainly for producing hard metals.080) .107 (.550) .250) .058-.220-.330-.070-.088) .620) .160) .090-.082 (.060 (.210 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.320) .

465) .091) .055-.326) .287) .500) .083) .120) .167) .317-.088) .150 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.133) . Patients with medically-inserted tungsten found at increased levels in drinking water.151 (.136-.116 (.065-.094) .088) .121-.081 (.538) .174) .122-.S.203-.353 (.074-.057-.061-.293 (.222-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.067-.333) .089 (.245-.100) .150-.125) .255-.176-.071-.267) . 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.148) .133) 90th .317 (.098-.146) .181 (.739) .158) .197) .186 (.122 (.063-.300-.462) .063-.301) .077-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH. or exposure that a control group of non-metal workers had mean levels differences.060-.136-.179-.275 (.085 (.085-.667 (.067 (. similar to those in this Report (Schramel et al.095) Selected percentiles ( 95% confidence interval) 50th .068 (. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.139) .090-.078-.. 2003.379 (.065 (.667) .198-..150-.354) .053-.605) .066 (. (1987) found possibly due to methodologic.261-.279 (.065) .554) .133) . 2005).414) .174 (.098 (.062 (.071) .634 (.253-.301) .100 (.333 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.190) .074 (. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.079) .079 (.216-.201) .197) .300 (.214-.105 (.333 (.582) .079) .063 (.217-.119 (.170-.306) .727) .148 (.267-.484 (.205-.439) Total .079 (.439 (.167-.265 (.075) .071 (.071 (.099-.075) .154) .138 (.144-.091) .385 (.333-.272-.090-.063-.077-.091 (.375) .459) .071) . 2001-2002.103-.285) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.250 (.188-.061-.098-.283) .068-.056-.797) .216 (.359 (.084 (.091 (.176-.197-.302-.083) .109-.094) .216-.144 (.231 (.161) . and 2003-2004 (Paschal et al. 1998).152-.198) .880) .084 (.279 (.131-.299 (.075 (.360 (.065-.168 (.049-.075-.329 (.058-.078) .108-.130 (.331-.184 (.079) .224) .071) .057-.308) .138) .083 (.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 .237) .078 (.071 (.078 (.136-..075-.120) .218 (.482 (.(Kraus et al.214) .353 (.074) 75th .286-.317) .199 (.080 (.080-.136-.125 (.124-.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 .078) .164 (.484) .064-.465) .070 (.116) .157) .284) .075 (.300) .383 (.329-.410-.333) .126-.392) .065-.555 (. population from the National Health and Nutrition Examination Survey.081 (.096) .436-1.158) .426) .S.347 (.139 (.153-.136 (.080 (.073 (.067 (.216-.143 (.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 .056-.179-.497 (.054-.086) .060-.250 (.253 (.344-.059-.081) .215 (.079) .341 (.091) . population (CDC.082) .431) .060 (.237) .370) 320 363 290 679 744 725 1339 1544 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .217-.086-.169 (.155-.359 (. interval) .073 (.200-.823) .086) .083-.199 (.146 (.255 (.124 (.077) .130-.072 (.084) .278-.240-.258 (. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.197 (.119-.104-.200-.094-.083 (.354-.209-.302-.106 (.064-.092) .073 (.169) .439 (.180-.100) .386) .116-.339 (.109 (.333-.059-.059-.222) .167) .065 (.154) .138 (.081-.412 (.308) .059 (.091) .085) .158 (.098-.107-.074) .231-.453) . Nicolaou et al.117) .315-.143-.237-.233-.258-.206-.270 (.145 (.082) .086) .201 (.069-.340 (.364 (. 2001).426) .333 (.250-.098) .054-.122-.095-.253) 95th .187) .069 (.070 (.333 (.108) .294 (.093) .431) . Using neutron activation analysis to 2000.139-.431) .158) .28) .165) .S.087) . 1997).300-.061-.121 (.093-.072-.167-. measure urinary tungsten.069 (.358) .279 (.153) .080-.339 (.111 (.084) .074-.089) .301) .215) .082 (.208-.063 (.381) .146 (.072-. population.117 (.077) .063-.211 (.073 (.087 (.216 (.105 (.255 (.066 (.452-.436) .

Pietra R. Angerer J. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. 4/15/09 Centers for Disease Control and Prevention. mercury. urine. Paschal DC. Int Arch Occup Environ Health 1997. platinum.58(10):631-634. tellurium.cdc. Pirkle JL. Schramel P. The determination of metals (antimony. 238 Fourth National Report on Human Exposure to Environmental Chemicals . Cassina G. 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. Atlanta (GA). Schramel P.htm. Centers for Disease Control and Prevention. Zobelein P. Weber A. References Bachthaler M. Ting BG. Nevada Exposure Asssessment. Wendler I. Paetzel C. palladium. Manke C. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. lead.Metals blood. 2005.76(1):53-59. 2004). Sampson EJ. Seghizzi P. Trace metals in urine of United States residents: reference range concentrations. bismuth. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. and hair (Bachthaler et al. Sabioni E.62:380-384. Lenhart M. thallium. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Churchill County (Fallon).(2):73-77. cadmium. Nicolaou G. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Catheter Cardiovasc Interv 2004. Jackson RJ. Mosconi G. Occup Environ Med 2001. J Trace Elem Electrolytes Health Dis 1987.gov/nceh/clusters/Fallon/study.. Kraus T.69(3):219-223. Feuerbach S. Schaller KH. Link J. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. Available at URL: http://www. et al. [online] 2003. Angerer J. Environ Res 1998. National Center for Environmental Health. Morrow JC. Cancer Clusters. Third National Report on Human Exposure to Environmental Chemicals.

063) .006-.011) .013 (.006-.023) .065) .008 (.055 (.006 (.024 (.009-.026 (.017-.013 (.006 (.010) * .011-.067) .040) .007-.088) .127) .017-.017-.007 (.027 (.016) .022-.013) 90th .010) .018) .010-.041 (.005-.158) .021 (.007 (.006-.037) .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 .033 (. interval) .007 (.008 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.006-.010) * .011) .009 (.008) .037) .064 (. and 0.048) .008 (.011-.020 (.007 (.013) .031 (.027 (. nuclear fuel.040) .005-.029 (.006-. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks. Since the 1990’s.007-.016) .019-.014 (.027) .054) .051) .017) .009 (.021-.028 (. 0.037) .011) .005-.007-.007) .065) .067) .017) .010 (.010) .050) .006-.028 (.009 (.008) Sample size 2464 2690 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 . In workplaces that involve uranium mining.011) .018-.030-.039) .020-.052 (.045) .012-.021 (.007 (.012) . or processing.010 (.006 (.007-.022-.046-.015) .011 (.023-.021) .009) .006-.012 (.011) .069) .027) .031 (.008-.027 (.015 (.031-.009) .054-.007-.026 (.005-.044 (.009 (.007) .008) .038 (.008 (.042) .008 (. see Data Analysis section) for Survey years 99-00.017 (.022-.011-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.007-.036-.013-.009) .011 (.030 (.010) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.009) .017-.026) 95th .056) .026) .007 (.015 (.010-.009 (.012-. 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. 235U (about 0.008 (.009) * .010) .016) .006 (.033) .046 (.062) .016-.021) .030 (.013 (.036) .023-.031 (.010-.011) .036 (.023 (.010) .S.014 (.008) .007-.017) .043) .030 (.027-.034-.020-. and 234U. respectively.012 (.035) .007) .020-.010) .023-.007-.008 (.023) .006-.019-.035-.009 (. 01-02.023 (. human exposure occurs primarily by inhaling dust and other small particles.009 (.009) Selected percentiles ( 95% confidence interval) 50th .028 (.015 (.014 (.011-. milling.040-.010) . population from the National Health and Nutrition Examination Survey.026 (.009-. in some ceramics.012 (.028-.009) .032 (.007 (.045) .048 (.012-.023 (.013 (.007) .011-.035) .027-.019 (.017) .008 (.016) .020) .039) .016-.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.72%). Variable concentrations of uranium occur naturally in drinking water sources.026-.016) .008-.036-.040 (. Thus.015-.012-.008-.027) .006-.030) .028-.012 (.013 (.046 (.014 (.020) .009) .007-.072) .014 (.019-.008 (.013 (.010 (.012-.010) .009 (.009) .024-.007-.009-.006-.006-.021 (.040-.046) .053 (.007-.012) .007-.015) .009 (.008-.007-.005.027) .016-.279) .008-.010-.049) .027 (.007 (.029-.018 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.031 (. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.008 (.114 (.008 (.007-.050) .008 (.026) .060 (.034) .037-.Metals Uranium CAS No.054) .007) 75th .042 (.005-.026-.012-.020-.043 (.031 (. including nuclear weapons.007-.022) .009) .008 (.008 (.014 (.018) .008-.011-.023) .009) .009-. and as an aid in electron microscopy and photography. Fourth National Report on Human Exposure to Environmental Chemicals 239 .007 (.039-.010-.037 (.008) .015 (.007) .019-.009) .017) .008 (.025-. and 03-04 are 0.046 (.008) .009-.034-.011) .021-. Uranium has many commercial uses.010-.013-.006-.012 (.013 (.007 (.004.021) .023-.018) .009-.004.024-.017-.017 (.012) .066) .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 .006-.008 (.018) .009 (.008 (.012 (.009-.036 (.008-.020-.038) .010 (.017-.009) . 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.027-.040 (.053) .007-.024-.009-.007-.073) .016 (.009-.013-.009) . Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).009) .018 (.036) .056) .010 (.046 (.011-.007-.016) .029-.009-.033 (.033-.008-.037) Total .049) .041 (.012) .047 (.022 (.007 (.

1%-6% of an ingested dose may be absorbed.009 (.009-.008 (.014-.008) .016) . the shrapnel acts as a source of chronic.010) .007 (. where limited absorption occurs (less than 5%). Uranium is eliminated in feces and urine.019) .016-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.019-.014) 90th .020-.011-.027 (.006-.016-.006 (.033 (.016) .032) .011-.008-.056) .011) .010 (.020) .013 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.007 (.009 (.023-.015-.006-.Metals impact.010 (.019 (. Inhaled uranium-containing particles are retained in the lungs.022-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. After inhalation.025 (.006 (.074) .045 (.007 (.007) .008 (.006) .025-.011-.033 (.005-.027-.034 (.034-.018-.016) .026 (.010) .029) .024-.006-.005-.020 (.011 (.029) .017) .030) .028) .010) * .017-.013 (.010 (.042) .009) * .008 (.008 (.024) .006-.008) Sample size 2464 2689 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .034 (.008) .018-.015-.011 (.006-.027-.009) .009) .009-.021 (.006-.008) .039) .011-.020-.014 (.024) .034) .010 (.058) .007 (.041) .033 (. which can occur occasionally from high occupational exposure.031 (.020-.029) .024 (.016) .039) .047) .018-. In cases of retained DU shrapnel.006-.008-.015 (.011-.007 (.011-.016) .013 (.043 (.030 (. interval) .019-.006) .033) .007 (.006-.017-.007-.032) .013 (.063) .006 (.010-.006-.012 (.009) .050) .007 (.007-.006-.048) .015-.027 (.051 (.020 (.028) .014-.009-.021-.028) .020 (.019-.018-.006) .014) .007 (.010-. After exposure to soluble uranium salts.019) . 2005).012 (.019-.008 (.022) .033 (.044) .005-. Depending upon the specific compound and solubility.025-.015) .042-.008) .050) .067) .011-.013) .013 (.006-.009) .022 (. After long term or repeated exposure.012) .019-.029 (.042) .034 (.025-.054) .006-.008 (.007 (.013) .014-.012 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.025 (.007 (.009) .008) .006 (.007 (. which represents distribution and excretion. liver.013 (.006-.012) .012 (.080) .015) .007-. kidneys.030-.016) .014) .028 (.030 (.027-.010-.015-.006-.015-.048) .006-.010-.006) .100 (.009 (.008-.024 (.007-.006-.007 (.021 (.015 (.022 (.034 (.008) .009) .006-.013 (.009) .017 (.146) .010 (.015 (.017) .021) .007-.010-.008-.005 (.008 (.016) .013-.011) .051) .029) . the initial half-life of uranium is about 15 days (Bhattacharyya et al. Health effects from uranium exposure result from chemical toxicity to the kidney.009-.012-.009) Selected percentiles ( 95% confidence interval) 50th .016-.009) .021 (.013 (.007 (.016-.008) .020-.019 (.026) .005-.007-.017 (.008 (.008-.008) .010) ..035 (.053) .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.030) .024-. 0.029 (.010-.035 (.039) Total . and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.006-.007 (.050 (.027-.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 .011) * .008) .030 (.008-.012 (.010-..007 (.040 (.016 (.005 (.006-.006) .027) .006-.012) .024) .016) .006-.014) .270) .007 (.007) .015) .013 (. 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.007 (.041) 1227 1334 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 . low level exposure.015) .010) . 240 Fourth National Report on Human Exposure to Environmental Chemicals .010-.007 (.018 (. with much slower elimination from bone.027 (.011-.005 (.025-.026 (.008) .051) .030-.017) .039) .008) 75th .009-.006-.022-.061) .005 (. Radiation risks from exposure to natural uranium are very low.024) .004-.008) .053) .031-.018) .029 (.034 (. 2003).009 (.009) .007 (.027) .007) .012 (.S.012 (.007-.007 (.018-.009) .026-.011) .013 (.059 (.004-.010-.010-.011-.010-.005-.008 (.006-. population from the National Health and Nutrition Examination Survey.021 (.007-.028-.013) .077) .010) .006 (.017-.024-.017-.015 (.037 (.019 (.009) .012-.028) .006 (.051) .022 (.005-..007-.007 (.026 (.007-.028 (.005-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.006-.025) 95th .024 (. 1992).008 (.009-.014 (.009 (.058) .010) .024) .034-.022-.

