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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3.4.1.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.4.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.html.6.1. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.1-Dichloroethene (Vinylidene chloride) cis-1.2'. Paradichlorobenzene) 1.3.4’.4'-Pentabromodiphenyl ether (BDE 85) 2.4.3'.2'.3.3’.1-Dichloroethane 1.6'-Hexabromodiphenyl ether (BDE 154) 2.5'-Tetrachlorobiphenyl (PCB 49) 2.6-Pentabromodiphenyl ether (BDE 100) 2.3-Dichlorobenzene (m-Dichlorobenzene) 1.4'.1-Trichloroethane (Methyl chloroform) 1.5'.4-Dichlorobenzene (p-Dichlorobenzene. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.5.2-Trichloroethane Trichloroethene (Trichloroethylene) m.4.5.4.3.2-Dichlorobenzene (o-Dichlorobenzene) 1.2'.4.4.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4'-Tribromodiphenyl ether (BDE 28) 2. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4'.5'-Tetrachlorobiphenyl (PCB 44) 2.2'.4'-Tetrabromodiphenyl ether (BDE 47) 2.5.5-Pentabromodiphenyl ether (BDE 99) 2.3-Tetramethylbutyl] phenol) Triclosan (2. Table 1.4.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .2'4.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.2’.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.6-Heptabromodiphenyl ether (BDE 183) 2.2-Dichloroethene trans-1.5. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2.4’.2'.5’.2-Dichloroethene Dichloromethane (Methylene chloride) 1.gov/exposurereport/chemical_selection.4-Tribromodiphenyl ether (BDE 17) 2.cdc.4'.4'.2-Dichloropropane 2.5'-Hexabromodiphenyl ether (BDE 153) 2.2'.2'3.2'.2'. The process for selection is described at http://www.2'.4.What’s New in this Report What’s New in this Report In this Fourth Report.4.4.1.4'.4'-Tetrabromodiphenyl ether (BDE 66) 2.2-Dichloroethane (Ethylene dichloride) 1.4.1.

4-dichlorophenol and 2.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. urinary 2.5-dichlorophenol for the 1999-2002 survey periods. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. 2001-2002. and these data will be included in the next release of the Report. Data for other pesticides are included only for 1999-2000 and 2001-2002. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. Fourth National Report on Human Exposure to Environmental Chemicals 3 .1).. 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. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. the presence of an interference) that produced results of inadequate quality. Percentiles for all three NHANES survey periods (1999-2000. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. Explanations for each change are provided in Appendix B. five results that all have the value 90..g. Details of this procedure are provided in Appendix A.g. 2003-2004) have been re-computed by use of this improved procedure.

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

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

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

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

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

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

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

6-104) 82.7 (63.4-60.0 (69.9) 75.5) 66.1 (88.9 (69.2 (75.1) 53.2-70.4) 57. mineral processing.1-61.1) 55. acrylamide is synthesized and used in the production of polyacrylamide polymer. Natural substances in the food are converted to acrylamide.1 (47. widely distributed in tissues. and is either metabolized to the reactive epoxide. drinking water.7) 58.2-91.6 (56.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. FDA.3 (53. Fennell et al.0-49.9 (54. and binding agents. 2005).6 (81. 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. 1994).1) 101 (95. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.6 (51.7-64. gels.5-85.S.6-75. it was discovered that acrylamide is formed when starch-rich foods.4-83. pulp and paper production..9-105) 86. 2002).5 (74.3-71. In the general population. Survey Geometric mean (95% conf. such as potatoes and some grains. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.0 (53.5) 58.4 (54.8 (52. smoking. In 1997.7) 96. 1990.9) 63. Acrylamide is not thought to accumulate in the body at environmental doses.4 (59. 2005).7) 54.0 μg/kg for adults (FAO/ WHO. 2006.1) 46.7 (55. Elimination occurs mainly in the urine as mercapturic acid conjugates. EPA.3-2.Acrylamide Acrylamide CAS No. (NTP-CERHR. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.2 μg/kg/day (U. 2005).2) 57.6-66. ocular and dermal irritation from direct contact with acrylamide containing materials.2-77.9-52.7-64. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.6-65.4) 100 (89.9) 57. in permanent press fabrics. EPA reference dose of 0.5 (79. but can covalently bind to form adducts with proteins. 2004.7 (65.5-80. and from dermal contact with products that contain residual acrylamide. In humans. 2005).3) 63.8-55. but are generally above the U.S.6) 71.S.0-66. 2006).0 (67.2-114) 163 (147-191) 96. Fourth National Report on Human Exposure to Environmental Chemicals 11 . Animal studies indicate that acrylamide is well absorbed.4 (51.6) 50.9) 58.S.3) 86.4-89.6-108) 61.4 (53. as an absorbent in disposable diapers. These estimated intakes are hundreds of times lower than occupational exposures.8 (81. and in some cosmetics. Tareke et al. and well below doses known to cause nerve damage or carcinogenicity in animals.2-93. soil conditioners.4-76. see Data Analysis section) for Survey year 03-04 is 3.S.2 (58. 2005. and an average daily intake is estimated as 0.4-60.1 (83. 2005). in some sealing grouts.2-118) 98.5 (44.7-60.4 (54. acrylamide has produced upper airway irritation following inhalation of high levels.2-59.2 (62.1-57.0-108) 152 (139-175) 126 (111-142) 108 (86. and cosmetics (NTP-CERHR.5 (52. or to glutathione conjugates (Calleman et al.0.8 (57. 2004). the main source of exposure is from the diet. Commercially.0 (57.3) 70.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.7) 75th 79.1 (52. Polyacrylamides are useful water-compatible polymers used in water treatment.6) 73.0-58. FAO/WHO. interval) 61.2-67. Since acrylamide has limited volatility and high water solubility. glycidamide.6) 90.1) 62.0-104) 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. Estimated intakes in children are about twice that of adults (DiNovi and Howard. Recently. population from the National Health and Nutrition Examination Survey.2) 57.1 (73. EPA.1-64.6-61.8-57.8 (91.4) 57. 217 million pounds of acrylamide were produced commercially in the U. are heated at temperatures used for frying and baking..3 (55..7 (58. and in the synthesis or compounding of dye materials. People may be exposed to acrylamide from foods.1-64.0) 57.9 (60. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.7) 73.9-61.0) 85.4) 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.

U. 2005.0-103) 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 64.6-90. uterine. 2005.. presynaptic nerve terminal binding (LoPachin. 2001). 12 Fourth National Report on Human Exposure to Environmental Chemicals .S.9) 87.8 (51. EPA at: http://www. Vesper 2005) and smoking (Bergmark.. 2005..7-86...4 (56. Animal studies have shown that acrylamide can cause nerve damage (neuropathy). Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. Rice.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.9) 59. reproductive effects (reduced litter size. IARC classifies acrylamide as probably carcinogenic to humans.1-62.4-103) 79. adrenal. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.9-78..S. In addition. U. 2005). 2005.0. 2006.1 (70.3) 59.9-64. 2002.5-66..4-98. 2006) have been demonstrated after acrylamide dosing. 2005.9 (58. dominant lethality).2) 87..6-64.2-91. Glycidamide has been shown to react with DNA (Doerge et al.. 2005.0 (70. interval) 59. 2004. 2008).1 (56.Acrylamide occupational exposures. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.1-70.5 (83. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. 2005) and sperm DNA adducts (Xie et al..8-49. 2005). 2005.9) 65..2) 55. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.epa.8-61. 2005.2 (56. 2004).5-92.2-68. 2006).2-90.2 (63. 2005. 2005. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.0 (75.4 (61.4-59.8-48.. EPA.. 2005).1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59. 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. Klaunig et al. 1997.. Puppel et al..5 (56. Schettgen et al.4) 46.9) 75.5-64.2 (72.7) 90.7-62.who.3) 85. respectively) are markers of integrated acrylamide exposure over the preceding few months. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.7 (57. 2005) have been demonstrated in animals.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.3-78. population from the National Health and Nutrition Examination Survey.7 (87.6 (66.1) 60.9-138) 143 (130-159) 96.4 (90.1 (66. glycidamide (NTP-CERHR.1) 62.9-77.4 (57.4) 83.3) 59.8) 45.5) 71. most non-smokers had levels less than about 100 pmol/gram hemoglobin.7) 60.. Schettgen et al..7) 74..int/ ipcs/food/jecfa/summaries/summary_report_64_final. AHA levels have been shown to increase with dietary intake (Hagmar et al.5-94.3) 59.7) 61. 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.5) 75th 85. 2005).0) 118 (103-126) 121 (112-134) 113 (94.5) 87. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. and neuronal DNA reactivity (Doerge et al. 2009)..5 (59. scrotal.6 (90.1-60.7 (61. fetal death. EPA. see Data Analysis section) for Survey year 03-04 is 4.4 (81.9 (57.5 (42.9-62. Acrylamide is clastogenic and can produce dominant lethal mutations.8) 60. Survey Geometric mean (95% conf.7 (84. Hagmar et al.3-101) 95.. and other sites) (FAO/WHO. 2006). Vesper et al.8 (44. although different analytic methods can affect results.4) 53. Additional information is available from U.9 (81. 1997.0) 94. 2005.7-64. 2008).9-76. male germinal cell injury. 2003. altered gene expression in testicular tissues (Yang et al.6-62.0-93.1 (82. Maniere et al. Axonal degeneration.1-56. After exposure ceases. 2002.1) 56.4-65.3 (56. Puppel et al. and cancer (mammary. Mucci et al.0 (80. probably through its epoxide metabolite. NTP-CERHR.S.0-62.2) 65.pdf.0 (52.1 (57. thyroid.S.4 (51.

DiNovi M and Howard D. Available at URL: http://cerhr. Spicer R. Churchwell MI. Nordander C. Kamendulis LM.561:49-62. 6013-6019. [Epub ahead of print] Dybing E. Kautiainen A. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Calleman CJ. Chem Res Toxicol 1997 Jan.. Malmberg B. and Research Strategies. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Axmon A. Osterman-Golkar S.Toxicol Appl Pharmacol 1994.fda. Bridson WE. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . 64th Meeting: Summary and Conclusions (FAO/WHO).120(1):45-54. Food and Drug Administration (FDA).cfsan. 2001). Toxicol Appl Pharmacol 1993. da Costa GG. Italy. Acrylamide intake through diet and human cancer risk. Available at URL: http://www.. Calleman CJ. Toxicol Sci. et al. Wu Y. Mutat Res 2005. He F. Laurentie M. Tian G. et al. Illinois. Human exposure and internal dose assessments of acrylamide in food. Available at URL: http://www. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide.. 2001. Mutat Res 2005. Scand J Work Environ Health 2001. July. Fennell TR. morphological and molecular endpoints in animal models. Beland FA. 054472. Paulsen JE. Toxicol 2005. The Updated Exposure Assessment for Acrylamide. Mutat Res 2005.. Adv Exp Med Biol 2005. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Food Chem. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. gov/~dms/acrydata.who. Costa LG.43:365–410. NIH Publication No. LoPachin RM. Rome. Paulsson B. Perez et al.85:447-459. McDaniel LP. 2006.niehs. February. National Toxicology Program. Chicago. 2/3/09 Hagmar L. Becher G. Godard T. Alexander J. Cheong HK. 2005. 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. Maniere I. J Agric Food Chem 2008. 1994).Acrylamide In occupational settings.3:406-412.pdf. He F. Guffroy M. Bergmark E. Zhang S. Calleman CJ. Yang JS. et al. In another study.580(1-2):157-165. Mucci LA. Bruze M. Burgess J. Adv Exp Med Biol 2005. Churchwell MI.. CFSAN/Office of Plant and Dairy Foods. Costa LG. Joint FAO/WHO Expert Committee on Food Additives. Metabolism and hemoglobin adduct formation of acrylamide in humans. Magnusson AL. Aprea P. Summer SCJ. Toxicol Sci 2005. 8-17 February 2005. Farmer PB. Haugen M. 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. Mechanisms of acrylamide induced rodent carcinogenesis. Tornqvist M.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. 2009 Jan 8.56. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Uncertainties. smoking habits and gender. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide.nih. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Bergmark E. smokers and nonsmokers. Tornqvist M. et al. Hagmar et al. Andersen M. Survey data on acrylamide in food: individual food products. Rosen I. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Twaddle NC. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. 2004. et al. Acrylamide neurotoxicity: neurological.27(4):219-226.html#u1004.126(2):361-371.10(1):78-84. Doerge DR. Wilson KM. Doerge DR.580(1-2):119-129. Bergmark E. 1993. Duale N. Hagmar L.pdf.580(1-2):131-141. 2004 Acrylamide in Food Workshop: Update Scientific Issues.561:21-37.gov/chemicals/ acrylamide/Acrylamide_Monograph. Chem Res Toxicol 1990. Fennell TR. 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. Granath F. 1999). References Bergmark E. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Wirfalt E. 2/3/09 Klaunig JE. Bjellaas T. 2/3/09 Perez HL. April 13-15. Snyder RW.

et al. Eriksson S. Chemical Summary for Acrylamide. Yang HJ. Meyers T. U. 2/3/09. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Ospina M. Hemoglobin adducts of ethylene oxide. Toxicological effects of acrylamide on rat testicular gene expression profile. Ospina M. Licea-Perez H. Environmental Protection Agency (U. Myers GL. EPA). Angerer J.580(1-2):3-20. J Agric Food Chem 2002. Slimani N. Vesper HW. Tornqvist M. 1994. U. The carcinogenicity of acrylamide. Lee SH. Mutat Res 2005 Feb 7. Analysis of acrylamide. Adv Exp Med Biol 2005. et al.epa.20(6):959-64. Tjaden Z. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Puppel N. Tjønneland A. Han CH. September. Toxicol Lett 2006.274(1):59-68. Angerer J.206(1):9-14.134(1-3):65-70.207(6):531-9. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Int J Hyg Environ Health 2004. Fueller F. Integrated Risk Information System (IRIS). Smith A.Acrylamide glycidamide by gas chromatography-mass spectrometry. Ingham L. Tareke E. Acrylamide. Weiss T. Vesper HW. Benetou V. Toxicol Lett 2002.htm. Choi JH.gov/chemfact/s_acryla. Drexler H. Angerer J. Meyers T. Environmental Protection Agency (U.163(2):101-8.580(1-2):71-80. 2/3/09 Vesper HW.19(4):527-34. Office of Pollution Prevention and Toxics. EPA). Fu D. a carcinogen formed in heated foodstuffs. Liu K. Washington (DC).S. Kutting B. Mutat Res 2005.epa.txt. Letzel S. revised 1/3/06. Gray JG. J Agric Food Chem 2008. Rydberg P. Agudo A. Anal Biochem 1999. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population.56(15):6046-53.gov/iris/subst/0286. Marko D. Broding HC. Rice JM. Rapid Commun Mass Spectrom 2006.50(17):4998-5006. Hallmans G. Drexler H. Schettgen T. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Xie Q. Jin Y.561:89-96. Chae C.S.S. Sun H.S. Karlsson P. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Int J Hyg Environ Health 2003. Available at URL: http://www. Rossbach B. Liu Y. propylene oxide. Han DU. Reprod Toxicol 2005. Lee MH. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Schettgen T. Available at URL: http://www. Drexler H. Ding X. Schettgen T. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry.

65 (1.302) .120 (.073) < LOD .60-2.23 (.39) 3.160) .920 (.19) 1.990) .20 (.540-. acute respiratory illness.50 (1.88 (1.094) .070) 75th .62 (2.220) .175 (.071 (.730 (.050 (<LOD-.990 (.089) Age group 3-11 years 99-00 01-02** 03-04 .190-.21-1.040-.060-.120 (.26-1.087 (.360) .57) 2.030-.48-2.090-.49) 1.106-.35 (2.94) 1.140 (.09-3.040 (.310) 90th 1.75) 1.210 (.180 (.14) . emphysema.068) .79) 3.726) .310-1.570 (.02) 1. 83% of measurements had an LOD of 0.S.234) .09-3.45) 1. DHHS.200) 1.53 (1.87-3. stroke.060-.428-.086 (.066-.140 (.077) .030 (.063) .84-3.110) ..96-4.23 (1. acute respiratory infections.050) .78) 2. and various other disorders (U.54) 1.580) .17 (1.630 (.139) * .190-.047-.99) 2.030-.059-. which may vary for some chemicals by year and by individual sample.540 (.052 (<LOD-.480-1.080-.860 (.620 (.68 (1.080) < LOD .47-3.630 (.55-2. see Data Analysis section) for Survey years 99-00.11) .770) . cardiovascular disease.39 (1.060 (<LOD-.54 (1.150) .910-1.180) .00) .42-4.997-3.230) .220) .160 (.308 (.20) .81-2.20) 1.470-.690 (.19) .50-1.163) .320) .164 (. < LOD means less than the limit of detection.059-.240 (.580-1.570-1.05) 1.68) .050-.060 (<LOD-.33-2.130 (. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.20 (1.145) .30) 2.110 (.124 (.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .076-.960-1.070) .63-2.150) .44 (1.115-.12 (2.066) .99) 2.052 (<LOD-. Survey Geometric mean (95% conf.430-1.22) 2.137-.5% nicotine by weight (Kozlowski et al.950-1. Cigarettes contain about 1.040 (.120) .43 (1.111-.230 (.950 (.090-.110-.21-1.05 ng/mL.080 (.70-2.02) 1.071) .180) .153-.77 (1.820) .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 exacerbated asthma (U.09-2.770) .140-.142-.21 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. 1998).15) 2.050-.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.410) .090-.96) 2.160 (.260-1.510 (.110 (.12-4.88 (.01) 3.400-.160) .66 (1.28-1.061) < LOD .050 (<LOD-.075 (.44 (2.062 (.930 (.110 (.110) .55 (1.131 (.533-.38-2.193) .060 (.12 (1. 2006). 2004).42 (1. Serum Cotinine Metabolite of nicotine (component of tobacco smoke) Geometric mean and selected percentiles of serum concentrations (in ng/mL) for the non-smoking U.110-.180) .054 (.40) .77 (1.505 (.625) .187) .85 (1.70) 2.070) .108) * .05.350-.220-.043-.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .120 (.32) 1.S. DHHS.350 (.070 (<LOD-.17) .197) .080-.95) 1.14) . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.015.500 (.370-.087) < LOD < LOD .201) .14-1. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.83-2.350-.310) .130) .630 (. ** In the 2001-2002 survey period.180) . population from the National Health and Nutrition Examination Survey.76 (1.50-4.040-.23-2.66-3.050 (.300) .580 (.506 (.50) 3.790) .00) 1.110-.080-.30) * .89) 1.28) .080 (.080) < LOD < LOD .088-.480-.04 (1.144 (.050 (<LOD-.198) * .93) . and 0.060 (.163 (.710 (.20-2.770-1.213) .120 (. Children exposed to ETS are at increased risk for sudden infant death syndrome.053 (<LOD-.110 (.32-2.154-.260) 1.02 (.S.137 (.18-3. maternal exposure during pregnancy can result in lower birth weight.312) .060) .53-4.310-1.160 (.Cotinine Cotinine CAS No.44) 2.63 (2. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.164 (.16) .015 ng/mL.140-.34 (1. 2004).110 (.100-.15 (2.19-2. Fourth National Report on Human Exposure to Environmental Chemicals 15 . ear problems.520 (.080-.020-.48-3.087-.066 (.54 (1. respectively.96 (1.621-1.084) .077) .167 (.180) .068) .740-1.68) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.057-.900-1.620-1.77 (2.92 (1. and 17% had an LOD of 0.840) 3.216 (.058 (.17 (. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.850 (.180 (.600-1.62) 2.160-.040 (.120 (.188) .050 (<LOD-.740-1.800 (.44) 2.30) 2.32-2.190-.148-.280 (.660) .030-.120-. 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.047-.49) 1.120-.66) 1.126) .23 (2.450-.670) .060-.070-.12) 1.01 (1.050) . and 03-04 are 0.104-.

1991). nausea. non-Hispanic blacks metabolize cotinine more slowly than do non-Hispanic whites (Benowitz et al. and hair. The serum cotinine levels seen in the NHANES 20032004 appear approximately similar to levels seen in the previous survey period (NHANES 2001-2002) for the total population estimates. The Federal Aviation Administration has banned the smoking of tobacco products on both domestic and foreign air carrier flights in the United States. Nicotine stimulates preganglionic cholinergic receptors within peripheral sympathetic autonomic ganglia and at cholinergic sites within the central nervous system. (CDC. 1999. Non-Hispanic blacks had higher serum cotinine concentrations compared with either non-Hispanic whites or Mexican-Americans. Hukkanen et al. and peppers. 2005. Wilson et al. Nicotine can also be absorbed from the gastrointestinal tract and skin by using snuff. and increased appetite. the primary sources for ETS exposure are in a workplace where smoking occurs and in a residence shared with one or more smokers. nasal sprays. Nicotine also indirectly causes a release of dopamine in the brain regions that control pleasure and motivation. Soliman et al. Nonsmokers exposed to typical levels of ETS have serum cotinine levels of less than 1 ng/mL. Higher levels of cotinine have previously been reported for non-Hispanic black smokers (Caraballo et al. Measuring cotinine is preferred over measuring nicotine because cotinine persists longer in the body with a plasma half-life of about 16 hours (Benowitz and Jacob. which include potatoes. cognitive and sleep disturbances. and death.. Active smokers almost always have levels higher than 10 ng/mL and sometimes higher than 500 ng/mL (Hukkanen et al. Nicotiana tabacum. 2005). seizures.. Inhaling tobacco smoke from either active or passive (ETS) smoking is the main source of nicotine exposure for the general population. a process involved in the development of addiction. 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.. with levels showing similar or slightly higher results (depending on the degree of ETS exposure) than those reported in the previous NHANES (CDC 2005. is currently regarded as the best biomarker in active smokers and in nonsmokers exposed to ETS. The IARC and the NTP consider tobacco smoke to be a human carcinogen.. contains nicotine in larger amounts than other nicotine-containing plants. Perez-Stable et al. saliva. 2006).. 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. In homes with one or more smokers. 1999). mean air concentrations typically range from 2 to 14 µg/m3 (NTP. Up to 90% of the nicotine delivered in tobacco smoke is absorbed rapidly from the lungs into the blood stream (Armitage et al. 1975. Hukkanen et al. NIOSH guidelines consider ETS to be a potential occupational carcinogen and recommend that exposure be reduced to the lowest feasible concentration. vomiting. with higher levels measured in restaurants and bars. Serum cotinine has been measured in many studies of nonsmoking populations. 1996). 1998). chewing tobacco. html. Cotinine. salivation. 2005).. Mean air concentrations of nicotine in public spaces where smoking is allowed range from 0. tomatoes. Over the previous decade. 2004).3 to 30 µg/m3.gov/researchreports/nicotine/nicotine. 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. Acute tobacco or nicotine intoxication can produce dizziness. diarrhea.nih. nicotine has a half-life in blood plasma of several hours (Benowitz. 1998). Iwase et al. However.. For an adult.. craving. Nicotine is also used commercially as an insecticide in its sulfate and alkaloid forms. 1996).. 2006. Children are primarily exposed to ETS by parents and caregivers who smoke. 2005). 1999. 2004). eggplants.. More information about the effects of smoking and nicotine can be found at: http://www. 1994). with heavy exposure to ETS producing levels in the 1–10 ng/mL range.nida. or skin patches that contain nicotine. Once absorbed.. levels of exposure to ETS appeared to decrease since geometric mean cotinine serum concentrations in nonsmokers had fallen by approximately 70% and the rate of detectable cotinine in nonsmokers fell from 88% to 43% when NHANES 1988–1991 was compared to NHANES 1999–2002. During each previous NHANES survey. Biomonitoring studies of serum cotinine will help physicians Fourth National Report on Human Exposure to Environmental Chemicals . or chewing gum. The tobacco plant. urine.. Symptoms of 16 nicotine withdrawal include irritability.. the primary metabolite of nicotine. diaphoresis. 2006). Nonsmoking is usually defined as a serum cotinine level of less than or equal to 10 ng/mL (Pirkle 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. NCI. Cotinine can be measured in serum. variable changes in blood pressure and heart rate.. Biomonitoring Information Serum cotinine levels reflect recent exposure to nicotine in tobacco smoke.Cotinine 1994. Pirkle et al. 2005..

7:369-375.S. Jacob P. Racial/ethnic differences in serum cotinine levels among adult U. National Center for Chronic Disease Prevention and Health Promotion.291(3):1196-1203. Curtin LR. Hukkanen J. Benowitz NL. Modin G. Mehta NY. Turner DM. 1991. Richter PA.280:135-140. JAMA 1998. Herrera B. Sosnoff CS. Am J Public Health 2004. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Summary of Data Reported and Evaluation [online] 2004.pdf. Pickett MA.nih. Perez-Stable EJ. National Institute for Occupational Safety and Hygiene (NIOSH). Houseman TH.gov/eid/rmca/critdocs/ criteriadoc/33.cancer. DHHS). iarc. In Report on Carcinogens. Metabolism and disposition kinetics of nicotine. Caraballo R. Sweeney CT. et al. Department of Heath and Human Services. 1988-1991. Etzel RA. Tob Control 2006. IARC Monogr Eval Carcinog Risks Hum. Vol 83. Exposure of the U. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Brody DJ.56:483-493. Tobacco related exposures. cigarette smokers: the Third National Health and Nutrition Examination Survey. Available at URL: http://monographs. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.S. et al.57(1):79115. Dollery CT.niosh. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Centers for Disease Control and Prevention. Soliman S. Schober SE. Nicotine metabolism and intake in black and white smokers. Pollack HA. Department of Heath and Human Services. Centers for Disease Control. 1999.275:1233-1240.63:139-43. Int Arch Occup Environ Health 1991. Available at URL: http://monographs. Benowitz NL. References Armitage AK. Kozlowski LT.S. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.niehs. Maurer KR. Aiba M. Bernert JT. 1999-2002. Pirkle JL. Pechacek TF.94(2):314-320. June. Vogler GP. Trends in the exposure of nonsmokers in the U. Benowitz NL. population to secondhand smoke: 1988-2002. Pharmacol Rev 2005. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. U.S Department of Health and Human Services (U. 4/13/09 Perez-Stable EJ.280:152-156. Smoking and Tobacco Control Monograph 10 [online]. Epidemiol Rev 1996. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Fong I.S. Benowitz NL. Ethnic differences in N-glucuronidation of nicotine and cotinine.15:302-307. Summary of Data Reported and Evaluation [online] 1986. Office on Smoking and Health [online] 2006.surgeongeneral. National Toxicology Program (NTP). Brody DJ. Jacob P III.fr/ENG/Monographs/allmonos90.gov/tcrb/monographs/10/. 4/13/09 Iwase A. Warner K. Absorption and metabolism of nicotine from cigarettes. Benowitz NL.cdc.S. U. Coordinating Center for Health Promotion. George CF. International Agency for Research on Cancer. Kira S. Giovino G. JAMA 1998. Caudill SP.S. Mowery PD.4:313-316. Respiratory nicotine absorption in non-smoking females during passive smoking. Pirkle JL.php.S Department of Health and Human Services (U. Available at URL: http:// cancercontrol.fr/ENG/Monographs/ allmonos90. Schwartz SS. 11th ed. Strauss WJ. Third National Report on Human Exposure to Environmental Chemicals. Tobacco Smoke and Involuntary Smoking. Vol 38. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . 1988-1991. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects.114(6):853-858. 4/13/09 Centers for Disease Control and Prevention (CDC). Tobacco Smoke. 4/13/09 International Agency for Research on Cancer. 4/13/09 National Cancer Institute (NCI). Coordinating Center for Health Promotion. Available at URL: http://www. Environ Health Perspect 2006.S. BMJ 1975. Pechacek TF. Atlanta (GA): 2005. Flegal KM.php. Clin Pharmacol Ther 1994. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Lewis PJ.gov/library/ secondhandsmoke/. U. Bernert JT.gov/ntp/roc/eleventh/profiles/ s176toba. and the United States. Jacob P III. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace.18:188-204. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. DHHS). Cotinine as a biomarker of environmental tobacco smoke exposure. [online]. Herrera B. 4/13/09 U. available at URL: http://mtn. IARC Monogr Eval Carcinog Risks Hum. Jarvis MJ. JAMA 1996.iarc. Tob Control 1998. J Pharmacol Exp Ther 1999. Jacob III P. Available at URL: http://ntp.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. the United Kingdom. Giovino GA. Centers for Disease Control and Prevention.pdf. 2004.

18 Fourth National Report on Human Exposure to Environmental Chemicals .cdc. Kahn RS. Environ Health Perspect 2005.113(3):362-367. htm#full. Available at URL: http:// www. Khoury J Lanphear BP.gov/tobacco/data_statistics/sgr/sgr_2004/index. 2004. [online].Cotinine Chronic Disease Prevention and Health Promotion. Racial differences in exposure to environmental tobacco smoke among children. 4/13/09 Wilson SE. Office on Smoking and Health.

180 (. Urinary N.130 (. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . < LOD means less than the limit of detection.130-. DEET is not genotoxic. Neurological effects in humans. 134-62-3 General Information N. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.250) < LOD .N-Diethyl-meta-toluamide (DEET) CAS No..100-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1.110-. EPA.240) < LOD .N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. Additional information is available from U.220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .100 (<LOD-.140) < LOD . 1995.140) < LOD .110 (.180 (. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.170 (.110 (.S. About 3-8% of dermally applied DEET is absorbed.170 (.130-. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. 1998).270) 688 678 518 700 598 956 Limit of detection (LOD.220 (.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .. 2003).100-. After absorption.S. Fourth National Report on Human Exposure to Environmental Chemicals 19 . 2002).130-. (U.150) < LOD .110 (<LOD-. (Kolpin et al.EPA.449 and 0.180) < LOD .140-.130) < LOD .520) < LOD .210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S. DEET is not registered for use on agricultural commodities.S. and they range in concentration from 4% to 100%.S.S.140 (. DEET is also used in combination with dermal sun screens (U.130 (.140) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . DEET can be applied to clothing and the skin to repel biting insects. 2002).N.560) < LOD .100-. 2005). General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. including seizures and encephalopathy. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.gov/pesticides/. 1998).210 (.N-Diethyl-meta-toluamide (DEET) N.120-.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. DEET has low acute toxicity.120-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.110 (.130 (.100-.110-. Sudakin and Trevathan. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.160) < LOD .epa.. There are over 225 insect repellents brands containing DEET. One survey detected DEET in 74% of sampled streams in the U. 2003).130-.EPA. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.100-. have been reported as result of self-poisoning by ingestion or excessive dermal application.180 (. Its use is recommended for prevention of several vector-borne diseases.110 (<LOD-. and it has not been rated by IARC or NTP with respect to human carcinogenicity.130) < LOD . DEET is not a developmental or reproductive toxicant in animals (U.110 (.190) < LOD .EPA at: http://www.100-. which may vary for some chemicals by year and by individual sample.140) < LOD .

320 (.140-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD ..350-.440) < LOD .300 (.150-.580) 964 1191 1013 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .250-.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 .370-.250) < LOD .270 (.170-. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.150) < LOD . 1992)..250 (. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.93) < LOD .330 (. In this survey period.230) < LOD .N.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.320) < LOD .490) < LOD .500 (. 2005).640 (.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.270) < LOD .410-.280-1.130 (<LOD-.290-.200 (.270-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.370) < LOD .410 (.350) < LOD . representative subsamples from NHANES 2001-2002. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.240-.230-. 20 Fourth National Report on Human Exposure to Environmental Chemicals .N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure. population from the National Health and Nutrition Examination Survey. 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.190 (. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.S.630) < LOD .330 (.190 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.280 (.350) < LOD . Urinary DEET levels as high as 5.190-.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 .270 (<LOD-.230-.480 (.410 (.390-.240) < LOD .190 (<LOD-. 2007). Urinary N.

Grzywacz JG. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Zaugg SD.2:341352. Meyer MT. Fundam Appl Toxicol 1995.pdf. metabolism.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. Pharmaceuticals. Available at URL: http://www.N-Diethyl-meta-toluamide (DEET) References Arcury TA. Centers for Disease Control and Prevention (CDC). Barr DB. Sudakin DL.gov/oppsrrd1/REDs/0002red. and excretion of N. Toxicity and Exposure Assessment in Children’s Health. 4/9/09 U. U. Chen H.115(8):1254-1260.25:95-100. Int J Toxicol 2002. hormones. Page BC. Quandt SA.EPA). Environmental Protection Agency (U. 1-118. Selim S.S. 1999-2000: a national reconnaissance. streams. Hartnagel RE Jr. 1993-1997. pp. EPA 738-R98-010.EPA. 2005 Kolpin DW. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. EPA.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. DEET: a review and update of safety and risk in the general population. Lowry LK. Diethyltoluamide (DEET). Environ Sci Technol 2002.N. Furlong ET. Environ Health Perspect 2007. Veltri JC. Osimitz TG.N-diethyl-mtoluamide following dermal application to human volunteers.S. 2005.EPA). Smallwood AW. Third National Report on Human Exposure to Environmental Chemicals. J Toxicol Clin Toxicol 2003. et al. and other organic wastewater contaminants in U.epa. Trevathan WR. pdf. Human exposures to N.epa. J Anal Toxicol 1992.36(6):1202-1211. Schoenig GP. N. Washington (DC): U.16(1):10-13.S. Absorption.S. U. Available at URL: http://www. Reregistration Eligibility Decision (RED): DEET. September 1998. Gabriel KL. Atlanta (GA). DeBord KE. Chemical Summary.S.S.gov/teach/chem_summ/ DEET_summary. Thurman EM. Barber LB. Bell JW. Tapia J.41(6):831-839.S. Environmental Protection Agency (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

Hum Ecol Risk Assess 2004. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP).137(3):353-362. Kawamura N.S. Needham LL. N. Exposure of the U. Yoshinaga J.113(4):391-395. 5: 505-523. Tyl RW. 2007. Rhomberg et al. Park S. Human Health. Available at URL: http://cerhr. Hlywka JJ.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report..eu/ health/ph_risk/committees/sct/documents/out156_en.nih. C. Twomey K.59(4):403-408.niehs. Italy. Koulova AI. Yang M.780(2):365-370.europa. Han SS.36(6):1202-1211. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Meyer MT. Gender differences in the levels of bisphenol A metabolites in urine. Thurman EM. Hughes C. Munro IC. Tsugane S. Ecotoxicity and the Environment (CSTEE). 2/4/09 Fujimaki K. Zaugg SD. 2008.S. Life Sci 2001. hormones. Richter CA.nih.14(2):149-157. National Toxicology Program. Rubin C. Joint Research Centre Institute of Health and Consumer Protection. National Institute of Environmental Health Sciences. streams. Brine DR. Cunha G. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Biochem Biophys Res Commun 2003. Serizawa S. Available at URL: http://ec.nih. vom Saal FS. European Commission.116(1):39-44. 2003. November 26. and other organic wastewater contaminants in U. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Chung MK. 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. Lynch BS.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Ekong J. Harazono A. Available at URL: http://ntp. Szigeti-Buck. Occup Environ Med 2002. Koh WS. An evaluation of the possible carcinogenicity of bisphenol A to humans. Pyo MY. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Cohen JT. Sottas CM. Watanabe S.145:592-603. Arakawa C. Brussels. May 22. Imai H. McConnell EE. Kroes R.69(22):2611-2625. Hanaoka T. niehs. MacLusky.J.gov/chemicals/bisphenol/BPAFinalEPVF112607.68(1):121-146. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Furukawa M. Research Triangle Park. Han SY. Kim YH. Available at URL: http://cerhr. Ispra. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Kiguchi M. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).pdf. Howdeshell KL. Calafat AM.jrc. Available at URL: http://ecb. Marr MC.Environmental Phenols References Akingbemi BT. Joskow R. niehs. Ema M. Kuklenyik Z. Kim JC. Barr DB. 32 Fourth National Report on Human Exposure to Environmental Chemicals . K.pdf . Fujii S. Ye X. Environ Sci Technol 2002. Thomas BF. Needham LL. Caudill SP. Cha SW. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Barton L. NC. and Hajszan. 2002. U. Ikka T. et al. et al. Endocrinology 2004. Proc Natl Acad Sci USA 2005. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.pdf. Nippon Eiseigaku Zasshi 2004.. Regul Toxicol Pharmacol 2002. Barr JR. Zacharewski TR. Barber LB.59(9):625-628. Klinefelter GR. Reidy JA. Kim CS. Shin HC. Reidy JA. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. 2/4/09 European Commission.35(2 Pt 1):238-254. et al.pdf . Wong LY..it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Needham LL. Environ Health Perspect 2005.Scientific Committee on Toxicity. Matthews JB. 2/4/09 Ouchi K. Haighton LA. Department of Health and Human Services.S. Timms BG. Calafat AM. Watanabe C. September. 4.pdf. Toxicol Sci 2002. 1999-2000: a national reconnaissance.312(2):441-448. Gray GM.102(19):7014-7019. Myers CB. Calafat AM. Endocrinology 2008. August 2001. J Am Dent Assoc 2006. T. Kolpin DW. Bisphenol A. In vitro and in vivo interactions of bisphenol A and its metabolite.gov/chemicals/bisphenol/bisphenol. Rat two-generation reproductive toxicity study of bisphenol A. and Hardy MP. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Furlong ET. Leranth. bisphenol A glucuronide. Reprod Toxicol 2001. DirectorateGeneral Health and Consumer Protection. with estrogen receptors alpha and beta. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Environ Health Perspect 2008. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Bradley S. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Keimowitz AR. National Institutes of Health. Belgium. Hara K.10:875-921. Doull J. Pharmaceuticals. Chem Res Toxicol 2001.149:988-994.

Large effects from small exposures. Witorsch RJ. Chuang JC. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure.113(8):926-33. An observational study of the potential exposures of preschool children to pentachlorophenol. Biological monitoring of bisphenol a in a Korean population. Morgan MK. Food Chem Toxicol 2002. Filser JG. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Sheldon LS. Jang JY. Chang SS. Csanady GA. Kim SY. and nonylphenol at home and daycare.44(4):546-51.103(1):9-20. Environ Res 2007. Colnot T.15:12811287. Vom Saal FS. bisphenol-A.Environmental Phenols Volkel W.40(7):905-12. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. vom Saal FS. Hughes C. Environ Health Perspect 2005. et al. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Yang M. Kawamoto T. Lordo RA. Nagel SC. III.147(6 Suppl):S56-69. Wilson NK. Endocrinology 2006. Lee SM. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Chem Res Toxicol 2002. Arch Environ Contam Toxicol 2003. Dekant W. Welshons WV.

50) 1. 2006.600) . Indoor and to a lesser extent. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.700-1.80 (1.600) 1. During the 1980s and 1990s.497) * .500-1. and from contact with some personal care products and detergents. 140-66-9 General Information 4-tert-Octyphenol.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 .10 (1.300 (<LOD-.00) 1229 1288 03-04 03-04 03-04 * .3. Less frequently.600-1. population from the National Health and Nutrition Examination Survey. Laws et al.30) 1.900 (. orally administered 4-tert-octylphenol was well absorbed.10-2. 2002).00 (.30-2. In the 1990s.70 (1. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.20 (1. Bian et al. altered neonatal sexual development.60-3. In 1999-2000.600-1.300-.600-1.500) .60) .30) 90th 1. 34 Fourth National Report on Human Exposure to Environmental Chemicals . and some of their degradation products are toxic to aquatic life.500) 75th .600) .20-2.900 (.20) 2.200-.30 (1. The alkylphenols can bioaccumulate in some fish.90) 2.30 (1.30 (.400 (.S. and impaired spermatogenesis (e. 1997. did not bioaccumulate.40 (1.5% of 139 U. Ying et al. 4-octylphenol monoethoxylate was detected in 43.60-3. is used to manufacture alkylphenol ethoxylates.90) 2.900 (.40) * 03-04 03-04 03-04 .389 (. Katsuda et al.20-2.60) 613 652 1092 Limit of detection (LOD. to shorter chain alkylphenol ethoxylates.00 (.80 (1.20-2.10 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. Survey Geometric mean (95% conf.60-3.20-2.60-3. the various alkylphenols have also been used as emulsifiers and modifiers in paints.10 (.600-1. and through manufacturing waste streams (Warhurst.40) 2.. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.30) 2. The alkylphenol ethoxylates enter the environment through human use of products containing them.g.600-1. Saito et al.20) 314 715 1488 03-04 03-04 * * .500-1. testicular atrophy.357 (.369 (. altered estrus cycles and reproductive outcomes.400 (.500 (..30 (1. and was quickly eliminated from the blood (Certa et al..50-2.20) 1. over 500. industrial cleaners. Several alkylphenols.40) 2.Environmental Phenols 4-tert-Octylphenol CAS No.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.500) .70 (1. which may vary for some chemicals by year and by individual sample.900 (. 1996).600) .10) 2.477) . 2004).300-.900 (. 2000. through sewage.20-2. In rats.60-3.00 (1.. Urinary 4-tert-Octylphenol (4-[1.600-1. 2003. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.200-..000 tons of alkylphenol ethoxylates were produced annually worldwide. and some personal care products.60) 1.60-3..50) 1.300 (<LOD-.300 (<LOD-.507) * < LOD .40) 1. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.274-.20-2.268-.400 (.. pesticides.300 (<LOD-.300 (<LOD-. fish) and drinking water.30 (1.g. and emulsifiers.80 (1. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.50) . Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.50) .70 (1.. < LOD means less than the limit of detection. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol)... an alkylphenol.400) 1.40) 1. and to alkylphenoxycarboxylates.50-3. 1995. 2000.10) 1.299-.70 (1. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.80) 2.500) .S.800-1. and the polyethoxy chain may consist of up to 50 ethoxy units. streams in 30 states (Kolpin et al. Blake and Boockfor. see Data Analysis section) for Survey year 03-04 is 0. which are anionic surfactants used in detergents. have demonstrated estrogenic effects particularly when injected at high doses in animals.50) 1. leading to inhalation as another potential exposure route (Rudel et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. including 4-tert-octylphenol. Disposition in humans has not been studied sufficiently. impaired steroidogenesis. textiles. 2002).50 (1.1.2.

850 (.337-.410 (.65-3.02-4.S. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.85 (1.640-1.11) 1. nonylphenol.349) * < LOD . Kawaguchi et al.420) .96-4.450) . Nagao et al. Tyl et al.500-1.Environmental Phenols Myllymaki et al.33 (2. IARC and NTP have not rated octylphenol. 2001.00 (.17 (..270-. Urinary 4-tert-Octylphenol (4-[1. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.610) .05-2.560) .630-1.270 (.64 (.620) .62) .380 (<LOD-.78 (1.620-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.160-.11-2.. representative subsample of NHANES 2003-2004.53-3.14) 314 713 1487 03-04 03-04 * * .550-1. 2003..43) 1.370 (<LOD-. Yoshida et al.08) 1. Sweeney et al.00 (.00) 1.00) 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 . Calafat et al.11) 2.31 (1.170-.00) 2.33) 3. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.41) . 2004.860 (.78) 1228 1286 03-04 03-04 03-04 * .740 (.450) 1. at lower or environmentally relevant doses (Blake et al..40 (1.280-.470-1.62 (1.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..1.03 (1.S.320 (<LOD-. In a small number of adult Japanese volunteers.25) 2.730-1.207-.18-4. It is unclear if estrogenic or other effects occur in animals through oral dosing.15) 1.20 (1.76 (2.00) 2.03 (1.40-4.68-2.540-1.62 (1.36-3.384) * . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.29) 2.300 (<LOD-.50 (2.59) 1.10-2.06 (2. 2001).435 (.276 (.22) .260 (<LOD-.770 (. population from the National Health and Nutrition Examination Survey. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.31-2.530) .740 (.71) 2.03-6. 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.269 (.54) * 03-04 03-04 03-04 .24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2005.59 (1.270 (.67-2.68) 2.570) .73) 2. 2000. 2004).43-3.25) 90th 1. or their corresponding ethoxylates with respect to human carcinogenicity.890-2.470) 75th .199-.60 (1.910 (.43) 1.25-2.81 (1.460 (. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 35 .400) . 4-tert-Octylphenol is not considered directly genotoxic..470-1. 1999).3.78) 3.

McCoy GL. Takenaka A. Bolt HM. Indoor air pollution by alkylphenols in Tokyo. Karjalainen M.uk/resource/reports/ethoxylates_alkylphenols. hormones. Saito Y. Takai N. Sweeney T. Yoshida M. Marr MC. pesticides. Song L. Ye X.141(7):2667-2673. Williams B. Environ Health Perspect 2008.71(1-2):112-122.121(1):21-33. Spengler JD. Makino T.116(1):39-44.pdf. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Zaugg SD. Qian J. Raychoudhury SS. Anal Chim Acta 486:41-50. Reprod Toxicol 2001. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. nonylphenol. Available at URL: http:// www. Two-generation reproduction study with para-tert-octylphenol in rats. Brody JG. Nicol L. Nakagomi M. Paranko J. Saito I. Nagao T. Taya K. 2/4/09 Ying GG. Warhurst AM. Tyl RW. Izumi S. Environ Sci Technol 2002. Katsuda S. Thurman EM. and testosterone. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Laws SC.14(5):325-332.36(6):1202-1211. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Taya K.44(8):1355-1361. Millette CF. Environ Int 2002. Onuki A. Muller AM. Haavisto TE. streams. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Cooper RL.foe. Fail PA.37(20):4543-53.S. prolactin. Toxicol Lett 2001. Maekawa A. et al. Bodman GJ. Brine DR. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Camann DE. Endocrinology 2000. Usumi K.54(1):154-167.57(2):255-266.co. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Estrogenic activity of octylphenol. Horie M. Sakui N. Watanabe G. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Toxicol Appl Pharmacol 2005. Arch Toxicol 1996. and other endocrine-disrupting compounds in indoor air and dust. Ferrell JM. Food Chem Toxicol 2006. Blake CA. Environ Sci Technol 2003. Wiegand HJ. Furlong ET. et al. Barber LB.30(2 Pt 1):81-95. 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. Brooks AN. Xu L. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Inoue K. Needham LL. Inoue K. Pharmaceuticals. Exposure of the U. Boockfor FR. Toxicol Appl Pharmacol 2000. Maekawa A. Toppari J. Carey SA. et al. polybrominated diphenyl ethers. and sertoli cell number. alkylphenols. Kawaguchi M. Watanabe G. Regul Toxicol Pharmacol 1999. Boockfor FR. Okada F. testis size.folliclestimulating hormone. Toxicol Sci 2000. Certa H.15(6):683-692. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Yoshimura S. Phthalates.S. Korn LR. et al. Reidy JA. Ono H. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Kolpin DW. and other organic wastewater contaminants in U. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Yoshimura Y. Indoor Air 2004. Wang X. bisphenol A and methoxychlor in rats. Roche JF. Kawaguchi M. Blake CA. Biol Reprod 1997.18(1):43-51. Wong LY. Katsuda S. 2003. 1995. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Myllymaki SA. Meyer MT. Calafat AM.Environmental Phenols References Bian Q. Yoshida M. Ito R. Seto H. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Fedtke N. Myers CB.799(1):119-125. Chen J. Kookana R. Seely JC. 1999-2000: a national reconnaissance.165(3):217-226. Nair-Menon JU. Rudel RA.28(3):215-226.207(1):59-68. Reprod Toxicol 2004.

2002). Triclosan has a low bioaccumulation potential in fish. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al.. toys. 1996.. In a study of 90 U.. Calafat et al... Triclosan has been added to soaps. 2007). Biomonitoring studies on levels of triclosan provide physicians and public health officials with a reference values so that they can determine whether people have been exposed to higher levels of triclosan than are found in the general population.Environmental Phenols Triclosan CAS No. It acts by inhibiting bacterial fatty acid synthesis. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al..S. Matsumura et al. 2000). it has low acute toxicity. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard..S. In 1999-2000. (Sandborgh-Englund et al. Triclosan formulations may rarely cause skin irritation. It can be photochemically and biologically degraded. mouthwashes. Calafat et al.. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. 2005. Triclosan enters the aquatic environment mainly through residential wastewaters. a process that can result in the formation of small amounts of 2. Some reports show endocrine effects are observed in amphibians and fish (Foran et al.. Triclosan is not considered teratogenic at maternally toxic doses. IARC and NTP do not have ratings with respect to human carcinogenicity. Mezcua et al. 2007. and has also been impregnated into some kitchen utensils. representative subsample of NHANES 2003-2004.2 µg/L was comparable to the median level (8. the median urinary triclosan level of 7. young girls. 1988. 2008). General population exposure results from dermal and oral use of products containing triclosan.8-dichlorodibenzo-p-dioxin (Aranami et al. 2006). Biomonitoring Information Urinary triclosan levels reflect recent exposure. 1976. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. deodorants.. In animal and human studies. In a U.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. 1987). In the body it is conjugated to glucuronides and sulfates (Bodey et al. In animal studies. 1969).S.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. acne medications. 2007. toothpastes. Fourth National Report on Human Exposure to Environmental Chemicals 37 .. Triclosan can be absorbed across skin into the blood stream. 2004). There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al.6% of 139 U.. but not by race/ethnicity and sex. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent.. 2000. 2008 has shown higher levels during the third decade of life and among people with the highest household income. Lyman and Furia. Moss et al. Veldhoen et al. 2007).. and wound disinfection solutions. triclosan was found in 57. streams sampled in 30 states (Kolpin et al. and medical devices.

29-12.3-67. see Data Analysis section) for Survey year 03-04 is 2.3-35.0-19.6 (9.48 (8.5-86.72-13.2 (27.0-73.3 (11.00 (4.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.0) 65. population from the National Health and Nutrition Examination Survey.90-10.3 (9.10-9.80 (5.16 (6.4 (38.9 (33.1) 9.0 (26.1) 9.8) 7. Survey Geometric mean (95% conf.4) 75th 43.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.6-111) 33.21 (6.4-18.45 (5.2 (25.3) 6.82 (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 16.3) 10.8) 116 (39.45-13.4) 317 (231-433) 144 (96.1) 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 9.2 (37.3.6-37.4 (11.5) 66.1 (8.1) 13.4.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.45-10.6 (10.50) 10.8) 9.2 (11.2-58.2) 9.74 (5.55 (4.6) 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 9.7) 123 (36.3) 47.1) 11.40-17.4.Environmental Phenols Urinary Triclosan (2.5) 20.2) 13. Urinary Triclosan (2.94 (7.S.1) 9.9-236) 193 (90.9 (50.7 (39.1 (45.3 (8.8-63. population from the National Health and Nutrition Examination Survey.9) 8.S.54 (8.00-8.5-14.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.18 (5.3-31.0 (11.20-13.7 (28.3-15.6) 31.20-10.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.6 (30.48-10.40-11.50-10.2-46.6-14.7 (9.9 (11.8-112) 30.4) 25.0) 49.6-20.9) 32.30-14.4) 90th 249 (188-304) 03-04 03-04 03-04 8.0 (34.7) 10.89-11. interval) 12.20-11.0 (36.9-61.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.32-14.5) 13.1) 14.60 (6.4-19.92-12.9) 7.2-14.6-14.5) 11.6) 10.8) 14.86-12.4 (12.6-65.4) 357 (225-456) 203 (87.38-18.10) 84.9) 75th 47.4) 73.9 (8.93 (7.3 (26.8-60. interval) 13.0) 9. Survey Geometric mean (95% conf.60 (8.1) 50.4) 7.6) 12.6-15.7) 292 (151-432) 132 (78.5 (11.43-13.2-58.1) 9.2) 12.0-15.0 (8.0-15.20 (7.0-213) 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 (15.20 (7.6) 39.4) 51.1) 7.8 (21.4 (32.70-16.2 (10.8-85.2 (13.8-127) 37.6) 90th 212 (172-241) 03-04 03-04 03-04 9.7 (11.1-39.22-10.11-11.7 (14.6 (12.

Levy SB. Food Chem Toxicol 2000. Photolytic degradation of triclosan in freshwater and seawater. Leonard PA.524:241-247.116(3):303-307. Skirrow RC. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Percutaneous penetration and dermal metabolism of triclosan (2. Adolfsson-Erici M. 4’-trichloro-2’-hydroxydiphenyl ether. Wolff MS. 4. Meyer MT. population: 2003-2004. Br J Clin Pharmacol 1987. Aguera A. Wigmore H. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Wong LY.4’-trichloro-2’hydroxydiphenyl ether). Kaneshima H.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples.17(5):637-644. Ogawa H. Evidence of 2. J Invest Dermatol 1976. Pharmacokinetics of triclosan following oral ingestion in humans. Ishibashi H. Williams PE. Calafat AM. Pilot study of urinary biomarkers of phytoestrogens. Benson WH. Zaugg SD. and phenols in girls. phthalates. Arch Environ Contam Toxicol 1988. Osachoff H. Chelimo C. 1999-2000: a national reconnaissance.4. Pharmaceuticals. Larson EL. Aquat Toxicol 2006. Chemosphere 2007. Gilbert RJ.67(4):532-537. Matsumura N.24(3):209-218. Veldhoen N. Okui T.66:1052-1056. Clapson DJ. Moss T. Reidy JA. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice.Environmental Phenols References Aiello AE. Environ Health Perspect 2007.115:116-121. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis).7/2.50(1-5):153-156. Hong HC. Bodey GP. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Furlong ET.23(5):579-583.28(9):1748-1751. Watanabe N. Bennett ER. Britton JA. Urinary concentrations of triclosan in the U.S. Aranami K.38(4):361370. Environ Health Perspect 2008. Erratum in: Aquat Toxicol 2007. IMS Ind Med Surg 1969. and other organic wastewater contaminants in U. Ebersole R. Ye X.83(1):84. Furia T. streams. Hirano M.80(3):217-227. Hernando MD. J Toxicol Environ Health A 2006. Am J Infect Control 1996. et al. Barber LB. Needham LL. Nagao Y. Toxicology of 2. Mar Environ Res 2000. Thurman EM. Anal Chim Acta 1004. Bhargava HN. et al. Odham G.. et al. Ferrer I. hormones. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007.45 Suppl 2:S137-S147. Sandborgh-Englund G. Gunderson MP.38(2):64-71. Triclosan: applications and safety. Foran CM.69(20):1861-1873. Ekstrand J.S. Kanetoshi A. Teitelbaum SL. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Windham G. Shiratsuchi H. Lyman FL.36(6):1202-1211. Howes D. Williams FM. Fernandez-Alba AR. Biol Pharm Bull 2005. Kolpin DW. Environ Sci Technol 2002. The oral retention and antiplaque efficacy of triclosan in human volunteers. Gomez MJ. Readman JW. Pinney SM. et al. Mezcua M. Katsura E.

mollusicide. < LOD means less than the limit of detection. plants.350-.94 (1.S.350-. and metabolic acidosis were observed in CAS No.04) 1.73 (1.350-. bactericide..90) 1.350-. General population exposure to PCP may occur by inhalation of contaminated air.30) 1.00) 2.75) 2.30 (1.80) .30) 1.850-2. Human exposure to PCP has become less common.70) 2.660 (.510-3.350-2.90 (1.70) .990 (<LOD-2.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .350 (.350) < LOD .350 (.650 (.51) 1.350 (. other polychlorinated benzenes. algaecide and insecticide.350 (. ingestion of contaminated food or water.350-2.54-2.10) 1.91 (1.350) < LOD .350-1.42) 696 680 521 696 603 951 Limit of detection (LOD. PCP cannot be used on wood in residential or agricultural buildings. PCP use in the U. 1976.890 (.650) 1.18 (<LOD-1.350-.10 (1.60) 1.33-2.350-.980 (.350) . so it is relatively non-persistent.350-.350 (.350-2. 1986).350 (.390 (.g.350 (.390 (.960) 1. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350 (.45-2.65 (.350-.350 (.00 (.48-2.350 (.500-2.350) < LOD .350) < LOD . and it is used primarily as a preservative for wood to be used outdoors (e. PCP is absorbed rapidly and well by all exposure routes.350 (.350-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. along with small amounts of tetrachlorohydroquinone and conjugates. PCP has been detected in soils.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .78) 1.S.350-.37) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation. 1997).860-2.76) . and dermal contact with PCP-treated products. Survey Geometric mean (95% conf.350-.47-5.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. water and sediments because of the large amounts that were produced and used historically. are eliminated in the urine.350-. 40 Fourth National Report on Human Exposure to Environmental Chemicals .350-1.. see Data Analysis section) for Survey years 99-00 and 01-02 are 0..350) < LOD .10 (<LOD-1.350-2.350 (. has been restricted.350-.83 (2.350 (.350) 90th .350 (. and possibly of lindane (IPCS.350-1.48 (.350-.350) < LOD . After absorption. 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.67) 1.65 (.40 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . and animals.00) 1. Effects including hyperthermia.350-.630 (.510-5.90) 2.350-. with repeated or chronic exposure.350 (.350) < LOD .01 (<LOD-1.60) 1.350) < LOD . PCP is distributed to most tissues and is not extensively metabolized. hypertension.350-.64) 1.350-.770 (.58-2.350) < LOD .09) . utility poles and fence posts).25 and 0. To-Figueras et al.590-1..350-.350 (.58-2.480-2.33) .30 (.10) 1.50) 1. air.350 (. herbicide. 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.990-2.890-1.47-3. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Acute.23 (.30 (.680-1.350) < LOD .98 (1.32 (.350) < LOD .94 (1.62 (.350) < LOD . PCP is degraded by sunlight and metabolized rapidly by microorganisms.350 (. Kohli et al.350-.350) < LOD .08-3.350) < LOD < LOD 75th .350-1.350 (. 2002. population from the National Health and Nutrition Examination Survey. Since 1984. the elimination half-life may be a week or more (Uhl et al.350) < LOD . 1979).76) 1. PCP is eliminated over a few days (Braun et al.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 .350-2.350 (..350) < LOD .350 (.530) 1.5.350-.350-.350) < LOD .37 (. which may vary for some chemicals by year and by individual sample. After a single dose. In the environment.00) 1. The parent compound and conjugates.30) .10 (.

18 (1.30) 1.250 (.30) 1.52 (<LOD-1. 1995).330-.560-. and adversely affected thyroid function (U.270-.94 (1.830) < LOD . IARC has determined that pentachlorophenol is possibly carcinogenic to humans..950-1.25-2. carcinogenic.57 (.35-2.560) < LOD .990 (.cdc.950-1..52 (<LOD-1.25-1.00-1.920 (.18) .16-1.19) 2.280) < LOD .650 (.67 (1.850 (.630 (.e. environmental levels) and health effects is available from the U. 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. 1989).69 (1.09-1.470 (.atsdr.S.430) < LOD . OSHA has established an occupational standard. 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.320) < LOD < LOD 75th .67 (1. EPA at: http://www. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.67 (1.67 (1.S.S. Among adults in the NHANES 1999-2000 subsample.290-.710-1.510-.30-2. 2000). Survey Geometric mean (95% conf.08 and 5.300 (.83 (1.310-...78) 1.57 (1.82) 1.800) < LOD 1.510-.06 (.310) < LOD .epa.51) 1.35-2. More information about external exposure (i.35) 1. 2003).52 (1.10 (1.730) < LOD .19) 2.78) 1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.700-2.67-3.320 (.220-. 2004. EPA has developed standards for PCP in drinking water and the environment.79) 1.26 (1.00) 1.590-1.19) 2. inhalation. respectively) (Becker et al.340-.56) 1.40) 1.82 (1.40) 1.300 (.25 (1.S.250 (.30 (. chronically administered high doses of PCP were hepatotoxic. In animals.13 (.260 (.48-2.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .Fungicides adults and children severely exposed to PCP through ingestion.400 (.S.610 (.40) 1.90) 1. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.290-. 1989). In a small sample of U.9 mg/L.10-2.800-1.67-2. respectively) (Seifert et al.35) 1. and the FDA has established a standard for bottled water.09 (<LOD-2.490) < LOD .gov/ toxpro2.370 (.21-2.19 (1. van Raaij et al.440 (. 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..26 (1.320) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.780) < LOD .570 (.67-3.36) .950-1.780-1. Urinary PCP levels at the 95th percentile in this Report are approximately half the corresponding 95th percentile values found in German adults evaluated in 1998 (Becker et al.430-.94 (1. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al. In NHANES 2001-2002 subsamples.29-3.25) 1.92) 1. 1991). population from the National Health and Nutrition Examination Survey.84 (1.910-1.95) 3.75) 1..67 (1.560) < LOD .760 (.06-3.00-1.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .21 (.34 (.25-2.EPA.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * . children in the 1980’s.590) < LOD ..75 (<LOD-2. 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 (4.40-2.09) 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 .350) < LOD .52) 1. The U.84-4.gov/ pesticides/ and from ATSDR at: http://www.900-1.6 and 14.420) < LOD .360 (.240-.360-.84) 1.500-.650) 90th 1.25 (1.html.55) 1.220-.40) 1.500 (.40) 1.580-.500-1.300 (. Fourth National Report on Human Exposure to Environmental Chemicals 41 .94-3.73 (1.16 (.0 mg/L. Death can result from seizures and cardiovascular collapse.320) < LOD .650 (.290) < LOD .11) 2.06) 1. or skin absorption.270-.380-.. Pentachlorophenol is not mutagenic or teratogenic. 2003).

Engel R. Phillips DL. Kaus S. Environmental Protection Agency (U. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Barrot C. hair.10:552-65. Becker K. Pesticide residues in urine of adults living in the United States: reference range concentrations. 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. Arch Environ Contam Toxicol 1989. van den Berg KJ. Sala M. Notten WR. Baker S. drinking water and indoor air. et al. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Schulz C. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Hill RH. Otero R.S.org/documents/jmpr/jmpmono/2002pr08. Needham LL. Environ Health Perspect 1997. Seifert B. Arch Environ Contam Toxicol 1989. EPA).Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Environ Res 1995. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. International Programme on Chemical Safety (IPCS). Cline RE. 2002. 4/21/09 Kohli J. The metabolism of higher chlorinated benzene isomers. Lindane. Schulz C. References Becker K. house dust. Int J Hyg Environ Health 2003. Hill RH Jr. et al. Head SL.18:475-481. Bailey SL. Shealy DB. Toxicology 1991: 67(1):107-16. Can J Biochem 1976. To T. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Uhl S. et al. available at URL: http://www. Pharmacokinetics of pentachlorophenol in man. Seifert B. Krause C. Santiago-Silva M. Schlatter C. r e g u l a t i o n s . urine. Needham LL. 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. U. Arch Toxicol 1986.S.inchem. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Gregg M. 206:15-24. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Jones D.4:289296. Seiwert M. Safe A. Available at URL: h t t p : / / w w w. To-Figueras J. 11/30/2004.105(1):78-83. htm. Rodamilans M. Dev Toxicol Environ Sci 1979. Seiwert M. Chenoweth MB. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Bragt PC. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Holler JS. Hill RH Jr. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. PCP: Human Risk Characterization [online]. Braun WH.54(3):203-208. Blau GE. Smith SJ. 4/21/09 van Raaij JA. Schmid P.58:182-186. J Expo Anal Environ Epidemiol 2000.71:99108.18(4):469-474. Helm D. Fast DM.

Fungicides ortho-Phenylphenol CAS No.610 (. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.570-2.90 (1.80 (2.433-.820 (. Both chemicals degrade within hours to weeks in the environment (U. or apply these chemicals may be more highly exposed than the general population. in paints.20 (1.23) 695 680 520 695 603 953 Limit of detection (LOD.742) * .690) < LOD .389-. < LOD means less than the limit of detection.50-2.50-3.40-2.500-2.S.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 . OPP is volatile.07 (.610-1. OPP is efficiently absorbed from the gastrointestinal tract and through the skin. and it has limited water solubility.496 (. on ornamental plants and turfs.386-.30-7. population from the National Health and Nutrition Examination Survey.490 (<LOD-.50 (1.28 (.450 (<LOD-.14 (<LOD-3.570 (.508 (.600) < LOD 1. but OPP and SOPP are still used on pears and citrus (U.S. or 2-phenylphenol) and its water-soluble salt.770 (.760-2.480-1.600) < LOD .00-2.890 (.364-.00) .493 (.30) < LOD 1.30-2.33 (.570 (.497 (.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .50) < LOD . and as a wood preservative.840-1.490 (<LOD-.EPA. 2006).890 (. General population exposure can occur via dermal.61) 2.. such as fruits and vegetables.10-1. 2006).10) 2. whereas SOPP is not volatile and is more water soluble.550-1. are antimicrobial agents used as bacteriostats.389-.560-8.830 (.450 (<LOD-. Both have been used in agriculture to control fungal and bacterial growth on stored crops.590-2.00 (1. 2006).800-3.600-1.3.710) 3.520 (.19 (.350-1.780) < LOD .450 (<LOD-.645) * .90) 1.40 (.690-1.670) 2.85) 2.600) < LOD 75th .27 (.80) 1. Most agricultural food applications have been revoked.76) 1.20-2.696) * .890) 1.40-7.80) 1.30) 1. EPA.60 (1.10) .600-1. Estimated human intakes have been below recommended intake limits (U.50 (1.90) 2.750-2.836) * . inhalational. formulate. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.3 and 0.50-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.770 (.10) .950) < LOD .. leaving the chemical residue OPP.S.370-.40-5.10) 1.370-.20-3.60 (1.740 (.630) < LOD . 2002.60-3.10 (1.20 (. 90-43-7 General Information Ortho-phenylphenol (OPP.860 (. and sanitizers.00 (1.20) 2.636) * .90) .EPA. which may vary for some chemicals by year and by individual sample.600-1.624) * .580-1.50) < LOD .03) 1.90 (1. SOPP is applied topically to the crop and then rinsed off.00) < LOD .10-2. sodium ortho-phenylphenate (SOPP).880-2. however.. 1989).490 (<LOD-.498 (. interval) . or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment. it was used in home sanitizers for surfaces.370-.00 (1.00 (1.470 (<LOD-.09) 2.570-1.50) 1.490 (<LOD-.509 (.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.00) .600) < LOD .30 (1.88) 1.60-2.850 (.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .570-.466 (.20) < LOD 1.20) < LOD 2. 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.638) * .10 (1.50) . Cnubben et al.390-. Timchalk et al.420 (<LOD-.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .22 (.20 (1.970 (. OPP is considered to be moderately toxic after acute oral doses in animal studies. Fourth National Report on Human Exposure to Environmental Chemicals 43 .30) < LOD .10) 1. 1998. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.40-5. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.60 (1.790) 2.80-3.17 (.34) 1.22) 2.50 (1.90) . 2006). fungicides.621) * . OPP is still used as a disinfectant fungicide for industrial applications. 1998).552 (.10) .S.410-. In the past. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.92 (.640) < LOD . Workers who manufacture.50) < LOD . Available evidence suggests that OPP does not accumulate in the body.930 (.567 (.710-2.402-.02) 1.349-.28-3.490 (<LOD-.30) < LOD 90th 1.540-2.

900-1. 2002. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.13) 1.780 (. Bomhard et al. Biomonitoring Information Urinary OPP levels reflect recent exposure.990) < LOD . 2002.910-1.43 (1.93 (1.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .480-.07) 2.47) .. Murata et al.96) 1.301-.00 (.43) 3.Fungicides anemia.09-6.810) < LOD .26) 1. less likely.500) < LOD . OPP was not found to be mutagenic.S.59) 1.17) 2. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.08-2.11 (.78 (2.444 (.88-4.61 (1. 1999.27) < LOD .860 (.11 (. IARC has classified SOPP as a possible human carcinogen.11) 4.S.666) * .320 (<LOD-.96-4..S.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.470 (<LOD-.0) 1.420 (<LOD-.560-2. 2005.510 (<LOD-.28 (<LOD-4.568) * . leading to production of two metabolites. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.18) 2.4) 3.38) 2. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.53) 1.880-1.06-5.21-2.950) < LOD .38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .550) < LOD .04-4.61 (2.38-3.620-1.496 (..86 (1.69 (1.455-.59) . 1984. Kwok et al.270-.510-.75 (1.484) * . 44 Fourth National Report on Human Exposure to Environmental Chemicals .93) 1.353-.11-1.44 (1.46) < LOD 1. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .93) .96 (1.410 (<LOD-.09 (1.460-. 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.21 (.. In high dose animal studies.580-1.840 (.75 (1.670 (.311-. 1999. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.810-1. Ito et al.360 (<LOD-. and it has classified OPP as not classifiable with respect to human carcinogenicity. CDC.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 .33-2.91 (1.29) 1. reproductive. Nakagawa et al.EPA 2006).640-1. or developmental toxicity was observed (Bomhard et al. Brusick.473) * .24-2.38) 1. 1984.560) < LOD 75th . U.750-2..02 (.93) .32) 1.74 (1.910 (<LOD-1.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.980 (<LOD-1. Pathak and Roy.00 (1.620-1.12-2. ortho-phenylhydroquinone and ortho-phenylbenzoquinone. 2005). 1993.900) < LOD .980 (.970) 1. 2000. Smith et al.550 (.610) < LOD 1. 2002).600-1.440 (.52 (.291-. Volunteers exposed to 0.25-6.S.33) .656) * .385 (. U.28 (2.514 (. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC. 1992. Zhao et al. population from the National Health and Nutrition Examination Survey.770-2.329-. Additional information is available from U.380 (.12) < LOD 1.4 mg dermally had urinary levels of OPP that were several hundred times higher than median levels found in NHANES 1999-2000 and 2001-2002 (Bartels et al.403-.343 (.S.410 (<LOD-.62) .570) < LOD 1.580) < LOD . Detectable levels were seen in over half the U.248-. Survey Geometric mean (95% conf.750 (.17 (..61 (.40-13.08) 1.97 (2..780-14. 1997.58) 2.650-1. 1998..690 (.17 (.06 (1.gov/pesticides/.29) 1.670) < LOD . 1986).epa.64 (2. 2005).800-1.670 (..43-2. interval) .910 (.89 (1.81) 1.84 (1.420 (<LOD-.750 (.31) < LOD .43-2.590) * .09-3.940-2.550-.470) < LOD .508) * .51-3.860 (.791) * .96 (1.453 (.08-1.05-2.01) 1.11) < LOD 90th 1. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.06-4.20) < LOD 3. but no neurologic. or..24-2.21) 1.EPA at: http:// www. by possible genotoxic mechanisms (Hagiwara et al.361-.382 (.32) 3.

Narang A. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. 2005.50(11):3351-3358. Bartels MJ. Turteltaub KW. Smith RA. Brendler-Schwaab SY. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). et al. IARC Sci Publ 1984. Zhao S. Meuling WJ. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Identification of SARA compounds in adipose tissue. Nakagawa Y. Centers for Disease Control and Prevention (CDC).pdf. 1989. Christenson WR. Murata M. Stanley JS. Vogel JS. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. 90-43-7) in Swiss CD-1 mice (dermal studies). Tayama S. J Agric Food Chem 2006.20(5):851-857. Arch Toxicol 2000. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries.. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No.45(5):460-481. July 28. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Hagiwara A. Christenson WR. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol.159(1):18-24. Fukushima S. Third National Report on Human Exposure to Environmental Chemicals.43(7):14311437. Mendrala AL. Moldeus P. van de Sandt JJ. Bomhard EM. 2006. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Inoue S. Xenobiotica 1998.74(2):61-71.54(16):5731-5735. Hirose M. Carcinogenesis 1999.28(6):579594. Selim S. National Toxicology Program (NTP). St John MK. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Sangha GK. U. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Shirai T. Hakkert BC.epa.niehs. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Bromig KH. Bartels MJ. Richter M. Food Chem Toxicol 1984.gov/oppsrrd1/REDs/ phenylphenol_red. Kwok ES. 4/13/09 Onstot JD.286(2):309-319. McNett DA. Bormett GA. Environmental Protection Agency (U.S. March 1986. Fukushima S. Available at URL: http://www. Freyberger A. Eadon G. Toxicol Appl Pharmacol 1999.nih.35(2 Pt 1):198-208. Atlanta (GA). Imaida K. Roberts AL. Arnold LL. Kawanishi S. EPA-560/5-89-003. Brzak KA. Brusick D.S. Glas K. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. J Chromatogr B Biomed Sci Appl 1997. Regul Toxicol Pharmacol 2002. Herbold BA. Bartels MJ.Fungicides References Appel KE. Available at URL: http://ntp. Buchholz BA. Hum Exp Toxicol 1998. Moriya K. Cnubben NH. Elliott GR. Pathak DN. J Agric Food Chem 2002.EPA). Moore GA. rat and man. Eastmond DA. et al. Cano M. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Timchalk C.pdf. Timchalk C. Environ Mol Mutagen 2005.gov/ntp/htdocs/LT_ rpts/tr301. Drugs. Comparative metabolism of orthophenylphenol in mouse. Biochem Pharmacol 1992. U.150(2):402-413. Shibata M.(56):399-407.703(12):97-104. 4/9/09.17(8):411-417. Roy D. Office of Toxic Substances.22(10):809-814. Ito N. food additives and natural products as promoters in rat urinary bladder carcinogenesis.32(6):551-625.S. Toxicol Appl Pharmacol 1998. Sangha G. Crit Rev Toxicol 2002. Coelhan M. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Mutat Res 1993. EPA 739 R-06004. Bartels MJ. Gierthy J. Ito N. Hagiwara A. The carcinogenicity of the biocide ortho-phenylphenol.S. Environmental Protection Agency (U. Leser KH. EPA).

