2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

Fourth National Report on Human Exposure to Environmental Chemicals

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The process for selection is described at http://www.What’s New in this Report What’s New in this Report In this Fourth Report.2'.6-Pentabromodiphenyl ether (BDE 100) 2.6.5-Pentabromodiphenyl ether (BDE 99) 2.1-Trichloroethane (Methyl chloroform) 1.4'-Pentabromodiphenyl ether (BDE 85) 2.4.4.4.4'.4'-Tetrabromodiphenyl ether (BDE 66) 2.5'-Tetrachlorobiphenyl (PCB 49) 2.1.3'.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.5.3.4'-Tribromodiphenyl ether (BDE 28) 2.4-Dichlorobenzene (p-Dichlorobenzene. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.4.1-Dichloroethane 1.3-Tetramethylbutyl] phenol) Triclosan (2.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2’.6'-Hexabromodiphenyl ether (BDE 154) 2.2'.4'.4. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4'. 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 (2.2-Dichloroethene trans-1.3-Dichlorobenzene (m-Dichlorobenzene) 1.5.2'.2'3.2'.1.4.4-Tribromodiphenyl ether (BDE 17) 2.html.5'-Hexabromodiphenyl ether (BDE 153) 2.2'.2-Dichloroethene Dichloromethane (Methylene chloride) 1.1.5’.2-Trichloroethane Trichloroethene (Trichloroethylene) m.2-Dichloroethane (Ethylene dichloride) 1.gov/exposurereport/chemical_selection.5'-Tetrachlorobiphenyl (PCB 44) 2.5'.1-Dichloroethene (Vinylidene chloride) cis-1.2'.2'4. Paradichlorobenzene) 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 2.5.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .4'-Tetrabromodiphenyl ether (BDE 47) 2.4.2.cdc.1.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.4.3’.3.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.3.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.4.2'. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.3.2-Dichloropropane 2.4’.4.4’.6-Heptabromodiphenyl ether (BDE 183) 2.4'. Table 1.4.4'.2-Dichlorobenzene (o-Dichlorobenzene) 1.5.2'.4.2'.

2003-2004 data for these other pesticides will be provided on this website as soon as they are available. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. and these data will be included in the next release of the Report. 2001-2002. 2003-2004) have been re-computed by use of this improved procedure. Fourth National Report on Human Exposure to Environmental Chemicals 3 . Only slight differences should be noted when one compares the recomputations to previous releases of the Report. the presence of an interference) that produced results of inadequate quality.. urinary 2.5-dichlorophenol for the 1999-2002 survey periods. Percentiles for all three NHANES survey periods (1999-2000.g.4-dichlorophenol and 2.1). Data for other pesticides are included only for 1999-2000 and 2001-2002..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. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period. Explanations for each change are provided in Appendix B. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. five results that all have the value 90. Details of this procedure are provided in Appendix A. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods.g.

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

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

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

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

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

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

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

EPA.S.. 2006). 2004).8 (81.2 μg/kg/day (U.1 (73.7) 73.7) 96. Animal studies indicate that acrylamide is well absorbed.8 (52.7 (55.4-89.4 (54.0. Commercially.1) 62.7-64. Survey Geometric mean (95% conf.6) 73. ocular and dermal irritation from direct contact with acrylamide containing materials.9) 58.3 (55. 2002)..4-60.4 (53.6) 71.S.2-93.9-105) 86. or to glutathione conjugates (Calleman et al. but are generally above the U.9) 63.4 (54. pulp and paper production.0-108) 152 (139-175) 126 (111-142) 108 (86. gels. and cosmetics (NTP-CERHR.6-61.S.0 (53. and is either metabolized to the reactive epoxide.2-118) 98.1-61.4 (51. 1990.1) 53. drinking water. and well below doses known to cause nerve damage or carcinogenicity in animals.6-75. 2004.0 (69.6-108) 61.S. People may be exposed to acrylamide from foods.4) 100 (89.8 (57.5) 58.5-80. and in the synthesis or compounding of dye materials.2) 57. EPA reference dose of 0.1 (47.Acrylamide Acrylamide CAS No. Fourth National Report on Human Exposure to Environmental Chemicals 11 .7-60. population from the National Health and Nutrition Examination Survey. soil conditioners. in permanent press fabrics.4 (59. In the general population. Estimated intakes in children are about twice that of adults (DiNovi and Howard.5 (52.2-91.2-59.9) 75. 2005). mineral processing. 2005).4) 57. and an average daily intake is estimated as 0.7) 54.0-66.2 (75.3) 86.7-64.9 (54. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.2-114) 163 (147-191) 96. such as potatoes and some grains.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. Natural substances in the food are converted to acrylamide. 2005. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. widely distributed in tissues. interval) 61. it was discovered that acrylamide is formed when starch-rich foods.4-60.6-104) 82.7 (65.5 (79.1-64. FDA. smoking.5) 66.6 (56.2-70.2 (62. 217 million pounds of acrylamide were produced commercially in the U. as an absorbent in disposable diapers. see Data Analysis section) for Survey year 03-04 is 3.9-61.8-57.0-58.3 (53.4-83.1-64.0 μg/kg for adults (FAO/ WHO. but can covalently bind to form adducts with proteins. (NTP-CERHR.1) 55. Tareke et al.2 (58. 1994).9 (69.5-85. Polyacrylamides are useful water-compatible polymers used in water treatment. Since acrylamide has limited volatility and high water solubility. EPA.0) 57.6) 50. These estimated intakes are hundreds of times lower than occupational exposures.4-76. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. 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. 2005).3) 63.9-52. 2005). Acrylamide is not thought to accumulate in the body at environmental doses. Elimination occurs mainly in the urine as mercapturic acid conjugates. acrylamide has produced upper airway irritation following inhalation of high levels.6 (81.2-67.1 (52.8-55.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. and from dermal contact with products that contain residual acrylamide.5 (44. FAO/WHO.1 (83.7) 58.1 (88.9) 57.. 2005).1) 101 (95. are heated at temperatures used for frying and baking.0-49.1-57.0) 85. and binding agents. In 1997. Recently.5 (74.2) 57. the main source of exposure is from the diet.7) 75th 79.3-71.8 (91. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U. In humans.1) 46.0 (57. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.7 (63.6-66.3-2.2-77.9 (60. glycidamide.7 (58.0 (67. acrylamide is synthesized and used in the production of polyacrylamide polymer.S. in some sealing grouts.6) 90.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. Fennell et al.4) 57.6-65. 2006. and in some cosmetics.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 61.3) 70.6 (51.