Radiation protection dosimetry. Byrne AR. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. In 17 U. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Zimmerman I. Squibb K. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. McDiarmid et al. et al. Komaromy-Hiller et al.. (May et al. Information about external exposure (i.. soldiers evaluated before.. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. Karpas et al. eds. In a study of 105 persons exposed to natural uranium in well water. and 2003-2004 (Dang et al. in that the levels were below their respective detection limits (Byrne et al. IARC and NTP have no ratings for uranium human carcinogenicity. Mil Med 2003. Centers for Disease Control and Prevention (CDC).. respectively. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U.. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. 2002). 1978). Muggenburg BA.cdc. 1994. 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.110 to 45 μg/L (Ejnik et al. Atlanta (GA). and no consistent effects on multiple endpoints of kidney function were found. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. 2002.1996. 2006). Galletti.62:562-566. but in whom no shrapnel was embedded. the median urinary concentration was 0. ingestion. 28 soldiers who may have been exposed to DU by inhalation. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.65 μg/L). McDiarmid M. the geometric mean urinary uranium concentration was 0. In: Gerber GB.S.. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Durakovic A. Breitenstein BD. population.. 2000).. Metivier H.168(8):600-605. Drinking water and other environmental standards have been established by U.1992.gov/ toxpro2. Dietz LA.S. during.107:143-157. 2006). Tolmachev et al. 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. 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. Health Phys 2000... 2004). Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.078 μg/L (ranging up to 5.. with emphasis on quality control. 2006. Fourth National Report on Human Exposure to Environmental Chemicals 241 . NRC. Health Phys 1992. Benedik L. Carmichael AJ. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000.. 2000). 2004). EPA. Dang HS. 2005.. environmental levels) and health effects is available from ATSDR at: http://www. Pullat VR. Hamilton MM. or wound contamination..Metals injury associated with elevated urinary uranium levels (Kurttio et al. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. In the same study. Thomas RG.S. 1991. Volf V. pp. 2001-2002.S. Guidebook for the treatment of accidental internal radionuclide contamination of workers... Boyd P. References Bhattacharyya MH.S. 2004). Vol. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Third National Report on Human Exposure to Environmental Chemicals. (Kurttio et al. 2004). Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U.61 μg/g creatinine. Horan P. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. 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. Six workers in a depleted uranium program showed concentrations of 0. although slightly increased during and after deployment. Pillai KC.S. 2006). the median urinary uranium concentration was 2. Stradling GN. Sci Total Environ 1991.78:143-146. 1992.066 μg/g creatinine (Gwiazda et al.162 μg/L) (Orloff et al. A cohort of 46 U.e. 2003. Hamilton et al.html. Kent (England): Nuclear Technology Publishing. Uranium content of blood..atsdr.. 2006). 41 (1). Ejnik JW.011 μg/L (McDiarmid et al. had a mean urinary uranium concentration of 0. 1-49.55 μg/L (median 0. urinary levels of uranium were as high as 9. The U.

NRC). Saha H. Review of elements in blood.110(4):337-342. Pekkanen J. Li WB. Costa R.91(2):144-153.94:319-326.82(4): 527-532.86:12-18. Saha H. Howerton K. Health Phys 2004. July 1978. Kurttio P. Andrews WS.22–Bioassay at uranium mills. Oliver M. Marko R. Biologic monitoring for urinary uranium in Gulf War I veterans. Renal effects of uranium in drinking water. Van der Venne MT. Harmionen A. Environ Health Perspect 2002. Jackson RJ. Pirkle JL.S. D’Annibale L. Kurttio P. Kuwabara J. Metcalf S. Roth P. Health Phys 2002.44:29-40. Auvinen A. et al. Hollriegl V. McDiarmid M. Jarrett JM. J Toxicol Environ Health A 2004. Hamilton EI. Cremisini C. Lewis BM. Lorber A. Wahl W. Shelly T. Am J Kidney Dis 2006. Washington (DC): NRC. Kidney toxicity of ingested uranium from drinking water. Environ Res 1999. Smith D. Oberbroekling KJ. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Ough EA. concentration and daily excretion of uranium in urine of Japanese. Ting BG.S. Karpas Z.47(6):972-982. patient population and literature reference intervals for urinary trace elements. Salonen L. McDiarmid MA. Human exposure to uranium in groundwater. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Health Phys 2006. Health Phys 1996. Roiz J. Uranium and thorium in urine of United States residents: reference range concentrations. Mistry K. Sci Total Environ 1994. Ejnik J. Nuclear Regulatory Commission (U. Engelhardt SM. Komulainen H. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Karpas Z. U.296(1-2):71-90. McDiarmid MA. Gucer P. Makelainen I. et al. Gwiazda RH. Element reference values in tissues from inhabitants of the European community. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Kalinsky V. Charp P. Inductively coupled plasma mass spectrometry as a simple. Health Phys 2004.87:51-56. Paretzke HG. Salonen L.S. et al.158:165-190. Halicz L. Uranium daily intake and urinary excretion: a preliminary study in Italy. Pinto V.81:45-51. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Tolmachev S.Metals Galletti M. Heller J. Paschal DC. Environ Res 2004. Oeh U. Squibb K.71(6):879-85. et al. Auvinen A. Sabbioni E. Cordero S.S. VI. rapid. Katorza E. Int Arch Occup Environ Health 2006. Radiat Environ Biophys 2005. Orloff KG. et al. Englehardt SA. et al. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF.79(1):11-21.67(8-10):697-714. Nuclear Regulatory Commission (NRC) Guide 8. Clin Chim Acta 2000. Marino R.85:228-235. Wilson PD. Hancock RG. Scott K. Health Phys 2003. U. Bennett LG. Sampson EJ. Squibb K. Komaromy-Hiller G. Ash KO. Biokinetic modeling of uranium in man after injection and ingestion. May LM. Comparison of representative ranges based on U. Noguchi H. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Kane R.

0 (9.40) 3. lettuce) can be the main sources of intake for humans (FDA.10 (6.40-7.80) 7.30) 6.10) 5. population from the National Health and Nutrition Examination Survey.00-5.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.74-3.0) 13.40 (4.90-11. 2002).0 (11.90 (3.20) 7.0 (9.0 (11.0-23.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.75-3.0-17.50) 5.EPA.0) 11.40) 4.10-11. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.0 (9.05.90-11. 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.80 (3.0 (11.0) 15.10-11. Perchlorate is stable under most environmental and physiological conditions.20 (4.50-4.93-3.20 (8.50-11.0) 14.90-3.90) 5.67-5.0 (8. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.16) 3.10 (6.60 (4.0-17.22 (2.20 (2.65) 3.50 (5. 2005).30-17.40-4.0 (8.0-18.70 (3.10 (5.70-12.81) Selected percentiles ( 95% confidence interval) 50th 3.0 (9.31) 2.0) 9.40 (8.10) 3.00) 5.80-12.20) 3.40) 6.00) 3.0 (12.90 (5.20 (2.0) 9. or ammonium salt. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.03) 3.62 (3.0) 12.30-7. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.0-19. It is normally found and produced as the anion of a sodium.44-4.38) 5.01 (2.84) 14.11) 3.0 (11.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.S.20-4.70-11.29-3.0) 11.40) 2.12) 3.20) 4.0 (12. potassium.0-18.0) 15.08-3.0) 95th 14.50) 11.50 (3.0 (8.0) 13.0-15. leather tanning.05 (2.76) 4. matches.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.0) 13.0) 8.51 (3.30 (5.20-4.88) 3.00-6. but has strong oxidant properties in the presence of concentrated acids. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7..90-9.90 (4.60) 5.60-6.0) 9.0 (11. fabric dyeing.40-11. certain catalytic metals.18-3.0) 19.0) 9.70-5.70-9.10-12.50-3.76 (3.80-6.60) 3.50-4.70) 3. and electroplating. 2007). and limited applications in pharmaceutics.0 (11. laboratory analysis.20-3.30-19. and reducing agents.0) 14.79 (2.0) 16.0-29.0-17.66) 3.40-5.30-7. 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.0-14.90-3.0 (9.30) 6.87-3.30 (5.00) 7.07-4.80 (3.0 (11.70 (3.g.00-6..96 (3.0 (9.47-4.90) 6.60-7.90-9.46) 3.40) 3. Survey years 01-02 03-04 Geometric mean (95% conf. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism. In addition.80-4.80) 12.20 (4.0 (8.26 (2.80) 75th 6.75 (3.50) 3.56) 3.09) 3.30-6.80-4.89-3.70-3.70-7. Perchlorate was added to the U.0-18.0 (11. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.90-10.11) 4.90 (2.10 (7.35 (3.0) 8.90-12.70-3.0) 13. 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. and certain plants with high water content (e.10-4.05 and 0.5 hours and has a small estimated volume of distribution (Crump and Gibbs.00) 3.0 (12.0-17.0 (10.0) 10. interval) 3. milk. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 . Other manufactured uses include fireworks. 2005).45-4.S.50-7.40) 3.20 (5.20 (6.40-6.21 (2.80-15.60 (7.Perchlorate Perchlorate (Urbansky.81-16.93-4.0) 9.0 (13.51 (3.40 (4.39-4.0) 13.90 (5.68) 4.30 (2.20-12.20-11.80) 3.10) 12.32 (3.90 (5.0-17.0 (8.40 (5.00) 4.0) 11.40 (5.50) 6.0-20.0 (12.80-8.20 (7.93 (4.40 (5.0-17.0-15.19 (3.0) 10.70-6.54 (3.50) 5.0 (9.S.49-3.0) 9. 1998).10 (2.70 (3.0) 10.40 (3.60) 8.50 (8.19-4.30 (2.80 (7.40) 90th 10.22-5.02 (3.40-4.0) 13.10) 3.60 (4.40 (3.90-6.0) 708 617 681 652 1228 1092 Limit of detection (LOD.40-13.0) 14. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.10-7.10) 5.0 (11.0 (11.80 (6.0) 13.0) 13. Drinking water.