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

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

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

S. Hines CJ. Environ Health Perspect 2003. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor.24(10):1003-1012.pdf. Rose RL.S. Thurman EM. Hsiao JJ. Burkhardt MR. Occurrence of sulfonylurea. Barr JR.S.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Comparative metabolism and elimination of acetanilide compounds by rat. sulfonamide. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor.39(17):6561-6574. Roberts AL. Linhart SM. EPA).108(12):1151-1157. Tinwell H. Volume 65. Feil VJ. Heederik D.248(2-3):123-133.37(4):10881093. Casida JE. Battaglin WA. Sci Total Environ 2000. epa. Green T. Linderman R. imidazolinone. Hein MJ. acetochlor. 5/30/06 U. 2000.15(6):500-508. Hum Exp Toxicol 1996. Available at URL(non U.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Lefevre PA. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Atlanta (GA). Jefferies PR. Available at URL: http://www.html. EPA). Deddens JA. Barr DB. Number 15. Centers for Disease Control and Prevention (CDC). Xenobiotica 1994. Ward EM. Feng PCC. Reynolds SJ. and metolachlor herbicides in rats. Barr DB. Alavanja MC. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. 1998. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. J Expo Anal Environ Epidemiol 2005. Furlong ET. Andrews HF.S. et al.EPA): http://pmep. Larsen GL. Sanderson WT. et al. Hodgson E. Curwin BD. Hladik ML. Chem Res Toxicol 1998. Environ Health Perspect 2000. Camann DE. 2005. and other herbicides in rivers. Environmental Protection Agency (U. Third National Report on Human Exposure to Environmental Chemicals.111(5):749-756. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.S.248(2-3):115-122.Herbicides References Ashby J.cce. March 2006. Olsson AO. EPA 738-R-00-009. Sci Total Environ 2000. J Expo Sci Environ Epidemiol 2007. Federal Register: January 24. et al. 5/30/06.cornell. Kier L. Davison KL. Quistad GB. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.11(4):353359.17(6):559-566. Striley CA. Dialkylquinonimines validated as in vivo metabolites of alachlor. Bravo R. Acetochlor (Harness) Pesticide Petition Filing 1/00. Environmental Protection Agency (U. Environ Sci Technol 2005. Wilson AG.15(9):702-735. Kinney PL. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. J Agri Food Chem 1989. Peter CJ. pages 3682-3690. Barr DB. Wratten SJ. Kolpin DW. Coleman S. Whyatt RM. U. reservoirs and ground water in the Midwestern United States.

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

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

Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Hsiao JJ. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. WHO/ FAO Data Sheets on Pesticides.248(2-3):115-122. 1996.usgs. March 2006. Heydens WF.47(6):503-517. 2005. Alachlor in Drinking-water. 1999. Third National Report on Human Exposure to Environmental Chemicals. Hill RH Jr. Barr DB. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Kolpin DW.56(9):883-889. Tolos W. 2/27/09 Jefferies PR. Sci Total Environ 2000. Comparative metabolism and elimination of acetanilide compounds by rat. J Ag Food Chem 1995. Furlong ET. Gilliom RJ). Environ Health Perspect 2003. Camann DE. U. 1992-2001.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.htm. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Shoemaker DA. California. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. et al. Environmental Protection Agency (U.S.18(6):363-391. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Geneva. Environ Sci Technol 2005. Hines CJ. Hum Exp Toxicol. Feil VJ. Geological Survey (USGS). J Agri Food Chem 1989. Mutat Res. Casida JE. Henningsen G. Thelin GP. Barr JR.pdf. Davison KL.43(25):2087-94. Andrews HF.S.S.37(4):10881093.11(4):353359. Life Sci 1988. Thake DC. reservoirs and ground water in the Midwestern United States. Lau H. 2007. World Health Organization (WHO). Circular 1291. Martens MA. 1998. December 1998.gov/oppsrrd1/ REDs/0063. Casida JE. Sanderson WT. 98-4245 (by Barbash JE. Thurman EM. Clark JM. who. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. sulfonamide. Shealy DB. Hines CJ. EPA 738R-98-020. Occurrence of sulfonylurea. Deddens JA. World Health Organization. ALACHLOR. Jefferies PR.44(18):1325. Roberts AL. Background document for development of WHO Guidelines for Drinking-water Quality. Brown KK.S. Wilson AG. Dialkylquinonimines validated as in vivo metabolites of alachlor. Feng PCC. MacKenzie B.int/water_sanitation_health/dwq/chemicals/en/alachlor.org/documents/pds/pds/pest86_e. Linhart SM. Erratum in: Life Sci 1989. Sci Total Environ 2000. Kinney PL. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Supplemental Technical Information (available on-line only). Available at URL: http://water. Chem Res Toxicol 1998. Hill AB. Ann Occup Hyg 2003. imidazolinone. Wratten SJ. Available at URL: http://www. 1997. Available at URL: http:// www.24(10):1003-1012. Striley CA. Quistad GB. DNA adduct formation by alachlor metabolites. No. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Hladik ML. Reregistration Eligibility Decision (RED) Alachlor. Bull Environ Contam Toxicol 1996. Brown MA. acetochlor.56(6):853-859. 2/27/09 U. Sacramento. et al. Geological Survey (USGS). International Programme on Chemical Safety (IPCS). 86. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Atlanta (GA).39(17):6561-6574. Casida JE. Biagini R. An evaluation of the carcinogenic potential of the herbicide alachlor to man.pdf. 2003. revised February 15. 4/2/09 U.Herbicides References Battaglin WA.111(5):749-756. Am Ind Hyg Assoc J 1995.395(2-3):159-171.inchem. Kier LD. Kimmel EC. Peter CJ. Whyatt RM. Xenobiotica 1994.epa. Larsen GL. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Biagini RE. Burkhardt MR.43(9):2504-2512.php. Hull RD. Available at URL: http://www. Kolpin DW. EPA). Quistad GB. Centers for Disease Control and Prevention (CDC). Driskell WJ. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. and metolachlor herbicides in rats.248(2-3):123-133. 1999. and other herbicides in rivers. Tessier DM.

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

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

Agency for Toxic Substances and Disease Registry (ATSDR). Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Ferioli A. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Wetzel LT. et al. Gillis JH. Curwin BD. Clayton CA. et al.html. Stuart AA. Barbieri F. Quandt SA.47(6):503-517. Barr DB. Seiber JN. Wetzel LT. International Programme on Chemical Safety (IPCS).cdc. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Environ Health Perspect 2001. Atlanta (GA).. Carr WC Jr. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Gillis JH.43(2):155-167.69(2):217-222. Vonk A. 2005). diamino-S-chlorotriazine and hydroxyatrazine. A risk assessment of atrazine use in California: human health and ecological aspects.org/documents/pds/pds/pest82_e. Noriega N. et al. Reynolds SJ. 2005). Striley CA. et al. Cooper RL. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.htm. Toxicol Sci 2000. Centers for Disease Control and Prevention (CDC). Toxicological profile for atrazine. Sanborn JR. Third National Report on Human Exposure to Environmental Chemicals. Ann Occup Hyg 2003. Cottica D. Biological monitoring of human exposure to atrazine. Hayes TB. Environ Health Perspect 2007. Goldman JM. J Agric Food Chem 1982. Extrom PC. Chen H. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Available at URL: http://www. Tapia J. WHO/ FAO Data Sheets on Pesticides. Blewett C. Toxicol Sci 2000. The geometric mean of urinary atrazine mercapturate was 1. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. J Toxicol Environ Health 1994.64(9):672-678.58(2):366-376. Lioy PJ. McElroy WK. Simpkins JW. Collins A. 1996. Stevens JT. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Toxicol Lett 1993. Eldridge JC. Lee M. Lucas AD. Steroids 1999. Toxicol Sci 2003. Hines CJ.. Grzywacz JG. Saiz SG.15(6):500-508.. Gammon DW.. Ferrell JM. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Shoemaker DA. Moseman RF. Eberly LE.109(6):583-590.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. In small studies of Maryland residents in 19951996 (MacIntosh et al. 3/11/09 Arcury TA. 3/11/09 Laws SC. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Mendoza M. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Hermaphroditic. Tyrey L.inchem. J Toxicol Environ Health 1994. Breckenridge CB. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. 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. In a study of 60 farm worker children. Jones AD. Eldridge JC. Heederik D.. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Geneva. Catenacci G. ATRAZINE. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . atrazine was detected in only four children (Arcury et al. et al. levels of atrazine mercapturate were generally not detectable (CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.atsdr. Pfeifer KF. Maroni M. Fleenor-Heyser DG. Stoker TE. Available at URL: http:// www. 2007). Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Ferrell JM. 2000). In a small number of field workers. Laws SC. Goodrow MH. References Adgate JL. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Cooper RL. No. 2001). Hein MJ. 2001 [online]. Stoker TE. 82. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. 2005.gov/toxprofiles/tp153.99(8):5476-5480. J Expo Anal Environ Epidemiol 2005.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al.61(4):331-355. Bradway DE.115(8):1254-1260. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Proc Natl Acad Sci USA 2002. Biagini RE. Sanderson WT. 2003. et al.76(1):190-200.43(2):155-167. Aldous CN.. Schmid J. Barr DB. Brown KK.30(2):244-247. Bersani M. Freeman NC.53(2):297-307. Perry et al. In the NHANES 2001-2002 subsample. Barr DB. 1993). Pest Manag Sci 2005. World Health Organization. Deddens JA.. Stoker TE. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Cooper RL.

A review of epidemiologic studies of triazine herbicides and cancer.S. Singzoni B.56(2):69-109.S. Tortorelli J. Breckenridge CB. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Washington (DC).27(6):599612. Ann Epidemiol 2000. March 2006. revised February 15. Toxicology 1990. Dagenhart D.S.182(1):44-54.61(1):27-40. Needham LL.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. 6/1/09 U. EPA Office of Pesticide Programs.6(1):107-116. Stoker TE. Toxicol Appl Pharmacol 2002. Osborne DW.10(7):479. Stoker TE. 2003b. Geological Survey (USGS). The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. J Expo Anal Environ Epidemiol 1999. Supplemental Technical Information (available on-line only). Kastl PE. Environmental Fate and Effects Division. Available at URL: http://water. The Quality of Our Nation’s Waters. Sanderson JT. Wetzel L. Interim Reregistration Eligibility Decision For Atrazine. Fenton SE. Environmental Protection Agency (U.S. MacIntosh DL. 0062. Available at URL: http://www. Timchalk C. Circular 1291. U. 1992-2001. Office of Prevention. Rayner JL. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Perry M. Toxicol Sci 2000. Delzell E. Laws SC.epa. Environmental Protection Agency (U. Boerma J. J Toxicol Environ Health A 1999. Dryzga MD. Laws SC. Wood C. Case No.9(5):494-501. Pesticides and Toxic Substances. EPA). EPA). Crit Rev Toxicol 1997. White paper on potential developmental effects of atrazine on amphibians. Chem Res Toxicol 1993.S. Available at URL: http://www. Ryan PB. 3/11/09 U. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats.195(1):23-34.67(2):198-206.pdf. Lansbergen GW. Guidici DL. Stevens JT. Cooper RL. Cooper RL. Langvardt PW. Hammerstrom KA. May 2003a.58(1):50-59.usgs.pdf. A risk characterization for atrazine: oncogenicity profile. Guidici DL. 2007. Toxicol Sci 2002. Sathiakumar N.php. A longitudinal investigation of selected pesticide metabolites in urine. van den Berg M. Pesticides in the Nation’s Streams and Ground Water.epa.Herbicides development of a biomarker of exposure. Christiani D. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Toxicol Appl Pharmacol 2004.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.gov/oppsrrd1/REDs/ atrazine_ired.

60) 1.330 (.730 (. in 2001 (U. Sauerhoff et al. < LOD means less than the limit of detection.310) < LOD .350) < LOD < LOD < LOD . It was first registered with U. 2005). It is not well absorbed through the skin.910) < LOD .32 (1..560-. General population exposure to 2.260 (<LOD-.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. As much as 62 million pounds of 2.03) 695 659 520 668 589 892 Limit of detection (LOD.690 (.250 (<LOD-.760 (.10 (<LOD-1. Similar to other chlorophenoxy herbicides. and by consuming food or drinking water contaminated with 2.80) 1.210-..670-1.S.930 (. It is rarely detected in ground waters (USGS. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.420-.20 (. and mecoprop).07 (.810-1. abdominal pain.70) 1. 2. and aquatic environments.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.250 (<LOD-.560-1.EPA in 1948. renal and hepatic injury. it acts as a plant growth hormone. 4-D. Recent estimates of chronic intakes of 2.EPA.660) 1. Kohli et al.S.10 (<LOD-1.22) < LOD .230-.680-1. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.27-2.550-1. the chlorophenoxy herbicide 2.00-2.490 (.440-1.690 (.S.4-D) controls broadleaf weeds in residential.890) < LOD . population from the National Health and Nutrition Examination Survey.952 and 0.S.13) < LOD .610 (. 94-75-7 General Information Widely used throughout the United States. nausea.30 (<LOD-2.. Fourth National Report on Human Exposure to Environmental Chemicals 57 .4-D is rapidly absorbed via oral and inhalation routes.20 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.27 (.48) < LOD 1. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.S.2.4-D has low acute toxicity. with a half-life of several days to several weeks.55 (1.43) 1.420) < LOD .02-1. 2004).230 (<LOD-. 1989.66) < LOD 1.40) 1.210 (<LOD-.4-dichlorophenoxyacetic acid (2. myotonia.740 (.930-1.540-.05-2. 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 1974.690 (.4-D may occur during residential applications.690-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4-D have been below recommended intake limits (U.370-. 2.400) < LOD .610-. MCPA.16) < LOD . Survey Geometric mean (95% conf.10) < LOD 1. headache. agricultural. which may vary for some chemicals by year and by individual sample. 1977).320) 90th .490) < LOD < LOD < LOD .960-1. and delayed Urinary 2.4-D or exposed for prolonged periods.410) < LOD .890 (. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.08) < LOD . Once absorbed. but at higher levels they are herbicidal.4-D were used in the U.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . hypotension.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .4-Dichlorophenoxyacetic Acid CAS No.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . 2007).21) 1.Herbicides 2. 2.51 (1.4-D can be applied either as an aqueous salt or as oil-soluble esters. Human health effects from 2. dizziness.310 (.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 .EPA.24 (. At low levels. these herbicides can enhance plant growth. by direct contact with agricultural and residential areas after applications. It is poorly bound in soils.910) 1.27 (1.

560-.41 (1.780 (.620-.39) < LOD 1. myotonia. 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.410) 90th .S.13 (.17 (. It is unclear whether these associations are related to the chlorophenoxy herbicides. Kolmodin-Hedman and Erne. population (Hill et al..850) < LOD .gov/pesticides/. Survey Geometric mean (95% conf. 1995. 1985. 2005).19) .810-1.340 (.380-.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . CDC.7. 2004).epa. 2005). 1989).490 (.740 (.920) < LOD 1..670 (.930-1.640 (.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.780) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. in small samples of children (Hill et al. 2005.08 (.660) < LOD .4-D reflect recent exposure.570) < LOD .4-D does not have significant reproductive.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .590 (<LOD-1. 2005).8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. IOM.S. or to contaminants in the herbicide formulations (specifically 2. adrenals and gonads (NTP.24) 1.S. IPCS.S.470) < LOD .Herbicides neuropathy (Bradberry et al. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.560-.08 (.410) < LOD 1.. IPCS. 1996. IPCS. Frank et al.350 (<LOD-.670 (. 2001.720 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..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.410) < LOD < LOD < LOD .380 (<LOD-. 1994).73) .4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. 2.S. 2002. 1992). U. urinary 2.32 (<LOD-2. Epidemiological studies have reported associations of several types of cancer.S.980) < LOD 1.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. and evidence of histological injury to the kidneys. liver. Average post-application urinary levels of 2. 2005. 2002. developmental.270 (<LOD-. Hill et al. Knopp et al. Pearce and McLean.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 .820-1. 2005.990-1.670 (<LOD-1.EPA. or teratogenic effects in chronic rodent studies (Charles et al. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.660 (.790) 1.08 (. other exposures. 2. U.440 (.EPA.380 (<LOD-.4-D levels were detectable in less than a quarter of the individuals studied. U.380) < LOD .. Acute high doses administered to laboratory animals produced ataxia.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . eyes.14 (.810-1. In previous samples of the U. and of adults and children (Baker et al.390) < LOD < LOD < LOD . 2000).520-. The acid and salt forms of 2.780-1.4-D are eye irritants.270-. 1980. U. 2006. 2005.EPA 2005)..480 (. 2.550-. 2005). thyroid.340-..580-.590 (<LOD-1.56) .4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. 1996. Kutz et al.410 (<LOD-.13 (.610-.4-D production plant workers and a few forestry workers spraying 2.890-1.3.EPA.. 1996. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. Additional information is available from U. population from the National Health and Nutrition Examination Survey.790) < LOD .EPA at: http://www.890) < LOD 1.35) < LOD . Post-application levels in farmers and home gardeners were dependent on Urinary 2.S.27-1. 2003.610-.330-.05) .700 (.16) 1... Biomonitoring Information Urinary levels of 2.680) < LOD . 58 Fourth National Report on Human Exposure to Environmental Chemicals . 1995).

Stephenson GR.32(4):233-257. Arch Environ Contam Toxicol 1985.4-Dichlorophenoxyacetic Acid). Alexander BH. Environ Res 1995. Developmental toxicity studies in rats and rabbits on 2.4:427-435. Scand J Work Environ Health 2005. Dichlorophenoxyacetic acid. Biomonitoring for farm families in the farm family exposure study. Tables. Sirons G J. geometric mean urinary levels of 2. Baker SE. Murphy RS.htm. Crit Rev Toxicol 2002.4-D) epidemiology and toxicology. J Expo Anal Environ Epidemiol 2005 Nov. Beasley VR. Finding a measurable amount of 2. Sircar KP.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. TOX-63 Peroxisone Project (2. Dhar MM. Cook BT. Board on Health Promotion and Disease Prevention. Updated March 7.S. Hill RH Jr. 3/17/09 Institute of Medicine (IOM). Frank R. Campbell RA. Available at URL: http:// www.inchem. 2005 Charles JM. In farm families.4-D). Hill RH Jr. van Ravenzwaay B. Gupta BN. Pesticides residues in food: 1996 evaluations Part II Toxicology.nih. Holler JS. Tandon JS. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. TOX-63: TOXICITY REPORT CURVES. Available at URL: http:// www. Honeycutt R.60(1):121-131. References Arbuckle TE. Xenobiotica 1974. et al. Third National Report on Human Exposure to Environmental Chemicals. Assessment of exposure to 2.php?record_id=10603. Survival and Growth Curves from NTP Toxicity Studies. Washington (DC): National Academies Press. 2005. 2003.. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Selected pesticide residues and metabolites in urine from a survey of the U.4-D were highest in the farmers who applied the 2. the number of acres to which it was applied (Curwin et al.org/documents/jmpr/jmpmono/v96pr04. Pesticide residues in urine of adults living in the United States: reference range concentrations. Estimation of occupational exposure to phenoxy acids (2. Brody D. 3/17/09 Knopp D. Toxicol Sci 2001. Shealy DB. Arch Environ Contam Toxicol 1989. Forestry workers involved in aerial application of 2.18(4):469-474. Smith SJ.4-D will result in an adverse health effect. Available at URL: http://ntp. J Toxicol Environ Health 1992. Sanderson WT. Beeson MD. Kolmodin-Hedman B. International Programme on Chemical Safety-INCHEM (IPCS).4-. Reynolds SJ.5-T). 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .4-D): exposure and urinary excretion. Kutz FW. Hein MJ.4-dichlorophenoxyacetic acid in man.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study.4-D than levels found in the general population. Baker BA. Harris SA. Mandel et al. Barr DB. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. the amount of pesticide applied.27(1):23-38. Carter-Pokras OD. 914. Biomonitoring of herbicides in Ontario farm applicators.4 dichlorophenoxyacetic acid (2. Curwin BD.4:97-100. Wilson RD.4-dichlorophenoxyacetic acid (2.4-dichlorophenoxyacetic acid and its forms. Arnold EK. J Expo Anal Environ Epidemiol 2000. Philbert MA. Needham LL.4-dichlorophenoxyacetic acid (2. Exposure of homeowners and bystanders to 2. Biomonitoring studies of 2. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. 2005. Needham LL. Harris et al. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.niehs. Acquavella JF. Bailey SL. Driskell WJ.4-D and 2.51(3):152-159.4. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. 2006. Arch Toxicol Suppl 1980. Atlanta (GA). Mandel JS.37(2):277-291. Gregg M. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Veterans and Agent Orange: update 2002.10(6 Pt 2):789-798. et al.gov/index.Herbicides the time since application. Barr DB. Occup Environ Med 1994.4-D in urine does not mean that the level of the 2. Ripley BD.31 Suppl 1:98-104. and the use of protective clothing or equipment (Arbuckle et al. Centers for Disease Control and Prevention (CDC). Chapman P.. Erne K.71(2):99-108. Ritter L. 2. Scand J Work Environ Health 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Cole DC. Vet Hum Toxicol 1989. Kohli JD. To T. Heederik D. Baker S. Head SL.4:318-321. Khanna RN. 2005).31 Suppl 1:90-97. J Environ Sci Health B 1992.4-D.edu/catalog. National Toxicology Program (NTP). 1992).. general population. Solomon KR. Hanley TR Jr.15(6):500-508.nap. Absorption and excretion of 2. 2005). Review of 2. Bus JS. et al. Garabrant DH. Fast DM..31(2):121-125.

3/17/09 U. 3/17/09.4-dichlorophenoxyacetic acid (2.php.htm. Circular 1291.pdf. 2004. EPA 738 F-05-002. Pesticides in the Nation’s Streams and Ground Water. Blau GE. Environmental Protection Agency (U. Environmental Protection Agency (U. Pesticide industry sales and usage . Geological Survey (USGS). Gehring PJ.epa.EPA). 4/2/09 U. Available at URL: http://www. revised February 15.4-D RED Facts. gov/oppbead1/pestsales/01pestsales/market_estimates2001. March 2006. 1992-2001. Washington (DC): U.EPA).Herbicides Sauerhoff MW.S. Available at URL: http://www.S. Braun WH.epa.4-D) following oral administration to man.8:3-1U.gov/oppsrrd1/ REDs/factsheets/24d_fs.usgs. May. Toxicology 1977. The Quality of Our Nation’s Waters. Available at URL: http://water.S. Supplemental Technical Information (available on-line only). The fate of 2.2000 and 2001 market estimates. 2007. June 2005. S.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. 2. 60 Fourth National Report on Human Exposure to Environmental Chemicals .S. Office of Prevention Pesticides and Toxic Substances.S.EPA.

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

Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 01-02 is 0.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 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 .440 (<LOD-. population from the National Health and Nutrition Examination Survey.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 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. Survey Geometric mean (95% conf. 62 Fourth National Report on Human Exposure to Environmental Chemicals .670 (<LOD-.S.200 (<LOD-. population from the National Health and Nutrition Examination Survey.2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 831 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-. < LOD means less than the limit of detection.240) 679 701 957 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.740) 679 700 957 < 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.

2005. Hein MJ. Third National Report on Human Exposure to Environmental Chemicals. Gillion. Curwin BD. Linderman R. California. Geological Survey (USGS). R. 4/2/09 U.39(17):6561-6574.108(12):1151-1157. Kinney PL. Comparative metabolism and elimination of acetanilide compounds by rat.gov/oppsrrd1/ REDs/0001.usgs. Hladik ML. Roberts AL. April 1995. Deddens JA.S. Coleman S. Environ Sci Technol 2005.gov/nawqa/pnsp/pubs/files/051507. EPA 738R-95-006.epa. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. et al. Barr DB. Sci Total Environ 2000.15(6):500-508. Andrews HF.ESTfeature_gilliom. Circular 1291. Burkhardt MR. Reregistration Eligibility Decision (RED) Metolachlor.who. 3/26/09 U. EPA).php. Sacramento. Ward EM. Feil VJ.248(2-3):123-133. Rose RL.Herbicides References Battaglin WA.pdf. Supplemental Technical Information (available on-line only).111(5):749-756. 1998. J Agri Food Chem 1989. World Health Organization (WHO). Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Xenobiotica 1994. et al.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. usgs. Heederik D. Environ Health Perspect 2000.pdf 3/30/09 Hines CJ. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.gov/nawqa/ pnsp/pubs/wrir984245/text. Casida JE. Available at URL: http://www. Hodgson E.S. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. 1999. sulfonamide. March 2006. Peter CJ.S. Chem Res Toxicol 1998. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.24(10):1003-1012.11(4):353359. Geological Survey (USGS). Furlong ET. Available at URL: http://water. Available at URL: http://water. reservoirs and ground water in the Midwestern United States. Shoemaker DA. Sanderson WT. Ann Occup Hyg 2003. acetochlor.S. Atlanta (GA). Quistad GB. 2007. Pesticides in U.S. U. Camann DE.html.pdf. Kolpin DW. Gilliom RJ). Hsiao JJ. Striley CA. Jefferies PR. Occurrence of sulfonylurea.47(6):503-517. 2003. Larsen GL. Kolpin DW.usgs. Wratten SJ. Dialkylquinonimines validated as in vivo metabolites of alachlor.int/water_sanitation_health/dwq/chemicals/ metolachlor. Alavanja MC. Barr DB. and metolachlor herbicides in rats. Barr JR. Davison KL. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Environ Health Perspect 2003. Reynolds SJ. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. 6/1/09 Whyatt RM. Linhart SM. Thelin GP. Background document for development of WHO Guidelines for Drinking-water Quality. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 .41:3409-3414. J Expo Anal Environ Epidemiol 2005. Metolachlor in Drinkingwater. Available at URL: http://water. imidazolinone. Brown KK. Biagini RE. and other herbicides in rivers. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.248(2-3):115-122. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Feng PCC.37(4):10881093. Environmental Protection Agency (U. revised February 15. 1992-2001. Sci Total Environ 2000. Thurman EM. Centers for Disease Control and Prevention (CDC). Available at URL: http://www. Environ Sci Technol 2007. streams and groundwater. 98-4245 (by Barbash JE.

dizziness. Nelson et al. 2004). ranging from several weeks to many months.5-T was once applied as either an aqueous salt or as an oil-soluble ester.4. with an elimination half-life of approximately 19 hours (Arnold et al.5-T is eliminated mostly unchanged in the urine. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. 64 Fourth National Report on Human Exposure to Environmental Chemicals . renal and hepatic injury.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.g. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.4. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. 2007). Kohli et al.4. The half-life of 2. 93-76-5 General Information 2. At low levels. Although 2.. Given the commercial unavailability of 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.1.5-T use as a herbicide in 1985.. but higher levels are herbicidal. 1974). population from the National Health and Nutrition Examination Survey. Omer. Human health effects from 2.5-trichlorophenol and other degradates.5-T degrades to 2. these herbicides can enhance plant growth.5-Trichlorophenoxyacetic acid (2. it is not well absorbed through the skin. headache.4. 2.4. Ester forms of 2.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.S. the general population is unlikely to be exposed to it.5-T has been rarely detected in ground waters (USGS. Once absorbed into the body.Herbicides 2. 2. Mohammad and St.5-Trichlorophenoxyacetic Acid CAS No.3.2 and 0. and delayed neuropathy (Bradberry et al. abdominal pain.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5-T and 2. Chlorophenoxy herbicides act as plant growth hormones.7. Survey Geometric mean (95% conf. 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. and concern about contamination with 2.4. 2. 1989. Epidemiological studies have reported associations of several types of cancer. 2..8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.4. myotonia.4. 1992. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.4.5-T in soil varies with conditions.. 1986. nausea. Agent Orange).4.4. < LOD means less than the limit of detection. 1992).4. hypotension.5T is rapidly absorbed via oral and inhalation routes.4.5-T.5-T (Holson et al.4.4-D were used as defoliants in the Vietnam War (e..4.. which may vary for some chemicals by year and by individual sample.

. 1980). Finding a measurable amount of 2. in which urinary levels of 2.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.4.5-T also were below the limit of detection (Kutz et al. or to contaminants in the herbicide formulations (specifically 2.4.5-T itself is not mutagenic.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. Mean urinary levels of 2. similar to results of NHANES II (19761980).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. U. 2003.S.5-T were generally below the limit of detection. Urinary 2. Additional information is available from U. 2002. It is unclear whether these associations are related to the chlorophenoxy herbicides.4. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2004).4.4. IOM. urinary levels of 2.4. other exposures.Herbicides or contaminated herbicides. 1996. population from the National Health and Nutrition Examination Survey. 2005). 1992).4.EPA at: http://www. 2.5-T reflect recent exposure. Pearce and McLean. Biomonitoring studies on 2.gov/pesticides/.S. 2005.3.epa. Biomonitoring Information Urinary levels of 2.4. Survey Geometric mean (95% conf.S.5-T does not mean that the level will result in an adverse health effect.7. Fourth National Report on Human Exposure to Environmental Chemicals 65 . 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 the NHANES 1999-2000 and 2001-2002 subsamples (CDC.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. IPCS.5-T than levels found in the general population.EPA.

Gaylor DW.19(2):298-306.4-dichlorophenoxyacetic acid (2. et al. McLean D. Selected pesticide residues and metabolites in urine from a survey of the U. Gupta BN. Washington (DC): National Academies Press.4. 3/17/09 Institute of Medicine (IOM). St Omer VE. Philbert MA.epa. 2. Available at URL: http:// www.4:318-21. 3/17/09 Kohli JD.4. Scand J Work Environ Health 2005. 2003. Developmental toxicity of 2. Tandon JS.4.4.php?record_id=10603. 2005.5-t mixture. Centers for Disease Control and Prevention (CDC).5-T). LaBorde JB. Available at URL: http://www.2000 and 2001 market estimates. et al.S. Behavioral and developmental effects in rats following in utero exposure to 2. U. Crit Rev Toxicol 2002. Atlanta (GA). Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. discussion 5-7. Washington (DC): U.inchem. Pesticides residues in food: 1996 evaluations Part II Toxicology. 2004. gov/oppbead1/pestsales/01pestsales/market_estimates2001.31(2):121-125. Poisoning due to chlorophenoxy herbicides. Toxicol Rev 2004. S.5-trichlorophenoxy acetic acid in man.4.4-D) epidemiology and toxicology.19(2):286-297. Pearce N. Sircar KP. Carter-Pokras OD.37(2):277-91.23(2):65-73.8(5):551-60.nap. Fundam Appl Toxicol 1992. Agricultural exposures and non-Hodgkin’s lymphoma. Developmental toxicity of 2.EPA. Cook BT. 210:250-255.pdf. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. LaBorde JB. Wolff GL. Nelson CJ. Bradberry SM. Nelson CJ.org/documents/jmpr/jmpmono/v96pr04. Holson JF. Veterans and Agent Orange: update 2002. Third National Report on Human Exposure to Environmental Chemicals. International Programme on Chemical Safety-INCHEM (IPCS). Office of Prevention Pesticides and Toxic Substances. Kutz FW. May.4.edu/catalog. Gaines TB.S. Absorption and excretion of 2. Dichlorophenoxyacetic acid. Khanna RN. Available at URL: http:// www.S.31 Suppl 1:1825.4. McCallum WF. Vale JA. Brody D. Neurobehav Toxicol Teratol 1986.4-D and 2.EPA). Arch Toxicol Suppl 1980. general population. Mohammad FK.4. Dhar MM. Environmental Protection Agency (U. II. Kolmodin-Hedman B. Garabrant DH.4-D/2. Board on Health Promotion and Disease Prevention. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . 914. Vet Hum Toxicol 1989. Review of 2. Beasley VR.5-T). Gaines TB. Arch Int Pharmacodyn Ther 1974.5-T). Pesticide industry sales and usage . Murphy RS. J Toxicol Environ Health 1992.4-.5-T in four-way outcross mice. I. Holson JF.5-trichlorophenoxyacetic acid (2. Estimation of occupational exposure to phenoxy acids (2.32(4):233-257.htm. Fundam Appl Toxicol 1992. Proudfoot AT.5-trichlorophenoxyacetic acid (2. Sheehan DM. Multireplicated dose-response studies with technical and analytical grades of 2.Herbicides References Arnold EK. Erne K.

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

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

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

100-.50 (8.3 (18.9 (12.064 (.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .100) .083-.1) 20.120 (.5-17.110 (.158) . 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 9.149) .60-10.4) 21.112-.40-10.242) .8-17.4) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.4) 20.4 (12.100-.110 (.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 .054-.5) 15.080 (.00 (8.130) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.073-.077-.6-33.5-15.160) .130) .4) 19.5) 21.8) < LOD 8.2-15.055 (.113 (.120 (.117) < LOD .9 (12.120-.4-18.8-19.S. population from the National Health and Nutrition Examination Survey.080-.110) .1-24.140-.90) 90th 15.116) .062 (.098 (.109-.060) .048 (<LOD-.5 and 7.1) 10.9-22. which may vary for some chemicals by year and by individual sample.6) 9.054-.103 (.062 (.070-.8 (9.130-.3 (18.1-19.1 (18.112) 95th .170) .2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.8) 15.056-.5 (16.077 (.7) 15.160 (. 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.059 (.1) 15.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.109 (.1) < LOD 9. population from the National Health and Nutrition Examination Survey.3 (13. see Data Analysis section) for survey years 01-02 and 03-04 are 10.063-.70 (7.8.109-.9 (14.3 (14. Survey years 01-02 03-04 Geometric mean (95% conf.9-38.80-10.4) < LOD < LOD 16.4) 14.120) .139 (. which may vary for some chemicals by year and by individual sample.9-23.054-.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9. Fourth National Report on Human Exposure to Environmental Chemicals 79 .053 (<LOD-.8) 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 .1) 15.088-.140 (.6-24.8-25.100) .138) .101) .100 (.S.0) 21.2) 12.130 (.086-.2) 11.058) < LOD .108-.084-.138 (.2) 15.139 (.4 (12.8-24.4) 539 456 484 487 980 885 Limits of detection (LOD.062-.049-.130-.30 (8.6) 16.090 (<LOD-.30 (8.80-9.089 (.0-21.070 (<LOD-.9 (13.180) .124) .190) .3 (19.0 (10.4-17.130) .7 (14.3-21.8-17.0) < LOD 9.7 (15.093) .090-.140) .1-18.4) 95th 20.1) 14.190) .150 (.00-14.8 (11.130-.0) 19.147 (.50) 15.150 (.7-19.0-25.6 (15. Survey years 01-02 03-04 Geometric mean (95% conf.0 (15.2) 14.0 (10. < LOD means less than the limit of detection.096-.070) .40-9.110 (.9 (13.1 (13.7-22.103 (.0 (11.090 (.064) 90th .180) .6-24.110) .080) .6 (14.1) 13.120 (.5 (<LOD-11.5) 19.075) < LOD .80 (<LOD-10.10 (<LOD-16.8 (18.090-.6 (15.160 (.6) 19.5-17.102 (.110-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.100-.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .069) < LOD < LOD .7 (<LOD-15.1-16.090-.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.

Ellis H. 15. 1992-2001. 2 Classes of Pesticides. PA.html. Chlorinated Hydrocarbon Insecticides.91(1):122-126. Lancet 1998. Grajewski B.cdc. Patterson DG Jr.gov/~dms/ pesrpts. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Fernandez MG.27:405-421. Roy ML. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Priestly BG. References Agency for Toxic Substances and Disease Registry (ATSDR). et al.26:701-719. plasma dieldrin. Song S. Reprod Toxicol 2000. Environ Health Perspect 2001. 1991.352:1816-1820. Inc. Schulte P. toxicology. Neurotoxicol 2005.109(Supp1):113-139. Olea N. Kanthasamy AG. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Eds. Handbook of Pesticide Toxicology. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Chapin RE. Li AA. Mink PJ. bioaccumulation.gov/ circ/2005/1291/. Environmental Health Criteria 91. Cox. Vol. Part A 2000. J Toxicol Environ Health. Available at URL: http://www. International Programme on Chemical Safety (IPCS). No:429-436.inchem. Anantharam V.103(Suppl 7):113-122. Cancer Epidemiol Biomarkers Prev 2000. and epidemiology in the United States. Pesticides in the Nation’s Stream and Ground Water. Jorgensen T. 2007 [online]. Academic Press. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress.org/documents/ehc/ ehc/ehc91. Environ Health Perspect 1995. Kitzazwa M. 4/21/09 Bates MN. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.atsdr. Grandjean P. 1989.59:229-234.14:95-102.150:263-271. In Hayes WJ.66(4):229-234. Needham LL. Aldrin and Dieldrin [online]. Serrano FO. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. J Occup Environ Med 2005. David VL. Organochlorine exposure and risk of breast cancer. Chung KL. 4/21/09 Hoyer AP. Rosellini RA. Psychopharmacology (Berl) 1987. Narahashi T. Int Arch Occup Environ Health 1994. Turner W. Food and Drug Administration (FDA). Mann D. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Andersen A. Hartvig HB.html.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). pp. Stehr-Green.gov/toxprofiles/ tp1. Sonnenschein C. Kanthasamy A. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Mumtaz MM. Sanchez-Ramos J. and lymphocyte sister chromatid exchange. Wienburg CL. Edwards JW. Available at URL: http://pubs. Tully DB. 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. Ginsburg KS.htm. Six high-priority organochlorine pesticides.54:1431-1443. Facca A. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Jr and Laws ER. Shore RF. Revised Feb. 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. Available at URL: http://www. Available at URL: http://www. et al. Exp Neurol 1998. September 2002. Teta MJ. Toxicol Lett 1992. Toxicological profile for aldrin/dieldrin [online]. Basit A. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. VT.usgs. New York. Daniel SE. either singly or in combination.cfsan. Smith AG. Finley B. J Toxicol Environ Health 1989. Brock JW. 731-915. Frey JM. Soto AM. Jr. are nonestrogenic in transfected HeLa cells. Corrigan FM. August 2008.fda. Carlson JN. Patterson DG Jr. Demographic and seasonal influences on human serum pesticide residue levels. Buckland SJ. Chemosphere 2004. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. United States Geological Survey (USGS). Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.64-65 Spec.9:1357-1367.47:1059-1087. Garrett N. 6/1/09 Ward EM. 80 Fourth National Report on Human Exposure to Environmental Chemicals . McIntosh LJ. 4/21/09 Jorgenson JL.

1994).6) 20.8-32.1-25.82-11.8-33.8-61. 57-74-9 Heptachlor CAS No. 1994.8) 52.5) 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 * * * * 11.4 (30.9 (26.0 (32.5 (33.5) 37.8-42.0 (37.0 (<LOD-12.9-42.5-43.2-49.1 (40.5-13.6 (43.1-50.6-53.3) 18.3) 37.6) 48. the technical grade product of each chemical contains 10%-20% of the other chemical.4 (30.2 (10.63 (8.9 (31.3) 41.4 (35. Chlordane is not currently produced or used in the U. 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.5-40.8) 53.5 (31.3-24.1 (17. Fourth National Report on Human Exposure to Environmental Chemicals 81 .70 (<LOD-10.5.10-11.2-28.0) 41.9 (11. 10.7-56.2 (21.1 (20.1 (44.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.2 (39.4 (31.3 (21.3 (27.0-18. 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.9 (36. which may vary for some chemicals by year and by individual sample.5-44.5) 56.8) 44.20-10.5) 9.0) 37. and dairy products are the usual sources of exposure to these chemicals in the general population.8) 27. 01-02.2 (36.5-38.6 (9.6 (16.2) 33.3) 18.0 (20.5 (<LOD-12.1) 90th 34.7-12.6 (25.1 (<LOD-12.4 (<LOD-12.6-24.3-43.37 (8.4) < LOD < LOD < LOD 23.1 (<LOD-12. Since 1992.4) 39.7-39.0-61.8) 18.9-38.7 (10.4 (22.9 (15.9-21.7-25.S.9 (15.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.36-11.1) 30.1-25.0-12. 2007).4) 37.2-56. Technical grade chlordane had contained 7% trans-nonachlor.4-51.3 (20.2 (37.9) 11. population from the National Health and Nutrition Examination Survey.8-23. from the early 1950’s until the mid-1980’s.0) 31.1) 22.2-26.7 (43.6) 48.1 (27.4-14.S. As a result of the manufacturing process.90 (8.2) < LOD 11.8 (10.6-45.7) 31.7-70. Until 1988.9 (26.7) 35.3) 10.7 (32. Survey Geometric mean (95% conf.0-13.9 (21.5) 21. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.6-24.10 (8.5) < LOD < LOD < LOD < LOD 13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8 (40. in addition to trace amounts of numerous other related compounds (ATSDR.3) 10.7 (19.7 (34. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00.5.3 (26.9-40.8 (10.4) 29.8 (42.6) < LOD 11.9 (17.9 (11.20 (<LOD-11.2 (9.3-32.7) 19.74 (<LOD-10.Organochlorine Pesticides Chlordane CAS No.3 (9.0) 27. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.8 (18.2 (28.6) 39..5-65.2) * 12.9) 23.6) 23.8-73.9) 39.9) 17.9) 11.30-11.1) < LOD < LOD < LOD < LOD < LOD 8.5) 38. respectively.0 (26.9 (29.9) 10.5-32.0 (16.3 (25.4) 18.5 (34.2-21. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues. buildings.1 (<LOD-12.5-41.7) 42.5-47.8) 52.6 (9.2) 34.1 (11.1-51.6) 9.20-11.4) 12. Consequently.2) < LOD 11. fish.5) 10.2) 46.7) 19.4 (10.4-40.2) 36.2) 22.7 (34.5 (8.4) < LOD 11.1) 30.1) * 11. and 7.8-43.5) 44.0) 75th 20.0) 21.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.1-19. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44. and 03-04 are 14.5 (41.2) 37.6) 11.4) 22.8 (17. and in soil.3 (28.9) 47.6) 49. lawns.9) 13.3 (<LOD-19. heptachlor use has been limited to treatment of fire ants near power transformers.3 (11.4-21. 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.1-65.6) 9.8.8 (17.0-67.1-15.5) < LOD < LOD 9.8-33.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.7 (<LOD-13.9) 37.69-10.10-18.8-20.7 (<LOD-32.2-49.9) 36.1 (16. foods high in fat such as meat.1) 16. 2007).7 (17.9 (18.6-18.7 (42.4-45.89-10. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.9-21.1) * 11.1 (15.6) 8.1 (25.9) 31.2 (41. chlordane was used to kill termites and other insects on agricultural crops.7) 9.6) 36.3-49.7-14.6-12.9) 23.0) 20.3-45.8-31.7) 28.S.0-33.5-42.3-45.0-25.

280-.108-.057) * . which is also persistent in the body (ATSDR. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.104-.180-.300) . and heptachlor epoxide in foods and bottled water.240-.050-.115-.068-.245-.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .199-. heptachlor.246-.200-. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.062) < LOD .170) . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.S.070) .066 (.056 (.300-.240 (. 1986). 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.270 (.063) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.063) * . Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.231) .130) .310) .091) ..280-.230 (.440) . 1977a.203-.080) .160 (. 1986).280-.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.140 (. and breast milk is a major excretion route in lactating women.253-.092) . and inhalation exposure. 2006).290-.120-.280 (.130-.210 (.300) . 2007. Shindell and Ulrich.053-.350 (.104) .220-.320 (.250-.216-.067 (. Smith.146) . EPA has established environmental criteria for chlordane and heptachlor.061-.200-.290 (.077) .058 (.210-. Elimination of all these chemicals from the body occurs over months to years. FDA established allowable residues of chlordane.150 (.315 (.510) .190-.320) .066-.079) .300) . IARC.150 (. Le Marchand et al.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .207 (.410) .120 (.270 (.058-.082 (. dermal.230) . 82 Fourth National Report on Human Exposure to Environmental Chemicals .320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .240-.119 (.064) < LOD . characterized by seizures and paralysis.170) .070 (.170) .370 (.270 (. Takahashi et al.260 (.310 (. which may vary for some chemicals by year and by individual sample.310) .560) .090-.290) .080) .230 (.271 (.180) .258-.S.073) < LOD < LOD < LOD < LOD .070 (<LOD-.189 (.280 (.050 (<LOD-.380) .230-.070 (<LOD-.450) .220-. chronic doses of heptachlor have produced liver enlargement and injury.100 (<LOD-.130 (.130-.066 (<LOD-.450) .058-. Rogan.200 (.090) .070 (<LOD-.126) .Organochlorine Pesticides (Dallaire et al. neonatal mortality.063-.150-.210 (.180-.190-.074-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .069 (<LOD-.057-. and the U.290-. 1977b..242-.300 (.049 (<LOD-.350 (.430) . 2002.149 (.077) .208 (.148) .207) .250 (.077) .140 (.071 (.053-.S.146) < LOD < LOD .320 (.287) .260 (.080 (.079) < LOD < LOD < LOD .286 (. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.213) * .165-.080) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.128 (.170) .057 (.170-.087-.225 (..080 (. population from the National Health and Nutrition Examination Survey.370 (. 2007).348) .133) 90th .110-.075 (.350) .148-.130 (.068) 75th .340) .160) .310-.330 (.120-.112 (.063 (. Survey Geometric mean (95% conf.140-.180) .090) .083 (.280) .068) . 1996.204 (.063 (.130-.100-.070-.227) < LOD .430) . The major metabolite of heptachlor is heptachlor epoxide. Acute.150) .048-.066-.240) .160) .300) .223) .110 (<LOD-.160) . IARC considers chlordane and heptachlor as possibly carcinogenic to humans.220 (.070-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.230-.140 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.083) .060 (<LOD-.400) .136) . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.260 (.189-.269 (.373) .310) .168-.320 (..070 (<LOD-.130) .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 * * * * .258 (. 1991).076) < LOD .290) .077) .070) < LOD < LOD < LOD < LOD < LOD . The U.140) .130 (.150 (.260-. In laboratory animal studies.100 (.190-.360) .047 (<LOD-.302) . to heptachlor.063 (.070-.126 (.200-.230-.130-.140-. 1991.400) .065-.340) .073 (.320) .170) .063 (.115 (.106-. 2001.320 (. and alterations in immune function of offspring. OSHA has established occupational exposure criteria. Chlordane and heptachlor are absorbed after oral.290-. 1981).140 (.120-.130-.100-.250 (.370 (.055-.286 (.

cdc... In serum samples obtained in between 1994 and1997 from Inuit women in different Arctic countries. In the Hawaii episode. resulting in human exposure to heptachlor epoxide that was excreted into the milk. mean serum heptachlor epoxide and oxychlordane levels were about sevenfold and threefold higher. 2003). 2000). environmental levels) and scientists plan and conduct research on exposure and health health effects of chlordane and heptachlor is available effects. transnonachlor. 2004). 2006).atsdr.org/documents/cicads/cicads/cicad70. 1993). and 2003-2004 subsamples were comparable to levels measured in Swedish women from 1996-1997 (Glynn et al. or heptachlor epoxide causes an adverse health effect.gov/toxpro2. 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.. transnonachlor. respectively.. Biomonitoring Information Serum oxychlordane and trans-nonachlor levels in NHANES 1999-2000. A small sample of Polish women had mean levels of oxychlordane and trans-nonachlor that were about fivefold lower than in females in the NHANES 20012002 subsample (Jaraczweska et al.. or heptachlor epoxide in serum does not mean that the level of oxychlordane. 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. Finding a measurable amount of oxychlordane.Organochlorine Pesticides about external exposure (i.. than the 90th percentile values of NHANES 1999-2000 (Stehr-Green et al. the mean serum heptachlor epoxide and oxychlordane levels were more than twice as high. from ATSDR at: http://www.. trans-nonachlor. For the exposed persons drinking milk in the Arkansas episode. 2001-2002. inchem. A recent assessment of heptachlor is available at: http://www. 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 studies on levels of oxychlordane. 2002). 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.html. 1988). 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.e.htm#ref. Biomonitoring data can also help Fourth National Report on Human Exposure to Environmental Chemicals 83 . respectively. than the 90th percentile values of NHANES 1999-2000 (Baker.

0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.2) 20.0 (15.2-17.7-19. and 7.0-17.1) 23.2-27.8) 13.8) 19.3) 23.6-21.2-16. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.6 (12.5.0-19.8) 16.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.2) 15.8.0-17.3) 16.3) 22.5 (18.6) 14.1) 20.3 (<LOD-25.9-23.2 (<LOD-62.10-13. see Data Analysis section) for Survey years 99-00.40) 15.8 (<LOD-23. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-24.8-24.9-16.8-46.0-54.9 (15.9) 15.90 (<LOD-9.8 (13.9 (12.8-24.6 (16.4 (15.0-16.5) < LOD 14.6) < LOD < LOD < LOD 27.6.9-25.6) 22. and 03-04 are 14.3-18.1 (19.8 (13.3 (13.4 (11.7 (13.4) 18.5 (<LOD-32. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.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) 18.1) 13.6 (8.0 (11.4 (11.8-23.6 (13. Survey Geometric mean (95% conf.2) 26.6 (14.3) 18. < LOD means less than the limit of detection.2-27.0) 13.3) 10.1-38.1 (16.8) 21.8 (15.2 (18.4) 21.7 (16.7-25.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) 13.8 (18.5) 19. 10.0) 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) 18.3) 27. 01-02.5 (11.7 (10.5 (11.8) 20.7-18.6 (11.8) 15.8) 14.6 (<LOD-27.50) < LOD < LOD < LOD 17.20 (<LOD-9.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.2 (<LOD-16. respectively.6 (16.1-16. 84 Fourth National Report on Human Exposure to Environmental Chemicals .9-29.5 (<LOD-21.1-15.6) 13.8) 13.4 (<LOD-19.9-29.8) 14.2 (<LOD-25.6-17.S.8 (18.5 (10.8) 19.4 (<LOD-54.1-29.

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

5-87.2) 17.8 (30.1) 17.9 (66.6) 13.0 (60.4 (67.3 (56. respectively.8.1) 62.1-55.9-65.2 (7.4) 20.5) 36.0) 18.2) 19.0-68.0 (19.0 (13.8 (42.5-36.5-20.5-95.5) 26.8 (49.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.9 (36.1) 78.9 (47.6) 54.0 (15.8 (15.3-74.0) 40.2-18.1 (48.4-23.4) 19.3-58.6-22.4-35.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.9 (15.3-86.2-18.1) 17.0-59.8 (26.3) 15.1) 17.7 (16.6 (16.8-90.9-35.2) 59.9-40.8-41.6-82.3-39.7 (35.1-18.3) 19.7 (59.5) 14.7-35.2 (15.3 (17.8) 80.0-93.8 (19.1) 31.1) 17.1-22. 01-02.8-77.5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4 (28.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.3-21.1) 17.5 (45.6 (50.10 (<LOD-11.6) 25.4 (45.5) 77.8 (28. and 7.4 (11.0-38.8) 19.7) 52.6-20. population from the National Health and Nutrition Examination Survey.1-34.1) 16.2 (25.5) 20.0) 75th 31.7) 73.1) 18.1) 78.2) 34. which may vary for some chemicals by year and by individual sample.9-22.0) < LOD < LOD 8.0-143) 112 (68.0-23.3-57.4-22.3) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.7-160) 86.2) 30.7 (13.2 (14.3) 18.9 (16.0 (62.7-38.5) 48.8 (26.0-113) 68.5) 22.4-67.8 (28.7) 59.4-18.2 (19.7-32.2-88.3-50.2-21.5) 78.9-69.3 (16.4) 59.7-20.4) 107 (84.7) 15.0 (29.3-32.5) 30.6-88.4-62.2) 20.3) 32.3 (14.6) 34.1) 30.8 (17.2 (14.5 (15.6) 82.1) 32.6 (32.0) 49.2 (59.5) 19.8-16.7-34.9) < LOD < LOD < LOD 20.8 (26.4 (12.7-21.7) 17.4-52.8-90.1) 18. interval) 18.0 (14.1 (47.8-67.3) 16.1-126) 67.0 (16.7-113) 68.3) 36.9-45.9 (<LOD-14.8 (<LOD-20.0-123) 74.7) 78.2 (27.1-34.4-36.1-28.3) 25.9 (15.3 (58.7) 35.8) 47.1) 17.0-22.5) 35.6 (56.6 (12.8-19.7 (11.9) 14.2) 39.5-69.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.2 (36.3 (14.6 (<LOD-14.8-110) 59.0 (16.6) 56.8 (45.4) 16.8 (16.5 (15.7-18.9 (29.3) 18. 86 Fourth National Report on Human Exposure to Environmental Chemicals .8 (11. Survey Geometric mean (95% conf.6-54.2-23.8 (28.1-16.2 (64.1 (10.1 (17.6) 60.0 (15.7-22.9-65.9-64.5-111) 68.8-16.3-30.5-17.0 (42.0-24.9-20.4) 48.0 (13.6-19. see Data Analysis section) for Survey years 99-00.6 (52.3) 30.0) 19.7 (18.6 (15.9-58.5 (13.4 (16.8-21.7-23.6 (57.7 (59.9) 51.8 (71.2) < LOD 10.0 (42.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.3 (45.9) 14.0) 13.8-19.5 (44.7) 14.1 (65.8-79.86-13.8-129) 74.7-29.9 (51.7-17.S.9) 51. < LOD means less than the limit of detection.3) 32.0) 33.7) 28.6-66.5-19.2 (60.2-37.7 (74.1) 14.8 (13.0-37.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.7 (28.2-16.4 (30.1) 17.2 (26.7 (30.1-51.8) 51.3) 30.5) 14.5) 9.0-20.1-16.5 (25.6 (56.6) 10.1-20.70 (<LOD-12.5.6) 56.0 (48. and 03-04 are 14.0-93.1 (41.2-17.1 (22.0-23.7) 78.9 (51.9 (19.8 (13.3 (49.6) 84.4) 55.9 (28.9-36.5) 90th 55.9-89.7-77.7) 56.8 (12. 10.

458 (.370 (.565) .410-1.450) .310-.108 (.600 (.191 (.380 (.397-.651) .120-.470-.092 (.085-.S.220 (.096-.079-.640 (.600) .122) .250) .080-.390 (.340-.110 (.190-.183 (.272-.180-.510 (.103 (.190-.237) .082) .260) .232) .490 (.430-.190-.079-.129) .100-.690) .078 (.279-.093) .110-.230 (.126) .080-.390) .580 (.210) .840) .150) .405) .290-.288 (.071 (<LOD-.300-.414 (.069-.830) .119) Selected percentiles ( 95% confidence interval) Sample 95th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.186-.158-.100-.211) 90th .130 (.680 (.367) .081-.087 (.041 (<LOD-.220 (.061-.210) .590 (.090-.830) .320-.590) .460) .520 (.440-.145-.062 (.690) .340) .190-.340-.106 (.090-.930) . population from the National Health and Nutrition Examination Survey.125) .960) .186 (.098) .095-.114) .420) .131) .130) .100 (.120 (.130) .395) .090 (<LOD-.090) .330 (.054-.250) .559) .110 (.119) < LOD < LOD < LOD .324 (.108) 75th .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.177-.395-.580 (.220 (.109 (.286-.250) .500) .060) .390-.090-.099-.630) .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 .460-.173-.460) .140) .234) . which may vary for some chemicals by year and by individual sample.400 (.594) .470 (.120 (.310-.110 (.110 (.680) .081 (.440) .327 (.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.111-. Fourth National Report on Human Exposure to Environmental Chemicals 87 .090 (.161-.410-.112 (.120) .220) .090-.409-.310-.310) .100-.520 (.430-. interval) .120) .096) .060 (<LOD-.080-.120-.150) .330-.540) .171-.390 (.170 (.260) .135 (.400) .130) .130 (.093-.070 (.094 (.205 (.106 (.630) .108) .270-.220 (.134) .180-.090-.317 (.080-.120) .461 (.078-.220 (.242) .104-.120) .105 (.116-.160-.240) .220 (.237) .240) .202 (.100 (.190-.100-.047-.096-.141) .098-.092 (.400-.480) .080) .510-.128 (.112 (.093-.280) .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .117) .084-.400-.470-.343 (.113) < LOD .565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .490-.110 (.301-.285-.099-.390 (.240 (.497-.091) .310 (.210) .160 (.420 (.220 (.060-.125 (.085-.630) .210-.210 (.106 (.124) .490) .130) .141) .470 (.417 (.210-.684) .090-.116) .122) .370 (.210 (.390) .127) < LOD < LOD .20) .320-.360-.069) .130) .161) .360-.220 (.120-.573 (.800) .350 (.390 (.068-.104 (.430-.111 (.240-.080 (.190-.310-. Survey Geometric mean (95% conf.113) .350-.330-.288-.210 (.098 (.760 (.130) .558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .371) .089 (.240) .470 (.355 (.109 (.093-.550 (.098 (.580 (.590 (.116 (.097) .180-.110 (.300) .091-.085-.120 (.103 (.400 (.520) .490 (.110) .130) .055 (<LOD-.

Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Muckle G.cdc.inchem. Hawaii Med J 1991. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Jr. Academic Press.html. Environ Health Perspect 2002. Environ Res 2000. maternal serum and milk from Wielkopolska region. Keller JA. et al. KalubaSkotarczak A. 9/25/07 International Programme in Chemical Safety (IPCS).Summaries & Evaluations. Gilman A. Ayotte P. Bjerselius R. Environ Health Perspect 2003. In Hayes WJ. Available at URL: http://www. Arch Environ Health. Wohlleb JC. 1979-1980. 1991 pp. Willman E. Stehr-Green P.htm. Loo S. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Bull Environ Contam Toxicol 1981:27:506-511. Available at URL: http://ntp. Shindell S and Ulrich S. Hertz-Picciotto I.41:145–148. 1994-1997 organochlorine compounds. Concise International Chemical Assessment Document 70 Heptachlor [online]. May 1994. Circumpolar maternal blood contaminant survey.nih. Organochlorine exposures and breast cancer risk in New York City women. Inc. August 2007. et al. 79. 2 Classes of Pesticides.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 4/21/09 Baker DB. Baker DB. 1986. et al. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Vol. Chlorinated Hydrocarbon Insecticides. Tartter P. Available at URL: http://ntp. 6/1/09 National Toxicology Program (NTP). Available at URL: http://www.gov/ntp/ htdocs/LT_rpts/tr008. Distribution of polychlorinated biphenyls. Kolonel LN. Laliberte C.111:349355. LeMarchand L. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Chashchin V. et al. Handbook of Pesticide Toxicology.inchem. 2001. Saidein D. Jr and Laws ER. Wolff MS.cdc. Bleiweiss IJ. Sci Total Environ 2004. Aune M.niehs.atsdr.gov/ntp/ htdocs/LT_rpts/tr009. Covaci A. Jaraczewska K. Siegel BZ. Available at URL: http://www.nih. Toxicological profile for heptachlor and heptachlor epoxide [online].org/documents/iarc/ vol79/79-12. Available at URL: http://www. Bioassay of heptachlor for possible carcinogenicity. Dendle WH.9:1-109. Head SL. Toxicological profile for chlordane [online]. Wong L. Sci Tot Environ 2006. Mortality of workers employed in the manufacture of chlordane: an update. Lawrence River (Quebec. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. JAMA 1988. Smith AG.28:497501. 731-915. 1963-1967. Lulek J.org/site/foundation/ research/projects2. Berkowitz GS. Environ Health Perspect 2002.html.gov/toxprofiles/tp31. Senie R. Arch Pediatr Adolesc Med 1996.atsdr. Natl Cancer Inst Carcinog Tech Rep Ser 1977a.niehs. Chlordane and heptachlor [online].8:1-123. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States.110(8):835-838. 2006. Charles MJ. Granath F. Pollutants in breast milk.htm. Bioassay of chlordane for possible carcinogenicity. International Agency for Research on Cancer (IARC). Dewailly E. gov/toxprofiles/tp12. 1993. Available at URL: http://www.heptachlor. Van Oostdam JC.pdf. Voorspoels S. Dewailly E. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Poland.372:20-31. Hansen JC.org/ documents/cicads/cicads/cicad70. Takei G. Barker J. Natl Cancer Inst Carcinog Tech Rep Ser 1977b.pdf. Vol. J Occup Med 1986. 4/21/09 Dallaire F. Royce W.150:981-990. National Toxicology Program (NTP).84:151-161.330:55-70. Eds. Canada). International Agency for Research on Cancer (IARC) .50(3):108-118. A Report to the Hawaii Heptachlor Research and Education Foundation. Takahashi W.259(3):374-377. Organochloride pesticide residues in human milk in Hawaii. 4/21/09 James RA. Glynn AW. Brower S. Darnerud PO. Drews K. 6/1/09 Rogan WJ. New York.110:617-624. Atuma S. Organochlorines in Swedish women: determinants of serum concentrations. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii.html. Odland JO.

3-590) 293 (104-541) 48.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 1991).2-95. 01-02.2 (<LOD-40. In the body. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR. and trace amounts of several related compounds.4 (23.3) 22.7 (15.8-39.7) 677 756 595 1002 1549 1370 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 10.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. inhalation.9) 14.1) 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 12.8) 36. population from the National Health and Nutrition Examination Survey. 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.5 (23. DDT is converted in the environment to other more stable chemical forms.0-155) 83.2-bis(p-chlorophenyl) ethane (DDD).Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.90 (<LOD-12. which is a mixture containing p. 2002.1 (33. which may vary for some chemicals by year and by individual sample. Smith.1’-dichloro-(2. resulting in fetal exposure.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) 12.2) < LOD < LOD 9.4) < LOD < LOD < LOD 61. or dermal exposure.3 (<LOD-31. DDT was used at one time as a treatment for head and body lice.p’-DDT (65%-80%).10 (<LOD-12.0) 20. In the general U.2 (11.1 (<LOD-39. Only a small proportion of DDT is metabolized and excreted (Smith.8.6-33.00 (<LOD-10.0 (18. including 1.9 (10.S.0) 26.0 (18.6 (31.1 (23. 17.S. after World War II until 1972. and water.9 (21.5 (15.5) 25.p’-DDD (4% or less).2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.p’-DDT (15%-21%).7) < LOD 18. Food imported from countries that still use DDT may contain the chemical or its residues. and 03-04 are 20.2-65. see Data Analysis section) for Survey years 99-00.8) 30.1’-(2.0-27.9) 17.4. continues to be the primary source of DDT exposure. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.6 (9.1) 31.2) 30. < LOD means less than the limit of detection.9) < LOD < LOD 9.5 (23.7.0-15. DDT is converted to DDE and several other metabolites.5) 23.8) 15. population.70 (8.4) < LOD 17.8-26. and 7. sediments.6 (25. as well as in plant and animal tissues.8-23. respectively. when virtually all use of it was banned.2) 155 (59. DDT usually refers to the technical product.3) 21. and dairy products.1-27. although DDT and DDE intakes have decreased over time (FDA. air.8-17. It was produced and used in the U.7 (19.9-34. Gunderson.3 (27.9 (10.3-236) 24.5-36. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (<LOD-25. depending on conditions.5) < LOD < LOD 9.3) 28. 1988).9-28. It is still used in some countries.3-16.9 (<LOD-20. Survey Geometric mean (95% conf.3 (<LOD-21.0-37.9 (10.9) 29.5 (14. p. Fourth National Report on Human Exposure to Environmental Chemicals 89 . DDT can be absorbed after ingestion.5-54. particularly for endemic vector and malaria control.0 (10. particularly meat.7-16.50-11.3) 21. These chemicals are highly persistent in soil. fish.S.10-13. 2008.8) 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 8.0 (21.0-35. 1991). The biodegradation half-life of DDT in soil varies from 2 to 15 years.6 (22.0) 40. Both Serum p.1-71. o. DDT and DDE can cross the placenta.0-53. food.0) 19.

both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. dioxins and furans).170) .098-. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.142 (. 1998). 2006).201 (.180) .108 (. which may vary for some chemicals by year and by individual sample. 2006). interval) Selected percentiles ( 95% confidence interval) Sample 95th . population from the National Health and Nutrition Examination Survey. Gray et al.g.130 (<LOD-. and o. 2002. 2006.260) ..189-. Hayes et al.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .084 (..051 (<LOD-.078-.106) .p’-DDD and p. and seizures.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 .62 (.079) < LOD < LOD . In high dose.. 1995. and leukemia have also been inconclusive (ADSDR. Snedeker.530) .130 (<LOD-.220) ..170 (. reproductive organ abnormalities.132-. 2001). Calle et al..106-. 2002. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. and altered behavior after neonatal exposure (Eriksson and Talts.313 (. A workplace standard for DDT has been established by Serum p.627) . It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.143) < LOD < LOD . 2000.048 (<LOD-.180 (. 2006.140-. overt signs of acute human toxicity include vomiting. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.530 (.190 (.114-.230) .400 (.00 (. Beard. 90 Fourth National Report on Human Exposure to Environmental Chemicals .078 (.063 (<LOD-. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. Animal studies reported reduced fertility. and duration of lactation.S.130-.. 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.112 (. Reproductive effects in humans affecting birth weight.086 (.105-. 2002.061) < LOD < LOD < LOD .343) < LOD .095) < LOD .330-4.150 (<LOD-. fertility. 1996).069) .190-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.230) . Mariussen and Fonnum. premature delivery.p’-DDE can produce anti-androgenic effects (Gray et al.. 2001).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 .190 (. 1997).Organochlorine Pesticides chemicals are excreted in breast milk. Survey Geometric mean (95% conf.220) . accidental exposures.120-..068-.087 (.146 (. 2001).01) .570-4.150-.290) .150-.170-. have not been consistently demonstrated (Beard. polychlorinated biphenyls.150) . 2006). Jusko et al.180-.150 (<LOD-.130 (<LOD-.065-.059-.. 1956). tremor.250-1. Gladen and Rogan.160-. Jusko et al. lung cancer.00) . 2004.240 (.203) .071 (.240) .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.120 (<LOD-.180 (.200 (. 2002.074-.064 (. resulting in exposure to nursing infants (Rogan..420) .250 (. DDT may bind to estrogen receptors (Chen et al. 2006.140) . 2001). other organochlorines.400) ..180) .054-. Studies of DDT exposure and pancreatic cancer.146 (.080-.34) .106) < LOD < LOD .128 (.075) 1. Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR. In laboratory animals.26) 1.071-..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 .

and 7. see Data Analysis section) for Survey years 99-00.cdc. respectively. Compared to females in the NHANES 1999-2000 subsample. Declining DDE levels over time have also been observed in the German population.html.e. Biomonitoring Information DDE persists in the body longer than DDT. 1991).6 (81. 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. 2004). mean serum levels of DDT and DDE in the U.. respectively.atsdr... IARC classifies DDT (p. population declined by about fivefold to tenfold. Fourth National Report on Human Exposure to Environmental Chemicals 91 .S. population from the National Health and Nutrition Examination Survey. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. Stehr-Green. 2003). Heudorf et al.. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al.epa. 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. 1989). 2005)..S.p’-DDT) as a possible human carcinogen..7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. EPA at: http://www. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.7-119) 113 (100-140) 93.gov/ toxpro2. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.Organochlorine Pesticides OSHA and a guidance established by ACGIH. 1998. In a population-based sample of men and women from eastern Slovakia. NTP considers DDT as being reasonably anticipated to be a human carcinogen. Smith. 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.8. 2004). 01-02. In general. Since the 1970’s. 8.6.. Link et al. compared to levels observed in this Report (Anderson et al.3. 2002.S. Survey Geometric mean (95% conf. More information about external exposure (i.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. for males and females in the NHANES 19992000 subsample (Pavuk et al. and 03-04 are 18.gov/ pestcides/ and from ATSDR at: http://www.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. 2002. environmental levels) and health effects is available from the U.. 2003.

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.07 (5.3 (9.62-6. less than one percent had detectable serum levels of o.16 (2. In the NHANES 1999-2000.55 (2.72) 1.49) 8.15-4.12 (6.69) 8. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.30 (1.30-1.36) 3. 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.56) 2.03-1.22 (7. 309 versus 268 ng/g lipid.66-17. serum levels of o.7) 9.54 (1.36 (3.47) 3.01) 1.90) 22. o.01-11.534-.6 (7.91-2.8-90.88-35.32-1.796 (.32-9.87-16.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.12 (.p’-DDT.6) 9.9-17.4) 13.91) 3.40-8.21) 3. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.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 .40-4.13) 4.48 (6.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.01-1.3) 16.55-9.71) 12.07) 1.68) 2.6) 9.58) 1.p’-DDT (Stehr-Green.385-.39) 1.41-12.40-4.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.02 (2.92 (3.623 (.63-15.20 (.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.57-3.77 (1.70) 1. 2005).1) 12.63 (6.03-4.1 (8.53-15.32 (1.32) 1.36-1.9-38..51) 3.01-15.7-19.26-10.7 (8.611-1.53 (2.35) 1.26-2.54-7. 2001-2002 and 2003-2004 subsamples.68 (2.90-8.69 (2.4) 9.520 (.600) .80 (2.2 (19.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.75 (8.01) 1.1) 40.00 (.59 (1.Organochlorine Pesticides nearby agriculture (Botella et al. considerably higher than levels in this Report (Smith.4-19.81 (1.9 (15.54) 8.32 (1.14-9.25) 1.5) 16.65 (1.76) 1.25 (1.06) 1.34) 6.726) .57-2.18-1.47 (1.561 (.87 (5.39 (3.53) 7. population from the National Health and Nutrition Examination Survey.75) 6.25) 8.5) 5.10-1.963-1.85-10.01-1.51 (1.43-4.46 (1.43-8.50-17.6 (8.50 (2.8 (9.59) 3.7) 13.11-1.37-1.24) 1.75) 1.8 (14.71 (5.456 (.7-20. Finding a measurable amount of p. 2004).24-17.17 (3.31-12.31 (1.3) 10.76) 1.26 (1.11 (2.3-43.29 (1.p’-DDT were below the limits of detection.69) 4.730) .91-3. or p.22-1.430-.97 (3.0) 2.00) 7.25-14.37 (1.69 (1.3) 13.39-1.52 (3.78 (4.32-1.76 (2. Survey Geometric mean (95% conf.58) 75th 3.0 (9.96) .21) 90th 7.25 (.13 (1.45 (1.99) 1.14 (1.30 (1.71 (6.10) .28) 1.33-1.56-3.85 (1.40 (3.84 (3.06) 3.27) 3.58) 1.22) .6) 9.9) 5. In a subsample of NHANES II (19761980) participants.04 (6.82) 1.18-1.34) 2.7) 16.51) 1.488-.91 (6.64-2.63 (1.61-2.59 (4.419-.66) 4.43-4.71) 32.9) 7.44) 1.83 (1.97-4.79) 4.51-15. Serum p.6) 13.27-1.18-4.1 (9.07) 1.76-3.19-14.516 (.680-1.19) 4.52-6.80) 1.68-4.57 (1.61 (1. 1971).14) 2.30-1.965-1.66) 1.2 (6.10-5.37-10.5) 10.82 (1.. High mean levels of whole blood DDT (about 3.92 (3.72) 1.4 (12.00 (6.93 (7.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.5) 22.18 (6. 1991).85-4.02-8.75) 2.0 (12.557) 1.01-11.860 ng/L) and DDE (about 14.6) 8.37-16.57) 2.10) 2.84-3.59) 6.80) 1.60-13.870 (.14) 2.81-5.890-1.37-4.75 (4.64) 3. interval) 1.59 (1.3 (8.57-13.88 (2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.820-1.590 (..77 (1.05 (3.36-11.52 (1..2 (9.18) 1.00-1.92) 1.80) 3. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.4 (8.70-3.96) 1.66-2.46-2.5) 7.14-1.6) 9.31-2.24 (1.2) 19.8) 15.500-.45 (1.6 (9.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .39-2.63 (1.41 (1.S.36-2.57 (1.23 (7.81 (7.13-2.49 (1.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.2-32.34 (7.1) 7.26) 3.04-1.16-1.43 (5.2) 26.38 (1.56-2.18-3.635) 1.09-1.57 (3.4) 14.646) .38 (1.8 (13.05) 1.81) 11.69 (.53) 1.46 (1.2 (9.8 (13.17-3.56-6.81-18.66) 3.51-49.994-2.65) 1.6) 12.34-11.9 (26.25-16.6) 11.49 (1.66) 1.01-5.48-4. 2004).51-8.49 (6.34-3.12-1.7-48. 1989).6 (17.02) 1.66-4.p’-DDT.