8) 60.2 (72.1 (57.S.5-92. dominant lethality)..3 (56.0-62.4-65.7-86. EPA.9 (57.2 (63.5 (42. 2005. respectively) are markers of integrated acrylamide exposure over the preceding few months.0..7 (84. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. probably through its epoxide metabolite. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.3) 59..epa.4 (61.8) 45.3-101) 95.3) 59.0 (70.1 (56.5 (83. Acrylamide is clastogenic and can produce dominant lethal mutations.5) 75th 85. see Data Analysis section) for Survey year 03-04 is 4. 2005) and sperm DNA adducts (Xie et al.8-61. After exposure ceases.7) 61. 2005. scrotal. Hagmar et al.4 (56.9) 65.2 (56. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.. although different analytic methods can affect results. 2004.9-62.1 (70.9-78.2-91. Mucci et al. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. IARC classifies acrylamide as probably carcinogenic to humans.9-64.1-70. population from the National Health and Nutrition Examination Survey. Schettgen et al.4) 46.S. 2009).5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.pdf. glycidamide (NTP-CERHR. In addition.4) 53. most non-smokers had levels less than about 100 pmol/gram hemoglobin.3) 85.4 (81. 2005). Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. Maniere et al.4 (57.who. fetal death. 2005.S.7-64.. AHA levels have been shown to increase with dietary intake (Hagmar et al.1) 62.5) 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. and neuronal DNA reactivity (Doerge et al. The degree of formation of the more toxic glycidamide and levels of GHA can be influenced by polymorphisms in several of the enzymes that metabolize acrylamide (Duale et al. reproductive effects (reduced litter size.0 (75. 2005) have been demonstrated in animals.7) 90.7 (57. 2002. interval) 59.1-60.0-103) 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 64.5-94.9-77.6-90.. 2005).9 (81.. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.. 1997.9 (58..8-48.4-98.5-64. U.2-68.7) 60.7-62. 2005.1) 60. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. 2006).... EPA.0 (52.7) 74.7 (87.9-76. EPA at: http://www. altered gene expression in testicular tissues (Yang et al.9) 87. 2001).5-66. Glycidamide has been shown to react with DNA (Doerge et al.S.1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59.. 2004). Vesper et al.. 2006. 2006). 2005). 12 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf. NTP-CERHR..0-93.int/ ipcs/food/jecfa/summaries/summary_report_64_final.Acrylamide occupational exposures.0) 118 (103-126) 121 (112-134) 113 (94.0 (80.8 (44.7 (61.. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).6-62. 2006) have been demonstrated after acrylamide dosing.0) 94.4-59. Vesper 2005) and smoking (Bergmark. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 2008).1 (82. 2005.8 (51. and cancer (mammary.. 2002. 2005.3) 59. adrenal... Puppel et al. 2003.6 (66. Rice. 2005. Schettgen et al.2) 55.5) 71. and other sites) (FAO/WHO.1 (66. Axonal degeneration. 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.4 (51.5 (56.8-49.9) 59. 2008). 2005. thyroid.6 (90. uterine. U.9) 75.5) 87. 2005. 1997.1-56.4) 83. Additional information is available from U.1) 56.2-90. Puppel et al. 2005.4 (90.1-62. 2005. Klaunig et al.. 2005).5 (59.6-64.4-103) 79.2) 87. male germinal cell injury.2) 65.9-138) 143 (130-159) 96.3-78. presynaptic nerve terminal binding (LoPachin.

Costa LG.56.. Tornqvist M.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Fennell TR. 1999). Food Chem. Paulsen JE. Toxicol Sci. National Toxicology Program.who. The Updated Exposure Assessment for Acrylamide.561:21-37.html#u1004. Magnusson AL.85:447-459. Laurentie M. Maniere I. 2009 Jan 8. Doerge DR. Toxicol Sci 2005. In another study. Rome. Churchwell MI. Calleman CJ. da Costa GG. 8-17 February 2005. Alexander J. Adv Exp Med Biol 2005. July. Andersen M. Mutat Res 2005. Doerge DR.580(1-2):119-129. gov/~dms/acrydata. 2005. 2/3/09 Perez HL. NIH Publication No. 2004. 64th Meeting: Summary and Conclusions (FAO/WHO).580(1-2):157-165. Godard T. 1994). Becher G. Cheong HK. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR).10(1):78-84. Uncertainties. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Farmer PB.Toxicol Appl Pharmacol 1994. 2006. 054472. He F.27(4):219-226. Bruze M. LoPachin RM. Aprea P. He F.pdf. J Agric Food Chem 2008. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Food and Drug Administration (FDA).43:365–410.120(1):45-54. 2/3/09 Hagmar L. et al. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Bjellaas T. Burgess J. et al. Available at URL: http://www. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide.126(2):361-371. Acrylamide neurotoxicity: neurological. Kautiainen A. Rosen I. Illinois. Human exposure and internal dose assessments of acrylamide in food. DiNovi M and Howard D. Wilson KM.Acrylamide In occupational settings. Zhang S. Granath F. Tornqvist M.niehs. and Research Strategies. Bridson WE. AHA levels correlated with a neurologic symptom index and specific physiologic measures in an occupational setting and correlated better with clinical signs and symptoms than urinary excretion of the mercapturic acid metabolite (Calleman et al. Churchwell MI. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Metabolism and hemoglobin adduct formation of acrylamide in humans. Acrylamide intake through diet and human cancer risk. Malmberg B. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. 2001). Wu Y. Hagmar et al. smokers and nonsmokers. morphological and molecular endpoints in animal models. Mutat Res 2005. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Duale N.nih. Perez et al. Joint FAO/WHO Expert Committee on Food Additives. Survey data on acrylamide in food: individual food products. 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.561:49-62. Wirfalt E. Haugen M. et al. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Chicago. Toxicol Appl Pharmacol 1993. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Summer SCJ. Axmon A. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Calleman CJ.. Costa LG. Scand J Work Environ Health 2001. April 13-15.580(1-2):131-141.cfsan. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Calleman CJ. Italy. Tian G. 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. [Epub ahead of print] Dybing E. et al. References Bergmark E. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Available at URL: http://cerhr.3:406-412. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Bergmark E. smoking habits and gender. Toxicol 2005. Mucci LA. Hagmar L. Adv Exp Med Biol 2005. 2001.gov/chemicals/ acrylamide/Acrylamide_Monograph. Chem Res Toxicol 1997 Jan. Beland FA. February. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Mechanisms of acrylamide induced rodent carcinogenesis. Snyder RW. Yang JS. Available at URL: http://www. 1993.fda. Paulsson B. Nordander C. Bergmark E. Bergmark E. McDaniel LP. Twaddle NC. Fennell TR. Chem Res Toxicol 1990. 2/3/09 Klaunig JE. Kamendulis LM.pdf. Guffroy M. CFSAN/Office of Plant and Dairy Foods. Spicer R.. Mutat Res 2005. 6013-6019. Osterman-Golkar S..