04-3.25 (3.33 (7. 2000).39) 2. During gestation and infancy.60-15.87-3.58) 2.74) 7.20) 3.75) 3.30) 3.0) 11.70-3. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.37 (4. menopausal status.90 (7.60) 10.3) 11.66) 3.EPA.83 (5.44-6.45-2.77 (3.0-44. 2007).76 (3.3) 12.22-6.4 (11.10) 13. Survey years 01-02 03-04 Geometric mean (95% conf.30-5.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3. Many factors may be important in consideration of perchlorate action on the thyroid: dose.30) 75th 5.80) Selected percentiles ( 95% confidence interval) 50th 3.80 (7. medications).96) 2.93-8.46 (3.20-3.70-5..87 (7. population from the National Health and Nutrition Examination Survey.30 (3..90-9.22-4. chronicity of exposure. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.12 (6.39-4.35 (4.64-3.29-6.60-5.70-4.30-10.50 (3.25) 5.00 (6.25) 5.90) 5.40) 17.43) 6.10 (1. 2003.10 (4.3) 8.56 (3.51 (3.90 (2. 2002.0-14.70) 10.07 (2.15-12.10 (6.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3. 2001.20-3.61 (5.60-3.S.60-5. 2002. 2005).g.70 (4.3-14.61-10. perchlorate is negative in most genotoxic assays (U.40 (4.40) 3.10) 6.EPA.S.6) 12.80 (4.99 (5. up to 68% RUI has been demonstrated.90-15. levels and sufficient in most participants (Tellez et al.87) 2.12-2.0 (11.0) 13.60) 3.09 (7. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al..26 (3.34-3.60-11.46-4.40 (3.33-12.0) 12.93-5. Lawrence et al.0) 9.2) 8.40-10.97-5..45) 3.0 (9.18-3.4-16.0) 6.0) 12.20 (3.41-9. 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.90-3.0-14. in a representative sample of U.26) 4.51-4.4) 13.93) 3.56-3.10) 3.00 (2.52 (8.67) 5.20 (4.60-8.59) 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.1 (11..81-3.00-3.44) 3.90-20.0 (8.35 (2.50) 6.0) 9.19-10.80-3.0) 10.60) 8.89 (2.02-4.54 (3.90 (2.20-9.61-5.08 (3.60-11.76-3.30) 5.87) 7.30-5.0 (10..90-11.S.24 (4.37-13.22-4.21 (2. 2005).09) 3.00) 4.70-15. Li et al.53 (2. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.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 . 2002).22 (2.10 (4.95 (2.04-3.S. 2006.80-3.03 (2.40 (7. nitrate.90 (4. Lamm and Doemland.S.70) 2.00-11.50) 95th 12.50-5.5 (13.4 (8. dietary iodine intake.52-9.25) 5.35) 3. 2005.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5. In the U.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.29) 2.20) 8.6-17.50 (6.10 (2.90-2.46-13.32) 5.70 (2.87 (5.4) 8.16-3. interval) 3.0 (11.50-3. and the presence of other substances known to affect thyroid function (e.20 (7.20 (6.19-6.4 (10.1-14.05 (4.20 (2.50) 2.10-7. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability..64) 5.36 (8.6) 20.70 (2. levels.84) 2.2) 8.0) 13.. 2005.1-16.10) 4.0 (8.0 (11.20-10.30) 90th 9.98) 3.42 (3. In these small short-term experimental studies on males and studies of male perchlorate workers with doses or estimated exposures thousands-fold higher than known environmental exposures..99-3.0) 4. However.40) 5.73) 3.0 (9.1-13. although iodine intake was higher than U. women with urinary levels of iodine less than 100 micrograms per day.60-8.0) 7.24-2.5) 8.0) 12. gender. U.86) 4.50) 2.14 (2.S.Perchlorate inhibition (RUI).20-4.82 (5.4 (11. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses. age.47) 2. altered thyroid function was not found in Chilean pregnant women or their newborns with mean urinary perchlorate levels about 40-fold higher than average U.1-22.60 (3.0-19.50) 9.80 (7.50-9. 2005).54 (2. Steinmaus et al.39 (3.50) 5.30 (6. Greer et al.0-17. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al. NAS.0) 14.93-7.00) 9.7 (11. 1999.40 (3.3 (10.93-5.08) 3.02) 3. thiocyanate.0) 12.60-6.89-3.1 (8.00) 3.91) 4..72 (3.30 (5. Also.00-2.00 (4.71 (5.S.0 (9.10-3.33-6.8 (11.1) 8.

Dasgupta PK. Analysis of relative source contributions to the food chain. Greer SE. (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.46(5):509. J Occup Environ Med 2000. and nitrate on thyroid function in workers exposed to perchlorate long-term. Available at URL: http://www. Blount BC. EPA reference dose (Blount et al. Crump KS. Primary congenital hypothyroidism. Kirk AB.113(8):10011008. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Lamm SH. Goodman G. Environ Sci Technol 2006. Howd R.html and from ATSDR at: http://www. Page Last Updated: 05/28/2009. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lamm SH. 2007). Pleus RC. Washington (DC): National Academy Press. National Research Council of the National Academies. Environ Health Perspect 2005. Dyke JV. Lamm S. Blount BC. Pino S. Valentin-Blasini L. and environmental perchlorate exposure among residents of a Southern California community.S.17(4):400-407. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Skeels MR. Kelsh MA. Caldwell KL. et al. et al. epa.10(8):659-663. Daaboul JJ. CFSAN/Office of Plant & Dairy Foods. Erratum in: Environ Health Perspect 2005. Also. Cross M. Chacon PM. Valentin-Blasini L.html. Li FX. Food and Drug Administration (FDA). 2005. most of the population is considered to be below the U. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. He X.90(2):700-706. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. J Expo Sci Environ Epidemiol 2007. Richman K. Mauldin JP. Tellez RT. Osterloh JD. Blount et al. Thyroid 2001. Osterloh JD. Environ Health Perspect 2002. The effect of short-term low-dose perchlorate on various aspects of thyroid function. 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. Neonatal thyroxine level and perchlorate in drinking water. J Occup Environ Med 2003. Braverman LE. Lau EC.htm. Jackson WA. Additional information about exposure and health effects is available from the U. 2005). Low dose perchlorate (3 mg daily) and thyroid function. Perchlorate Exposure of the US Population. Abarca CR. Braverman LE.S. 6/2/09 Greer MA. Barnard JC. et al. Pino S. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Health Implications of Perchlorate Ingestion.gov/safewater/ccl/perchlorate/perchlorate. Steinmaus C.11(3):295. Magnani B.atsdr.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. J Clin Endocrinol Metab 2005. Erratum in: J Occup Environ Med 2004.EPA at: http://www. Pirkle JL. Byrd D. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Thyroid 2000. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Braverman LE.fda. Pirkle JL.42(2):200-205. Miller MD. Deyhle GM.. Gibbs JP. Lawrence J. thiocyanate. Sesser DE. Buffler PA. 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. newborn thyroid function. Lamm SH. Lawrence JE. Environ Health Perspect 2007.115(9):1333-1338. et al. Perchlorate in the United States. May 2007. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Doemland M. Rutherford GW.45(10):1116-1127.110(9):927-937. 2001-2002. Landingham CB.113(11):A732. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. population. The effect of perchlorate.40(21):6608-6614.. 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.41(5):409-411.cdc. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. 2005).Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Crump KS.S. References Blount BC. Li Z.114(12):1865-1871.gov/toxpro2. Environ Health Perspect 2006. National Academy of Sciences (NAS). Benchmark calculations for perchlorate from three human cohorts.. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans.

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

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

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

developmental and teratogenic effects were demonstrated in offspring.00 (.400-. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. 2003a. development in offspring was stunted and hypothyroxinemia was observed. 2007a.108 times higher than background serum levels in humans (Butenoff et al.500-3. 2003a).. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. 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.. the potential to estimate risks to humans from animal doses is uncertain.800 (. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. population from the National Health and Nutrition Examination Survey.400 (<LOD-. 2004).. see Data Analysis section) for Survey year 03-04 is 0.. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.400-1.. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.80) 485 538 962 Limit of detection (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 .300-1. Lau et al. Harada et al..00) . At doses causing maternal toxicity. 2001. PFOS.900 (. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.10) . Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al.. 1999.50) .800 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . perfluorohexanesulfonate (PFHxS). 2005). 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.40) . Animal studies of PFOS have demonstrated weight loss..20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .500-1. 2003a.700 (. < LOD means less than the limit of detection.10 (. 2004a. EPA. 1992..S. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. possibly related to lung immaturity (Lau et al.. Thibodeaux et al.. reproductive. 2005).600 (.300 (<LOD-.20) . 2003.900 (. which may vary for some chemicals by year and by individual sample. elderly and children.600 (.500) 90th . and there was no clear evidence of excess all-cause or diseasespecific mortality. 2007a. 2003).300 (<LOD-.500) . In such studies. PFOS. hepatotoxicity. 2007b.400-1. Olsen et al.. At high but non-toxic maternal doses of PFOS.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al.400 (<LOD-.00) . 2003a.900 (.. 2003.500) . and no substantial age trends were seen within adults ages 20-69 (Olsen et al.600-2..500 (. Olsen et al.500 (<LOD-1.400-1.300 (<LOD-. 2003. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) . monkeys.. 2003).500 (.800) 1.3.. 2007.700) . and humans.500) . Cook et al. 2003a).S.800 (.10) * 03-04 03-04 * * < LOD < LOD < LOD .500-. 2007b). U.400-1.400) .00) . 2004b).. PFOA. 2004). and changes in thyroid hormone concentrations (Grasty et al. EPA. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.. However. Olsen et al.400-1.. thyroidal).500-1. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. PFOA.80) 640 1454 03-04 03-04 * * < LOD < LOD .500) .800) 1. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. population.600 (. Fourth National Report on Human Exposure to Environmental Chemicals 249 . 2004. 2003).500-1. or increased cancer rates (Alexander et al..400 (<LOD-. 2007). U..800 (. and perfluorononanoic acid (PFNA) are detectable in a high percentage of the participants and PFOS levels are generally 3-10 times higher than PFOA levels (Calafat et al. Fei et al.S.500-1.S. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.400-. Kennedy et al. Survey Geometric mean (95% conf. 2004. In comparing three separate reports on adults.

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

Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. < LOD means less than the limit of detection.S.500-. < LOD means less than the limit of detection. 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.3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (<LOD-.600) < LOD .400 (.500 (<LOD-. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 1.600 (.300 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.S. Fourth National Report on Human Exposure to Environmental Chemicals 251 .300-.900) < LOD . which may vary for some chemicals by year and by individual sample. which may vary for some chemicals by year and by individual sample.0. population from the National Health and Nutrition Examination Survey. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th .400) .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-.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500) 485 538 962 Limit of detection (LOD.300 (<LOD-.

90 (1. see Data Analysis section) for Survey year 03-04 is 0.00) 2.00-7.826-1.70-5.20 (1.80-6.5) 8. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20 (1.30 (6.40) 1.60) 3.00) 1. Survey Geometric mean (95% conf.10) 4.40) 640 1454 03-04 03-04 2.20-2.77-2.01 (1.10 (.00 (2.20-1.80-4.700-1.30 (3.10 (1.90 (4.50 (1. 252 Fourth National Report on Human Exposure to Environmental Chemicals .60) 2.1) 485 538 962 Limit of detection (LOD.90) 8.20) 1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.90) 1.10) 5. population from the National Health and Nutrition Examination Survey.70 (2.00-1.10) 1053 1041 03-04 03-04 03-04 .70-2.20 (1.30 (1.80-8.00 (5.20 (1.40-1.67-2.10) 1.86 (1.70) 2.60-3.73-2.5) 5. interval) .30-9.30-6.60 (6.20-1.40 (2.800 (.50 (1.26) 2.40 (1.10-9.40) 1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.70) 1.10-5.20 (6.70) 2.50-6.09 (.30-12.80-3.861 (.03) 1.60-4.14 (.00) 1.90) 1.00) 3.721-1.90 (1.50 (2.912-1.80-3.91) 2.80) 5.60) 9.90) 3.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.80-7.50) 2.70 (1.852 (.90) 90th 5.20-1.80 (1.20) 2.900-1.12) .20-3.60-2.60-4.40-3.50 (6.62-2.0) 8.900-1.3.900) 1.20 (6.42 (1.20) 485 538 962 Limit of detection (LOD.40 (1.00-1.92 (1.93 (1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80-2.60 (1.800-1.70) 13.00-6.10) 75th 1.60-3.60 (1. Survey Geometric mean (95% conf.00 (1.586-.60-8.00 (1.80) 90th 2.80-7.70) 1.80-4.900 (.10) 6.3 (9.00 (.60-2.00 (1. interval) 1.70-10.00 (.54) .40) 4.30 (1.30 (7.90 (1.90-19.30 (2.90-2.40) 640 1454 03-04 03-04 1.700 (.10) 4.50-6.70-6.80 (1.10) 8.60-7.16) .900-1.30 (2. see Data Analysis section) for Survey year 03-04 is 0.S.44 (2.00 (1.40) .80) 1.835-1.50-3.10 (.27) 1.20-1.10) 75th 3.600-.0) 1053 1041 03-04 03-04 03-04 1.80 (4.834-1.20) 1.30) 03-04 03-04 .04) .20) .S.90-10.87-2.20) 03-04 03-04 2.50 (4.40 (1.60-2.80) 3.10) 1.30 (1.60 (1.90 (4.10) 6.05-2.80-4.984 (.900-1.72 (1.50) 2.08) 2.10-9.40-1.689 (.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.70-2.80-12.40 (1.56-1.30) .50 (1.1.30-2.50 (4.900 (.40) 2.50 (1.70-7.60) 1.6) 7.10 (4.80) 4.963 (.30) 3. population from the National Health and Nutrition Examination Survey.10 (.816-1.51) 1.697-1.80-8.50) 6.900-1.10 (4.900-1.809) 1.50 (6.17 (1.00-8.30 (1.966 (.30) 3.17-1.30) 3.50-10.90) 1.90 (1.90 (2.70) 3.72) 1.