7. < LOD means less than the limit of detection. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 01-02. and 03-04 are 20.8.Organochlorine Pesticides Serum o. 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.4. and 7. respectively. see Data Analysis section) for Survey years 99-00. Fourth National Report on Human Exposure to Environmental Chemicals 93 .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. 17. population from the National Health and Nutrition Examination Survey.S. which may vary for some chemicals by year and by individual sample.

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

hypospadias. Aune M.111:349355. et al. Swanson MK. Am J Public Health 1995. et al. Willman EJ. DDE. Ellis H. Gray LE Jr. Beard J.53(8):1161-1172. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Longnecker MP.cdc. Available at URL: http://www. Gabrio T. FDA total diet study. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Maternal serum level of 1. Schulz C. Chen CW. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Vena JE. Barr DB. April 1982 to 1984. Talts U. HCH. JAMA 1956. Jr.155(4):313-322.html. et al. Glynn AW. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Environ Health Perspect 2003. Charles MJ.72:261265. Olson JR.58:1185-1201. hexachlorobenzene.atsdr. Int J Hyg Environ Health 2002. Kulkarni PK. Biochem Pharmacol 1997. Organochlorines and breast cancer risk. and DDD [online]. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Needham LL.gov/~dms/ pesrpts. Krause C. Hurd C. Neurotoxicol 2000. Maternal DDT exposures in relation to fetal and 5-year growth. Chemosphere 2004.17(6):692-700. Lambright C.162:890-897.54:1431-1443. The Great Lakes Consortium. Effects of environmental antiandrogens on reproductive development in experimental animals. Lepom P. and polythelia among male offspring. Bull Environ Contam Toxicol 2004.112(17):1761-1767. Food and Drug Administration (FDA). Paepke O.355:7889. Rogan WJ. Eriksson P. Epidemiology 2006. Gunderson EL. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Hanrahan L. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. India. Bjerselius R. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Bates MN. Durham WF. lindane (g-HCH). Needham LL. Henley SJ. Brock JW.html. Levels of DDT. Jusko TA. Klebanoff MA. Thun MJ. Sci Tot Environ 2006. J Assoc Off Anal Chem 1988.gov/ toxprofiles/tp35. Olea-Serrano MF. Calle EE. Burse VW. Vorojeikina DP. dietary intakes of pesticides. Jr.. Zhou H. Zaidi SS. Parks L. Becker K.97(2):178192. Toxicological profile for DDT. Granath F.fda. et al. Hediger ML. Rivas A. selected elements. Link B.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. CA Cancer J Clin 2002. Herrman T. and other chemicals. Environ Health Perspect 2004. Olson J. Baker RJ. Arnold SF.85:504508. Organochlorines in Swedish women: determinants of serum concentrations. Davis MD.21(1-2)37-48. Botella B.1-dichloro2. Buckland SJ.7(3):248-264. Klebanoff MA. Gladen BC. Notides AC. Drexler H. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Falk C. 4/21/09 Gladen BC. DDT and human health. dichlorodiphenyldichloroethylene. Savitz DA. 4/21/09 Anderson HA.cfsan. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. et al. Seiwert M. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Hayes WJ. et al. Profiles of ortho-polychlorinated biphenyl congeners. et al. Int J Hyg Environ Health 2003. Kaus S. Koepsell TD. Longnecker MP. Bloom MS. Zhou H. Bhatnagar VK.96:34-40. Crespo J. Furr J. Am J Epidemiol 2002.358:110-114. FDA Pesticide Program Residue Monitoring 1993-2006 [online].206:485-491. Klebanoff MA. Kashyap R. Gray KA. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Cueto C. Greenfield TA. September 2002. Cerrillo I. Environ Res 2005. Environ Health Perspect 1998. Saiyed HN. Ostby J. DDE and shortened duration of lactation in a northern Mexican town. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Darnerud PO. Garrett N. Environ Res 2004. Heudorf U. et al. Zoellner I. Lancet 2001.71(6):1200-1209. Katz SH. Exposure of women to organochlorine pesticides in Southern Spain. Angerer J. Frumkin H. Biomonitoring of persistent organochlorine pesticides.52:301-309. August 2008. Needham LL. Available at URL: http://www. Wolf CJ. Hum Reprod Updat 2001. Piechotowski I. Brock JW. and dichloro(diphenyl)ethylene (DDE). Patterson DG Jr.205:297-308. Chemosphere 2005.106(5):279-289. Atuma S. and HCB residues in human blood in Ahmedabad. Moysich KB. Olea N. et al.

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1991). 1981). Over time. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.40-5. 2008).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. unlike aldrin and dieldrin. Because it is metabolized so rapidly. All uses of the pesticide in the U. and occasionally at low levels in sediment and surface waters.. EPA. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. endrin is converted rapidly to its major metabolite. Smith. unless the dose is high and the exposure is very recent. fatty infiltration. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces..40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD.8.09 and 7. IPCS.20 (<LOD-5.30) < LOD 5. 72-20-8 General Information Endrin. or discarded. Endrin was not widely used as a termiticide. is no longer manufactured in the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.S. 1979.60 (5.40) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. An epidemic of acute endrin poisoning. Endrin does not accumulate in body tissues (IPCS. Fourth National Report on Human Exposure to Environmental Chemicals 97 . 1987).S.S. At high doses. manufactured. rodenticide and avicide. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. anti-12hydroxyendrin. In the body.. 1996.50) < LOD 5.40 (<LOD-6. total diet surveys (FDA. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al.10 (<LOD-5. Survey Geometric mean (95% conf. endrin has been detected with declining frequency in U. a stereoisomer of dieldrin.30 (<LOD-6. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. have been cancelled by the U.Organochlorine Pesticides Endrin CAS No. inhalation or dermal exposure routes. 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 was used as an insecticide.S. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. endrin can persist for years. Endrin has been detected in soils.50) < LOD < LOD < LOD 5.10 (<LOD-5. Endrin is absorbed rapidly after ingestion.S. 1992). 1992). Hepatic effects of endrin exposure have included necrosis. endrin usually is not detected in serum of exposed individuals. Kavlock et al.20 (<LOD-5. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. or from contact with contaminated soils and sediments in areas where endrin was applied.40) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. 1992). Depending on soil conditions. 1991). < LOD means less than the limit of detection. Ketoendrin is a major photodegradation product (IPCS. 1992.

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

Narahashi T. Whitehouse DA. New York. Rogers E. Kavlock RJ. Perinatal toxicity of endrin in rodents. pp. 4/21/09 Bates MN. Fourth National Report on Human Exposure to Environmental Chemicals 99 . Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Eds.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Turner W. Hardjotanojo W. Perinatal toxicity of endrin in rodents. Chernoff H. Gray JA. Toxicology 1981.64-65 Spec.96:34-40. 1992. Gray LE.cfsan. 4/21/09 International Programme on Chemical Safety (IPCS). Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. No:429-436. et al. Toxicol Lett 1992.html. Gray LE.gov/~dms/ pesrpts.79(6):928-934. Ward EM. Liddle J. Pediatrics 1987. Academic Press. Environmental Health Criteria 130. 4/21/09 Kavlock RJ.inchem.9:1357-136.13:155-165. Sokal D. 1991. Fetotoxic effects of prenatal exposure in rats and mice. Ginsburg KS. et al. Roy ML. Patterson DG Jr. 731-915. Available at URL: http://www.html. Chlorinated Hydrocarbon Insecticides. In Hayes WJ. Cancer Epidemiol Biomarkers Prev 2000. Botella B. Rowley DL.htm. Garrett N. Fetotoxic effects of prenatal exposure in hamsters. Environ Res 2004. Gray J. Ellis H. Food and Drug Administration (FDA).gov/toxprofiles/tp89. Rab MA. Patterson DG Jr. Chernoff N. Hanisch RC. Schulte P. Rivas A. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.54:1431-1443.21:141-150. Jr. et al. 2 Classes of Pesticides. August 2008. Hanisch RC. Chemosphere 2004. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Frey JM. Burse VW. Andersen A. Available at URL: http://www. Toxicology 1979. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Exposure of women to organochlorine pesticides in Southern Spain. Handbook of Pesticide Toxicology. August 1996.atsdr. Available at URL: http://www. Olea-Serrano MF.fda. Toxicological profile for endrin [online]. Inc.cdc. Olea N. Saleem M. et al. Needham LL. Cerrillo I. Jr and Laws ER. Grajewski B. Crespo J. Buckland SJ. Smith AG. Vol. I. Endrin [online]. II. Convulsions caused by endrin poisoning in Pakistan.org/documents/ehc/ehc/ ehc130.

air. particularly by consuming fish. population from the National Health and Nutrition Examination Survey.0-25.4 (22.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and has been detected in soil.0-19.7-29. Survey Geometric mean (95% conf.6-TCP) (To-Figueras et al. 1976). 1988). and elimination occurs by renal and fecal routes.6 (23.2-15. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U. HCB is well absorbed after oral administration.8.6) < LOD < LOD 24.0-28.3 (14.9 (25.6) 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. distributes widely throughout the body.2 (13. and 7.7-21.4) < LOD < LOD 33. 2002).9-20..3) 24.S.2-31.6-33.0) * * 15.1-16. Although it is not manufactured as an end-product in the U.9 (14.6-trichlorophenol (2.. wildfowl.5-15.S.7-16.7 (15. and accumulates in fatty tissues where it persists for years. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.9-32.5) < LOD < LOD 18.3 (22. see Data Analysis section) for Survey years 99-00.7-16.0) < LOD < LOD 15. 100 Fourth National Report on Human Exposure to Environmental Chemicals .7-22.8) < LOD < LOD 27.5-14. EPA cancelled its use in 1984. which may vary for some chemicals by year and by individual sample.4.3-22. breast milk is an additional route of elimination in nursing women.5-TCP) and 2.6) < LOD < LOD 26.9) < LOD < LOD 16.4.3) < LOD < LOD 29.4) < LOD < LOD 19. primarily as a fungicide and seed treatment until the U.0 (25. and foods with a high fat content. and 03-04 are 118.4) < LOD < LOD 18.9-15.6-32.6 (24. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14. and sediment (Barber et al. 31.5 (13.9) < LOD < LOD 20.0) < LOD < LOD 15. 2.9) < LOD < LOD 19.0-16.0 (14.1 (14. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.9) 19.2 (17.S.6-44. water.5 (13.0.0) < LOD < LOD 24.7-30.9-30. Gunderson.5-18.7 (27.4 (18.8 (26. 2008.7) * * 14.4-15.0 (18. Urinary metabolites include pentachlorophenol (PCP).4 (11.6) < LOD < LOD 14.2-15.6) < LOD < LOD 25.9-24.5-14.3-26. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.7 (15.9 (25.3 (20.7) < LOD < LOD 24.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. 2005). HCB is slowly metabolized.3) * * 15. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al..8 (22.1-20.1 (13.4.1 (14.6-19.6) < LOD < LOD 26.7-26.9) < LOD < LOD 20.4) < LOD < LOD 14.4) < LOD < LOD 23.. HCB has been detected in fewer foods since the 1980s (FDA. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.Organochlorine Pesticides Hexachlorobenzene CAS No.1) < LOD < LOD 15.4 (18.4.4) < LOD < LOD 22.6-26. or game taken from areas with HCB contamination. 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-trichlorophenol (2.1 (17. respectively.5-15.2 (24. The general population may be exposed to HCB through diet. Therefore.8-15. 01-02.S.5-33.1) * * 15.7-15.2 (14.3 (12.7 (19.8 (15. The FDA dietary surveys have shown that over time.0 (18.5 (14.3) < LOD < LOD 20.2 (14.9) < LOD < LOD 28.9) < LOD < LOD 15.4-16.3 (22.9 (23. < 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.9-17.2) < LOD < LOD 29.7) 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 * * 16.2) < LOD < LOD 13.6 (21. 1997).4.3-20.3 (16.

163-.174-. 1982.171 (.114-.109) * * .069) < LOD < LOD . 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.065 (.163) < LOD < LOD .086-.140 (.176-.gov/pesticides/ and from ATSDR at: http://www.088-.094) < LOD < LOD .118-.090 (. EPA has established a drinking water standard. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.082-. IARC classifies hexachlorobenzene as possibly carcinogenic to humans. which may vary for some chemicals by year and by individual sample.143-. EPA at: http://www.102) < LOD < LOD .169-.089-.095 (.088-.069) * * .182 (.S. Fourth National Report on Human Exposure to Environmental Chemicals 101 .072-.203) < LOD < LOD . acute doses produce central nervous system depression and seizures. population from the National Health and Nutrition Examination Survey.132) < LOD < LOD .157 (.092 (.147-.095) * * . and weakness.090 (.115 (.225 (.145-. and the FDA has established a bottled water standard for HCB.120 (.097) . 2002).085-.100) < LOD < LOD .092 (. ACGIH has developed workplace exposure limits for HCB.atsdr.111) < LOD < LOD .118) < LOD < LOD .123 (.099) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Schmid. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.091-. The U.079 (. Survey Geometric mean (95% conf. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.081-. 1960). In humans.099) < LOD < LOD .060-.gov/toxpro2.086) < LOD < LOD .092-.095) < LOD < LOD 75th < LOD < LOD 90th * * .113-.175) < LOD < LOD .html.062-.095 (.111-.155) < LOD < LOD .098 (.092 (. and many died before 2 years of age (Peters et al.186 (. Biomonitoring Information Serum concentrations reflect the body burden of HCB. as well as hypertrichosis.258) < LOD < LOD .156 (.129) < LOD < LOD .S.178-.083) < LOD < LOD .191 (.107-. More information about external exposure (i.118-.122) < LOD < LOD .102 (.095-.073-.196) < LOD < LOD .159-..167 (.e.157-.cdc.141) < LOD < LOD .173) < LOD < LOD .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 * * .121 (.097) < LOD < LOD .090 (.089-. and liver and thyroid cancers (ATSDR.077-.epa.135-.147 (.125 (.114-..Organochlorine Pesticides chemical. very high. With chronic exposure. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD . 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.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .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 * * . This condition. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.190 (.163 (. environmental levels) and health effects is available from the U.081 (. arthritis.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.099) < LOD < LOD . Chronic feeding studies in animals have demonstrated kidney injury.203) < LOD < LOD . Infants were exposed transplacentally and through breast milk.097 (.160 (.090-.094 (.123 (.064 (.088-.127-. immunologic abnormalities.148-.130) < LOD < LOD .078 (.S.085) * * . anorexia.104 (. HCB interferes with normal heme synthesis.123 (.107) < LOD < LOD .176) < LOD < LOD .212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD . thyromegaly.152) < LOD < LOD .087 (.145-.126) .179 (.086-. reproductive and developmental toxicities.

Piechotowski I. selected elements.. HCB levels were directly related to age. Krause C. Environ Health Perspect 2002. et al. Bradman A. 2005).349:144.html. 2005).77:173182. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. van Wijk D. Lawrence River (Quebec. Jones KC. Arch Neurol 1982. 2006). Schwartz JM. Fenster L..58:1185-1201. Lepom P. Darnerud PO. Dogramaci I.54(3):203-208. 2002. Chemosphere 2005. Bertram et al.17:388–399. September 2002. Biomonitoring studies on levels of HCB provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of hexachlorobenzene than are found in the general population. Food and Drug Administration (FDA). Herrman T. Sci Tot Environ 2005.gov/~dms/ pesrpts. Eskenazi B. 4/21/09 Glynn AW. et al. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Biomonitoring of persistent organochlorine pesticides. Link et al. Bertram HP. however. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. 1986. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Biol Neonate 2002. Paepke O. In a representative sample of the 1998 German adult population. et al.cdc. levels. In the 1976-1980 NHANES subsample. In Spain..39(12):744-749. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Muller C. J Exp Sci Environ Epidemiol 2007.110(8):835-838. Otero R.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Canada). Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Santiago-Silva M. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates.gov/ toxprofiles/tp90. Zoellner I. 102 Fourth National Report on Human Exposure to Environmental Chemicals . and the geometric mean concentration of HCB in whole blood was 0. Kohli J. Kaus S..html. Seiwert M. 2002. Peters HA. April 1982 to 1984.cfsan. August 2008. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. trends and processes. Available at URL: http://www.71(6):1200-1209. The metabolism of higher chlorinated benzene isomers.205:297-308.. 2003). Laliberte C. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Safe A. only 4.44 mg/L.fda. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Reference values updated. Ozalla D. Lecha M. Bryan GT. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. and other chemicals. 2002) and among children (Link et al. Bjerselius R. Gabrio T. dietary intakes of pesticides. References Agency for Toxic Substances and Disease Registry (ATSDR). Herrero C. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Jones D. Hexachlorobenzene in the global environment: emissions. Gunderson EL. J Assoc Off Anal Chem 1988.81(2):82-85. Dewailly E. Muckle G. Glynn et al. HCB detection in serum also was proportional to age. Holland NT.. Lackman. Sala M. Can J Biochem 1976. Ayotte P.111:349355. Organochlorines in Swedish women: determinants of serum concentrations. Atuma S. Dallaire F. Environ Health Perspect 2003. 2005. Barr DB. Available at URL: http://www. but overall. Lackmann. Gocmen A. more HCB levels were quantified. Kemper FH. Granath F. 2002. respectively. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Sweetman AJ. 1989).. 1999). Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years..atsdr. et al. Toxicological profile for hexachlorobenzene update [online]. Becker K. Int J Hyg Environ Health 2002. Lackmann GM. Arch Dermatol 1999. Over the past two decades. Bradman et al. 4/21/09 Barber JL. As a result of the lower limit of detection in NHANES 2003-2004.9% of participants had quantifiable levels (Stehr-Green. distribution. 2002). FDA total diet study.. 2002. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Cripps DJ.135(4):400404. Schulz C... 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. IARC Sci Publ 1986. Link B. Aune M.

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

7 (53. In 2006. Technical grade HCH is a mixture of all four isomers.36.1 (9.6) 35.5) 16.7) 23.3) 34.1 (11.6-20.3 (42.5) 29. each result has been multiplied by 1. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.8-16.70 (8.3-56.6-42.9-56.5) 11.89 (<LOD-9. 2005).0-23.6-37.9 (50.4-111) 84. beta. formerly referred to as benzene hexachloride.2-52.1-49.0 (8.7 (25.1-36.2) 36.8-54.5) 22.20-16.70-12.9-81.3 (42. exists in several isomeric forms. See the section “What’s New” at the beginning of this Report for details.2 (34.8.70-19.0 (19.7 (30.0) 8.6-89. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-20.S.S. respectively.7-69. environmental levels declined.1) 31.0-70.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.2-55.5 (37.0 (37.S.46-11. Lindane has a half-life of about two weeks in soils and water.8 (10.2) 9.68 (<LOD-10. containing about 64% alpha and 10%-15% gamma isomers. the U. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.4 (8.56-12. 104 Fourth National Report on Human Exposure to Environmental Chemicals . 6.6) 50.4) 11.7-69.60-13.3-85.8 (17. 2005).7) 18.6) 18.5 (8.2 (31.6-47. including alpha.7) 97.4 (50.7) 73.0 (35. which may vary for some chemicals by year and by individual sample.7) 56.4 (11. It is no longer produced or sold in the U. so they can accumulate in fatty tissues of animals.3 (26.8) 27.4 (52.1-32.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.9) 17. gamma.90) 7. commonly known as lindane.2-20.1 (18. As pesticide applications of HCH were increasingly restricted or eliminated.0) 17.3) 37.7-20.0-111) 70.5 (16. The other isomers can be formed during the synthesis of lindane.0 (33.7-166) 70.8) 52.8-68.8 (32. 01-02.4) 44.7 (13.9 (32.3) 25.4 (16. < LOD means less than the limit of detection.8) * * * * * * 15.2-87. and delta.7-96.4) < LOD < LOD < LOD 46. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.0) 41.6-18.1 (12.8) < LOD 10.2 (29.8) 95th 68.4) < LOD 9.9) 15.8-87.0 (<LOD-12.04-10.4) 901 1067 952 992 1224 1007 Females 11. and have been used either as fungicides or to synthesize other chemicals.6-62.6) 47.6 (33.1 (27.7-96.9 (11.6) 16.80 (6.5 (11. HCH isomers.8 (33.2-67.90-8.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.1 (21. interval) 9. water.5) 90th 42.7) 27.0-21.8-19.6) 653 758 589 1240 1533 1370 20 years and older 10.70 (6.7) 10.0) 7.9 (9.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.5) 40. particularly alpha and gamma have been detected widely in air.2) 13.2 (18. 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.87 (9.5) 67.7 (29.6-14.2) 62. soil.1-27.9-51.6) 36.80 (<LOD-14.9) 45.7-26. and 03-04 are 9.1-16. 608-73-1 beta-Hexachlorocyclohexane CAS No.7) 32.Organochlorine Pesticides Hexachlorocyclohexane CAS No.9 (26. see Data Analysis section) for survey years 99-00.2 (9.0) 71.0-34.0) 35. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.5-29.0 (14.1) 71. and 7.2 (50.6 (22.6 (17.3) 51.8-199) 134 (85.0-70.8 (21.3 (13.4) 27. HCH isomers are lipophilic.5 (24.9 (62.4-45.1 (30.3) 14.9-24.1-32.9) 81.9 (30. However.4) 10.4) 21.7 (<LOD-16.5) 14.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.2-98.6 (16.8 (9.7) 10.1) 12.2 (48.5528.1 (16. **In survey period 2001-2002.2-42.50) 8. The gamma isomer. EPA cancelled agricultural uses of lindane (ATSDR.9-21.2-46.1-37.1) 12.1 (9.30-11. and sediment as a result of historic production and use.90-8. 319-85-7 gamma-Hexachlorocyclohexane CAS No.9-14.5 (14.9 (40.9-178) 48.43 (<LOD-9.7 (35.2) 142 (99. population from the National Health and Nutrition Examination Survey.3 (62.5-123) 49.4) 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 21.4) 51.4 (12. 58-89-9 General Information Hexachlorocyclohexane (HCH).6 (40.8 (64.4-73.1) 13.8) 12.8 (23.61-12.4-50.7 (62.3-38.6-135) 69.2-22.8) 7.8) 39.6 (10.1-15.76.66-12.5 (43.2-17.

070-.130) .330-.410) .090 (.120) .620-1.065 (.297-. U.412 (. hepatic enzyme induction.190-.150) .060) . Rogan. population from the National Health and Nutrition Examination Survey.220 (.090 (. or dermal exposure. The beta isomer accumulates in fatty tissues and is metabolized more slowly.560) .056-. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.072 (.280-.521 (.450 (.S.S.050 (. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans. the serum half-life was about 20 hours among children (Ginsburg et al.287 (.040-.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.460) . Fourth National Report on Human Exposure to Environmental Chemicals 105 .140) .047-.230-. paresthesias.Organochlorine Pesticides exposure to HCH is through the diet. HCH isomers are absorbed after inhalation.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 ..190-1.320 (.290 (.600) .244-.01 (.146-.050) .098 (.090-.073-.510) .480 (.057-.580-1. and nephropathy developed (IPCS.220) .372 (. tremors.064) .250) .140 (.089) . from 6% of samples in 1982-1984 to 2% in 1994 (FDA.250-.140) .340) .32) .700) .070 (.170-.100-.250 (.840) .110) .091) .092 (.120 (.083 (.057-.070-.580 (.210-.460 (.160) .190) .056-. EPA has established a drinking water standard.057 (<LOD-. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.086) < LOD < LOD < LOD < LOD < LOD < LOD .382-.048 (<LOD-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways. Workers who directly handled HCH have complained of headache.200-.360 (. 2002).089-.200-.250 (.100 (.100-..210 (.290) .125) < LOD < LOD < LOD .410-. After dermal application of lindane 1% lotion.131-..250 (.308-.081-.620) .5528.050-.078 (.100) .680) .254) 95th .175 (.120) .050-.118 (.124-.070) .069) .220-.350 (.100-. 1986).077) < LOD .119) . Saxena et al.310) .050-. for lindane.260) .068-.260) . 2008. each result has been multiplied by 1.420-.210) .170-.103 (.290 (.150-.234 (.400) .096) .080-.250-.150 (.294-. OSHA and ACGIH have established workplace standards and guidelines.080 (.110) .450) .587) 653 758 589 1240 1533 1370 20 years and older ..160 (.067 (.051-.191-.051 (<LOD-.173-.214) .220-.103-.240-. Gunderson 1988).390-.05) .080-.080) * * * * * * .120-. Distribution is mainly to fatty tissues.059-.404) .065 (.305) . enlarged livers.470 (.120 (. respectively.270 (.067) .050 (.070-.480 (.S. 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. interval) .222 (.090 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.360-.319) .118-.410 (.260-. which may vary for some chemicals by year and by individual sample.661) 901 1067 952 992 1224 1007 Females . 1977).501) . HCH crosses the placenta and is also excreted in breast milk (Radomski et al.080-.050 (<LOD-. ingestion.331 (.380 (.400) .350) .160-.064 (.200 (.370-.100 (. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.130-.140) .340-.210 (.180-.120-.410) .290) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .191-. 1981).110) . resulting in a half-life of about seven years.144 (.281 (.050-.310) .103) 90th . ataxia.390 (. 1983). The U.300-. probably by blocking inhibitory neurotransmitters in the central nervous system.221-.139 (.174) .062 (.077) < LOD .240 (.690) .150) .050 (<LOD-.450-. See the section “What’s New” at the beginning of this Report for details. and memory loss (Nigam et al.814) .062 (.280-.120 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .910 (.310 (.570 (.360) .120-. and FDA has established a bottled water standard and food residue tolerances for lindane. and seizures.480) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .710) . 1971.070 (.290 (.058 (<LOD-..083) . **In survey period 2001-2002.442 (.190) .080) .37) 1.470) .080 (.216 (.167 (.110-.130 (. 1996.100) . When animals were chronically fed lindane at high doses.560 (.330 (.

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

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

Environ Health Perspect 2003. Heinrich R. Crespo J. Herrman T. Atuma S. Rogan WJ. Stehr-Green. Maass R. Angerer J. children and newborn infants. Chemosphere 2004. Bhatnagar VK. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Demographic and seasonal influences on human serum pesticide residue levels. Sturgeon SR. Radomski JL.cdc. Nigam SK. Link B. selected elements.htm. 2002. Deichmann WB. Environ Res 2004. Placental transfer of pesticides in humans.9(4):417-424. Astolfi E. Garrett N. Int J Hyg Environ Health 2002. Saiyed HN. et al. et al. Gunderson EL. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Kutty D. Bhargava AK. Aune M. Available at URL: http://www.54:1431-1443.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).72:261265. Int Arch Occup Environ Health 1986. Olson J. Seiwert M. and HCB residues in human blood in Ahmedabad. The Great Lakes Consortium. Metabolism of gammahexachlorocyclohexane in man. Majumder SK. Exposure of women to organochlorine pesticides in Southern Spain. FDA total diet study. Hanrahan L. Kaus S. Available at URL: http://www. Organochlorines in Swedish women: determinants of serum concentrations. Lindane. Occupational exposure to hexachlorocyclohexane.106(5):279-289. Bates MN.gov/~dms/pesrpts. VI. Buckland SJ. Becker K.27:405-421.cfsan. Ellis H.inchem. Granath F.48:127-134. Biomonitoring of persistent organochlorine pesticides. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. et al. April 1982 to 1984. J Toxicol Environ Health 1989. Zaidi SS. Bai KM. Toxicological profile for hexachlorocyclohexanes update [online]. Needham LL. Rothman N.205:297-308.20(2):186-193. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Brinton LA. Wood PH. Toxicol Appl Pharmacol 1971.atsdr. Bottimore DP. Patterson DG Jr. Reisch JS. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Karnik AB. et al. Int Arch Occup Environ Health 1983. Botella B. J Pediatr 1977. International Programme on Chemical Safety (IPCS).57(4):315-320. Glynn AW. Needham LL. Piechotowski I. Potischman N.96:34-4Food and Drug Administration (FDA).71(6):1200-1209. available at URL: http://www. Chemosphere 2005. Falk C. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.120:1-82. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Kulkarni PK. Brock JW. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). J Assoc Off Anal Chem 1988. Needham LL. Krause C. Lepom P. Krishna Murti CR. August 2008.58:1185-1201. Cancer Causes and Control 1998. Absorption of lindane (g benzene hexachloride) in infants and children.fda. FDA Pesticide Program Residue Monitoring 1993-2006 [online].html. Olea N. Arch Toxicol 1981.91:998-1000. Rey AA. Siddiqui MKJ. Visweswariah K. PA. Darnerud PO. dietary intakes of pesticides. Environ Health Perspect 1998. 4/21/09 Anderson HA. et al. Arch Pediatr Adolesc Med 1996. Gabrio T. Bull Environ Contam Toxicol 2004. Bjerselius R.52(1):59-67. Olea-Serrano MF. India. Paepke O. Rev Environ Contam Toxicol 1991. August 2005. et al. Cerrillo I. Pollutants in breast milk. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Rivas A. Schulz C.111:349355. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Burse VW. Zoellner I. Kashyap R. and other chemicals. Levels of DDT. HCH. org/documents/jmpr/jmpmono/2002pr08. Lowry W. Saxena MC.150:981-990. gov/toxprofiles/tp43. 4/21/09 Ginsburg CM. Raju GS. et al. 4/21/09 Kutz FW.html.

1 (<LOD-104) < LOD < LOD < LOD < LOD 39. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.10 (<LOD-15.70 (<LOD-15.3 (15.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.70-40.5-82.40 (<LOD-13.Organochlorine Pesticides Mirex CAS No.10-37.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5 (<LOD-42.0 (14. animals. water. 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.5 (<LOD-115) 153 (30. 1995).6-305) 15. < LOD means less than the limit of detection.2) 51. population from the National Health and Nutrition Examination Survey.7) < LOD 66.90-29.8 (<LOD-73.3) 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. 1991).4) < LOD 15.S. In studies conducted in the 1970’s and 1980’s.6) 9. Occupational exposure is limited to workers at sites where mirex contamination is present..3 (15. 1985.2-230) 13.8 (12.7 (<LOD-47.3-225) 15.1 (<LOD-65.6 (<LOD-108) 9. aquatic organisms. where it has a half-life of 12 years.0-374) 11.S.6) < LOD < LOD < LOD < LOD 71.5 (9. 10. (Kutz et al. Some states and the U.S. or pesticide application. 01-02.2 (7. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. soil.5-291) 11.4 (8.70-24. Formerly. and 03-04 are 14. Mirex can cross the placenta and be excreted in breast milk. 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.6.4) < LOD 63. see Data Analysis section) for Survey years 99-00. respectively.1 (13. and 7. Mirex has been detected in air. Fourth National Report on Human Exposure to Environmental Chemicals 109 .S. after which it is widely distributed in the body and stored in fat. since 1977. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. which may vary for some chemicals by year and by individual sample.7 (12.7) 8.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. where it was applied directly to soil and by aerial spraying.0 (12. Mirex is not metabolized in the body. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.6 (<LOD-31.6 (<LOD-23. 2385-85-5 General Information Mirex has not been produced or used in the U. Survey Geometric mean (95% conf. it is a highly persistent chemical in the environment.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 contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.8) < LOD 15.8. and foods.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. mirex was detected in human adipose samples. resulting in exposure to newborns and nursing infants. disposal.0 (<LOD-108) < LOD < LOD 50. Mirex is absorbed through the skin and from the gastrointestinal tract.5. especially those from persons living in the southeastern U.1 (8..4-230) 18.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Mirex binds strongly to soil.5-425) 40. sediments.

79) . 110 Fourth National Report on Human Exposure to Environmental Chemicals . 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.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 .220) .92) .090-1.093 (. 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. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.112 (. population from the National Health and Nutrition Examination Survey.510) < LOD < LOD .8. as well as in a subsample of NHANES II (1976-1980) participants. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.100 (<LOD-.108 (.37) . 2005).610) < LOD < LOD < LOD < LOD .79) .077 (<LOD-.. IARC classifies mirex as possibly carcinogenic to humans.053-. More information about external exposure (i.310 (.cdc.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.220 (<LOD-.079 (<LOD-. Laboratory animals fed high doses developed liver enlargement and liver tumors.064 (<LOD-.140 (<LOD-.102) < LOD < LOD < LOD < LOD .106) < LOD .215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . reproductive toxicity included decreased fertility and testicular damage.110 (<LOD-. 7. In samples obtained between 1994 and 1997. 2004).73) .070-1. which may vary for some chemicals by year and by individual sample.090 (<LOD-.055-.470 (.089-. 1991).html.090-1.256 (.470) .106 (.170) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . The U.100 (<LOD-. EPA has established environmental standards for mirex.. Smith.450) 1.054 (<LOD-.052-.690) .450 (. environmental levels) and health effects is available from the ATSDR at: http://www. and 4.430 (.7 ng/g of lipid.370 (.S.gov/toxpro2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .080-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170) < LOD .170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .090 (<LOD-. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.268) < LOD . 1995.080-1. The geometric mean mirex levels of the Inuit mothers were 8.02) .41) . 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. 1989).059 (<LOD-. which is approximately twofold to threefold lower than the 90th percentile for females in the NHANES 20012002 subsample but similar to 95th percentile for females in the NHANES 2003-2004 subsample (Van Oostdam et al. 2001-2002.090 (<LOD-.Organochlorine Pesticides exposures are unknown..635) < LOD .08 (.S.410 (.062-.090-1. In addition.470) .e.170-3. Survey Geometric mean (95% conf. Biomonitoring Information In the NHANES 1999-2000. serum mirex levels were generally below the limits of detection (Stehr-Green. and 2003-2004 subsamples.atsdr.

Fourth National Report on Human Exposure to Environmental Chemicals 111 . The human body burden of mirex in the southeastern United States. 1994-1997 organochlorine compounds.atsdr. PA.gov/toxprofiles/ tp66. Sci Total Environ 2004. Vena JE. Jr and Laws ER. Smith AG. 731-915. Rev Environ Contam Toxicol 1991. Carra JS. Leininger CC. et al. 2 Classes of Pesticides. Toxicological profile for mirex and chlordecone [online]. Profiles of ortho-polychlorinated biphenyl congeners. Kutz FW.120:1-82. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. dichlorodiphenyldichloroethylene. Environ Res 2005.330:55-70. J Toxicol Environ Health 1985.cdc. Circumpolar maternal blood contaminant survey. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. hexachlorobenzene. References Agency for Toxic Substances and Disease Registry (ATSDR). Vol. August 1995. Handbook of Pesticide Toxicology. Watts DL. Odland JO. New York. Stroup CR. Stehr-Green. 4/21/09 Bloom MS. Demographic and seasonal influences on human serum pesticide residue levels. Olson JR. Chlorinated Hydrocarbon Insecticides.27:405-421. et al.97(2):178192. Swanson MK.html. 1991 pp. Eds. Available at URL: http://www.15:385-394. Hansen JC.Organochlorine Pesticides effect. Wood PH. Gilman A. In Hayes WJ. Moysich KB. Kutz FW. Dewailly E. Jr. Inc. Bottimore DP. J Toxicol Environ Health 1989. Chashchin V. Van Oostdam JC. Strassman SC. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Academic Press.

4.00 (2.72) < LOD 1.60 (.S.5-trichlorophenol (2. public drinking water systems did not detect 2.50-16.60 (4.0) < LOD 21.30-11.50-25.4.0) 14. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR. 2.40-11.0) < LOD 5. Historically.5-TCP) and 2.0 (4.40) < LOD 1.60) < LOD 8.900-2.30-27.S. other organochlorines. Occupational exposures.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.40 (2.40) < LOD 6. < LOD means less than the limit of detection.6-TCP in any of the samples (U.5-Trichlorophenol CAS No. 2. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.9 (<LOD-121) 9.30) < LOD 4. EPA.3.9.0) 2.60-8.71 (<LOD-8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.27) 696 661 521 696 603 939 Limit of detection (LOD.0 (4.0 (5.0 (8.0) 2.6-trichlorophenol (2. recent sampling of U.19 (<LOD-6. 2.0 (4.63) 18.0 (3.40 (2.0) < LOD 5.27) 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 1.42 (<LOD-12.4. Formation of 2.40 (2.57 (<LOD-15. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.20-36.80 (1. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols. Exposure to trichlorophenols also may result from metabolism of lindane. 1976).S.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. usually at herbicide production or waste incineration facilities.90-33.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.4.40) < LOD 4.50) < LOD 1.42 (<LOD-8.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . population from the National Health and Nutrition Examination Survey.0) 2.80 (2.30) < LOD < LOD < LOD < LOD < LOD 1. may occur by inhalation or dermal routes.0) < LOD 11. 2006).00-8.4. soils.20) < LOD 1. Trichlorophenols are no longer manufactured commercially. 1999).Organochlorine Pesticides 2.60 (2. Survey Geometric mean (95% conf. are metabolites of several organochlorine chemicals. surface water.80) < LOD 1.8) 21.30-27. Both chemicals have been detected in air.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 5.0 (3.30-27. and sediments. 95-95-4 2.9 and 0.4. hexachlorobenzene.50 (2.980-3.20) < LOD 5.4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30-3.4. 112 Fourth National Report on Human Exposure to Environmental Chemicals .4.71 (<LOD-8.50-63.50 (1. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.40 (.0) < LOD 5.10-3.940-3.5TCP and 2. including hexachlorobenzene and hexachlorocyclohexanes.00-3. and polychlorinated benzenes (Kohil et al.4.40 (1.30 (.60-18.920-3.950 (<LOD-1.40 (2.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.40 (.6-TCP).980-3.5-trichlorophenol. 1999).20-71.00-3. however.40-18.20 (4.0) 2. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. Such workers would probably Urinary 2.0) 2.30-40.40 (1.6-TCP were used as intermediates in the production of certain pesticides.31 (<LOD-9.0) 2.20) < LOD 90th 5.4. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. which may vary for some chemicals by year and by individual sample.50 (.7.30-44.03) 9..7) 24.80-41.6-Trichlorophenol CAS No.00 (3.0) < LOD 11.

8) < LOD 9.. In the same 2-6 year old children. in addition to dioxins.e.5) 11. 1995) and up to 19 times higher than the 95th percentile value of 1.6-TCP as reasonably anticipated to be a human carcinogen.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.980 (<LOD-1. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.73 (<LOD-8.79-4.3 mg/L reported in German adults aged 18-69 years (Becker et al. 2003.4.1) 2..5-TCP and limited for 2.53-3.9) 12. 2003).75 (<LOD-6.7 (4.95 (3.69 (2. 7.67 (1.13-13.32) < LOD 4.53-3.81 (<LOD-9. leukemias.atsdr. However.29 (1. animals showed hepatocellular abnormalities.4.6-TCP levels at the 95th percentile were up to eight times higher than 3..4.86 (3.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.4.78) < LOD 1. NTP classifies 2.69-18. Laboratory animals chronically fed high doses of 2.00-19.55 (4.1 (<LOD-58.4. More information about external exposure (i. 1989)..4.11) 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 2.17) 9.4) 5.9 (5.82 (<LOD-32.44 (1.00) < LOD 4. 1995) were similar. as being possibly carcinogenic to humans.2 (2.0) 7.02) < LOD 7.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.57 (3.24) < LOD 6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.68 (<LOD-8.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al. and other chlorinated compounds.920-2.4.4 (6.93-11. Fourth National Report on Human Exposure to Environmental Chemicals 113 .cdc.02-3.31) < LOD 2. Among 6-11 year old children in NHANES 1999-2000.6) 4. population from the National Health and Nutrition Examination Survey.67 (1.16 (.43 (2.37) 16.4) < LOD 3.83-12.47-8.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.88-16. the 95th percentile urinary 2..44 (.19-4. The 95th percentiles for 2.75 (3.Organochlorine Pesticides be exposed to mixtures of chlorophenols.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).80 (1.5-TCP nor 2.gov/toxpro2.43) < LOD 12.57 (<LOD-7.15) < LOD 2. At lower doses.820-2.8) 4. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.46 (1. IARC classifies combined exposures to polychlorophenols. the 95th percentile urinary 2.64 (4.78 (3. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.20-6.49 (1.24 (3.4. Neither 2..S.2) 2. Human health effects from 2.0 mg/L.74) 11.00-29..8 (5..78-19. Radon et al. 2004).4.5) < LOD 12.4.16) < LOD 90th 5.2) < LOD 5.05-17.6) 4.5-TCP or 2. which includes trichlorophenols.28-25.90 (4.. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples. Urinary 2.4.4) < LOD 3.24) < LOD 1.html. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.6) 4.68-4.6-TCP had increased rates of hepatic tumors. 2003).4.6-TCP.50) < LOD 2.60-3.24) < LOD 5.5-TCP.24-11. furans.3 (5.27-17.62-20. and lymphomas. Survey Geometric mean (95% conf.57 (<LOD-7. urinary 2.36 (1.19-12. environmental levels) and health effects is available from ATSDR at: http://www.4.33) < LOD < LOD < LOD < LOD < LOD 2.05-8.37-11. 1989).5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.

65 (5.36 (1.0) 7.57 (<LOD-2.53) 2.67-12.52 (2.00 (2.0) 12.54) 6. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.0) 13.4.01-6.5-TCP and 2. 114 Fourth National Report on Human Exposure to Environmental Chemicals .55-3.0 (14.4 (9.4.47 (3.0 (15. Finding a measurable amount of 2.2) 25.3 (11. was about six times lower than the median urinary levels for males in this Report (Radon et al.1 (10.49 (6.58 (1.40) 3.6-19.09) 15.4.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.89 (3.35-3.40-2.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.76) 3.4.04) 2.3-26.68 (<LOD-2.0-38.60 (2.23) 2.20-3.7-3.30-33.8-15. In harbor workers exposed to chlorophenol-contaminated river silt.0-54.80-7. similar to the limit of detection for this Report (Anderson et al.7 (13.8-13.30) 4.3-17.0-37.0 (15. 1991).4.80-20.0) 10.70) 5.3 (11.44) 75th 4.08 (2.98-11.00-4.4.50 (2.90 (3.0 (13.4 (10.4-17.30-11.10 (5.60-21.40) 4.4.5-TCP level of 0.6) 21.0 (14.92 (2.20-23.0 (7.0) 14.0-50.1-25.56 (3.0-43.87-14.9) 13.2 (14.0-18.18-3.0 (20.70) 3.6-TCP in urine does not mean that the level of 2. Urinary 2.45) < LOD 11.40 (2.9 (13.20) 4.0 (6.33-4.9) 694 677 519 696 602 931 Limit of detection (LOD.90) 2.20 (3.70-3.0) 13.6 (12.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.0) 13.4 (17.14 (2.6-TCP level. for males in NHANES 19992002 (Agramunt et al.0) 17.28) 24.60) < LOD 5.0 (16. the median urinary 2.0-38.4.4.30-2. < LOD means less than the limit of detection.5-46.95) 3.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.9 (11.0-44.50-5.0-41.60 (3. interval) 2. 0.70-6.0) 11.36-5.4.6 (11.5-TCP and to the median 2.2) 12.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.91-4.5-TCP or 2.58-3.6TCP causes an adverse health effect.40-7. population from the National Health and Nutrition Examination Survey.5-TCP or 2.60) 6. Urinary 2.3.0 (14.45 (5.0 (12.65) 15.1 (8.98-7.63) 90th 15.07 (<LOD-3.5-TCP or 2.0) 9.0) 10.4.40) 2. Biomonitoring data will also help scientists plan and conduct research about 2.40-2..8) 32.6-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.25-11.60 (3.6TCP values.32) * 3.0 (8.5-TCP (0.00-21.0) 6. respectively.09-7.70-6.0) 14.0) 15.40-14.90 (4.4.40-32.85) * 3. 2004).0 (20.28) * 2.70 (2.7 (9.0) 9.9) 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 2.00 (4.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.10-3.70) 1.95 (4.20-6.0 (6.6-17.0) 7.8-24.3) 37.75 (8. 2003). Survey Geometric mean (95% conf.59-6.23-2.31 (3.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.85 (2.72-10.8 (9.4.66 (8. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.0) 19.46-3.4.40-4.3) 20.3) 23..36 mg/g creatinine.80-6.79 (5.5-TCP and 2.0 (8.8) 18.48-26.0 and 1.80 (2. Biomonitoring studies on levels of 2.12) 2.6 mg/g creatinine) and 2.4.7-16.0) 13.24 (2.78 (2.6-TCP than are found in the general population.10) 2.1) 16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.7 mg/L.84) 2.69 (3.10-3. Mean values of 2.80 (3.5-TCP or 2.31) * 2..45 (2.78 (2.0 (11.30-2.4.00 (1.51-12.89-6.53) 4.6-TCP exposure and health effects.80-25.6) 26.80 (2.7) 21.5 mg/g creatinine) were similar to the limit of detection for 2.45-9.0) 11.0 (4.S.32) 3.67) 4.74 (2.32-4.90-8.6-22.60-3.0 (9.0) 19.52-3.73-9.0) 17.95-6.70 (2.70) 5..4.40) 2.99) 6.4.02) 2.06) * 2.40 (2. 1998).2-0.23) 3.59) 4.74-3.0-68.4 (8.4.20 (3.10-2.0 (6.60-37.10) 6.26 (2.6-TCP (0. which may vary for some chemicals by year and by individual sample.80) 1.7) 33.

04-16.29-4.0 (11.82 (8.5 (8.06) 11.6-31.18-4.82) 2.25 (3.6 (22.6) 8.5) 9.91-2.62-15.11) 10.42 (2. Survey Geometric mean (95% conf.53 (3.29-4.88) 4.0) 8.15 (6.53) * 2.5) 12.35 (3.46-14.1) 14.10 (6.22-9.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.53-11.2 (7.72) 32.6) 12.63) * 4.3) 8.3-37.60 (4.20-2.87) 2.88 (2.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.19-5.2 (8.56) < LOD 11.1-21.51 (2.52) 2.76) 2.13 (1.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.7-36.4) 8.5) 11.67-17.17-4.9) 8.01 (3.6 (10.55-2.22 (3.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.2) 19.09-3.76-8.16-10.23) 4.02) 3.8) 19.47-5.58 (4.63) 4.25-17.7 (14.95-2.22 (1.38) 22.23 (1.00) 4.89) 10.54 (2.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.92) 4.65-2.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.32 (2.33) * 2.9-64.66-4.00) 4.7) 6.3-23.65-21.56-5.71 (3.33 (1.0) 10.63-13.51-21.14-13.73-22.88-7.5 (7.9-29.83-5.73) 5.4 (12.9 (9.63 (<LOD-2.77) 2.53) 4.59 (2.4) 4.8) 21.51) 18.24 (1.98 (1.5) 8.49) 4.00 (2.9 (9.9-34.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.77-4.41 (3.48-2.9) 19.14-2.33 (7.50-8.83-6.6 (6.10-9.87) * 2.76) 4.63-15.52 (5.17) 13.42) 2.81) 2.9-32.06-2.90) 2. interval) 2.6 (9.Organochlorine Pesticides Urinary 2.41-6.30-2.87-6.72-16.79-17.68) 2.13-6.1 (8.82-2.52 (3.25-15.88) * 2.2 (12.76) 1.S.60-2.17) 2.89-2.3 (9.98) 10.9) 8.10) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.04-2.7) 25.83 (3.8 (7.15 (1.91 (7.75) 75th 4.88) 4.26-13.0 (9.00 (3.33-2.1 (13.4.2 (13.6 (12.43 (<LOD-2.26 (6.56 (7.4 (11.02 (1.83-6.6 (5.44 (3.81-9.91 (3.50 (2.88) 5.40 (7.25-2.05 (6.22-2.29 (6.78) 2.38-5.87 (3.63 (2.18-2.4) 9.82 (3.99-2. Fourth National Report on Human Exposure to Environmental Chemicals 115 .8 (8.5 (10.27-9. population from the National Health and Nutrition Examination Survey.5) 11.06) 4.65) 2.38 (4.96) < LOD 4.08-2.65) 18.25 (3.90 (1.38 (2.1) 11.28-4.1-32.21-11.68) 2.6 (9.87-7.88) 1.78) 90th 12.43-7.32-19.70-9.52) 2.49-3.43 (2.5-28.05 (3.22 (<LOD-2.8) 12.78 (2.6) 13.0 (6.40 (2.8) 11.9) 7.94-13.

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

EPA. Certain organophosphorus insecticides (e. have accounted for a large share of all insecticides used in the United States. An estimated 73 million pounds of organophosphorus insecticides (70% of all insecticides) were used in the United States in 2001. In general.. chlorpyriphos) are initially metabolized to the more toxic “oxon” form. the organophosphorus insecticides have better gastrointestinal than dermal absorption.Dimethylthio. and a low persistence in the environment.DimethyldithioDiethylDiethylthio. General population exposure to organophosphorus insecticides may occur by ingesting contaminated food and from hand-to-mouth contact with surfaces containing organophosphorus insecticides. and manufacturers of these insecticides may have greater exposure than the general population. Approximately 40 organophosphorus insecticides in a wide variety of formulations are registered for use in the United States by the U. slight to moderate water solubility.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Organophosphorus Insecticides: Dialkyl Phosphate Metabolites General Information Organophosphorus insecticides.. 1993). with usage declining 45% since 1980 (U. most residential uses have been phased out in the United States as a result of implementation of the Food Quality Protection Act of 1996. Most organophosphorus insecticides undergo hydrolysis with excretion of major hydrolytic metabolites in the urine. which are active against a broad spectrum of insects. Farm workers.g. florists. naled) are also registered for public health applications (e.S. The thiophosphate type organophosphorus insecticides (e. Mammalian elimination halflives can range from hours to weeks. mosquito control) in the United States.S. 2004). In general. moderate to high soil binding. pesticide applicators. EPA. less common routes include inhalation and dermal contact.g.g. the various organophosphorus insecticides demonstrate low vapor pressures (with some exceptions).Diethyldithiophosphate phosphate phosphate phosphate phosphate phosphate (813-79-5) (1112-38-5) (756-80-9) (598-02-7) (2465-65-8) (298-06-6) • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • Fourth National Report on Human Exposure to Environmental Chemicals 117 . gardeners. Although organophosphorus insecticides are still used for insect control on many food crops.. malathion. 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. widely varying degrees of soil leaching or runoff potential. 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.

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

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

37 (3.07-10.33-18.70 (2.56 (1.970-2.80) 2.890 (<LOD-2.16) 4.82-12.56 (4.1) 95th 13.5) 20.50 (.22 (.4) 18.02-5.30 (2.05-7.66) * * 1.02) 4.2) 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 1.60-11.80-24.4) 17.1.14) * * .0) 5.60-18.13-2.9) 14.80-4.95) 5.70) < LOD < LOD 75th 3.0-27.27-15.34-7.19) 9.0) 5.0 (9.1-23.55-6.8 (8.44 (2.03 (.2 (9.0 (4.0) 6.2 (9.6) 18.00 (4.20-30.61) 4.40-19.0 (7.35-16.81) 11. 01-02.2-20.70) .0 (7.40-1.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.85 (3.717-1.0) 11.290 (<LOD-.810-1.80) 11.58 (3.10 (2.58 (5.10 (2.50 (4.4 (7.44-3.70 (4.54 (3.10 (.79 (5.38-5.86-15.98-5.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.70-19.0) 10.80-22.80) 4.39 (3.97) 90th 7.620-1.2) 16.23-5.00-19.0 (7.71 (2.74 (8.670-1. 120 Fourth National Report on Human Exposure to Environmental Chemicals .60 (1.04) < LOD 1.08-15. respectively.57-7.90-5.80) .8) 11.13 (2.47) 5.98-12.579-1.51) 2.80 (2.0 (7.81) 1.11 (. see Data Analysis section) for Survey years 99-00.20 (.50-5.0) 6. and 03-04 are 0. and 0.3-15.0) 20.00-27.46) 10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2 (7.70-23.0) 11.30 (2.30-4.0) 5.2.90 (1.758-1.91) 4.00) 3.80) 2.63) 1.60-25.0) 10.40-14.00-12.4 (9.0) 11.12) 4.40-16.3) 14.28) 1.1-17.490-2.50 (2.79-7.70-14.30 (4.26-8.52) * * 1.1 (9.3) 16.15-12.8) 19.40 (.4) 20.08-2.2) 14.72) 5.600 (<LOD-1.700-1.20 (2.20-4.90) 3.0 (8.60) .71-9.42-3.80) 2.1 (10.4 (7.60 (5.26-6.955 (.42) .2 (7.8 (12. 0.32 (.94) * * .17-3.2 (14.00-27.0 (9.83 (5.840-1.0 (8.1) 10.981 (.29) * * 1.81) 11.4 (9.80) .9 (8.55-8.45 (2.21) 9.70) < LOD < LOD 1.74 (8.97) 8.90-4.7 (14.8) 7.61 (3. which may vary for some chemicals by year and by individual sample.5-16.34-3.47) * * 1.80) 3.32) 1.00 (5.39 (8.68-7.20-7.16 (2.43-12.21 (.0) 9.10) < LOD .2) 16.76 (2.52) 6.10) < LOD < LOD 4.00-7. interval) 1.623-1.00 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.0 (5.8) 7.56 (6.36-4.10 (.2 (7.0) 12.8 (14.860-2.780) < LOD 3.15) 14.08 (<LOD-2.30-6. < LOD means less than the limit of detection.599-1.0) 10.27-3.6) 7.530 (<LOD-2.60) < LOD < LOD 4.5-17.58 (2.01) * * 1.53) 4.70-11.35-11.290 (<LOD-1.2 (11.40-5.82) 10.40-11.0 (12.0) 7.93-24.00) 3.1) 13.13 (2.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.52-11.954 (.00-12.8-32.93 (4.20 (.3) 17.830 (<LOD-3.2.5 (11.0) 15.9) 8.67) 3.0 (6.2 (14.33 (5.89) 9.20 (.0 (8.0) 6.0) 11. population from the National Health and Nutrition Examination Survey.740-2.9) 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 1.12-19.8 (9.2) 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 1.50) 2.80 (4.94) 3.757-2.9-18.56-13.99 (5.0) 10.10-7.26 (5.44-38.7) 11.5 (8.20 (.0-28.35-12.750-1.48-7.86 (1.90) 2.5) 15.0) 10.50-36.73) * * .0 (6.96-3.7 (12.

900 (.7 (8.40) < LOD < LOD 75th 2.05) .4 (9.05 (.95 (3.66 (5.02 (2.549-1.04 (1.1) 4.83 (7.43) 2.88-10.37 (4.870-2.94-10.80 (7.94-23.03) 2.02-2.9) 12.69-10.9-28.00-19.650-1.3) 5.19 (4.920 (.89) * * 1.57) 4.533-1.68-4.1) 4.41-12.28-9.5) 11.5-16.92-5.09 (.6) 8.8) 7.78 (2.4) 13.75-7.57-10.37-5.35) < LOD < LOD 3.9 (5.3) 16.3) 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 1.2) 7.60) * * .87 (3.42) 12.10 (3.98 (3.83) 8.7) 5.94 (2.4 (4.74) 90th 7.34 (6.37-3.47 (3.75 (7.82-6.4) 4.932 (.2) 5.26) * * .820 (.14 (3.8 (10.38 (1.00-13.40-12.2) 8.69 (4.608-1.81-5.36) * * 1.46) 2.41) Selected percentiles ( 95% confidence interval) Total * * 50th .47 (3.23) 4.2) 5.6) 9.2 (6.02-14.1-15.2) 13.82-14.2 (8.98) 9.67) 4.8) 16.500-1.28 (2.98) .92-2.90-8.98) .2) 95th 12.09) 2.89-3.45-5.1 (10.42 (3.0 (8.1 (7.60-9.75 (3.890 (<LOD-1.30) 2.440 (<LOD-2.56) .40-14.54) .30 (1.69) 2.04-6.960 (<LOD-2.73 (1.75) 2.510-1.924 (.64-5.10-13.8) 12.4) 4.570-1.3) 15.7 (9.93) 9.62) .38) .9 (9.773-1.84 (5.7) 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 .43 (.52) 4.76-4.95) 2.45-5.44 (2.53) 9.61 (1.51-5.90-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.77 (6.53 (6.8) 6.5-32.40 (3.5) 12.790 (.860 (.75) 14.8) 8.2) 9.66-15.71) 10.00) 8.87-5.31 (3.28) 10.9 (9.79-3.87 (1.82-26.29 (2.88 (5.29) * * .57 (4.05 (1.98-22.47) 2.85 (6.6) 11.818 (.84) 7.750 (<LOD-1.94 (4.1 (6.883 (.94-22.5) 8.03-6.13) 4.7) 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.1 (11.61-29.07 (. interval) .98-5.960 (.34) * * .54-4.67-19.01-2.34) < LOD < LOD .9) 11.54-2.5-20.93-5.0) 6.81 (1.72) 11.28 (4.68) < LOD < LOD 3.9) 16.996 (.0) 7.53-11.80) 9.35 (1.855 (.03) 2. Fourth National Report on Human Exposure to Environmental Chemicals 121 .40-3.7 (10.710 (<LOD-1.88) 2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.23 (4.18 (.66 (1.620-1.88-15.54-15.7) 18.28 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.15-10.1 (9.69) 4.47) * * .56-13.74) 4.39 (2.5 (4.61 (1.3) 12.37 (5.67) 1.1) 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 1.7) 12.11-6.09-11.50) 7.03 (2.5) 7.03 (7.82-14.56) 7.93-9.25) 6.60) 2.20-8.40-5.00 (4.2 (10.62-5.6) 13.31-14.40) 4.00-17.32-12.430-1.1 (8.80 (6.6 (9.540-1.85) 2.66-34.27) < LOD 2.41) .5) 7.40-28.61-13.566-1.79-9. population from the National Health and Nutrition Examination Survey.37) 9.57 (6.780 (<LOD-1.02 (7.574-1.43 (3.45-11.54-11.56) 4.55-20.71-2.94-9.S.06-2.80 (2.34 (6.00 (4.633-1.66 (2.46-5.21-23.830-1.560-1.5-13.6 (10.58) * * 1.47 (1.25) < LOD .890 (<LOD-1.76) < LOD .24-3.

80-14.24-5.3 (12.3) 10.77-3.47-6.27) 4.20) .34 (6.66-13.88) 3.6) 18.52 (6.53 (3.0) 7. and 03-04 are 0.8) 8.0) 11.4 (10.9 (7.0 (10.0) 14.0) 6.20) 3.6) 14.7-21.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.90-15.12 (4.18 (3.15-2.3) 8.00) 7.4 (10.0) 12.04 (3.30) 3.96) 90th 7.0-24.5 (9.10) 6.0-24.10 (<LOD-1.77-14.27 (3.0 (14.0) 13.42 (1.7 (11.40 (2.5 (8.8-20.50-5.90-31.910 (<LOD-2.15-6.80 (5.00-9.3 (6.0) 23.90 (6.35-3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.39-13.S.41) 3.35 (6.37 (3.5) 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 * * * * * * .73) 7.0 (8.00) < LOD .0 (9.20 (<LOD-2.14 (6.80-3.28 (7.30) < LOD < LOD .60) < LOD < LOD 2.40 (2.00) 8.80) .8 (12.46-4.7) 10.10 (.0) 12.6) 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 * * * 1.00) 3.95 (5. which may vary for some chemicals by year and by individual sample.98-9.30) 3.72) 2.9) 10.650-1.8 (12.80) 5.58 (1.90) 8.50) 3. respectively.01 (2.3 (9.90 (1.88) 10.40) < LOD < LOD 75th 2.7) 14.97-4.92-17.10-4.0 (13.20-4.80-6.1 (10.6-41.0) 18.670 (<LOD-1.70-9.3) 22.99 (3.34-10.580-2.22-12.89) 2.0-19.34-3.90 (6.5-26.00 (.00-16.49-4. 0.80-8.10-10.90 (6. population from the National Health and Nutrition Examination Survey.11-6.50) . < LOD means less than the limit of detection.00) 3.9 (12.0) 14.80) .39 (5.29) < LOD < LOD < LOD < LOD 3.970 (<LOD-2.3) 20. 122 Fourth National Report on Human Exposure to Environmental Chemicals .80 (2.70) 2.46-28.3 (11.33-11.7 (10.6 (10.00-4.70-8.75 (3.80-12.4 (14.0) 9.90 (6.60 (5.2 (9.22 (6.1) 11.9) 95th 14.8-21.90 (2.9-14.95-9.58.00-18.80 (2.0) 13.51) < LOD 1.8-17.16-1.78) 5.0) 12.31-7.80-21.62-17.31-12.17 (7.9-17.00-18.20-18.4) 7.92) 9.30) 8.0) 11.670 (<LOD-1.89 (2.3) 14.20) 3.75 (2.29-4.90 (2.4) 11.20-8.96) 3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80-4.90 (2.6) 11.670 (<LOD-1.7) 15.61 (3.66) 4.790 (<LOD-1.0-29.70 (1.30) < LOD < LOD 4.0) 9.1-23.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5.7) 16.8-20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740 (<LOD-1.680 (<LOD-1.84-4.64) 10.18) * * * * * * * * 1. see Data Analysis section) for Survey years 99-00.63-14.74) * * * * * 1.9-15.67) 3.00-4.81-6. and 0.27) 9.8) 9.41-5.2 (7.82) 8.0 (10.67) 4.22) 8.50) 5.45 (3.06 (2.7-19.5 (8.90 (5.90) 4.86-10.0 (9.25 (2.5.10-15.59-3.60 (6.22 (6.27) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .70-9.37) 2.70 (8.31) 1.2) 14.0 (7.5) 21.1 (10.90-9.0 (15.9) 16.4-17.6-19.70-5.34-5.67-10.6 (10.35) 4.9) 9.0-33.0 (5.670 (<LOD-1.90-15.61-32.27 (7.95 (2.60 (2.7) 22.3 (7.50-4.0) 19.24 (2.3 (9.6) 14. 01-02.

7) 14.15 (1.0 (8.5 (10.2) 12.59-3.0-21.0) 14.5-17.6) 7.53-8.03) 3.910 (<LOD-1.3-17.2) 12.42) 7.7 (10.38) 1.27) < LOD .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 1.38 (2.3 (7.34) < LOD < LOD < LOD < LOD 3.30) 8.7) 15.4 (11.3) 6.2) 8.29 (5.41 (7. population from the National Health and Nutrition Examination Survey.68-10.00) 8.89-13.0 (13.91) 3.89-10.8 (10.9 (9.93-10.25-9.6) 13.51-10.42) 8.1 (8.06 (<LOD-1.86-3.33-10.850 (<LOD-1.8 (8.77 (2.92) 3.21) * * * * * 1.7) 12.80) 3.0-19.58 (4.00 (<LOD-1.973 (.70-35.0 (10.30) 7.11 (5.6 (11.68-4.99) 2.7) 14.81 (7.15) < LOD < LOD 75th 2.920 (<LOD-1.55) 16.2 (9.91-9.07-3.44-6.85-8.590 (<LOD-.29-2. Fourth National Report on Human Exposure to Environmental Chemicals 123 .7-23.2) 12.5) 10.780-1.88 (1.9-17.28 (1.73 (5.83 (6.39-17.4-18.07 (5.38 (1.4) 16.6 (13.5) 22.34-18.03 (6.530-1.78) 4.68-19.86 (3.86) 9.79-6.18) 2.94-14.6) 12.95) 3.2) 15.37) 3.21-21.78 (6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.54-5.32) 2.1 (13.72-4.28-12.27-13.27) 1.78 (4.12) < LOD < LOD 4.07) 2.50-17.75-3.6) 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 * * * * * * .23-3.00) 2.27) * * * * * * * * 1.97) < LOD .04) 9.09-11.01-5.29) 3.72) 4.83 (7.4-16.2) 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.4) 15.30) 2.64-11.75-3.7-19.9-25.6) 6.5 (15.3-34.00 (3.38-13.93 (6.00 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .28) 6.5 (9.0 (11.77) 3.74-4.78-10.77 (2.6 (10.19) 3.97-4.890-2.51-7.85-17.7 (11.9) 19.9 (9.3-21.5) 8.2) 16.2) 10.760 (<LOD-1.55 (2.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.25 (4.54 (7.12 (7.1 (19.71) < LOD < LOD 2.32-8.2-15.89 (3.8) 11.4) 7.9 (9.89) 5.S.74-19.00 (7.4) 7.54) 9.68) .45) 6.30-5.14 (2.4-15.03 (2.3-15.96-11.67 (7.93 (<LOD-2.16-14.5 (11.82-11.9) 16.1) 20.8) 16.50 (6.55) .950) .89 (2.93 (2.67 (1.37-5.96-10.99 (4.36 (2.33) 3.89-3.89-3.6) 95th 16.7) 9.16 (3.06) .7 (8.52-3.11-3.43 (2.3) 9.810 (<LOD-1.940) < LOD < LOD 1.87 (3.79-9.3-17.5) 13.4) 6.70-2.05-3.4) 7.92 (5.2) 19.6) 952 1187 945 997 1331 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * .63 (2.6) 14.5 (8.8) 14.95) 90th 8.2-30.6 (12.07) 2.71 (1.620 (<LOD-.4) 9.7 (10.27) 5.45) 3.00 (2.38 (.69-11.6 (13.1) 13.690 (.3) 12.4-16.88-7.82-8.2 (9.94 (5.48 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20-3.47-9.42-19.02-4.95 (2.09-11.63 (6.61 (2.6 (11.29 (2.6-19.00 (5.1) 10.3) 8.

50-2.87-3.27 (3.57 (1.990-1.260 (<LOD-.79) .36-4.670) .19-1.336-.580-.96-3.17-4.970) .450 (<LOD-.80) 2.78) 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 * .700) .201-.76-6.960) .15) 2.50 (1.750-1.46-3.94 (3.70-7.980) 1.57 (2.86 (1.600-.26 (2.30-1.18 (.70 (1.18 (1.74-5.73 (2.380) . see Data Analysis section) for Survey years 99-00.810) .61 (1.30 (.587) * * .60 (2.10) 1.750) 1.83 (2.45 (2.46) 1.08 (2.98-3.20-2.29-2.30 (.970) 1.14 (1.20-2.880 (.89) 1.457 (.740 (.549 (.20) 3.73 (1.50 (1.22-2.27 (2.30 (1.720-1.90-4.15) 2.590-.350-.690-1.98) .20) 1.64 (1.455 (.01) .50 (1.680-1.20 (2.790 (.720-1.910 (.60) 3.10-1.32-1.585) * * .49) .960) 1.210 (<LOD-.780 (.74) 3.80) 3.280-.95 (2.550 (.820 (.11-3.759) * .560-.710 (.31-3.21) 3.960 (. interval) Selected percentiles ( 95% confidence interval) Total * .22 (1.620-1.930) < LOD .467 (.730) .23-3.20 (1.25-1.540 (.930 (.34) 2.20 (1.50) 1.570 (.45-4.570-1.40 (1.830 (.94) .75-2.47 (1.960) .70-2.58 (1.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.657) * * .46 (2.453 (.600-1.90) 3.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.00) 1.20) 3.33-2.22-3.749 (.30) 4.90 (1.83) 2.00-2.690-.55 (3.79) .86) 3.80) 3.597) * .54) .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 * .400) .48 (2.75 (2.10-1.592) * . 124 Fourth National Report on Human Exposure to Environmental Chemicals . < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.10) 1.382-.16-3.425 (.20) 1.45 (1.49) 2.00 (1.740 (.94 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740-.840 (.80 (2.09 (.592) * 50th .710) .68-5.570) * .505 (. and 03-04 are 0.41 (2.16) 2.30) 4.54 (2.490 (<LOD-.390-.650-.880) < LOD .90) 2.30) 2.10) 1. 01-02.63 (1.69-4.70 (1.26) .97 (2.353-.850) < LOD .34) 2.91) 2.780 (.760 (.41-5.03) 1.80) 5.910-1.95-5.08 (2.00-4. respectively.449 (.46 (1.710 (.00) 2.38) 1.S.30-3.89-6.77 (1.78) .459 (.860) < LOD < LOD .910) 1.20-3.47) 2.350-.89) .80 (1.880) < LOD 75th .16) 1.510 (<LOD-.10) 3.240 (<LOD-.65 (2.77-2.29) 1.70 (1.88) 1.59-6.343 (.949) .01-3.22-3.04) .950) 90th 1.500 (<LOD-.550 (.380-.37-2.05-3.30-3.45 (1.510 (.35) 1.820 (.303-.160 (<LOD-.940) < LOD . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.09.720 (.73-5.59-2.398-. 0.30) 1.780) .90) 2.04) 1.83) 1.14-1.20-1.570 (<LOD-.83) .618) * .680-1.95) 2.17) 1.690) .960-1.76 (1.60-4.39) 2.930-1.42-2.20) 2.690 (.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 * .54-2. and 0.20) 2.32 (1.60) 2.05-2. population from the National Health and Nutrition Examination Survey.30 (.83 (2.13) .31) 2.700) .580-1.80) 3.440-.600 (<LOD-.11-3.31) 95th 2.592-.800 (.13) 2.388-.40 (1.50 (1.01-1.570 (<LOD-.380-.1.930) 1.32) 3.570 (.740-1.2.390-.48 (1.31-3.50-2.340-.96-5.20 (1.359-.22-8.80) 2.50 (1.17) 1.98 (2.460-.584) .

560 (.61 (3.740) .16-2.05) < LOD .05) 1.08-2.57-2.84-6.73 (2.07-3.136-.90) 2.700 (.22-3.72 (2.66) .67 (1.00-3.990-1.97 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 * .720 (.560-.550) .72-4.08-2.39 (1.470) .42-8.510-.790) .840) 1.60 (2.305 (.98) 1.38 (2.330 (<LOD-.310-.270-.700 (.08-2.20-7.82 (2.22-2.67 (1.08 (.22 (2.05 (1.70 (2.S.89-3.87 (2.640 (. population from the National Health and Nutrition Examination Survey.84 (2.60) 1.16) 1.403) .52 (1.870 (.23 (.840) 1.460 (.800) < LOD .640 (.850) 1.580) .380-1.49-4.320-.790 (.07) 5.97) 2.25-3.485) * * .447 (.348-.930-1.550-.590-1.520-.92 (1.444-.45 (2.300-.560-.680 (.58 (1.99) 1. Fourth National Report on Human Exposure to Environmental Chemicals 125 .280 (<LOD-.47 (1.42-6.310 (<LOD-.77-4.840) .500-.50 (1.30) 3.270-.53) .16-1.23) 2.760) .97 (1.490 (.47-4.07 (.38 (1.22-3.830 (.32) 1.17-2.97) 672 678 478 509 694 552 595 948 744 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.04) 95th 2.47 (1.61) 2.72 (1.88) .07) 1.22) 4.13 (1.06-2.55 (1.830) 90th 1.95) 1.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.33 (1.535 (.75 (2.49 (1.42) .77-3.910) < LOD .380-.29-4.509 (.07-2.04-5.22) .471-.515) * * .540-.440-1.23) 3.61-3.580 (.330-.368) * .04-1.32-1.580-.64 (2.28 (1.69 (1.32) 2.60) .78) 3.73-3.89 (1.739) * .590) * 50th .79) 1.11) 1.393 (.64 (2.730) .62 (2.08 (2.72) 1.08-3.800-1.950-2.470 (<LOD-.552 (.670 (.253-.900) 1.710 (.92) 3.880) 1.750 (.80) 2.31-1.310 (<LOD-.43) 2.645) .65) 2.43) 2.412-.250 (<LOD-.05-4.20-2.300 (<LOD-.23) 2.72) 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 * .71 (1.94) .58) 3.453 (.742) * * .43 (1.460) .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 * .318-.91 (1.820) .760) < LOD 75th .448 (.03-1.320-.660-.67-3.75-3.750 (.234 (.20) 1. interval) Selected percentiles ( 95% confidence interval) Total * .820) 1.710 (.66 (2.75) 6.30-2.250 (<LOD-.82) 2.81) 2.720-1.590 (.377-.32 (.57-4.24) 4.270 (<LOD-.460-1.710 (.870) .520 (.97) 1.52) 3.77 (3.71) 2.63 (1.17) 2.11-2.71) .75 (1.510 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.19 (1.08) 1.480) .23) 1.02-3.03-2.597) * .42 (.480-1.05-2.61-3.02-3.99) 2.67) .88 (1.740) < LOD 1.43) 1.00 (3.79 (1.640 (.22) 1.50) 1.370-.18-2.06) 4.390-1.390) .688) * .350) .57 (3.76) 1.44-2.08) 2.920) .180 (<LOD-.380) .57 (1.67) 1.69 (3.00-1.55-3.530 (.690) < LOD < LOD .550-1.58-6.510 (.08-3.07) 1.08-3.372 (.980-1.700 (.62 (1.45 (1.34 (1.14 (2.10) 2.39) 2.09) .33) .11 (.07) 1.17) 2.41 (.32) 5.335-.60 (1.550-.02-6.630) * .44) 2.230 (<LOD-.70 (3.38-3.591 (.92-8.08-3.285-.36) 3.400-1.940-1.400) .