Drexler H. Han DU. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Hemoglobin adducts of ethylene oxide. Int J Hyg Environ Health 2004. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry.134(1-3):65-70.207(6):531-9. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study.50(17):4998-5006.20(6):959-64. Meyers T. September. Jin Y. 2/3/09 Vesper HW. Vesper HW. Fueller F. Liu Y. EPA). Analysis of acrylamide. Broding HC. Rossbach B. Gray JG. U. Anal Biochem 1999. Available at URL: http://www. Office of Pollution Prevention and Toxics. Chemical Summary for Acrylamide. Chae C. et al. Benetou V. Mutat Res 2005. Ingham L. Yang HJ. et al.epa. Angerer J. Tjaden Z.gov/iris/subst/0286. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine.19(4):527-34. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Washington (DC). Rapid Commun Mass Spectrom 2006.561:89-96. Choi JH.S. Drexler H. Kutting B. Toxicol Lett 2002.580(1-2):71-80. Ospina M.S. Rydberg P. Int J Hyg Environ Health 2003. Tareke E. Agudo A. Sun H. EPA).S. Licea-Perez H.htm. Schettgen T. J Agric Food Chem 2008. Puppel N. The carcinogenicity of acrylamide.Acrylamide glycidamide by gas chromatography-mass spectrometry. Angerer J. Ospina M. revised 1/3/06. Tornqvist M. Schettgen T. Slimani N.163(2):101-8. Drexler H. Ding X. Liu K.gov/chemfact/s_acryla. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Schettgen T.S. Toxicological effects of acrylamide on rat testicular gene expression profile. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany.txt. Integrated Risk Information System (IRIS). Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Acrylamide. Lee SH. Smith A. Angerer J.580(1-2):3-20. Han CH.206(1):9-14. Toxicol Lett 2006. Letzel S. Available at URL: http://www. Tjønneland A. Environmental Protection Agency (U. 2/3/09. Adv Exp Med Biol 2005. Mutat Res 2005 Feb 7. 1994.274(1):59-68. a carcinogen formed in heated foodstuffs. propylene oxide. Karlsson P. Weiss T. Marko D. U. Vesper HW. J Agric Food Chem 2002. Myers GL. Meyers T. Eriksson S.56(15):6046-53. Xie Q. Lee MH.epa. Fu D. Hallmans G. Rice JM. Reprod Toxicol 2005. Environmental Protection Agency (U. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population.

and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.054 (.110 (.080 (.050-.139) * .120 (.063) .63-2. acute respiratory infections.180) .02) 1.S.12-4.84-3.16) .17 (. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob. DHHS. and 0.540 (.108) * .198) * .28-1.32) 1.990 (.77 (1.160 (.110 (. cardiovascular disease.23-2.63 (2. Cigarettes contain about 1.21-1.20-2.02) 1.120 (.32-2.312) .052 (<LOD-.950-1.163) .060 (.050) .22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .080) < LOD .260-1.17) .62 (2.20) 1.310) .110) .310-1.580 (.370-.060-.68 (1.18-3.620-1.00) .48-3.57) 2.48-2.060 (<LOD-.23 (2.350-. DHHS.150) .130) .060 (.50-1.01) 3.043-.167 (.188) .164 (.050 (<LOD-.900-1.Cotinine Cotinine CAS No.080-.690 (.26-1.520 (.110-.94) 1.187) . Survey Geometric mean (95% conf.120 (.210 (.140 (.180) .04 (1.34 (1.131 (.77 (2.850 (.65 (1.76 (1.200) 1.088-.090-.180 (.240 (.62) 2.047-.480-1.15) 2.160-.85 (1.50) 3.115-.81-2.400-.580) .086 (.510 (. and 17% had an LOD of 0. < LOD means less than the limit of detection.068) .175 (.450-. 1998).14) .140 (.05) 1. Fourth National Report on Human Exposure to Environmental Chemicals 15 .154-.047-.96-4.080 (.50-4.220) .137-.92 (1.066) . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.12 (2.142-.104-.20 (.040-.45) 1.220) .050 (.22) 2.40) .77 (1.621-1.32-2.470-.193) . which may vary for some chemicals by year and by individual sample.S.430-1.12) 1.05 ng/mL. see Data Analysis section) for Survey years 99-00.92) 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 .770-1.05.180) .230 (.19-2.015 ng/mL.12 (1.160 (.075 (.30) * .077) .144 (.53 (1.860 (.070-.88 (.20) .145) . and 03-04 are 0.96 (1.180) .60-2.740-1.88 (1.070 (<LOD-.93) .066 (.950 (.00) 1.124 (.073) < LOD .533-.040 (.02 (.052 (<LOD-.160 (.670) .505 (.076-.160) .68) 2. ear problems.55 (1.01 (1.630 (.061) < LOD .050 (<LOD-.990) .060) .35 (2.153-. and various other disorders (U.66) 1.110) .220-.310) 90th 1.600-1.068) .060 (<LOD-.580-1.730 (.071 (.110-.080) < LOD < LOD .300) .428-.020-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. ** In the 2001-2002 survey period.78) 2.770) .20 (1.49) 1.060-.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .350-.19) .410) . 2004). emphysema.54 (1.17 (1.480-.68) .83-2.160) .930 (.99) 2.44) 2.910-1.19) 1.14) .030-.030-.30) 2.080-.66-3.89) 1.54) 1.015.070) .660) .30) 2.800 (.360) .75) 1.09-2.620 (. population from the National Health and Nutrition Examination Survey. Children exposed to ETS are at increased risk for sudden infant death syndrome.163 (.066-.310-1.44) 2.840) 3.087) < LOD < LOD .43 (1.70) 2.920 (.201) . and exacerbated asthma (U.071) .23 (1.070) 75th .100-.790) .120-. acute respiratory illness.087-.5% nicotine by weight (Kozlowski et al.110-.120 (.087 (.084) .030 (.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.080-.280 (.190-. respectively.234) .09-3.090-.120-.053 (<LOD-.126) .630 (.S.120) .54 (1.190-.99) 2.23 (.180 (.39 (1.030-.42 (1.540-.213) .302) .740-1.350 (.180) .21-1.070) .710 (.197) .50 (1.150) .820) .33-2.140-.14-1.66 (1.997-3.040 (.320) .42-4.060-.148-..080-.094) .050 (<LOD-.47-3.570 (.059-.059-.95) 1.79) 3.770) .500 (.15 (2.960-1.050 (<LOD-.55-2.49) 1.39) 3.625) .062 (.570-1.21 (.726) . Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.058 (.040-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110 (.44 (2.38-2.140-.11) . 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.44 (1.308 (.53-4. stroke.057-.110 (. 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.130 (.137 (.87-3.190-.28) .260) 1.050-. 83% of measurements had an LOD of 0.09-3.120 (.077) .050) .164 (. 2004).70-2.216 (.040 (.089) Age group 3-11 years 99-00 01-02** 03-04 .230) .110 (.090-.106-.96) 2. 2006). maternal exposure during pregnancy can result in lower birth weight.111-.506 (.630 (.