80-4.5-62.50) 4.89 (3.8-30.60) 03-04 03-04 3.50-13.40-6.0) 90th 41.0) 03-04 03-04 19.6) 21.6-24.8 (45.9) 22.80 (7.0) 21.2 (28.60-14.60 (6.70-7.40 (6.4-17.2) 30.60 (6.37 (2. Fourth National Report on Human Exposure to Environmental Chemicals 253 .6 (19.9 (19.4 (23.18 (3.47-4.7-53.10 (3.7 (35.90-4.0) 485 538 962 Limit of detection (LOD.7 (35.80 (6.2 (27.20) 7.8) 27.40-6.90) 6. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.0) 21.2 (21.3 (44.79) 4.8-35.5) 57.20 (4.60 (3.1.7 (19.60-6.5 (28.84-3. see Data Analysis section) for Survey year 03-04 is 0.0) 43.1 (23.1-24.11 (2.3) 41.20-9.5) 8.3) 28.82) 4. see Data Analysis section) for Survey year 03-04 is 0.20) 4.90 (7.10-3.80-9.40-10.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.40-17.9-23. population from the National Health and Nutrition Examination Survey.70 (5.2 (19.60-13.00) 3.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.0 (20.9 (17.40) 75th 5.7-33.7-49.5) 1053 1041 03-04 03-04 03-04 14.50 (4.5) 7.1) 15.6 (42.30-11.20 (4.99-3.70-9.20-5.9-38.8-78.20-4.S.30-5.7-30.50 (3.2 (16.60 (4.6-45.50-4.S.3-22.7) 39.20) 10.65-4.5 (28.60-9.7-69.6) 42.90 (7.4) 21.7-23.0-66.1-52.6) 7.00 (5.3 (35.6) 9.0-20.4 (19.30) 6.53) 3.1) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 4.67-4.8-22.30 (3.20) 7.70) 4.40 (4.9-19.4 (28. population from the National Health and Nutrition Examination Survey.4 (19.50) 7.9) 9.70-10.40) 3.30 (3.0) 23.10 (6. Survey Geometric mean (95% conf.8-22.3 (28.00 (3.6) 62.4 (17.6) 18.10 (3.5) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 21.20) 5.1) 57.3-61.70) 6.4) 56.30 (5.6 (44.0-16. interval) 3.5) 19.5) 18. Survey Geometric mean (95% conf.5-33.8) 32.5) 32.4) 20.50-6.30-6.6-50.7 (7.30-8.7 (13.40-14.2 (18.8-81.2) 45.30) 7.2-22.21-3.9) 22.1-35.8-22.70 (3.0) 36.3 (17.3 (35.2) 640 1454 03-04 03-04 4.90 (7.4-25.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.35) 3.20) 5.90 (5.1 (24.4-42.9 (22.91) 3.4) 640 1454 03-04 03-04 23.8) 46.4.80 (6.90-12. interval) 20.7 (43.9) 27.80) 8.70) 3.00 (5.85-4.7 (43.80-12.5) 9.90-4.70 (5.07-4.4) 75th 30.70-7.96 (3.6 (35.1 (19.95 (3.5-23.5-21.1-25.8 (37.6) 35.0-70.40) 90th 7.30-3.1-33.80 (5.60 (5.6) 1053 1041 03-04 03-04 03-04 3.27) 4.60 (7.8 (34.40) 5.2-57.1-36.70-5.47 (4.0 (27.3) 42.2) 30.3) 485 538 962 Limit of detection (LOD.9 (13.60) 8.10) 5.

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) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .300 (.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.300) . Survey Geometric mean (95% conf.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 .400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .4.S.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300-.200-.500) .300 (.300-. 254 Fourth National Report on Human Exposure to Environmental Chemicals .300) .300 (.300 (.200 (<LOD-.S. see Data Analysis section) for Survey year 03-04 is 0.300-. population from the National Health and Nutrition Examination Survey.300 (.200-.300) . < LOD means less than the limit of detection.300 (.500) .300 (.300 (.400 (<LOD-.300 (.300 (.500) < LOD 485 538 962 Limit of detection (LOD. see Data Analysis section) for Survey year 03-04 is 0.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500) 485 538 962 Limit of detection (LOD. 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. which may vary for some chemicals by year and by individual sample.200-. population from the National Health and Nutrition Examination Survey.300 (.200-. Survey Geometric mean (95% conf.500) .2.300) .300-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200-.200-.300) .200-. which may vary for some chemicals by year and by individual sample.300) .200-.200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.

600 (<LOD-.400 (<LOD-1. < LOD means less than the limit of detection.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 0.60) 640 1454 03-04 03-04 * * < LOD < LOD .10 (.10-1.10 (.900-1.700 (<LOD-.10-1.700 (<LOD-. Survey Geometric mean (95% conf. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .800) .300 (<LOD-1.30) 1.700 (<LOD-2.60) 485 538 962 Limit of detection (LOD.00 (.700) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .30 (1. population from the National Health and Nutrition Examination Survey.900) 1.20-1.900) 485 538 962 Limit of detection (LOD.80) 1. which may vary for some chemicals by year and by individual sample.00) < LOD .300 (<LOD-.600 (<LOD-1. which may vary for some chemicals by year and by individual sample.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.6.900) .300-2.80) 1.20) 1.600) .00 (.10) 1.700 (<LOD-.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .50 (1.900-1.700 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. * 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.10) 1. < LOD means less than the limit of detection.900-1.600 (<LOD-1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .700 (<LOD-.900 (<LOD-1.10-1.40) 1.3.30 (1.900-1.10) .900-1.30) .40) < LOD < LOD .30 (1.20 (1.800) .600 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (.900-1.00-1.700 (<LOD-.30) 1.10-1.10) .700) 1.800 (<LOD-.S.70) 1.00 (.900 (.900-1.400 (<LOD-.500 (<LOD-.10) * 03-04 03-04 * * < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 255 .10 (1.700) .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 .10 (.90) .50 (1.700) 90th 1.

Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Ye Y. Cook JC. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Lau CS. Caudill SP. Holmstrom KE. Saito N. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Laane RW. Environ Health Perspect. The influence of time.Perfluorochemicals References Alexander BH. Evans TJ. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Toxicol Sci 2001.113(2):209-217. de Voogt P.1968--2003.7(4):371-377. Kawashima Y. Tully JS.39(3):363-380. Morikawa A. Biegel LB. Olsen J. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Toxicol Appl Pharmacol 1995. Taniyasu S. Birth Defects Res B Dev Reprod Toxicol 2003. Calafat AM. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Reidy JA. Mandel JS. Calafat AM. Environ Health Perspect 2007. Regul Toxicol Pharmacol 2004. Chlorinated. Environ Sci Technol 2005.46(2):141-147. Environmental and toxicity effects of perfluoroalkylated substances. Environ Sci Technol 2005.Koizumi A. Day RD. Guruge KS. et al. Chem Biol Interact 2000. Mohotti KM. Yun SH. Frame SR. Reidy JA. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion.60(1):44-55. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. et al. Biegel LB. Kannan K. in vivo.115(11):1677-1682. et al. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Olsen GW. Yamashita N. Inoue K. Arendt MD. Rogers JM. Perfluorinated chemicals in selected residents of the American continent.39(23):9101-9108. Environ Sci Technol 2004. Aguilar-Villalobos M. Kuklenyik Z. Harada K. Witter FR. Ingall GB. Calafat AM. Environ Sci Technol 2007a. Hekster FM. and perfluorinated contaminants in livers of polar bears from Alaska. Perkins RG. Occup Environ Med 2003. Crit Rev Toxicol 2004. Murray SM. Reidy JA. Yoshinaga T. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Kumar KS. Characterization of risk for general population exposure to perfluorooctanoate. Butenhoff JL. Yamashita N.40:21282134. Harada K.115(11):1670-1676. Tarone RE. Kudo N. Mabury SA. Cook JC.63:490496. J Environ Monit 2005. Mandel JH. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Kannan K. Needham LL. Katakura M. Seneviratne HR. Kennedy GL Jr. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Halden RU. Saito N. Kuklenyik Z. Mandel JH. Burris JM. Reidy JA. McLaughlin JK. Butenhoff JL. Bignert A. Grey BE. Serum concentrations of 11 polyfluoroalkyl compounds in the U.124(2):119-132. Needham LL. Kuklenyik Z. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Wong LY.S. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Androgenic deficiency in male rats treated with perfluorodecanoic acid.60(10):722729. Hurtt ME. The toxicology of perfluorooctanoate. O’Connor JC. Toxicol Appl Pharmacol 1990. Keller JM. Yoshinaga T. Environ Sci Technol 2004. Dinglasan MJ. Environ Health Perspect 2007. Gaylor DW. Wijeratna S.39(23):9057-9063. Peterson RE.68(6):465-471. Kuklenyik Z. 2007b. Hurtt ME. O’Connor JC. Sasaki S. Corsolini S. Koizumi A.115(11):1596-1602. and ex vivo studies. Calafat AM. Liu RC. Jarnberg U. Frame SR. Suzuki E. Fluorotelomer alcohol biodegradation yields poly. Loganathan BG. Environ Sci Technol 2006a.34(4):351-384. Hurtt ME. Moore RW. Rodricks J. Olsen GW.99(2):253-261. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Herbstman JB.S. Falandysz J. Needham LL. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats.179:99-121. Seacat AM. Chemosphere 2006b. et al. Rev Environ Contam Toxicol 2003. brominated. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort.41:2237-2242. Cook JC. Fillmann G. Taniyasu S. Olsen GW. Environ Res 2005.38(17):4489-4495. Environ Sci Technol 2005.and perfluorinated acids. Needham LL. Grasty RC. Moore JA. Bandai N. et al. Toxicol Appl Pharmacol 1992.38(10):2857-2864. Inoue K. 256 Fourth National Report on Human Exposure to Environmental Chemicals . J Occup Health 2004. Bookstaff RC.39(1):80-84. Edwards EA.134(1):18-25. Fei C. Caudill SP. Tully JS. Apelberg BJ. Kamiyama S.104(2):322-333. et al. Polyfluoroalkyl chemicals in the U. Kannan K. Calafat AM. Watanabe T. et al.

Zobel LR. Washington. Toxicol Sci 2002.68:105–111.111(16):1892-1901. Prevedouros K.74(2):382-392. Buck RC. Butenhoff JL. Rogers JM. Coordinate induction of acyl-CoA binding protein. Mar Pollut Bull 2005. A global survey of perfluorinated acids in oceans. Grey BE. Hanari N. Church TR. Ellefson ME. Butenhoff JL. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Butenhoff JL. van Belle G. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts.S. Lundberg JK. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Larson EB. The developmental toxicity of perfluoroalkyl acids and their derivatives. (Erratum in: Environ Health Perspect. fast foods. Miller JP. Church TR. Olsen GW.40(1):32-44. et al. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Seacat AM.198(2):231-241.54(11):1599-1611. fish. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. II: postnatal evaluation. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Lau C. Korzeniowski SH. Historical comparison of perfluorooctanesulfonate. Rogers JM. Burris JM.2(1):53-76. et al. Butenhoff JL. Taniyasu S. Butenhoff JL. Mandel JH. Hansen KJ. Olsen GW. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water.epa. Ehresman DJ. Environ Health Perspect. Thibodeaux JR. et al. Toxicol Appl Pharmacol 2004. Kannan K. Hansen KJ. Mandel JH.111(16):1900) Olsen GW. Burris JM. Taniyasu S. Environ Health Perspect 2003a. Bronson R.. J Occup Environ Med 1999. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Environ Sci Technol 2003. Toxicol Sci 2003. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Cousins IT. Thomford PJ. 1/15/06 Vanden Heuvel JP. Environ Health Perspect 2005. Chemosphere 2004a. Hansen KJ. htm. Half-life of serum elimination of perfluoroo ctanesulfonate. Kannan K. 2003. Burlew MM. Biochim Biophys Acta 1993. Nesbit DJ. (Erratum in: Toxicol Sci 2004. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. and food items prepared in their packaging. Hanson RG. Toxicol Sci 2003. Mair DC.perfluorohexanesulfonate. Peterson RE. Thibodeaux JR. Yamashita N. J Children’s Health 2004b.115(9):1298-1305. 2007a. U. Froehlich JW.26(1):47-51. Kawashima Y. Butenhoff JL. Church TR. Moisey J. Olsen GW. Hansen KJ. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys.) Tittlemier SA. Helzlsouer KJ. Seacat AM. Sterchele PF. Petrick G. Lundberg JK. Horii Y. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse.gov/opptintr/pfoa/pfoara. Olsen GW. perfluorooctanoate andother fluorochemicals in human blood. Case MT. birds. Olsen GW. EPA). and humans from Japan. Lau C. fate and transport of perfluorocarboxylates. fish. Olsen GW. Environmental Protection Agency (U. Seymour C.37(12):2634-2639. et al. Burris JM.1177(2):183-190.55:3203-3210. Richards JH. Mandel JH. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors.113(5):539-545.Perfluorochemicals Kudo N.68(1):249-264. I: maternal and prenatal evaluations. Horii Y. Biol Pharm Bull 2003.51(8-12):658-668. Sources. J Ag Food Chem 2007. Ehresman DJ. Gamo T. et al.82(1):359. Chemosphere 2007b. Available from URL: http://www. 2003a.S.45(3):260-270. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Hansen KJ. Rogers JM. Burris JM. Burris JM.74(2):369-381. and perfluorooctanoate in retired fluorochemical production workers.41(9):799-806. Barbee BD. Mandel JH. Huang HY. Environ Sci Technol 2006. Grey BE. Cao XL et al. Yamashita N. Hanson RG. Olsen GW. Pepper K. Stanton ME. et al. Olsen GW. Reagen WK. J Occup Environ Med 2003b.