1 (11.0) 8.610 (<LOD-1.5) 30.35-6.48-2.53) 1.83-2.25-3.0) 16. and 03-04 are 0.0-58.1-25.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.1-20.12) 1.2-26.7) 20.53) * 2.79 (1. see Data Analysis section) for Survey years 99-00.1-47.0) 17.79 (2.0) 28.0) 20.70-6.40) < LOD 2.30-14.50-7.70 (.44) 2.06 (1.0 (37.99 (2.77) 38.60) < LOD 1.9) 17.16) * 1.9 (10.31-6.0-53.33 (5.54 (1.3 (14.0-230) 35.18. < LOD means less than the limit of detection.50-17.0 (24.8) 39.91 (4.4.3 (24.0 (40.10-4.10) .1) 95th 48.83 (1.3) 28.0-43.13) 12.0) 33.5.4) 38.75-14.3) 38.8 (22. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-50.53) 40.0) 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 2.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0-69.0 (38.64-3.0 (38.88) 1.5-74.57-2.10-13.10) 39.4-76.1 (10.8) 62.52 (4.21 (3.3 (23.0 (32.0 (26.85) * 2.30) 4.0) 30.6-54.5-40.80-18.48-2.72 (1.0-110) 42.1) 38.40-4.41) 5.20-4.64-8. 0.93-3.6-27.4 (19.83 (3.70 (1.0) 42.0) 4.0) 45.1-19.92-5.0-52.0) 28.61 (1.98 (1.20) 1.41 (1.2 (12.7 (12.23-2.0 (38.9-51.46 (.60 (2.90 (1.9 (19. which may vary for some chemicals by year and by individual sample.2 (19.1) 140 (46.0) 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 2.66-5.21 (4.12 (3.0) 15.50-2.0 (33.0-62.6 (15.10 (1.80-2.48) 5.18) 14.92) * 2.1 (25.0-31.9 (27.30) 11.0) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6) 52.85 (1.53 (1.78 (1.0 (19.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0-260) 34.5-45.0 (8.4) 19.5 (24.0-53.44-7.0) 32.10 (1.8 (12.27-6.81-3.10 (1.9) 48.6 (26.67 (1.6 (9.80) 90th 38.5) 69.11 (4.50-5. and 0.23-2.78) 9.0) 16.9) 18.30 (.29-9.63-6.71 (4.20 (2.59 (1.95 (5.0 (38.3) 26.0) 4.0-62.9 (19.46-6.0) 6.0 (6.0-47.0) 3.18) 20.0 (20.8-24.26) 75th 11.9-21. interval) 1.10 (1.86 (1.0 (7.0) 19.13 (1.0 (38.1) 38.4 (10.S.2-47.0 (21.14) 5.13 (1.0 (11.0-39.3) 31.0) 31.71) 5.43-7.7-41.2-33.80) < LOD 1.2-62.71-2.04 (<LOD-2.6 (11.46-2.90) 11.0-41.44) 3.1) 18.82 (1.7 (28.3 (12.1-46.61-2.3 (12.2-39.05-3.8 (12.0-39.76 (2.02 (2.41) 1.600-2.21 (1.8-21.0 (38.70) 1.0-29.17-2.80) .4-22.00 (.77 (1.58) 16.1 (26.70-17.660-2.0) 17.81-2.470 (<LOD-1.41-4.7-22.19-2.87-7.05) * 2.9 (23.11) 2.70 (7.07-5.16) 2.26 (.97) 6.8) 41.04-8.0) 15.9) 38.0-92. 01-02.0) 3.42) 1.32 (2.5-27.1 (25.7 (12.94 (1.0) 3.79-2.58-2.49-2.65 (4.0 (8. respectively.6-22.45) 2.59 (1.5-20.54 (3.8) 32.2) 16.7) 47.05) 1.36-2.80) 1.830-4.41) 1.4 (15.74-2.0 (25.00 (.70 (1.19) 2.2-80.0) 3.10 (7.96) 5.45) 2.90 (1. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0-49.0-110) 34.2-27.44) Selected percentiles ( 95% confidence interval) Total * 2.0) 5.1-40.18) 6.29-4.2) 31.50 (2. population from the National Health and Nutrition Examination Survey.98) * 2.70) 1.90-8.04) 3.0 (17.83-2.0) 18.0 (8.50-20.09 (4.6-45.76 (2.0) 20.86-3.2-27.00-24.0) 13.69) 2.0 (20.830-3.0 (38.8 (26.70) 5.0 (13.0-41.1 (22.23) 9.57-2.29) 2.0-41.40) 50th 2.3 (10.88) 3.40-16.3) 33.530-4.690-3.40) < LOD 1.06) * 2.0-58.

75 (1.2-70.4 (9.83 (.899-2.18-1.9-37.1) 52.2 (8.7 (24.2-28.4) 12.7-47.5 (6.2) 33.6) 3.2) 13.1 (34. interval) 1.50-5.3-19.99-4.7 (10.0 (25.47 (3.9 (13.19-14.71) 8.7) 26.75-6.11-2.88 (1.7) 95th 51.5-190) 30.5 (13.12 (1.6-38.0) 48.17) 2.1) 27.06) 1.57) 4.33) < LOD 1.9) 24.7 (18.40 (5.4-21.9-36.72) 2.95 (2.2 (22.22-2.5) 70.8-26.00 (4.7-109) 22.9) 3.4 (11.27) 10.6-32.19 (1.19) 5.71 (1.30) 28.36-13.2 (16.6 (11.6 (7.66) 8.2) 13.57 (6.48) 1.8-43.3-27.14 (.8) 11.9) 24.71-2.95-16.7-38.58-2.00-16.4-34.16 (1.1 (25.0 (23.28) 1.1) 25.32 (3.35) 1.16-2.79 (2.70-4.36 (4.82) 1.2) 471 575 310 664 821 715 813 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.888-1.5 (34.2 (21.1) 36.0 (14. population from the National Health and Nutrition Examination Survey.69-5.38) 5.23) 37.94-20.54-2.8) 31.52 (1.03) 1.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.7 (18.5 (15.6) 23.4) 14.54-15.52-4.61 (1.46-6.0) 10.4 (25.890-4.68 (1.67 (1.9 (26.67-3.61-2.25-3.0-118) 29.6) 7.0 (39.24 (1.0) 30.63-5.62 (2.06) 75th 9.0 (17.9) 54.59-2.45-1.5-43.0 (19.80-8.84-13.31) 2.0) 3.0) 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 1.06-1.19) 5.08 (1.680-4.91 (6.7-19.6) 11.2) 36.1) 25.26-4.35 (2.66 (1.94) 1.8) 3.86) * 2.36) 10.96) 2.68) 47.5 (15.38-1.22-3.47-17.38-5.43) * 2. Fourth National Report on Human Exposure to Environmental Chemicals 127 .4-67.22 (.43-12.96-16.7) 23.2) 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.3-42.08) 1.1) 15.56) 1.59-2.4 (19.76-2.11) < LOD 1.9-95.3 (10.16 (1.0-71.7) 66.33) 2.0 (23.4 (12.88 (4.5 (41.8-45.79-17.1) 17.2-34.3 (20.930 (<LOD-1.9) 12.7-43.3) 13.44) 9.5-36.5 (17.27-3.0 (32.1-60.20-5.21 (4.1) 13.9-18.7) 30.00) 1.17-3.6-49.80 (1.9 (39.0-70.870-3.1 (50.82 (2.1 (12.2) 41.23) < LOD 2.9-41.7 (11.58-17.75 (1.61-22.91-2.0) 47.66 (1.8-37.69-18.46-22.37 (1.7-20.0) 25.07-2.750 (<LOD-1.06) 1.2 (15.4 (25.60 (.8) 23.6-51.18) 3.3) 28.14-8.33-5.97 (1.38 (3.95) 90th 32.95-16.3 (10.00) 6.90 (.60) 4.1) 27.64 (1.94) 19.1-63.35) .88 (1.4 (21.50 (2.4) 3.3-22.22 (2.1 (33.1) 13.12) 3.51) < LOD 1.51) .870-3.870-3.9 (19.18) * 2.93) 5.5) 27.29-5.860 (<LOD-1.0 (6.83) .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.27 (6.0) 13.02) 1.5 (8.6 (27.20) Selected percentiles ( 95% confidence interval) Total * 1.67-16.70 (1.03-2.0-40.56 (2.34) * 1.9 (7.6) 112 (40.23-1.86) * 3.33) 1.3 (9.26-2.40 (2.46) 1.39 (1.55 (2.5-97.88 (4.59-15.4-71.53) 1.9-52.47 (1.2 (9.4) 12.43-2.S.40-4.6 (24.8) 32.6) 19.16 (1.67 (1.45 (1.27) 50th 2.9) 3.19-6.28 (1.7) 61.4 (5.15 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.41 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.37-2.1 (39.8 (7.7) 15.6) 3.75) * 1.1-22.2-47.3 (8.07-2.670-1.7-37.8-34.62) 4.46-5.2-38.02) * 1.7) 34.4-39.2) 4.40-7.48 (4.07) 9.9 (10.09 (5.01 (.8) 15.32-3.02 (.

300-1.180) .110-.640) .300-.240 (<LOD-. < LOD means less than the limit of detection.620 (.10) .42) .05.20) .13) .150) .1.58) .12 (.160) .600 (.640) .171) * * .460-.090 (<LOD-.830) < LOD .410-.540 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10) .990 (.760) < LOD .770) < LOD 95th .130) .610 (.870) < LOD .210 (.700-1.099-.700-1.770 (. 0.860) .700-1.410-.470-1.470 (.860-1.370-.270 (.320 (.140-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .540) .650-1.630 (.380-.870 (.230) .120 (<LOD-.450 (. respectively.090 (<LOD-.540) .32) .700) 952 1187 946 997 1329 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .150 (<LOD-.840) .140) .190 (.370-.350) .560 (.350) < LOD < LOD < LOD < LOD .410-1.60) 1.820 (.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 * * * * * * .650-1.360-.10 (.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.990) .610-1.640 (.310 (.160) .130 (.S.720 (.140-.15) .390 (.900 (.100 (. and 03-04 are 0.190 (. and 0.820 (. 128 Fourth National Report on Human Exposure to Environmental Chemicals .940 (.390) < LOD < LOD .660 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .650 (.290) < LOD < LOD < LOD < LOD 90th .050-.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 * * * * * * * * * .510-1.310-.530-.162) * * * * * .440-1.640-1.140-.090 (<LOD-.730-.310) < LOD < LOD < LOD < LOD .650) .30) .630 (.990) .730) . which may vary for some chemicals by year and by individual sample.720-1.290) < LOD < LOD < LOD < LOD .160-.410) < LOD < LOD < LOD < LOD .700-1.130-.260 (.380-.084-. see Data Analysis section) for Survey years 99-00.430-.290 (<LOD-.830 (. 01-02.10) .090 (<LOD-.420-.200) < LOD < LOD .220 (.090 (<LOD-.30) .120-.080 (<LOD-.550) .680-1.1.870 (.460 (.430 (.830) .560 (.870 (.690-1.400-.680) .00) .850 (.780) < LOD 1.230-.740) < LOD .320-.130-.830 (.380-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) .310 (.450 (.850 (.130) .090 (<LOD-.117 (.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.680 (.490 (.130-.930 (.720) .610 (.840) .870 (.210 (.30) .170-.36) .570) .220 (<LOD-.42) . population from the National Health and Nutrition Examination Survey.080 (<LOD-.650) .310) < LOD < LOD < LOD < LOD .280) < LOD < LOD < LOD < LOD .450 (.360-.190 (.850) < LOD .610-.870 (.680-1.120-.330-.03) .

700-1.880-1.490-1.580 (.550 (.67) .86) .180-.880 (.66) 1.730) .150-.110) .410-.58) 1.990) .090 (<LOD-.116 (.540) . population from the National Health and Nutrition Examination Survey.080) .230-.370 (<LOD-.190 (.580) < LOD .060-.03 (.300-.360) < LOD < LOD < LOD < LOD .100 (<LOD-.200 (.460 (.03 (.730) .670 (.300-.360-.710-1.860 (.43) .730 (.870) .070 (<LOD-.580-1.650) < LOD .510-.960) .070 (<LOD-.600) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .850 (.140) .380-.60) .62) 1.940) .970) .01 (.090 (.540 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.78) .190-.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 * * * * * * * * * .410-.660-1.700 (.260-.740 (.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.02) .720 (.140-.190 (.110) .600-1.500) .170 (.750) < LOD 95th .740) < LOD 1.500 (<LOD-.03 (.S.540 (.86) .380-1.780) < LOD 1.380 (.450 (.260) .450) .330-.29 (.360 (.270) < LOD < LOD < LOD < LOD .250-.080 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .470 (<LOD-.440 (.400) .390-.12) < LOD .570-1.500-1.330-.330 (.780 (.170 (.760) .890 (.410) < LOD < LOD .19 (.730) .161) * * .110) .120) .220 (.220) < LOD < LOD < LOD < LOD .650-1.860-2.400 (<LOD-.640-1.380-.140-.24 (.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 .084-.410) .560 (.800-1.580) .670 (.860 (.340-.330 (.700 (.140-.320 (<LOD-.700) .360-.200 (.290) < LOD < LOD < LOD < LOD 90th .940) .410 (.09) .310) < LOD < LOD < LOD < LOD .111) * * * * * .410 (.670-1.20) 1.070 (<LOD-.24) .390-.990) .280) < LOD < LOD < LOD < LOD .14) 1.520-.570-.02-1.140-.610-1.720 (.170) < LOD < LOD .550 (.300 (.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.110) .080 (<LOD-.120) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .110-.38) 1.570 (.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 * * * * * * .440-1.100-.03) .580 (.057-.270 (.330-.140-.210 (.070 (<LOD-.230) < LOD < LOD < LOD < LOD .810 (.050 (<LOD-.380-.240-.36 (1.00) < LOD .230 (<LOD-.

70-30.65) 1.0 (16.0-38.0 (17.830 (.260-.10 (3.770 (<LOD-1.00-17.30 (2.0) 5.840 (.76 (1.07) 1.30-6.10 (. and 03-04 are 0.70-50.49 (1.0 (5.20 (1.70-7.07 (3.640 (.6) 5.47 (3.90-28.720) 2.00) .14) .30 (.67 (2.0) 4.70-17.55-4.46 (1.60) .21-3.29-10.42) .85-3.12-1.360-1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.36-3.63 (3.11) 13.49 (1.0-40.40) 2.0) 4.14-5.10-3.48) 13.20) < LOD < LOD < LOD < LOD < LOD 1.11) .28) 1.0-39.425-1.31-10.51 (2.40-4.53 (2.42) 2.0 (17.83-3. 130 Fourth National Report on Human Exposure to Environmental Chemicals .330 (<LOD-1.67 (1.480-.01) 5.39) .88-3.510-.83) 2.13 (3.00 (.83-3.080-1.0 (17.960 (.35) 11.0-38.S.18) 1.110 (<LOD-.97) 20.730 (.90 (2.52 (1.0) 2.3) 952 1187 935 997 1331 995 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .0 (5.32 (1.00-17.24-7.08.1.66) 4.99) 19.55-8.1.80 (4.51-8.40-7.600 (.0 (5.52 (1.63) 32.30 (1.68) 2.39 (2.32-9.0 (7.691 (.45 (2.750-1.370-. population from the National Health and Nutrition Examination Survey.86) 4. 01-02.99) 11.11 (1. which may vary for some chemicals by year and by individual sample.800-4.0) 2.20 (1.170-1.90) .0) 7.0 (17. respectively.50) 2.210-1.07-3.26 (2.0-44.05 (3.07-3.74 (3.70) 2.30-7.40) 1.21) 3.580 (.30 (1.350-.30-3.0) 5.800) 90th 13.53) 20.87) 5.15) 14.40 (1.0) 4.0 (5.20-17.50) .20-4.00) 1.10-9.90 (1.890 (.190-1.620-1.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4. < LOD means less than the limit of detection.0) 2.90) .99 (1.0) 2.250 (<LOD-.590 (.840-3.880) 5.12) * * * * * * * * .0 (6.70-3.43-4. see Data Analysis section) for Survey years 99-00.14) 2.770) 2.53-7.20-4.07 (3.30 (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.23-6.07 (1.74) 5.0 (4.610 (.62-8.0) 2.0 (4.0) 2.60) 1.850) 16.90-37. and 0.49) 17.94-3.31) .0-40. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.750-2.35-10.800) 17.90-20.28-9.87) 12.0 (5.0) 4.90-9.35) 5.640 (.30) .96 (1.0) 5.36-3.94 (1.00 (1.59-5.90) .37) .94-8.15) 19.05-3.0 (13.40-20.62) 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 * * * * * * .350-.400-1.52) 5.740 (.00) .840 (<LOD-1.40-8. 0.16) 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 .900 (.82-4.0) 5.05 (2.0 (17.0-38.690 (.67) .40 (1.38-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.960 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.0) 3.380-.10 (3.28) .33 (4.0) 2.0 (3.03 (.97) 20.48 (2.610) < LOD < LOD < LOD < LOD < LOD 2.10-3.30) 95th 19.61 (1.910) 2.870) < LOD < LOD .

670 (.2 (8.38 (2.61) Sample size 1949 2517 1927 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .1 (7. population from the National Health and Nutrition Examination Survey.53) 27.88 (2.86) .75) 5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.84) 9.90-6.3) 2.69-7.0) 4.650) 90th 10.40) 1.37) 4.4 (4.7 (12.580-1.83-11.04 (1.12-4.500 (.02 (.96-25.830 (.370-1.48-42.09-3.62-17.51-44.60 (1.35 (.340 (.69) 2.11) .51-4.590) 2.1) 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 * * * * * * .150 (<LOD-.25-9.32-6.340-.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 * * * * * * * * * .600 (<LOD-1.53) .04-16.80 (.40 (.8) 2.700) < LOD < LOD < LOD < LOD < LOD 1.470 (.970-3.22) 2.8-33.47) .14-6.430 (<LOD-.18) * * * * * * * * .790) 11.840-3.12 (4.940-4.660) < LOD < LOD .05) .56 (1.47) 5.930) .13 (2.02 (1.370 (.57) 8.7) 5.30 (4.33-3.55) 21.25 (1.250 (<LOD-.700) 6.50 (2.79 (.7) 3.10-3.03) 2.830-3.88-3.748 (.3) 3.8) 4.67 (2.77 (.860-2.8 (20.06 (.73 (4.5-40.260-.31-7.17 (1.370) < LOD < LOD < LOD < LOD < LOD 1.4-34.40-2.91) 2.88) 17.67) 2.21-3.65 (2.47-10.0 (4.44) .11-5.340-.540-1.23-7.71 (2.710 (<LOD-1.5 (11.07 (2.540 (.00-19.790 (.64-4.49-2.07-21.800-2.580) 16.2-38.1) 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.9) 5.56) .18) 95th 21. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.02) .5 (9.8) 2.730-3.27 (2.33 (1.50) 11.270 (<LOD-.560 (.33-4.8) 1.48 (4.85-3.67) 1.97) .71 (.580 (.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.890 (.29 (4.96-8.08) . Fourth National Report on Human Exposure to Environmental Chemicals 131 .66-47.31) .82-11.10) 2.8) 7.96) 2.474-1.820) .28-6.39) 20.5) 2.31) .240-.57-40.36 (.33 (3.850-3.25-38.330-1.48-7.620-3.45 (1.8) 7.14 (1.0 (9.56) 2.430) 1.02-4.360 (.52 (.89 (2.57 (.7) 6.650 (.270-.00) .260-.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.1) 2.91-4.22-27.57) 1.29-4.55 (3.770) .450 (.03) 16.41 (4.960 (.33-5.7 (6.43) .10 (2.190-1.50 (4.18) 1.74 (2.310-.340-.390-.580) 1.44-11.630-1.92 (2.740-1.32) 9.41) 18.4) 2.5 (8.80) 3.31-18.1 (5.S.62 (1.59 (1.67-6.01 (1.5) 7.9) 6.780-4.5) 2.88 (.64) 30.86 (3.820 (.50) .47-10.81-17.55) 21.83 (4.40-12.24) 3.98 (4.85 (1.17) 5.9 (11.15) 9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.690-5.7) 4.320-1.

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Caltabiano LM. Rothlein J. Myers JE. Muniz J. Steenland K. Vitayavirasak B.epa. Weerasekera G.S. Heaton RK. Neurotoxicity among pesticide applicators exposed to organophosphates. Environmental Protection Agency (U. metabolite clearance. Buccafusco JJ. Wickremasinghe AR. Irish RM. Russo J. Levy LS. Chronic neurological sequelae to organophosphate pesticide poisoning.84(5):731-736. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Arch Environ Health 1988. Ruberu DK. Hore P. discrimination.2000 and 2001 market estimates. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Weisskopf C. EPA). Daniell WE. Aprea C. Calvert IA. Smit LA. The Pesticide Health Effects Study Group.20(2):115-22.338(8761):223-227. Lambert WE. National Research Council (NRC).44(4):352-357. Scherer J. Gladstone EA. Am J Ind Med 1987. et al. Lancet.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates.edu/ openbook.12(2):153-172. Eskenazi B. Beach J. Stark A. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Thompson ML. and spatial learning in monkeys and rats. et al. McCauley L. et al. Berry H.php?record_id=2126&page=1. Rodnitzky RL. Available at URL: http://www. Hansen S. Bradman A. Nell V. Savage EP. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Environ Health Perspect 2005. low-level organophosphate exposure on delayed recall. Tumino R. Pesticide industry sales and usage . J Occup Environ Med 2002. Seiber J. and cholinesterase status of date dusters and harvesters in California. Santana J. Masala G. Frasca G. Effects of long-term organophosphate exposures on neurological symptoms. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Keefe TJ.26(2):199-209. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments.114(5):691-696.pdf. Jenkins B. Washington (DC). A behavioral evaluation of pest control workers with short-term.52(10):648-653. Pedersen L. Buchanan D. 4/7/09 Young JG. Bravo R. Burcar PJ. Pilkington A. 1991. Dinoff TM.nap. Schenker M.113(4):504-508. Washington (DC): U.345(8958):11351139. Petchuay C.38(4):546-563. Phillips J. Stokes L. Sci Total Environ 2004. Salvini S. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Lu C. Office of Prevention Pesticides and Toxic Substances.68(3):209-227 Maizlish N. Mounce LM.24(1):18-29. Samuels S.43(1):38-45. Ames RG. Effects of chronic. Environ Health Perspect 2006. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Prendergast MA. Jamal GA. Terry AV Jr. Narang A. Rosenstock L. Visuthismajarn P. McConnell R. vibration sense and tremor among South African farm workers. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Saieva C. Occup Environ Med 2001. et al. Johnson C. Available at URL: http://books. Lewis JA. van der Hoek W. J Toxicol Environ Health A 2005. 2004. et al. Bull Environ Contam Toxicol 1994. 1993 [online]. Barr DB. May. Chrislip D. Kidd M.S. Scand J Work Environ Health 1998.52(2):190-195. Pesticides in the Diets of Infants and Children. Robson MG. Int J Occup Environ Health 2006.30(2):98-103. Neurotoxicol Teratol 1998. National Academy of Sciences. Neurotoxicology 2005. Arch Environ Health 1975. U. low-level exposure to the organophosphate diazinon. Claypoole K. Marshall E.12(2):134-141. Lasarev M. Rothlein J. Stephens R. Lancet 1995. Gillham R. Arch Environ Contam Toxicol 2000. Malathion deposition. Rohlman D. O’Malley M. Keifer M. 1/12/09 Peiris-John RJ. Fourth National Report on Human Exposure to Environmental Chemicals 133 . EPA. Am J Public Health 1994. London L. Takamiya K. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides.58(11):702710.332(1-3):71-80. Chronic central nervous system effects of acute organophosphate pesticide intoxication. An epidemiological study of the relations between exposure to organophosphate pesticides and indices of chronic peripheral neuropathy and neuropsychological abnormalities in sheep farmers and dippers. Lasarev M. Spurgeon A. Muniz J. Occup Environ Med 1995. S.

In addition to reflecting exposure to the parent insecticide. malathion is metabolized to malathion dicarboxylic acid.5. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report.6-Trichloro-2-pyridinol (6515-38-4) 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol 2-Isopropyl-4-methyl-6-hydroxypyrimidine (2814-20-2) Malathion dicarboxylic acid (1190-28-9) para-Nitrophenol (100-02-7) 2-(Diethylamino)-6-methylpyrimidin-4-ol/one 134 Fourth National Report on Human Exposure to Environmental Chemicals .Organophosphorus Insecticides: Specific Metabolites Organophosphorus Insecticides: Specific Metabolites General Information The specific metabolites of the organophosphorus insecticides discussed in this section are those that are often measured in biomonitoring studies.” Organophosphorus insecticide (CAS number) Chlorpyrifos (2921-88-2) Chlorpyrifos-methyl (5598-13-0) Coumaphos (56-72-4) Diazinon (333-41-5) Malathion (121-75-5) Ethyl parathion (56-38-2) Methyl parathion (298-00-0) Pirimiphos-methyl (29232-93-7) Primary urinary metabolite (CAS number) 3. For general information about the organophosphorus class of insecticides. For example. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides. parathion and methyl parathion are metabolized to para-nitrophenol. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. the level may reflect exposure to the environmental degradation products of these pesticides.

and sprayed to kill mosquitoes.4.52-2.19-3.74-9.04-10.50 (2.63 (8. 2002).6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40) 2.32) 2.40 (6.90 (1.59-2.97-7. 2005).26) 7. chlorpyrifos was no longer registered for indoor residential uses in the United States.55-5.01) 1.24-1.20 (2.09 (2.5.0) 12.90-4.30) 4.80) 12.50-8.51) 1.30-11.70-17.7) 9.76 (1.80 (7.64) 3.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.EPA.3 (10. applied to structures to kill termites.95) 7.70-16.17 (1.39-2.80 (1.20) 2.50-5.8) 10.0) 18.94 (4.4 (8.0) 12.30) 5.39) 4.00-8.32-1.95 (4.0) 7. Chlorpyrifos is degraded in agricultural soils with a half-life of several months. and inhalation routes.0) 12.0) 8. It also has been applied directly on animals to kill mites.46-2. Chlorpyrifos is Urinary 3.63 (2.3 (8. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.77-15.0 (7.90 (1.90) 3. and on plants for days to several weeks.50 (1.7) 13.50-4.15 (1.10) 2.0 (13.38 (3.80-10.9) 697 660 521 701 602 947 Limit of detection (LOD.and post-construction structural applications for termite control were to be phased out by 2005 (U. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.9 (7.50 (2.70-5.62-2.3 (11.5) 7. and is infrequently detected in ground water (IPCS. 1999.5 (8.80) 4.0) 10.20-4.28) 2.60) 5. Estimated intakes from diet and water have not exceeded recommended intake limits.02 (7.5-24. 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.30 (2.30-5.10) 6.35) 2.50 (2.50-2.00) 3.20) 10.21) 3.77 (1.37 (4.9-18.28-3. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.44-2.1-16.40-13.05-5.0 (7.97) 4. Survey Geometric mean (95% conf.66-4.60-3.10 (5.91 (1.97) 2.90-8. USGS.45 (1.88 (1.66-15. in 142 urban homes and preschools in North Carolina.78 (7.10 (1.59) 2.20-16.81-2.51 (1.0) 11.74 (1. 2007).90-2.0 (9.90) 7.00-24.60-4. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.70-11.40-26.80) 1.02 (1.70) 1.71 (6. The general population may be exposed to chlorpyrifos via oral.67 (2.4 (9.57 (2.43-2.4 (10.63 (1.9 (9.51-2.00) 1.30 (2.79-2.77-6.30 (4.20) 2.0) 8.40-10.2 (10. and dust.72) 2.90 (2.37) 5.60 (4.71 (1.7-23.0-28.20-14. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.8-15.60 (5.77) 1.35) 1.0) 6.24-3.30-12.20) 4.89 (2.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.47) 1.47-9.87-6.20 (4.44 (3.0 (10.92 (1.0 (7. Fourth National Report on Human Exposure to Environmental Chemicals 135 . Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.43-2.00) 2.60 (2.37 (1.29) 90th 7.72-4.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1. interval) 1.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.5.0) 12.53 (1.47-11.4-15.0) 12.40 (5.86) 4. 2921-88-2 Chlorpyrifos-methyl CAS No.03) 99-00 01-02 99-00 01-02 99-00 01-02 2. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.30-9.40) 9.25) 1.22) 2.7) 8.13-3.10 (3.83) 1. pre.20-2.S.05) 1.61-7.96) 3. air.91) 16.27 (7.44-5.97) 2.22 (1.70 (1.16) 2.61) 75th 3.09 (3.67 (1.50-14.04-10.10 (4.0) 9.10-17.50-4. 2002).80-8. 5598-13-0 General Information The chemical 3.13 (1. For instance.47-13. After 2001.02) 1.03) 1. dermal.40 (5.68 (7.30) 4.20-11.52-12.71 (2.90 (6.4 and 0.36 (4.S. Exposure can also result from contact with contaminated surfaces.0) 10. staying bound to soil particles.90 (3.0) 15.97) 7.6) 7.84) 1. It has low leachability.19 (1.31-2.0) 10.9 (10.90-7.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.89-2.8) 9. Approximately 80.0 (7.50-2.EPA.9) 11.3) 8.70 (1.000 pounds are used per year.30-1.30-2.0) 14.67 (2.61 (1.20-3..47 (4.70-15. Approximately 21-24 million pounds per year were used domestically from 1987-1998.60-3.S.40-2.60-2. population from the National Health and Nutrition Examination Survey.29-1.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No. but can be detected in streams receiving runoff from application sites.50 (1.98-15.31-2.80) 2.99-4.25) 3.68-2.1) 5.76 (1.0 (7.34) 1.

05-3.82) 8. 2005. Howard et al.58 (4.24) 5.2) 6. 2006.64-2.02) 7. Urinary 3.49-2.75) 6.74) 1.91-4.46 (2.44 (1.42-2.68) 6. 2005. and other metabolites.83) 1.1 (10.53 (2.S.5 (6.63 (5. Thus.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.22) 1.5) 5.83-2.02 (5.55 (1.2 (7.6-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.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 1.28) 2. Once absorbed.99) 1.01) 3.49 (1.33 (1.1 (7.97) 3.30-4. Slotkin et al.93 (4.85 (2.56) 5.98 (6.19-2.30-1.01) 1.19-1.86 (3.50 (4.87-3.85 (3.91) 1.3) 8.48 (1.56 (4.94-14.00 (7. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.93) 2.64 (1.45 (1.54) 5.80-6.43 (4.07) 5.S.05-1.44 (5.93) 5.84-6.17-4.01) 3. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.11) 7.33) 2.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.39 (4.24-5.69 (1. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.93 (1..92) 3.64-7.39 (2.57-2. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.81) 2. population from the National Health and Nutrition Examination Survey.00-8.99-8.33-7.11 (2. 2006a. Based on animal data and human cholinesterase monitoring during occupational exposure.54 (2.82 (2.58) 1.22-6. Survey Geometric mean (95% conf.3) 8.24) 75th 2.57) 2.70-4.71) 3.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.4) 4.47 (5.42 (6.88-8.12) 1.43-10.56 (1.44 (1. cholinergic effects.62) 90th 5.1-38.88) 6.35) 2.33 (.38) 3.71 (1.96) 3.58 (1.31) 1.09-1. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.66 (1.39-1. weakness.05-4.0) 6. Ricceri et al. TCPy is more persistent in the environment than chlorpyrifos itself (U.06 (5.09 (1.08) 6.45-1.06-4.94-12.12-3. Metabolic hydrolysis leads to the formation of TCPy.47 (1. 1984).95 (1.24 (1.73 (1.77) 1.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.11 (2.76 (2.35) 1.34-1.. resulting in excess acetylcholine at nerve terminals.20 (2.24-24. interval) 1.20-1.29 (3.57-2.47 (1.0) 10.25-12.86 (1.06 (1.92-2.07) 1.32) 1.88 (1.80-4. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.82-4.6) 9. Betancourt et al.95 (3.24-1.58 (1. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.00-13.63-2.58-5..6) 10..65-15. TCPy can also occur in the environment from the breakdown of the parent compounds.25-11.57) 9.79-13.7) 7.23-1.23) 14. paralysis.91-13.1-21.85) 4.9 (12. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.09-2. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.55 (4.49-2. and producing acute symptoms such as nausea.46 (1.58) 5.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .19) 6.09-3.49-2.68) 1. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.14-8. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al..97 (3.91 (4.8) 9.36) 1.88-9. 2005.62-7.72) 1.0) 16.98 (7.75 (1.15 (4.26-14.11-9.97 (2. 2006. 2000).86 (1.92 (1..89) 4. 2006b).5.66) 1.56) 2.16 (4.42 (5.59-2.35-1.39) 6.51 (1.81 (3.19) 3.22 (4.31-1.91) 2.88-8.72-2.90-9.88 (1.72) 2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).91) 10.21-1. 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.85-4.28) 2.17-4. In pesticide applicators.21-6.12-1.48 (2.940-1.88-10.40) 1.05) 3..83-11.37 (1.EPA. vomiting.59) 3.62) 1.05-8.16) 6.97) 3.80-11..25-1.93 (2.22 (6.03) 1.44 (6.41 (1.78 (1. 2002).97-3.44-6.85) 1.31-4.63 (4. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.44 (5.91 (3.65-11.27-7.91) 1. Roy et al.27-1.66-11..60 (1.76 (3.24-4. and seizures.3 (7.53-5.0) 12.14) 1.56-2.82 (3.3) 9.55) 1.47-2.00) 1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.52 (5. neurotransmission.60-3.33 (5.80) 3.

the weighted population mean of TCPy measurements was approximately three times higher (Adgate. Koch et al. Burns CJ. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. In Iowa farm families using several different pesticides. 2005).. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. 2002).. Additional information about external exposure (i.. 2005). Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP.EPA..S. urinary TCPy levels in children were reported not to have increased (Hore et al. U. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. 2005. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos.S. 2000). Lotti A. Aprea C. Levels of TCPy in the U.. Betta A. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. but levels were roughly four to six times higher than the geometric means in the U. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. 1992. MacIntosh et al.. 2005.63(3):218220.Reference values of urinary 3. Eberly LE. Barisano A.S. et al. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Barr DB. representative subsample of NHANES 19992000 (CDC. Environ Health Perspect 2001. population (CDC. but not chlorpyrifos. CDC. EPA at: http://www. Carr RL. the geometric mean urinary TCPy levels were similar in parents and children. 2005). 2005). Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. In Minnesota and South Carolina farmers who used chlorpyrifos. References Adgate JL. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. In a probability-based sample of 102 Minnesota children aged 3-13 years.atsdr.gov/pesticides/. Toxicol Sci 2006. Haidar S.cdc. 1999). Seidler FJ. Curwin et al.. Whyatt et al. 2004). Garabrant D.5. 2003. Following crack-and-crevice application of chlorpyrifos in their homes. Perera et al. Burgess SC. Of 482 pregnant women living in an agricultural community. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. Albers JW.html and from U. Betancourt AM.92(2):500-506. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy.gov/toxpro2. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. 2005).Organophosphorus Insecticides: Specific Metabolites 2004.. 2007). 2001). Magnaghi S. Fourth National Report on Human Exposure to Environmental Chemicals 137 . Environ Health Perspect 2005.. 2005.. Freeman NC.epa.. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al.109(6):583-590. Giordani B. Clayton CA. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect..S. Aldridge JE. et al. Lioy PJ. Occup Environ Med 2006. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC.e. 2004). Slotkin TA. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. 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. Biomonitoring Information Urinary TCPy levels reflect recent exposure. 2006). 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. environmental levels) and health effects is available from ATSDR at: http://www. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. Chlorpyrifos exposure and biological monitoring among manufacturing workers. 2005).82(2):305-312. Berent S. Catenacci G. Meyer A..113(8):1027-1031.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study)... et al. J AOAC Int 1999. 2001) and Italy (Aprea et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S..

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Available at URL: http://www. Third National Report on Human Exposure to Environmental Chemicals. Levin ED. Chlorpyrifos. Hardt J. Mandel JS. Seidler FJ. et al. International Programme on Chemical Safety-INCHEM (IPCS). Environ Health Perspect 2005. 2005.5. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals .6-trichloro-2-pyridinol.204(2-3):175-180. Roy TS. Shealy DB. Eskenazi B.73:8-15.niehs. Jewell NP. Environmental Health Criteria 198.108(4):293-300. Chlorpyrifos: pharmacokinetics in human volunteers. gov/ntpweb/index. Needham LL. Environ Health Perspect 2006a. Head SL. J Expo Anal Environ Epidemiol 2005. Barr DB. Irish R. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Chrislip DW. Exposures of preschool children to chlorpyrifos and its degradation product 3. J Expo Anal Environ Epidemiol 2005. Yang D. Environ Health Perspect 2006. Bennett DH. Seidler FJ. MacIntosh DL.71:99108. Ryde IT. Environmental Protection Agency (U. Neurologic function among termiticide applicators exposed to chlorpyrifos. Herrick RF. Freeman N. et al. Weltzien E. Kromhout H.10(4):327-340. Ann Occup Hyg 2007. Robson M. et al.93(1):105-113. Biomonitoring for farm families in the farm family exposure study. Sharma V. Chuang JC.S.

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

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

population from the National Health and Nutrition Examination Survey.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.380 (<LOD-. 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 . Survey Geometric mean (95% conf.S. Fourth National Report on Human Exposure to Environmental Chemicals 141 . which may vary for some chemicals by year and by individual sample.27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2.560) < LOD 659 700 920 < 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. Survey Geometric mean (95% conf.270) < LOD 659 701 920 Limit of detection (LOD.200 (<LOD-.210) < LOD < LOD 567 815 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1312 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 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. 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 .670 (<LOD-1.

S. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Third National Report on Human Exposure to Environmental Chemicals. Olsson AO. EPA). September 2000.epa. Sadowski MA. Reprod Toxicol 1998. Atlanta (GA).12(6):619-645. Freshwater KJ. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. Available at URL: http://www. Nguyen JV. Centers for Disease Control and Prevention (CDC).gov/oppsrrd1/ REDs/0018tred. Eigenberg DA.S. Anal Bioanal Chem 2003.pdf. Barr DB. 2005.376(6):808-815. U. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. EPA 738-R-00-010. Environmental Protection Agency (U.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals .

Before these restrictions.S. 2007).05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). see Data Analysis section) for Survey years 99-00 and 01-02 are 7. diazinon cannot be sold for residential use.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. seed and foliar applications are planned to be phased out (U. Once absorbed. USGS. Diazinon is not well-absorbed through the skin.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No.49 (<LOD-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks.EPA. diazinon was widely used in residential and garden application.7. in the past.S. but is rapidly absorbed orally (IPCS. It is also used for cattle ear tag applications to control flies and ticks and. vegetable. 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. population from the National Health and Nutrition Examination Survey.S. which may vary for some chemicals by year and by individual sample.EPA. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. an organophosphorus insecticide that is used to control insects on nuts. Most granular formulations. < LOD means less than the limit of detection. 2004). 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. diazinon produced wild bird kills before use restrictions were in place. 2004). since 2004. 1998). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1842 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. and forage crops. but these uses have been phased out. It is toxic to birds. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. fruits. Prior to 2000. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 143 . Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. 1998. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. Inhalational and dermal routes of exposure can be significant for pesticide applicators. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. aerial.2 and 0. and other metabolites. Estimated intakes from diet and water do not exceed recommended intake limits (U. and particularly when it was ingested in granular form. in some pest strips.45 (<LOD-3.

subsamples of NHANES 1999-2000 and 20012002. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate.EPA considers diazinon unlikely to be carcinogenic in humans. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants. Diazinon is not considered to be a mutagen. weakness.49 μg/L.. In animals. resulting in excess acetylcholine at nerve terminals. Thus. 2000.html and from U. and producing acute symptoms such as nausea. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1.45 and 1. diazinon does not accumulate in tissues (IPCS.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. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. Additional information about external exposure (i.S. respectively.cdc. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection.S. in the 2001-2002 subsample (CDC. 144 Fourth National Report on Human Exposure to Environmental Chemicals .e..atsdr.72 (<LOD-4. paralysis. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. Diazinon has moderate acute toxicity in animal studies. 1998). 1986.epa. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. cholinergic effects. population from the National Health and Nutrition Examination Survey.S. respectively (Baker et al. In the U. In addition to being a human metabolite of diazinon. Olsson et al. Survey Geometric mean (95% conf. EPA at: http://www. and seizures. or reproductive toxicant (IPCS. The U. Seifert and Pewnim..76 (<LOD-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. 1986 Rajendra et al..gov/pesticides/. and indoor applications have been documented.48) < LOD < LOD 644 678 484 699 554 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. environmental levels) and health effects is available from ATSDR at: http://www.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al.. 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.S. 2003). At high doses. 2002).. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1842 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 1998). animal carcinogen. 1992). teratogen. In two nonrandom samples of United States adults and children.gov/toxpro2. Intoxications in humans from intentional overdose. agricultural. vomiting.

et al. Dumas P. Baker SE. Sadowski MA. revised February 15.44(11):2243-2250. Banister EW. Geological Survey (USGS).S. Bouchard M.gov/circ/2005/1291/. Swan et al.114(2):260-263. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. 1/14/09 U. Carrier G. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. EPA 738-R-04-006. Driskell WJ. Toxicol Lett 2002. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Oloffs PC. Toepel K.37(4):501-507.htm. Barr DB.inchem. EPA).111(12):1478-1484. Bravo R. J Expo Anal Environ Epidemiol 2000. 2006). Atlanta (GA). Olsson AO. Liu F. 2006). Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Brunet RC. Biomonitoring studies of 2-isopropyl-4-methyl-6-hydroxypyrimidine provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of diazinon than are found in the general population.S. Interim reregistration eligibility decision (IRED. International Programme on Chemical Safety-INCHEM (IPCS). Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Barr DB. Environmental Protection Agency (U. Environ Health Perspect 2003.376(6):808-815.org/documents/ehc/ehc/ehc198.S. Pesticides in the Nation’s Streams and Ground Water. 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. Garfitt SJ. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Drug Chem Toxicol 1986. Rajendra W. Available at URL: http://www. Irish R. Available at URL: http://pubs. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Semen quality in relation to biomarkers of pesticide exposure. Centers for Disease Control and Prevention (CDC). Study for Future Families Research Group. Pewnim T.134(1-3):105-113. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. U. Nguyen JV. May 2004. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Effect of sublethal levels of diazinon: histopathology of liver. Environmental Health Criteria 198.pdf.50(5):505-515. Barr DB.9(2):117-131. 4/7/09 Lu C. Third National Report on Human Exposure to Environmental Chemicals.usgs. References Anthony J. Drobnis EZ. Available at URL: http://www. Kruse RL.10(6 Pt 2):789-798. In a small number of men visiting fertility clinics in Missouri and Minnesota. 2007 [online]. Anal Bioanal Chem 2003.gov/ oppsrrd1/REDs/diazinon_ired. Biochem Pharmacol 1992.. Seifert J. Swan SH. Bull Environ Contam Toxicol 1986. Diazinon. 1992-2001. Cocker J. Beeson MD. Oloffs PC.epa. Needham LL. Redmon JB. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Environ Health Perspect 2006. In 23 children. Noisel N. Diazinon. The Quality of Our Nation’s Waters. Banister E. March 2006. Jones K. Ann Occup Hyg 2006. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses.Organophosphorus Insecticides: Specific Metabolites 2005). Fenske RA.. Barr DB. Mason HJ. In 54 Canadian greenhouse workers. 1998. 2005.

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

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

6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals .S. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.usgs. Environ Health Perspect 2004. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Curl CL. A longitudinal investigation of selected pesticide metabolites in urine. Centers for Disease Control and Prevention (CDC). Petitti D. International Programme on Chemical Safety-INCHEM (IPCS). Kedan G. Barr DB.15(2):164-171. Ryan PB. Flessel P. Freeman NC. 6/1/09 U.gov/circ/2005/1291/. Environ Mol Mutagen 1993. Rappaport E. et al. Genetic toxicity of malathion: a review. Needham LL. Harris JA. et al. Malathion (addendum). Arch Environ Contam Toxicol 2000. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Bradman A.132(4):794-795.gov/oppsrrd1/REDs/ malathion_red. 1992-2001. Irish R. Toxicol Sci 2003 May. July 2006. Reregistration eligibility decision (RED) Malathion. Mutat Res 1999. Bravo R. Hammerstrom KA. Prasad SB. Mutat Res 2002. MacIntosh DL. Jewell NP.109(6):583-590. Lu C.22(1):7-17. Environmental Protection Agency (U. Brunet RC. htm. and cholinesterase status of date dusters and harvesters in California.445(2):275-283. Giri S. Lioy PJ.56(10):2393-2399. Carrier G. J Expo Anal Environ Epidemiol 1999. Albertini RJ. Eskenazi B.inchem. Jaloszynski P. O’Neill JP. Hertz-Picciotto I. Sharma GD. Clayton CA. Cancer Res 1996. Pesticides in the Nation’s Streams and Ground Water. Lu C. Harley K. Dumoulin MJ. revised February 15. Neutra R. 2007 [online]. Fenske RA.S. Eberly LE. Samuel O. Hooper K. Thomas D.77:1009-1010. Szyfter K. Nicklas JA. Blasiak J.74(2):following table of contents. Atlanta (GA). U. et al. Barr DB. Barr DB.epa. EPA 738-R06-030. Am J Epidemiol 1990. Goldhaber M. metabolite clearance.38(4):546-553. Available at URL: http://pubs. Toepel K.514(1-2):223231. Krieger RI.Organophosphorus Insecticides: Specific Metabolites References Adgate JL.114(2):260-263. Bouchard M. Environ Health Perspect 2001. Dinoff TM. Erratum in: Toxicol Sci 2003 Aug. EPA). Griffith W. Malathion deposition. Trzeciak A. J Expo Anal Environ Epidemiol 2005.org/documents/jmpr/jmpmono/v2003pr06. Grether JK. Weltzien E. Geological Survey (USGS). Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.112(10):1116-1124.9(5):494-501. 2005. Swan SH. Giri A. March 2006.S. Quintana PJ. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Available at URL: http://www.73(1):182-94. Environ Health Perspect 2006. Reproductive outcome in women exposed to malathion. Am J Public Health 1987. The Quality of Our Nation’s Waters. Gosselin NH. Third National Report on Human Exposure to Environmental Chemicals. Barr DB. Pluth JM. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. 4/7/09 Kissel JC. Available at URL: http://www. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.pdf. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues.

70 (2. Methyl parathion is not registered for residential use in the United States.40) 2. more slowly absorbed through the skin.0) 3.12) < LOD < LOD 1.60-24.57) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60-36. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.46 (3.0) 3. was once a restricted-use insecticide with limited applications on certain agricultural crops.61) < LOD 1.00 (2.70) 2.700 (<LOD-.85 (2.19 (.S.20 (<LOD-2. It had been applied to cotton.50 (1. Morgan et al.18-3.EPA.11-4.70 (2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.92-2.01) 4.72 (3.28-4.S.60-5.30-16.10-1. peak domestic use was as high as 5-6 million pounds per year.50) 3.70-6.10 (3.15-3.90 (1.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . methyl parathion was rapidly absorbed after ingestion.37-4.80) 2. but by 2003.990-1.0) 3.860 (<LOD-1.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .30 (2.940 (<LOD-2.37-2.32-1.48) 90th 2..11) 2.61) < LOD 1.33 (1.910) < LOD .80 (2.850) < LOD .36-1. and aquatic invertebrates.10 (<LOD-6.30 (1. 2003).. Both are toxic to birds.33) 2.70 (2.40) 1. 2006).62 (1.300-. Methyl parathion use is highly restricted.790 (<LOD-. ethyl parathion. Ethyl parathion. In the 1990s.26 (1.70-3. fish.770 (.91-3.79) 4. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.0 (3. first registered in 1948.69) 4. In animal studies.32-3.71 (3.13-1. which may vary for some chemicals by year and by individual sample.1.92) 5.50-9.09-1. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. Once absorbed. Methyl Parathion. 1977).28 (1.50 (2.10) 22.60-19. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 149 .30-5.70 (<LOD-3. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. Given its limited use.22-3.298-00-0 Ethyl Parathion CAS No.05) 4.01-4.70) 2. 2007).0) 4.02-6. pulmonary.45 (1.45) 5.28 (1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50 (2.70) 2.40-3. on cereal grains.50) 2.21-1.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .01) 695 660 518 679 603 941 Limit of detection (LOD.70-3.70-6.80 (2.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.37-4.40) 4. and to a lesser extent.60) 1.50) 3.70-6. 2000).44) 2.74) 5. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.58) 3.89 (2.21 (2.0) 3.47) 2.0) 2.50 (1.50 (1.71 (2. and of the chemical nitrobenzene. binds tightly to soils resulting in low leachability.34 (3.60 (4.910) < LOD < LOD .20 (2.50-14.S. Estimated intakes from diet and drinking water have been below recommended limits.50) 1. Survey Geometric mean (95% conf. Increased risk of exposure via dermal.90-11.20-5.00) 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 1.57-4.40 (1.00) 3.10) 4. with limited applications in agriculture.80 (1.27) 2. 2002.32-1.40-4.10 (3.20) 5. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.70 (3. < LOD means less than the limit of detection.. and eliminated rapidly from the body after absorption (Kramer et al. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion. and oral routes can occur in pesticide and agricultural workers (Muttray et al. Methyl parathion has low water solubility. and has a short half-life in soils and on plants.66 (2.16) < LOD 1. all registered uses were voluntarily cancelled (U.8 and 0.32 (1.50 (1.30-3.67) < LOD 1.40-4.37) 2.0) 3.69 (2.41-4.67 (1.910) < LOD < LOD < LOD 1.49 (1. Many previous registered agricultural uses of methyl parathion have been cancelled (U.EPA.10-11.90-9.730 (<LOD-.00 (2.

but lists ethyl parathion as a possible human carcinogen.7) 3. 2004). Zurich et al.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 .88) 1.4 (3.94-4.79 (1. 1995).97 (2. 1990.10) 90th 2.96 (1.26) 17. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2006. Additional information about external exposure (i.04) 1..82) < LOD .39) 1. Survey Geometric mean (95% conf.26 (1.11-4.690-1. Orsorio et al.41-2. gov/toxpro2.17) ..25) 1.15-10.530) < LOD < LOD < LOD .73 (1.57) 6. methyl parathion.08) < LOD .71 (1.EPA considers methyl parathion unlikely to be carcinogenic to humans. resulting in excess acetylcholine at nerve terminals.79) 1.14-3..67-2.980 (.9) 1.01 (2. 1991). EPA at: http://www. 2004).92 (2. and seizures.370 (<LOD-.83 (1. ethyl parathion.55) 2. 2003.33-3. accidental exposure.84) 3.html and from U.680 (<LOD-1.730-1.cdc.77-7.08-3.80 (1. Methyl Parathion.35-3.43) 4. WHO. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.30-1. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.94-47.10 (1.61) 4.500) < LOD < LOD .23) 1.31-3.720 (<LOD-.88 (1. In large doses.S.970 (.20) .13-12. and unintentional acute or chronic high-level occupational exposure (Hill et al.16-4.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . 150 Fourth National Report on Human Exposure to Environmental Chemicals ..96 (1.78-2. environmental levels) and health effects is available from ATSDR at: http://www. does not inhibit acetylcholinesterase enzymes. 1995.59 (1..20) 3.Organophosphorus Insecticides: Specific Metabolites Metabolites”).970 (.60) 2. Slotkin et al.840 (.430 (.20 (3.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .48-4.540) < LOD .850-1. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.39 (1.790-1.60 (1.89 (2.90 (1.atsdr.76-14.33-6.01 (.15) 3.57-7.880 (.11) 1. vomiting. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene. U.44-3.00 (1.930 (.440 (<LOD-. and producing acute symptoms such as nausea.950) < LOD .37-1.78 (2.72-2. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.55 (<LOD-3.95) 1.870) < LOD .17-4.87 (1. Jaga and Dharmani. Karanth and Pope et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Lores et al. and other metabolites. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.29 (2. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.00 (1. cholinergic effects.2) 2.67 (3..80 (1.56-2. Methyl parathion is not considered genotoxic. Parathion and methyl parathion have high acute toxicity in animal testing. gov/pesticides/.07 (1.09) 2. weakness. paralysis.930 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.08 (1.97-10.70) 3.86 (2.940 (<LOD-1.31) < LOD .78) 2. paranitrophenol.00) 2.91 (1.35-3.720-1.310-. 2006. population from the National Health and Nutrition Examination Survey.29) 2.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD ..89 (2. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.13) 4.57-2..640) < LOD < LOD 1.3) 2.830-1.30) 3.25 (2.800-1.1) 2. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.790-. The metabolite.44-3.71) 1.e. Thus.98-7.33-3.S.29) 1.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. In addition to being a metabolite of methyl and ethyl parathion. 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.400 (<LOD-.05) 4. teratogenic.2) 2.01-3.97 (<LOD-4.07) 2. At high animal doses of methyl parathion.04 (2.S.epa.82 (2.60-2.91) 1.38-3.21) 1.78-2.21-21. 2005.93 (2. 1978.

Needham LL. Lu C. Barr DB.110 Suppl 6:1085-1091. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. 1999). 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. general population (CDC. Centers for Disease Control and Prevention (CDC). Bailey SL. Head SL. 2005. Environ Health Perspect 2002. a range of values several hundred times higher than levels found in the U. 2002). et al. 1995. Pope C. Rev Environ Health 2006. 2002. References Barr DB.71:99108. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Kramer RE. ACGIH recommends a BEI of 0.21(1):5767. Bradway DE. Hill et al. Leng G. Chicago area methyl parathion response. Occup Environ Med 1999.14(4):213-216.112(10):1116-1124.htm.. Available at URL: http:// www. et al. Arch Environ Health 1978. Rockhold RW. Gregg M. J Anal Toxicol 1990.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Guizzetti M.215(3):182-190. Pesticide workers may have much higher levels following pesticide applications.25(5):599-606. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation.9:311-320. Wellman SE. Rubin et al. 2005). end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Role of individual susceptibility in risk assessment of pesticides.inchem. Baker S. Moomey CM. CDC. Barr DB. Parathion-Methyl (addendum).15(2):164-171. and levels were similar or slightly lower that those in a small convenience sample of the U. Curl CL. 1995). and many residents were symptomatic (Barr et al. Runkle KD. McClure PC. Giordano G. Head SL.... Pathak S. Lewalter J. International Programme on Chemical Safety-INCHEM (IPCS). et al. Turner WE. Costa LG.. Slach EF. Karanth S. Kedan G. Toxicology 2005. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Hryhorczuk DO. Morgan DP. Laboratory investigation of a poisoning epidemic in Sierra Leone. Dharmani C. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Alley CC. Griffith W.S. 2004). 2002.110 Suppl 6:1075-1078. McCann KG. Environ Health Perspect 2004. Third National Report on Human Exposure to Environmental Chemicals. 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. McCann et al. 2005. 2005. DiPietro E. Shealy DB. et al. In a study of workers who handle parathion. et al.5 mg (500 µg)/g creatinine for workers at the end of shift.S. Environ Health Perspect 2002. Harley K. oral or dermal administration. Lores EM. Jewell NP. Barr DB. 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. Atlanta (GA). 4/7/09 Jaga K. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Baker SE. Hill RH Jr. Arch Environ Contam Toxicol 1977. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Pharmacokinetics of methyl parathion: a comparison following single intravenous.. Pesticide residues in urine of adults living in the United States: reference range concentrations. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Ashley DL. Bradman A. 2005).33(5):270-276.org/documents/jmpr/jmpmono/v95pr14. Cline RE. Clark JM. Levels of para-nitrophenol in the NHANES 1999-2000 and 2001-2002 subsamples were similar or slightly lower than those in a nonrandom subsample of NHANES III (19881994) participants (CDC. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.6(2-3):159-173.. Neurotoxicol Teratol 2003. population (Olsson et al. Hetzler HL. Barr JR. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.56(7):449553. J Expo Anal Environ Epidemiol 2005. Baker RC. Lin LI. Weltzien E. Environ Res 1995. Hill RH Jr. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Methyl parathion: an organophosphate insecticide not quite forgotten. J Biomed Sci 2002. Moseman RF. Kissel JC. Eskenazi B.

gov/circ/2005/1291/. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Sadowski MA. revised February 15. pdf. 6/1/09 World Health Organization (WHO). 1992-2001. EPA). Backer G.E. EPA-738-FOO-009. Available at URL: http://www. Environmental Protection Agency (U.S.pdf. 0153. Investigation of a fatality among parathion applicators in California. Environ Health Perspect 2002. Methyl parathion in drinking water. Ames RG.201(2):97-104.376(6):808-815. Levin ED.S.epa. Ryde IT. Environ Health Perspect 2006.epa. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Letzel S.S. 1995-1996.usgs. Schilter B.pdf.Organophosphorus Insecticides: Specific Metabolites Muttray A. Toxicol Appl Pharmacol 2004. The Quality of Our Nation’s Waters. Monnet-Tschudi F. Hill RH Jr. gov/oppsrrd1/REDs/methylparathion_ired. Pesticides in the Nation’s Streams and Ground Water. 2007 [online].114(10):1542-1546. External and internal exposure of wine growers spraying methyl parathion. Slotkin TA. Ethyl parathion. Rosenberg J. U.int/water_sanitation_health/dwq/chemicals/ methylparathion.S. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. EPA). et al. Case No. Kieszak S.S. Available at URL: http://www. Rubin C. Dunlop B. March 2006. Costa LG. Available at URL: http://pubs. Barr DB.162(2-3):219-224.110 Suppl 6:1047-1051. Honegger P. Facts.who.04/106. Nguyen JV. 152 Fourth National Report on Human Exposure to Environmental Chemicals . September 2000. 1/14/09 U. Geological Survey (USGS). Yacovac R. Tate CA.gov/oppsrrd1/REDs/factsheets/0155fct. Olsson AO.D. Mengle DC. Am J Ind Med 1991. Ohio. May 2003. 5/19/09 Zurich MG. Anal Bioanal Chem 2003. 1/12/07 U. Jung D. Toxicol Lett 2006. 2004. Hill G.20(4):533-546. Environmental Protection Agency (U. Seidler FJ. Available at URL: http://www. Osorio AM. WHO/SDE/WSH/03. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. R. 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. Esteban E.

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

08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .740-1.210-.820) < LOD < LOD .300-1.780 (.700-1.64) .15) < LOD .580-1.850 (.21) < LOD .780 (.17 (.470 (.250 (<LOD-.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .410 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th . population from the National Health and Nutrition Examination Survey.500 (.840 (.07) .210 (<LOD-.31) . 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.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.950) < LOD < LOD 1. Survey Geometric mean (95% conf.2.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0.430 (<LOD-.210-1.S. population from the National Health and Nutrition Examination Survey.610 (<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.670 (<LOD-1. 154 Fourth National Report on Human Exposure to Environmental Chemicals .780 (<LOD-1.840) 669 687 929 Limit of detection (LOD.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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.55) .680 (<LOD-.700-.780 (<LOD-1.27) .200-.740 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.760 (<LOD-.94) .670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .S. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.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 . < LOD means less than the limit of detection.

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

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

2001.gov/toxpro2. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Zhao RC. Hu et al. 1998. Lewalter J. Fredriksson A.gov/toxprofiles/ tp155. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. neurochemical changes in cholinergic. Regul Toxicol Pharmacol 2002. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides.300(3):161-165. Guillot TS. Toxicological profile for pyrethrins and pyrethroids. WHO.27(12):1273-1283. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. EPA at: http://www. Neurotoxic effects of two different pyrethroids.. Agrawal AK.. Garey J. Lazarini et al. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation.atsdr. Environ Health Perspect 1999. Elwan MA. Seth PK. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Kang IH. 2005). Moniz et al. Idel H. Richardson JR. September 2003. Toxicol Appl Pharmacol 1991. Kim TS. Garey and Wolff. dopaminergic.205(6):459-472. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Shaw IC. Shukla Y. Lazarini CA. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. et al.8(1):18-21. Eriksson and Fredriksson. Shafer. Elwan et al. and permethrin) in the Hershberger and uterotrophic assays. Bull Environ Contam Toxicol 1999. fenvalerate. and seizures (ATSDR. Wolff MS. Leng G.. 2005). salivation. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. 1999. Kim et al. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Abell AD. Go V. 2005).211(3):188-197. Bernardi MM. Effects of prenatal exposure to deltamethrin on forced swimming behavior.. Sunami O. Levsen K. In California. Int J Hyg Environ Health 2002. Kim HS. Leng G.. Neurotoxicol Teratol 2005.251(3):855-859. Florio JC. J Reprod Dev 2004. Lee SJ. motor activity.23(6):665-673.. Varoli FM. Okuno Y. 2006. Sugiri D. 2006). and striatal dopamine levels in male and female rats. Idel H. Pauluhn J. choreoathetosis. Neurotoxicol Teratol 2001. Toxicol Appl Pharmacol 2006. epa. Pogo BG. 2006. Kamita Y. Cruz-Casallas PE. Yang J. Spinosa HS. Ose K. Lemonica IP.62:101-108. Kunimatsu et al.html. McCarthy et al. Caudle WM. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Hu JY. tremor. Thomson BM. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Neurosci Lett 2001.50(2):245-255.. Available from URL: http://www. Song L. McCarthy AR.. et al. Kuhn KH. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Pyrethroid pesticide-induced alterations in dopamine transporter function. Berger-Preiss E. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al.27(4):609-614. Salzgeber SA. Eriksson P. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Soderlund et al. Wolff MS. 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. Estrogenicity of pyrethroid insecticide metabolites. J Environ Monit 2006. bioallethrin and deltamethrin. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Kim IY.. 1991.atsdr. Ranft U. Moniz AC. 2001.. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. 2000. 2003.8(1):197-202. Kuhn K. Go et al. Biochem Biophys Res Commun 1998. 2004. Yamada T.html. Leng G. Garey J.108(1):78-85. 2005)..S. Generally. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line.107(3):173-177. Ray et al.gov/pesticides/ and from ATSDR at: http://www.cdc. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.1/15/09 Aziz MH. et al. 2003. 2003. Wang SL. Shin JH. 2002. Fourth National Report on Human Exposure to Environmental Chemicals 157 .. et al.35(2 Pt 1):227-237.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Bernardi MM. Leng A. Kunimatsu T. hypersensitivity. Miller GW. In developing rodents. Xenobiotica 1997.. 2003. 2002). Adhami VM. Chen JH. References Agency for Toxic Substances and Disease Registry (ATSDR). 2002). Additional information about pesticides is available from U. cdc. Wieseler B.

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

the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. Studies in Germany of 396 children and adolescents (Becker et al. 2004). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Baker et al.. 2001) showed that urinary levels of 4-fluoro-3-phenoxybenzoic acid at the 95th percentile ranged from either slightly higher or lower than the detection limit in the U. Cyfluthrin is rapidly metabolized and eliminated from the body... 2001.68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin. 2006) and 1177 urban adults and children (Heudorf et al. Following an indoor application exposure. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. most of which were dermal and respiratory irritations (Spencer and O’Malley. 2003). the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. 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... but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment. 2003). 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. Fourth National Report on Human Exposure to Environmental Chemicals 159 .S. representative 2001-2002 NHANES subsample (CDC. 2005. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. 2003).95 µg/L. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). Leng et al.Pyrethroid Pesticides Cyfluthrin CAS No. Urinary levels for adults and children in these studies were similar (Heudorf et al. 2005). 2005).. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.S. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. 2006). Thus. representative subsample in NHANES 2001-2002 (CDC. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0..2 μg/L) in the U. 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. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002.

2 and 0. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Survey Geometric mean (95% conf.2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 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.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. 160 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 830 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 700 594 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey Geometric mean (95% conf.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid (creatinine corrected) Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 161 .

Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. 2005. J Expo Anal Environ Epidemiol 2003. Leng G. Ball M. Angerer J. Hadnagy W. Butte W. Idel H.Pyrethroid Pesticides References Baker SE. Heudorf U. Environ Health Perspect 2001. Bernard CE. Rev Environ Contam Toxicol 2006. Kolossa-Gehring M. Atlanta (GA). Centers for Disease Control and Prevention (CDC).77(1):67-72.209(3):221-233. Drexler H. Seiwert M. Sugiri D. Int Arch Occup Environ Health 2004. Heudorf U. Hoppe HW. Third National Report on Human Exposure to Environmental Chemicals. Angerer J. O’Malley M. 19962002. Ranft U.209(3):293-299. Schulz C. Heudorf U. Spencer J. Angerer J. Becker K. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int J Hyg Environ Health 2006. Pyrethroid illnesses in California. Arch Environ Contam Toxicol 2004. Angerer J.109(3):213-217. Human exposure to indoor residential cyfluthrin residues during a structured activity program. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Int J Hyg Environ Health 2003. Olsson AO. et al. Krieger RI. Williams RL. Barr DB. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.206(2):85-92. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.186:57-72. Berger-Preiss E.46(3):281-288. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.13(2):112-119. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Int J Hyg Environ Health 2006.

Similarly.490-.68) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.310) .68) .180 (.77 (.850 (.490-1. trans-cypermethrin.2-dichlorovinyl)- CAS No.790) .44 (.270 (.300-.510 (.670 (.610) .Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.2-Dichlorovinyl)-2. but can also reflect exposure to trans-3(2.680-3.500 (. transcypermethrin and trans-cyfluthrin.600) .52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.330) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.150 (.340-.570 (.650-1.120-.340) .350) .68 (. and trans-cyfluthrin. Cyfluthrin.740-2.220) .730 (.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.920) 1.580) 1.220-. 1985.28) 671 680 518 701 591 957 Limit of detection (LOD.670-1.250 (.420-.470 (.68359-37-5 Cypermethrin Permethrin CAS No.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.170 (. 1999).820 (. 1999).160 (.110-.202 (.490-1. 1985.280-.680 (.790-1.270 (.2dichlorovinyl)-2.510 (.200-.13 (. 52315-07-8 CAS No.or trans-3-(2.910-5.280 (. Biomonitoring Information Urinary levels of cis.380-.220-.230) .330 (. cis-permethrin. and ciscyfluthrin.155-.2-dichlorovinyl)-2.630) .35) 1..15) .54) .08) .370 (.43) .960 (.220-.470-1.890 (.12 (.430-.110-.640 (.210) 90th .28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .260 (.220-.110-.890 (.S.670-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.410) .200-.900 (.200-.80) .2-dichlorovinyl)-2.410) . which may vary for some chemicals by year and by individual sample.50) .120-.120-.200) < LOD < LOD < LOD .740) 1.700) .790 (. population from the National Health and Nutrition Examination Survey.160 (.710-1.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .11) . < LOD means less than the limit of detection.300-.730 (.460 (. Survey Geometric mean (95% conf.2-dichlorovinyl)2.730 (.550) . Generally.670-2.880 (.380-..210-.2dichlorovinyl)-2.490-.400-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.530 (.770-1.460-.950-2.1 and 0.24) 1.200 (.740-1.21) .510 (.630-.240) .570-. ciscypermethrin and cis-cyfluthrin.2-dichlorovinyl)-2. cis-3-(2.300 (.262) * * * < LOD < LOD .2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.160 (<LOD-. more of the trans-metabolite than Urinary cis-3-(2. Kuhn et al.340) . In the body.630) . Fourth National Report on Human Exposure to Environmental Chemicals 163 . cis-cypermethrin. The presence of cis-3-(2.110 (<LOD-. but it can also reflect exposure to cis-3-(2.630 (.690) .and trans-isomers.35) .780) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.270-.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.870) 1. the presence of trans-3-(2. trans-permethrin.370-.460-1.240) .07 (.300 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.520) .600 (.1.770) .440 (.140 (.180) . The chemical trans-3(2.610) .47 (.740 (.380) .140 (<LOD-.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .200) . Kuhn et al.380-.580-1.500 (.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.250-.790-1.710) .270 (.600-1.200) .210) .32) .120-.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.53) .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 .380 (.

530 (. urinary trans-3-(2.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .550-1.780) 1.200-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. Schettgen et al. Studies in Germany of 396 children and adolescents (Becker et al.890) . 2006.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .780 (.550) . Other studies have provided evidence that urinary levels of cis.360-1.440-.12-2.150-.540) .and trans-3-(2.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.250-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.190 (.880) .21) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.182) * * * < LOD < LOD .33 (.. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.920 (..700) .640) 1.11) .400 (.37) .180 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.080-.2-dichlorovinyl)-2.580) .380 (.380-.300-.640-. 2001.400-1.2-dichlorovinyl)-2.260 (.67 (.49) . 2005).600 (.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.570) ..300) .540 (.450-1.190) ..230-. 2004).680-1.410) .2dichlorovinyl)-2.200 (.300 (.250-. representative NHANES 2001-2002 subsample (CDC.29 (.250) .370-.290) .550) .12 (.280-.440 (.550-1.840 (.470-1. 2002).230-.530 (.280 (.540 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al. Cyfluthrin. In the same residents.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al. 2005) In a small group of indoor pest-control operators.270) .450-.2-dichlorovinyl)-2.240 (<LOD-.260-.170 (.200) .2-dichlorovinyl)-2.220 (. 2006) and 1177 urban adults and children (Heudorf et al.24) .59) .270) .320) .370-.2-Dichlorovinyl)-2.250-.350 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..380) . urinary levels of cis-3-(2.390-.700) . In a study of urban residents in Germany (Berger-Preiss et al.560) 1.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.840 (.590 (.130-.750-1.640-1. 2001) showed urinary levels of cis.250) . 2003).59 (1.260 (.640 (.390 (.Pyrethroid Pesticides 2.200-. In a study of volunteers.170 (. Survey Geometric mean (95% conf.260) .. 2002).150-.500 (. the median and 95th percentile of urinary levels of cis-3-(2..560) .590) .390-.260 (.and trans-3(2. 2005).510-1. 2006).140-.2-dimethylcyclopropane carboxylic acid did not increase.180-.290 (.31) .59) .33) .440 (.750 (.170) < LOD < LOD < LOD . In these volunteers.210-.120 (.03) 1.890 (. 164 Fourth National Report on Human Exposure to Environmental Chemicals .270-.138 (.230-.680-1.340-.800 (.270 (.340) . 2003).340) .320-. 2006.11) 1.830) .220) .810 (. 2005).80) .430 (.190) .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 . though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.450 (.710-3.150-. post- Urinary cis-3-(2.11 (. median urinary levels of trans-3-(2. 2004.430-1.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.420 (.290-.350) .700-2..690-1. population from the National Health and Nutrition Examination Survey.S.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2005).430-.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.S. 2006).710 (.250) 90th .580-1.67) .160 (<LOD-..550 (.680 (.440-.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .104-.230 (. Lu et al.220 (..370-.290) .900 (.640-1.11) .2dichlorovinyl)-2.300) .300 (..250 (<LOD-.