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

National Toxicology Program (NTP). Schober SE.gov/tcrb/monographs/10/. Benowitz NL. Department of Heath and Human Services. [online]. Hukkanen J. Ethnic differences in N-glucuronidation of nicotine and cotinine. Aiba M. Brody DJ. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Caudill SP. Soliman S.cdc. Tobacco Smoke and Involuntary Smoking. Warner K. Benowitz NL.S. Mehta NY. Curtin LR. References Armitage AK. Schwartz SS. BMJ 1975. 11th ed. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Tobacco related exposures. Available at URL: http://monographs. Summary of Data Reported and Evaluation [online] 1986. Smoking and Tobacco Control Monograph 10 [online]. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Lewis PJ. Clin Pharmacol Ther 1994.nih.S. Jacob P III. Metabolism of nicotine to cotinine studied by a dual stable isotope method. 1988-1991. 4/13/09 Centers for Disease Control and Prevention (CDC).7:369-375. Jarvis MJ. Vol 83. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Metabolism and disposition kinetics of nicotine. Pirkle JL. Epidemiol Rev 1996.gov/ntp/roc/eleventh/profiles/ s176toba.94(2):314-320.18:188-204.S. Tob Control 2006.280:152-156.pdf. Benowitz NL. Brody DJ.iarc. Turner DM. In Report on Carcinogens. Department of Heath and Human Services. Centers for Disease Control and Prevention.cancer. Houseman TH. National Institute for Occupational Safety and Hygiene (NIOSH). Mowery PD. 1999-2002. Sweeney CT.gov/library/ secondhandsmoke/. International Agency for Research on Cancer. Int Arch Occup Environ Health 1991. JAMA 1996. Office on Smoking and Health [online] 2006. Giovino GA. Sosnoff CS. Cotinine as a biomarker of environmental tobacco smoke exposure. Jacob P III. Pirkle JL.S. Tob Control 1998.291(3):1196-1203.114(6):853-858. 4/13/09 Iwase A. and the United States.S. 4/13/09 National Cancer Institute (NCI). U.56:483-493. DHHS). Jacob III P. Dollery CT. IARC Monogr Eval Carcinog Risks Hum. Nicotine metabolism and intake in black and white smokers. Pechacek TF. Pechacek TF. Etzel RA. Exposure of the U. Centers for Disease Control. Perez-Stable EJ.4:313-316. Coordinating Center for Health Promotion. DHHS). Pickett MA.php. Flegal KM. Herrera B. Am J Public Health 2004. U. Benowitz NL. 1988-1991. Kira S. available at URL: http://mtn. 1991. Available at URL: http://monographs.surgeongeneral. Vogler GP. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Bernert JT. Modin G. Pollack HA. JAMA 1998. Tobacco Smoke. iarc. Racial/ethnic differences in serum cotinine levels among adult U. J Pharmacol Exp Ther 1999. Richter PA. Vol 38. JAMA 1998.S. Jacob P. population to secondhand smoke: 1988-2002.S Department of Health and Human Services (U.63:139-43. Fong I. U. George CF. cigarette smokers: the Third National Health and Nutrition Examination Survey. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Bernert JT. Available at URL: http:// cancercontrol. Maurer KR. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Third National Report on Human Exposure to Environmental Chemicals. 4/13/09 U. Centers for Disease Control and Prevention. Available at URL: http://ntp. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Strauss WJ.pdf. Available at URL: http://www. Coordinating Center for Health Promotion. Giovino G. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 2004. Absorption and metabolism of nicotine from cigarettes. Benowitz NL.php. 4/13/09 Perez-Stable EJ. June.S Department of Health and Human Services (U.fr/ENG/Monographs/ allmonos90.fr/ENG/Monographs/allmonos90. et al. Summary of Data Reported and Evaluation [online] 2004. Trends in the exposure of nonsmokers in the U.S.280:135-140.gov/eid/rmca/critdocs/ criteriadoc/33.15:302-307. IARC Monogr Eval Carcinog Risks Hum.niehs. Caraballo R. Environ Health Perspect 2006. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey.57(1):79115.275:1233-1240. National Center for Chronic Disease Prevention and Health Promotion. Kozlowski LT. 1999. Respiratory nicotine absorption in non-smoking females during passive smoking. et al. 4/13/09 International Agency for Research on Cancer. Pharmacol Rev 2005.niosh. the United Kingdom. Herrera B. Atlanta (GA): 2005.