Mortensen et al.. vinyl tiles and flooring. corresponding monoester metabolites. inhalation. Pan et al. 2001. lubricating oils. plastic raincoats. For the general population. blood product storage bags. hair spray. several of the phthalates produced testicular injury. Albro and Lavenhar. Harris et al... Phthalates are also used as solubilizing and stabilizing agents in other applications. 1998)... not all phthalates Phthalates and Urinary Metabolites in this Report Phthalate name (CAS number) Benzylbutyl phthalate (85-68-7) Dibutyl phthalates (84-74-2) Dicyclohexyl phthalate (84-61-7) Diethyl phthalate (84-66-2) Di-2-ethylhexyl phthalate (117-81-7) Abbreviation BzBP DBP DCHP DEP DEHP Urinary metabolite (CAS number) Mono-benzyl phthalate (2528-16-7) (some mono-n-butyl phthalate) Mono-isobutyl phthalate Mono-n-butyl phthalate (131-70-4) Mono-cyclohexyl phthalate (7517-36-4) Mono-ethyl phthalate (2306-33-4) Mono-2-ethylhexyl phthalate (4376-20-9) Mono-(2-ethyl-5-hydroxyhexyl) phthalate Mono-(2-ethyl-5-oxohexyl) phthalate Mono-(2-ethyl-5-carboxypentyl) phthalate (40809-41-4) Mono-isononyl phthalate Mono-methyl phthalate (4376-18-5) Mono-(3-carboxypropyl) phthalate Mono-n-octyl phthalate (5393-19-1) Abbreviation MBzP MiBP MnBP MCHP MEP MEHP MEHHP MEOHP MECPP MiNP MMP MCPP MOP Di-isononyl phthalate (28553-12-0) Dimethyl phthalate (131-11-3) Di-n-octyl phthalate (117-84-0) DiNP DMP DOP 258 Fourth National Report on Human Exposure to Environmental Chemicals . 1998. 1985. Nielsen et al. intravenous medical tubing. lotions. solvents. Because they are not chemically bound to the plastics to which they are added. 2004. 1995). fragrances. The table shows the phthalate diesters. shampoo. and other oxidized metabolites included in this Report. indoor dust. 2001).. and. and nail polish. such as plastic bags. dietary sources have been considered as the major exposure route.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. detergents. 2003). dermal contact with products that contain phthalates. In chronic rodent studies.. Phthalates are metabolized and excreted quickly and do not accumulate in the body (Anderson et al.. The intravenous or parenteral exposure route can be important in patients undergoing medical procedures involving devices or materials containing phthalates. automotive plastics.. in humans. Infants may have relatively greater exposures from ingesting indoor dust containing some phthalates (Clark et al. and sediments (Clark et al. garden hoses. Various phthalate esters have been measured in specific foods. water sources. and toys (ATSDR. to a lesser extent.. Phthalates are often used in polyvinyl chloride type plastics.. Dirven et al. liver injury. Absorbed monoester metabolites are usually oxidized in the body and. Ingested phthalate diesters are initially hydrolyzed in the intestine to the corresponding monoesters. Human milk can be a source of phthalate exposure for nursing infants (Calafat et al. 1982. 1989). and personal-care products. 2003). 1997. deodorants. 1985. 1982.. urinary metabolite and air phthalate concentrations are roughly correlated (Liss et al.. however. and teratogenicity.. 2000. inflatable recreational toys. In settings where workers may be exposed to higher air phthalate concentrations than the general population.. 1997.. Phthalates have low acute animal toxicity. 2002). Okubo et al. Zacharewski et al. some medical devices and pharmaceuticals. 2003.. People are exposed through ingestion. which are then absorbed (Albro et al. Jobling et al. followed by inhaling indoor air. but these effects either have not been demonstrated when tested in non-human primates or are yet to be studied. 2005). 1993). such as soap. indoor and ambient air. In vitro studies showed that certain phthalates can bind to estrogen receptors and may have weak estrogenic or anti-estrogenic activity (Coldham et al. There are numerous products that contain phthalates: adhesives.. Parks et al. phthalates can be released into the environment during use or disposal of the product. liver cancer. 2006). but in vivo studies did not support phthalates having estrogenic effects (Milligan et al. 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.

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

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Orton TC. Barlow NJ. Caudill SP. Jackson SJ. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Abbott BD.58:339349. Peck CC. Malek NA. Barr DB. Rhodes C.65:299-308. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Toxicol Sci 2000. Bratt H. et al. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Toxicol Sci 1998.45:11-17. Parks LG.S. Peters JM. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Meek MD. Wu ZF. Ostby JS. Silva MJ. Clemons JH. Albro PW. Crit Rev Toxicol 2006. Environ Health Perspect 1982. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Pratt IA. Environ Health Perspect 1986. et al. Environ Health Perspect 2004. Batten PL. Matthews JB. Lambright CR. Cunningham ML. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Zacharewski TR. Urinary levels of seven phthalate metabolites in the U. Environ Health Perspect 2006. Rusyn I.114(11):1643-1648.36:459-479. Hodge CC. 112(5):A270].112(3):331-338. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat.Phthalates phthalate (DEHP): a cross-sectional study in China. Reidy JA.46:282-293. Klinefelter GR. Fielden MR. et al.

5-41.5 (67.9) 18.4 (10.2-33.8 (21.3-125) Total 15.7-16.0 (33.2 (19. because it is not bound to products in which it is incorporated.6-132) 103 (84.7-170) 169 (134-198) 152 (99.3-161) 99.6 (13.1) 29.0-26.8-72.7 (80.S.7-119) 99.2-17.9 (12.8 (50.8) 24.8 (53.6) 16.1 (10.6) 95th 103 (94.1-18.7 (70.9) 49.2) 12.9 (16.2-183) 101 (78.2-20.4 (63. sealants. residents (Blount et al. and 03-04 are 0.7-16. including MBzP.2) 33.4) 98.1-116) 122 (93.4 (32.2) 32.4-15. 2000). IARC considers BzBP not classifiable with respect to human carcinogenicity.7-172) 103 (74.8-17.0) 90th 67.4) 71.9) 43.3-18.4-120) 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 13.3-130) 122 (88.4-92.2) 14. High dose BzBP and its monoester metabolites.1) 76.3 (44.5 (57.6) 29.6) 14.5-94.4-127) 80.9-28.5 (55.6-79.0 (34.7) 23.1) 67.3-21.2-19.3) 13.6) 13.2-38.8-16.2-40.8 (86.6-39.7-14.8-64.6 (13.9) 13.0) 33.7-15.0 (55. interval) 15.5 (27.Phthalates Benzylbutyl Phthalate CAS No.9 (39.5-84.9-87.1-90.8 (80. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.6-18.2) 17. population from the National Health and Nutrition Examination Survey.5) 82.7) 38. 01-02.4) 81.1 (13. some personal care products.3 (12.6) 25.8) 28.0-130) 101 (86.2-116) 122 (102-143) 101 (84.1-16.4) 35.4 (13.6) 63.1 (20.0 (30.3 (29.5-35.6) 13.5-36.8) 33.1-38.1-43.5) 27.4 (59.4 (10.6-116) 122 (102-142) 101 (85.1) Selected percentiles ( 95% confidence interval) 50th 17.4 (31.3-18.3-27.9-27.8 (71.8) 63.0) 20.2 (10.2-16.8 (10.4) 12.9 (11. 262 Fourth National Report on Human Exposure to Environmental Chemicals .4) 75th 35.9) 11.3) 54. particularly male animals (McKee et al.6) 15.6) 35.1 (19.0) 34.0 (20.3 (30.0) 70.1-214) 166 (116-191) 145 (110-213) 88.4) 129 (98.9-16. car care products. and to a lesser extent.6) 37.6 (12.7 (13.3-34.2-39.0) 32.3) 37.2 (19. 2001-2002.3) 23.5) 15.4 (53.7-25.0 (30.0) 24.1) 32.5 (47.3 (12.4 (48.2-115) 113 (91. 0.5 (26.5-33.6 (21.4) 35.8-133) 89.6 (13.6-17.0 (14.0 (15. NTPCERHR.7-17.3) 13.7 (15.7-58.3-91.8 (14.9-62.3-75.8.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.9) 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..8-14.2 (47.5-36.9 (21.9-49.4) 108 (96.4) 65.5 (76.3) 15.1 (14.0-55.4 (27. 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 (43.2 (14.9-190) 86.5 (61. see Data Analysis section) for Survey years 99-00.8-18.5-62.9 (13.9 (22.1) 31.6 (32.1-15.7-35.1 (13.6 (66.8-17.1) 14.9 (28.S.1-16.1-61.6 (53.5) 30.3) 63.5) 15.6 (13. 2000).6) 14.6-43.6-38.2-16.6) 50.7 (11. Food crops take up BzBP.2-31.4) 80.8-48.9) 12.8) 14.5-145) 138 (106-241) 143 (127-179) 120 (99.2) 66.0 (23.4 (53.3 (13.0 (11.3-88.5) 23.6) 67.1 (14.0 (15. can produce developmental and reproductive toxicity in rodents.0-85.5) 55.4 (68.9) 15.2 (25.3 (12.7-82.4 (29.1) 68.6 (41.8 (71.8-41.4 (32.0-106) 58.8 (28.9-47. vinyl tile.6-150) 94.3 (29.3-82.5-25.3 (54.8 (38.5) 16.1) 12.0) 23.9 (70.5 (66.4) 51.2 (11.2) 69.1-35.4) 33.2-155) 91.2) 22.1) 13.8-16.4-25.6-92.1-15. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2004. respectively.9-30.3) 94.1-120) 52.9) 14.7 (51.1-39.5-14.9 (12.3 (22. BzBP can be released into the environment during its production and.0 (27.4-24.2) 14.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9-14.8-14.6-92.2) 15. and 0.7) 40.8 (30.1.8-121) 79.1 (55.1 (58. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.5-97.5 (13.5) 65.6-72.6) 35.8-13.8-98.8-76.4) 49. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.4) 38.1 (32.7 (53.3-74.4-62.8) 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 16.7-13.7 (12.7-16.3..3-12.8 (12.0 (12. it can be released into the ambient air during use or disposal of the products.8-35.6-29.6) 24.3 (33. and 2003-2004 were generally similar those reported in U.2) 13.7 (82.0) 16.4) 14.9) 14.4-16. and diet is the major source for general population exposure.0 (43.5-18.5-40.3-43.0 (26.2) 78.