58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .500-. trans-Cypermethrin.660) 1.14-6.41 (1.730) .08-4.91 (1.17-1.60) .68-3.14-2.23 (.520-.87 (1.410 (<LOD-.43) 2.09 (.560 (.410 (<LOD-.400 (<LOD-.2-dichlorovinyl)-2.20 (.410-.60) 1.550 (.460-.520) .11-1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.530) .670) .94 (1.56) 2.910-1.500) .01) 4.69 (1.77 (1. 2005). interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.54) 4.11-2.700-1.460-.12-6.50 (1.760) .08) 1.4.620) < LOD 2.55-4.42 (2.55-3. < LOD means less than the limit of detection.66) 691 680 518 690 595 954 Limit of detection (LOD.2-dichlorovinyl)-2.59 (1.19) 1.81) 2.410-.89 (2.7) 2.26 (.35) 1. which may vary for some chemicals by year and by individual sample. Finding a measurable amount of cis. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.2-Dichlorovinyl)-2.49-3.570) 90th 1.40 (1. 2005).95) 2.70) 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 .480-.25 (1.20 (.07-3.20 (.23) 2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.56 (1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.470 (<LOD-.66) .95) 3. The maximum post-application urinary levels.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .19 (3.or trans-3-(2.03-1.90) 1.68) 2.76-4.63) 1.440 (<LOD-.42) 1.54 (1.420 (<LOD-.13) .41-14.55-5.560 (.28 (2.780 (.64-4.76-3.560 (.77) 2. however.970 (.700) .60-4.800-1.68) 1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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.840-1.28 (1.49-5.68-2.22 (1.820) .56 (1.77) 1.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .Pyrethroid Pesticides application median urinary levels of summed cis. Biomonitoring studies on urinary levels of cisor trans-3-(2.17 (.10) 2.17 (.62 (1.920-1.37 (1.63) 1.97-11. population from the National Health and Nutrition Examination Survey.400-.03-1.580 (.500 (. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.39 (1.5) 2.07 (1.69) 1.16) 1.68) 1. Urinary trans-3-(2.01 (1.610) 1.830-1.910-1.14) 1.08-6.84 (1.940 (.and trans-3-(2.S.860) .56) 2.85) 4.670) .490-1.810-1.2dichlorovinyl)-2. Survey Geometric mean (95% conf.470 (.39-5.48) 4.710 (.19 (2.850-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.27 (1.49-3.25-3. Fourth National Report on Human Exposure to Environmental Chemicals 165 .4 and 0.490 (<LOD-.680-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.750) .

530 (<LOD-.86 (2.00) 1.33-2.16 (1.30-6.15-3.35 (1.19) .08 (.08 (.31 (2.42 (. trans-Cypermethrin.15) 3.530 (.60) 2.55 (2.20 (1.10) 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 .39) 1.35) 1.750) .27-2.91) 1.57) 3.570-.900 (<LOD-1.670) .470 (.720-1.770) < LOD 2.89) 2.720 (<LOD-.47-2.31 (.44) 2.15-3.07-3.37 (1.850) .850-3.3) 2.15) 2.700-.740) .80) 1.48 (1.45-2.Pyrethroid Pesticides Urinary trans-3-(2.27-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (.87 (1.74) 2.19 (1.57 (1.07-1.87) 1.30-3.540) .800-1.33-1.850) 1.26 (1.70 (.440-.31) 1.07) 2.55 (2. population from the National Health and Nutrition Examination Survey.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .13) .570 (<LOD-.640) .11) .410-.42) 1.15 (1.56 (1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.470-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.780) .34-4. Survey Geometric mean (95% conf.720-1.930-1.22-2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.15-3.880 (.81 (2.560 (.34-3.36) 2.41) 1.56-5.60 (1.660) .730) .36 (1.29) 1.S.91-11.780) 90th 1.48-2.33 (1.880-1.500-.87-8.780 (<LOD-.760 (.07-2.2-Dichlorovinyl)-2.61) 1.880 (<LOD-1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .74) .00) 1.65) 1.00-5.67 (2.55 (2.65 (2.480-.610-.56-2.700 (.28) 2.22-1.87-3.800-1.00 (1.39 (1.75 (1.520 (<LOD-.580) .60) 2.580 (.02-1.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.64 (1.12 (.47 (1.820-2.45 (1.68) 3.22) 1.00) 5.20-2.970 (.47-2.570 (.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.13) 1.91 (1.12-1.98 (1.40-2.87) 1.07) 2.

A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Int Arch Occup Environ Health 2003. Environ Health Perspect 2001. Atlanta (GA). Sugiri D. Hadnagy W. Bull Environ Contam Toxicol 1999.62:101-108. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Kuhn K. Ranft U. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Leng G. Berger-Preiss E.134(1-3):141-145. Bartell S. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Hoppe HW. Drexler H. Int J Hyg Environ Health 2002. Int Arch Occup Environ Health 2004. 2005. J AOAC 1985. Hardt J. Angerer J. Schettgen T. Angerer J. Schulz C.209(3):293-299. Permethrin and its two metabolite residues in seven agricultural crops. Angerer J.Pyrethroid Pesticides References Becker K.77(1):67-72. Centers for Disease Control and Prevention (CDC).109(3):213-217.205(6):459-472. Int J Hyg Environ Health 2006. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Berger-Preiss E. Int J Hyg Environ Health 2003. Idel H. Heudorf U. Barr DB. Angerer J. Idel H. Heudorf U. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Drexler H.114(9):14191423.68(6):1160-1163. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Ball M. Ranft U. et al. George DA. Environ Health Perspect 2006. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Heudorf U. Leng G. Levsen K. Butte W. Kolossa-Gehring M. Sugiri D. Pearson M. Wieseler B.206(2):85-92. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.76(7):492-498.209(3):221-233. Int J Hyg Environ Health 2006. Angerer J. Bravo R. Third National Report on Human Exposure to Environmental Chemicals. Lu C. Angerer J. Biological monitoring of workers after the application of insecticidal pyrethroids. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Idel H. Leng G. Seiwert M. Heudorf U.

Deltamethrin can degrade to cis-3(2.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.39 µg/L. Baker et al.. (2004) reported a geometric mean concentration of cis-3(2. 2001) showed that urinary levels of cis-3-(2. 52918-63-5 General Information Cis-3-(2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. 2001. Finding a measurable amount of cis-3-(2. Urinary levels for adults and children in these studies were similar (Heudorf et al.Pyrethroid Pesticides Deltamethrin CAS No. mean peak urinary levels of cis-3-(2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..2-dibromovinyl)-2. Biomonitoring Information Urinary levels of cis-3-(2. Following residential spraying with deltamethrin for malaria protection in Mexico. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population.2-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. 2006) and 1177 urban adults and children (Heudorf et al.2-dibromovinyl)-2. In an analysis of 217 urine specimens from a nonrandom sample of United States residents..3-0.2-dibromovinyl)-2.S.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.. Outside the U.2-dibromovinyl)-2. Thus. In the NHANES 2001-2002 subsample. Studies in Germany of 396 children and adolescents (Becker et al. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. 2005).2-dibromovinyl)-2.5 μg/L) than the detection limit (0.. in some situations replacing the use of DDT. deltamethrin has been used against mosquitoes that carry malaria.2dimethylcyclopropane carboxylic acid formed in the environment. in detection of cis-3-(2.2-dibromovinyl)-2.1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2-dimethylcyclopropane carboxylic acid of 0.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.. 168 Fourth National Report on Human Exposure to Environmental Chemicals .2-dibromovinyl)2. urinary levels of cis-3-(2.2-dibromovinyl)-2. 2004). 2005).2-dibromovinyl)-2. 2005). 1990).2-dimethylcyclopropane carboxylic acid in the environment (IPCS.

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) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD.1.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. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Fourth National Report on Human Exposure to Environmental Chemicals 169 .S.2-Dibromovinyl)-2.1 and 0. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Survey Geometric mean (95% conf.2-Dibromovinyl)-2.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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. 170 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.Pyrethroid Pesticides Urinary cis-3-(2.

Batres LE. Seiwert M. Lopez-Guzman OD. Atlanta (GA). Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Hoppe HW. Drexler H. et al. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. 5/26/09 Ortiz-Perez MD. toxicokinetics. International Programme On Chemical Safety (IPCS). Heudorf U. Kolossa-Gehring M. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. [online] 1990. Grimaldo M.org/documents/ehc/ehc/ ehc97. Angerer J. Angerer J.209(3):293-299. Int Arch Occup Environ Health 2004. et al.Pyrethroid Pesticides References Becker K. Deltamethrin. Angerer J.77(1):67-72. Schulz C. Heudorf U.109(3):213-217. Environ Health Perspect 2001.inchem. Environmental Health Criteria 97. Int J Hyg Environ Health 2006. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Angerer J. and genotoxicity in exposed children. 2005. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Int J Hyg Environ Health 2006. Torres-Dosal A. Available at URL: http://www.113(6):782-786.209(3):221-233. Heudorf U. Butte W. Carranza C. Environ Health Perspect 2005. Ball M.htm.

2003.. 2006. 2004). 2005). representative NHANES 2001-2002 subsample (CDC.. A study of 396 German children (Becker et al.. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. 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. 2003. urinary 3-phenoxybenzoic acid levels at the 95th percentile were about threefold lower than the levels at the 95th percentile in the 2001-2002 NHANES subsample (Berger-Preiss et al. 52918-63-5 use and house dust levels (Lu et al.. 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 . CDC. 68359-37-5 Cypermethrin Deltamethrin CAS No. 52645-53-1 Tralomethrin CAS No. Fenpropathrin Permethrin CAS No. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. 2006). 2005. Baker et al. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. In one study of 145 urban residents in 80 private homes in Germany. 2005). median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. Hardt and Angerer. (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. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides.52315-07-8 CAS No. 2005). 39515-41-8 CAS No. CDC. 2003). 2005). Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. CDC. Saieva et al.. mean peak urinary levels of 3-phenoxybenzoic acid in children increased at least sixtyfold over non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (OrtizPerez et al. 2005). Thus. 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. 2002. 2005).. 2005). Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al. 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. In the New York City study. 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.Pyrethroid Pesticides Cyhalothrin CAS No.. Becker et al. In a small group of indoor pest-control operators. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides.. 2005.

population from the National Health and Nutrition Examination Survey.41) 3.60) .276-.45 (2.427) .430-.267 (.530-.71 (1.320 (.35) 1.226-.29-1.830-2.390) .277-.190-.1.430-.27-2.41 (1.740 (.364) .960 (.86 (1.273 (.78) 6.33 (1.46) .30) 3.253-.41-2.350-.63 (3. Survey Geometric mean (95% conf.428-.45-5.65 (1.320) .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 .740 (.16-1.12 (.8) 3.33 (2.51-6.04-5.41-3.35 (1.369) .210-.830) 90th 1.05) 1.601) .315 (.25-4.370) .340) 1.43) 3.246-.14-6.200-.12) 4.247-.13 (.600 (.417 (.520 (.54) 1.34 (2.79) 3.352-.260-.750-1.56-5.83-11.420) .530-.210-. Fourth National Report on Human Exposure to Environmental Chemicals 173 .93 (1.1 and 0.62-6.160-.190-.90) 1.595) .730 (.510-.300 (.38 (2.27-2.62) 5.800) 1.490) .1) 3.69) 3.570-1.32-21.32 (2.238-.373) .311 (.750) .34) 8.560-1.18 (1.250 (.34-6.710 (. interval) .590-.1) 3.190-.297 (.39) 2.610) .05) .320) .321 (.300 (.230-.230-.233-.620-1.25 (2.49-2.27-11.35) 2.200-.340) .560-.18 (2.680 (.35 (2.470-.35) 2.33) .360) .01 (1.640 (.340) 75th .250 (.28) 1.454 (.490-.336 (.560-.292 (.384) .36) 1.586) .990) .325 (.280 (.25 (2.250 (.700 (.810) 1.298 (.300 (.760 (.314) .48-2.52-5.13) .75 (1.270) .81 (1.300) .65-2.320) .S.26-2.940) 1.1) 3.330) .76 (1.44) 5.89-71.240 (.670 (.320) .288-.290 (.800 (.260 (.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .78) 1.250-.23 (2.53) 1.230 (.02-6.26) 2.180-.55 (1.550-.46) 2.16) 1.25-7.78) 1.590 (.362) .230 (.50 (2.32 (1.840-1.330) .04) .510-.260 (.650 (.42-2.292-.25-1.49-2.52-4.270 (.49 (1.850) .220-.30 (.374) 99-00 01-02 99-00 01-02 99-00 01-02 .700-1.21 (2.38 (2.227-.710 (.73) 1.328 (.630) .314 (.63-3.387) .160-.353 (.440) .820) .450 (.260 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.92-3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.780) 4. Deltamethrin.69 (1.200-.30 (1.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.62-8.12) .72 (1.266-.434) .190-.507 (.295) .230-.78 (1.51-3.406) .240 (.26) 2.64) 697 680 524 701 603 957 Limit of detection (LOD.49 (1.265-.570-.870 (.48-2.03 (3.355) .820) .750) .53-3.850) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.288 (.271-.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .

300-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.02-1.94 (1.224-.229-.246 (.670) .62) .329) .261 (.35) .860-1.48 (1.534) .06-3.240 (.43 (2.480 (.270 (.210 (.07) 2.590) .840-1.220-.328) .200-.320) .490-.S.240 (.63) 1.274 (.372) .21-4.316 (.323 (.91) 9.280 (.02 (2.160-.52) 2.32 (2.378 (.67 (1.43) 1.930) 1.62) 1.240-.490 (.190-.272 (.220 (.570) .510 (.09 (.61-2.240-.41) 1.490 (.35 (1.760) .49) 3.37) 1.04 (3.410) .88) size 1998 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .357) .09-2.264 (.09-2.480-.27) 1.35) 1.22 (1.63-3.630) .250 (.275 (.311 (.290) .225-.677) .00) 1.41-4.36 (1.365) 99-00 01-02 99-00 01-02 99-00 01-02 .72 (1.35-3.0) 3.380-.510 (.52 (1.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .04 (.55) 3.11 (. Deltamethrin.25-5.280 (.370 (.380 (.423 (.51-7.91) .400-. population from the National Health and Nutrition Examination Survey.230) .335-.330) 1.329) .216-.202-.19 (2.190 (.54 (1.15-2.238-.13-1.19-6.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.420-.400) .437) .86 (1.234 (.10 (2.03-1.330) 75th .274-.73-4.500) .44) 2.40) 2.640 (.610 (.580 (.810) 1.200-.88-5.83 (1.80) 4.640 (.300-.750-1.83) 1.67 (1.400-.930) .261-.253) .390-.362 (.309 (.330) .290-.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .860 (.272) .312 (.280) .227 (.240 (.230-. interval) .73) 1.43-64.200-.321-.387) .64-5.650) .440-.460-.91-4.40 (1.03 (.07-5.250 (.13 (.720 (.270) .210-.720) 90th 1.530-.84 (1.350 (.173-.309) .550 (.49) 1.90) 3.43 (1.460-.17-1.21 (1.530-.550 (.330) .280-.440-.25) 2.60-4.81 (1.96 (1.190-.330 (.580) .00) 5.11 (.401) .240-.670) 3.290) .75-8.440-.19) 2.730) .240 (.280) .17 (.370-.25-2.240-.271-.550 (.270-.53 (1.280 (.590) .304) Selected percentiles ( 95% confidence interval) Sample 95th 3.67) 1. Survey Geometric mean (95% conf.55 (1.150-.16-4.730) .700-1.05-3.210 (.44 (1.230-.200-.446) .00) 1.74) 3.270) .590-1.250) .960-1.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .13-1.09) 3.226-.510 (.410-.540 (.95) 1.60) 1.49 (1.590) .37 (1.91 (2.860-1.270 (.39) 1.740) .178-.730-1.49-2.278) .350) .560 (.299-.310) .36-6.450 (.

Sugiri D. Leng G. Int J Hyg Environ Health 2003. toxicokinetics. Biological monitoring of workers after the application of insecticidal pyrethroids. Atlanta (GA). Angerer J. Hadnagy W. Bartell S. Ranft U. et al. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides.76(7):492-498. Kolossa-Gehring M. Carranza C. Berger-Preiss E. Becker K. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Environ Health Perspect 2005. Seiwert M. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Pearson M. Lopez-Guzman OD. Hardt J. Leng G. Ortiz-Perez MD. Barr DB. Int Arch Occup Environ Health 2003. Hoppe HW.114(9):14191423. Liu Z. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Idel H. Lu C. Levsen K. Sugiri D.209(3):221-233. Environ Health Perspect 2003. Olsson AO. Third National Report on Human Exposure to Environmental Chemicals. urban cohort. Environ Health Perspect 2006. Arch Environ Contam Toxicol 2004.Pyrethroid Pesticides References Baker SE. Obel J. et al.111(1):79-84. Exposure to indoor pesticides during pregnancy in a multiethnic. Lapinski R.206(2):85-92. Berger-Preiss E. Godbold J. Bravo R.46(3):281-288. Idel H. Grimaldo M. Int J Hyg Environ Health 2006.113(6):782-786. Torres-Dosal A. Angerer J. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Fourth National Report on Human Exposure to Environmental Chemicals 175 .205(6):459-472. 2005. Berkowitz GS. Centers for Disease Control and Prevention (CDC). and genotoxicity in exposed children. Barr DB. Int J Hyg Environ Health 2002. Deych E. Batres LE. et al. Ranft U. Ball M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.

300-.120) .04.154-.370) .130-.200-.220) 95th .230 (.280-.140) . 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.320 (.400 (.110 (.280-. and glass.400) .170-.134-.190-.130-.160) .150 (.207) .260) .210) . solder.320 (. and refuse incinerators that process or release antimony. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.390) .180-.350 (.360) .190-.130 (.280 (.190) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.150-.110-.330 (.140-.080) .360-.260 (.250) .184) .210 (.310 (. People are exposed to antimony primarily through food and.390) . or other substances containing antimony is another means of exposure.120-.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.090 (<LOD-.330-.160) .260 (. interval) .200 (.140) .117-.340 (.400) .330) .148-.280-.103) .120-.04.144) .320) Total .350 (.170-.130 (.350) .095-.130 (.310 (.150-.110) .410) .087-.210) .250 (.120-.197) .300-.390) .240 (.330) .07.230 (.230) .110-.169 (.180 (. metal bearings.290-.170) .130 (.190 (.220-.070-.180) .180 (. distribution.090-.340) .260 (.360 (.250-. from air and drinking water.090 (.370-.080 (<LOD-. water.140 (.220) .570) .410-.430 (.070 (<LOD-.220 (.350-.230-.280) .350 (.140 (.200-.460 (. fireworks.170 (.710) .230 (.142 (.240 (. 01-02.120) .200 (.137) .390) .080-.110-.100) .134 (.095 (.350 (.230) .470 (.200) .460 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3. and excretion of antimony vary depending on its oxidation state.120 (.200) .160) .100-.260) . and +5.120 (. < LOD means less than the limit of detection.250-.270 (.090) 75th . population from the National Health and Nutrition Examination Survey.160-.114) .400) . The absorption.400-.130 (.146 (.175 (.290-.131-.130-.150) .500) . to a lesser extent.190) .150-.150-.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 .320-.230-.120 (.330) .490) .360 (. ceramics.130) . enamels.160-.170-.079-.157) .220 (.120-.180) .280-.220-.470) .440) .158 (.190) .210) .110-.390-.300-.210) .200-.130-.190 (.330) .109-.150 (.250 (. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications. and as a fire-retardant in textiles and plastics.600) .410) .S.300) .150) .122 (.500) .115) .160 (. It is used in metal alloys.190) .126 (. and pewter.120-.130 (.108-. and 03-04 are 0.310) .120-.430 (.120 (.270 (.150-. Dermal contact with soil.164-.460 (.070 (<LOD-.510) .290 (.120-.099 (.460) .220-.320-.176 (.117-.140 (.490 (.161) .210-.210 (.530) .180 (.119) .270) . It is also used in paints.133) * .180-.280) .390 (.350-.150 (.250-.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 .210-. 7440-36-0 General Information Antimony is found in ores or other minerals.190 (.143 (.145) Selected percentiles ( 95% confidence interval) 50th .156-.088-.440) .390-.120-.180-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.098-.154) .300) .125 (.280) .200) .120) .130-.100 (.330 (.180-. 176 Fourth National Report on Human Exposure to Environmental Chemicals .130 (.170-.350-.120 (.160-.420) . castings.330 (.310-.160) .128 (.080) .560) .Metals Antimony CAS No.105 (.440 (. Workplace exposures can occur at smelters.100 (.280 (. which may vary for some chemicals by year and by individual sample.128 (.180 (.220) .310 (.132 (.310 (.190) .140 (.220-.112-.135) * .350) .160 (.350 (.140) .140) .240 (.140) .160) .200) .160-.190-. 0.190-.090-.150) 90th .400 (.280-.230-.210) .260-. Antimony enters the environment from natural sources and from its use in industry.470) .320-.093 (.160) .260-.350) .200 (.108 (.390-.130) .119-.130-.300 (.250-. see Data Analysis section) for Survey years 99-00.130 (.140) .136-.130) .430 (.250 (.190-.310-.178) .120-.130) < LOD .200-.270-.280) .190 (.340 (.230-.123 (.180 (.141-.270 (.330-.120) .115-.240-.300) .200 (.200 (.310) . ammunition.145 (.320-.240 (.400 (.270 (.360) .180-.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 .150) .132 (.220) . Stibine is a metal hydride form of antimony used in the semiconductor industry.136) * . respectively. storage batteries.220-. 0. +3.350) .230-.260) .240-.230) .137) .220-.200 (. sheet and pipe metal. coal-fired plants.320) . and 0.170-.154) .300 (.190 (.126-.160 (.240) .180 (.130-.170 (.240 (.270) .100-.

364 (.417) .125 (.320-.137 (.104-.108-.191 (.150-.107-.248) . interval) .265-.117-.265 (. and kidney have been demonstrated in high dose animal studies depending on the dose.247) .245) .112 (.195-. 1986).080 (.114 (.741 (.122 (.099-.438) .138) * .156-.173-.118 (.230-.086 (.124 (.162-.127) .333 (.176-.109 (.278 (.161) .159-.118 (.209) .238) .116-.153 (.338 (.109 (.096-.263-.081) . skin.371 (. 1986).085) .185 (.133) .178-.124-.203) .167 (.198) .111-. population from the National Health and Nutrition Examination Survey..130) .079 (<LOD-.121 (.131-.173 (.357) .164 (.146-. Acute antimony poisoning may cause a metallic taste.115-.132) .228 (.195-.159-.250-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.081 (<LOD-.146-.172-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.250) .115 (.310) .196 (.250-..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.318-.271-..140) .278) .364 (.193 (.068 (.103-.146-.268) .333-1.261) .089) .444) .167 (.148-.159-.727) .189 (.152) .315) .087) .121) .485) .211) .185 (.241-. 1988. Ming-Hsin et al. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.145) .233-.134) .126-.391) .164) .229-.480) .253-.121 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine. 1995).417) . and gastrointestinal symptoms such as vomiting.130) .333-.127) .357-.146) .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 .233 (.107-.385 (.206-.741) .176 (. 1954).115) .333-.267 (.352 (.129 (.199-.127) .183) .138-.129) * . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.140) < LOD .125-.405) .213 (.192 (.181) .129) .161) .092) .226 (.248-.108 (.429 (.430) .132 (.277 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30) .214) .333) .250 (.135 (.116 (.105-. myocardium.320 (.147-.080 (<LOD-.181) .100 (.288 (. resulting in hemolysis with abdominal and back pain (Dernehl et al.179-.S.167-.230) 95th .238) .151) .112-.188-.Metals than for trivalent compounds (Elinder and Friberg.108-.176 (.104-.127 (.429) .257) .255) .069-.294) Total .310 (.338) .178 (.242-.113-.250 (.421) .084) .320-.200-.500) .338 (.225 (.250-. 1953). species.195 (.117-.154-.321) .131) .138-.281-.228-.192) .253 (. 1944).102-.135 (.130 (.295 (.128-.109-..171) .150-.256 (.115 (.163 (.241-.263 (.123 (.298 (.310) .115 (.148) * .192-.255-.119-. 1962).182 (.333 (.119-.308) .129 (.123) .259 (.414) .138 (. liver.120 (.095-.120 (.320 (. 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.139 (.208 (.127) .111 (.068-. diarrhea.227-.400 (. 1973).267) .194-.099-.318-.425) .205-.280-.076-.391) .276 (.373) .135) .209 (.173 (.126 (.209-.222 (.122 (.250-.106-.113-.075 (.082) .082 (<LOD-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.143) 90th .204-. abdominal pain.136) .164-.112 (.300 (.228 (.320) .106-.280 (.107-.130) .207) .185-.209) . Inorganic antimony salts irritate the mucous membranes.167 (. Fourth National Report on Human Exposure to Environmental Chemicals 177 .186) .076-. Histopathologic inflammatory and degenerative changes in the lung.200) .200-.173) .238 (.098-.208-.187) .333 (.200-.203) .115-.152) .103-. 1958) and occupational exposures (Briegner et al.160 (.131 (.147) .308-.267-.317) .120 (.135) .170 (.181) .086) 75th .224 (.193) .071-.272) . and ulcers (Werrin.117-.317) .124-.233) .236 (.343 (.239-.075 (.139 (.188) .143 (.074 (.119 (. and eyes.317) .108-.149-.135) .143) .077) .149) .078 (.143) Selected percentiles ( 95% confidence interval) 50th .175 (.069-.286 (.163 (.126) .097-.114 (.235-.447 (.217 (.082) .352) .444) .098) .124) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman. and route of exposure (Elinder and Friberg.102-.120 (.269 (.244-.300) .220) .313-.156 (.148-.300) .153-.471 (.095-.061-.092-.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 .380 (.266 (.144-.113) ..143) .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 .333-.098-.471) .114 (.225) .

. eds. Sabbioni E. Lenert G. Br J Ind Med 1991. Weltle D. and hydrogen sulfide. Chin Med J 1958. Biomonitoring of a worker population exposed to low antimony trioxide levels.158:165-190.59:469-474. Urinary antimony in infancy. or exposure differences. Antimony in blood and urine of infants. Antimony trioxide is rated by IARC as a possible human carcinogen.. Fuchs A. Friberg L. Pulmonary edema of environmental origin. Sci Total Environ 1994. Iavicoli I. 1997). Ju-Sun P. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect.cdc. Hamilton EI. Centers for Disease Control and Prevention (CDC). Matthews T. Roland H. Atlanta (GA).10(3):560-586. Buchet JP. Mahieu P.. Cordasco EM. Caroli S. Schaller KH. Cullen A. Review of elements in blood. Van der Venne MT. 1998. External and internal antimony exposure in starter battery production. Dezateux C. 1998). Information about external exposure (i. Bailly R. O’Regan M. Schacke G. Industrial Medicine and Surgery (Dec.)1954. Trace element reference values in tissues from inhabitants of the European community I. 1986. 26-42. Nordberg GF. 1998) or compiled reference ranges (Hamilton et al. even when exposure levels were below workplace air standards (Bailly et al. Sabbioni E. VI. Lauwerys R.46:931-936. Ming-Hsin H. 1987). 1990. Piatnek DA. which may be due to methodologic. Mayne P. stibine. and a drinking water standard has been established by the U.atsdr. HH. Chest 1973. et al. Stasney J.. J Clin Pathol 1998. Third National Report on Human Exposure to Environmental Chemicals. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Rev Infect Dis 1988. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Delves HT. Luedersdorf R. Briegner H.e. 2004. and 2003-2004. Handbook on the toxicology of metals. Antimony. environmental levels) and health effects is available from ATSDR at: http://www. gallium. Konings J. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Iavicoli et al. Dunkelberg.. Paschal et al. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Wu M-T. arsenic. Liao Y-H... Shao-Chi C. 1994) have reported values slightly higher than those in this Report. Elinder CG. Skulsukai G. respectively. Pozzoli L. 2005. Kuo-Juie Y. Kentner et al. Stone FD. Liao Y-H et al.521-523. Yu H-S. Chia-Yu H.Metals to antimony have been established by OSHA and ACGIH. and antimony in optoelectronic industry workers. Yang C-Y. Alimonti A. Vouk VB. Bolten C.76:432436. Earlier measurements in general populations (Minoia et al.S. References Berman JD. Costeloe K. Arch Dis Child 1997. Environ Health Perspect 1998. Wade A. Stead FM. Stocks J. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. clinical efficacy. 2nd ed. Apostoli P. Dezateux et al. Chen J-R. Gebel TW.76(2):103-115. 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. Ludersdorf et al. population. et al. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al.51:238-240. Kiberd B.. gov/toxpro2. Arsine. EPA. J Trace Elem Med Biol 2002. Element reference values in tissues from inhabitants of the European community.48:93-97. In: Friberg L.106:33-39. and future strategies. 2002.64(2):182-185. Chemotherapy for leishmaniasis: Biochemical mechanisms. Mayer P. Int Arch Occup Environ Health 1987. Biological monitoring of exposures to aluminum. Int Arch Occup Environ Health 1995. Industrial Medicine 1944. 1995.13:361-362. Cheng-Wei L. Pilgrim L. 20012002. Pietra R. Carelli G. pp. Leinemann M. Kentner M.67:119-123.. Petrucci F. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Suchenwirth R. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Gallorini M. Semisch CW. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Dernehl CU. et al.html. Nau CA. Biological assessment of exposure to antimony and lead in the glass-producing industry. Industrial antimony poisoning.. Ho C-K. Minoia C.16: 33-39. J Occup Environ Med 2004. New York: Elsevier. 1991.. indium. Delves HT.

Pirkle JL. Morrow JC. Trace metals in urine of United States residents: reference range concentrations. blood. Werrin M. Paschal DC. Chemical food poisoning. Ting BG. 27:38-45. Sampson EJ. et al. Sci Total Environ 1990. and serum of Italian subjects. Industrial Hygiene and Occupational Medicine 1953.76(1):53-59. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Jackson RJ. Antimony poisoning in industry. Environ Res 1998. Quarterly Bulletin of the Association of Food and Drug Officials 1962.95:89-105.Metals in urine.99-108. Renes LE.

Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. 2001). arsenocholine. ocean and fresh waters.1) 1281 1276 03-04 03-04 03-04 9. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. and in lead-acid storage battery grids. arsenites.41 (7.30 (6.0 (22.3) 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 7.000 metric tons annually.9-34.1) 15.6) 11.5 (36.6) 618 722 1074 Limit of detection (LOD.90) 75th 16.0 (43.5 (40.90-14.5 (23.8-61.8) 7. grain. and foods. Arsenic and its compounds have had many uses in the past and present as medicines.2 (12.4 (48. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.1-40.8) 30.5) 43. sodium arsenite.90 (5.90 (7.40) 7.10-10. and gray forms). General population exposure to inorganic arsenic can occur through consumption of drinking water and. and play sets.90-8.7) 65. Gallium.19-9.84) 8.2) 15. Before the 20th century.55 (7.2 (41.50 (8.9 (8. In nature.5-52.6 (32.2-93. Although it is still widely used in the United States.10) 10. lead hydrogen arsenate. semiconductors.4) 60.2-20.74.10 (6.80 (5.6 (13.6-141) 53. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.29 (8. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.Metals Arsenic CAS No. were used as treatments for syphilis. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.30 (7.9-62. aluminum. arsenic as elemental metalloids may be used in some ammunition.90-7.90 (7. +3 and +5).5 (34. solders. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.9 (17. alloys. mental disorders. and as homicidal poisons.8) 34. and as a cosmetic to lighten complexion. Since the 1940s.0-60.8-77. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. such as arsenopyrite (FeAsS) and realgar (As4S4). pesticides. 2005).3-19. from coal burning. trimethylarsine oxide.4 (24.2 (51.7-95.57) Selected percentiles ( 95% confidence interval) 50th 7. retaining walls.9) 21.12 (6.0 (15.27) 9. Arsenic trioxide (As2O3.90) 16. and produce.2 (13.3-15.6-35.7 (11. The United States no longer produces arsenic from mining but imports about 22. Arsenic is measurable in most soils.70-9. it is found in over 200 crystalline or mineral forms. as alloy in metal bearings.34-9. In the last century. and indium arsenides are used in the semiconductor industry.4) 40. Survey years 03-04 Geometric mean (95% conf.12-10. 180 Fourth National Report on Human Exposure to Environmental Chemicals .2-17. interval) 8.00 (6.00-9. the smelting of copper.7-83.0 (14.5-41. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.97) 8.4) 13. and arsenates (oxidation states of -3.5) 41. meats.25-9.5) 95th 65. Water sources contain mostly inorganic arsenate.0 (11.6 (9.50-14. cancers.2-61.80-9.8) 7. population from the National Health and Nutrition Examination Survey. particularly arsenic trioxide.13-8.90-8.66-8. Various arsenic compounds were used in paint pigments and for tanning animal hides. Arsine (AsH3) is a reactive.5-19.08 (5.1 (38. and other metals.4 (26. to a lesser extent.70) 8.20 (8.S. psoriasis.3) 10. mostly for use in wood preservation (ATSDR. though in some locations arsenite may be prevalent (WHO.77) 6.1) 7. gaseous hydride manufactured in small quantities for use in the semiconductor industry.70 (6. lead.8) 33.4-65. black.9-46. referred to as inorganic arsenic compounds. to a lesser extent. cacodylic acid.6 (15. see Data Analysis section) for Survey year 03-04 is 0.6-43.34-10.8) 29.5 (14.7) 24. arsenic compounds.9) 68.02-8. and arsenosugars.2) 46.1) 290 725 1542 03-04 03-04 9.0-19.1-18.80) 6.5) 66.8) 17.8 (48. and. Also.4 (7.30) 17.84) 8.5-178) 46.10-7. Arsenic trioxide is approved to treat acute promyelocytic leukemia.90-11.7) 90th 37. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4 (31.1 (32. copper arsenates. or rarely as elemental metalloids (yellow.3-111) 78.

88) 7. 2007.99-9.. Extremely high groundwater arsenic levels.5) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2557 03-04 03-04 03-04 8.0-26. 2007. mine tailings).3) 9.9 (45.4 (11.44) 6. 2001). EPA.4 (24. Though modest bioconcentration occurs in some aquatic life.7-17.0) 1281 1276 03-04 03-04 03-04 8.3-41.47 (7. Inorganic forms of arsenic demonstrate high acute toxicity. so exposure to the general population is extremely limited.2-46.75) 13.06 (4.0) 26.2) 40.2-15.33-10.5) 290 725 1542 03-04 03-04 8.3 (24.0 (31.8 (12.31 (6. interval) 8.2 (12.25-9.S. 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.6 (10. though some reduction may occur in the gut prior to absorption. selenium. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.25 (6..01) 11. arsenocholine.50 (6..11 (5.7 (9.40) 8.5-17. dust.28-7. age. 2001). arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.4 (12. NRC. kelp.8) 27. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established. as observed in Bangladesh where millions of people have been exposed.9) 53..Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.76 (6. Fish. Arsenate is reduced in the body to arsenite (oxidation state +3).44-11.5 (9.4 (40.3-53.4-64.8-62.23-7.58-10. arsenic does not show biomagnification in the food chain (WHO.7-35. In aquatic organisms.0-38..04) 7.6 (17. inorganic arsenic is widely distributed within the body. WHO.1) 6.1) 58. population from the National Health and Nutrition Examination Survey. 2001). trimethylarsine oxide (TMAO).7) 95th 50.7 (11.8 (11. but is poorly absorbed dermally (WHO. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. 2001). dose level. WHO.6-17. 1988).93-9.g. 2001).0) 12.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .93-8.5-120) 40.S.81-9. 2001). TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. and some other seafood can contain organic forms of arsenic including arsenobetaine. and arsenosugars.6 (35.0 (17.8 (21.66-8..8 (20. After absorption. are used in enclosed ultraclean operations within the semiconductor industry.1) 24.4) 54. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.1-36.2) 15.3 (27.10-8.41) 6.8-32. Chowdhury et al.86-17. 2006.3-62.4 (26. cacodylic acid and monosodium methyl arsenate.64 (7.12-10.6) 45.7) 28.20-9.1) 8.30-9. U.8 (27.3-64.01) 7.7-34.66-8. EPA’s maximum contaminant level (Hughes.45) 5.5) 17.13) 8. 2006. Tseng. The reduced form of MMA (oxidation state Urinary Total Arsenic (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.7-18. shellfish. and folate status (Chen et al.04 (5.7-188) 27. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.0-69.S. 2003.8-75.18 (5.24 (7.0) 33.66 (7.1 (11.59) Selected percentiles ( 95% confidence interval) 50th 7.96) 12. The semiconductor dopants.10-16.88 (5.47-6. Direct exposure to DMA and MMA may result from use of the two pesticides.1) 7.47 (6.4 (42. Gamble et al. 2001. have caused clinical arsenic poisoning.9) 13. 2001).3) 6.9-56.7 (25.00 (6.51) 75th 14. 2007.33 (6.0) 14.38-10. and contact with CCA-preserved wood structures. gallium arsenide and indium arsenide.0-18. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.2) 90th 30. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.75 (5. 2001. Steinmaus et al.07-9. Children may have additional exposures from ingestion of contaminated soils (e. 2001).8) 22.32 (5.0) 42. Survey years 03-04 Geometric mean (95% conf.1 (14.4) 32.61 (7. organic arsenic can be converted back to methylated and inorganic arsenic. In aquatic sediments. Smoking tobacco is also a source of inorganic arsenic.35) 7.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (<LOD-1. Arsenic has many actions demonstrated in cellular studies. vomiting. and it also will inhibit succinate dehydrogenase. Studies of arsenic at levels typical of U. hematocytopenias. and by uncoupling oxidative phosphorylation (NRC. NRC. arsenic trioxide) includes hemorrhagic gastritis with nausea.30) 1.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al.50) 1. population from the National Health and Nutrition Examination Survey. 2006) or when exposure occurs in smokers (Chen et al..30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Chronic elevated arsenic intakes have been associated with diabetes. Survey years 03-04 Geometric mean (95% conf. Chile). WHO. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. 2004. 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. Acutely. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al.. 2004). Such actions may lead to decreased energy production. can cause peripheral sensorimotor neuropathies.50) 621 725 1078 Limit of detection (LOD.20 (<LOD-1. Although arsenate is reduced in the body to arsenite..60) 1. noncirrhotic portal hypertension.. 2001). Cohen et al. WHO.10 (<LOD-1. but additional or confirmatory research is needed (Kapaj et al. Cardiac arrhythmias. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. gluconeogenesis. apoptosis. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al.. 2001. drinking water have not been associated with increased cancer rates (Schoen et al. Chronic arsenic exposure in humans is considered to be a cause of skin. 2006. substitution in phosphate metabolism.20 (<LOD-1. and DNA repair inhibition (Cohen et al. see Data Analysis section) for Survey year 03-04 is 1. 2001).. and production of glutathione may be affected as well. and diarrhea.10 (<LOD-1. which can lead to dehydration and shock. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. respectively.. 2001). including inhibition of numerous enzymes.S. hyperkeratosis. Bangladesh. leading to a decrease in adenosine triphosphate energy production. and hyperpigmentation of the skin (NRC. 2000. interference in signal transduction pathways.S. some of these effects may take years to develop. hepatotoxicity. renal failure.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. 2007. food residue.20 (<LOD-1. 1998.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. and environmental standards for arsenic and arsenic Urinary Arsenic (V) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.EPA has established drinking water. 2006. peripheral vascular disease. cell transformations. 182 Fourth National Report on Human Exposure to Environmental Chemicals . Raml et al.0. and childhood neurodevelopmental effects in observational human studies. 2001). U. Chronic human intake of arsenic at less than acutely toxic doses..60) 1.. 2001). including drinking water sources with elevated arsenic levels (e. 2004).80) 1. and altered gene expression.. 2001). increased oxidative stress.S. Taiwan. Laboratory studies using inorganic arsenic have shown chromosomal aberrations... 2007. fatty acid oxidation.g. which may vary for some chemicals by year and by individual sample.S.10 (<LOD-1. NRC. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. < LOD means less than the limit of detection. WHO. and endothelial injury (Kumagai and Sumi. 2001. WHO. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells.10 (<LOD-1. and bladder cancer (IARC. hypertension. Cellular glucose uptake. 2007). Bredfeldt et al. 2006. The organic forms of arsenic occurring in seafood have little known toxicity.EPA.20 (<LOD-1.g. cytotoxicity. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. The U. lung. With chronic exposure.

S. 2000).19) 3. 2006. 1986). DMA produced bladder cancer in some chronic rat studies (Cohen et al. Consequently.69 (<LOD-3.html. Additional information about external exposure (i.61 (<LOD-3.80 (<LOD-4. Offergelt et al. and the FDA has established a bottled drinking water standard..S.18) 3.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.50) 1. 1999.. 2004.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2007. urinary arsenic levels have been accepted as a good biomarker of dose (WHO.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine..18 (<LOD-3. 1992. Levels of total urinary arsenic in the U. hand washings from children playing on CCA-treated wood compared to children playing on non-CCA-treated wood playground equipment were slightly to fivefold higher (Kwon et al... Vahter et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. environmental levels) and health effects is available from ATSDR at: http://www. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. population from the National Health and Nutrition Examination Survey.. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U...00) 1.atsdr.. 2006. In animal studies.. Pellizzari and Clayton.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2.04 (<LOD-3. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al.cdc. In the German Environmental Survey III of 1998. arsenic has been fetotoxic and teratogenic.. 2003.75 (<LOD-2. In a Nevada town where groundwater levels were naturally elevated. 2008. but generally only at maternally toxic doses (WHO. Valenzuela et al. Compared with this Report. 2006).S. Meza et al. population in NHANES 2003–2004 (Schulz et al. Josyula et al. 2007. 2004..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.. 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... Calderon et al. WHO. 2008). had decreased since the prior 1990– 1992 survey.41) 3. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. 2001). Pellizzari and Clayton.33 (<LOD-3. Shalat et al. Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. population (Rubin et al. 2008). 2000. 2001).. 2006). Shalat et al. 1999). 1999...e.75 (<LOD-2. 1998. 2006). and were about two-fold lower than those for the U. although urinary arsenic levels were not associated with CCA contact (Shalat et al. Several studies have shown that urinary arsenic levels are not correlated with low levels of arsenic measured in house dust or in washings taken from hands (Hysong et al. 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. Survey years 03-04 Geometric mean (95% conf... 2006. median urinary total arsenic levels in 4052 adults varied with seafood intake. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..Metals compounds.. 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. 2006). Fourth National Report on Human Exposure to Environmental Chemicals 183 ..S. Caldwell et al. Pellizzari and Clayton 2006). 2001). gov/toxpro2. Caldwell et al.

Caldwell et al. arsenocholine.30 (1.5) 32.62) 2. Survey years 03-04 Geometric mean (95% conf. vasospasm.4-35. and TMAO.0 (26. methylation capacity.80 (3.50) . MMA. 2003)..5) 29.19 (. In most human studies.2 (6.8) 35.S. Sun et al.700-1.800) 1.29 (1.7) 15.3) 1284 1284 03-04 03-04 03-04 1.1) 18.S. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. 2000.3-39. Blom et al. Also.8. 2008).90-7. interval) 1. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.80 (.S. population in the NHANES 2003–2004 subsample.5 (26. 2008)..50-6.. 2008. 2000. arsenite.9) 13. 2006). 1990. and other factors such as nutrition..00-6.800-1.00-12.20-3.20 (2. in NHEXAS 1995–1996. Valenzuela et al.900-1.68) . and 0.g.. 1985.83) Selected percentiles ( 95% confidence interval) 50th 1. 1996.8 (12.40) 75th 5.900 (.50) .8-50.0 (27.17-1.3% of a representative sample of the U. 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.1-25. arsenite.37 (1.20) 3. arsenobetaine.30 (2..6 (13.700-1.70 (3. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al..3 (9. population from the National Health and Nutrition Examination Survey.600 (.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 * * 1.50) 90th 16.3) 35.3) 95th 35.S. Arsenate.800-4. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.70) 6. Measurable organic arsenic species in this Report are three biologically generated environmental forms.2-38. In the residents of a Chilean town who consumed water with high levels of arsenic.500-1.8 (17. 2001.48-2. These associations are stronger at higher urinary levels.7-22.10 (4. 2008). 1. 2000. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.6. 184 Fourth National Report on Human Exposure to Environmental Chemicals .80) 1.7) 13.e.0-23..6.28) 1. which may vary for some chemicals by year and by individual sample. 2001).20 (4.20-190) 31. Chowdhury et al.55 (1.80 (4.30) 2.00 (1..4.05) < LOD .20-25.4 (16.800 (. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. see Data Analysis section) for Survey year 03-04 is 0.66 (1.4) 23.9 (7..70-21. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.. The higher percentiles of total urinary arsenic levels in the U. Individually measurable species resulting from inorganic arsenic exposure are arsenate.60-3.90-29.Metals other areas of the world (Ahsan et al.9 (6. when seafood organic arsenic is subtracted).. Caldwell et al.0) 4.4) 31.1-94.20) 7.93) 1.20 (. After recent seafood ingestion.11-1.8-40. China.S. 2008.10) 8. In the late 1980s. < LOD means less than the limit of detection.45 (1. 2005.00) 3.40-6. respectively. Caldwell et al. Some noncancer effects of arsenic (e...6 (25. with DMA. population (Sun et al.60) 1.6-44. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. and TMAO were detected in only 7..5) 621 725 1078 Limit of detection (LOD.43-1.20 (1.74 (1.70-21.00-4. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.80-5.5) 292 728 1548 03-04 03-04 1.0) 29.400-. Tseng et al. dermal keratosis. and duration of exposure are also considered important.31-1. DMA and MMA. 2007) with higher levels of arsenic in the drinking water.871-1. geometric mean levels were about 70-fold higher than for the U.. population (Ahsan et al. When seafood intake is avoided. 4.10) 4. Total arsenic measured in the urine includes all species of inorganic and organic arsenic. WHO. 2008).6 (11. For residents of Inner Mongolia.3 (21.. arsenocholine.40) 5. 2005.00 (. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.800 (.9-23. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-35.20) 18. population showed a higher contribution of arsenobetaine (Caldwell et al. Caceres et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 45. and two methylated metabolic products.7 (13. Pellizzari and Clayton. 2005.7 (21.. 2007). and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.40-7. Aposhian et al.5 (14.30) 10..1-51.00-1..70 (5.

Vahter et al.4 (24.6-46.13-39.612-1.21) 5.4-82.54 (1.73-6. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. Information about the biological exposure indices is provided here for comparison.83) 8.88 (5.531 (. 1986. Fourth National Report on Human Exposure to Environmental Chemicals 185 . Offergelt et al.62-6.3) 95th 29. population for the sum of inorganic related species was 18.3-24.25 (.9) 32.2 (12.30-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.64-29.50-7.51) 5. not to imply a safety level for general population exposure.44 (1.S. WHO.51-2.15-4.29 (4.1-18.4) 13.6) 19.11 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.88) 2..61-6. 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.6-29.638) 1. population from the National Health and Nutrition Examination Survey.14 (1.79 (1.18-1.43) 14. 2008).5-20.833-1.91 (4.36) 2.959-1.50-15. Survey years 03-04 Geometric mean (95% conf.53 (.1) 26. Sun et al. 2003.3) 1284 1284 03-04 03-04 03-04 1.2 (12.4-21.901-2.82) Selected percentiles ( 95% confidence interval) 50th 1.45) 1.4) 292 728 1548 03-04 03-04 1.58 (3.55) 1. Studies of small groups of metal and sulfuric acid smelter workers with varying industrial hygiene conditions have reported urinary inorganic arsenic levels (arsenate + arsenite + DMA + MMA) ranging as high as several hundreds of μg/L during or after work exposure (Jakubowski et al.909-1. The 95th percentile of the U.67) 4. 2008).80) . 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.9 (25..00 (3.2 (4.25-7.786-1. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.400-.65 (1.6-32.S.3 (10. Caldwell et al.83) 2.0 (9.82) 4.7) 30.9 μg/L.32-7.6 (6.7) 17.81 (4.28) 1.9-18.78-5.93 (1.1-36.43) 75th 5..1 (26.15-1. Biomonitoring studies of urinary arsenic can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of arsenic than are found in the general population.40 (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. 2001).70) 5.4 (11.877 (.4-28..9 (13.Metals as with DMA.40) 1.6 (9.10 (.29-14.30) 1.4) 32.12) < LOD .19-2.39-3.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.78 (3.8) 29..5 (18.3 (10.37-2. 2001).68 (1..47 (1. 1992.72) 12.5 (18.4) 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. 1998.67) 1. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.91) 90th 16.80-153) 17. 2006.16 (.938-1..76-27.0-36. In recent years.05 (.05) 1..5) 17.9) 14.00 (1. 2007).2 (13.7) 9.15-1.5) 26. which is below the ACGIH BEI (Caldwell et al.47 (2. interval) 1.

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

08 (<LOD-4.76) < 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.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey years 03-04 Geometric mean (95% conf. * 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.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 2.80) < LOD 621 725 1078 Limit of detection (LOD.S.2.44) 2. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.00) 1.40 (<LOD-1.00 (<LOD-2.00 (<LOD-3. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. < LOD means less than the limit of detection. Survey years 03-04 Geometric mean (95% conf.20 (<LOD-1.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Fourth National Report on Human Exposure to Environmental Chemicals 187 .29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.95 (<LOD-2. see Data Analysis section) for Survey year 03-04 is 1.

00-12.45) 3.95-3.0 (9.S.27 (2.0 (10.0 (10.00-9.0) 14.03-6.03 (3. Survey years 03-04 Geometric mean (95% conf.00-7.6) 292 728 1548 03-04 03-04 3.50-15.17 (2.0-19.0 (9.7-16.71 (4.86-21.0) 11.8) 7.78 (4.84-8.31) 4.28) 2. interval) 3.0) 17.0-17.00) 9.5 (11.22) 4.00 (6.79 (3.00-4.3 (8.27-2.00) 6.00 (3.0-18.38 (3.49) 10.9) 5.44 (2.9 (7.48 (2.39-3.65-8.17-6.81 (5.88 (4.62) 4.94) 3.00) 90th 11.0-16.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 621 725 1078 Limit of detection (LOD.69-3.00) 12.57-5.82-9.0) 9.6) 1284 1284 03-04 03-04 03-04 4.9) 13.9 (11.2) 10.0 (10.48 (3.5) 95th 13.00) 75th 6.80-3.27-5. interval) 3.00-7.69-6.3 (8.60-7.80-6.15) 4.73) 6.12 (3.10) 6.00 (7.0) 9.37 (3.80) 2.9) 12.7.05) 10.09 (7.82-5.S.17-4.30) 3.61-16.08 (2.33-4.00 (5.00 (5.29-4.05) 5.32 (8.70 (3.06) 5.10) 3.95-6.00 (5.0 (10.42) 3.0 (8.0) 95th 16.77 (3.16 (4.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.92) 3.60-3.80 (4.0) 16.24) 3.00-4.34 (3.65-6.0 (8.50-5.00 (5.00-12.95-4.0) 13.8) 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 3.4 (7.00 (5.11 (3.71 (3.98) 4.00 (4.0 (12.00-4.00-15.00 (6.19) Selected percentiles ( 95% confidence interval) 50th 3.00-4.78) 4.1 (8.16-11.46 (4.84-18.00 (3.7 (10.0 (9.34 (3.00-10.14) Selected percentiles ( 95% confidence interval) 50th 3.0 (12.97-3.86 (2.20-12.00-3.14) 3.5) 12.00-15. see Data Analysis section) for Survey year 03-04 is 1.9) 11.31-4.86-7.82) 3.18 (6.45) 8.0) 292 728 1548 03-04 03-04 4.80-5.69 (3.0 (13.0-12.30 (7.60-6.67) 8.71-4.0) 13.00-11.70-4.32 (4.27 (3.34-4.00-4.1-18.00-11.44) 5.89 (3.70) 5.61-11.71) 3. population from the National Health and Nutrition Examination Survey.00-22.7) 1284 1284 03-04 03-04 03-04 4.00) 3.16 (2.00-13.90) 2.11) 4.0 (13.00) 4.69 (3.55 (2.00-3.00) 7.00-5.3 (7.70-12.8) 7. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0 (14.00 (3.00-7.0) 16.94-3.00) 5.0) 12.33) 3.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .05) 3.91) 75th 5.6-18.13-4.7) 13.57 (3.34-4.74) 90th 9.85 (3.52) 3.00) 6.95 (4.0-17.00-15.45 (8.00) 4. Survey years 03-04 Geometric mean (95% conf.00 (3.0 (11. population from the National Health and Nutrition Examination Survey.73 (3.74 (2.32-10.00) 3.0) 17.1-22.00-4.60-4.0-25.12-4.59 (6.72 (4.00) 6.0-16.00) 6.1-15.0) 11.00 (7.00 (3.00 (3.80) 7.70-3.0) 10.24-4.00 (6.92-12.7) 12.6 (9.0) 9.20) 11.34) 3.00-11.00-8.90 (3.90) 5.20-4.00-7.25 (4.50 (4.49-4.67) 9.37 (2.

61-3.10 (.23) 1.46-2.45) 3.79) 2.71-2.00) 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 1.85) 1.50 (1.33 (1.80 (1.36) 1.43-3.00) 2.61) 2.00) 2.00 (<LOD-1.40-3.60) 1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.34) 2.00 (<LOD-1.10 (1.88 (1.20 (1.70-2.84-3.36 (1.30) 2.900-1.07) 2.40-3.40 (1.30-1.20 (1.60) 292 728 1547 03-04 03-04 * * < LOD < 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 1.07-3. see Data Analysis section) for Survey year 03-04 is 0.70-2.00-2.86) 3.86) 2.58) 2.31 (1.50-2.50 (<LOD-1.40-2.70-3.60) 2.82-2.10 (<LOD-1.82-2.93) .53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.35-3.80 (2.18-1. Survey years 03-04 Geometric mean (95% conf.86 (2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.14-1.20 (1.07 (1.20 (1.18-1.00-2. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.60) 2.30 (2.40) 1.90) 2.10-1.37 (1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00-1.80 (1.20 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey years 03-04 Geometric mean (95% conf.88 (1.28 (1.33 (1.90) 2.40 (2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00-1.90) 1.90 (2.60 (1.S.30) 1.17) 2.20) 2.80-2.52 (2.62) 2.60-2.22) 3.77) 1.00-4.46 (1.50) 621 725 1077 Limit of detection (LOD.20 (1.20-3. population from the National Health and Nutrition Examination Survey.53-2.816 (<LOD-.81) 1.50 (2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .00 (2.80 (1.50) 1.53 (1.15-1.10-1.90 (1.73-2.40) 2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.86 (2.88-2.80) 1.10-3.S.10) 2.80 (1. < LOD means less than the limit of detection.11-1.80) 1.40) 1. population from the National Health and Nutrition Examination Survey.00) 1.30) 1.30-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (1.30) 90th 1.20-1.00) 1.9.70-2.50 (1.57) 95th 2.40-2.70-2.30 (1.54) 90th 2.63 (<LOD-1.10) 95th 2.853-1.30 (1.30-1.985) 1.80-2.30 (1.96-2.10 (1.16 (2.31-3.00 (2.28 (1.22 (1.85) 2.10 (.60 (2.05-1. which may vary for some chemicals by year and by individual sample.70) 2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

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

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70(2):159-170. Jones RL.367(1):80-88. Black K. et al.96(2):119126. Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites. Belson MG. GSTM1 and T1. Sonora. J Toxicol Environ Health A 2007. Speciation of arsenic compounds in urine from occupationally unexposed and exposed persons in the U. Environ Res 2004. Kieszak SM.inchem. Rey OA. Shipp M. Rumpler A. Lauwerys R. Kopplin MJ. 8/8/07 192 Fourth National Report on Human Exposure to Environmental Chemicals . Offergelt JA. Environ Health Perspect 2007.S.20(8):1120-1125. U. Xu Y. Hoet P. et al. Vahter M. Lu X. Environ Health Perspect 2005. et al. CruzGonzalez MB. Urinary trivalent methylated arsenic species in a population chronically exposed to inorganic arsenic.114(2):220-227. Naranmandura H. html. Ibata K.113(3):250-254. Huang YK. Roels H.epa. Arsenic drinking water exposure and urinary excretion among adults in the Yaqui Valley. EPA). Valenzuela OL. Chen CJ. Boeckx M. Environmental Protection Agency (U. Marshall G.S. Fok N. Mason H. 8/7/07.gov/safewater/arsenic/regulations_factsheet. Urinary arsenic metabolites in children and adults exposed to arsenic in drinking water in Inner Mongolia. Steinmaus C. Jimenez M. Washington (DC) National Academy Press. Friberg L. Lewis Publishers. Int Arch Occup Environ Health 1986. Becker K. Clayton CA. Tseng CH. Francesconi KA. Kolossa-Gehring M. Arsenic in Drinking Water. Thio-dimethylarsinate is a common metabolite in urine samples from arsenic-exposed women in Bangladesh. Available at URL: http://www. Environmental Protection Agency (U. Smith AH. Raml R. 2001.htm. Boca Raton (FL).S.36-37. urinary arsenic speciation. Lauwerys RR. Buckley BT. Toxicol Appl Pharmacol 2005. Chem Res Toxicol 2007. A pilot study of children’s exposure to CCAtreated wood from playground equipment.49(6):387-393. Liaw J. Li L. Genetic polymorphisms in MTHFR 677 and 1298. Available at URL: http://www. Geneva 2001. et al. and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. Borja-Aburto VH. Calderon-Aranda ES. Arsenic. using a routine LC-ICP-MS method. Wang Z. Investigating childhood leukemia in Churchill County. inorganic. Integrated Risk Information System. China. Seifert B. Arsenic exposure. Environmental Health Criteria 224.115(1):151-157. Jhangri GS. Vahter M.30(5):293-301. Ferreccio C. Chung CJ. Buchet JP. Flanders WD.115(4):648-652. Fact Sheet: Drinking Water Standard for Arsenic. Twenty years of the German Environmental Survey (GerES): human biomonitoring--temporal and spatial (West Germany/East Germany) differences in population exposure.epa. Nolinder P. Available at URL: http://www. pp. Suzuki KT. Shalat SL. Environ Health Perspect 2007. 3rd Ed. 1998 [online].222(3):374-380. Guidelines for Biological Monitoring. Garcia-Vargas GG. Environ Health Perspect 2004. Solo-Gabriele HM. Moore LE. Assessing the measurement precision of various arsenic forms and arsenic exposure in the National Human Exposure Assessment Survey (NHEXAS). Arsenic methylation. Tseng CH. Sun G. Jin Y. Rahnster B. Yang MH. Toxicity of dimethylmonothioarsinic acid toward human epidermoid carcinoma A431 cells.S. von Ehrenstein O. Seiwert M. Environ Health Perspect 2006. Kalman D. Mexico. Environ Health Perspect 2006. 8/7/07 U. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 2007. January 2001 [online]. Fleming LE. EPA).112(14):1375-1380. Arsenic on the hands of children after playing in playgrounds. Li X. Conrad A. Nygren A.org/documents/ehc/ ehc/ehc224. Li B. Yuan Y. 2001. National Research Council (NRC). Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers. Arsenic.htm. Arsenic and Arsenic Compounds. Arsenic in drinking water-2001 update.114(8):1293-1296. Burgess JL. Toxicol Appl Pharmacol 2007. et al.211(2):175.206(3):299-308. Int J Hyg Environ Health 2007. Huang YL.Metals Kwon E. et al.K. 2nd ed. Nevada. Zhang H. urinary arsenic metabolites and human diseases: current perspective. Rubin CS. Goessler W. and metabolism of arsenic. et al. Schulz C. EPA 815-F-00-015. Morton J. Meza MM. Gandolfi AJ. Br J Ind Med 1992. Biggs ML. J Anal Toxicol 2006. Holmes AK. Sun X. In:Industrial Chemical Exposure. Pellizzari ED.210(3-4):271-297. Sci Total Environ 2006.25(1):1-22. Ochi T. Garcia-Montalvo EA. World Health Organization (WHO). Erratum in: Toxicol Appl Pharmacol 2006.57(2):79-91.gov/iris/subst/0278. Increased mortality from lung cancer and bronchiectasis in young adults after exposure to arsenic in utero and in early childhood.

93-8.48) 1.88) 1.70 (1.34 (1.65-1.50 (2.56) 1. barium sulfate and barium carbonate).94-6.14-1.60-3.90) 1.21 (1.90 (6. fireworks.50-1.12) 6.43 (1. 0.54) 2.12 (2.S.25 (1.32) 8.9) 5.82) 2.21-8.30-1.65) 3.50 (4.76-2.14 (6.40 (5.50-6.48-4.28-1.10-4.10 (4.64-3.15 (2.49-1.35-4.90-2.27 (1.80) 6. such as barium chloride.12-1.11 (2.41-3.64) 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 2.00 (2.50 (1.78) 1.87-9.86) 6. and ceramics.73) 3.65) 1.59) 3.70-3.52 (1.57) 3.61 (2.10) 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 1.40) 3.50 (1.01-7. The general population can be exposed to low amounts of barium in air.06-2.59-11.63 (5.50 (6.61-8.40 (1.35-1.81-2.46) 1.24-1.54) 1.12.70-5.90) 2.29-1. soluble forms of barium.97 (1.10) 5.45 (1.81-2.61 (3. Small amounts of barium can be released into the air during mining and other industrial processes.62 (1.53-5.73-5.75) 2.20-6.67) 6.10 (2.88) 7.04-2.35 (3.70-2.00-3.57-7.19-1.30 (5.61 (1. Barium salts have also been available as rodenticides.87-14.00-76.20-5.73 (5.62) 1.43) 6.17-1.00) 1.77 (3.55-7. it combines with other chemicals such as sulfur or carbon and oxygen.75-3.52 (4.36) 5.34 (2.64 (1.30-5.08 (6.50 (4.11 (3.51) 1.18) 3.15 (1.85) 1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. bricks.76) 1. Fourth National Report on Human Exposure to Environmental Chemicals 193 .37) 1.87 (5.78-2.05-2.71) 2.20) 2.70) 4.20-8.38 (1.56 (1.49) 4.26) 2.35 (1.30 (1.76-3.63) 1.10) 3.30-3.80 (2.80) 7.71) 95th 6.38) 8.78) 1. glass.28) 90th 5.48) 1.22) 6.86 (4.74-3.00-8.42 (1. 2001).20-8.65-5. and 03-04 are 0.30) 5.15-11.31 (2. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).55-3.39-1.47) 4.51) 2.32-7.90 (4.60) 4.66 (4.80-3. Barium compounds are used by the oil and gas industries to make drilling muds.08-8.50 (3.74-2.76-7.02 (7.99-5.63 (2.70-8.41-1.72) 75th 3.96-2..20 (3.30 (5.54 (6.68 (1.00) 1.70) 5.80-7.30) 8.35) 5.56) 4.50) 1.54) 1.88) 4.18-1.51) 7.00) 6.20-8.39) 4.57 (5.80 (1. tiles.40) 7.61 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.34) 2.15 (6.30) 4. respectively.44-5.11-1.20-1. such as brazil nuts.31.87-7.82-6. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80 (5.80-2.87-3.30-2.30-1.37 (4.31-2.1) 9.30-2.93 (4.60-6.25-1.71 (2.46) 1.50) 2.95 (4.63) Total 1.18 (6. and 0.76 (3.56 (1.16) 5.34 (1. depilatories.98) 1.29) 5.27 (1. 7440-39-3 Medically.35 (2.54-1.70) 1.90-9.56 (6.30 (3.86-5.16 (1.65 (5.36-1.05% of the earth’s crust.4) 6.44-2.60) 3.82) 1.65) 1.86-4.50-6.72) 1. and food.36-1.Metals Barium CAS No.63) 1.77-3.90) 2.37) 5.93-2.12.95-6.50-1.63 (8.g.86 (4. rubber.49) 11.30) 5.54-8.8) 9.70) 1.77) 1.87 (6.21-2.62) 1.60) 1.40 (4.41) 1.22-1.29-5.06-1.80 (1.10-5.38 (1.90 (1.69 (1.43 (1. In single dose animal studies.60-10.80 (2.33 (1. are high in barium (Genter.32-1.40 (1.90) 4.62 (1.50) 2.15-1.20 (1.53) 2.51 (1.49) 2. 01-02.35-1.27) 2.00) 4.78-3.40 (1. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.92) 2. In nature.80-5.45) 7.37-1.48 (6.60) 1.07 (2.66) Selected percentiles ( 95% confidence interval) 50th 1.09 (1.04-6.65-8.49) 8.25-11.73 (6.50 (4. Barium compounds are also used commercially in paint.87) 7.71-9.2) 6.39) 1.73) 1.47-1.81-3.36 (1.40 (5.54-1. see Data Analysis section) for Survey years 99-00.39 (1.50 (1.91) 2.24-1.71) 1.43 (5. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.37-8.8 (6.48-4.70 (5.85 (2.21 (1.11 (3.20-1.24 (4.50 (1.38) 2.74) 3. whereas others are practically insoluble (e.30) 2.80 (1.36 (4.56 (2.99 (4.53) 1.91) 6.50 (1.72) 4.54 (2.15) 5.70) 3. Certain foods.50) 4.88 (5.50 (5.61 (5. water.46-1. interval) 1.00 (1.19) 2.20 (4. Workers employed by industries that make or use barium compounds can be exposed to barium dust.40 (5.44 (1.22-1.85) 1.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.01 (4.14-6.70-2.03 (1.90-13.49 (1.80) 1.30 (2.49-9.60 (2.15-1.60 (1.20-1. population from the National Health and Nutrition Examination Survey.47-1.20-1.70-6.40-13.26) 5.43) 2.30) 5.12) 7.4) 7.63 (1.91 (2.26-7.84) 5.10 (3.09 (2. Some barium salts are freely soluble in water.26-1.40) 7.12 (2.60-6.8) 5.39 (1.4) 9.70) 7.60-2.30) 3.

80-6.51-3.96 (4.75-3.00 (3.49 (1.32 (1.61 (4.76 (3.25-11.76 (4.54 (2.97 (5.20 (1.58 (2.77) 1. hypertension.37-2.16 (1.710-1.20-1.25) 4.48-3.88 (2.53 (2.35-3.4 (5.81-7.51) 4.04) 5.39-10.68 (2.14-2.43-6.00-7.34-3.51) 4.56 (1.73-2.91 (3.70) 1.2) 6.26-1. chemical form.45-6.48) 2.02-5. Chronic high doses in animals resulted in kidney damage (McCauley et al.29 (3.59) 2.60 (1.47) 1.52) 2.11) .73-4.26-1.30) 2.8) 4.26) 4.51 (1.39 (2.10 (6.58) 4.00) 4.68-3. The health effects of exposure to barium compounds depend on the dose.46) 3.71 (5.60 (5.31 (4.36 (3.13-3.29-4.92) 2.24-1.23-2.55 (1.28) 5.54) 1.00) 6.19-1.99 (4.69-9.89 (2.33 (1.38 (1.91-2.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.832-1.34) 1.38) 1.51 (1.16) 11.29 (1.60 (1.34-1.5) 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 1.20) 4.57-7.09) 6.58) 1.2 (3.47) 4.703-1.36-2.79) 1.99) 1.28-11..34 (1.72 (2.41 (2.64 (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 2.48 (1.50 (4.22-4.50) 1.50) 2. water solubility.64 (1. and route of exposure.48-5.59) 1.91) 2.47 (5.77) 1.59 (1.3 (6. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.42) 1.00 (3.880-1.68-3.61) 2.29-3.36 (5.76-3.76) 2.75-22.881 (.24-6.29-1.23-1.31-1.62 (1.46) 1.41 (1.26-4. vomiting.754-1.01 (4.22-2.15-4.96) 4.28-7.08-2.11-2.97-3.03-1.56-3.55 (1.33-4.87) 1.33 (5.81-6.03) 2.00 (5.29-7.42) 1.10-1.44 (1.55) .36-1. paralysis.36 (1.32 (2. NTP.47 (2.06) 2.06) .39 (3.77-5.72) 6.82) 1.73) 2.33 (1. in urine.39) 4.31-1.46) 2.24-1.90-2.52 (3.86-7.38) 4.57-10. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.77) 5.55 (4. 2001).18 (1.0) 5.24-3.76 (2.S. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.26-1.97 (4.19-1.81-6.38-7.39-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 7.49 (1. weakness.26-1.38) 1.74 (5.21 (1.55-5.27-3.891 (.64 (1.921 (.79-5.68) 3.46 (2.55 (5.39 (2.30 (1.37-1.58 (4.25 (1.96 (4.33) 1.48 (1..77) Total 1.40 (1.57 (6.42 (4.28-6. 1985.60 (2.36 (3.03-1.63) 1. Insoluble barium salts.45 (1.02) 4.86 (2.39-5.08-1.76) 2.36 (1.18 (1. population from the National Health and Nutrition Examination Survey.Metals was eliminated primarily in feces and to a lesser extent.75) 1. 1990).24-6.49-1.46-22.40 (1. 1986).98 (2.84 (3.77) 1.59-7.38 (1.32) 2.57) 2.04 (2.51) 6.3) 6.0) 6.28-1.24) 3.65 (2.19-2.49-1. Barium is not rated for human carcinogenicity.74) 1.16-1.80) 3.57-5.83) 3.39-1.19-1.52) 7.00) 1.70) 4.45) 95th 6.47) 1.13-2.34-5.27-1.97-4.68) 1.41) 4.915 (.2) 5.84-5.38 (4.52-4.76) 1.67-6. a benign condition that may occur among barite ore miners.96-6.10-2. Toxicity from soluble barium salts is rare.38-1.963 (.02 (3.59) 1.45) 1.85-5. 1994.31) 5.64) 7.68 (3.56) 4.45-1.01) 1. and cardiac dysrhythmias.96) 4.35-1.05-1.50) 1.52-10.35-1.52) 1.82) 1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.83) 2.03) 1.69 (5.68 (3. interval) 1. 1984.48 (1.10) 6.92 (4.00 (2.22-1. diarrhea.41) 5.03) 3.27 (2.41 (1.31 (1.29-4.64) 7.36-1.60 (2.4) 5. Symptoms following acute high dose include perioral paresthesias.56) Selected percentiles ( 95% confidence interval) 50th 1.27) 7.40 (1.96) 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.62 (2.38 (4.24 (5.37 (1.53) .65 (5..91 (3.58-6.62) 2.12) 2.905 (.11) .04) 1. Perry et al.33-1.64 (1.96) 7. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis. 1989).38-5.27) 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 .58) 75th 2.47-8.39 (2.777-1.99 (2.30 (1.74) 1.49-1.55-6.37) 2.56 (1.44-2.97) 1.66 (1. Following intravenous injection in animals.72) 4.80) 4.54) 2.22-1.45-1. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves. are not absorbed when administered.37 (1.00-1.63-4.88 (6.20-8.75) 2.33) 6.47) 10.70) 10.45 (3.78 (2. such as those used in medical radiographic procedures.02) .23-5.24 (3.89) 90th 4.75) 2.53-21.20-2.24-11.40-1.01 (5.51 (3.00) 4.43) 1.62 (4.44-2.45-8.32) 2.86) 5.59 (1.84-2.32 (1.31-1.28 (1.48-1. Wones et al.75) 1.54 (1.29) 1.84) 2.10) 3.

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

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.346 (<LOD-.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. population from the National Health and Nutrition Examination Survey. 2002). Skin exposure can result in delayed hypersensitivity reactions. 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 . Chronic beryllium disease. based upon excess lung and central nervous system cancers in studies of workers.273) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .231 (<LOD-. EPA. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. S. 1990).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 . or berylliosis.281 (<LOD-. respectively.391) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine. IARC has classified beryllium as a human carcinogen. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. Maier. and drinking water and environmental standards have been established by U. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. NTP considers beryllium to be a known human carcinogen. Fourth National Report on Human Exposure to Environmental Chemicals 197 .. 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. including contact dermatitis and subcutaneous nodules.S. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2003. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure.