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

130-.130-. DEET is not genotoxic.210 (.110-.epa.110 (.1.560) < LOD .S.140 (.100 (<LOD-.S.220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .170 (.140) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130 (. There are over 225 insect repellents brands containing DEET.160) < LOD .180 (.N-Diethyl-meta-toluamide (DEET) N.220 (..110 (.150) < LOD . 1998).N-Diethyl-meta-toluamide (DEET) 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. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.240) < LOD . have been reported as result of self-poisoning by ingestion or excessive dermal application. Survey Geometric mean (95% conf. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. Additional information is available from U.170 (. (U.180 (.110 (. EPA. DEET has low acute toxicity. < LOD means less than the limit of detection.180 (. 1998). 2003).110-.520) < LOD .449 and 0.. Neurological effects in humans. DEET is not a developmental or reproductive toxicant in animals (U.S.100-. About 3-8% of dermally applied DEET is absorbed. Sudakin and Trevathan.130-.110 (<LOD-.270) 688 678 518 700 598 956 Limit of detection (LOD.130 (. After absorption. DEET is also used in combination with dermal sun screens (U. DEET can be applied to clothing and the skin to repel biting insects.130-. 134-62-3 General Information N.N-Diethyl-meta-toluamide (DEET) CAS No. One survey detected DEET in 74% of sampled streams in the U. population from the National Health and Nutrition Examination Survey. and they range in concentration from 4% to 100%.130) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 19 .140) < LOD .S.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. 2002).100-.120-. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.gov/pesticides/. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .EPA.130) < LOD .100-. including seizures and encephalopathy. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.EPA at: http://www.120-. 2003)..100-.100-.250) < LOD .140) < LOD .180) < LOD .S.140-. Its use is recommended for prevention of several vector-borne diseases.S. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.130 (.190) < LOD . (Kolpin et al. 2002).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 .210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.110 (<LOD-. DEET is not registered for use on agricultural commodities.110 (. and it has not been rated by IARC or NTP with respect to human carcinogenicity.100-.N. 2005). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140) < LOD .EPA. Urinary N. 1995.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.370) < LOD .170-.490) < LOD .N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.480 (.230) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .390-.230-.370-.150) < LOD . Urinary DEET levels as high as 5. In this survey period. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.190 (.410-.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 .S.410 (.200 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.640 (.190 (<LOD-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.350-.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Urinary N.280-1.93) < LOD .270-.N. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.300 (.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.190 (.330 (.350) < LOD .S.250 (.280 (.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 .240-. Survey Geometric mean (95% conf.270 (..440) < LOD . 20 Fourth National Report on Human Exposure to Environmental Chemicals .410 (. Biomonitoring studies on levels of DEET provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEET than are found in the general population. 2005).330 (.320) < LOD .630) < LOD .290-.140-. 1992).250-. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.500 (.. population from the National Health and Nutrition Examination Survey.320 (.230-.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 .250) < LOD .190-.350) < LOD .270) < LOD . representative subsamples from NHANES 2001-2002.130 (<LOD-.240) < LOD .150-. 2007).500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .270 (<LOD-.

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

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

pdf. Needham LL. Calafat AM. Occup Environ Med 2002.312(2):441-448. Kiguchi M.nih.35(2 Pt 1):238-254. Ye X. Biochem Biophys Res Commun 2003. 2003. Ecotoxicity and the Environment (CSTEE).nih. Belgium. Reidy JA. DirectorateGeneral Health and Consumer Protection. and Hardy MP. et al. Munro IC. Chung MK.137(3):353-362. Koulova AI. Joskow R. Twomey K. T. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats.. Watanabe C. Available at URL: http://ecb. MacLusky.10:875-921. Available at URL: http://ec. Barr DB. Ispra. Kuklenyik Z. niehs. Pyo MY. 1999-2000: a national reconnaissance.S. Tsugane S.149:988-994. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Lynch BS. National Institutes of Health. Fujii S. Exposure of the U. Chem Res Toxicol 2001. Kroes R. Yang M. Marr MC. and other organic wastewater contaminants in U. Brussels. Needham LL. Reidy JA. Haighton LA. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. European Commission. J Am Dent Assoc 2006. NC. Doull J.europa. Environ Sci Technol 2002. 2007. Toxicol Sci 2002.59(9):625-628. Calafat AM. National Institute of Environmental Health Sciences. Harazono A.pdf. Brine DR. McConnell EE. An evaluation of the possible carcinogenicity of bisphenol A to humans. Han SS. Italy. Available at URL: http://ntp. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).Scientific Committee on Toxicity. Gray GM. Hara K. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. 32 Fourth National Report on Human Exposure to Environmental Chemicals .780(2):365-370. National Toxicology Program. et al. Research Triangle Park. Kim YH. Barr JR. Proc Natl Acad Sci USA 2005. Kolpin DW. Hanaoka T. Imai H. Kim CS. Matthews JB. Ikka T.gov/chemicals/bisphenol/BPAFinalEPVF112607. Arakawa C. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Serizawa S. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Zaugg SD. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Leranth. 5: 505-523. Hum Ecol Risk Assess 2004.69(22):2611-2625. May 22. Sottas CM. Cunha G.pdf . August 2001. Joint Research Centre Institute of Health and Consumer Protection. November 26. September. Hlywka JJ.S.68(1):121-146. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Ekong J. K.145:592-603. Cohen JT. Timms BG.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Barber LB. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Watanabe S. Hughes C.. Keimowitz AR. Ema M. Richter CA. niehs. streams.nih.gov/chemicals/bisphenol/bisphenol. Nippon Eiseigaku Zasshi 2004. Bisphenol A. Park S. Barton L. Myers CB. Available at URL: http://cerhr. Regul Toxicol Pharmacol 2002. 2002.36(6):1202-1211. et al. Furlong ET. Available at URL: http://cerhr. hormones. Meyer MT. Szigeti-Buck. Rat two-generation reproductive toxicity study of bisphenol A.eu/ health/ph_risk/committees/sct/documents/out156_en.59(4):403-408. Cha SW.J. Caudill SP.niehs.. 2/4/09 Ouchi K. Klinefelter GR.113(4):391-395. 2/4/09 European Commission.14(2):149-157. Bradley S.jrc. Furukawa M. bisphenol A glucuronide. Rubin C. 2/4/09 Fujimaki K. Calafat AM.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Howdeshell KL. U. Zacharewski TR. Tyl RW. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Thurman EM. vom Saal FS. C. Rhomberg et al. and Hajszan. Endocrinology 2008. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Environ Health Perspect 2005. Department of Health and Human Services.pdf. Kawamura N.102(19):7014-7019. Han SY. Yoshinaga J. with estrogen receptors alpha and beta. 2008. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Human Health. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Koh WS. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Environ Health Perspect 2008. Pharmaceuticals. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Endocrinology 2004.116(1):39-44.pdf . Needham LL. Shin HC. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. N. Thomas BF. 4. 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. Life Sci 2001. Wong LY. Reprod Toxicol 2001. Gender differences in the levels of bisphenol A metabolites in urine.S. Kim JC.Environmental Phenols References Akingbemi BT. In vitro and in vivo interactions of bisphenol A and its metabolite.