6 (11.7 (18.5-31.3-16.2) 12.8-27.1) 27.7-61.1 (9.7-15.8 (49.5) 16.7 (19.5-23.2 (69.4-15.5-26.0-53.9) 42.5) 20.7-56.9) 12. 2005.8-13.9-62. A small study of African-American women in Washington.3 (12.2) 11.4) 90th 50.6 (36.6 (51.1-29. population from the National Health and Nutrition Examination Survey.4 (25.2-49.2) 26.8 (10.7 (14.7 (54.6) 13.6) 75th 25.2 (56.6) 30.3-38.1 (19.9) 100 (80.9 (15.4-19.0) Selected percentiles ( 95% confidence interval) 50th 13.4 (10.8) 54.3) 67.3) 89.5-38.5 (42.4) 28.4) 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) 58.8-64.1-14.1 (53.4 (63.3) 14. 2004.6-81.4-27.1 (11.4-17.4-116) 73.5-13.9 (10.6 (11.8-42.3) 90.5-76.4 (74.5 (12. and females compared to males (Silva et al.0-109) 65.1) 24.4-42.5 (10.4) 17.5-58.5 (35. 2005).8) 80.4) 60.9 (24. 2002.7-397) 70.8-85.0 (41.3 (38.7-123) 77.4-18.8) 71.1) 35.8-15.8) 16.8-69.6) 25.7-15.4) 104 (89. in men attending a Boston infertility clinic (Duty et al. 2004).2-13.4) 44.3 (13.9-13.7-14.6-47.4 (11.4) 51.S.7) 56.9 (12.3) 37.9 (39.0) 24.6 (11.5) 41.4-23.4) 12.4 (69.5) 95th 77.4 (21.4 (60.0 (13.3 (60.6-12.4-14.8 (11.8) 108 (75.2) 11.3) 73.3 (23.3 (35.0) 15.8 (46.8-14.2-117) 95.6 (57.0-15.8-15.5-58.4 (12.7 (55.1) 17.4) 13.8) 68.7 (13.7) 46.5-79.3) 12.0) 12.6-20.1-125) 86.6) 12.4) 15.9-13.3) 36.1 (13.9-69.9-115) 57.8) 33.6 (19.6) 53.9 (54.4-99.0-26.8) 15.9) 11.8-13.2) 32..5-61.5) 78.8) 11.2-13. 2007).9 (12.6-15.2-21.1 (41.5 (11.1 (21.4 (11.9-23.8-13..9 (51.3) 16. adolescents compared with adults.8) 53. Weuve et al.4 (33.7 (11.3) 29.6-86.4-90.5-99.8 (57.3) 55.7 (13.4) 14.1 (14.6-26..7-19.7 (59. 2003).3) 21.2-51..1) 142 (99.3) 13.0-48..1-35.7) 38.4) 50.5) 23.2 (41.6-99.1-12.9-14. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.3-34.7) 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) 14.7) 25.9 (15.7-19.2 (27.6-40.2) 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. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.5-16.4-14.6 (15.9) 24.7-31.8) 26.0 (49.8-173) 195 (121-305) 229 (99. 2002).7-29.4 (46.9 (10.1 (18.1-27. 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.0) 60. Hoppin et al.2-17.3 (39.0 (62.7-90.5) 17.8 (64.5) 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 . median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.8-34.7 (23. and in a small sample of German residents (Koch et al.8-60.1 (34.1-12.0) 24..8 (50.3-73.2-57.4-142) 134 (116-176) 136 (85.73-12.1 (21.7-14. In an annual sample of German university students. In NHANES 1999-2000. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.4 (26.9 (22.5-42.0-27.9 (29.1-58.6 (14.95-14.4-102) 70.9-83.5) 13. 2007).6-13.6 (24.4-79.1 (25.8-39.2-15.8) 33.3-11.1 (46.6 (22.1) 39.9-28.1-120) 77.3-64. in young Swedish men (Jonsson et al.9 (43.9-16.1-79.0) 11.1) 80.6 (30.3) 13.0 (10.1 (21.8) 34.5 (56.8 (12.0 (33.4-93.2 (40. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.0 (12.2) 67.8) 46.7 (11.1 (13.2) 11.1 (15. 2006).9 (55.0 (12.8 (30.4) 13.7-12..7-20.8 (13.3 (15.0-90.8 (69.5 (9.0) 13.2-78.5) 10.4) 21.5-57.1 (43. 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.7 (12.8-16.7) 19.3 (24.5 (49.0 (38.9) 52.4 (11.3) 18..1) 23.6) 38.8-48.7 (11. Hauser et al.8-80.5 (10.7) 11.0) 49.8-14.1 (23. interval) 14.69-11.5) 46.0-51.9-40.8) 53.1) 12.5 (48.2-26.1) 24.2-15.Phthalates York City (Adibi et al.0 (67.4 (13.6 (30.7-20. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5-26.3) 13.9 (9.6) 12.6) 73.5-29.9 (24.7-69.8) 56.9) 64. 2003).9-104) 62.6 (34.4 (34.9) 12.1 (21.9) Total 14.3) 14.8) 13.4-60. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..7 (21.5-213) 49.2) 15.9) 12.9) 11.8) 24.6-116) 74..0 (41.4) 25.2-12.0 (11.7 (38.

Poland. 112(5):A270]. Environ Health Perspect 2004.110(5):515-518. Hauser R. Baird DD. Environ Health Perspect 2000. Calafat AM. Koch HM. Bull Environ Contam Toxicol 2002. Hoppin JA. et al. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Caudill SP.S. Environ Health Perspect 2006. Hum Reprod 2007. Rossbach B. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Prenatal exposures to phthalates among women in New York City and Krakow. Sampson EJ. Helm D. Reprod Toxicol 2004. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Ryan L. Ryan L. Pirkle JL. Singh NP. Meeker JD.93:177-185. Urinary levels of seven phthalate metabolites in the U. Green RA. Hodge CC. Sanchez GN. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Atlanta (GA). Centers for Disease Control and Prevention (CDC). Available at URL: http://cerhr. Brock JW. Drexler H. Jacek R. Needham LL. Barr DB. McKee RH. Needham LL. Dobler L. Levels of seven urinary phthalate metabolites in a human reference population. Reidy JA. Wittassek M. Environ Health Perspect 2002. Silva MJ. et al. Duty SM. Chen Z.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Blount BC. Davis BJ.108(10):979-982.nih. Research Triangle Park (NC). et al. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.210(3-4):319-333. Weuve J. Wiesmuller GA.Phthalates References Adibi JJ. Hagmar L. 4/20/09 Silva MJ.112(3):331-338. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.niehs. Barr D. Third National Report on Human Exposure to Environmental Chemicals. 2000 [online]. Caudill SP. Hilborn ED. Silva MJ. Epidemiol 2005. Environ Res 2003. Reproducibility of urinary phthalate metabolites in first morning urine samples. 2005. Phthalate monoesters levels in the urine of young children. Malek NA. Brock JW. Jedrychowski W. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Calafat AM.114(9):1424-1431. Perera FP. Rylander L. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].16(4):487-493. Camann DE. et al. Environ Health Perspect 2003. NTP-CERHR. et al. J Androl 2004.25(2):293-302. Eckard R. Schettler T. David RM. et al. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Hu H. Duty S.html.22(3):688-695. Angerer J. Caudill SP.18(1):122. Gans G. Brock JW. et al. Giwercman A. Koch HM. Richthoff J. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Int J Hyg Environ Health 2007. Jonsson BAG. Silva MJ. Butala JH.68:309-314. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Silva MJ.111(14):1719-1722.

80 (5..60 (8.3-43.3) 33.96) 3.7 (17.7) 15.10) 11..5) 18.60) 3.90 (3. population from the National Health and Nutrition Examination Survey.10) 9.70-4.20-12.6 (9.8 (9.67 (5.1-20.20) 7. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.40) 5. 2003). DBP can produce reproductive toxicity in male rodents (McKee et al. in men attending a Boston infertility clinic (Duty et al.70-8.0) 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 2.5) 18.33 (2. and in a small sample of Japanese adults (Itoh et al. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.9-14.3 (16.7) 18.48 (2.46 (3.5) 12.73-5.5 (27.97-7.80 (2.8) 40.S.30-13.56-4.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2. pharmaceutical coatings.2-22.6) 16.0-25.3-48.0) 9.6 (10.2 (11.60 (4. 2005).4 (14.0 and 0. CDC.10) 3. 84-74-2 Di-isobutyl Phthalate CAS No.5 (11.30-6.3-19.30) 10.9-23.7 (9. and also in some printing inks.1-25.73 (2.5) 19.82-3.3 (11. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.5) 23.70 (2.1 (13. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.5) 14.S.97) 4. NTP-CERHR.1) 25.00-6.3-20.90 (6.40-3.3.6 (29.40-9. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.97) 2.4 (20. 2004.3) 3.0 (11.3) 18.6 (13.37) 6.90 (4.00) 7.72-3.30) 10.6 (11.9) 15..68 (2.0) 20. When total DBP metabolites have been measured.2 (12. 2000.50-6.6 (14.49-2.85-6.1) 16.20 (3.20 (7.30-2.55 (3.10 (4.40-17.30-11.6) 12.40 (7.1-12.43) 6.7 (17.63) 3.00 (5.30 (4.3 (18.10 (3.1-17.30) 5.5-29.00) 4.50-2.4) 22.6 (13.00 (7.7) 14.70-4.20) 4. interval) 2.9) 10.60-6.66) 2.46-5.6 (10. Fourth National Report on Human Exposure to Environmental Chemicals 265 .0) 24.50) 8.3-24.70) 5.7-20.90 (4.0-18.9 (16.60 (2.8) 21.30 (1.00-4.28-5.17) 4.22) 3..71 (2.5-16.30) 2.30) 6.84) 4.3 (13.. OSHA has established a workplace air standard for external exposure to DBP.6) 26. In addition.19-3.80 (5.50) 18. about 65% to 80% of a dose is eliminated in urine within 24 hours.2-14. mostly as MnBP (Anderson et al.7-31.07 (3.6-26.5 (20.11-3.00-9.60 (5. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.5-16. residents (Blount et al.6-18.24-8.80-5.5-24..50) 5.22 (3.8) 677 652 703 699 1216 1088 Limit of detection (LOD.00) 6. and insecticides.50 (3.6) 17.7 (7.00) 4.30-6.9 (16.90-7.6-20. 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.10) 2.0 (13.30-7.4) 5. Koch et al. Biomonitoring Information Median concentrations reported in the NHANES 19992000.4) 12.6 (14.0) 13.10 (4.10-9.26 (2. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.02) 4.20-9.10-2.0-14.50-10.Phthalates Di-n-butyl Phthalate CAS No.46) 2. Studies of children found age-related differences in urine MBP levels.7) 4.00-6.17 (2.80-5.46 (2.4-27.80 (2.20 (6.7 (18.0-38. they have been referred to as monobutyl phthalate (MBP).6) 10.5) 22. Hauser et al.50 (6.2) 5.40-12.10) 8. Following oral administration of DBP to humans.3 (19.40 (3.40-4.20-2. 2003). 2000).5 (17.5) 25.40 (2.90) 12.20-12.2 (8. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.7 (16.3 (13.6-34. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.80) 75th 5.80 (3.50) 7.70) 3. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.50) 2.90-4.00) 10.3-18.20-6.1) 22.44-2.81 (3.40-5.56 (3. in a small sample of pregnant women in New York City (Adibi et al.70 (5.0) 12.6-14. 2004.6) 17.25) 01-02 03-04 01-02 03-04 01-02 03-04 4. Survey Geometric mean (95% conf.0 (19.59) 3.30 (3.. 2005.40 (6.3-30. 2007).2-33.0 (13..94) Selected percentiles ( 95% confidence interval) Sample 95th 17. 2005).4-12.1 (8.6) 16.90-2.56 (5.7-31.10-9.3 (16.50) 90th 12. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.7) 7.55) 2. 2001).00-11.90-4.50-4.7-18.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3. 2005).40-4.40-3..56) 3.30-3.5 (10.91) 4.40 (2.