McCanlies EC. blood. VI. environmental levels) and health effects is available from ATSDR at: http://www. Available at URL: http://www. Howerton K.12 to 0. Third National Report on Human Exposure to Environmental Chemicals.. Minoia et al. Given these results.cdc. and 2003-2004. In other studies.157:388-398..95:89-105.S. 2001).html. Environ Res 1998.inchem. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures.gov/toxpro2. Comparison of representative ranges based on U. Gallorini M. and serum of Italian subjects. Genetic and exposure risks for chronic beryllium disease. Paschal DC. Sabbioni E.13 μg/L. They reported urinary beryllium levels ranging from 0. A study of 46 elements in urine. patient population and literature reference intervals for urinary trace elements. Levels of beryllium in urine for the U.23:827-839. and the fact that most NHANES participant levels were undetectable.. Paschal et al.. Pietra R.atsdr. Beryllium [online]. Andrew M. Ash KO. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Maier L. Jackson RJ. et al.e. Kriess K. less than 0.org/documents/ehc/ehc/ ehc106.htm. Review of elements in blood. 1990. Hamilton EI. 3/27/08 Komaromy-Hiller G. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Am J Epidemiol 2003.Metals (i. Trace element reference values in tissues from inhabitants of the European community I. Hamilton et al. 106. Ting BG. Weston A. Sci Total Environ 1990.76(1):53-59. Int Arch Occup Environ Health 2001. Element reference values in tissues from inhabitants of the European community. Sci Total Environ 1994.. Trace metals in urine of United States residents: reference range concentrations. 20012002. 2000. Environmental Health Criteria. Minoia C. Clin Chim Acta 2000. Costa R.74:162-166.e. Atlanta (GA) 2005.296(1-2):71-90. which approximate this Report’s limit of detection. Pozzoli L. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Pirkle JL. Morrow JC. 1998). 0. HLA-DPB1 and chronic beryllium disease: a HuGE review.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Apostoli P. Schaller KH. Clin Chest Med 2002. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Van der Venne MT. population are lower than levels in workers.S.S.158:165-190. Sampson EJ. References Apostoli P. 198 Fourth National Report on Human Exposure to Environmental Chemicals . urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al.1 μg/L). Centers for Disease Control and Prevention (CDC). et al. 1990. population were generally undetectable in NHANES 1999-2000. it is likely that urinary beryllium levels in the U. and the 95th percentile for males in NHANES 2001-2002. 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. Sabbioni E. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. International Programme on Chemical Safety (IPCS).

235 (.S.300) .300-.900 (.900-1.426-.00 (.500 (.403) .500-.300-.200-.412 (.255) .500-.600 (.400) . 7440-43-9 General Information Cadmium is a soft.00-1.600-.424) * .400 (.300 (.700-1.403 (.10) 1.400) .70) 1.600) 1.00-1.60 (1.20) 1.20) 1.400 (.10 (1. as zinc sulfide) and to a lesser extent.425 (.20) 1.60) Total * .20) 1. malleable.400 (.40-1.50) 1.300 (.300-.900-1.600) .700-1.00 (.300-.300-.449) Selected percentiles ( 95% confidence interval) 50th .600) .20 (.368-.10 (1.500-.200 (.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 .50-1.500 (.266-.400-.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 * * * * * * .275-.500-.20-1.50 (1.300 (.S.30-1.393 (.600) 90th 1. 0.500) .289-.300-.300 (.10 (1.359-.300-.500-.3.700) .300-.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .400) < LOD < LOD < LOD . respectively.362-.40 (1.600) .500-.40 (1.600 (.400 (.300-. during refining of lead and copper from sulfide ore.10 (1.500-.50-1.600 (.421 (.800) .376-.500 (.50) 1.200 (<LOD-.30) . Fourth National Report on Human Exposure to Environmental Chemicals 199 .600 (.300-.00 (.400 (.00-1.80 (1.60 (1.400 (.427) * .400 (.00-1. EPA.20) 1.600 (.400) .20 (1.300-.30) 1.30) 1.00 (1.300 (.400) < LOD .400) < LOD . population from the National Health and Nutrition Examination Survey.70) 1.800 (.90) 1.300 (.367-.600 (.70) 1.600 (.300 (<LOD-.700 (.800 (.600) . interval) .400) .600 (.80) 1.200-.300 (<LOD-.00) .gov/minerals/pubs/commodity/cadmium).400-.200 (.500-.386-.60 (1.344) .300) .600 (.300-.400-.200) .10) 1.20-1.300-.600 (.400-.700) .395 (.366) * * .60 (1. and 03-04 are 0.200) .300 (.300 (<LOD-.500-.500-.441) * .00 (.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.40 (1.600 (.400 (.500 (.300) .500 (.304 (.900-1.300) .30-1.700) .10) 1.3.900-1.10 (1.500) .382 (.600) .300 (.400 (.00-1.10 (.400) .20-1.60) 1.800) 1.400-. and nonferrous alloys. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.400) .400 (.800) .216-.700-1.400-.800-1.20) 1.300-.300) .700) .300) .500) .400-. and 0.600 (.300) .500-.00 (. The predominant commercial use of cadmium is in battery manufacturing.60 (1. 01-02.300) 1.10) 1.50-1.283 (.50 (1.398) < LOD < LOD < LOD < LOD < LOD < LOD .470) * .900-1.333 (.300 (<LOD-.10) 1.00 (.900-1.300-.40) 1. lead.00-1.304 (.20) 95th 1.300-.400) .500 (.60-1.500-.400) .900-1.700) .900-1.500-.600) .00 (.400) .300) .400 (.900-1.600) .500-.400 (.900 (.500-.361-.700) 1. and incineration of municipal waste materials.20) .800-1.300 (.20) 1.400 (.300) .513) .00 (.300-.20-1.S.600-.452) .00 (.50) 1.60) 1.10) 1.60) 1.700) .Metals Cadmium CAS No.40-1.00-1.200 (<LOD-.600-1.400) .400 (.500) . bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.20) . U.usgs.300-.460) .300 (. plastic stabilizers.20) 1.313 (.300-.700) .00 (.300 (. Other uses include pigment production.500-.20-1. coatings and plating.70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .400-.300 (.30) 1.600-.00-1.20-1.600) .296-.400) .337) .400) .300-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00.40) 1.420 (.80) 1.900-1.30 (1.40 (1.304-.40 (1.300) .500) . Cadmium also may be emitted into the air from zinc.14.326 (. or copper smelters (U.400 (.200 (.400-.00-1.500 (.10) 1.400 (.500 (.600) .300) 75th .200-.50-1.30-1. which may vary for some chemicals by year and by individual sample.50 (1.40 (1.600 (.00) .300-. Since 2001.30-1.700) .500-.200-.500) .400 (.30-1.400-.400) .500 (. cadmium use has declined in response to environmental concerns (http:// minerals.400-.400) < LOD .300-.70) 1. < LOD means less than the limit of detection.600 (.468 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.10 (1.500-.200-.10 (1.300) .300 (.50 (1.400) .378 (.40 (1.20-1.309-.00 (1.10) 1.500) .300) .331) .378-.

72) 1.220-.813 (.38) .115-.607) .15) 1.210 (.790 (.067-.277 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.433-.83) 1.800 (.160 (.295) ..300) .490) .211 (.860) 1.06.191-. Cadmium is absorbed via inhalation and ingestion.306 (.220-.940-1.221 (.230 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg. potatoes.530 (.210 (.400-.890 (.195-. 2004a. 2003).198) .196-.390-.03) .350 (.202-.214-.714-1.114-.818 (.490) 1.203) .596) .886) .190-.519) .28) 1. rice.476-.980) .06) .165-.475 (.748-1.170-.189) .12 (.210) .230) 75th . Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.470-.963-1. Inhalation of cigarette smoke is a predominant source of exposure in smokers.243-. and various seeds.06.700-.090) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.551) . 1999.336) .387) .112-.326) .189-.226) . wheat.209 (.272-.539) .530) .25 (1. calcium.060-.20 (1.481) .989-1.870) .265 (.43) 1.01) .440 (.37) 1121 1335 1277 1136 1355 1266 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 .551 (. drinking water is a source for cadmium intake.240-.299) .492 (.456-.260-.192-.249-.263) .10 (1.177-.886-1.284) .179-.310) .257) .260-.261-.741-1.229) .320) . Kikuchi et al.820-1.972 (.493-.980) . however.210 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.187 (.763-.04 (.510-.240) .479) .061-.167-.733-. With chronic exposure.199 (.237-.559 (.232 (..280 (.01-1.270 (.191 (.190-.12-1.262) .110-.28 (1.219 (.430) .980-1. see Data Analysis section) for Survey years 99-00.090) . 2003).220) Selected percentiles ( 95% confidence interval) Sample 95th 1.128 (.220) .806) .235) .150) . Cadmium in soil is absorbed by plants.38) 1.184-.308) .175 (.210 (.74) 1.447 (.265) . respectively.360) .151-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .817 (.078 (.28-1.20 (1.545 (.51 (1.466 (. population from the National Health and Nutrition Examination Survey.13) .260 (.170 (.211-.231) . 2003).160) . cadmium accumulates in the liver and kidneys where it is bound to metallothionein.836-1.193 (.221) .733) . 01-02..810-1. including many food crops such as cereal grains.180 (.372) .222) .22 (.160) .157) .087-.249) .** Survey Geometric mean (95% conf.426 (.279 (.06.960) 1.977) .848 (.077 (.200-.339) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.233) .238) .313) . To a lesser extent.875 (. 2001).208-.455 (.204 (. 2003.450 (.289-. Renal tubular and glomerular damage.148) .880) . Diamond et al.700-.290-.06-1.171-.203 (.390 (.458 (.34) 1.130 (. 0.193-.181 (.135 (.980-1.354) .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.134) .153-.234 (.24) 1.140 (.790 (.09-1.440 (.462 (..229) .316 (.820) 1.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .990) .251) .48 (1.227 (.800-.633 (.270 (.30-1.351-..633-1.540) .17 (.169-.753-.440-.329 (.817 (.273 (.194-.077 (.430-.281 (.141 (.918-1.20-1. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.01 (.121 (.241) .100-.507) .157-. an inducible metal binding protein.282 (.717-.191-.230) . Horiguchi et al.500) 90th .216 (.233) .713) .081) .15) .366) .065-.200 (.381-.207-.580) .067-.201 (.452 (.17 (.136) . a factor that may contribute to the higher absorption of cadmium by women (Diamond et al. and 0.109 (.17 (.192-.482) . 200 Fourth National Report on Human Exposure to Environmental Chemicals .S.202 (.32 (1.Metals 2000).640) .107-.875) .170-.52 (1.175 (.388-.04 (. ingestion through food is the largest source of exposure.255) .820 (.061 (<LOD-.892 (.686-.283 (.190-.20) 1.150-. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.302 (.220 (.173) .390-.36) 1.092) .366-.07-1.238-.19) 1.239 (.82) 1. and 03-04 are 0.210 (.247) .450 (.183-.498-.20 (1.445 (.15 (.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 .101) .705-.680 (.855-1.623) .219 (.47) 1.310 (.480) .730-.092 (.120 (.160-.960 (.255) .. whose body burdens of cadmium can be approximately twice that of nonsmokers. copper) and protein.206) .02-1.17) .232) .766 (.500) .189-.589 (.261-.38) 1.412) .200-.550 (.57) 1.300 (.366-.38) .394-.519) .980 (.255) .520-. zinc.126) .22 (1.330-.436-.892-1.109-.322 (.858 (.178-.890-1.919) .285-. 1994).700-.219 (.135-.362) .510) .229-.200 (. For nonsmokers who are not exposed to cadmium in the workplace.253-.839 (.843-1.610) .41 (.327 (.400-.06-1.206 (. interval) .393-.210) .246) .223 (.13 (. Cadmium absorption may be increased with iron deficiency (Berglund et al.13-1.445 (.257-.25) 1.080 (.148-.423-.

184) .071 (.941 (.091) .00 (.667) . most often a result of occupational exposure (Roels et al.631) .501 (.38) .795) 1. 1996.688-.311) .350) .241) .253) .187) .293-.560-. 2002.084-.093 (.136-.212 (.919 (.696-.757 (.931 (.484 (.177) .387 (.168-.194-.08) .470) .308 (.240) . 2002.097) .335 (.274) 1.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .289) .906) .876-1.181 (.191 (.156) .440) .607) .173-.404 (.391-.940 (.827) .536 (.147-.381-..388-. can result from high dose chronic exposure.304-.200 (.712 (.09 (.856) .137 (.382) .591 (.163 (.343-.205 (.377-.487 (.336-.219 (.884) .07) .077-.268 (.075-.255-.270 (.227-.170-.247-.308) .135) .783) .830) .219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .476) .084 (.207) .806-1.219 (.247-. Horiguchi et al.136-.123-.226) 75th .159 (. 1999).950) . 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.985 (.191-.690 (.154 (.678-.784) .253 (.201-..130-.137-.979 (.240) .614) .490 (.228-.235) .. 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.281) .414 (.204-.185) .622 (.234) .242) .154-.267 (.267 (.182) .404) .273 (.412 (.210 (.418) .653) .232) .479 (. interval) .146-.101) .340) .331 (.157-.541) .718 (.757) .725-1. 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.562-.263-.507-..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.700) .074-.147-.740 (.261-.288) .438) 90th .929) .190 (.917 (.198) .261 (.098) . Fourth National Report on Human Exposure to Environmental Chemicals 201 .190 (.176 (.321) .174-.470) .325 (.719 (. Olsson et al.234 (.645-.220 (.107) .398-.266) . 1999).818) .690-.222-.491-.216-.211 (.063-.143-.434 (.02 (.215 (.143-..067-. 2004).183 (.150-.181 (.106) .210) .826-1.856 (.833-1.07 (.236-.16) .183) ..085 (.318 (.850) .232) .426-.225) .500-.13) .813-.184-.551) ..338 (. population from the National Health and Nutrition Examination Survey.182) .382-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.303) .083-.094) . At lower environmental exposures.687 (.289) .206-.708-1.143) .171-.850) .691-.716-.927-1.178-.261) .813-1.779 (.700 (.147 (.533) .184-.159 (.123-.300-.538) .209) Selected percentiles ( 95% confidence interval) Sample 95th .288 (.686 (.157-.518) .617 (.224 (.104) .096) .187-.716) . 2000.329 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.175 (.472) .245 (.05) 1. 2002.199 (.449) .176 (.208 (. 1999).166 (.126 (.090 (.423-.113-. However.668-.767) .091 (.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 .144-.229) .722-.481 (.196 (.00 (.075 (<LOD-.085-.316 (.909-1.250) .473 (.170 (.252 (.415) .998) .10) 1.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.278) .156 (.178) .418-. During the 1950’s and 1960’s.281) .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 .304) .175-.297) .140-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.917) .282 (.208-.122 (.12) 1.263 (.221 (.086 (.100 (. 2004b). Staessen et al.223) .162 (.441-.192) .545) .873 (.678 (.131-..225) .729 (.17) .432 (.288-.06 (.630-.727-.238-.962) .690-.239-.292) .789 (.647-.444-.156-.663 (.650-.537-.769 (.181-.163) .830-1.210 (.161-.191) .104) .674-1.280 (.181) .202 (.218) .209) .173 (.112) .839) .423 (.792 (.802 (.175 (.111-. 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.168 (.440) .189-.148 (. 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.221-.421 (.433-.078-.828) .387-.234-.247-.826-1.091 (.516-.266-. Noonan et al.051-.256-.438-.666-.352) .283 (.078 (.531 (.818) .783 (.16) 1.940-1.233 (.207-.185 (.238) . 2003.S.158-.767 (..414-.197-.865 (.754) .431) .140-.168-..687-.446) .693 (.874-1. Jarup et al.364) .** Survey Geometric mean (95% conf.182) .296 (.559-.316) .199-.

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

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. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Fayers PM. Komaromy-Hiller G. Stock AL. Ukai H. Ezaki T. Chislovska NV. Consonni D. Oguma E. diabetes mellitus. population. Howerton K. Toxicol Lett 2004. Bo M. Comparison of representative ranges based on U. Gadea E. Zhu G.html. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Thorax 2004.atsdr.102:83-89. ShkiryakNizhnyk AZ. Kaus S. Oguma E. possibly better than b2microglobulin. Darbyshire J. Vahter M. Bellerup P. Environ Res 2004. et al. Ash KO. iron deficiency.1(8587):663-667. Elinder CG. environmental. Pickering CA. Greves HM. Lancet 1999. Ikeda Y. Int J Hyg Environ Health 2002. Davison AG.96:353-359. Holguin F. Lidfeldt J. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Nermell B. Kumagai N. Dekio F. Seiwert M. Toffoletto F. Thayer WC. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Mannino DM. Hotz P. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Fukui Y. Fatal chemical pneumonitis due to cadmium fumes. Buchet JP. Tsukahara T. Carlsson MD. Toxicol Appl Pharmacol 2004a. Choudhury H. Environ Res 2004b. Krause C.57:668-672. Savage-Brown A. Taylor AJ. Toxicological profile for cadmium update. Jarup L. et al. et al. et al.76:186-196. Mascagni P. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Kundiev YT. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. patient population and literature reference intervals for urinary trace elements. Ikeda Y. Kikuchi Y.148(1-2):11-20. 206:15-24. Grubb A. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10.59:194-8. Seiwert M.S. Becker K. Machida M. Okamoto S. Schulz C. Mucha A. Sanz P. Persson B. Nerbrand C. Jones RL. Serra J.000 women in the Japanese general population: a nationwide large-scale survey. Neurotoxicology 2003. Hellstrom L. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Clin Chim Acta 2000. Moriguchi J. 4/8/09 Alfven T.95:20–31. Horiguchi H. Becker K. Fukui Y. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.45:43-52. Lauwerys R. Environ Health Perspect 1994. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Int Arch Occup Environ Health 2003.59:497]. Sasaki S. et al. et al. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.24:717-724. Bernard A. Bregante G. Occup Environ Med 2000. Horiguchi H. Berglund M. Alfven T. Vahter M. Atlanta (GA). Agency for Toxic Substances and Disease Registry (ATSDR). Moriguchi J. et al. Cadmium fume inhalation and emphysema. J Occup Health 2003. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Comprehensive study of the effects of age. Nomiyama T. Costa R. 1999 [online]. Environ Res 2006. et al. Ye T. Takebayashi T.66(Pt A):2141-2164. J Toxicol Environ Health 2003. Lepom P. Lukyanova EM.296(1-2):71-90.110:699-702. Palomar M. Furuki K. Diamond GL. Available at URL: http://www. Venables KM. Third National Report on Human Exposure to Environmental Chemicals. Miyamoto K. Miyamoto K.13(11):1627-1631. 102:10581066. Uemura T. Ezaki T.46:372-374. Akesson A. Schulz C. Anthropometric. Environ Health Perspect 2002. Friedman LS. Sasaki S. Seifert B. Lundh T. Nordberg G. Jin T. 2005.cdc. 196:114-123. et al. References Akesson A. Jarup L. Kaus S. Occup Med 1996.205:297-308. Lancet 1988. et al. Int J Hyg Environ Health 2003.gov/toxprofiles/tp5. Furuki K. Fernandez MA. Centers for Disease Control and Prevention (CDC). Lison D. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Machida M. Tsukahara T. Environ Health Perspect 2005. Wang H. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Chiappino G.S. et al.354:1508– 1513. Olfactory function in workers exposed to moderate airborne cadmium levels.

Honda R.30(5):395-399. Revised 2000 [online]. Staessen J. Emelianov D. Environ Res 2006. Nordberg GF. 4/8/09 Waalkes MP. In: Clarkson TW. Wang JX. dietary intake. 2004. Merlino MV. et al.html. Vangronsveld J. Liu QF. Cadmium in blood and urine – impact of sex. Cadmium carcinogenesis. age. et al. Hazard Summary. Honda R. eds. 151-168.epa. Mueller PW. 204 Fourth National Report on Human Exposure to Environmental Chemicals .533(12):107-120. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. pp. lead. 2001. Gallmans G. Fan YG. Ren Fail 1999. and risk of fractures: prospective population study. Mutat Res 2003. Nakagawa H. Schwenk M.gov/ttn/atw/ hlthef/cadmium. Relationship between newborn size and mother’s blood cadmium levels. Bruiglia S. Skerfving S. et al. Tanebe K. Environ Health Perspect 2002.353:1140-1144. Nakagawa H. et al. Ottosson H. Tawara K. Tanebe K. Suwazono Y.39:2507-2515.110:151-155. Cadmium compounds. Roels HA. Lancet 1999. created 1992. Oskarsson A. et al. Biological monitoring of cadmium. Roels HA. Okubo Y. Nakagawa H. EPA). Lybarger JA.100:330-338. lead. J Cardiovasc Risk 1996.110:1185-1190. et al. Time trends in burdens of cadmium.S. Staessen JA. Usefulness of biomarkers of exposure to inorganic mercury. Kathman SJ. Saito S. Wennberg M. Zhang YL. J Environ Sci Health B 2004. Int J Hyg Environ Health 2006. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. cadmium. Friberg L. iron status. Environmental exposure to cadmium. Roels H. Wilhelm M.209:301305. Lundh T. Minciullo PL. 2000. Lison D.21(3-4):251-262. Noonan CW. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. Sager PR. and former smoking – association of renal effects. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Kido T.3:26-41. Revised and new reference values for arsenic. Zhao YC. Thijs L. Available at URL: www. Zhu HD. J Perinat Med 2002. Nordberg GF. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Schultz C.Metals Nishijo M.84 (Section A):4455. Sarasua SM. United States Environmental Protection Agency (U. Japan. forearm bone density. and mercury in the population of northern Sweden. Kuznetsova T. Toyama. lead. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Bensryd I. Stegmayr B. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Nordberg M. Nogawa K. Salpietro CD. Jansson J-H. Gangemi S. Occup Environ Med 2002. Environ Res 2000. Stelitano A.59:394-397. Biological monitoring of toxic metals. Kobayashi E. Lauwerys R. Bergdahl IA. Arch Environ Health. Ginucchio G. New York: Plenum Press. Olsson IM.59(1):22-25. Environ Health Perspect 2002. Hoet P. Buchet JP. Campagna D. Lijnen P. Nishijo M. Lundh T.

57-5. the body half-life is estimated to be 70-109 days based on 137Cs exposures.91-8.1) 9.87 (4. However.40) 7.26) 7.5-14.03 (4.98 (7.55 (7.70 (6.2 (9.2-13.05) 5.97 (7.47-8.62 (5.1) 11.96 (6.12-11.02 (4.00) 7.80 (8.90 (4.87 (4.60 (8.59-5.7 (8.40-5.6 (9.3-13.68) 9.00-8.14.40) 5.Metals Cesium CAS No.91 (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. Little is known about the health effects of this metal. infrared lamps.33 (6.0) 12.64-5.20-7.27 (7.99) 9.42-7.10-8.9 (11. nausea.53-11.93 (4.86 (7.7-14.40-5.7) 11.00) 4.60-5.66 (7.95) 5.94 (4.1 (10.3) 10.88 (8. Most human exposure to cesium occurs through the diet. and clay.77 (4.76-6.84-9.0) 11.1-13.0) 10.20-8.7 (9.08) 7.81 (4.8) 12.80-11.40 (4.7) 10.25 (3.3) 10.98 (7.33-5.20) 4.04 (4.50) 5.9) 8.9 (11.7) 11.94-4.70 (6.62) 4.89) 4.5 (8.70-8.8 (10. although cesium was generally of low toxicity when given to animals.80) 7.50) 9.54) 4.04) 7.90) 5.6) 11.60-7. 01-02.81) 4.52-9.83) 6.55-11.9) Total 4.70-5. Inorganic cesium compounds are used in photomultiplier and vacuum tubes. and high-power gas-ion devices.71-9.08 (6.26 (3.56) 5.56-11.90-10.72-7.8) 12.90-10.62 (5.60 (7.27-5.60-7.S.27) 4.00-4.49) 4.8) 11. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.43 (5.6 (11.59) 7.3) 10.23-4.59-5.1-12.80-10.5 (10. respectively.30-5.36 (3.7) 10.20) 5.52) 7.84 (4. photographic emulsions.13 (7.6 (9.9 (11.90-8.46) 7.30) 5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.47-4.84-5.10 (6.0-13.16-6.12) 5. diarrhea.74-5.44 (8.13 (8.69-6.80 (4. scintillation counters.71 (4.8 (10.9) 11. 0. and as polymerization catalysts.82) 5.81-14.5-14.08-5.79 (4.22-4.10-5.07-11.21) 90th 9.64) 4.74) Selected percentiles ( 95% confidence interval) 50th 4.80-6.90-12.70) 5.49 (4.4) 9.95 (3.34) 9.3) 10.20-4.50 (4.9) 12. Whether cesium compounds are carcinogenic is unknown.61-6.1 (9. soil.20 (6.17-6.30 (6.71-5.7 (9.13-8.99) 7.8 (11.8-13.26-11.12-5.64) 5.73-11.87-7.01-6.00-8.83-4.72) 4.4 (10.39-4.31-8.8) 9.99-6.33 (5.68 (7.0) 12.60) 5.99-11.94) 4.4 (9.90-12.2-12.90-10.30) 7.8) 11.80 (4.2-13.29) 4.00-9. cesium hydroxide is corrosive and irritating at high concentrations.81) 4.80-10.32 (3.86-11.38) 5.97-7.10-9.43-8.3 (8.80-13.7 (10.22 (4.92-13.40-11. Fourth National Report on Human Exposure to Environmental Chemicals 205 .54-11.97) 4. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.3 (8.90 (6.05-5.74 (4.20) 7.84) 8. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.50 (6.73-5.39) 7. and 03-04 are 0.4) 12.80 (8.59-5.89) 5.32-5.34 (4.56 (4.70 (4. interval) 4.37) 5.60) 7.5-13.90) 7.6) 10.00) 6.7 (11.90) 5.67 (4.50-7.50 (7.70) 7.49) 75th 7.1-12.5) 10.9 (10.77-8.15-8.9 (10.63) 6.5) 12.50 (4.84) 5. see Data Analysis section) for Survey years 99-00.1 (11.71-8.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.16-6.40-7.70) 5.81) 9.60-12.9 (11.0) 12.90) 9.4-13. 2004).5) 9.63-4.01) 7.8) 12.50 (4.10 (8.2) 11.80 (4.10 (8.4) 95th 11.3) 9.70 (8. and cardiac arrhythmia (ATSDR.40-11.1) 10. Radioactive 137Cs has been used medically to treat cancer.03 (4.40-5.87 (4.30 (6.6 (9. semiconductors.86-12.4) 10.14.70 (9.49 (5.20 (4.64 (4.64-10.70 (8.36) 3. For absorbed cesium salts.77 (9.32) 4.3-15.00 (7.07) 4.4) 12.14 (4.2 (9. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.01-8.45-5.09) 5.70 (5. population from the National Health and Nutrition Examination Survey.90) 4.13 (5.25-5.8) 9.63 (4.10 (6.35-5.60-6.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.29 (4.20) 8.4 (9.37) 7.0 (9.1) 9.2-14.35 (4.09-5.23) 9.6 (9.08 (7.10-7.71) 4.3-13.71 (8.20-5.2-13.21 (4.0 (10.5-16.94 (4.56 (4.03-4.26) 4.17) 4.59 (5.0) 11. and 0.82-4.1) 11.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4.05) 5.0-15. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.17 (6.61) 7.7 (10.00-10.40-5.99-11.60-6.4) 10.89-5.40) 5.80-10.12 (4.45-8.80 (8.42) 7.60) 7.42) 6.35 (4.08-5.95-4.36 (6.77 (9.87) 5.64) 5.24) 4.7 (10.2) 12.0) 9.53 (6.6 (11.25) 4.4) 11.3) 12.7 (9.05-5.2.30-10.55 (4.

8) 10.37) 4.35-7.95) 4.7-12.06 (5.53 (4.30 (4.08) 4.09) 8.33 (5.29-3.07-4.99-4.30-4.43-11.11 (5.56 (4.03-6.54 (5.95) 8.84-11.07 (5.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.00) 6.20) 5.35-11.42-6. 2005.87 (5.S.61 (7.36-10.08 (6.43 (3.74 (5.00 (8.99-9.54 (4.67 (5.99 (3.68-11.05) 3.65 (6.98 (6. interval) 4.22 (3.05-3.8) 5.0) Total 4.93-9.64 (8.65-4.93-7.66-6.38) 10.75-11.14-6.24-10.04-11.51) 4.72 (4.50) 8.57) 3.91-7.0) 7.79-5.03-5.58 (6.64) 4.83-6.2 (8.00-9.27 (6.78) 4.16-8.46 (8.09) 4.33 (5.04) 5.64 (4.63 (7.39 (5.63-6.3 (10.71 (7. Minoia et al.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 3.87-4.64-6.44 (8.84-7.92) 3. Komaromy-Hiller et al.02 (5.08-7..9 (10.00-5.2) 11.60) 3.88-10.17-4.13-9.36-3.41-7.48-6.56-10.63 (6.22) 6.18-7.88-4.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5. Two small studies of European populations reported urinary cesium levels similar to U.50 (7.28) 7.07) 8.27 (8.1) 11.38-7.46-8.S.3) 9.99-9.39) 8.79) 6.7) 10.63-6.42 (4. (2000) found urinary cesium levels that were slightly lower than those reported for the U.53) 6.3) 11.41 (5.10) 7.30 (7.08) 4.26 (3.28 (4.18-6.34 (5.72) 4.14) 4.21-4.27 (6.3 (9.04-5.78 (3.3-15.81 (4.16-5.25) 4.95 (5.9) 10.74-11.19-6.82) 7.70) 7.06) 4. population.14-7.43 (4.59) 4.94 (5. and were also roughly similar to those in this Report.52-5.77 (6.17) 4.43 (8.28 (5.20-4.46 (7.05 (4.90 (7.97-5.08 (5.55) 4.13) 7.0 (7.27-4.60-10.17) 9.82-4..97-4.30 (3.27-6.08) 3. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect. 2004).79) 9.51 (3.91-6.44) 3.31 (4.44-5.47) 6.13 (3.92 (5.61-3.38 (3. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.39) 5.15-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.46) 6.4) 10.5 (9.07) 8. 1990).78 (3.21-5.95 (3.5) 9.43) 8.76-6.90-8.09 (4.05) 6.40) 7.53) 3.06) 5.03) 5.95-6.74) 3.15) 95th 8.80) 6.85) 4.44-9.29-3.98) 5.72-5.43 (4.73-4.85) 5.99) 4.01-8.00-4.95) 10.91) 4.33-8.00-5.90-3.96-4.38-12.56) 4.91 (5.5) 9.47) 4.91-9.98 (7.55 (3.79) 4.50 (6.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .14 (6.53 (6.11 (5.76-9.26-6. Using clinically submitted specimens.40-5.31-4.58) 3.64) 9.6 (9.62-8.13-9.29) 4.98) 5.67) 5.17 (6.41) 4.65-3.30-4.77 (4.78) 4.49) 3.83-7.79 (5.87) 5.91) 5.54 (3.37-3.22-11.90-8.47) 7.41 (8.60 (3.08 (3.27) 4.35 (3.84-9.64) 5.68 (4. population from the National Health and Nutrition Examination Survey.16-8.62) 5..66 (5.48) 7.30) 10.26 (4.59-8.31-6.29) 4.41-4.60 (5.36-6.60-20.91) 5.50-5.56) 3.84-7.S.5) 7.63) 6.30) 10.12-6.77 (7.35) 3.68) 6.10-4.74) 75th 5.04) 6.14) 4.41) 9.2 (8.51 (4.20-4.15 (7.50 (5.51 (4.94) 7.66 (6.33-3. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.48) 90th 7.29) 5.47) 6.10 (3.10 (5.05-4.58 (4.31 (4.05-3.18) 8.12) 3.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.42 (5.75 (7.68) 4.12 (3.20-4.23 (7.50) 4.96) 4.21-3.25) Selected percentiles ( 95% confidence interval) 50th 4.85-4. 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.45-6.18 (7.7) 10.56) 4.10 (3.14-4.50) 4.08-3.20-8. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.24 (3.89-4.95-12.51 (3.70) 6.41 (4.73 (3.46-4.06 (3.96-4.16) 5.96 (4.86 (4.54 (4.70 (7.44 (4.75 (6.42-4.81 (4.40) 6.38 (3.3 (8.97) 8.96) 4.19-3.63 (4.83) 8.15-11.74 (4.91 (5.28) 8.58-5.9 (9.02-4.55-5.6) 6.6 (9.45 (4.42-4.84-9.00-8.03) 6.47 (7.67 (6. population results shown in this Report (Alimonti et al.68) 3.50) 4.77) 4.8) 6.77-5.51 (7.47 (4.00-10.71) 6.66 (5.35 (4.21 (2.24-4.58) 8.8 (9.43-6.

Forte G. Pietra R. Ronchi P. Sabbioni E. J Expo Anal Environ Epidemiol 2004. Gallorini M.296(1-2):71-90. Sci Total Environ 1990. Howerton K. Atlanta (GA) 2005. Wolfe MI.19:3131-3138. Gatti A. et al. Voorhees RE. Rapid Commun Mass Spectrom 2005. Trace element reference values in tissues from inhabitants of the European community I. patient population and literature reference intervals for urinary trace elements. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. Spezia S. and serum of Italian subjects. Komaromy-Hiller G. Clin Chim Acta 2000. et al. Costa R.gov/toxprofiles/tp157. cesium.cdc. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Available at URL: http://www. Toxicological profile for cesium. Mott JA. Paschal D. Wood CM. Ash KO. Pozzoli L. Mincione G.2004 [online]. 2000. blood. Third National Report on Human Exposure to Environmental Chemicals. Centers for Disease Control and Prevention (CDC).Metals References Agency for Toxic Substances and Disease Registry (ATSDR). antimony and tungsten.S. Minoia C. A study of 46 elements in urine.html. Assessment of urinary metals following exposure to a large vegetative fire. Apostoli P.atsdr.95:89-105.14:120-128. Comparison of representative ranges based on U. et al. Sewell CM. New Mexico. 4/8/09 Alimonti A.

316-.03) .390-.350-.430) .830-1.870 (.36) 1.900-1.59 (1.850) 1. Cobalt occurs naturally in airborne dust.454 (.790-. 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.570) . 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.520) .410 (.640) .570 (.02-1.291-.410 (.352 (.890) .320 (.460-.583) .540-. diamond-polishing wheels.424) .431) .450-.419) Selected percentiles ( 95% confidence interval) 50th .330-.372) .650 (.64) 1.416) .770) .26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. hard metal or in combination with other elements.380-.37-1. Cobalt compounds are used as catalysts in producing oil and gas.550 (.800) .355-.428-.910-1.348-.810) .16 (1.19) .750 (.450) .03) 1.410) .390) .46 (1.310 (. 208 Fourth National Report on Human Exposure to Environmental Chemicals .47 (1.460) .560 (.22-1.393-.12) 1.388-.390 (.44) 1.930 (.01 (.390 (.16) 1.670-.32 (1.09) .370 (.790) .270-.710 (.330 (.06 (.343 (.543) .820 (.350-.690-.50) 1.740-.399) .331-.47) 1.900) .53) 1.333-.680 (.520-.16 (.540-.313) .290-.750 (.340) .523) .520 (.65) 1. respectively.850-1.900-1.430 (.340) .800-.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 .364-.04 (.530 (.16-1.348-.461 (.590-.499 (.340-.67) 1.S.700) .510) 1.339 (.410 (.740-.01-1.870 (.380 (.380 (.490-.690-.660) .01-2.880 (.870-1. varnishes. large appliances.580 (.463-.338-.580 (.300 (.270-. and soil.760 (.47 (1.890-1.940-1.350) 75th .07 (.420) .410 (.330) .07-1.316 (.680) .56) 1.14) 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 .930) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.24 (.16) 1.810) .850-1.469-.333-.340-.820 (.48) 1. hard metal (alloys of cobalt and tungsten carbide).03-1.418 (.398 (.610) . and 03-04 are 0.48) 1.940-1.450) .410-.08.410-.305-.50 (1.480 (.52 (1. and in synthesizing polyester and other materials.800-.09 (.336-.23-2.960-1.25-1.750 (.680 (. blue-colored pigments.660) .380 (.860 (.890-1.06 (.400-. and fertilizers.810-.270-.670 (. It is emitted into the environment from burning coal and oil and car and truck exhaust.550-.14) . It is also a component of porcelain enamel applied to steel bathroom fixtures.520-.22) 1.42) 1.670-.680) .73) 1.740 (.350 (.370-.880-1.600) .580 (.515 (.950-1.15-1.700) .450) .430 (.39) 1.427-.650 (.09 (.840) .640) .440-. industry is imported or obtained by recycling scrap metal that contains cobalt.26) 1.640) .610) .60 (1. 01-02.460) .369 (.327-.920) 1.377-.950-1.308-.33 (1.540-.08) .520 (.26-2.520-.450-.710) .04-1.590-.900) .75 (1.434 (.370-.452 (.300-.374 (.23) .470) .370-.16-1.32-2.47) 1.16 (1.81) 1.920-1.410) .05) 1.373-.410-.32 (1.386) .28 (1.610-.07-1.670 (.487) .660-.28 (1. 0.99) 1.465) .259-.367 (.360-.500) .28 (1.620-.04) 1.760) . and kitchenware.950 (.08-1.420) .03) 1.285 (.26) Total .24 (1.350-.05 (.17 (.379 (.33-1.620) . automobile airbags.319) .600-.750-. and inks.930-1.32) 1.470 (.520-.520 (.371 (.15 (1.04-1.520) .430-.620-.05 (.530) .04-1.600 (.530-.540-. Usual human exposure is from food sources.12) 1.280-.590 (.460) .610 (.379 (.980) .550) 90th . Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.13) 1.03 (.375 (.540) 1.360-.07.301 (.950) .21) 1.294 (.435 (.81) 1.310-.890) 95th 1.980-1. see Data Analysis section) for Survey years 99-00. Cobalt is used as a drying agent in paints.520 (.630 (.17-1. The cobalt used in U. seawater.373) .620-.480-.650-.390 (.410 (.480 (.22 (1.394) .590) .790 (. population from the National Health and Nutrition Examination Survey.710) 1.14-1.519 (. and magnetic recording media.340 (.92) 1.07.460 (.17 (1.500 (.490-.00) .570-.570) .690 (.630 (.630-. steel-belted radial tires. interval) .430) .900) .564) .460 (.S. shiny.370) .502) .850) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.Metals Cobalt CAS No.450) .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 .68 (1. and 0.29 (1.380-.334) . Cobalt compounds are also used in manufacturing battery electrodes.17 (1.581) .820 (.890-1.430 (.404) .26-1.950 (.420 (.32) 1.360-.405-.570-.414) .03 (.670 (.359 (.06-1.45 (1.940 (.431) .417) .01 (.730) 1.28-2.398) .496) .20 (1.

324-.562) .515 (.372) .434-.50) 1.324) .282-.00 (.301-.327-.457-.615) .513-.349) .03 (.355) .404-.329 (.599) .792-1.16 (1.382-.282 (.250) .691 (.457 (.753-.513 (.955) .368) .296) .09) 1.392 (.667-1..360) .429) 1.611) .369 (.337) .323) .348) .826-1.237-.365) .955) .937 (.736-.632-.975 (.727 (.394) .36) 1.781) 95th 1.00 (.339-.352 (.35) . Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.23 (1.667-1.707) .33) .328 (.344-.280-.248-.327 (.361 (.388 (.738 (.468) .704-.368) .850 (.00 (.10) Total .362 (.488) .548 (. 1994).976 (.561) .737 (.495 (.554 (.15 (.16 (.900-1.259-.487-.333-. 1972).334) .16 (.830 (.303-.25 (. cobalt is excreted predominantly in the urine.574-.396) .335 (.898 (.27) 1.479-.54) 1..362-.608 (.313-.11-1.847) .895-1.290 (.277-..554 (.408 (.462) .609) .857-1.673-.471 (.391 (.275-.243-.297-.421) .733-1.547 (.274-.591 (.409) . using hard metal cutting tools.83) 1.851 (.393 (.278-.990-1.581) .508-.306) 75th .310) .60) 1.29 (1.257 (.234 (.635 (.314 (.00 (.239-. and to a lesser extent.433) .35) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.505) .391) Selected percentiles ( 95% confidence interval) 50th .449) .428-.537 (.983) .938) .00) .313-.328) .452-.00) .378 (.273 (.425) .533 (.331-.563-.753) 1.543) .560-. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.272-.50 (1.343 (. interval) .419) .S.Metals fabricated from cobalt alloys (Lhotka et al.293 (.529 (.306 (.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 .353-. or using diamond-polishing wheels that contain cobalt metal.792 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.00-1.963) .247 (.290 (.960 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.10-1.848 (.626-. Exposure in the workplace may come from electroplating.12 (.872 (.342-.952 (.417 (.708) . 1994.298 (.523 (.895-1.33) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .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 .17) .949) .378-.781-1.821-3.700 (.33) 1.534 (.317 (. 2003).50) 1.44 (.297) .990) .278 (.594) .57) 1.425-.728) .552 (.313 (.861 (.365-.363) .352) .407 (.550-.660-.500-.449-.358 (.387) .905) .24) .73) 1.542 (.294-.644 (.380-.319-.929) .804) 1.500 (.503-.28) 1.279) .279 (.777-.522) .774 (.333-.634-.381) .29) 1.352 (.606 (.593) .296-.481) 90th .346 (.353 (. A portion of cobalt retained for long periods is concentrated in the liver.30 (1.289) .25 (. population from the National Health and Nutrition Examination Survey. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.06 (.290 (. Once absorbed and distributed in the body.15) 1.248-.611) .14 (.281) .842) .03-1.259) . Cobalt is absorbed by oral and pulmonary routes. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.738 (.963-1.463-. respectively.426 (.313-.29 (1.585) .760-1.442-.313-.679-.10 (.963) .562) .963-1.291 (.662) .750) .302-.384) .400 (.728 (.964 (.638-1.329-.750-.256-.378-.251-.60) 1..756 (.286) .598 (.361 (.36) 1.786-.476-.938-1.378-.640) .49) 1.29 (1.457) .361-.376 (.740-1.833-1. Smith et al.917) .757-1.879-1.333 (.932-1.333-.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 .838 (.362) .647) .326-. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).694) . but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.600-.616-.343-.850-1.703-.824 (.328 (.16) .467-.669) .300) .479) .911-1.337 (.386 (.02 (.04-1.301) .259 (.. 1972).630-.55) .471-.435-.630-. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.469-.309) . an essential human nutrient.861-1.689 (. refining or processing alloys.257-.04 (.275-.438) .10) .304) .471-.500-.435 (.723 (. 1979).444 (.582-.396) .455 (.534-.595) .829-1.829) .487-.475 (..215-.19) .983-1.388 (.368 (.513) .417) .393-.402 (.461) .268 (.12-1.785) . in the feces.27) 1.844 (.700 (.361-.523 (.407) .271 (.29) . Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.439) .11-1.821 (.316 (.744) 1.304-.683-.313-.

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

Occupationallyinduced “isolated cobalt sensitization. Salvatori S.150(1-3):167-171. et al. Szekeres T. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. 2001. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Peltier A. Romazini S. Weyher I. Int Arch Occup Environ Health. Zhuber K. Lison D.69(3):193-200. Sabbioni E. oxides. Schramel P. Linnainmaa M. Smith T. J Bone Joint Surg Br 2005.533:135-152. et al.150. Pisati G. Kriss JP. Falcone G. Science 1988. Sci Total Environ 1997. Occup Environ Med 2001. Sci Total Environ 1994. Vitali MT. Daniel J. Blunn G. J Bone Joint Surg Br 2006. Laippala P. Cleland D. Hedge AG. Robinson C. Rorabeck CH.58(10):631-634. Arch Intern Med 1990. Jarvis JQ. Meier R. et al. Oksa P. Absorption and retention of cobalt in man by whole-body counting. Occup Environ Med 1994. Leghissa P.45:246-247. Bacis M. Fujimura N. Bourne RB. Trace element reference values in tissues from inhabitants of the European Union. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds.36:732-734. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Cresti R. DeSantis V. Kuska Y. Buchet JP. Sabbioni E. Zedda S. Dunstan E. Dickel H.” Contact Dermatitis 2001. Lhotka C. Long-term clearance of inhaled 60Co. et al. Lung cancer risk in hard-metal workers. Molders J.50(9):835-842.55(4):269-276. Mosconi G. Alessandrelli M.95:29-37. Sabbioni E. J Occup Med 1992. Ichikawa Y. Hoet P. Mutat Res 2003. Meyer zum Buschenfelde K-H. 3rd ed. HoffmannB. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Moulin JJ.157:117121. 1985.88(4):443448. Steffan I. Kusaka Y. Lison D. Iversen BS.48:172-173. Bozec C. Lasfargues G. McCalden RW. Zobelein P. Health Phys 1979.87(5):628-631. Am J Epidemiol 1998.22:359367.28(5):1121-1128. Unwin P. Linna A. Gross RT. Schank M. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Cannon SR. Co-sensitivity between cobalt and other transition metals. De Boeck M. Palmroos P. Lison D. X. Barnaby CF. Goto S. Lisi P.242:1412-1415. McMinn DJ. Health Phys 1972. Kirsch-Volders M. Goldberg MA.(1-3):133-139. J Trace Elem Med Biol 2006.20(1):25-31.148:241-248. Biological monitoring of workers exposed to cobalt metal. Br J Ind Med 1993. Kiilunen M. Am J Ind Med 2003. Bunn HF. Kristiansen J. Wild P. Industrial Chemical Exposure: Guidelines for Biological Monitoring. et al. Angerer J.44:124-132. Edmonds CJ. Chess DG. The release of metals from metal-onmetal surface arthroplasty of the hip. Int Arch Occup Environ Health 1997. Tilley S.21(2):189-195. Contact Dermatitis 2003. Buchet JP.34:620-626. and cobalt metals. Sci Total Environ 1998. Cobalt cardiomyopathy. Goto S. cobalt salts. Outcome of occupational asthma due to cobalt hypersensitivity.Metals effects of cobalt.216:253-270. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Lauwerys RB. Salama A. Epidemiological survey of workers exposed to cobalt oxides.406:282-296. Shirakawa T. Boca Raton (FL): Lewis Publishers. Kraus T. Iavicoli I. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Stanescu D. Hoher T. Heki S. Swennen B. Clin Orthop Relat Res 2003. Schaller KH. Cobalt and antimony: genotoxicity and carcinogenicity. salt. Thabe H. Carnes WH. Dunning SP. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Pradhan C. Ghat IS. A report of two cases from mineral assay laboratories and a review of the literature. Zweymuller K. Lauwerys R. Kato M. Radulescu M. Thakker DM. et al. Chest 1989. J Orthop Res 2003. Lauwerys R. a study of 13 elements in blood and urine of a United Kingdom population.51(7):447450. Roto P. Ziaee H. Sanghrajka AP. Weber A. Thomassen H. Diepgen TL.150:177-183. White MA. Swennen B. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Uitti J. Respiratory health of cobalt production workers. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Hammon E. Christensen JM. and hard metal dust. J Rheumatol 2001.204:147-160. MacDonald SJ. Sci Total Environ 1994.

52-1.90) 2.80 (4.40-2.60 (1.20) 4.20 (2. Lead has a variety of uses in manufacturing: storage batteries.50 (2.10-4.70) 4.60) 2.3.86) 1.20 (3.800-1.90 (3. and 03-04 are 0.19 (1.50-3.70) 4.50) 7.70 (1.70 (2.60) 4.60) 3.70 (1.50-1.40) 1. bronze).90) 2.90-2.90) 1.40) Total 1.60-1.60 (3.50-1.20) 90th 3.70 (2.30-1.40 (1.09) 1.10-1.20-3.40) 5.60 (1.70) 4.60-1.3.900 (.75-1.60) 2.50-1.20 (3.20 (3.40) 1.78 (1.00) 1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.60) 3.80 (2.20-3.25) 1.40-3.10) 2.40 (2.71-1.50) 1.40) 2.50) 5.900 (.20 (3.30-2.50 (1.40-2.10-2.60) 4.46 (1.30-6.50 (4.60) 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 2.75-2.30 (3.80-4.50-5.60) 4.10-3.55-1.20-6.S.50 (3.60 (2.90-2.77 (1.30-4.00) 3.20) .30) 2.40-3.30 (4.50-2.20) 3. and 0.40) 4.30) 5.20-2.30-1.52 (1.30-2.60-4.50 (1.31) 1.10-2. respectively.70) 2.65 (1.75) 1.80-3.50) 3.43) 1.50 (4.00) 6.10 (2.30-1.80-3.00) 4.80 (1.10-3.80 (1.10-2.30-1.17) .40 (2.00-4.20 (3.75 (1. Since lead has been eliminated from gasoline.90) 2. leaded glass.40) 1.50-3.00) 2.25 (1.50-4.30 (1.986) .28.20 (1.90 (1. 7439-92-1 General Information Elemental lead is a soft.60-1.900-1.40 (3.10-1.69 (1.87 (1.60 (2.40-6.90-4.90) 3.96-2.40-5.91) 1.45-1.20) 4.87) 1.83 (1.10) 4.70) 4.62-1.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.20-3.40 (1.80) 2.50) 4. Elemental lead can be combined with other elements to form inorganic and organic compounds.60) 4.00-5. plastics.20) 3.40-4. metal alloys (e.S.80-5. population from the National Health and Nutrition Examination Survey.45 (1.30-1.30 (2.20-3.80) 1.60) 1. see Data Analysis section) for Survey years 99-00.37 (1.10) 3.70 (3.80-3.30) 1.60 (2.10) 1.20) 5. brass.942 (.30 (2.01 (1.14-1.80) 1.60-1.20 (1.10-3.30) 2.80 (4.90 (3.00-2.90 (2.66 (1.60 (2.60) 2.30 (2.90-4.81) 1.10 (1.50) 1.00) 1.70) 1.60 (2.20 (1.60) 2. ammunition.70-2.37 (1.90) 2.00) 5.50-4. Lead was used in plumbing for centuries and may still be present.80 (5.60 (1. Before the 1980’s.80 (1.00) 2.50-5.60) 2.60-6.70-2.20) 1. antique-molded or cast ornaments.20 (3.10 (4.10) 3.60 (2.50 (2.10-6.40) 2.90) 1.60) 1. dense.30) 95th 5.60-2.00 (3.70-5.10-2.66) 1.40) 3.00 (2.70 (1.60-2.g.30-2.69 (1.40-1.10-6.60) 5.70) 3.80-4.50) 1. 0.20) 2.04-1.40-2.62) 1.80 (3.60) 5.14-1.80 (2.70-2.30 (2.90-6.40) 2.00) 2.60 (3.50) 2.00 (1. the main source of lead exposure for the general U. interval) 1.878-1.10 (2.80) 1.00) 2.70 (2.00) 1.70-6.70-3.00) 1.20 (1.48) 1.40 (4. such as lead phosphate and tetraethyl lead.70) 1.70) 1.50 (1.00 (6.60 (1.00) 1.80) 2.50-6.20-4.70) 3.90) 2.50-2.50) 4.93-2.00-1. blue-gray metal that occurs naturally in soils and rocks.30-2.90 (3.49-1.51) 1.36-1.69) 1.69) 1.50) 5.80-3.90-3.10) 2.20-2.39) 1.43-1.90 (4.80-4.30 (2.50-2.10) 5. Lead is most often mined from ores or recycled from scrap metal or batteries.10 (1.40) 2.00 (5. solders.40-1.70) 1.80 (5.36) 1.23 (1.70) 3.00-6.70 (3.00-4.60 (1.90) 3. 01-02.50 (3.60) 1.20) 3.70-1.00) .90-4.30 (4.90 (2.80) 1.60) 3.00) 3.30-1.10-2.62 (1.89) 1.50 (2.37-1.40 (1.10 (1.90 (3. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.50 (1.60) 1.80 (1.80 (2.70 (5.50-1.60 (1.20) 3.43) 1.22 (1.80 (1.30 (2.10) 1.55-1.00-4.70-1.43 (1.10 (2.00 (1.80) 3.10) 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.32-1.90 (3.90-2.43 (1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.40-1.14-1.40 (5.12-1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.60) 1.20-1. and for radiation shielding.30 (4.40-1.34-1.40-1.10-2.68-1.50) 75th 2.60 (1.40 (1.80 (1.00 (4.20 (4.70) 1.70-4.40-1.00 (4.95) 1.80) 2.72) Selected percentiles ( 95% confidence interval) 50th 1.56 (1.50 (2.90-2.10-1.80) 2.10) 3.50) 2.30-5.00-1.70 (1.20 (3.60-4.36-1.80-2.80) 1.50-2.50) 1.10-3. In the past.30 (2.30 (1.25 (1.30 (1.51 (1.40-3.20-1.50) 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 2.70-1.00) 4.90 (1.946 (.10-8.10 (3.52-1.90) 1.30) 2.60) 3.20 (2. malleable.30 (1.60 (4.53) 1.02) 1.50-1.40-6.10-4.60 (3.Metals Lead CAS No.90) 5.20 (1.50 (2. ceramic glazes.55 (1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .39-1.899-.32-1.90-4.60-3.60 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.

680) .641-.70 (2.80) 1.10 (.91) 2.595-.833-1.30-2.70) 1.. or water contaminated by mining or smelting operations.900 (.31-3.00 (.86 (1.800 (.570-.00) 2. Approximately half of the absorbed lead may be incorporated into bone.04 (.10-1.90-2.700-1.70) 1.40) 3.80) 2.540 (.80-3.g.862) .21 (2.40) 1.29 (2.31 (1.50-2.30) 1.90-2.72) 1.10 (1.50 (2.700-.700 (.86) 95th 2.10 (1.808 (.20-1.625-.66 (2.60 (1.900) . battery and radiator manufacturing) and recreational sources.766 (.70-3. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.27) 1.03-2.33-2.680-. interval) .773) .572-.540-.10) .40 (2.49) 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 .70) 3.960 (. dust.738) .52-1. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient.900) .30) 2.526-.828) Selected percentiles ( 95% confidence interval) 50th .00) 2.660) .688 (.986) .20) .40-2.33 (2.600) . imported children’s trinkets and toys.40 (1.753 (.970-1.800 (.70 (2.40 (1.50) 1.40 (1.10-3.10 (1.60-3.690) 75th 1.20) .560-.00) .18-1.07 (.90-3.620 (. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead. 2007.70-2.50) 1.636 (.Metals occupational (e.900 (.10) 1.810-1.60-1.40-3.82 (1.60 (1.80) 2.13-3.09) 1.708-.80) 2. 01-02. However.30) 1.00) .700 (.30) 2.00 (2.610 (.800-.20 (1.960-1.20 (1.86) 1.90 (2.640-.40-1. pewter utensils and drinking vessels.50) 2.580-.90) 1.40-1.70) 1.616) .82 (2.33.800) .20 (1.20-2.13) .73 (1.700-.700 (.12) 90th 2.600-.900-1.850 (.818) .640 (.90-2.931) .535-.558 (.04) 2.80) 1.90) 2.04 (.40-5.20 (1. older plumbing systems with leaded pipes or lead soldered connections.40-1.600-.40) 2.900) .10 (1.80 (2.800-1. lead-containing folk remedies and cosmetics.731 (.40) 1.90 (2.20 (2.935) 1.62) Total .60-2.20-1.700 (.955-1.24-1.900-1.00 (1.745-.04-2.718) .600) .752 (.50 (1.605) .600 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60 (1.50-2.900) . 0.579-.600-.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.680-.700) .990) 2.80) 3.800 (. and contact with soil. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.700 (.29) 2.915-1.10-1.80) 2.848 (.80-2.11 (1.10-3.10-1.23) .80) 3.620) 1.00) 1.661-.50 (2.613) .00 (1.50-1.600 (.70 (2.642 (.785) .89) 2.75) 3.80 (1.90 (2.20 (1.80-2.40 (2.60) 2. In the blood.90-3.06) .40) 2.651) .30-3.70 (2.07-1.00 (1.628) 1.00-1.90) 2.40) 2.700 (.00-2.857) . 2000).630 (.64) 2.40) 1.80 (1.00-1. or after soluble lead compounds are ingested. and 0.700-.591 (.30 (1. and 03-04 are 0.700-. CDC.30-1.30) 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.49 (1.730 (.50-3.35 (.75) 4.506-.70) 2.10-1.11) 2.60-2.600-.40-1.590 (.02) 1.00) .30 (2.710-.90-2.900) .800-1.60 (1.564 (. lead-contaminated dust in indoor firing ranges.20) 1.40 (1.900) .97) 4.625 (.90 (1.20) 1.20) .553-.00 (1.40) 2.10 (.800 (.30-1.579-.20-1.900-1.. see Data Analysis section) for Survey years 99-00.815 (.62-4.659 (.50 (1.840 (.90-4.800-.691-. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.650) 1.17 (1.20-2.78-2.00-1.30) 1.00-2.14-1.14 (1.44-2.10-3.920 (.941) .10) 2.920 (.02 (.700) 1.757-.30) 1.40) 1.20) .50) 1. lead-based painted surfaces undergoing renovation or demolition.20 (1. Fourth National Report on Human Exposure to Environmental Chemicals 213 .30) 1.500-.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 1.32 (1.41) 2.66 (2.60 (2.10) 2.1.40) 1.710-1.800) .833 (.00) .556-. respectively.30) .70) 3.S.600-.20) 1.960-1.14 (1.23-4.10) .695 (.59) 1.90 (1.50) 3. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.700-.80) 1.52-1.10-1.900 (.27 (1.820-1.800) .60-3.20 (3.940 (.729-.20 (2.78-2.78-2.70 (1.30) 2.30-5.90) 2.677 (.573 (.480-.52 (1.30-1.04) .40 (1.800) .30-1.40 (2. population from the National Health and Nutrition Examination Survey.50 (2.80) 2. stained glass framing.30 (3.40 (2. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.604 (.671-.90 (1.795 (.790 (.589-.1.822-1.00-2.900-1.923 (. 1991).674) 1.50-2.701) .990) 1.10 (.10-5. Lead is absorbed into the body after fine lead particulates or fumes are inhaled. bullet fragments retained in human tissue.03 (1.22) 1.86-2.19 (1.637-.910-.800) .20 (2.749) .50) 2.59-2.

838) . zinc.98 (1.61) 1.. 1995).31) 1.659-.26) Total .882-1. abdominal pain.971 (.940 (.62) 2.02) 1.586-.655) 75th 1.671 (.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 .50) 1.992-1.50-2.47) 1.496 (.22) 1.700-.812-1.43 (1.31) 1.11) .551-.08) .51 (1.645-.28) 2.19-5.41-1.654) .722 (.594-.633 (.49 (1.55 (1.34-1.746) .50-1.37-1.342-.89-5.720 (.09-1.701 (.432 (.639 (.00 (1.722 (.15-2.75 (2.400) .11-1.04) 2. encephalopathy.03) 2.679) 1.617-.10 (.876-1.07-1.698) .887 (.41) .623 (.725) .632 (.918 (.88-2.97 (1.603-.53) 1. population from the National Health and Nutrition Examination Survey.05 (.404 (.639 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.87) 1.64-2.618 (.88) 2. Large amounts of lead in the body can cause anemia. The toxic effects of lead result from its interference with the physiologic actions of calcium.97-18.62-1.S.04-3.676) .85-2.65 (1. 2007).720 (. Schwartz.56-3.33 (1.20-3.67-4.742) Selected percentiles ( 95% confidence interval) 50th .61) 1.914-1.755 (. Approximately 70% of lead excretion occurs via the urine.31 (1.79) 2.56) 3.82) 1.50-2.828-1.78-4.436) .61) 3.23 (1.588-.46 (1.870 (.593 (. 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.571-.94-2.793-1.09) 1.718) .52) 1.615 (.383-.46 (2. 1995. 1991.645-. kidney injury.914 (.36-2.56-2.Metals 90% of the body lead burden in most adults.38 (2.962 (.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 1.681-.00 (1.920-1.10) 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 .98-2.63) 4.03 (1.26) 2.862-.11 (1.603-.652 (.710) .11 (1.52 (1.28) .790) .696 (. Lead can cross the placenta and enter the developing fetal brain.11 (.657) 1.01) .682) .71-2.75-2.64) 2.72-2.569 (.981-1.851) .48 (1.70 (1.33) 1.51) 1.701) .88) 1.644 (.01 (. 1993.725) .375 (.988-1.571-. seizures.. For instance.605-.508) .22-1.66) 2.730) 1.35) 2.679-.77) 2.65-2.734) .08-2.43) 1.997-1.20) .88 (1.698) .74 (1.11) 1.. O’Flaherty.18) .83) 1.24 (1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR. In 1991.44 (1.529-.79 (1.592-.712 (.742) .18 (1.50-2.677-. interval) .18) 1.19) 1.66 (1.10 (1.53-1.03 (. scant amounts are lost through sweat.63) 1.765) .29 (1.608-.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 .541-.731-.639) .428) .58) 1.62-2.621 (.98) 2.702-.828) .658 (.62-3.461) .00) . Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.47 (2.380-.22) .938 (.41 (1.44 (1.721 (.933) .06) .73-2.918-1.408-.510-.988 (.469 (.85 (1.615 (.89-2.708 (.97) 1.43-1. through the inhibition of certain enzymes.72-2.12-1.914 (.22) 1.25-1.03 (.635 (.15) 1.673) .05 (1.79) 1.946-1.535) .43) 2. 1996).677 (.587-.893) .71 (1.603 (.64) 95th 2.703) .609 (.17 (.72) .917-1.14) 1.758) .608 (.09-1. The skeleton acts as a storage depot.693 (.648 (.898) .73) 2.55 (1.404 (.18) 2.61) 1. and through binding to ion channels and regulatory proteins.709 (.56 (1.668-.641 (.83 (2. with lesser amounts eliminated via the feces.992-1.681-.86 (1.38 (2.460-.979 (.78 (2.40-1.677) .977) 1.957-1.718) 1.17-1.975-1.68 (1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.03) .03 (.03) 1.990 (.33-1.739) .38 (2. and paralysis.03-2.50 (1.15-3.10) 1.938-1.00 (.11 (.05-1. with a half-life of years to decades.08) .22-2.753) .03) 2.37-1. CDC. and iron.44) 1.14 (1.96 (1.27 (1.06 (1.594-.963-1.03) 1. Nash et al.561-.0) 3.31 (1.03) .583-.774 (. 2004.644) .69 (1.404-.810 (.655-.667-.607-.638 (.85-2. Staessen et al.841-1.07) .97) 1.625 (.05-1.655) .926 (.92) 2.601-.606-.03) 90th 1.43 (2.492-.683-.18) 1.07 (. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.61) 1.763) .15-2.781-1.649 (.604-.612-.59-3.853-1.688) .09-1. and nails (Leggett.02-1.88) 2.15) 1.707 (.20) .933-1.588-.900 (.06) 1. BLLs and associated toxic effects differ in children and adults.559-.623 (.702) . 2003.667) .579-.670) 1.66 (1.94 (1.639 (.47 (1.31 (2. based on prospective population studies.28-1.686) . hair.702) .85) 1.796-1.622 (.25-1.00 (1.06 (.800-.45 (1.33) 2. 1993).64 (1.39-1.667-.

IARC considers inorganic lead compounds probable human carcinogens.S.6%) were lower than those from NHANES 1991-1994..gov/toxpro2. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. Staessen et al. BLLs higher than 40 mg/dL can result in proximal tubular dysfunction and decreased glomerular filtration rate leading to interstitial and peritubular fibrosis when high body burdens persist. 2003. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. 1998). A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3.. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. Information about external exposure (i.. environmental levels) and health effects is available from ATSDR at: http://www. Surveillance data reported by U. 2002. approximately 11.Metals µg/dL or higher as the level of concern in children. 1995.6% in NHANES 1988-1991 to 1. and organic lead compounds not classifiable with respect to human carcinogenicity. and spontaneous abortion (Baghurst et al. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. Both drinking water and ambient air standards for lead have been established by the U. More recently. almost double the geometric mean of 1. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. Borja-Aburto et al. premature delivery. 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. 2003). 1994). 2002). and peripheral neuropathy generally occurring at much higher levels (e.07 µg/dL (Becker et al. 2005b..atsdr. adults in the 19992000 NHANES sample (Apostoli et al.. higher than 100-200 µg/dL). 2002a). may alter sperm morphology. Urine levels may reflect recently absorbed lead.4% in NHANES 1999-2004. seizures. 2006). 2003.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample. EPA. particularly in the skeleton.S.S. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. Payton et al.cdc. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al.. respectively. CDC. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. residing in housing built before the 1950’s..7 µg/dL and 4. 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. The U.. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. 2005b). urban residence.4% of children had BLLs of 10µg/dL or higher (CDC. the geometric mean BLL was 3. both the geometric mean (1..cdc. 2007). reduce sperm count. adults in the 1999-2000 NHANES sample.0 µg/dL in females (Soldin et al. including minority race or ethnicity. 2001). Schwartz. Telisman et al. usually with BLLs greater than 40 mg/dL... Fourth National Report on Human Exposure to Environmental Chemicals 215 ..21% of approximately 3. adult residents.. 2006). with overt encephalopathy. 1996. 2000). though there is greater individual variation in urine lead than in blood and greater potential for contamination. 1996. However. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. 1984.. For example.S. 1991. and low family income (CDC.. Jones et al.xls). 1999).g. Schwartz et al.2 µg/dL in males and 3.e. 2005a). which is an 84% decline. Overall. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. 1999). 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.75 µg/dL in U. 2003. 2000).. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. Bellinger 2005.. Pirkle et al. when the geometric mean BLL was 2. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. In occupationally exposed adults. Korrick et al. and decrease fertility (Alexander et al. the prevalence rate has declined annually since 1994 (CDC..3 million children tested had BLLs of 10 mg/dL or higher (http://www.. BLLs reflect both recent intake and equilibration with stored lead in other tissues. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. Lanphear et al. High dose occupational lead exposure. Data submitted through state public health programs from 2006 showed that 1.S..S..9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. At low environmental exposures. 2009).html. Muntner et al. In NHANES 1999-2002 in children 1-5 years old. 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.5 per 100. 1987.000 adults.. 1996.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006..

Bavazzano P. JAMA 1996. Payton M.cdc.atsdr. Int J Hyg Environ Health 2002. Borja-Aburto VH. Rotnitzky A.82:60-80. Homa DM. Available at URL: http://www.htm. Korrick S. Centers for Disease Control and Prevention (CDC). 4/14/09 Centers for Disease Control and Prevention (CDC). 2005. Adult blood lead epidemiology and surveillance—United States. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Lepom P. Weiss ST. Lanphear BP. Neurotoxicol 1987. Birth Defects Research (Part A). Bellinger D. Available at URL: http://www.gov/mmwr/preview/mmwrhtml/ mm5532a2. Baghurst PA. Ganzi A. Ronchi L.115:521-529. Kim R. McMichael AJ. Coresh J. et al. N Engl J Med 2003. MMWR Morb Mortal Wkly Rep 2005a.htm. Hernberg S.cdc. Luukkonen R. Canfield RL. Pediatrics 2009.89:330-335. Caldwell KL.73:409-420. Hu H. Jacobson SW. 2002 [online]. Ga. Preventing Lead Poisoning in Young Children. Ewers TG. Reese YR.gov/nceh/lead/ CaseManagement/caseManage_main. 4/14/09 Centers for Disease Control and Prevention (CDC). Atlanta (GA). Hänninen H. Aro A.htm.html. Blood lead levels measured prospectively and risk of spontaneous abortion. Scand J Work Environ Health 1984. Third National Report on Human Exposure to Environmental Chemicals. et al. Korrick SA. Henderson CR. Meyer PA. Schulz C. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Weiss ST.10:43-50.cdc. Seiwert M.348:15171526.205:297-308.53:411-416. Lanphear BP.26:359-371. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. References Agency for Toxic Substances and Disease Registry (ATSDR). Angle CR. Blanco J. Kaus S.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. IARC Monogr Eval Carcinog Risks Hum 2006. Apostoli P. Leggett RW. Wigg NR. Atlanta. Hu H. et al.htm. Hu H. Kaufman JD. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Vimpani FB. Cory-Slechta DA.87:1-471. Aug 2007 [online].123:e376-e385. van Netten C. Cox C. Neri A. Available at URL: http://www.113(4):1016-1022. Muntner P. Cox C.54(20):513-516. Auinger P. Jones RL.8(3):395-401. The relationship of bone and blood lead to hypertension. Available at URL: http://www. 2005b. Sparrow D. et al. Intellectual impairment in children with blood lead concentrations below 10 µg/dL.287:1-11. 4/14/09 Centers for Disease Control and Prevention (CDC). JAMA 1996. Acquisition and retention of lead by young children. Inorganic and Organic Lead Compounds. 1991 [online]. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study.150(6):590-597. Environ Health Perspect 1993. 1999-2002.55(32):876-879. Pirkle JL. et al. Toxicological profile for lead. 1988-2004.1542/peds:2007-3608. Hertz-Picciotto I. Checkoway H. Baj A.101(7):598-616. Becker K. Bellinger D. Public Health Rep 2000. Chiodo LM. Speizer FE. Teratogen update: lead and pregnancy.cdc. Krause C. Robertson EF. Sparrow D. doi:10.cdc. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Kuehnemann TJ. Semen quality of men employed at a lead smelter. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Blood lead reference values: the results of an Italian polycentric study. MMWR Morb Mortal Wkly Rep 2006. Atlanta (GA). Batuman V.275(15):1171-1176. Manton WI. Brody DJ. Rios C. CDC. Muller CH. Available from URL: http://www. Roberts RR. Am J Epidemiol 1999. Environ Res 2000. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 4/14/09 Centers for Disease Control and Prevention (CDC). Farias P. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Neurotoxicol Teratol 2004. Blood lead levels—United States. 2003-2004. Jusko TA.gov/nceh/lead/publications/ books/plpyc/contents. Managing Elevated Blood Lead Levels Among Young Children. 4/14/09 Alexander BH. Mantere P. Sci Total Environ 2002. Wager C. Am J Public Health 1999. Rotnitzky A. Lead and hypertension in a sample of middle-aged women. gov/mmwr/preview/mmwrhtml/mm5420a5. Dietrich K. Occup Environ Med 1996. Rojas LM. Age-specific kinetic model of lead metal in humans. Neurodevelopmental effects of postnatal lead exposure at very low levels. Vupputyuri S. Hunter DJ. Stanek KL. Jacobson JL. Pediatrics 2004.275:1177-1181.gov/toxprofiles/tp13. Lead.

Kaufmann RB. Physiologically based models for bone-seeking elements. Payton M. Schwenk M. Toxicol Appl Pharmacol 1993. Int J Hyg Environ Health 2006. Association of blood lead. Low-level lead exposure and renal function in the Normative Aging Study.9:303-327. Kidney Int 2003. Telisman S. Blood lead concentrations in children: new ranges. Hwang KY. Weiss ST. Am J Epidemiol 2001. Environ Health Perspect 1996.327:109-113. Blood lead. and tibia lead with neurobehavioral test scores in South Korean lead workers. Schwartz BS. Semen quality and reproductive endocrine function in relation to biomarkers of lead. J Hum Hypertens 1995. Am J Epidemiol 1994. stable lead isotopes to determine release of lead from the skeleton. Rubin R.289(12):1523-1531. Schwartz J. Brody DJ. Smith DR.Metals results from NHANES III. Hanak B. Pizent A. dimercaptosuccinic acidchelatable lead. JAMA 2003.104(1):60-66. Hickman T. Environ Health Perspect 1998. Wilhelm M. Use of endogenous. Hu H. Lee BK.118:16-29. Lead.63:1044-1050. cadmium. Soldin OP. Gunter EW.108(1):45-53. Osterloh JD. Environ Health Perspect 2000. Lee GS. Clin Chim Acta 2003. Rocic B. Staessen JA. blood pressure. O’Flaherty EJ. 50:31-37. Amery A. Paschal DC.209:301305. cadmium. Revised and new reference values for arsenic. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. IV. Pirkle JL.153(5):453464. zinc. Cvitkovic P. Lustberg M. et al. Gavella M. and hypertension in perimenopausal and postmenopausal women. Arch Environ Health 1995. Kinetics of lead disposition in humans. Exposure of the U. Jurasovic J. Nash D. lead. Fourth National Report on Human Exposure to Environmental Chemicals 217 . et al. blood pressure and cardiovascular disease in men. Low-level lead exposure and blood pressure. Schulz D. and copper in men. Magder L.S. Stewar WF. population to lead: 1991-1994. Sherwin R. Sparrow D.140:821-829. Soldin SJ. Lee SS. Roels H. Flegal AR. Kaufmann R.106:745-750. Lauwerys RR.