147(6 Suppl):S56-69. vom Saal FS. Sheldon LS. Food Chem Toxicol 2002. Kawamoto T. and nonylphenol at home and daycare.Environmental Phenols Volkel W.103(1):9-20. Colnot T. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Environ Health Perspect 2005. An observational study of the potential exposures of preschool children to pentachlorophenol.15:12811287. Arch Environ Contam Toxicol 2003.40(7):905-12. Kim SY. Morgan MK. Witorsch RJ. Wilson NK. Endocrinology 2006. Lordo RA.113(8):926-33. Hughes C. III. Filser JG. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Nagel SC. Jang JY. Vom Saal FS. Chuang JC. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Dekant W. Chem Res Toxicol 2002. et al.44(4):546-51. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Environ Res 2007. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Lee SM. Csanady GA. Welshons WV. bisphenol-A. Biological monitoring of bisphenol a in a Korean population. Yang M. Large effects from small exposures. Chang SS.

20-2.. leading to inhalation as another potential exposure route (Rudel et al.50 (1.600-1.30) 1. 34 Fourth National Report on Human Exposure to Environmental Chemicals . Laws et al. industrial cleaners..600-1. Indoor and to a lesser extent. 2000.900 (. and emulsifiers.10 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60-3.600) .274-.20) 1. the various alkylphenols have also been used as emulsifiers and modifiers in paints.S.20-2. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 0. did not bioaccumulate.60-3. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.389 (.70 (1.g.30-2. 2002).50) .20-2.500) .600-1.268-.60) 613 652 1092 Limit of detection (LOD.400 (. 2004).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 . 1995.500) . is used to manufacture alkylphenol ethoxylates.300 (<LOD-. over 500. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.60-3..400) 1..200-.30 (1. 2006.40) 1. altered neonatal sexual development.900 (. Survey Geometric mean (95% conf.80 (1. Katsuda et al.5% of 139 U. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. and through manufacturing waste streams (Warhurst.10-2. During the 1980s and 1990s.300 (<LOD-.500-1.40 (1.20) 2.30) 2.70 (1. 1997..369 (.00 (.20) 314 715 1488 03-04 03-04 * * .60) 1. 2002).507) * < LOD .20-2. The alkylphenols can bioaccumulate in some fish.30 (1.50) .900 (.50) 1. Saito et al.40) 2. Less frequently. Ying et al.Environmental Phenols 4-tert-Octylphenol CAS No.60-3.600) .. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. and some of their degradation products are toxic to aquatic life. textiles. 140-66-9 General Information 4-tert-Octyphenol. orally administered 4-tert-octylphenol was well absorbed. impaired steroidogenesis.. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).299-.40) 2. and impaired spermatogenesis (e.00) 1229 1288 03-04 03-04 03-04 * . In rats. Bian et al. < LOD means less than the limit of detection. altered estrus cycles and reproductive outcomes. to shorter chain alkylphenol ethoxylates.. 1996).50) 1. an alkylphenol. and to alkylphenoxycarboxylates.900 (.20-2.600-1. have demonstrated estrogenic effects particularly when injected at high doses in animals.357 (.300-.40) 1. population from the National Health and Nutrition Examination Survey.00 (.10) 2.90) 2.. and from contact with some personal care products and detergents.900 (.10 (1. Several alkylphenols.000 tons of alkylphenol ethoxylates were produced annually worldwide.20 (1.477) .200-.80) 2.20-2. Blake and Boockfor.10) 1.600-1.60-3. including 4-tert-octylphenol.30 (.70 (1.70 (1.1. Disposition in humans has not been studied sufficiently.00 (1. testicular atrophy.500-1. and was quickly eliminated from the blood (Certa et al. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.400 (.300 (<LOD-.600) .30 (1.80 (1.10 (.60-3.30) 90th 1.2.300-. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. 4-octylphenol monoethoxylate was detected in 43.300 (<LOD-. Urinary 4-tert-Octylphenol (4-[1. and some personal care products. 2000.800-1. pesticides. streams in 30 states (Kolpin et al.300 (<LOD-.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30 (1.600-1. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.497) * .500) 75th . and the polyethoxy chain may consist of up to 50 ethoxy units.. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.S. The alkylphenol ethoxylates enter the environment through human use of products containing them.50) 1.400 (. 2003.600) 1.700-1. which are anionic surfactants used in detergents.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.50-2. In 1999-2000.500 (. fish) and drinking water.40) * 03-04 03-04 03-04 .g. In the 1990s.500) . through sewage.60) .50-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.90) 2.3.