61-3.3) 28.28 (4.04) 3.9 (11.97-2.51) 2.07 (2.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.51) 15.6) 13..8 (10.75 (4.30 (6.6-19.4-16.33-9.0-18. Survey Geometric mean (95% conf.52-3.07-5.20-2.56-4.86-4.28-13.38-10.4) 7.99) 7.31 (2.66) 2.46-11.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.80-3.68) 3. Between 1998 and 2003.54 (4.47-5.6 (12.08) 75th 4.81 (3.52-20.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.21) 10.08-2.5) 15.15) 3.14 (4.65 (4.33 (3.8) 10.5 (11.7) 3.96 (3.3) 16.and gender.59 (4.29-3.79 (4.1-12.43) 3.4) 15.7) 10.5 (9.1) 10.20 (2.44 (3.25) 5.0 (10.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.18-4.67-5.53-4.3 (13.02-10.74-3.6 (15.7 (9.53-3.2 (10.1) 15.1-25..7-28.86) 6.52) 3.5) 13.95-3.S.81) 4.80) 7.11-2. to about two to fourfold higher (Fromme et al.3) 13.2-13.72-7. 2002.81 (6. the students’ median values for MiBP levels remained relatively unchanged.20 (7.0) 11.64-7.27-12.52 (2.73 (5.58-4.69) 6.9 (15.0 (12.98 (2.94-12.1 (10.62 (6.65-4..18) 3.31) 2.0) 7.1) 4.04) 7.8-18.20 (2.32 (3.0 (8.9-40.85 (2.41 (2.57 (3.18 (1.3) 18.89-5.8-36.36-2.69 (2.7 (21.75 (6.94 (5.51) 5.53-5.43) 3.00-7.54) 2.91-6.7) 11.31 (7. An analysis of NHANES 2001-2002 showed similar age.1) 13.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .2) 24. 2007).33 (2.17) 90th 8.76-15. 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.. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples. Finding a measurable amount of MnBP or MiBP in urine does not mean that these levels or the parent compound cause an adverse health effect.1) 7.34 (3.17-12.95) 10.7) 19.00 (3.92 (7.9-16.76-3.42) 2.56) 5.78) 9.02 (7.29-8. 2004).69) 4.64-7.57 (3.56) 2.38 (6.94) 6.35) 3.68) 5.6-19.03 (5.11) 5.09-2.18-10.78) 8.46 (2.20-4.5-19.1 (11. 2005). up to four and 13 fold.20-3.32) 7. population from the National Health and Nutrition Examination Survey. interval) 2.10-5.6 (8.26 (2.9) 12.62-12.89 (3.88 (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.55-6.8-18.6 (10.26-2. while MnBP declined (Wittassek et al.64-10.8 (8.03-11.74 (4.9 (9.32 (7.03-7.47-12.66 (8.78-8. Differences in urinary MBP population estimates by gender have also been shown (Silva et al. than adults in NHANES subsamples during the same time period.66) 10.11 (5.3) 13.84 (8. Over this time.22 (2.39-3.81) 9..18) 4.6) 11.57-4.6 (9.69-7.05) 2.72) 5.95) 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.7 (13.0) 3.43) 3.6 (8.76-3.82) 4.82 (4.84 (4. 2006).47 (3.56-15.2 (11.15-4.37) 3.3 (17.79-6.19 (2.24) 3.79-8.58-3.1-15.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.31) 2. 2005). Weuve et al.8 (9. ranging from more than one-tenth the NHANES median (Itoh et al. 2007).0) 15.33) 3.2) 8.13-6.1) 11.66) 4.83 (2..00-3.21 (5.2-15.4) 23.68 (2.7 (11.46) 3.4 (12.65-11.8-13. 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.18 (4.39) 5.54 (2.2) 9.00-3.13 (2.99-4.01-2. samples from German university students had consistently higher median urine levels of MnBP and MiBP.9-26.1-24.93-6.45) 3. In an analysis of NHANES 1999-2000.76 (3.04-5.30) 2.36-7. respectively.17 (2.6) 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.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC. 2004).89) 6.80 (3.

0-51.9 (20.7) 74.2) 26.4-42.2 (59.5) 31.0 (23.7-20.5-47.1-75.8) 23.2 (74.3 (30.2) 32.2) 62.2 (18.9-92.1) 23.2-23.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.9.3-96.9) 18.3 (23.8 (57.9-28.4 (19.3-145) 85.6-69.6 (19.2 (21.7) 52.6 (90.6 (65.6) 17.8-42.7-24.3-76.1) 36.7-121) 97.5) 40.7 (70.5 (59.5) 24.5-44.1 (51.1-27. *In the 1999-2000 survey period.7-111) 64.1 (26.6-36.0 (45.7 (33.3 (42.1 (62.2-93.6 (44.1 (19.2 (21.1 (18.1 (31. 1.5) 78.6 (48.6) 38. respectively.7-92.6 (61.4 (35.5-47.2 (79.7 (22.9) 75.3) 19.3) 24.5) 36.5) 19.8-29.1 (19.0-24.6-31.9-33.2) 20.0 (15.4) 22.6-49.8) 75th 51.3-85.6 (55. and 03-04 are 0.0 (30.3) 23.6-33.7-106) 69.9-87.1.1 (58.7-42.4-60.2-32.4 (23.1-92.3) 18.1-80.9-53.5-60.2) 90th 98.3) 21.7-91.0-58.9-101) 77.2 (19.5-27.5 (74.1 (41.8) 48.8) 58.5) 36. and 0.1 (17.4 (84.3 (17.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.0 (31.8-119) 90.2-49.3 (36.5 (28.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.2) 38.6-20.7 (28.1 (34.7-127) 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 22.6 (32.5) 85.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.4-31.0) 20.7-53.4 (35.5) 95.8) 62.4-20.7 (16.6-29.0) 21.1) 31.3-21.7-117) 118 (108-143) 93. population from the National Health and Nutrition Examination Survey.6-24.9-22.1) 20.2-33.2-114) 73.0 (72.8-25.3-60.5-121) 106 (94.0 (20.6-44. interval) 24.5-43.5 (29.3) 36.4 (38.7 (18.2) 42.4-25.3 (23.6-29.1) 19.2 (78.1-82.3 (30.5) 17.6-48.4 (25.7 (24.3-79.4 (35.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.6-143) 127 (99.9) 26.7-26.7-42.7 (19.S.4-44.2 (25.6-40.6-113) 108 (90.6-37.2-21.6) 46.4) 64.6) 39.7 (64.0) 30.1 (19.1) 23.3-40.7-34.3-136) 137 (107-162) 119 (90.6 (16.2 (75.2 (58.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.7 (18.8) 19.1) 23.0-24.2-24.7) 28.1 (19.0) 84.0) 31.8-22.6 (22.2 (17.5 (59.2 (20.7 (51.6 (26.0-21.4 (71.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.0) 27.0 (78.3 (37.6) 21.4) 52. 01-02.4-159) 107 (84. referred to as monobutyl phthalate (MBP).1) 30.6) 71.9-42.0 (18.3) 26.7 (43.5) 47.9 (79.9) 46. Fourth National Report on Human Exposure to Environmental Chemicals 267 .4) 20.4 (21.5) 21.5-117) 95.1) 47.8-123) 101 (90.8-132) 95.3-24.0 (17.0) 117 (104-131) 112 (84.3 (56.6) 35.5) 34.1) 25.7) 124 (98.0) 38.9) 29.0-19.7-34.0-73.8-111) 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 23.5) 65.9-22.1-29.1-20.5-53.9 (79.4) 59.4 (35.0 (25.4-26.8 (19.3-67.1) 17.2-63.1) 46.6) 80.1-24.1 (21.1-51.1-22.9-114) 116 (97.0) 120 (98.5) 20. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.3 (60.3 (51.2-159) 92.0-26.1 (28.7 (38.2) 68.1 (54.2-87.7) 92.7) 42. Survey Geometric mean (95% conf.7-116) 95.0 (36.9) 21.5-42.0-19.8) 43.9 (17.9 (17.2-56.5) 26.5 (30.9-79.4-18.3) 40.9) 36.5) 37.6) 20.9) 71.0-32.4 (36. see Data Analysis section) for survey years 99-00.1 (16.4 (72.4.2-22.1 (36.

interval) 22.1-21.2) 31.7 (28.6-27.0 (27.6-50.9 (64.2) 159 (102-263) 147 (93.3) 33.8-24.7 (16.5 (18.1 (61.5-30.4) 53.7-80.4-103) 117 (83.7-26.2) 65.3-49.9) 52.0-38.7) 42.4 (33. Survey Geometric mean (95% conf.1-128) 97.0) 108 (71.6-43.7 (73.4 (47.3 (28.6 (19.0-90.4) 21.7) 20.4) 51.4) 15.3 (55.7 (20.9 (20.0) 28.9-100) 86.4 (50.9 (56.9-68.3) 35.5-22.9) 24.2-48.1) 37.8) 40.1) 42.7 (27.7-51.3 (48.3 (16.6) 64.7 (14.2 (38.9 (35.8 (18.4-164) 96.1-32.7-42.3-38.0 (50.2 (19.6-53.8-43.2-18.6-92.3) 59.0-47.1) 20.6 (25.3-32.0) 70.3 (52.9-56.3-18.6-24.9-68.9) 19.0 (69.5-76.0 (20.4 (16.5) 60.1) 50.6-19.9 (30.1 (56.3) 19.3) 33.4-61.3 (17.6 (27.0-60.7-28.6 (61.7 (57.6) 65.2-28.4-47.2-16.8 (13.5) 90th 68.0) 53.3-21.1-23.1) 20.4) 20.4-34.3) 21.1-83.8 (17.3-17.0-92.6-26.8) 17.6-44.8 (33.0) 41.0) 94.6-24.8 (22.7-19.5) 17.0 (71.6 (57.7) 36.6 (41.9-49.7 (43.5-16.3-78.5) 91.9-26.5-21.1) 35.6) 24.2 (19.9) 39.5-142) 89.6-22.6) 39.9 (39.4 (50.4 (31.1) 21.0) 26.6) 38.3-20.2-179) 84.7 (60.7 (60.8 (16.0 (19.3-71.5 (30.8) 34.5-41.0 (18.4 (37.9 (35.8-23.5 (81.7) 19.0) 81.1) 53.8) 75th 38.4-131) 81.5) 134 (93.5 (64.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.1 (29.9-84.4-135) 71.4 (31.4 (19.1 (46. population from the National Health and Nutrition Examination Survey.2) 21.2-85.4-24.1-99.3-39.7 (12.3 (71.7-20.8 (18.6) 14.2) 16.1 (32.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.2-22.6 (74.7 (54.9-105) 85.6) 23.7 (19.6 (29.4 (23.6 (17.5 (15.1) 22.2-61.7-78.4-72.3 (42.4 (31.6-44.9-70.3 (24.6-128) 96.9 (73.8) 20.4 (45.0) 35.1) 44.5) 82.4 (56.0) 75.9-38.5-70.3 (76.4 (16.0-75.8) 20.0 (52.9) 30.4) 62.1 (21.1 (15.9 (30.6) 24.0-17.9 (19.5-18.0 (16.1) 17.0) 25.6 (31.8) 35.4 (53.1) 61.6 (25.7-21.6) 18.0 (43.8-235) 137 (108-198) 88.4 (13.5-142) 81.4) 16.2-108) 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.3 (17.6-28.8) 22.8 (18. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.3-23.2 (35.2-22.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6) 83.0-19.5) 39.8 (50.9) 49.3) 20.4) 19.9 (30.1-99.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.5) 21.5-37.3) 17.0) 19.9) 14.3-21.9-36.9-34.0 (15.2-21.2-86.S.3 (46.3-40. 268 Fourth National Report on Human Exposure to Environmental Chemicals .5-23.9 (21.8 (65.7 (81.6-155) 91.3) 19.6 (72.6) 25.5 (14.0-41.4 (17.2-22.4) 15.5-15.3 (17.6-119) 63.4-76.8) 34.3) 18.9) 20.0 (70.9 (16.4 (17.2-106) 64.3 (69.6-23.8) 28.2-27.6-32.8) 17.4-65.1 (34.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.5 (18.3 (52.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.2) 59.8) 13.9) 91.8 (25.6-23.0-113) 104 (83.3 (21.2) 74.6-42.4 (20.0 (34.8) 30.4 (68.6) 31.5) 84.3 (19.7-37.0) 59.1-62.8) 63.6-16.8) 17.9) 62.8) 23.0) 55.2 (83.9-14.8) 19.2 (16.3-81.3) 67.3-26.3) 52.5-64.4 (18.2-73.0 (61.3 (60.6) 34.1-18.8-24.9) 28.8-32.0 (26.0) 29.7-19.0 (18.6-74.7-23.6) 37.9 (58.7-39.3-106) 74.9 (37.