700) .400 (. 1999 .90-3.80 (3.776 (.60) 1.903) Selected percentiles ( 95% confidence interval) 50th .20 (2..886) ..50-2.50-3.00 (.418-.30-6.30-2.00 (2.g.900 (.S..500-. which can bioaccumulate in aquatic and terrestrial food chains.00 (.700-.30) 4132 4241 03-04 03-04 03-04 . Some cosmetic skin creams from countries other than the U. see Data Analysis section) for Survey year 03-04 is 0. and dental amalgam.00 (1.00 (. Accidental spills of elemental mercury. IARC. with the highest concentrations occurring in the kidneys (Barregard et al. constitutes the main source of dietary mercury exposure in the general population.g.50) 4.781 (. population from the National Health and Nutrition Examination Survey.30) 1. and organic forms.484) . silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.326 (.30 (1. The ingestion of methyl mercury.00) ..40-2.80) 4.20-4.800-1. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.40 (4. predominantly from fish and other seafood.30) 3.300-. Elemental mercury is a shiny.80 (1.700-.00-5.900) 1.10) . Kingman et al.10-3.60-5.672) .00) 1. solid-waste incineration. thermometers.700-.814 (. or oxygen.490 (.80) 3..372) . Poorly absorbed from the gastrointestinal tract.30) 3. Atmospheric elemental mercury can be deposited on land and water.90 (1.2.800-1. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.60) 2085 2293 3478 Limit of detection (LOD.500 (.30) 5. synthetic organomercury compounds were once used in pharmaceutical applications. and is distributed to most tissues.00 (.30) 1.927) .600) 1.40-2..400-. Also.703-.60-2. may contain inorganic mercury.400-.40) 3. Apart from methyl mercury.60 (1.50) 2.753-1. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.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 .80 (1.40-3.g.500) .60 (2.90) 90th 3. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).40 (4. and mercury compounds are still used as preservatives (e.900) 1. such as chlorine (e. sulfur.800-1.919) .00-1.600 (.90 (4. The kinetics of the different forms of mercury vary considerably. 1994.877 (. have often required public health intervention (Zeitz et al.30-4.472-.363-.20) 2.800 (. Other major uses include electrical equipment (e.900) 75th 1. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.60-3. 1980. and mining and smelting.60 (1.12) .700-.02) .g.70 (3. inorganic. thermostats and switches).40-1.90) 3.90) 95th 4. an organic form of mercury.800-1.40 (3.00 (2.30 (2. which create an episodic potential for volatization and inhalation of mercury vapor.70) 911 856 2081 4525 03-04 03-04 .979 (..900) .300 (. 1998. mercuric chloride). Woods et al.20-3.285-.30-5.419 (..700-.80) 1..714-.800 (. interval) . Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).689-. merbromin).50) 1.70 (4. 218 Fourth National Report on Human Exposure to Environmental Chemicals .500 (.70 (1.800 (.00 (2.800-1. elemental mercury is absorbed mainly by inhaling volatilized vapor.40) 1.563 (. electrical lamps.50) 5. thimerosal.300) .800 (.574) .700) .00) 1.40 (3.655-.Metals Mercury CAS No.500-.S.80 (1. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.00) 3.40-1.50-1. phenylmercuric acetate) or topical antiseptics (e.00) 4.60-6. After elemental mercury is absorbed. 1993). 2007).60-6.70-2.90 (1.20-4. sphygmomanometers and barometers. In addition. 2002). Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.860-1.900) 1. Hursh et al.700 (. to form inorganic mercury compounds or salts.60) 1.70 (1.797 (. Survey years 03-04 Geometric mean (95% conf.

600 (.407) .377 (.40-1..700 (.307 (.00) 7.40) 1.60) 2.00) 1. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.50-3.27) .40 (1.20 (2. Smith and Farris.70-5. Methyl mercury enters the brain and other tissues (Vahter et al. 1993).800 (.500-.40-2. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations..00-6.10 (1.90 (1.20) .80) 1.377) ..3) 4..70-6.14.200-.800) 1..35 (1.800-1.00) 4.70 (1.20-3.697-.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 .475) .00 (2. 2004.00) .10) .0) 4. 1969.7) 4.40) 2.30-3.30 (.825-1.10-1.30-2. 1996).269-.30) 1.500 (.20) . The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.00 (3. 1994. population.369) 1. Myers et al. Smith et al.20-3.20) 1.. 1991.329 (.299-. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola. and a useful marker of exposure in epidemiologic studies (Grandjean et al.40 (1.700-..00) 1.200 (.30-6. 1996.10 (1.268-. 1975.. 1992). thereafter.60) 3. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.800-1.200-.40) 5.50 (2.30-11.10) . 1992.265-.90) 5. a measure of accumulated dose (Cernichiari et al.500-. 1973).343 (. 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. 1992 and 1999.600) .200-.23) .60) 1. After exposure to elemental mercury.80-3. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al..00 (2.300 (.60 (3.824) 1..90) 2.20 (.900-1.800-1.50) 1.50 (1.02 (..700-1. Miettinen et al.800 (.60 (1.600) .297-.30-6.800 (.40-2.10 (.318 (.00 (1.256-.29) . 1994) and then undergoes slow dealkylation to inorganic mercury.10 (. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.500-.200 (...70) 4.80 (1.664-1.90) 90th 1. Methyl mercury is incorporated into growing hair.73) 1.200-.300) .726-1. Suzuki et al..820 (.374) .01) . 2003).800) .00-3.30-4. 1999).738-.833 (. Fourth National Report on Human Exposure to Environmental Chemicals 219 .500-1.50-12.14 and 0. for both acute and chronic exposures.50) 2.900 (. 1994). 1995. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.800) 1.30-6. Vimy et al..70-3.10-3.300) .70 (1.900-1..00) 6.667 (.317 (..30 (1.90 (3.30 (1. interval) Selected percentiles (95% confidence interval) 50th .900 (.60 (2.90 (4.940) Race/ethnicity (females.60 (3.20-2.700-.300 (.300) .90) 2.70) 4.395) .00-1. Geometric mean Survey years (95% conf.70 (1. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.20-11. with most elimination occurring through in the feces (Sherlock et al.900 (.80 (3.800) 75th .700 (.871-1.300) .10 (1.06-1.700-1.919) . 1971).300 (. Jonsson et al. 1990)..30-5.30-4.30 (1.50) 1..500-.20-3.10 (3. 1984.700 (. Sandborgh-Englund et al. National Health and Nutrition Examination Survey.90 (4.60 (1.00-2.700) 2.80) 579 527 370 436 588 806 Limit of detection (LOD.800) .00 (2.70-3.00) 2. 2003).06 (.90) 3.60) 1. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al. Vahter et al. 1998).300) ..50) 3. Excretion occurs by renal and fecal routes.300 (.500-.700 (.944 (. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .50) 95th 2.400-. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.70) 1.00-2.200-. 1993).S. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30) 3. McDowell et al. 2005). Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.. 1999-2002.200-.500 (. 1998).50-2.00-2.300) .60 (1.541-.70-5.90 (1.30) 1.Metals the tissues to mercurous and mercuric inorganic forms. 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.10 (5.10) 1.

2005. 2006. insomnia. 1951. 1963). 2004... see Data Analysis section) for Survey year 03-04 is 0.600) .700 (.. ataxia. Salonen et al.. 2000). Rissanen et al.. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. overt signs and symptoms of chronic inhalation may include tremor.. depression.700-.42. Bellinger et al.Metals may be more efficient for inorganic mercury (Grandjean et al. typically after a latent period of weeks to months. Sakamoto et al.700 (. which may vary for some chemicals by year and by individual sample. Smith et al.800) .700 (..500-. and progressive constriction of the visual fields. 1993). Acute. Stern 2005. and cerebral palsy (NRC. Survey Geometric mean (95% conf.. 2005). The constellation of findings may include anorexia. 2004)..700-.600) . and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600) .600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .800) . 220 Fourth National Report on Human Exposure to Environmental Chemicals . cerebellar ataxia. Rice.500 (.600-.600 (. the existence of a causal relation is unresolved (Chan and Egeland. Overt poisoning from methyl mercury primarily affects the central nervous system. maculopapular rash.500 (<LOD-.600 (.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 .700) . Once absorbed. short-term memory loss.500-.600) . 1983). Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. pain in the extremities. Smith et al.S. irritability. Inorganic mercury exposure usually occurs by ingestion.600-.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.500-.600-.600 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700 (. 2000.600 (..500-. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. 1995.500 (<LOD-. particularly irritability. Oskarsson et al.500-. fatigue. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. population from the National Health and Nutrition Examination Survey. hearing impairment. dysarthria. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. and sleep disturbance (Bidstrup et al. causing parasthesias.700) 2007 2240 3406 Limit of detection (LOD. Factor-Litvak et al.500 (.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .600) . 1995.600 (. 1970. 2004. 2003).500-. anorexia. limb deformities.700-.600) .. altered physical growth. 1987). 2000. < LOD means less than the limit of detection.500-.600) ..500-. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. DeRouen et al. The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.. dysarthria.700 (. gingivitis.500-. 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. and pinkish discoloration of the hands and feet (Tunnessen et al. Vupputuri et al. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. Sakamoto et al.600 (.. sensory impairments. At levels below those that cause acute lung injury.700 (.. 2004). 2006.600 (..500) . 1996). and neurocognitive and behavioral disturbances. 1998.600-. In recent epidemiologic studies. Drexler and Schaller.600) . 2002. hypertension.600) .600 (..

.250) .16 (.42) 95th 3.. From 1996 through 1998.14.408) .700 (.405-. Benes et al. Grandjean et al.58 µg/L for 4645 adults.350-.67-3. 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..96 (1. see Data Analysis section) for Survey year 03-04 is 0.. In NHANES 19992002.330-.78 µg/L for adults and 0.530-.78-2.280-. adult women in several ethnic subgroups (Hightower et al.88 (1. range 40 years to 78 years) had an average total blood mercury concentration of 2.05) 1.463) .24) 1. EPA.88-3.534) . the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.406-.460) .28) 1. 2009). Urinary mercury consists mostly of inorganic mercury (Cianciola et al.509) .19 (1.31) 1266 1272 03-04 03-04 03-04 .99-6. military veterans (mean age 52.960 (.400 (.433 (. 1998).492) Selected percentiles ( 95% confidence interval) 50th . Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Sanzo et al. environmental levels) and health effects is available from the U. Fourth National Report on Human Exposure to Environmental Chemicals 221 .61) 1.29) 1.930-1. the median concentration of blood mercury was 0.03-4.213-.63-2.05) 3.gov/mercury and from ATSDR at: http:// www. 2001. et al.68 (2..160-. 2001.570) .580) .S. 2009).16 (1.396-.413-.430 (.480 (...e.416 (. Information about external exposure (i. 2003).313-. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.442-. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.89) 3. average age 33 years.509) .330-.430) .08 (1.S.09 (2.atsdr.840-1.9 years). IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.555) .18) 2. who participated in a 1998 representative population survey (Becker et al.254 (. interval) ..14-2.31) 2. total blood mercury geometric mean levels in females aged 16-49 years did not change. EPA at: http://www. slightly higher total blood mercury levels were found in U.770-1. During the same survey periods. However.26 (1.340-. 2003).23) .24 (2.200 (..76-3.cdc.382-.549) .480) 75th 1.13-2..55 µg/L.01 (.290-.54 (2.420 (.. Over the NHANES 1999-2006 survey periods.360-.870-1. average age 9.360 (.30) 3.S. aged 18 to 69 years.370) .870-1.97) 2.12 (.93 (1.60) 619 713 1066 Limit of detection (LOD.520) .358 (.530) .96 (1. 1995.330-.46) 3.epa.52) 2.S. 2006).07 (.39-3. the total blood mercury concentration is due mostly to the dietary intake of organic forms. and the age-related changes differed across the groups (Caldwell et al.440 (. Kingman et al.840) 1.940 (.890 (.76-4.8 years. Biomonitoring Information In the general population. A cohort of 1127 U. 758 children.304) .14) 90th 2. Schober et al.840-1.460 (. 1997.476 (.700-1.430 (. particularly methyl mercury.S. These distinctions can help interpret mercury blood levels in people.441 (.60-2.08 (1. 1998). (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women..00) 1. 2004.420 (.60 (1..330 (.33 (2.90) 2. Survey years 03-04 Geometric mean (95% conf.610-1. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children. Among the three racial/ethnic groups. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.85-2.447 (. population from the National Health and Nutrition Examination Survey. total blood mercury increased with age.23) 2.410-.530) .gov/toxprofiles.88) 287 722 1529 03-04 03-04 .67-2.77-2.19 (2.65) 1.55) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2538 03-04 03-04 03-04 .34-3.00 (.20 (1.Metals standard for inorganic mercury has been established by U. In Germany the geometric mean for blood mercury was 0.495 (. 2000).76-3. Total blood mercury levels increase with greater fish consumption (Dewailly et al. Mahaffey et al. 2002). and increased slightly in non-Hispanic white children (Caldwell..66) 3.360-.46 µg/L for children.

265-. 2006. Levels in U.376-.67 (1.404-. An expert-panel report recently prepared for the U..784) 1.400-.62 (1. Czech (Benes et al.455-.667-1.400) .. women of childbearing age have generally been much lower than these levels (CDC.525 (. 2009).S.280-.800-1.03) 2.78-4.88 (1.532 (..696 (.587 (.67 (1.307-.07) 1.87 (1. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine. interval) . and Italian (Apostoli et al.31 (1.18-1.362 (. and on average. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.S..480) . ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.365 (.88-2.714-1.28 (.208-.535) 1.464 (.30) 2. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.545 (.13 (1. 1998).255 (.51-2.630) . Urinary mercury levels in recent German (Becker et al.652) .09) 1.486) Selected percentiles ( 95% confidence interval) 50th .785-1.588) . 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. 2005). Department of Health and Human Services noted that several studies have observed a modest.347) .44) 1.S.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 .508 (.392-.455-.64-2.964-1.54 (2.88-2.Metals 2000). 1988.599) .391-.447-. population from the National Health and Nutrition Examination Survey.25 (..309-.990) .01) 2. 2003). et al. 2006). military veterans with dental amalgams.768 (.46-2..455) .909 (. 1992).40-1.30) 1. not to imply a safety level for general population exposure. Urine mercury and the number of dental amalgams were correlated..196-.566) .687) .391) .. 2002) adult population surveys were similar to those in a U. a biomarker of perturbation in renal tubular function. Langworth et al.289) .79 (1.61) 1.87) 2.56) 1266 1271 03-04 03-04 03-04 .246-.301-. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.343 (.23-2.616) . In the study of U. reversible increase in urinary N-acetyl-glucosaminidase.297 (.13-2. 2002).79) 1. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.77 (2. mean urinary mercury was 3.11) 2.86) 95th 2.306 (.21) 1.225-. Information about the biological exposure indices is provided here for comparison.32 (1.358) ..365 (.04-3..368) .63) 1.11) 1.11-2.498) 75th .S.619-. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.41-2. et al.443 (.S.875-1.00) 90th 1.276 (. Survey years 03-04 Geometric mean (95% conf. DeRouen et al.417) . the urine mercury increased by approximately 0.385-.384 (.76 (1.522-.00 (.39) 1.12-3.476 (. 2009).1 µg/L for each surface with a dental amalgam (Kingman et al.16) 1.333-.06 (.06 (.485 (.537) .32-2.217 (.620-.970 (.40 (1.275) .472-.447 (.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .1 µg/L. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.35 (1.463 (. 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.00) 286 722 1529 03-04 03-04 .65 (1.969-1.

686) .636-.622-.30 (1.760 (.799) . National Health and Nutrition Examination Survey.23-1. 16-49 years) 99-00 01-02 .930) .685 (.27 (1.00 (3.810) .616-.92) 4.27 (2.24) 6.59-5.22-3.99) 1.06 (.68-3.92) 2.831) .56 (1.70 (2. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.Metals Urinary Mercury−Females Aged 16-49 Years Old.657 (.32 (1.596 (.09-1.540-. National Health and Nutrition Examination Survey.14) 3.500-.501-.410-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.740 (.62 (4. 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.22 (.45) 95th 3.28 (1.14-2.07-5.14 and 0.87-4.85) 4.632 (.806) . Geometric mean (95% conf.62 (1.832-1.30 (2.32-3.41 (1.77) 1.624-.10-4. population.553-.89 (2.35 (1.85-3.18) 3.18 (3.656-.600 (.615 (.00 (2.45-3.870) .16-5.51 (3.38) 4. Geometric mean Survey years (95% conf.592 (.790) .65-4.99 (2.21-3.691) .61) 1.97) 2.709) 75th 1.579-.710 (.772 (.S.77) 2.706 (.833) .426-. interval) Selected percentiles (95% confidence interval) Survey years 50th .46-4.76 (1.47) 1.62 (3.10-2.76) 2.909-1.43-1.55-3.07-2.79) 3.91 (2.650) 1. 16-49 years) 99-00 01-02 .670) 75th 1.605-.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .03 (.41 (1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.37 (1.S.420-.475-.05 (3.966) .69-3.709) .04-10.81-6.665) .48 (2.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .710) 1.81 (3.610-.92) 3.580-.557-.664) .631-.46 (1.03-2.14-1.56) 3.94) 1.24-1.580 (.57-4.21 (2.516 (.560-.526-.23-1.84 (2.95 (2.91-7.41 (2.655 (.53-3.520-.27-1.578-.13-4.41-6.45) 2.15 (2.76-5.724 (.99 (3.03 (.809) .846) .831) .00) 2.31-1.37) 1. population.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.582-.69 (1.650 (.46) 3.47) 1.98 (5.44) 3.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .07) 1.723 (.32) 2.09-1.45 (1.14.68 (3.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.99-2.522 (.650 (.508-.04-1.910) .21 (1. interval) Selected percentiles (95% confidence interval) 50th .540 (.13 (2.50-4.774) .97) 2.54) 595 531 381 442 594 826 Limit of detection (LOD.15-1.42-3.658 (.3) 5.51) .45) 2.17) 95th 5.68) 3.83-3.45-2.61-6.565 (.72) 1.450-.744) 1.52) 3.569-.824) .50 (2.50 (1.30-2.892) .721 (.42) 90th 2.79) 1.39-3.25) 2.620 (. 1999-2002.56) 4.639 (. 1999-2002.560 (.719 (.637) .42) 2.742-1.97 (1.30 (2.65) 1.03) 1.35) .387-.606 (.05 (2.710 (.16) 5.55) 90th 3.97) 2.31 (1.699) 1.520-.502-.84 (2.850-1.

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226 Fourth National Report on Human Exposure to Environmental Chemicals . Goldberg J. Amiano P. Suzuki T. Whittle K. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Smith JC. Smith RG.79:786789. Vahter M. Hum Toxicol 1984. Guo S.4(5):981-988. Topping G. Hall LL.98(1):133-142. Aguinagalde FX. Takahashi Y. Most B.289(13):1667-1674. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. McDowell M. Am J Physiol 1990. Tunnessen WW. Stern AH. Burbacher T. et al.31:687-700. Blood mercury levels in US children and women of childbearing age. Kaye WE. Turner MD. Friberg L. Smith PJ.115(10):1527-1531. Langolf GD. Acrodynia: exposure to mercury from fluorescent light bulbs. Smith JC. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Bernardo MF. Imai H. Am Ind Hyg Assoc J 1970. Toxicol Appl Pharmacol 1996. Nakazawa M. Lind B. Environ Health Perspect 2007. Stern AH. Longnecker MP. Sherlock J. Amurrio A.258(4 Pt 2):R939-945. 1999-2000. et al. Pediatrics 1987.128(2):25125-25126. Orr MF. Osterloh J. DeRouen TA. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Environ Res 2005. Public Health Nutr 2001. Jones RL. Newton G. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Vorwald AJ. The contribution of dental amalgam to urinary mercury excretion in children. Daniels JL. Toxicol Appl Pharmacol 1994. The kinetics of intravenously administered methyl mercury in man. The hair-organ relationship in mercury concentration in contemporary Japanese. Hislop D. Sinks TH.40:413-419.37:245-252. Mottet NK. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury.48(4):221229.111(12):1465-1470. Leitao JG. Schober SE. Dorronsoro M. Br J Ind Med 1983. Yoshinaga J. Methyl mercury pharmacokinetics in man: a reevaluation. Fisher HL. Environ Health Perspect 2003. Bolger PM. Environ Res 2005.Metals Sanzo JM. Sandler DP. Smith AE. Azpiri MA. Shen DD.110:129-132. Baser M. Lorscheider FL. Vimy MJ. Arch Environ Health 1993. Martin MD. 1993-1998. et al.97(2):195-200. Patil LS. Farris FF. Zeitz P. Hongo T. Toxicol Appl Pharmacol 1994. Effects of exposure to mercury in the manufacture of chlorine. Environ Health Perspect 2002.124:221-229. Effects of occupational exposure to elemental mercury on short term memory. Mooney TF. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. JAMA 2003.2:117-131. Woods JS. Matsuo N. Leroux BG. Vupputuri S. Allen PV. McMahon KJ.

0-56.5) 80.9-83.7) 78.7 (44.9-55.3 (37.1-88.5-68.7-41.0 (81.0 (76.3) 85.4-82.2 (49.3-91.0-101) 82.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.0 (46.9 (40.0-38.S.0 (41.3-108) 215 (161-278) 169 (145-194) 148 (136-163) 154 (132-180) 158 (130-177) 127 (114-139) 1121 1335 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 47.7) 78.2 (49. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1 (34.2 (38.4 (34.5-65.1) 35.0) 39.0-53.0) 54.3 (79.5) 80.7 (50. and xanthine oxidase (Kisker et al.9-55.7 (45.2-79. 1997).7) 75th 84. interval) 45.6 (43.2-53.9) 62.4 (72.7 (58. 01-02.7-122) 93.4 (80.1) 126 (106-147) 109 (94. WHO.3 (38.3 (46.7-50.1-52. 0. and in pigments for ceramics.0-65.8-90.2) 41.0-77.0) 84.8) 44.2 (83.Metals Molybdenum or ore deposits.7 (73..7) 46. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.8-49.8 (82.8) 48.6 (55.8. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.9 (33.6 (40.7-73.0-85. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.5 (49.7 (37.6-42.1 (91.9) 67.2) 37.9) 34. Fourth National Report on Human Exposure to Environmental Chemicals 227 .5-41.6) 51.3-75.5 (81.1-63.7) 51. population from the National Health and Nutrition Examination survey.1) 57.9 (32.1) 46.6-55. 1996).3-47.6 (40.5 (37.0) 55.6) 71.8) 40.5-91.4-75.1) 60.2-70.2 (56.7-47.5 (48.4) 56.9 (78.6 (55.5 (74.5) 85.7) 57.1-59.7-39. At a daily oral molybdenum dose of 24 µg. inks.6-96.7) 45.2 (63.9 (73.3 (53.6-111) 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 52.8-46.7-84.7 (36.1-51.5 (67.3 (84.6-82.3) 41.6) 71.0 (48. and 03-04 are 0.9-109) 97.8-94.3-44.7-96. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.3) 37.6-58.2) 48.3 (55.1 (71.5.0-62. More recently.7 (51.4) 42.6) 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. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.2) 79.8) 39.2) 52.9 (52.6-72.8) 75.4) 76.2 (69.6) Selected percentiles ( 95% confidence interval) 50th 50.7-91.3 (64.8) 46.4) 49.7) 86.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.3) 65.5) 47. 2001.4 (48.2 (55.5-52.2) 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 (98.6-46. see Data Analysis section) for survey years 99-00.1) 59.0 (42.3) 47. semiconductor and battery industries have begun to use molybdenum.9 (34. chemical reagents in hospital laboratories. Excretion occurs predominantly via the kidneys.3 (73.1) 82. and 1. urinary excretion over six days CAS No.2-42. aldehyde dehydrogenase.3) 83.0) 62. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.1-55.5-52. lubricants.2) 53. respectively.8 (67.1 (38.2-37.3 (47.5 (43.1-52.7) 77.1-44.7-68.7-105) 69.0-71.4-61.0) 60.7-92.3) 54.6 (52.5) 44. and paints.6 (73.2 (61.4) 45.8.9-85.5 (41.8-106) 88.8 (85.4 (79. 7439-98-7 General Information Elemental molybdenum is a silver-white.4) 52.5-46.0 (43.5) 60.9 (44.0-110) 90.7-51.2-59.1-48. Compounds of molybdenum are also used as corrosion inhibitors.7-60.4 (48.0 (42. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. hydrogenation catalysts.4-52.0) 45.2-91.0-100) 63.2-59.3 (55.5 (41.5-124) 108 (92.8 (42. 2001).5-66.7) Sample size 2257 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 78.2) 40.7 (71.3-115) 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.9-82.0) 97.6) 53.3 (71. In humans. which exert homeostatic regulation over molybdenum balance.2 (40.6) 93.9-56.8-108) 87.4) 41.9 (37.6-62.

6 (36. Based on studies finding adverse reproductive effects in rats and mice.9 (64.3) 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.S.9-68.1-100) 86.3-43.8-118) 81.5 (50.6) 43.1 (30.5) 60.4) 44.8-47.2 (40.0-56.3-59.9) 44.9 (39.2-46.8 (57.7-43.9-45.3) 44.4-106) 85.4-185) 106 (94.2 (40.5) 73.5 (37. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.1-112) 78.5-35.4) 77.6-63.9-96. at daily oral doses of 95 µg and 428 µg.03 mg/kg/day in humans (IOM. In industry. 1993).9) 173 (130-243) 159 (129-170) 132 (107-158) 85.4-107) 85.2 (40.8-47.8) 37.4) 60.3) 41.9 (40.4-41.2) 39.3-52.3) 61.8-66.2-96.1-43.3 (51.6) Selected percentiles ( 95% confidence interval) 50th 41.9-87.1 (37.1-43. and urinary levels reflect intake from all sources.0) 36.6 (57.0) 39.2) 58.0) 39.5 (54.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.8 (75.7-137) 129 (109-155) 112 (97.4-118) 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 ..3 (53. 1995).9) 92.2) 55.4) 58.8) 38.3-46.4 (53.0-133) 119 (88.0) 38.3 (36.0) 88.4) 116 (101-126) 104 (88.3 (71.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.0) 33.6-45.5 (35. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.6 (36.6 (59.2) 42.6 (38.7) 115 (93.5-48.4 (56.6) 36.0 (74.0) 62.3) 64.9-40.3) 56.3 (37.5 (34.8) 61.6-78. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0-46.4) 122 (107-133) 109 (99.2-65.4 (40. urinary excretion over six days rose to 50% and 67%.1) 101 (83.9 mg/kg/day and established a tolerable upper intake level of 0.3-56. 1961. EPA.6) 39.3-44.8-42.8 (36.1 (42.3-45.1 (82.1) 37.2 (43.4 (44.8) 79.2-49.4-42.9 (49.0-41.1-81.8) 62.6-41.9-71.9 (39.2 (33.7) 112 (95.5-99.1-39.5-97.2 (73.0-38.2 (57.4-120) 101 (84.6-88.6 (42.5 (65.5 (80. 1999). and molybdenum has not been systematically evaluated for carcinogenicity by IARC.0 (80.1-40.1-127) 90.7 (66.9-41.5 (59.0 (35.7) 62.6 (71. population from the National Health and Nutrition Examination survey.1-39.4 (59.5 (79.4 (55.2) 37..9 (35.2-80. 2001).7 (77.2-40.2) 37.S..2) 43. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.7-62.5-44.4-39.8) 38. respectively. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.1-41.7) 42.8-84.3 (58.2 (36.7-93.3 (71.7) 41.1) 65.2-96. Molybdenum is generally considered to be of low human toxicity.9) 79.8) 39.1 (38.0) 44.3) 40.5) 63. Biomonitoring Information Molybdenum is an essential element for health.2-47.9-45.0-120) 85.5 (39.1-34.5 (36.1 (54.5-69. interval) 43.5-60.5 (40.8-46.5) 90th 108 (97.Metals was 18% of the ingested dose.4 (37.0-103) 103 (90. U.8 (90.9) 40. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.4) 40.1 (39.8) 71.9) 31.9 (36.1) 56.2-41.8-52.6-76.5 (35.3 (83.3) 37.9 (79.4 (67.5 (41.9) 41.2 (69.8 (37.1) 37.5-92.5 (38.3-115) 98.9-61.4-66.7 (30.7-38.3 (37.5 (37.1) 43.4 (78.8) 45.7-100) 77.0) 72. and clinical or epidemiologic evidence of adverse effects is limited.5-50.9 (73.5 (65. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 (44. but available epidemiologic data are scant.1 (40.6-61.1 (49.3) 57.7-120) 87.2 (50.2-121) 107 (92.8-65.1 (38.7) 57.8 (56.7) 45.1-38.7-52.2) 42.4-76. 1997).7) 75th 63.0 (58.6) 48.6-61.7-40.2) 39.1-67.5 (41.2) 38.0) 53. of the ingested dose (Turnlund et al.5) 71.3-68.2 (37.3) 43.9-117) 57.5-62.3 (36.9-42.1-109) 89.5 (39.1-45.6) 39.5-45.1-79.9-118) 91.3 (55.3-141) 109 (81.7) 53.6-63.5-119) 90.4) 61.7-44.5) 72.9 (64.5 (83.2 (52.8-67.5 (78.3-102) 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 40.0-46.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.7 (75.5-70.4) 89.4) 47.5 (40.5-46.1) 40.4) 48.1 (33.

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

respectively. 230 Fourth National Report on Human Exposure to Environmental Chemicals .07. and 0. Platinum compounds are used in electrodes. however. and iron. 0. population from the National Health and Nutrition Examination Survey. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. Important properties of platinum are resistance to corrosion. dental alloys. and high catalytic activity. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Metals Platinum CAS No. copper. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. strength at high temperatures. and as drugs (e.. jewelry.g. carboplatin) in the treatment of cancer. 7440-06-4 General Information Platinum is a silver-gray. < LOD means less than the limit of detection.. 01-02. cisplatin.04.04. 1998). Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. and 03-04 are 0. 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. see Data Analysis section) for Survey years 99-00. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al.S. thick-film circuits printed on ceramic substrates. 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. which may vary for some chemicals by year and by individual sample. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. as oxidation catalysts in chemical manufacturing. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel.

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

ruthenium. Fruhmann G. 2004. 2003). Biomarkers 1999. pp.01 µg/L (Becker et al. Influences on human internal exposure to environmental platinum. 2001). Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Ruff F: Platinum and platinosis. et al. eds.19:685-691.. Herr et al. Occup Environ Med 1998. Rommelt H.35:313-321. Schierl R. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. References Becker K. Raab W. Several studies have shown that background concentrations in general populations were usually less than 0. palladium. Angerer J. Platinum concentrations in urban road dust and soil..70(3):205-208. Part 1: monitoring of urinary concentrations.htm.005 µg/L (Iavicoli et al. Kaus S. In: Bingham E.4(1):27-36.. Grimm CH. Platinum.Metals the International Programme on Chemical Safety at http:// www. Blanks R. Ewers U. Schulz C. 1999. Hysell D. osmium. Allergy and histamine release due to some platinum salts. et al. Ruff F: Histamine release by sodium cholorplatinate. 232 Fourth National Report on Human Exposure to Environmental Chemicals . 289-380.. Biomonitoring of traffic police officers exposed to airborne platinum. Cohrssen B.. 2003. Analyst 1998.org/documents/ehc/ehc/ ehc125. Hall L. et al. Neuendorf J. 2004).56(3):283-286. 2004) or less than 0. Farago ME. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure.. Schierl R. Boos KS. 2000.04 µg/L) in this Report.. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Seiwert M. Schulz C. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. 206:15-24. Urinary excretion of platinum from platinum-industry workers. Schierl. Int J Hyg Environ Health 2004. 1991 [online]. Arch Environ Health 2001. Moore W Jr. Urinary platinum levels associated with dental gold alloys. Parrot JL. Environmental Health Criteria 125. 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. van de Weyer C.. which elevate urinary platinum by five to twelve-fold (Begerow et al. Wilhelm M. Int Arch Occup Environ Health 2003.inchem.. and in blood and urine in the United Kingdom. Hauff K. 3/31/08 Moore W Jr. International Programme on Chemical Safety (IPCS).55(2):138-140. Iavicoli I.S. Duneman L:Long-term urinary platinum. Levels of platinum in urine for the U. 2003. Crocker W. Nowak D. et al.207(1):69-73. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Patty’s Toxicology. Gieler U. and platinum. 1997. Pethran A. J Expo Anal Environ Epidemiol 2003. Ensslin AS. 1998). Uptake of antineoplastic agents in pharmacy and hospital personnel. Kelly J. Herr et al. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Pethran A. Senofonte O. and gold excretion of patients after insertion of noble-metal dental alloys. Gromiec JP. 2003. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. New York: John Wiley & Sons. Kuster W. Nickel. Stilianakis NI. rhodium. Kazantzis G. 1998). Powell CH.htm. 5th ed. Environ Health Perspect 1975b. Hysell D.76(1):5-10. 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. Br J Pharmacol 1969. Campbell K. Herr CE. Wilhelm et al. Saindelle A. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Environ Res 1975a.9:152-158. Hebert R. population were below the limit of detection (0. Arch Environ Health:1969. Bocca B.. Kavanagh P.inchem. Pethran et al.13(1):24-30. Int Arch Occup Environ Health 1997. Schierl R. Czerczak S. Kulka U. Huber R. Available at URL: http://www. palladium. Fries HG. Biomonitoring Information Urinary platinum levels reflect recent exposure. Seifert B. Jankofsky M. Schierl et al. Occup Environ Med 2004. Petrucci F.10:63-71. Alimonti A. Carelli G. Thornton I.123(3):451-454. Begerow J. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies.org/documents/ehc/ehc/ehc125. Turfeld M. Saindelle A. International Journal of Hygiene and Environmental Health 2003. Schierl R..61(7):636-9.

134-.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 .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.480) .146 (.420 (.520) . respectively.350) .225) .350-.190 (.400) .460) .390-.210 (.290 (.330) .500) .181-.470) .200 (.300) .170-.290 (.400) 95th .210-.420-.360-.330-.260 (.350) .430) .270-.280) .230 (.350-.260 (.500) .370 (.160 (.184 (.170-.165) Sample size 2413 2653 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .380 (.300 (.290 (.440) . 2005).370 (.450 (.300 (.470 (.230-.201 (.188) .390) .147-.430) .420-.270 (.450) .220) .390 (.410-.390-.159 (.220) .180) 75th .360 (.190 (.330) .490) .200) .400) .147-.310 (.380) .163) .180 (.165 (.360-.217 (.170 (.220) .230-.149 (.440 (.400) .440 (.202 (. 01-02.260-.240) .370 (.147-.430 (.290) .330-.370) .300-. and 03-04 are 0.167 (.206) .450 (.250) .390) .300) .350-.180-.350 (.217) . however. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.290) .Metals Thallium depilatory cosmetics.310 (.440) .148-.260-.310-.410-.390-.360-.200 (.370 (.290 (.220 (.360 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.410 (.230) .480) .370 (.196) .400-.420) .520) .170) .410-.180-.250-.. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.178) .470 (. In addition.220 (. thallium readily crosses the placenta and also distributes into breast milk.310 (.230) .430-.200) .550 (.300 (.270 (.430-.150-.210 (.200-.135-.280) .410 (.460-.160-.191 (.340 (.450 (. 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. the latter being the current major industrial consumer of thallium in this country.270 (.S.179-.640) .500 (.460 (.450 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.220-. it has not been specifically mined or refined in the United States since 1984.171 (.187-.250-.410 (.159 (.360-.158) .230-.330-.200) .390 (.500) .370 (.240-.172 (.370 (.450 (.240) .250 (.160 (.410-.430-.160 (.420) .215) .270-.440 (.270 (.270 (.300) .202) .290-.170) .201 (.260-.280-.240-.200 (.150-.420) .162-.410) .190 (.520 (.137-.220) .190 (.410 (.180-.155 (.170 (.160-.400 (.420-.218) .450 (.290) .330) .470) .177) .440 (.400 (.170-. In the United States.450 (. interval) . see Data Analysis section) for Survey years 99-00.154-.450 (.400 (.330-.280) .320) .690) . Human health effects from thallium at low environmental CAS No.220 (.160-.145-.400 (.480) .218) .210) .197-.176 (.220) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .330-.200 (.02.260 (. From these and other sources.220) .390) .300) .180 (.243) .200-.400 (.02.440) .170-.360 (.450 (.410 (.230) .360-.290-.170-.330-.380 (.180) .410 (.270) .185 (.140-.167-.175) .370-.190 (.170-.270) .183) .370-. In the past.350 (.480) .260-.180-.220 (.400-.240-.200) .185-.410-.430 (.200) .150-.330) .400-.250 (.470) .183) .200 (. 0.310) .230) .430 (.159 (.520) .02.370-.350-.173-.170 (.280-.173) .510) .250-.200-.192) Selected percentiles ( 95% confidence interval) 50th .400-.400) .440-.400-.172) .330-. and 0.340-.360) .420) .510) 1200 1313 1281 1213 1340 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .380-.260) .145 (.410-.160-.490) .153-. thallium was obtained as a by-product of smelting other metals.290 (.320 (.170-.160 (.200) .590) .340-.260-.250-.430 (.290 (.156) .370) .180 (.133-.340) .390-.630) . Thallium disappears from the blood with a half-life of several days.196) .202 (.190 (.167-.290) 90th .200 (.340) .144 (.320-.380-.490) .390) .320) .480) .280 (.560) .350-.150-.170) .320) .590) .173) .420) .250-.157-.270-.510 (.490 (.280 (.420) .190-.250-.145-. representing distribution into other tissues.150-.160-.172 (.420) .340-.239) .280 (.360 (.290) .490) Total .160 (.182-. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.156) . population from the National Health and Nutrition Examination Survey.350-.156-.340-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.197 (.240) .250-.150-.220 (.370-.200-.250-.

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

Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L.47(3):223-231. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U.35(1):4-9. Minoia et al. Brockhaus A. 2005. 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. 1981. Martin J-C. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Morrow JC. 1980. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Apostoli P. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Available at URL: http://www. Pirkle JL. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium.216:253-270. X. Investigation of a working population exposed to thallium. Schmidt M.265 people living near a thallium-emitting cement plant in Germany. Sci Total Environ 1990. Ting BG. Paschal et al. Environ Res 1998. Sampson EJ. with concentrations ranging up to 76. 7/15/09 Blanchardon E. Celier D. 1990. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Jackson RJ. blood..html.cdc. Soddemann H. A study of 46 elements in urine.95:89-105. Minoia C.. Boisson P. (1981) studied 1. 1985). Wiegand H. 2005. Sabbioni E. Gallorini M. Atlanta (GA). 1998. Pietra R. White MA. Trace element reference values in tissues from inhabitants of the European Union.113(1):47-53. Ewers U. 1992 [online]. et al.gov/toxprofiles/tp54. Manke G. Challeton-de Vathaire C.. et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Buhlmeyer G. Sabbioni E. Trace element reference values in tissues from inhabitants of the European community I. Radiat Prot Dosim. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Valentin H.S. Investigations of thallium-exposed workers in cement factories. Int Arch Occup Environ Health 1981. Sci Total Environ 1998. J Soc Occup Med 1985. Trace metals in urine of United States residents: reference range concentrations. Toxicological profile for thallium.76(1):53-59. Kramer U. Cassot G. Brockhaus et al. 2005) and are shown with results from NHANES 2003-2004 in this Report. A study of 13 elements in blood and urine of a United Kingdom population.. 1998). Schaller KH. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Pozzoli L. Raithel HJ. and serum of Italian subjects.48(4):375-389. 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. Schaller et al. Int Arch Occup Environ Health 1980.5 μg/L.1 mg/m3 (Marcus.Metals (CDC. et al. Dolger R. Marcus RL.atsdr. White and Sabbioni. Third National Report on Human Exposure to Environmental Chemicals. Centers for Disease Control and Prevention. Paschal DC.

310-.580) .510-.056-.330-.360 (.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 .370 (.210 (.170) .220 (.290-.560) .170 (.110) .180-. 0.180-.260 (.088 (.450-.180 (.230) .056-.090-. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).330-.400 (.065-.180-.04.310 (.160 (.520) .510-1.180-. 01-02.200-.123-.300 (.160-.230-.100-.310-.400-.560) .109) .090) .050-.500 (.069) .100) .150-.110) .590) . see Data Analysis section) for Survey years 99-00.126) .570 (.340-.550 (.090 (.210 (.073 (.060-.093 (.140 (.064-. and as catalysts in the petroleum industry.170) .430-.250) .380-.300) .420-.210 (.073-.250) .360-.092 (.100 (.570 (.320 (.092) .090-.370-.360-.270-.060-.100-.360) .410 (.120-.640 (.060 (.090-.090) .110-.320) .140-.101 (.350 (.130 (.830) .087) .096 (.090-.170 (.210-.069-.210 (. and 0.137 (.062 (.180) .250-.062 (.260-.070-.100-.130-.120-.04.087-.210) .280 (.530 (.105 (.130 (.310-.073) . and 03-04 are 0.150 (.090 (.084 (.080 (.790) .080) .320-.120-.060-.190) . mainly as scheelite (CaWO4). Little information is available on the toxicity of tungsten.320 (.070) .300-.340-.082) .270 (.380 (.500 (.300 (.650) .290) .470 (.133) .107 (.060 (. Tungsten is used mainly for producing hard metals.120) .670) .460) .093) .230-.100) .440) .220) .330) .370-.140-.170) .113 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .150 (.220) .470 (.300) 95th .110 (.560 (.122) .135) .350) .058-.510 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.400 (.380 (.060 (.071 (.270-.068) .470) .490 (.370) .140 (. Evidence is lacking for the carcinogenicity of tungsten.360 (.770 (.160 (.190 (.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 .270 (.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 .100) Selected percentiles ( 95% confidence interval) 50th .690) .078-.460) .810) .290-.110 (.230) .190-.340) .150) .400) .430 (.080-.180) .180 (.100 (.070 (.113 (.330 (. which is used in the steel industry.270 (.105) .380-.080 (.260-.101-.130-.080-.100) .180) .380-.110 (.096-.250) .130) .310-.070) .050-.077-.116) .060 (.430 (.290-.081 (.620) .113 (.120) .360 (.100) .065 (.300 (.080) 75th . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.290 (.520) .120) .160) .080 (.050-.380) .400 (.104) .800) .53) .470-.090-.090) .480) Total .460 (.340-.240 (.190-.430) .260) .160-.110 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.066-.076 (.160 (. interval) .160 (.120) .070 (.220) .080) .430-.460 (.070-.073-.460 (.200 (.120-.450 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.082 (.270-.110 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.100 (.Metals Tungsten CAS No.530 (.420-.090-.500) . Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.090-.800) .091) .S.550) .550) .090) .120) .050-.560) .160 (.076 (.120) .090-.080) .160) .082 (.310-.060-.410-.950) .430 (.190-.140 (.170) .350-1.130) .095-.170-.250) .160-.250-.130) .070) .200) .390) .140 (.150 (.280 (.330) .074-. Tungsten compounds are used as lubricating agents.082-.097-.120-.320-.120 (.260 (.060-.270-.520) .00) . filaments for incandescent lamps.071-.084-.158 (.550) .560) .470) .084) .230 (.110-.113 (.160-.210 (.132) .060 (.086 (. respectively. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.370 (.092 (.630) .370 (.080 (.130-. population from the National Health and Nutrition Examination Survey.080-.100 (.088) .070) .04.130) .095-.093-.350) .490) .400 (.310) .620) .204) .350) .250) .090 (.190 (.070 (.070-. which are used in rock drills and metal-cutting tools.111-.180) .240-.120-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.230-.100) .130-.140) 90th . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.080 (.620 (.190-.070-.390 (.290) .060-.220-.151) .260-.110-.530 (.070-.060 (.250) . and for producing ferrotungsten.130) .280-. bronzes in pigments.380-.230-.

079 (.459) .130 (. population (CDC.462) .098-.300 (.098 (.205-.224) .133) 90th .058-.098-.358) .091) .287) .148) .082) .080-.353 (.136-.215) .28) .284) .302-.085-.080-.152-.605) .158) .071 (.065-.329 (.067 (. similar to those in this Report (Schramel et al.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 .049-.329-.154) .059-.078) .727) ..136-.308) .331-.275 (.174) .148 (.333 (.431) .065 (.174 (.179-.083-.122-.060-.073 (.217-.170-.087) .167-.167-.103-.301) .197-.056-.218 (. or exposure that a control group of non-metal workers had mean levels differences.299 (.216-.181 (. measure urinary tungsten.184 (.167) .078 (.267) .084 (.079) .340 (.497 (.283) .168 (.069-.059 (.054-.094) .426) .301) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf..344-.285) .070 (.131-.138 (.091 (.386) .065-.075-.081 (.138) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.270 (.555 (.169 (.538) .465) .245-.085) .392) .214-.085 (.056-.233-.120) .075) .116) .079) .091) .431) .315-.165) .167) .250-.075-.059-.255 (.354) .100) .439 (.074) .066 (.158 (.061-.083) .339 (.383 (.375) .206-.081-.124-.222) . interval) .431) .090-.121-.439 (.119-.482 (.333) .237) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.333 (.063-.197 (.061-.144 (.073 (.667 (.231 (.153-.130-.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 .186 (.079) .286-.122 (.250 (.222-.199 (.079 (.145 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.279 (.070 (.077) .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-.094-.215 (.078) .136-.302-..077) .093) .068 (.133) .484 (.582) .072-.082) .122-. population from the National Health and Nutrition Examination Survey.079) .083 (.154) .190) .063 (.091) .125 (.086) .067 (.078 (.360 (.326) .080 (.209-.797) .176-.067-.317 (.200-.133) .146) .317-.187) .086-.068-.075 (.158) . Using neutron activation analysis to 2000.081 (.(Kraus et al.089) .201) .216 (.333 (. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.379 (. 2003.099-.074) 75th .138 (.339 (.500) .333-.253) 95th .359 (.880) .739) .150-.116-.090-.069 (.188-.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 .096) .333) .453) .117) .250 (.146 (.087 (.086) .200-.098) .055-.077-.104-.092) .272-.198-.208-. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.083 (.071 (.074-. Patients with medically-inserted tungsten found at increased levels in drinking water.081) .214) .465) .061-.359 (.059-.216-.231-.300) .083) .093-.267-.065) .091 (.082 (.064-.105 (.333 (.176-.164 (.074-.116 (. 2001-2002.294 (.153) .098-.063-.089 (.308) .136-. 1998).073 (.075) .088) . Nicolaou et al.060 (.279 (.364 (.063-.053-.199 (.150-.439) Total .060-.078-.120) .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.069 (.057-.S.064-.095) Selected percentiles ( 95% confidence interval) 50th .S.144-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report. (1987) found possibly due to methodologic.125) .347 (.426) .634 (.071-. 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.301) .077-.279 (.119 (.073 (.071 (.211 (.084 (.071) .091) .203-.063 (.253 (.075 (.201 (.161) .146 (.197) .084) .414) . 2001).293 (.071) .143-.554) .072 (.412 (.139 (.072-.151 (.063-.237) .333-.106 (.667) .086) . population.094) .155-.436) .436-1.065-.108) .066 (.105 (.484) .054-.124 (.253-.157) . 2005).258-.169) .065 (.261-.341 (.300-.179-.265 (.823) .381) .237-.180-.216-.139-.080 (.109-.117 (.074 (.150 (.084) .107-.100 (.143 (.100) .300-.216 (.278-.139) .158) .353 (.258 (. 1997).240-.088) .410-.317) . and 2003-2004 (Paschal et al.306) .071) .111 (.197) .121 (.108-.109 (.126-.354-.136 (.385 (.452-.255-.255 (.095-.057-.S.062 (.198) .

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

036 (.014 (.017-.014 (.030 (.032 (.015 (.008 (.008 (.019-.019-.013 (.007-.015 (.009-.009) Selected percentiles ( 95% confidence interval) 50th .030 (.014 (.007) .056) .048 (.007-.036-.007-.008) .127) .022 (.027 (.006 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.060 (.007-.022-.005-.051) .019-.046 (.009-.035) .007 (.008-.017-.008 (.006-.069) .017) .006-.009-.008 (.011) .036) . Uranium has many commercial uses.009 (.016 (.023) .088) .020-.010) .012-.011) .010-.018) .033 (.009 (.024-.012-.006-. in some ceramics.013) .020 (.027 (.016) .007 (.020) .008 (.023 (.029-.053) . including nuclear weapons.011-.053 (.012-.072) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.013 (.010) .054) .007-.028-.017-.016) .012-.023 (.027) . and 0.020) . the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.010) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.009-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.046-.037) Total .011) .017) .038) .011) .114 (.054) .054-.009) .006-. 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.039) .007-.006 (.052 (.008 (.010) .011-.009) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Variable concentrations of uranium occur naturally in drinking water sources.011-.042 (.022-.016) .067) .026 (.004.009) .005-. 01-02.034-.041 (.031 (.031 (.017 (.038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .024 (.009 (. and 03-04 are 0.011-.007 (.030 (.008-.007 (.048) .009) .008) .009 (.009) .012) .022-. or processing.012 (.065) .006-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.008-.016-.011-.015) .022) .005-.027) .010 (.013 (. 235U (about 0.037 (.007 (.015) .008 (.007 (.062) .010) * .007-.015 (.023-.010) .031 (.027-.010-.014 (.009) .021) .005.S.046 (.043) .158) .040 (.008) . see Data Analysis section) for Survey years 99-00.016) .013) 90th .055 (.014 (.037-.006 (.007-.028-.008 (.023) .024-.033 (.007 (.008-.063) .029 (.006-.017) .007-.013 (.026-.018 (.027 (.017-.044 (.006-.026 (.026) .028 (.011 (.030-.012) .023-.009-.008) .017-.007) 75th .008) .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 .020-.007) . and as an aid in electron microscopy and photography.024-.017) .007 (.031 (.012 (.040 (. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).007-.040-.009 (.010) .011) . Since the 1990’s. 0. human exposure occurs primarily by inhaling dust and other small particles.009) .015-. Fourth National Report on Human Exposure to Environmental Chemicals 239 .013-.007) .034-.012-.021-.021) .009) .027) .017) .030) .008 (.008 (.037) .065) .006-. In workplaces that involve uranium mining.009-.012 (.010) .Metals Uranium CAS No.040) .049) .008-.021) .020-.008-.016) .036 (.004.009) .009-.011) .007 (.027 (.064 (.006-.008 (.013 (.007) .029-.010-.013 (.009) .008-.017 (.046 (.011-.018) .010-.021-.012) .025-.026 (.033) .027-.005-.006-.007 (.007-.035-.008 (. Thus.009 (.039) .041 (.009-.006 (.023 (.009-.038 (.036) .012 (.019-.009-. respectively.067) .039-.018) .016) .007-.011) .010) .045) .021 (.010 (.010) * .009 (.034) .010 (.050) .006-.008 (.037) .009) .047 (.013-.018-.021 (.037) .023-.010 (.007-.049) .008-.013 (.043 (.016-.013-.008 (.012 (.021 (.012 (.028 (. nuclear fuel.028 (.026) 95th .009) .012) .009 (.009) .042) .020-.027-.012-.019 (.040) .005-.046) .020-.018 (.010-.009 (. and 234U.026) . population from the National Health and Nutrition Examination Survey.010 (.007-.026-.040-. interval) .036-.027) .015 (.033-.279) .007) .046 (.006-.007-.066) .009) * .035) .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 .031-.007-.010-.011-.023) .056) .031 (.045) .006-.008 (.023-.009 (.72%).007-.014 (.008 (.073) .018) .008 (.016-.017-. milling.007-.050) .011 (. 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.007 (.

010) .014) .006) .014) .021-.058) .033 (. with much slower elimination from bone.014-.007 (.020-.007 (.011-. Inhaled uranium-containing particles are retained in the lungs. Uranium is eliminated in feces and urine.007) .016) .008) .080) .007 (. 240 Fourth National Report on Human Exposure to Environmental Chemicals .016-.024) .007 (.015-.029 (.008) .007) .S.008-. After exposure to soluble uranium salts. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.009 (.009-.008) .034 (. which can occur occasionally from high occupational exposure.018) .009) .034 (.010-.034 (.008-.006 (.009-.005-.017) .051) .023-.010-.017-.016) .009) .053) .035 (.024 (.006-.015 (.031 (.015-.020 (.013) .009-.016) .008 (.022 (.030-.007-.032) .028 (.032) .007 (.010-.027) .011) .008 (.015 (.008) .063) .034 (.007 (.014) 90th .015 (.028) .013 (.007-.025-.011) .007-.009) .028) .061) .027 (.007 (.011) * .006-.009) .005-.051) . liver.020-.006-.004-.009) * .031-.009-.010) * .051 (.044) .015-.013) .009 (. 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.016) .009) Selected percentiles ( 95% confidence interval) 50th .010) .006 (.010-.007 (.016) .043 (. the shrapnel acts as a source of chronic.006-. 1992).010-.010) .025-.005 (.009) .010) .013 (.029) .024-.037 (.020 (.009) .006-.018 (.048) .019-.015 (.005-.019-.013 (.047) .030-.012) .010 (.015) .012-.020-.027-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.029) .030 (.017-.100 (.026 (.012 (.024) .005 (.010 (.006) .009) .008 (.011-.007-.006-.010 (.017) .007-.029) .024-.011 (.077) .024) .042) . and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.039) .012 (.013 (.018-.005 (.016) .014-.010-.025) 95th .013-.074) .030) .030 (.006 (.024 (.018-.008) 75th .008-.007 (. In cases of retained DU shrapnel. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.010-.019 (.006-.005-.006-.008) .029 (.009-.033 (.051) .008 (.018-.024-.007 (.028) .006-.027 (.012 (.010) .006-.050) .006 (.029 (. 2005).019 (.054) .017 (.008 (.019 (.022-.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 .025-.019-.016-. interval) . low level exposure.017-.008-.013 (.017 (.007-.006-. 0.016 (.042-.011) .053) .019) .006) .016-.026 (.006-.006) .007-.034) .022 (.014 (.067) .005 (.029) .007 (.007-.005-.045 (.014-.006-.008 (.016) .028 (.030 (.006-.011-.028-.028) .033 (. After inhalation.020) .024) .040) 883 682 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites * Not calculated: proportion of results below limit of detection was too high to provide a valid result..011-.022-.010-.024) .024 (.008) .019-.014 (. kidneys.021) .011-.026 (.012 (.050 (.007 (.008-. where limited absorption occurs (less than 5%).011-.008) .018-.011-.025-.146) .027 (.007 (.009) .021 (. which represents distribution and excretion.033) .1%-6% of an ingested dose may be absorbed.012 (.022 (.006-.011-.017-.015-.015) .027-.035 (.008) .027-. Health effects from uranium exposure result from chemical toxicity to the kidney.013) .059 (.010 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.008 (.004-. 2003).011 (.021 (.010-.034-.041) .006-.009) .015-.Metals impact.012 (.006-.012 (.058) .015) .018-.040 (.034 (.007 (.007 (.007-..008-.034-.009) . the initial half-life of uranium is about 15 days (Bhattacharyya et al.012) .014) .006-.009) .022-.050) .039) .017) .010-.009 (. After long term or repeated exposure.013 (.015) .013 (.007-.033 (.019) .019-.027-.009 (.007 (.007 (.048) .021 (.270) . population from the National Health and Nutrition Examination Survey.013 (.006) .030) .010) .021 (.039) ..011-.056) .039) Total .008) Sample size 2464 2689 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .010-.020-.005-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.025 (.016) .008 (.010 (.006-. Depending upon the specific compound and solubility.006-.006-.007 (.007 (.006 (.022) . Radiation risks from exposure to natural uranium are very low.016-.005-.008 (.012-.027) .008) .009-.006-.025 (.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 .042) .006-.008) .008) .013 (.026-.006 (.009 (.026) .007 (.020 (.006-.008 (.012) .007 (.013 (.007) .

. 1978). Six workers in a depleted uranium program showed concentrations of 0. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. Karpas et al... Centers for Disease Control and Prevention (CDC).107:143-157.1992.gov/ toxpro2. Third National Report on Human Exposure to Environmental Chemicals.Metals injury associated with elevated urinary uranium levels (Kurttio et al. the geometric mean urinary uranium concentration was 0. 1992. 2002).S. 2006). Zimmerman I. A cohort of 46 U. 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. Pillai KC. McDiarmid M. Dietz LA.. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U..e. Muggenburg BA. Pullat VR. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.atsdr. respectively. Kent (England): Nuclear Technology Publishing. the median urinary uranium concentration was 2. (May et al. 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. 2003. Breitenstein BD. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.1996. but in whom no shrapnel was embedded. population. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. In: Gerber GB. ingestion.html.011 μg/L (McDiarmid et al. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. Ejnik JW.. 2006). Volf V. environmental levels) and health effects is available from ATSDR at: http://www. 2004).55 μg/L (median 0. and no consistent effects on multiple endpoints of kidney function were found. Radiation protection dosimetry. 41 (1). References Bhattacharyya MH.168(8):600-605.S. (Kurttio et al. or wound contamination.. 1994. 2000). Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Information about external exposure (i.78:143-146.S. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. 2006). 2005.110 to 45 μg/L (Ejnik et al.066 μg/g creatinine (Gwiazda et al. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. Benedik L. and 2003-2004 (Dang et al.. during.. Guidebook for the treatment of accidental internal radionuclide contamination of workers.65 μg/L).. in that the levels were below their respective detection limits (Byrne et al. 2004). Stradling GN. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure... Vol. In the same study. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. IARC and NTP have no ratings for uranium human carcinogenicity. In two studies of a Finnish population with high natural uranium concentrations in their drinking water.. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. 2000).162 μg/L) (Orloff et al. 2001-2002. had a mean urinary uranium concentration of 0. McDiarmid et al. Komaromy-Hiller et al. 2004). Hamilton MM. Carmichael AJ. 2006). 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. Squibb K. Galletti. The U.S. Atlanta (GA). Sci Total Environ 1991.. Boyd P. 28 soldiers who may have been exposed to DU by inhalation. Health Phys 1992. with emphasis on quality control. 1991. NRC. urinary levels of uranium were as high as 9. 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. pp. 2004). eds. Thomas RG. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Health Phys 2000. In a study of 105 persons exposed to natural uranium in well water. soldiers evaluated before. the median urinary concentration was 0. Fourth National Report on Human Exposure to Environmental Chemicals 241 . Hamilton et al. Dang HS. Tolmachev et al. EPA.. Drinking water and other environmental standards have been established by U.S.61 μg/g creatinine. Mil Med 2003. Uranium content of blood.078 μg/L (ranging up to 5... In 17 U. 2002.S. 1-49. Metivier H. et al. Byrne AR. 2006.cdc.62:562-566. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. Horan P. Durakovic A.. although slightly increased during and after deployment.

Komaromy-Hiller G. Salonen L.22–Bioassay at uranium mills. Health Phys 1996.71(6):879-85.47(6):972-982. et al. Gucer P. Jarrett JM. Washington (DC): NRC.296(1-2):71-90. Metcalf S. Shelly T. Roth P. Karpas Z. Sabbioni E. Review of elements in blood. Human exposure to uranium in groundwater. Katorza E.110(4):337-342. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Health Phys 2002. Ting BG. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Radiat Environ Biophys 2005. Engelhardt SM. Element reference values in tissues from inhabitants of the European community. Sampson EJ. Pirkle JL. Charp P. Paschal DC. Kurttio P. NRC). McDiarmid MA. Uranium and thorium in urine of United States residents: reference range concentrations. Hancock RG. Nuclear Regulatory Commission (U. Auvinen A. Wilson PD. Halicz L. Sci Total Environ 1994. Ejnik J. Health Phys 2004. Environ Res 1999. May LM. Renal effects of uranium in drinking water. Salonen L. Squibb K. et al. Van der Venne MT. Comparison of representative ranges based on U. Environ Health Perspect 2002. McDiarmid M. et al.81:45-51. Lewis BM. Health Phys 2004.158:165-190. July 1978. Li WB. Squibb K. Int Arch Occup Environ Health 2006. Noguchi H. Pinto V. Heller J. et al. Saha H. Biokinetic modeling of uranium in man after injection and ingestion. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Howerton K. Ash KO. VI. Komulainen H.S. Auvinen A. Marino R. Andrews WS. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Saha H. Environ Res 2004. Paretzke HG. Karpas Z. Nuclear Regulatory Commission (NRC) Guide 8. D’Annibale L. Ough EA. Cordero S.82(4): 527-532. Roiz J.94:319-326. Biologic monitoring for urinary uranium in Gulf War I veterans. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Cremisini C. Marko R. Englehardt SA. Kane R.S. J Toxicol Environ Health A 2004. Health Phys 2006. Uranium daily intake and urinary excretion: a preliminary study in Italy. Am J Kidney Dis 2006. Kurttio P. Clin Chim Acta 2000.S. U. Tolmachev S. et al. Pekkanen J. Jackson RJ. Harmionen A.87:51-56. Lorber A. Oliver M.67(8-10):697-714. Hollriegl V.79(1):11-21. Mistry K.S. Inductively coupled plasma mass spectrometry as a simple. patient population and literature reference intervals for urinary trace elements. Oberbroekling KJ. McDiarmid MA.91(2):144-153. Gwiazda RH. Orloff KG. U. Kalinsky V. et al. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Scott K.86:12-18. Hamilton EI.44:29-40.Metals Galletti M. Oeh U. Wahl W. Makelainen I. Health Phys 2003. rapid. plasma and urine and a critical evaluation of reference values for the United Kingdom population.85:228-235. Smith D. concentration and daily excretion of uranium in urine of Japanese. Kuwabara J. Bennett LG. Kidney toxicity of ingested uranium from drinking water. Costa R.

Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.40 (4.0) 10.0 (8.5 hours and has a small estimated volume of distribution (Crump and Gibbs.00) 4. In addition.50-4. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.40) 3.EPA.45-4.70-6.10-7.50) 11.20 (8.00) 3.76 (3.29-3. milk. population from the National Health and Nutrition Examination Survey.05 (2.40) 6.Perchlorate Perchlorate (Urbansky.90 (5.0) 11.0) 15.80-8. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .90 (3.60 (4.0-17. interval) 3.75-3.40 (4.40 (5. and limited applications in pharmaceutics.96 (3.79 (2.62 (3.12) 3.08-3.21 (2. 2005).90 (2.0 (9. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.50) 5.35 (3.11) 3.10-4.80 (3.80) 12.40) 3.50 (8.50-3.68) 4. lettuce) can be the main sources of intake for humans (FDA.80) 75th 6.30) 6.60-7. Inhibition of iodine uptake by competition for the sodium/iodide symporter in the thyroid can be estimated in humans by measuring radioiodine uptake CAS No.0 (12.0-14.0-19.0 (9.20-4.40-7.81-16. 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0-17.30-7.20 (4.20) 7.0 (11.50-4. It is normally found and produced as the anion of a sodium. Drinking water.0) 15.76) 4.30 (5.70-7.0) 13.89-3.0) 9.51 (3.40-11.01 (2. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.30 (5.40) 2.0 (11.0 (13.00-5.30 (2.g.20 (7.50-11.50 (5.80) 7.0) 10. Survey years 01-02 03-04 Geometric mean (95% conf.90-11.90) 5.51 (3.00) 3.0-23.0 (12.50 (3.10 (2.70 (3.39-4.0) 95th 14. and electroplating.19-4.0) 9.0 (11.0) 708 617 681 652 1228 1092 Limit of detection (LOD.90 (5.70 (3.00-6. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.40 (3.40 (8.0) 9.0 (11. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.67-5.10) 12.50-7.0 (11.70 (3.20 (4.30-6.90-3.80-15.40) 3.0-15.0) 9.0) 8.60 (7.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.0) 14.90 (5.0 (11.54 (3. Other manufactured uses include fireworks.20-12.66) 3.30-17.S.0) 13.0) 8. Perchlorate is stable under most environmental and physiological conditions.20 (5.0 (9. 2005).0 (8.0-29.0-18.20 (2.20 (6.70-3.0-15. 2002).80-4.80 (6.40 (5.05 and 0.70-9.26 (2.80-6.10-11.10) 3.0) 11.40-4.05.10 (5.32 (3.10-12.75 (3.0) 13.0) 13.20-3. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.0) 16.0 (9.70-12.40) 4.10) 3. leather tanning.90-11.22-5.0-18.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.84) 14.40 (5.16) 3.30-19.50) 3.0) 13.00) 5.90 (4.44-4.50) 5.0-20.70-3.65) 3.22 (2.40-6.00-6. potassium.0 (12.0) 14.0 (10.0) 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 3.0-17.0-18.30 (2.46) 3.20-11.10-11.20-4.88) 3.0) 13.47-4.0 (9.93-3.19 (3.80-4.0) 9.93 (4.20) 4.0) 13.0-17.30) 6.0) 10.S.60 (4.18-3.10 (6.20) 3.30-7.0 (9.00) 7. but has strong oxidant properties in the presence of concentrated acids.0-17.10 (7.49-3. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.20 (2.0) 9.90-6. certain catalytic metals.70-11.70) 3. matches. Perchlorate was added to the U.10) 5.0 (12.09) 3.87-3.0 (8.31) 2.90) 6.0 (11.60) 5.0 (11.0) 13. fabric dyeing.80 (3.60) 8.90-3.80) 3.93-4.0) 14.0 (11. and certain plants with high water content (e.0 (11.0 (8.11) 4.40-13.50) 6.90-10.40-5.10) 5.40) 90th 10.80-12.0 (9. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.38) 5.S.0 (8.40 (3.90-9.60-6. 2007). and reducing agents.0) 12.81) Selected percentiles ( 95% confidence interval) 50th 3.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4..90-12. or ammonium salt.56) 3.0-17.07-4.40-4.74-3.90-9.. 1998).03) 3. laboratory analysis.0) 11.0) 19.60) 3.80 (7.10 (6.02 (3.70-5.

61-5.77 (3.08 (3.00 (4.40) 17.40 (3.64-3.82 (5. Also.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 3.87 (5.7 (11.10-3.87) 2.90-15.1-22. 2005.90-2.4-16. 2005). Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.0) 6.g.30-5.90 (2. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.20-4. 2002.0) 12.50) 9.70 (2.60 (3..26) 4. up to 68% RUI has been demonstrated. 2003.0 (8.80-3.EPA.1 (8.36 (8.66) 3..14 (2.39-4.76 (3.04-3.5 (13..00) 4. population from the National Health and Nutrition Examination Survey.70-15.10 (4.20 (4.84) 2. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.1-13.2) 8.80-3. nitrate. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability. Many factors may be important in consideration of perchlorate action on the thyroid: dose.00-3.67) 5.60-5.70-5.3-14.60-11.0) 7.40) 3.12 (6.09 (7. gender.44) 3.S.00-2.60-8.93-7.30-5.0) 4.44-6.39 (3.0 (11.S. 2002.98) 3.60) 8.0) 9.0-14.70 (4.0) 13.20 (2.0) 12.25) 5.50) 2.S.70-4.30) 3.20 (3.90-9.90 (4. thiocyanate. 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.4 (11. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.90 (7.50) 2.58) 2.60-6..20) 3.70) 2.54 (2.6) 20.80 (4.47) 2.40 (3.59) 3.29) 2.1) 8. U. 2005).09) 3.03 (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.50-5. 2007).93-5.30 (5.46-13.60-15.19-10.1-14.S.50 (3..99-3.32) 5..72 (3.22-4.18-3.0 (10.50-9.10 (6.90 (2.S.76-3.51-4.10) 13. women with urinary levels of iodine less than 100 micrograms per day.45) 3. 2001. 2002).4 (8.40) 5.87 (7.90-3.0-19.87) 7.53 (2. 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.29-6.80 (7.50) 95th 12.73) 3. although iodine intake was higher than U.33-12.30) 90th 9.10 (1.96) 2.0) 10.22-4.52 (8.70-3.40 (4. chronicity of exposure.10-7.20) 8. Lamm and Doemland.61 (5. In the U.34-3.54 (3.39) 2.02-4.S..3) 8.64) 5. Li et al. levels.35 (4.24-2.10) 4.EPA.4) 8.12-2.. dietary iodine intake.91) 4.0 (8.26 (3.99 (5.52-9. 2005.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3..22 (2.0) 12.1-16.15-12. in a representative sample of U.33 (7.4) 13.30-10.50 (6.10 (2.90-20. However.0) 9.08) 3.10) 6. Steinmaus et al.19-6.40 (7. Lawrence et al.42 (3.Perchlorate inhibition (RUI).16-3.21 (2.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.37-13.4 (11.30) 5.25) 5.70) 10.97-5. 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.51 (3.0 (9. and the presence of other substances known to affect thyroid function (e.05 (4.86) 4.93-8.20-3.00-11.30) 75th 5. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.95 (2.41-9.89 (2.S.0) 11..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 .6) 12.33-6. Survey years 01-02 03-04 Geometric mean (95% conf.60) 10.02) 3.30 (6.93) 3.61-10.10 (4.20-3.60-3.3 (10.80 (7.93-5.6-17.3) 11.50) 5.25) 5.0-17.60-11.60-8.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5. menopausal status. age.00) 3. medications).00 (2.30 (3.35 (2.74) 7. 2006.75) 3. 2005).40-10.90-11.20-10. perchlorate is negative in most genotoxic assays (U.3) 12.50) 6.45-2.00 (6.0-14.0) 12.0) 13.20 (7.22-6.89-3.56 (3.46 (3.43) 6.60) 3.81-3. NAS. 2000).8 (11.0 (11.00) 9.07 (2.1 (11.90) 5.0-44.83 (5.4 (10.70 (2.87-3. During gestation and infancy.35) 3. levels and sufficient in most participants (Tellez et al. interval) 3.04-3. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.10) 3.20-9.71 (5.2) 8.46-4.0 (9.5) 8. Greer et al.60-5.80) Selected percentiles ( 95% confidence interval) 50th 3.56-3.20 (6.50-3.0) 14.37 (4.25 (3.24 (4.0 (11.0 (9. 1999.

Washington (DC): National Academy Press. Braverman LE. 2005. Perchlorate in the United States. Also. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. and nitrate on thyroid function in workers exposed to perchlorate long-term. Environ Health Perspect 2007.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653.46(5):509. Blount BC. Benchmark calculations for perchlorate from three human cohorts. population..40(21):6608-6614. National Academy of Sciences (NAS).gov/toxpro2. Barnard JC. May 2007. 2005). Tellez RT.. Crump KS.S. (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. thiocyanate.115(9):1333-1338. Available at URL: http://www. Environ Sci Technol 2006. Neonatal thyroxine level and perchlorate in drinking water. Howd R. 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. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. J Occup Environ Med 2000. Perchlorate Exposure of the US Population. The effect of perchlorate. Gibbs JP. Goodman G. Abarca CR.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Caldwell KL.html. National Research Council of the National Academies.90(2):700-706.41(5):409-411. J Clin Endocrinol Metab 2005.. Pleus RC. Valentin-Blasini L. Magnani B.42(2):200-205. Environ Health Perspect 2005. Buffler PA. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Braverman LE. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. et al. 6/2/09 Greer MA.11(3):295. CFSAN/Office of Plant & Dairy Foods. Low dose perchlorate (3 mg daily) and thyroid function.cdc.fda. 2001-2002. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.atsdr. Lawrence J. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Braverman LE. Richman K.17(4):400-407. Erratum in: Environ Health Perspect 2005. Blount BC. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Kirk AB.110(9):927-937. Miller MD. Mauldin JP. Li Z. epa. Chacon PM. Dyke JV. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. J Expo Sci Environ Epidemiol 2007. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Skeels MR. Lamm SH. References Blount BC.113(11):A732.EPA at: http://www. Li FX.S. Pino S. Doemland M. Pirkle JL. 2007). et al.113(8):10011008. Thyroid 2001. Page Last Updated: 05/28/2009. Pirkle JL.gov/safewater/ccl/perchlorate/perchlorate. Lamm S. Valentin-Blasini L. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. 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. Lamm SH. J Occup Environ Med 2003. Health Implications of Perchlorate Ingestion. Lau EC. Environ Health Perspect 2006. 2005). Osterloh JD. EPA reference dose (Blount et al. et al. Pino S. Primary congenital hypothyroidism. most of the population is considered to be below the U. newborn thyroid function. Greer SE. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Deyhle GM. Lamm SH. et al. Kelsh MA. and environmental perchlorate exposure among residents of a Southern California community. Blount et al. Food and Drug Administration (FDA).htm. Jackson WA.114(12):1865-1871. Cross M.S. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Sesser DE.10(8):659-663. Daaboul JJ. Osterloh JD. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002.45(10):1116-1127. Thyroid 2000. Dasgupta PK. Lawrence JE. Erratum in: J Occup Environ Med 2004. Steinmaus C. 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. He X.html and from ATSDR at: http://www. Landingham CB. Byrd D. Crump KS. Additional information about exposure and health effects is available from the U. Analysis of relative source contributions to the food chain. Environ Health Perspect 2002. Rutherford GW.