78) 1228 1286 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..3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.06 (2.550-1.410 (.03 (1.S. Nagao et al.29) 2.53-3.540-1.41) .. 2003.59 (1.00 (. Kawaguchi et al.11) 2..450) .00 (. 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. IARC and NTP have not rated octylphenol.. Sweeney et al.43) 1.199-.62 (1.14) 314 713 1487 03-04 03-04 * * . or their corresponding ethoxylates with respect to human carcinogenicity.71) 2. at lower or environmentally relevant doses (Blake et al.280-.560) .43-3.260 (<LOD-. 4-tert-Octylphenol is not considered directly genotoxic.570) .03 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.36-3.269 (.03-6. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U..S. representative subsample of NHANES 2003-2004.78) 3.300 (<LOD-.770 (.68) 2.15) 1.25) 90th 1.910 (. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.11) 1.349) * < LOD .54) * 03-04 03-04 03-04 .270 (.20 (1.276 (.530) .02-4.370 (<LOD-.50 (2.860 (.00) 1.450) 1.730-1.435 (.17 (. Survey Geometric mean (95% conf.380 (<LOD-.22) .890-2.00) 2. Tyl et al.85 (1.Environmental Phenols Myllymaki et al.470) 75th . 2001).33 (2. 2004.62 (1. Calafat et al.59) 1.850 (.60 (1. nonylphenol.740 (.31-2.500-1.76 (2.620-1.620) . 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.270-.337-.207-. 2000.1. 1999).40-4.610) .31 (1.67-2.470-1.65-3.40 (1.05-2.78 (1.11-2.460 (.740 (.18-4.73) 2.96-4.00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th . Biomonitoring 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.25-2. 2001.3.400) . Fourth National Report on Human Exposure to Environmental Chemicals 35 .630-1. It is unclear if estrogenic or other effects occur in animals through oral dosing. population from the National Health and Nutrition Examination Survey.33) 3.43) 1.270 (.64 (.170-.470-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-2.68-2. Urinary 4-tert-Octylphenol (4-[1. 2004).62) .08) 1.320 (<LOD-.640-1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.00) 2.160-.384) * .81 (1.420) . Yoshida et al. In a small number of adult Japanese volunteers..25) 2.

1995. Sweeney T. Raychoudhury SS. Boockfor FR. prolactin. nonylphenol. Saito Y. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Toxicol Appl Pharmacol 2005. Arch Toxicol 1996.799(1):119-125.Environmental Phenols References Bian Q.44(8):1355-1361. Watanabe G. Taya K.121(1):21-33. Wong LY. Xu L. alkylphenols. Horie M. Katsuda S. Paranko J.54(1):154-167. Sakui N. Chen J. Food Chem Toxicol 2006. Toxicol Sci 2000.folliclestimulating hormone.uk/resource/reports/ethoxylates_alkylphenols. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Anal Chim Acta 486:41-50. Inoue K. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Ito R. Haavisto TE. Nakagomi M. Nagao T.165(3):217-226. Toxicol Lett 2001. Brooks AN.foe. Two-generation reproduction study with para-tert-octylphenol in rats. Okada F. Warhurst AM.116(1):39-44. Blake CA. Carey SA.71(1-2):112-122. Cooper RL. and other organic wastewater contaminants in U. Ferrell JM.28(3):215-226. Toxicokinetics of p-tert-octylphenol in male Wistar rats.14(5):325-332. Yoshimura S. bisphenol A and methoxychlor in rats. Muller AM. Thurman EM. Inoue K. and testosterone. Furlong ET. Wang X. and other endocrine-disrupting compounds in indoor air and dust. 36 Fourth National Report on Human Exposure to Environmental Chemicals . pesticides. Barber LB. Spengler JD. McCoy GL. Watanabe G. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Indoor Air 2004. Karjalainen M.30(2 Pt 1):81-95.37(20):4543-53. Song L. Available at URL: http:// www. Certa H. Kookana R. Qian J. Endocrinology 2000. polybrominated diphenyl ethers. Ono H. Tyl RW. Phthalates. 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. Toppari J. Toxicol Appl Pharmacol 2000. Brine DR. Rudel RA. Yoshida M. Katsuda S. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Maekawa A. Seely JC. Zaugg SD. Korn LR. and sertoli cell number. Reidy JA. Yoshimura Y. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004.co. 1999-2000: a national reconnaissance. Maekawa A. hormones. Millette CF. Laws SC. Nicol L. Estrogenic activity of octylphenol. Kolpin DW. Camann DE. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. streams. Regul Toxicol Pharmacol 1999. Bolt HM. An environmental assessment of alkylphenol ethoxylates and alkylphenols. et al.S. Fedtke N.18(1):43-51. Indoor air pollution by alkylphenols in Tokyo. Takenaka A.207(1):59-68. Kawaguchi M. et al. Meyer MT. Environ Sci Technol 2003. Reprod Toxicol 2004. Yoshida M. Needham LL. Exposure of the U. testis size. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry.141(7):2667-2673. 2/4/09 Ying GG. Environ Health Perspect 2008.15(6):683-692. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Bodman GJ. Seto H. Blake CA. Brody JG. Williams B.57(2):255-266. Izumi S. et al. Reprod Toxicol 2001. Taya K. Makino T. Saito I. Nair-Menon JU. et al. Marr MC. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Environ Sci Technol 2002. 2003. Myers CB. Takai N. Roche JF. Fail PA. Myllymaki SA. Calafat AM. Kawaguchi M. Biol Reprod 1997.pdf. Pharmaceuticals. Environ Int 2002. Boockfor FR. Usumi K. Ye X. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Wiegand HJ.36(6):1202-1211. Onuki A.S.

. representative subsample of NHANES 2003-2004. and wound disinfection solutions. 2007). There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. 1987). mouthwashes. Mezcua et al. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect.2 µg/L was comparable to the median level (8.6% of 139 U. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. 2008 has shown higher levels during the third decade of life and among people with the highest household income. Triclosan has been added to soaps. It can be photochemically and biologically degraded. In 1999-2000. Fourth National Report on Human Exposure to Environmental Chemicals 37 .. Triclosan enters the aquatic environment mainly through residential wastewaters. it has low acute toxicity... 2007. streams sampled in 30 states (Kolpin et al.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. the median urinary triclosan level of 7. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. General population exposure results from dermal and oral use of products containing triclosan..S. young girls. Biomonitoring Information Urinary triclosan levels reflect recent exposure. (Sandborgh-Englund et al. 2007). Some reports show endocrine effects are observed in amphibians and fish (Foran et al. 1996. Triclosan can be absorbed across skin into the blood stream.. 1988. 2008). 2007.Environmental Phenols Triclosan CAS No. toys. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al. 2000....S. 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. It acts by inhibiting bacterial fatty acid synthesis. acne medications. and has also been impregnated into some kitchen utensils. Lyman and Furia. but not by race/ethnicity and sex. Triclosan has a low bioaccumulation potential in fish. Triclosan is not considered teratogenic at maternally toxic doses. In the body it is conjugated to glucuronides and sulfates (Bodey et al.8-dichlorodibenzo-p-dioxin (Aranami et al.. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and medical devices. toothpastes. IARC and NTP do not have ratings with respect to human carcinogenicity. triclosan was found in 57. deodorants. In animal studies. Veldhoen et al. Matsumura et al. 1976. In animal and human studies.... Moss et al. Triclosan formulations may rarely cause skin irritation. 2002). Calafat et al... 2000). 2005. In a U. Calafat et al. 2006). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. 1969). 2004). a process that can result in the formation of small amounts of 2. In a study of 90 U.