Perera FP. Environ Health Perspect 2006. et al.114(9):1424-1431. 4/20/09 Silva MJ.Phthalates References Adibi JJ. Drexler H. Helm D. Ryan L. Levels of seven urinary phthalate metabolites in a human reference population. 2000 [online].22(3):688-695.210(3-4):319-33. Hagmar L. Rossbach B. et al. Koch HM.18(12):10681074. Wittassek M. Itoh H. Meeker JD. Sampson EJ. Green RA. Dobler L. Jacek R.18(1):122. Masunaga S. Giwercman A. Caudill SP. J Androl 2004. Fourth National Report on Human Exposure to Environmental Chemicals 269 . population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Hilborn ED.112(3):331-338. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Weuve J. David RM.111(14):1719-1722. Hu H. Silva MJ. Environ Health Perspect 2003. Brock JW. Bull Environ Contam Toxicol 2002. Available at URL: http://cerhr. Chen Z. Centers for Disease Control and Prevention (CDC). Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Silva MJ. Schettler T. Jedrychowski W. et al.S. Jonsson BAG. McKee RH. Int J Hyg Environ Health 2007. Massey RC. Pirkle JL. Third National Report on Human Exposure to Environmental Chemicals. Springall C. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Castle L. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Hum Reprod 2007. et al. Ryan L. et al. et al. Reidy JA.16(4):487-493.208:237-245. Environ Health Perspect 2000. Angerer J. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Sanchez GN.25(2):293-302. Epidemiol 2005. Hauser R. Environ Res 2003. et al. Caudill SP. Drexler H.108(10)979-982. Singh NP. Calafat AM.niehs. Barr DB. Koch HM. Caudill SP. Phthalate monoesters levels in the urine of young children. Int J Hyg Environ Health 2007. Prenatal exposures to phthalates among women in New York City and Krakow. Silva MJ. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Angerer J. Koch HM. Boehmer S. 112(5):A270]. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Anderson WA. Hodge CC. Brock JW. Yoshida K. Richthoff J. Atlanta (GA). Duty S. et al. Needham LL.gov/chemicals/ phthalates/dbp/dbp-eval.93:177-185. Needham LL. Silva MJ. Fromme H. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. 2005. Blount BC. Poland. Reprod Toxicol 2004. Wiesmuller GA. Eckard R. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. NTP-CERHR. Bolte G. Butala JH. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Barr D.68:309-314. Rylander L. Gans G.210:21-33. Camann DE. Research Triangle Park (NC). Scotter MJ. Environ Health Perspect 2004. Malek NA. Food Addit Contam 2001. Int J Hyg Environ Health 2005. Urinary levels of seven phthalate metabolites in the U. Calafat AM.html. Duty SM.nih.

70) .300-.600) .500 (.70 (1. polyvinyl acetate.400) 1.300-.300-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. 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.200-.600) .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 . 01-02.400 (<LOD-. and 03-04 are 0.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.400-.500) .400) < LOD < LOD .400 (. 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.20) .300-.90) .400 (. only levels at or above the 90th percentile could be characterized.600) .400-.10 (.600 (.70 (1.300-.200-.80) . respectively. and 0.400 (.400 (<LOD-.400-.500 (.900-1.500-.700) .00 (<LOD-1. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.500) .S.200-. and polyvinyl chloride.50) .200-.300-.700) .400) 1. < LOD means less than the limit of detection.10 (<LOD-1.300-.10) .9.600) .500) . Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (.500) 1.300 (.500 (.300-. 0.400 (<LOD-.10 (<LOD-1.500) . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.50) .70) .00-3. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers. In this Report.400-.400 (.300-. resins.00 (<LOD-1.200-. Survey Geometric mean (95% conf.700) .400-.400 (<LOD-.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.300 (. including nitrocellulose.300) < LOD .500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .Phthalates Dicyclohexyl Phthalate CAS No.00-2.500 (.600) .300 (.500) 1.200-.300 (.00 (<LOD-1.400-.300) < LOD .300 (<LOD-. and polymers.500 (.400 (.2.500) 1. 270 Fourth National Report on Human Exposure to Environmental Chemicals .500) < LOD < LOD .500 (.400 (. population from the National Health and Nutrition Examination Survey.400) < LOD 1.300 (.500 (.3. see Data Analysis section) for Survey years 99-00.300-.600) < LOD .400 (.10 (<LOD-2.200 (<LOD-.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . 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. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.500) < LOD < LOD .500 (.500) < LOD 1.400-.300 (.00) .

36-1.06) .470 (.510-.530 (.830) 1.500) 3.800-1.05) .690 (.330 (.53) .330 (.530-.450 (.690-1.380-.410 (.450 (.770) < LOD 2.16 (<LOD-3.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.670 (<LOD-.06) .33) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.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 .400-.630 (<LOD-.310-.290-.00) .43 (1.500) 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 .740) .33 (<LOD-3.380 (.670-1.660) .12-1.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .510 (.910 (.14 (<LOD-3.710) .950 (.590 (<LOD-.390 (.690) < LOD < LOD .690) < LOD 2.16) .740) < LOD < LOD .67 (1.610 (.240-.770-1.270) < LOD .480 (.44) . population from the National Health and Nutrition Examination Survey.34) .470) 3.910 (.53) .54-6.620) < LOD .170-.770-1.690) < 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 1.370 (<LOD-.00 (<LOD-3.530-1.770-1.82) .54 (<LOD-2.220 (<LOD-.500 (.360-.310) < LOD .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. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.54) .420-.630 (<LOD-.530) 1.17) .660) < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 271 .11) .420-.82 (1.940 (.770 (.910 (.400-.880 (.10) .490) .S.790-1.250 (.560) 1.590 (.500-.22 (<LOD-1.350-.18) .74) .260-.910 (.420-.

Products that may contain DEP include perfumes. 272 Fourth National Report on Human Exposure to Environmental Chemicals .9.9 (61. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples..Phthalates Diethyl Phthalate CAS No. 2002).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. 2007).4 (62.4.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. respectively.1 (71.7 (70. 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. and 03-04 are 1. 2001-2002.S.7) 71.3 (74.. In contrast. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products..3 (82. deodorants. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. shampoos. DC (Hoppin et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 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. see Data Analysis section) for Survey years 99-00. 01-02. colognes.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.2. particularly those containing fragrances.8-111) 85. 0. Biomonitoring Information MEP levels in the NHANES 1999-2000. and hand lotions. soaps. 2003) and African-American women in Washington. and 0.2-102) 95. population from the National Health and Nutrition Examination Survey. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.5) 81. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.1-93. and also in men attending a Boston infertility clinic (Hauser et al.

2 (66.9 (82. This age-related trend is opposite the direction seen for other phthalates. In an analysis of NHANES 1999-2000. Analysis of NHANES 2001-2002 showed similar findings..6 (77.Phthalates 2002 (Brock et al. Other population estimates also differed by sex and race ethnicity (Silva et al.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-114) 101 (87.9-110) 96. the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups. population from the National Health and Nutrition Examination Survey..6 (65.S. 2005). 2004).3-105) 87. Median MEP levels found in a small sample of German residents (Koch et al. with adjusted geometric mean levels of urinary MEP that increased with age (CDC. 2003) were slightly lower than levels found in NHANES 2001-2002. 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Urinary Mono-ethyl phthalate (MEP) (creatinine corrected) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.0 (66. 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.5-113) 122 (93. 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 92.7-110) 81.0-156) 140 (111-180) 150 (123-184) 154 (136-177) 160 (146-182) 177 (147-202) 165 (127-208) 177 (135-224) 180 (145-203) 364 (275-495) 330 (249-409) 363 (292-485) 390 (336-452) 419 (363-486) 512 (423-632) 341 (219-554) 512 (290-802) 470 (310-596) 879 (676-1260) 808 (590-1100) 791 (589-1080) 1010 (803-1460) 1060 (884-1320) 1230 (989-1610) 625 (400-784) 843 (512-1320) 719 (470-1330) 1760 (1000-2000) 1330 (868-1840) 1470 (987-2220) 2170 (1790-3350) 2120 (1520-2790) 2290 (1770-3200) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 141 (124-159) 148 (130-168) 154 (139-171) 187 (165-211) 187 (166-210) 211 (180-248) 120 (107-134) 126 (110-147) 127 (108-150) 158 (142-179) 171 (148-188) 181 (148-217) 324 (249-415) 352 (282-425) 390 (341-465) 377 (307-495) 407 (355-473) 508 (379-634) 1000 (693-1480) 1100 (839-1480) 1070 (852-1360) 822 (697-1170) 860 (712-1100) 1120 (889-1400) 1950 (1460-2900) 2120 (1490-3030) 2000 (1610-2410) 1930 (1170-3410) 1430 (1190-2010) 2250 (1440-3330) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 164 (142-190) 213 (182-249) 241 (213-271) 208 (183-236) 247 (226-271) 254 (225-287) 149 (135-165) 157 (142-173) 165 (144-189) 154 (136-174) 199 (164-242) 233 (202-270) 196 (166-228) 227 (185-270) 212 (188-246) 128 (111-142) 136 (124-150) 135 (120-158) 382 (314-472) 461 (396-572) 533 (417-665) 443 (390-505) 557 (478-618) 619 (476-791) 313 (239-387) 338 (288-402) 386 (338-485) 814 (673-974) 1080 (860-1650) 1230 (956-1610) 1030 (762-1700) 1240 (961-1480) 1530 (1200-1970) 856 (655-1390) 919 (712-1160) 989 (831-1330) 1330 (974-1920) 1940 (1410-2630) 2270 (1810-3140) 1920 (1230-2590) 2090 (1550-2800) 2590 (2160-3500) 1950 (1480-2740) 1590 (1320-2170) 1920 (1400-2780) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 273 . 2002).

Prenatal exposures to phthalates among women in New York City and Krakow.111(14):1719-1722. Silva MJ. Environ Res 2003. Hoppin JA. Davis BJ. Drexler H. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Caudill SP. Angerer J. Malek NA. Centers for Disease Control and Prevention (CDC). Brock JW. Perera FP. Barr D. Environ Health Perspect 2003. Barr DB. Hum Reprod 2007. Baird DD. Bull Environ Contam Toxicol 2002. Phthalate monoesters levels in the urine of young children. Jedrychowski W. Singh NP. Ryan L. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Atlanta (GA). Reidy JA. Silva MJ.22(3):688-695. et al. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Environ Health Perspect 2002. Brock JW. Silva MJ.S. Environ Health Perspect 2004. 2005. et al. Duty S.112(3):331-338. Jacek R.93:177-185. Rossbach B. et al. Caudill SP.110(5):515-518.68:309-314. Reproducibility of urinary phthalate metabolites in first morning urine samples. Hilborn ED.Phthalates References Adibi JJ. Meeker JD. Hauser R. Koch HM. Poland. Third National Report on Human Exposure to Environmental Chemicals. Camann DE. 112(5):A270]. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Needham LL. Hodge CC. Urinary levels of seven phthalate metabolites in the U.

92-2.6 (20.41) 3.5-27.31 (3.1-48. Fourth National Report on Human Exposure to Environmental Chemicals 275 .0-84.6-38.92) 4.60) 8.10-3.10) 2. and 0.2) 4.6-60.10) 3. 01-02.00) 2. ATSDR.0 (13.9 (26.50-5.70-5.82 (3. respectively.70-4.15 (1.6 (16.80) 6.90 (4.0-29.30 (4.8-47.8 (19.5 (18. 1982.57 (3.6 (10.4-27.6) 14.8 (17.1-29.6-25.0) 35.96-5.10-5.2-17.50 (3.90) 4.9) 27.2 (11.20 (3.83) 2.60 (6.9-49.0) 11.84) 3. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).00) 3.10 (4.91-3.50-2.90) 7.41 (3.20 (1.80 (2.9) 5.40 (2.50-6.30-13.3 (19.85 (3.S.4 (13.50-3.9.7 (14.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90) 1.30 (6.3-49.98) 2.3-25.1) 25.46) 3.50 (3.10) 4.0-18.80-27.10) 2.90-3.79) 2.7-32.1) 22.92-2.4-20.30) 2.90-11. 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.80) 9.5 (12.1 (11.40 (4.16 (2.9 (16.4) 13.2.0 (17.62) 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 5.80-9.3 (15.0 (14.7 (17.6 (9.80-4.00) 1. Albro and Lavenhar.2) 29.5) 43.0 (21. which is used for many consumer products.5-28.03-2.90 (3.00 (7.50-8.00-5.50-2.7-58.9-48.40-8.1 (8.5 (30.3) 13.20 (4.70 (7.7) 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 3.6-130) 31.00 (2.96) 4.70 (1.2) 23.7) 27.27 (3.9 (29. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.80 (1.6) 95th 23.50-5.1 (10.5 (12. see Data Analysis section) for Survey years 99-00.9-57.10 (4.8-50.70-2.3) 52.1 (8.60) 90th 14.61 (3.70) 2.6-28.1) 29. as glucuronide conjugates (Albro et al.86) 2.7) 8.7) 35.60-7..50 (7.9 (13.10 (5.70 (1.4-40.1-17.3 (10.9-28.10 (3.3 (11.2 (10.6) 5.0) Total 4. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.26-2.60) 3.6-23.40) 9.70-3.50) 9.3-64.84 (2.43 (3.80 (8.5) 19.70 (5.2-39.10-5.70 (3.9) 18.54) 4.5) 40.87-2.40-1. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.34 (2.90) 4. 2002. mainly polyvinyl chloride.1-17. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).9 (17.6 (11.0) 39. DEHP has been removed from or replaced in most toys and food packaging in the United States.30-11.2 (29.37-4.60) 10.70-5.5) 37.70) 16.4) 6.5) 31.7) 6.10 (3.90 (1.50-20. packaging film.6 (12.75-4.40-8.5-17.80 (4.00-3. 1.5 (20.