246 Fourth National Report on Human Exposure to Environmental Chemicals .S. Thyroid 2005.S.epa. Available from URL: http://cfpub. Drinking Water Contaminant Candidate List. Doc. Integrated Risk Information System (IRIS). EPA/600/F-98/002 Washington (DC). EPA).9(3):187-192. U. EPA). 1988.Perchlorate pregnancy and the neonatal period.1/15/06 U. Perchlorate as an environmental contaminant.S. Environmental Protection Agency (U.S. Perchlorate. Environ Sci Pollut Res Int 2002. Revised 2/11/05. cfm?substance_nmbr=1007.15(9):963-975. No.gov/iris/quickview. Environmental Protection Agency (U. Urbansky TF.

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

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

. U.400-1. Harada et al.10) .500-1. 2003). interval) Selected percentiles ( 95% confidence interval) Sample 95th .400 (<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 .. 2004a.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al.500) .400 (<LOD-.10) . Kennedy et al. which may vary for some chemicals by year and by individual sample. 2007).300 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. thyroidal).3.800 (.700) .300 (<LOD-.500 (. 1999. 2003a.400-.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . 2007b.. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. Fei et al.. developmental and teratogenic effects were demonstrated in offspring...700 (. Cook et al. reproductive.600-2. 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. 2003a. 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. Lau et al. 2005). development in offspring was stunted and hypothyroxinemia was observed. At doses causing maternal toxicity..10) * 03-04 03-04 * * < LOD < LOD < LOD .400-1. 2003. In such studies. PFOS. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. 2007a...S.500-3. 2003. PFOA.400-1..400-1. 2003a). perfluorohexanesulfonate (PFHxS). 2004.400-.900 (. PFOS.500-1. Olsen et al.50) .S.00 (. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. and perfluorononanoic acid (PFNA) are detectable in a high percentage of the participants and PFOS levels are generally 3-10 times higher than PFOA levels (Calafat et al. U. 2001. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.20) .900 (.600 (. However. < LOD means less than the limit of detection.S. monkeys. possibly related to lung immaturity (Lau et al.. 2007a. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. EPA. and humans.500-1.500) . 2005).400) .400-1. see Data Analysis section) for Survey year 03-04 is 0. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. 1992. the median PFCs values tend to be roughly similar in these age categories (Olsen et al..80) 640 1454 03-04 03-04 * * < LOD < LOD .00) .300-1. and changes in thyroid hormone concentrations (Grasty et al..800) 1. Thibodeaux et al. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.80) 485 538 962 Limit of detection (LOD. 2003a.800) 1. In comparing three separate reports on adults..800 (. or increased cancer rates (Alexander et al. 2004.300 (<LOD-.600 (. 2003). PFOA. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 249 . 2004b).108 times higher than background serum levels in humans (Butenoff et al.10 (.500-..500) .400 (<LOD-. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.00) .500-1.. the potential to estimate risks to humans from animal doses is uncertain. 2007. EPA. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. 2004). elderly and children.500) . Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. Survey Geometric mean (95% conf.800 (. 2003a). Animal studies of PFOS have demonstrated weight loss. 2003.800 (.500 (<LOD-1. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. 2003).00) .. population.500 (. At high but non-toxic maternal doses of PFOS.. 2004).600 (.. Olsen et al.40) . Olsen et al. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. and there was no clear evidence of excess all-cause or diseasespecific mortality..900 (.S. hepatotoxicity. 2007b).500) 90th .

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

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 .500-.3.400) . Survey Geometric mean (95% conf.300 (<LOD-. < LOD means less than the limit of detection.500) 485 538 962 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .600) < LOD .400 (<LOD-. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 251 . see Data Analysis section) for Survey year 03-04 is 0. which may vary for some chemicals by year and by individual sample.S.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.900) < LOD . Survey Geometric mean (95% conf.300 (<LOD-.300-.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .S. population from the National Health and Nutrition Examination Survey. 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. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.600 (. see Data Analysis section) for Survey year 03-04 is 1.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (<LOD-.400 (.0.

14 (.51) 1.30) .40-1.20 (1.90 (4.50 (1.12) .80-4.70-7.73-2.40-3.50 (4.6) 7.816-1.50-10.826-1.586-. 252 Fourth National Report on Human Exposure to Environmental Chemicals .60) 2.42 (1.3 (9.80) 90th 2.54) .56-1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.3.70) 2.70-5.00 (1.10 (1.90 (2.50) 6.20 (6.700 (.1) 485 538 962 Limit of detection (LOD.0) 1053 1041 03-04 03-04 03-04 1.20) 1.10) 75th 3.40) 640 1454 03-04 03-04 1. population from the National Health and Nutrition Examination Survey.80-3.00 (.00) 2.10-9.00 (1. Survey Geometric mean (95% conf.00) 3.800-1.60-8.20-1.20) 2. interval) 1.900-1.90) 1.10-9.87-2.50 (6.721-1.30 (1.00-7.70-2.50-6.30) 03-04 03-04 .809) 1.60-4.20) 485 538 962 Limit of detection (LOD.900-1.70-2.10) 6.10 (.00 (1.60-2.S. interval) .00 (1.600-.60 (6.963 (.20-1.30-2.70-6.60-2.60) 1.20-1.80-4.20 (6.50) 2.80) 4.80-2.30 (1.90 (1.50 (1. see Data Analysis section) for Survey year 03-04 is 0.10) 5.90 (1.80 (1.80-8. see Data Analysis section) for Survey year 03-04 is 0.20) 1.00-1.03) 1.44 (2.70 (1.00-8.984 (.50) 2.20) .10 (.30) 3.70) 3.30 (7.90) 90th 5.20-3.50 (1.90) 1.900 (.80 (4.10) 1.00) 1.30 (2.10 (4.40) 2.60-3.90-19.01 (1.77-2.90 (4.900) 1.72 (1.697-1.80) 3.26) 2.900-1.91) 2.30-9.40 (1.08) 2.70 (2.50-3.30-6.92 (1.80-7.900-1.80-8.17-1.10) 1.30 (2.70-10.00-1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80-7.90) 8.30) 3.40) .20 (1.00 (.60 (1.50 (2. Survey Geometric mean (95% conf.10 (.10) 8.861 (. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.60) 3.10-5.90) 3.70) 13.10) 4.40) 1.80) 1.90-10.40-1.17 (1.70) 1.16) .30 (3.70) 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 1.50 (6.S.70) 2.5) 8.60) 9.50-6.20-1.70) 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 1.40) 640 1454 03-04 03-04 2.30 (6.20 (1.10) 1053 1041 03-04 03-04 03-04 .00 (2.05-2.90-2.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.40 (1.86 (1.10) 4.80-3.80) 5.00-6.00) 1.900 (.10) 6.90) 1.50 (1.30-12.80-4.30 (1.50 (4.30) 3.70) 1.27) 1.5) 5.00 (5.835-1.852 (.10 (4.90 (1.0) 8.40 (1.30 (1.900-1.40 (2.80-6.80 (1.60-3.912-1.04) . population from the National Health and Nutrition Examination Survey.20-2.966 (.60-2.60 (1.1.60-4.80-12.09 (.834-1.90 (1.20 (1.800 (.10) 75th 1.60-7.40 (1.72) 1.700-1.40) 1.20) 03-04 03-04 2.62-2.689 (.67-2.900-1.60 (1.93 (1.40) 4.

90-4. interval) 20.0) 21. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0.70 (5.30-6.5) 18.5 (28.1 (23.3) 42.8 (34. see Data Analysis section) for Survey year 03-04 is 0.2 (27.90-12.40-17.5) 7.89 (3.1-52.3) 41.40) 75th 5.40-6.4 (17.0) 23.4-17.90 (7.6 (35.4) 21.0-16.4) 75th 30.60 (6.4) 20.11 (2.30-3.40 (4.70 (5.9) 9.80 (6.1 (19.80-12.0) 03-04 03-04 19.2) 45.60 (7.07-4.3-22.60-14.6-50.70) 6.00 (3.3 (44.00 (5.0 (20.0-66.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.95 (3.50 (3.5) 32.50) 4.1-33.30) 6.5) 8.1 (24.8-35.27) 4.5-21.7-49.70) 3.2) 30.7) 39.0 (27.9 (19.30 (3.6 (44.60 (5.70-7.7 (7.65-4.60) 03-04 03-04 3.4 (19.2 (19.20-9.5) 57.6-45.60 (3.8-22.7-53.40) 3.8-78.20-5.7-30.3 (35.50-13.6-24.8-30.40) 5.20) 7.50 (4.00) 3.3-61.6) 18.60) 8.70-5.2-57.10 (6.90 (7.30) 7.30-11.8-22.84-3.6) 62.10) 5.9-38.30-8.0-70.9 (17.2 (16.4-25.0) 485 538 962 Limit of detection (LOD.50) 7.70 (3.90 (5.3) 485 538 962 Limit of detection (LOD.0) 21.9-23.7-69.20) 10.18 (3.7 (13.S.2 (18.20) 4.2) 30.8-22. Fourth National Report on Human Exposure to Environmental Chemicals 253 .2 (28.60-13.80 (5.5-62.91) 3.90 (7.7 (35. population from the National Health and Nutrition Examination Survey.2 (21. interval) 3.30 (3.60 (4.60-9.7 (43.7 (43.50-6.6) 7.0-20.2) 640 1454 03-04 03-04 4.5-23.47-4.90-4.21-3.40) 90th 7.7 (35.0) 43.8 (37.3 (35.6) 35.9) 22. Survey Geometric mean (95% conf.7-33.70-7.1-25.10 (3.7-23.5 (28.37 (2.1-24.S.2-22.6) 9.80-9.4-42.4 (19.35) 3.5) 1053 1041 03-04 03-04 03-04 14.1.60-6.1-35.4.3 (17.80-4.6 (42.40-10.80 (6.8) 32.30-5.79) 4.3 (28.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.10-3.80 (7.8) 46.60 (6.4) 56.9) 22.40-6.8) 27.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50-4.20-4.4 (23.90) 6.82) 4.20) 5.5-33.20) 5.9) 27.5) 9.6) 42.3) 28.20) 7.4 (28.40-14.00 (5.5) 19.70-10.10 (3.70) 4.9 (13.85-4.70-9.67-4.20 (4.1) 15.80) 8.7 (19. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.47 (4.1-36.5) 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 21.1) 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 4.40 (6.4) 640 1454 03-04 03-04 23.6) 1053 1041 03-04 03-04 03-04 3.8-81.53) 3.8 (45.1) 57.99-3.30 (5.9 (22.20 (4.6 (19.9-19.6) 21.0) 90th 41.96 (3.0) 36.

200-.300) .300 (.300) .300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.300 (.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .S.4.300) .300 (. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0.500) .200-.400 (<LOD-.500) . < LOD means less than the limit of detection.300-.200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-. Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.200-.200-.300 (.200-. Survey Geometric mean (95% conf.200-.300-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .300 (.300 (. which may vary for some chemicals by year and by individual sample.300 (.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.300 (.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.200 (<LOD-. 254 Fourth National Report on Human Exposure to Environmental Chemicals .300-.S.500) 485 538 962 Limit of detection (LOD.300) .500) < LOD 485 538 962 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.300) . Survey Geometric mean (95% conf.300) .200-.300 (.200-.300 (.300 (.300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300) .500) .200-.300 (.2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0.

Fourth National Report on Human Exposure to Environmental Chemicals 255 . Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.700) 1.800) .30) 1.10) 1.10-1.10) 1. < LOD means less than the limit of detection.30 (1.00 (.900 (<LOD-1.700 (<LOD-.900) 485 538 962 Limit of detection (LOD.70) 1.800 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .10) . see Data Analysis section) for Survey year 03-04 is 0.900-1.700) 1.10-1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .90) .400 (<LOD-1.10 (.600 (<LOD-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 .30 (1.S.30) .3.300 (<LOD-1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .900-1.10 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey.S.00-1.40) < LOD < LOD .600 (<LOD-1.900) 1.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (. population from the National Health and Nutrition Examination Survey.900-1.600 (<LOD-1.500 (<LOD-. Survey Geometric mean (95% conf.900-1.700 (<LOD-2.900) .80) 1.700) 90th 1. Survey Geometric mean (95% conf.6.10-1.10 (.00) < LOD .400 (<LOD-.10 (1.900-1.800) .700 (<LOD-.30 (1.900-1.700 (<LOD-.20) 1.60) 640 1454 03-04 03-04 * * < LOD < LOD . which may vary for some chemicals by year and by individual sample.80) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300 (<LOD-.700 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900-1.300-2.30) 1.900 (. < LOD means less than the limit of detection.50 (1.20 (1.10) * 03-04 03-04 * * < LOD < LOD .00 (.60) 485 538 962 Limit of detection (LOD.10) .20-1.10-1.700) .600 (<LOD-.40) 1.10-1.50 (1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .600) .700 (<LOD-.00 (.700 (<LOD-. which may vary for some chemicals by year and by individual sample.

179:99-121. Moore JA. Kumar KS. et al. et al.134(1):18-25. Seneviratne HR. Sasaki S.46(2):141-147. Apelberg BJ. Halden RU. Cook JC. Taniyasu S. et al. Arendt MD. de Voogt P.68(6):465-471.124(2):119-132. Biegel LB. Holmstrom KE. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats.S. Saito N. Birth Defects Res B Dev Reprod Toxicol 2003.63:490496. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Corsolini S. Saito N. Environ Sci Technol 2004. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. J Occup Health 2004. et al. Environ Health Perspect 2007. Environ Sci Technol 2006a. Loganathan BG. Butenhoff JL. Jarnberg U. The influence of time. Kannan K. Hurtt ME. Herbstman JB. Grey BE. Harada K. Ingall GB.39(23):9101-9108. Polyfluoroalkyl chemicals in the U. Evans TJ. Moore RW. J Environ Monit 2005.39(23):9057-9063. in vivo. Rogers JM. Edwards EA. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Day RD. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Calafat AM. Toxicol Sci 2001. Yoshinaga T. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Mandel JH.34(4):351-384. Kannan K.104(2):322-333. Regul Toxicol Pharmacol 2004. Ye Y.115(11):1677-1682. Calafat AM. Fillmann G. Perfluorinated chemicals in selected residents of the American continent. Environ Sci Technol 2007a. Olsen J. Environ Health Perspect. Aguilar-Villalobos M. Gaylor DW. Keller JM. Environ Res 2005. Katakura M. Mohotti KM. Tarone RE. Chlorinated. Laane RW. Kuklenyik Z. Toxicol Appl Pharmacol 1992. Characterization of risk for general population exposure to perfluorooctanoate. Frame SR.41:2237-2242. Hurtt ME. Needham LL. Olsen GW. Wong LY. Suzuki E. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats.115(11):1670-1676. Needham LL. Environ Health Perspect 2007. Calafat AM. Rodricks J.99(2):253-261. brominated. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. et al.60(1):44-55. Mandel JH. Reidy JA. et al. Reidy JA.39(3):363-380. Yoshinaga T. O’Connor JC. Calafat AM. Olsen GW. Fluorotelomer alcohol biodegradation yields poly. Bignert A. Reidy JA. Androgenic deficiency in male rats treated with perfluorodecanoic acid.39(1):80-84.and perfluorinated acids.115(11):1596-1602. Cook JC. Kuklenyik Z. Falandysz J. Perkins RG. Murray SM. Dinglasan MJ. Hekster FM. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Environ Sci Technol 2005. Grasty RC. Yamashita N. and ex vivo studies. Peterson RE. Caudill SP. Mabury SA.40:21282134.7(4):371-377. The toxicology of perfluorooctanoate. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Lau CS. Kuklenyik Z.S. Kudo N. and perfluorinated contaminants in livers of polar bears from Alaska. Tully JS.1968--2003. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Wijeratna S. Butenhoff JL. Taniyasu S. Environ Sci Technol 2005. Tully JS. Needham LL. Biegel LB. McLaughlin JK. Environ Sci Technol 2005. Yamashita N. Toxicol Appl Pharmacol 1995. Koizumi A. Witter FR. Kamiyama S. Toxicol Appl Pharmacol 1990. Cook JC. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Mandel JS. Fei C. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Inoue K. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Kuklenyik Z. Kennedy GL Jr. Guruge KS. Bookstaff RC. Hurtt ME. Frame SR. Chem Biol Interact 2000. Burris JM. Watanabe T. Occup Environ Med 2003. Rev Environ Contam Toxicol 2003.Perfluorochemicals References Alexander BH. 2007b. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Liu RC. Yun SH.60(10):722729. Crit Rev Toxicol 2004. O’Connor JC. Needham LL. Caudill SP. Harada K. Kawashima Y. Morikawa A. et al. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries.38(10):2857-2864. Chemosphere 2006b. Environmental and toxicity effects of perfluoroalkylated substances. Environ Sci Technol 2004. Olsen GW. Reidy JA. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Bandai N. Calafat AM.113(2):209-217. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Seacat AM. Kannan K. Inoue K.Koizumi A.38(17):4489-4495. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism.

68:105–111. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Half-life of serum elimination of perfluoroo ctanesulfonate. Ellefson ME. Yamashita N. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat.41(9):799-806. Toxicol Sci 2003. and food items prepared in their packaging. Olsen GW. The developmental toxicity of perfluoroalkyl acids and their derivatives. Available from URL: http://www.Perfluorochemicals Kudo N. Kawashima Y. Rogers JM. Ehresman DJ.1177(2):183-190. I: maternal and prenatal evaluations. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Bronson R. perfluorooctanoate andother fluorochemicals in human blood. Butenhoff JL. Fourth National Report on Human Exposure to Environmental Chemicals 257 .2(1):53-76. Pepper K. fate and transport of perfluorocarboxylates. Coordinate induction of acyl-CoA binding protein. Horii Y. Reagen WK. Rogers JM. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Kannan K. Environ Sci Technol 2003. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Hanari N. Thibodeaux JR. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Barbee BD. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Taniyasu S. Olsen GW. Toxicol Sci 2003. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Olsen GW. Chemosphere 2004a.) Tittlemier SA. Taniyasu S. Environ Sci Technol 2006. Olsen GW.perfluorohexanesulfonate. Mair DC. Mandel JH. Olsen GW. et al. et al. Larson EB. Hanson RG.82(1):359. Stanton ME. Environmental Protection Agency (U. Butenhoff JL.111(16):1900) Olsen GW. Mandel JH.68(1):249-264. Environ Health Perspect 2005. Zobel LR. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Yamashita N.epa. J Children’s Health 2004b. Mandel JH. II: postnatal evaluation. Butenhoff JL. et al. Hansen KJ. Toxicol Appl Pharmacol 2004. Burris JM. Petrick G. Mar Pollut Bull 2005. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Hansen KJ. fast foods. 2007a. Environ Health Perspect 2003a. J Occup Environ Med 2003b. Ehresman DJ.113(5):539-545. Helzlsouer KJ. Hansen KJ. (Erratum in: Environ Health Perspect. Hansen KJ. Miller JP. Burris JM. Burlew MM. Cao XL et al. Church TR. Lau C. et al. fish. fish. Sources.. Prevedouros K. Biochim Biophys Acta 1993. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Horii Y. Environ Health Perspect. Toxicol Sci 2002. et al.45(3):260-270.40(1):32-44. Washington. Olsen GW. Hanson RG.54(11):1599-1611.111(16):1892-1901. U. Seacat AM. Butenhoff JL.51(8-12):658-668.74(2):382-392. Mandel JH. Chemosphere 2007b. Burris JM. Lundberg JK. Moisey J. Burris JM. J Ag Food Chem 2007. Grey BE. Korzeniowski SH. htm. Lundberg JK. Thibodeaux JR. and perfluorooctanoate in retired fluorochemical production workers. Buck RC.26(1):47-51. et al. J Occup Environ Med 1999. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. and humans from Japan. Sterchele PF. Biol Pharm Bull 2003. Seymour C. Butenhoff JL.S. Peterson RE.S. 2003a. Froehlich JW. Case MT.55:3203-3210. Church TR. Grey BE. Church TR. 2003. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Rogers JM. (Erratum in: Toxicol Sci 2004. Lau C. Burris JM. Olsen GW.115(9):1298-1305. Gamo T. Thomford PJ.74(2):369-381. Olsen GW.gov/opptintr/pfoa/pfoara. Kannan K. Historical comparison of perfluorooctanesulfonate.198(2):231-241. EPA). Huang HY. Butenhoff JL. 1/15/06 Vanden Heuvel JP.37(12):2634-2639. van Belle G. Hansen KJ. A global survey of perfluorinated acids in oceans. Seacat AM. Richards JH. birds. Cousins IT. Nesbit DJ.

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

Sauer MJ. 2006). Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. at very high levels. 2000a. 4/20/09 Albro PW.html. Massey RC. Environ Health Perspect 1982. Available at URL: http://www. 1985. 2001. 2000c.niehs.e.. 2004. McKee et al. Clark K. variation also occurs in the same person during repetitive monitoring (Fromme et al. but there are known species-related differences in the hydrolysis of diester phthalates. Vol. phthalates have been shown to induce peroxisomal proliferation in rodents. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). Silvapathasundaram S.. References Agency for Toxic Substances and Disease Registry (ATSDR). 2002.. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al.21:13-34.html. Rhodes et al. Pharmacokinetics. Food Addit Contam 2001. 227-262. Needham LL. and race/ethnicity (Silva et al. Connor C. 2003. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. Matthews HB. Cousins IT.. Peck and Albro. The Handbook of Environmental Chemistry. 2004). Castle L. 2005. Hauser et al. pp.gov/toxpro2. atsdr. McDonnell DP. Hoppin et al.. 1982).. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. at higher doses. Metabolism of di(2-ethylhexyl) phthalate. Assessment of critical exposure pathways. Population estimates of concentrations of specific phthalate metabolites may differ by age. NTP-CERHR. Corbett JT. In Staples CA (ed). These differences may contribute to species-specific differences in toxicity (ATSDR. The monoester metabolites are thought to mediate toxic effects for some of the phthalates... dibutyl phthalate (DBP). 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. Kessler et al.atsdr. and extent of metabolite conjugation to glucuronide (Albro et al. Mackay D.. Schroeder JL.html. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. 2003. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. Anderson WA. reducing estrogen production. Silva MJ. 2004. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al.cdc.. 2007.. 2004.18(12):10681074. 2002)..cdc. 2006)..html). Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . Scotter MJ. 2001. gender. Springer.805:49-56.cdc.gov/ toxprofiles/tp9. Environ Health Perspect 1997. 105:734-742. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. Available at URL: http://www. Biomonitoring studies on levels of phthalate metabolites provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of phthalates than are found in the general population.atsdr. and Sertoli cell abnormalities in the male animals and. Drug Metab Rev 1989. Coldham NG. van der Broek PH. Jordan S. Information about external exposure (i. Evaluation of a recombinant yeast cell estrogen screening assay. interactions with macromolecules and species differences in metabolism of DEHP. High doses of di2-ethylhexyl phthalate (DEHP).45:19-25. 1986). 2001). Springall C. Lovekamp-Swan and Davis. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al.nih. 2000b. Calafat AM.3. testicular atrophy..New York.gov/ reports/index. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Toxicological profile for di-n-butyl phthalate update [online]. 2002). which may be a pathway to the development of liver toxicity and cancers in these animals. Also. Hauser et al. efficiency of intestinal absorption. In animals. Herbert AR. 2005). phthalates produced anti-androgenic effects by reducing testosterone production and...Phthalates and metabolites have been tested. 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. Albro PW and Lavenhar SR. 2004. ovarian abnormalities in the female animals (Jarfelt et al.gov/toxprofiles/ tp135. 2007). Part Q: Phthalate Esters. 1982. Dave M. Jongeneelen FJ. Slakman AR. However. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. J Chromatogr B 2004. Dirven HA.

103:582-587. et al. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Leffers H. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Environ Health Perspect 2004. Kano I. Chahoud I. Giwercman A. 2006 [online]. Ryan L. 2000b [online]. Ladefoged O. Environ Health Perspect 1998.19(4):505-515. Singh NP. Rylander L. Park MG. Reynolds T.niehs. Environ Health Perspect 2003. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.105:802-811. Am Ind Hyg Assoc J 1985. Mechanisms of phthalate ester toxicity in the female reproductive system. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Calafat AM. Silva MJ. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Davis BJ. Scand J Work Environ Health 1985. Duty SM. Brock JW. Anal Bioanal Chem 2005.html. Chen Z.nih.112(17):1740]. Meeker JD. Ryan L.niehs. Epidemiol 2005. Research Triangle Park (NC). National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Boehmer S. Hagmar L. Int Arch Occup Environ Health 1993. et al.Phthalates in human urine samples. and infant formula by tandem mass spectrometry (LC-MS-MS).html. Andersson A-M. Drexler H. Skakkebaek NE. Environ Health Perspect 2002. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets.niehs. J Androl 2004. Available at URL: http://cerhr.16(4):487-493. Main KM. et al.195:142-153. Mortensen GK. Jonsson BAG. Borch J. Toxicol Appl Pharmacol 2004. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Skerfving S. Davis BJ. Calafat AM.46(11):643-647. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate.210:21-33. Reproducibility of urinary phthalate metabolites in first morning urine samples. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Fromme H. Jobling S. Gans G.nih. Silva MJ. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. White R.nih.26(8):1219-24. Hauser R. Balasubramanian AV. Csanády G. Kalita JC. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004.25(2):293-302. Hauser R. Silva MJ.gov/chemicals/dehp/dehp-eval. Kessler W. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.111(2):139-145.11(5):381-387. McKee RH. 6/2/09 NTP-CERHR. Sumpter JP. Lovekamp-Swan T. Zhang S. Research Triangle Park (NC). Urinary phthalate metabolites and biomarkers of reproductive function in young men. Int J Hyg Environ Health 2007. Yoshimura M. Research Triangle Park (NC). Numtip W.html.110(5):515-518.nih. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Environ Health Perspect 1995. Richthoff J. Jacobsen H.64(8):555-560. Angerer J. Wang P. Meeker JD. Sumpter JP. David RM. Baird DD. Dalgaard M. Filser J. Park S. Pan G.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Harris CA. Duty S.18(1):122. Brock JW. Available at URL: http://cerhr. 6/2/09 Okubo T.gov/chemicals/ phthalates/dbp/dbp-eval. Stringer WT. Available at URL: http://cerhr. Akesson B. Bolte G. Parker MG. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Henttu P.22(3):688-695. Butala JH. Milligan SR. Hanaoka T.niehs. Tsukino H. 6/2/09 NTP-CERHR. Koch HM. Kano K. 6/2/09 NTP-CERHR.382:10841092. Nielsen J. Grote K. Hum Reprod 2007. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). consumer milk. Hartle RW. Reprod Toxicol 2005. Biol Pharm Bull 2003.html. Research Triangle Park (NC). 2000a [online]. Hass U. Liss GM. 2000c [online]. Decreased serum free testosterone in workers exposed to high levels of di-n-butyl phthalate (DBP) and di-2-ethylhexyl 260 Fourth National Report on Human Exposure to Environmental Chemicals . 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population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Peck CC. Pratt IA. Fourth National Report on Human Exposure to Environmental Chemicals 261 .S. et al. Batten PL. Reidy JA. Urinary levels of seven phthalate metabolites in the U. Environ Health Perspect 1986. Parks LG. Silva MJ.58:339349. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat.112(3):331-338. Peters JM.65:299-308. Jackson SJ. et al. Toxicol Sci 1998. Abbott BD. et al. Rhodes C. Orton TC. Barlow NJ.46:282-293. Clemons JH. Zacharewski TR. Environ Health Perspect 2004. Matthews JB. Hodge CC.36:459-479. Environ Health Perspect 2006. Meek MD.Phthalates phthalate (DEHP): a cross-sectional study in China.45:11-17. Wu ZF. Klinefelter GR. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Environ Health Perspect 1982. Ostby JS.114(11):1643-1648. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Caudill SP. Albro PW. Fielden MR. Barr DB. Crit Rev Toxicol 2006. Lambright CR. Toxicol Sci 2000. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Rusyn I. Cunningham ML. 112(5):A270]. Bratt H. Malek NA.

9) 43.5 (76.3) 63.2) 17.1 (13.4-16.0-130) 101 (86.6-150) 94.7-14.0 (34.2-183) 101 (78.3-161) 99.5-36.S. High dose BzBP and its monoester metabolites.Phthalates Benzylbutyl Phthalate CAS No.1) 13.9) 18.3) 13.0) 24.2) 12.2-116) 122 (102-143) 101 (84. and diet is the major source for general population exposure.5-36.4 (32.5) 15.6-79.7-16.5 (66.5) 16.0) 90th 67.2-40.0-106) 58.0 (11.1) 12. see Data Analysis section) for Survey years 99-00.9) 15.2-115) 113 (91.2-33.1.9-62.3) 15.2) 78.8 (80. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6) 37.4-120) 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 13.0 (43.4 (63.7-58. because it is not bound to products in which it is incorporated.1-16.6 (13.6-92.6) 63.4) 35.1) 32.5-40.3 (12.4 (10.0 (33.8 (50.2 (43.4 (53.8-121) 79. some personal care products.5-62.7-119) 99. and 03-04 are 0.3-18.9) 14.3) 37.4) 71.8 (21.5 (61.8-13.9-49. can produce developmental and reproductive toxicity in rodents.2-155) 91.2-38.6-92.1) Selected percentiles ( 95% confidence interval) 50th 17.3-21.3) 94.4) 49.3.4) 51.5) 30..8-14.3) 54.9) 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 (14.1-18.7 (82.3 (29.2 (11.5-94.0) 70.6) 35.8-17.8-133) 89.5 (26. interval) 15.6 (21.4) 108 (96.6) 35.6 (13.5 (57.6) 13.7) 40.5) 82.1 (10.9) 13.3-130) 122 (88.6) 95th 103 (94.1-15.9 (28.4) 14. residents (Blount et al.1-214) 166 (116-191) 145 (110-213) 88.8) 33.8-41.7 (11.3 (13.6-29.0 (27.6) 14.8 (12.7-16.2) 32.7-25.9 (39.5 (67. respectively.6) 25.5) 15.1 (55.1 (20.2 (25.0 (12.7-15.1 (58.7 (13.6) 13.0 (14.1) 29.7) 23.1) 31.7 (53. population from the National Health and Nutrition Examination Survey.8 (10.6) 29.3) 13.2-19. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.7 (80.8 (38.4) 12. 01-02.. and 0.3-82. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.6 (66.2) 14.4-127) 80.5) 55.8 (71.8-14.5-41.3-43.5-25.2) 22.6-116) 122 (102-142) 101 (85.4 (53.1 (13.S.8) 14.8-72.1) 14.2 (47.4 (31.9-14.9) 14. 2000).3 (33.9) 12.9-87.6-17. sealants.1-90.4 (59.3 (22.4) 33.8) 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. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.6 (13.9-16.8 (53.7-172) 103 (74. including MBzP.5 (47.1) 76.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.6) 67.4) 98.9) 11.3-34.0-26.0) 32.5-35.9-47.3 (30.3) 23.0 (30.5-84.2-31.7 (12.6) 24.9-30.9 (12.2-20.6-18.4 (68.9 (22.0 (15.1 (14.4-15.4 (29.2) 15.6) 50.2-39.2 (14.7-17.7-16.8 (30.7-170) 169 (134-198) 152 (99.3-88.4-92.2) 14.4) 81. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2 (19.4) 65.6) 16.7-35.5 (55.9 (16.8-35.8-16. 262 Fourth National Report on Human Exposure to Environmental Chemicals .0 (23.3-27.2) 69.8-18.1 (19.8-17.6) 14.7) 38.6 (41.1-35.1-116) 122 (93.4-24. car care products.8) 63.6 (53. vinyl tile. 2004.1-15.0 (26.6 (12.1-120) 52. NTPCERHR.4-62.7 (15.3 (29.5-145) 138 (106-241) 143 (127-179) 120 (99.4 (48.4) 75th 35.2) 13.4 (27.0 (55.2 (10.9 (70.1 (32.4-25.6 (32.3 (12.6-43.6 (13.1-38.8-64.3-125) Total 15.5 (13.4) 35.5-97.3 (12.3-91.9 (12.5 (27.6-72.1-43.3-18.9 (13.1) 67. IARC considers BzBP not classifiable with respect to human carcinogenicity.4) 129 (98.1 (14.1-16.5-18.1) 68.5) 65.7-13.1-39.9-190) 86.0) 16.2-16.5) 23.1-61.0) 34.0) 33. and to a lesser extent. it can be released into the ambient air during use or disposal of the products.3-75.4 (10.0-85.2) 66.4) 38. 2001-2002.4) 80.6) 15.8 (71.3-12.8.2) 33.8) 24. Food crops take up BzBP.8-16.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8) 28.8-48. 0.6-132) 103 (84.2-16.6-39.8 (86.8-76. BzBP can be released into the environment during its production and.0 (20.2 (19.4 (13.7 (70.3 (44.9) 49.0 (15.2-17.0) 23.5) 27.5-33.4 (32.6-38. 2000).0 (30.3-74. particularly male animals (McKee et al.5-14.9-27.9 (21.9 (11. and 2003-2004 were generally similar those reported in U.7 (51.9-28.8 (28.7-82.3 (54.0) 20.0-55.8-98.

2) 11.8 (10.7-20.1-125) 86. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.9-16.. adolescents compared with adults.9-14.6) 73.9) 52.4) 13..5) 41.8-39.3-11.5 (10.2-15.6-116) 74.2 (56.9-28.6) 12.7 (13.3 (35.1 (43.0 (11.2-12.1) 35.8-60.73-12.8 (64.9) 100 (80.9 (51.3-64.6 (30.8) 33.5) 10.5-26.7-20.9-69.9-83.0) 15.0 (49.6 (11.4-23.6 (15. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.5-58.8-48. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.2-13. and females compared to males (Silva et al.4-14.Phthalates York City (Adibi et al.6 (51.7 (38.5) 13.2) 26.3 (38.6-99.4-142) 134 (116-176) 136 (85.9 (22.4) 17.1 (21.7-90.1) 80.4-42.6-47.4-102) 70. 2005.6) 58.6-26.4 (13.2) 12.5 (11.8 (46.2 (41.1 (21.1 (18.1 (19.6 (30.95-14. 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.1 (23.6 (14.0 (67.2 (40.8) 16.8-15.4 (26.6) 38.2-51. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.3) 18.8) 46.5-38.3) 21.7-61..5 (56.5) 17.6) 30.0-27.6 (57.3) 13.0) 24.0 (13. 2007).4-60.7-15.6-15.3) 73.4 (21.7) 11.1-79.4 (10.8 (13.0-15..7 (13.0) 49.5-57.4-27. and in a small sample of German residents (Koch et al.9 (55.8-27.2) 15.3-73.7) 25.5) 16.3 (15.8-13. 2003). In NHANES 1999-2000.2) 11.1 (53.7 (11.5) 78.0 (62.9 (43.7-14. 2002).1) 24.0 (12.0) 60.4 (11.4-18.9 (39.9-23.9) 12.8-14.1 (34.1 (14.7-56.5-79.7 (14.7-69.6) 53.7-14.9 (9.5-61.2) 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 12.9) 64.4 (33.69-11.9 (10.0) 13.7-12.4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.8) 108 (75.2) 32.8 (12.5-31. 2003).2) 11.6-81.6 (11.8) 13.3) 14.7 (21.3) 37.4-79.1-12.9-115) 57.2-49.7) 19.4-99.2-57.8) 68.7-15.9) 12.7) 56.4) 15.7-31.6) 25.1 (13.5-42.1-120) 77.7 (18.1-58.4 (11.1 (21. in young Swedish men (Jonsson et al.7 (11.5-13.0-109) 65.7) 38.8-173) 195 (121-305) 229 (99.5 (42. Hoppin et al.1 (25.2-26.4) 60.8-85.2-15. A small study of African-American women in Washington.2-13.6) 12.3) 29.1) 24.2-78.0-26.6-13.2 (69.5) 95th 77.4) 28. 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.4) 50.6 (19.8) 15. 2005).1 (46. 2004.4) 104 (89.9-13.8) 11.8 (50.6) 13.6-20.3-38.6-86.8) 33.5 (12.8) 71.6) 75th 25.8-16.8) 54.7 (11.9-40.8) 80.3 (23.4 (25.6 (24.5 (9.4-116) 73. 2006).8-42.1-12.8) 53.3-16.4) 21.9 (15. 2007).3) 90.9) 11.6 (36.3 (60.5 (10.7 (59.4) 25.3) 89.4 (74.4 (63.7-29.7 (55.0) 11. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al..1-27.8-15.4 (60.9 (29.5) 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 . Hauser et al.5) 46.8-69.3) 67.0 (12. 2004).3) 12.7 (19.1-29.8-13.5-213) 49.7 (12.8) 24.8 (30.1) 12. in men attending a Boston infertility clinic (Duty et al.1-14.5) 20.8) 56.1 (41.4-19.3) 36. 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.2-21.4) 90th 50.0 (10.9 (54.3) 16.6 (34. population from the National Health and Nutrition Examination Survey.4 (11.7) 46.4) 51.4 (46.9-13. interval) 14.9 (15.5) 14.5-76.3) 14.5) 23.1) 17.7 (23.1 (15.3 (12.9-104) 62.5-23.8-64.4-90.8-13.0-48.1-35.1 (21.5-16.0) Selected percentiles ( 95% confidence interval) 50th 13.9-62.9) 12.1) 39.6 (22.0 (41.8 (57.0-90.8-34.8) 26.7-397) 70.4) 12.4) 13.8-80. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2002.9) 24.9 (12.6-40.1) 142 (99.7) 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 40.6-12.5-26.9 (24.8 (69.9 (24.0) 24.7-19.9) 11.3) 13.4) 14.5-29.3 (24.1 (13.7 (54..4 (12.3 (13.5 (48.5 (35.S.0-51.5-99.1 (9.7-123) 77..9) Total 14.4-15..3) 55.8-14.3-34. Weuve et al.4 (34.0 (33.9 (12.8) 34.0-53.4) 44.0 (38.6 (11.3) 13.5 (49.4-17.8 (11.1) 27.2) 67.3 (39..0) 12.1) 23.2-117) 95.4-14.9) 42.2-17.5-58. In an annual sample of German university students.2 (27.1 (11.8 (49.0 (41.9 (10.7-19..4-93.8) 53.4 (69.

et al. Third National Report on Human Exposure to Environmental Chemicals. 4/20/09 Silva MJ. Hilborn ED. Meeker JD. Calafat AM.112(3):331-338. Needham LL. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Barr DB. Silva MJ. 112(5):A270]. Urinary phthalate metabolites and biomarkers of reproductive function in young men.16(4):487-493. Weuve J. Dobler L.110(5):515-518. Available at URL: http://cerhr. Singh NP. Atlanta (GA). 264 Fourth National Report on Human Exposure to Environmental Chemicals . Reproducibility of urinary phthalate metabolites in first morning urine samples. Brock JW. Calafat AM. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Silva MJ. Green RA. Angerer J. Reidy JA. Jacek R. Centers for Disease Control and Prevention (CDC). Hum Reprod 2007. Sanchez GN.S. Butala JH. Research Triangle Park (NC).niehs. Helm D. Jedrychowski W. Ryan L. Rossbach B. Silva MJ. Jonsson BAG. Ryan L. Schettler T. Levels of seven urinary phthalate metabolites in a human reference population. David RM.210(3-4):319-333.nih. Int J Hyg Environ Health 2007. Urinary levels of seven phthalate metabolites in the U. Prenatal exposures to phthalates among women in New York City and Krakow. Hu H. Eckard R. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Baird DD.html. et al. Brock JW.25(2):293-302. Giwercman A. Malek NA. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Duty S.18(1):122. Richthoff J. Brock JW. Environ Health Perspect 2002. Environ Res 2003. Koch HM. Hodge CC.111(14):1719-1722.93:177-185. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Silva MJ. J Androl 2004.22(3):688-695. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). et al. et al.114(9):1424-1431. NTP-CERHR. Sampson EJ. Duty SM. et al. Epidemiol 2005.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Hagmar L. Bull Environ Contam Toxicol 2002. Gans G. Reprod Toxicol 2004. et al. Koch HM. 2005. Caudill SP. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Caudill SP. 2000 [online]. Perera FP. et al. Environ Health Perspect 2003. Caudill SP. Hoppin JA. Environ Health Perspect 2004.68:309-314. Wittassek M.Phthalates References Adibi JJ. Rylander L. Phthalate monoesters levels in the urine of young children. Barr D. Blount BC. Drexler H. Needham LL. Pirkle JL. Chen Z. Davis BJ. Camann DE. Hauser R. Poland. McKee RH. Environ Health Perspect 2000. Environ Health Perspect 2006.108(10):979-982. Wiesmuller GA. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.

56-4.10) 9.50) 2.4-27.3 (16.90-4.7-20.46) 2.Phthalates Di-n-butyl Phthalate CAS No.81 (3.3 (18.6) 12.46 (3.2-33. OSHA has established a workplace air standard for external exposure to DBP.5 (20. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC. they have been referred to as monobutyl phthalate (MBP).7) 4.3-18.30-3.80 (2.0 (11.30-2.3-24.56 (3.0) 12.49-2.80 (5.00) 4.7 (16.6) 17. 2004.7 (9. 2005).24-8.50) 5.6 (13.9-23.80-5.S.59) 3.3-30.30) 10.5 (11.20 (7.7-31.56 (5.7-18.10) 3..70) 3.4) 22. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.20-12. 2000.00) 7.17 (2.60 (2.1) 16. about 65% to 80% of a dose is eliminated in urine within 24 hours.0 and 0. When total DBP metabolites have been measured.60 (5.1) 22.. Survey Geometric mean (95% conf.6 (13.80-5.2 (11.50-4.40-12.00) 6.4 (20.1 (13. Fourth National Report on Human Exposure to Environmental Chemicals 265 .30 (4.1 (8.17) 4.6 (14.3 (13.28-5.50 (3. in men attending a Boston infertility clinic (Duty et al.7) 7.4) 5.1-20.00-6. 2000).5-24. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate. Following oral administration of DBP to humans.85-6. and insecticides.90 (6.0) 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 2.3 (19.6 (10.8 (9.7 (7. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.6-20.30-6.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.2 (8.7-31.10) 2.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.5) 14.9 (16. 2005). Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.73-5.6 (11.10 (3. 84-74-2 Di-isobutyl Phthalate CAS No.50-10.50-2.6) 16.0-14. 2005.0) 24.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.5 (10.20-2.5) 22.00-9.0-25.00-4.5-16.20) 7.80 (3.3-19.07 (3.4) 12.40-5.3) 33.6 (14.10-9.1-17.30-7.50) 7.55 (3.0 (13.3-48. 2003).5) 23.3-43.80 (2..6) 16.55) 2.30) 5.5 (17.00-6.2-22. NTP-CERHR.5) 25.70 (5.6 (10.20-12.67 (5.43) 6.56) 3.6-18.19-3.40 (2.5) 12.2-14.70-4. in a small sample of pregnant women in New York City (Adibi et al.5) 18.40 (7.4 (14. 2003).6 (9.9) 10. CDC..20) 4.63) 3.40-3.20 (6.90) 12..73 (2.90 (4.10) 11.22 (3. and in a small sample of Japanese adults (Itoh et al.3 (11.40 (2.40 (3.71 (2.72-3.9) 15.40) 5.10) 8.5 (27.26 (2.S.00 (5.90-4.7 (17.30) 10.50 (6.90-7. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U. 2007).5-29.40-17.7 (17.40-9.50-6. Hauser et al.40-3..6 (29. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity. In addition.50) 18.9-14.02) 4.5) 19.11-3.0) 13.84) 4. 2004.0-38. residents (Blount et al.20 (3.48 (2.60 (8.60) 3.1-12.6) 26. DBP can produce reproductive toxicity in male rodents (McKee et al.2) 5.00 (7.7) 15.97) 4.3.60 (4.90 (4. 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.3 (16. Studies of children found age-related differences in urine MBP levels.37) 6.96) 3.5) 18.97) 2.6-14.30-11.20-9.0-18.33 (2.82-3. mostly as MnBP (Anderson et al.60-6.20-6.30 (3. interval) 2.0) 20..1-25.7) 14.10-9.91) 4.30) 2. 2005). pharmaceutical coatings.4-12.44-2.30) 6.10 (4.40 (6.90 (3.30 (1..8) 21.00) 10.9 (16.3 (13.70-4.3) 18.97-7.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3. Biomonitoring Information Median concentrations reported in the NHANES 19992000.80 (5.80) 75th 5.40-4.90-2.00-11.10 (4.8) 40.50) 8.0 (13.6-26.30-6.3-20. population from the National Health and Nutrition Examination Survey. 2001).7) 18. and also in some printing inks.6-34.22) 3.70-8.5-16.66) 2. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.10-2..1) 25.00) 4.70) 5.2 (12.0 (19.40-4.0) 9. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.6) 17. Koch et al.6) 10.70 (2.68 (2.46-5.46 (2.8) 677 652 703 699 1216 1088 Limit of detection (LOD.50) 90th 12.3) 3.30-13.7 (18. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.

4) 23.39) 5. 2004).8-18. 2006).62-12.7 (11.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC. 2004). Between 1998 and 2003. than adults in NHANES subsamples during the same time period.6-19. 2005).79 (4.0-18.00-7.37) 3.96 (3.03 (5.18) 4.05) 2.7-28.2) 24.65 (4.47-12.20-4.6-19.15-4.8) 10.17-12.0) 11.57-4.7) 11.25) 5.54 (4.58-3..97-2.0 (8.66 (8.43) 3.08-2. 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.08) 75th 4.69) 6. Survey Geometric mean (95% conf.59 (4.13-6.66) 2.7) 19.1) 13. interval) 2.0) 3.53-5.57 (3.7 (9.56) 2.69) 4.69 (2.03-11.72) 5.8-13.67-5.76-3.73 (5.64-7.57 (3.6 (15.47 (3.32 (3.98 (2.7) 10.92 (7.69-7.18) 3. samples from German university students had consistently higher median urine levels of MnBP and MiBP.51) 15.3 (13.26 (2.1 (11.3) 16.66) 4.18 (4.65-4.6 (8.and gender. ranging from more than one-tenth the NHANES median (Itoh et al.4) 15.58-4.1-12.34 (3.75 (4. Over this time.21) 10.31) 2.0 (10.36-2.41 (2.04) 3.53-4.7 (21.8 (10.94-12.85 (2.1 (10.68 (2.27-12.13 (2.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.20-3.02 (7.78) 9.53-3.30 (6.9 (9.33 (3.38 (6.89) 6.03-7.81) 4.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.6 (8. 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. population from the National Health and Nutrition Examination Survey.11-2.39-3. 2005).5 (9.76-3.5) 13.31 (7.51) 5.8 (9.91-6.7 (13. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.82) 4.74 (4.2) 8.17 (2. up to four and 13 fold.1-24.84 (4.10-5.81 (6.42) 2.4-16.00-3.61-3.3) 13.95) 10.1) 7.38-10.56-15.29-8.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.55-6.52) 3. An analysis of NHANES 2001-2002 showed similar age.36-7.00-3. In an analysis of NHANES 1999-2000.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.46-11.81) 9.17) 90th 8..2-13.64-10.99-4.9-40.3) 18.32 (7.00 (3.S.78-8..44 (3. 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.64-7.0) 15.28 (4.56) 5.33 (2.35) 3.0) 7.76-15. 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.01-2.1) 10.20 (7.24) 3.15) 3.86) 6.79-8.46 (2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.20 (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 2.43) 3..45) 3.65-11.33-9.18-10.6) 13.54) 2. while MnBP declined (Wittassek et al.33) 3.04) 7.11) 5.32) 7.74-3.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .84 (8.14 (4.75 (6.3) 28.3) 13.2 (11.29-3.93-6. 2002.89-5.04-5.22 (2.78) 8.18-4. Weuve et al.80 (3.68) 5..95-3.68) 3.18 (1.8-18.31 (2.83 (2.51) 2.30) 2. 2007).62 (6.8 (8.5-19.72-7.52-3. to about two to fourfold higher (Fromme et al.4) 7.1) 4.9-16.7) 3.89 (3.6) 11.9 (15.2) 9.9-26.8-36.99) 7.. 2007). respectively.02-10.6 (10.1-25.07 (2.0 (12.46) 3.2 (10.47-5.1) 11.66) 10.09-2.94 (5.1-15.28-13.43) 3.6 (9.21 (5..20-2.52-20.07-5.94) 6.56-4.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.5) 15.6 (12.5 (11.20 (2.11 (5.88 (2. the students’ median values for MiBP levels remained relatively unchanged.3 (17.52 (2.82 (4.26-2. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.54 (2.19 (2.31) 2.4 (12.1) 15.80-3.9) 12.76 (3.79-6.81 (3.2-15.80) 7.95) 2.9 (11.86-4.

1-22.1-75.6-33.1) 47.4-44.2-49.1) 19.7 (16.3 (56.4 (35.0) 20.9 (17.5-121) 106 (94.1 (26.1 (16.6) 38.7-26. respectively.6-69.5) 34. 1.1-51.6 (26.1) 31.7) 52.7 (33.3 (42.9 (79.4 (35.8) 23.6-29.0-24.8) 19.9) 29.8) 62.6 (61.5-53.6-36.3 (23. interval) 24.3 (17.1 (51.5) 19.2-63.2-56.9-22.1 (19. *In the 1999-2000 survey period.6) 17.2 (17.2 (21.2 (18.2-32.0 (31.3-21. Fourth National Report on Human Exposure to Environmental Chemicals 267 .1 (19.3 (30.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.5) 37.9-53. and 03-04 are 0.6-20.3) 23.2) 42.1) 30.4 (23.1 (54.1) 17.2 (75.9) 18.4) 20.3) 24.8-42.1 (62.7 (64.5-47.2-93.7-111) 64.6) 21.2-23.0 (25.1 (28.6-113) 108 (90.3-76.6-48.1-27.2-22.2) 68.4-159) 107 (84.7-92.0-19.8-123) 101 (90.2-87.1-29. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.3) 26.1-92.2 (25.9-22.9) 36.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9 (17.3-40.1) 23.3-145) 85.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.1 (31.0 (36.6-49.8 (19.4 (72.3) 18.1 (58.1 (41.3-96.2 (21.0-26.8 (57.3) 21.7) 124 (98.2 (78.7-53.6-24.0-58.4-42.7 (70.5-43.5) 24.1-24.9-28.4) 52.4-26.2-33.7-24.8-22.6-143) 127 (99.2) 26.5) 85.5) 40.6 (22.7) 28.6-40.7 (18.6-31.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.6 (65.1) 25.1-80.4-20.3-85.5) 95.7 (43.2 (58.6) 39.3-60.5 (30.1) 46.7 (22.7) 42.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.7-121) 97.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.8-119) 90.0) 31. population from the National Health and Nutrition Examination Survey.9-33.4 (35.0) 38.2) 38.7-116) 95.4 (19.3 (30.7 (51.6) 20.9) 46.0 (20.4 (21.9-114) 116 (97.8) 75th 51.5) 47.7) 92.8-29.5 (29.2) 90th 98.7-34.4-25.1) 23.1 (36.5) 26.6 (44.5) 31.3 (36.5 (59.7 (19.4) 22.1 (17.6-29. 01-02.0) 21.2 (59.0) 120 (98.0-32.5) 17.1 (21.6 (90.5-117) 95.6-44.5) 65.3-79.6 (48.4) 64.8-132) 95.2) 20.3 (37.8) 48.2-21.1 (19.7-42.5-47.0-51.1) 23.5) 21.1 (19.5-42.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1) 36.0) 117 (104-131) 112 (84.3) 36.0 (18.7 (24.0-24.8) 58.5-44.5-27.6 (19. and 0.6 (16.4 (36.5) 36.3) 19.9-79.5 (59.7-106) 69.9) 26.8-25.2 (19.0) 27.2-159) 92.7) 74.0-19. referred to as monobutyl phthalate (MBP).9.0-73.5) 78.1-82.6) 35.8) 43.7 (38.3-24.0-21.2 (74.6-37.3 (23.7-124) 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.7-20.1 (34.5 (74.7-127) 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 22.7-117) 118 (108-143) 93.5-60.4 (35.9-101) 77.2 (20.0 (72.5) 36.3-136) 137 (107-162) 119 (90.9-42.5 (28.3 (60.0) 30.2 (79.0) 84.0 (23.1-20.7-42. see Data Analysis section) for survey years 99-00.9) 21.4 (71.9-87.3 (51.6) 46.7 (28. Survey Geometric mean (95% conf.9) 71.4-31.6 (32.9 (20.4) 59.4 (38.6) 80.S.4 (84.9) 75.3) 40.4 (25.0 (30.5) 20.3-67.1.7 (18.4-18.2-24.0 (17.6 (55.7-91.7-34.9 (79.0 (78.1) 20.4-60.1 (18.2) 32.0 (45.2-114) 73.0 (15.9-92.2) 62.4.6) 71.

S.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.0) 81.2) 21.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.2-48.9) 24.1) 42.8) 20.7) 20.4 (13.4-72.0-60.9 (35. interval) 22.4) 15.3 (48.3) 19.9 (35.3 (76.5-23.8) 19.9) 20.7) 19.8) 35.0-17.5) 91.1-21.2-22.7-26.6-32.5-21.4) 20.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.4 (19.9-70.3-38.5-18.9 (20.5-15.4 (31.4-135) 71.1-128) 97.0 (15.9-105) 85.0-19.9-38.3) 59.6-27.6) 83.1) 37.6) 25.0 (61.8) 34.6-128) 96.5) 90th 68.7 (60.6-53.9 (37.3-40.2-108) 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.7-19.0 (16.3 (17.0-47.7-37.7) 36.1) 44.7-51.4 (53.6) 37.9 (73.2) 159 (102-263) 147 (93.5-16.9) 91.2-61.9-56.2-18.4 (18.4 (31.6 (74.3-21.3 (52.8-24.5-70.7 (20.6-19.8) 23.4 (17.4) 21.0) 59.3-106) 74.2-27.2) 65.1 (15.8) 22.8) 17.4) 51.4) 53.9) 52.5) 21.7-20.8) 34.0) 25.3) 52.0) 53.5) 60.3-23.4) 15.4-131) 81.2-73.6 (17.8) 75th 38.5) 84.6-50.7-78.0 (70.5-76.0) 55.4 (50.9 (56.8 (25.2) 16.5) 82.1 (29.5) 17.0 (71.2-22.4 (68.4) 19.9-14.8) 20.6) 38.2 (19.5) 134 (93.0 (18.6) 18.5-41.6) 14.0 (34.5-64.1) 17.3 (21.3) 20.3 (60.6-44.5-22.0) 41.2-16.3 (28.7 (27.1-83.4-24.3 (24.3-26.6-24.6) 31.8-24.5-142) 81.1-18.9-84.3-20.1-62.5 (18.0-75.4-34.8) 13.3-49.5 (15.4-164) 96.4-76.9 (30.3-17.4 (23.3) 67.4-47.4 (16.6) 24.1 (34.1) 35.0 (20.8 (18.6 (57.4 (20.4 (31.6 (19.6 (31.5 (30.9-68.4 (16.0) 108 (71.3 (17.7 (73.0 (18.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.3) 33.3-71.0) 29.9-26.6 (27.1) 53.6-24.7 (16.1-99.8 (16.7-42.6-119) 63.4) 16.6-23.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.1 (56.8 (13.6-22.5 (64.1) 61. 268 Fourth National Report on Human Exposure to Environmental Chemicals .0-41.6 (61.9 (64.2 (83.9 (30.2) 74.6 (41.3) 18.0-92.8-235) 137 (108-198) 88.0) 70.8) 30.0-113) 104 (83.0 (52.7-21.3 (55.9) 49.6-42.4 (17.3 (71.2 (19.6-28.1) 50.4 (45.1 (46.8 (17.9) 14.6-43.4-103) 117 (83.0-38.3) 19.1 (32.0) 94.2) 31.0 (26.7-19.6-16.0) 28.3-18.8 (18.2-179) 84.9-100) 86. Survey Geometric mean (95% conf.8) 17.8) 17.5) 39.4-61.7 (57.1-99.4 (50.3) 17.9 (21. population from the National Health and Nutrition Examination Survey.9) 19.9 (30.9) 62.4 (33.5-30.5 (14. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.2-21.3-21.7 (12.3-39.3-78.2-22.6) 39.8) 63.4 (37.5 (81.6) 24.3-32.8-32.4) 62.7 (54.0) 75.2) 59.2-85.4-65.4 (47.5-37.4 (56.6) 34.9 (16.7 (60.0) 19.8) 40.7 (43.7-80.3 (69.7) 42.9 (39.1) 21.6-92.6 (25.8-23.7 (19.0 (43.6-26.9-36.5 (18.2-106) 64.1) 20.7-39.0 (50.0) 35.6 (29.1) 22.7-23.9-49.0-90.3) 21.6 (72.6) 23.6-155) 91.3 (52.3) 35.7 (28.1) 20.8) 28.8 (18.1 (61.9 (58.2 (35.7 (14.3 (42.9) 28.2 (16.8-43.0 (69.9) 30.3 (17.3 (19.2-28.9) 39.3-81.7 (81.8 (22.2-86.8 (33.6-23.0 (27.6) 65.7-28.0) 26.5-142) 89.3 (46.9-34.8 (50.1-23.6 (25.1-32.3 (16.6) 64.0 (19.1 (21.8 (65.3-114) 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 17.3) 33.9 (19.2 (38.9-68.6-44.6-74.

208:237-245. Reprod Toxicol 2004. Drexler H. Massey RC. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP).S. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Caudill SP.16(4):487-493. Caudill SP. et al. Camann DE. Needham LL. Helm D. Butala JH. et al. Environ Health Perspect 2004. Blount BC.111(14):1719-1722. Jedrychowski W. Hodge CC. Perera FP.gov/chemicals/ phthalates/dbp/dbp-eval. McKee RH. Malek NA. Hilborn ED. Hu H. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Drexler H. Epidemiol 2005. Koch HM. Calafat AM. Brock JW. Yoshida K. Eckard R. Jonsson BAG. Barr D. Bolte G. Caudill SP. Environ Health Perspect 2003. Barr DB. J Androl 2004. Richthoff J.22(3):688-695. Wittassek M. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Ryan L. Urinary phthalate metabolites and biomarkers of reproductive function in young men.nih. Int J Hyg Environ Health 2007. Environ Res 2003. Dobler L. Masunaga S. Fromme H. Giwercman A. et al. Silva MJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.Phthalates References Adibi JJ. NTP-CERHR. Jacek R. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Hagmar L. Sampson EJ.112(3):331-338. Ryan L. 4/20/09 Silva MJ. Duty S. Wiesmuller GA. Angerer J. et al.108(10)979-982. Third National Report on Human Exposure to Environmental Chemicals. Boehmer S. Urinary levels of seven phthalate metabolites in the U. Int J Hyg Environ Health 2005. Centers for Disease Control and Prevention (CDC). Hum Reprod 2007.html. Scotter MJ. et al. Itoh H. Springall C. Anderson WA. Int J Hyg Environ Health 2007.93:177-185. 112(5):A270].25(2):293-302. Phthalate monoesters levels in the urine of young children. Available at URL: http://cerhr. Koch HM. 2000 [online].68:309-314. 2005. Duty SM. Weuve J.210(3-4):319-33.niehs. Chen Z. Reidy JA. Rossbach B. Green RA. Fourth National Report on Human Exposure to Environmental Chemicals 269 . et al. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Brock JW. Bull Environ Contam Toxicol 2002.114(9):1424-1431. Needham LL. Environ Health Perspect 2006. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Poland.210:21-33. Rylander L. Singh NP. Pirkle JL.18(1):122. Food Addit Contam 2001. Atlanta (GA). Levels of seven urinary phthalate metabolites in a human reference population. et al. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.18(12):10681074. Calafat AM. Schettler T. Silva MJ. Koch HM. Castle L. Silva MJ. Hauser R. Gans G. Angerer J. Prenatal exposures to phthalates among women in New York City and Krakow. David RM. Meeker JD. Silva MJ. Sanchez GN. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Research Triangle Park (NC). Environ Health Perspect 2000. et al.

300-.80) .400 (<LOD-. 0.400) 1.300-. In this Report. only levels at or above the 90th percentile could be characterized.300-.500 (.10 (<LOD-1.300-.20) .90) .200 (<LOD-.10 (<LOD-2.300-.500 (.10) .70 (1.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.300 (. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.400 (.400 (<LOD-.400-.900-1.500) 1. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.500) 1. and 0.10 (.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 1.500) .600) .500 (.3.50) .600) < LOD .200-. resins.2.200-.400 (.400 (.600) . and polymers. see Data Analysis section) for Survey years 99-00.400) < LOD 1.400 (<LOD-.300 (.400-.400 (.400 (.500 (.300 (<LOD-.700) .500) .00 (<LOD-1.70) .500 (.600) .700) .400-.300-.200-.70 (1. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect. including nitrocellulose.200-.300-.500 (.500) < LOD < LOD .500 (. 01-02.400 (. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.200-.300-. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00 (<LOD-1.300) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.400 (.50) .300 (. Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population. population from the National Health and Nutrition Examination Survey.700) .9.400) 1.300) < LOD .500) .200-.500 (. respectively.600 (. 270 Fourth National Report on Human Exposure to Environmental Chemicals .300-.500) < LOD < LOD .500) 1. which may vary for some chemicals by year and by individual sample.00) .600) .00 (<LOD-1.600) .00-3.300) 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 .10 (<LOD-1. < LOD means less than the limit of detection. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. and polyvinyl chloride.S.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 .300 (.500) .500-.300 (.00-2. polyvinyl acetate.300 (.400-.400 (<LOD-.400-. Survey Geometric mean (95% conf.Phthalates Dicyclohexyl Phthalate CAS No. and 03-04 are 0.400) < LOD < LOD .400-.400-.500) < LOD 1.300-.500 (.70) .400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .300 (.

620) < LOD .53) .S.670 (<LOD-.12-1.790-1.16 (<LOD-3.400-.54) .530-1.44) .00) .500 (.36-1.770-1.770 (.530 (.470) 3.420-. Survey Geometric mean (95% conf.770-1.17) .770) < LOD 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.330 (.53) .10) .260-.360-.830) 1.880 (.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 1.950 (.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.34) .690-1.390 (.450 (.05) .170-.06) .910 (.490) .250 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.14 (<LOD-3.67 (1.54-6.530) 1.380 (.690) < LOD 2.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .740) .11) .630 (<LOD-.450 (.18) .500) 3.670-1.530-.82 (1.500-.590 (<LOD-.400-.270) < LOD .54 (<LOD-2.380-.16) . population from the National Health and Nutrition Examination Survey.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 .610 (.480 (.43 (1.800-1. Fourth National Report on Human Exposure to Environmental Chemicals 271 .310) < LOD .220 (<LOD-.350-.590 (.560) 1.690 (.33) .660) .22 (<LOD-1.740) < LOD < LOD .82) .06) .510 (.690) < LOD < LOD .470 (.510-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .410 (.370 (<LOD-.290-.33 (<LOD-3.940 (.710) .910 (.240-.910 (.Phthalates Urinary Mono-cyclohexyl phthalate (MCHP) (creatinine corrected) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.310-.660) < LOD < LOD .420-.330 (.74) .910 (.420-.00 (<LOD-3.630 (<LOD-.

see Data Analysis section) for Survey years 99-00.4 (62..7 (70. 2001-2002.4.. population from the National Health and Nutrition Examination Survey.9 (61. particularly those containing fragrances. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. 0. In contrast. 2002).9-92. respectively.1-93. 2007).8-111) 85. deodorants.. and 0. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. soaps.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75.Phthalates Diethyl Phthalate CAS No. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. and hand lotions.3-103) 193 (141-256) 184 (148-227) 221 (165-294) 180 (140-221) 181 (152-212) 188 (158-219) 197 (129-249) 183 (142-217) 196 (170-241) 564 (419-818) 479 (387-651) 557 (432-695) 482 (390-590) 498 (441-567) 533 (471-629) 378 (290-730) 451 (315-636) 521 (295-571) 1510 (1050-2150) 1260 (983-1480) 1250 (973-1560) 1340 (1010-1660) 1350 (1060-1660) 1590 (1220-2070) 756 (379-1070) 808 (572-1090) 827 (542-1440) 3260 (1550-4420) 2070 (1470-3050) 2310 (1360-3310) 3480 (2230-4640) 2720 (2160-3670) 2980 (2250-3800) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 179 (149-215) 182 (157-211) 197 (173-224) 178 (154-206) 174 (153-198) 189 (160-225) 154 (119-197) 171 (139-199) 171 (148-201) 174 (138-210) 167 (139-194) 182 (138-219) 523 (372-650) 502 (419-603) 536 (449-654) 425 (350-508) 427 (387-498) 478 (392-564) 1440 (1020-2280) 1450 (1060-2110) 1520 (1210-2070) 988 (880-1230) 1050 (879-1310) 1260 (969-1640) 3500 (2130-4560) 3100 (2110-4390) 2910 (2210-3480) 2230 (1370-3880) 1860 (1490-2500) 2590 (1800-3420) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 181 (157-209) 226 (195-262) 267 (239-298) 322 (275-377) 352 (324-384) 357 (310-412) 152 (133-175) 158 (141-178) 167 (145-193) 174 (146-210) 220 (190-264) 249 (212-307) 306 (256-350) 357 (290-407) 306 (253-414) 134 (108-157) 147 (119-177) 148 (125-175) 441 (390-541) 530 (444-660) 597 (523-688) 789 (635-949) 853 (709-1090) 948 (769-1150) 367 (287-482) 413 (366-451) 418 (366-477) 1280 (851-1510) 1490 (1050-2110) 1640 (1320-2180) 1890 (1410-2270) 2160 (1620-2470) 2500 (1840-2980) 986 (798-1340) 1020 (905-1230) 1210 (954-1480) 1720 (1460-2130) 2630 (1540-4460) 3050 (2230-4300) 3610 (2130-4640) 3540 (2810-5070) 4370 (2780-5910) 2470 (1590-3880) 2320 (1560-2720) 2250 (1590-3290) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. shampoos. 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. 01-02. and also in men attending a Boston infertility clinic (Hauser et al.S. Products that may contain DEP include perfumes. colognes. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. DC (Hoppin et al. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.3 (82.5) 81.2-102) 95. 272 Fourth National Report on Human Exposure to Environmental Chemicals . Biomonitoring Information MEP levels in the NHANES 1999-2000. 2003) and African-American women in Washington. and 03-04 are 1.9. 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.7) 71.3 (74. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1 (71.2. 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.

2005). Other population estimates also differed by sex and race ethnicity (Silva et al.6 (77.6 (65. 2002). 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.7-110) 81. 2003) were slightly lower than levels found in NHANES 2001-2002.3-105) 87. In an analysis of NHANES 1999-2000. 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. 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 92.0 (66...S. population from the National Health and Nutrition Examination Survey.9 (82.5-114) 101 (87. 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..2 (66.0-156) 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 . 2004). This age-related trend is opposite the direction seen for other phthalates. with adjusted geometric mean levels of urinary MEP that increased with age (CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Analysis of NHANES 2001-2002 showed similar findings.5-113) 122 (93. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9-110) 96.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.Phthalates 2002 (Brock et al. 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. Median MEP levels found in a small sample of German residents (Koch et al.

Hodge CC. Reidy JA. et al. Angerer J. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Bull Environ Contam Toxicol 2002. Baird DD. Brock JW. Davis BJ.110(5):515-518.112(3):331-338. Hum Reprod 2007. Singh NP. Hilborn ED. Phthalate monoesters levels in the urine of young children. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Silva MJ. et al. Rossbach B. Silva MJ. Prenatal exposures to phthalates among women in New York City and Krakow. Caudill SP. Drexler H. Caudill SP. Barr DB. Atlanta (GA). Barr D. Environ Health Perspect 2004. et al.S. Poland. Environ Res 2003. 2005.Phthalates References Adibi JJ. Perera FP. Camann DE. Reproducibility of urinary phthalate metabolites in first morning urine samples. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Malek NA. Hauser R. Koch HM. Centers for Disease Control and Prevention (CDC). Urinary levels of seven phthalate metabolites in the U. Brock JW. Environ Health Perspect 2003. Meeker JD.22(3):688-695. Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 2002. Needham LL.68:309-314.111(14):1719-1722. Hoppin JA. Silva MJ.93:177-185. Ryan L. Duty S. Jacek R. Jedrychowski W. 112(5):A270].

68 (3.30-6.5) 37.3 (24.25-3.30 (4.70 (1.1) 25.7) 6.20 (3.4-40.40-1.40) 9.2 (29.10-5.2-28.10 (6.70) 7.5 (12.40-8.9 (29. see Data Analysis section) for Survey years 99-00.75 (3.8 (19.10 (2. 1.1982).60) 4. as glucuronide conjugates (Albro et al.70 (3.70 (8.00) 9.5-28.0) 23.0 (18.2 (31.9-57.50) 4.26-2.50-3.21 (2.0) 23.1) 22.7) 8.4-27.5) 23.80-5.00 (5.90-11.10-2.7) 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 3.7-32.80 (8.70-5.63-4.0-18.94-3.0 (9.70-8.30-8.2 (7.70 (5.80) 6.35) 4.5) 40.40 (6.70-6.90) 1.4) 20.0 (19.10) 3.2-35.0-19.6-25.20 (3.21 (2.7) 35.92-5.4) 22.5-36. After parenteral administration.00) 1.00-3.2 (10.9) 18.9 (13.9 (7.03-2.60 (6. Following ingestion.0-18.00) 5.30-13.5 (30.5-41.1 (8.50 (7.31 (3.77 (2. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.44) 4.2) 4.7 (14. and in humans.98) 2.60) 7. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).4) 6.5-17.50 (7.3) 13.60) 4.00) 1.79) 2.20 (1.0) Total 4.50-8.0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.6) 5.9-19.84) 3.8 (17.10-5.5) 19.4-42.90-5.80) 13.41 (3.6-23.6) 39.9-48.6-28.86) 2.60) 9.10) 2.0 (21.0) 23.0 (16.90) 4.50 (3.50-5.1-17.15 (1.90) 3.7 (17.50-3.61 (3.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.27) 2. Peck and Albro.80) 9.2-39.50 (8.70) 16.80-4.10) 2.51) 4.30 (6.93) 6.00-3.3 (15.4 (21.3) 28.10 (5.40-12.1 (8.90 (4.10-3.2) 23.67-4.8-36.6 (9.85 (3.00) 2.5 (12.0 (14.7) 19.82 (3.2 (11.37-4.00) 3.6 (11.9-28.4) 13.00 (2. and 0. 1989.4) 5.6 (12.2-17.42) 3.9) 15.34 (2.4-20.92) 4.75-4.50 (3.5) 43.30 (7.7-58.3-64.4) 22.1-48. population from the National Health and Nutrition Examination Survey.20 (4.70) 2.90) 7.2) 29.S.40 (2.32 (3.5) 31. which is used for many consumer products. 2002.5 (18.82) 3. Concentrations in plastic materials may reach 40% by weight.41) 3.3-26. 1982.9-49.57-7.80-8.50-5.10) 3.9 (16.16-3.6) 14.40 (4. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.50-2.9 (26.8 (19. mainly polyvinyl chloride.10 (3.4) 23.30) 2.40-8.10-4. 01-02.85) 4.3 (19.3) 52.7) 37.70-4. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).5 (11.Phthalates Di-2-ethylhexyl Phthalate CAS No.5-40.70 (1.6) 95th 23.5 (24.4) 33.9-26.70-5.40-11.10) 8.8-47.86) 2.9) 27.42-5.19-3.0 (17.6) 9.4-53. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).40-8. Fourth National Report on Human Exposure to Environmental Chemicals 275 .23 (2.90) 4.89-3.35 (1. packaging film.30-11.40 (4.50-11.10-11.2) 6.90-8.54) 4.6 (20.50-20. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.9 (17.