S.10) 84.2 (37.1) 13.4) 73.6 (9.S.6) 12.3.2 (10.7 (11.4 (12. Urinary Triclosan (2.0 (36.5) 20.3) 10.7 (28. population from the National Health and Nutrition Examination Survey.0 (34.2-58.45-13.2) 9.7 (9. interval) 12.0-73.9 (50.4 (38.29-12.4) 51.82 (8.60 (6.3 (11.8-127) 37.3-67.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.94 (7.4) 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 9.40-17.1-39.4-18.6-14.3-31.6) 10.20 (7.43-13.2 (25.6) 90th 212 (172-241) 03-04 03-04 03-04 9.2-14.1) 9.5) 66.6 (30.3-15.0) 49.2 (13.18 (5.40-11.4 (32.6-65.4 (11.32-14.3 (9.00-8.20-11.4) 75th 43.38-18.1 (8.6-20.50) 10.9) 7.48-10.8) 14.86-12.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.4-19.20 (7.8) 116 (39.4) 25.0) 9.2-58. Survey Geometric mean (95% conf.1) 50.9 (8.3) 47.45 (5.6-37.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8-85.2-46.5-14.93 (7.92-12.48 (8.5-86.4.1) 11.54 (8.00 (4.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.2 (11.4) 7.72-13.8-60.1) 9.89-11.50-10.7 (14.1) 9.6 (10.10-9.7) 292 (151-432) 132 (78.8-63.1 (15.6-15.6-14.7) 123 (36.5) 13.30-14.1 (45.9) 32.7) 10.4) 357 (225-456) 203 (87.6 (12.3 (8.2) 13.9) 75th 47.Environmental Phenols Urinary Triclosan (2.45-10.8) 9. interval) 13.3-35.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.5) 11.90-10. population from the National Health and Nutrition Examination Survey.0 (26.16 (6.20-13.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.6) 31.0-15.1) 9.22-10.74 (5.70-16.0 (11.6-111) 33.4.9 (11.55 (4.0-19.0 (8.5 (11.0-15.60 (8.6) 39.1) 7.20-10.9-236) 193 (90.21 (6. Survey Geometric mean (95% conf.3) 6.1) 14.2 (27. see Data Analysis section) for Survey year 03-04 is 2.8) 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 .3 (26.80 (5.6) 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 9.2) 12.4) 90th 249 (188-304) 03-04 03-04 03-04 8.11-11.7 (39.0) 65.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9 (33.8-112) 30.9-61.8 (21.9) 8.

Needham LL. Fourth National Report on Human Exposure to Environmental Chemicals 39 . et al. Osachoff H. The oral retention and antiplaque efficacy of triclosan in human volunteers. Moss T. and other organic wastewater contaminants in U. Shiratsuchi H..115:116-121.45 Suppl 2:S137-S147. Arch Environ Contam Toxicol 1988.116(3):303-307. et al.36(6):1202-1211. Thurman EM. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Foran CM. Gunderson MP. Gilbert RJ. Bhargava HN. 4. Fernandez-Alba AR. Biol Pharm Bull 2005. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007.80(3):217-227. Evidence of 2. Ishibashi H. Watanabe N. Environ Health Perspect 2007.69(20):1861-1873. Pilot study of urinary biomarkers of phytoestrogens. Nagao Y.67(4):532-537. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Gomez MJ. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. 1999-2000: a national reconnaissance. Larson EL. population: 2003-2004. Benson WH. Calafat AM. Chemosphere 2007. Williams PE. streams. Environ Sci Technol 2002.S. Readman JW.66:1052-1056. Teitelbaum SL. Bennett ER. Wolff MS.7/2. Ye X. Matsumura N. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Toxicology of 2. Levy SB. Aquat Toxicol 2006. et al.17(5):637-644. J Invest Dermatol 1976. Katsura E. Britton JA. Bodey GP. Furia T. 4’-trichloro-2’-hydroxydiphenyl ether. Kanetoshi A.24(3):209-218. Ebersole R.23(5):579-583.28(9):1748-1751. Windham G.50(1-5):153-156. Ekstrand J. and phenols in girls. Wong LY. Leonard PA. Veldhoen N. Okui T. Ogawa H. Barber LB. hormones.Environmental Phenols References Aiello AE. Aguera A. Howes D. Kaneshima H. Meyer MT. phthalates. Clapson DJ. Mezcua M. J Toxicol Environ Health A 2006. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Anal Chim Acta 1004. Photolytic degradation of triclosan in freshwater and seawater. Odham G. Williams FM.4. Pharmacokinetics of triclosan following oral ingestion in humans. Mar Environ Res 2000.38(2):64-71. Pinney SM.38(4):361370. Furlong ET. Aranami K. Hirano M. Ferrer I.83(1):84. Chelimo C. Sandborgh-Englund G. Lyman FL. Skirrow RC.4’-trichloro-2’hydroxydiphenyl ether). Food Chem Toxicol 2000. IMS Ind Med Surg 1969. Percutaneous penetration and dermal metabolism of triclosan (2. Pharmaceuticals. Erratum in: Aquat Toxicol 2007. Br J Clin Pharmacol 1987. Adolfsson-Erici M.524:241-247. Kolpin DW. Reidy JA. Am J Infect Control 1996. Wigmore H. Environ Health Perspect 2008. Hong HC. Triclosan: applications and safety.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Urinary concentrations of triclosan in the U.S. Zaugg SD. Hernando MD. et al.

plants. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene. bactericide..60) 1.90) 1.350 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350 (.350-.350 (.40 (.350-.350-. and possibly of lindane (IPCS.350-. Survey Geometric mean (95% conf.350-.350-.80) .350) < LOD .590-1. other polychlorinated benzenes.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350-.51) 1.350 (. the elimination half-life may be a week or more (Uhl et al.350-.350 (. are eliminated in the urine.58-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.350-.23 (.530) 1.350-.350 (.g.04) 1.350) < LOD < LOD 75th .890 (.350) 90th . To-Figueras et al.680-1. 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.350) < LOD .33-2.73 (1.48-2..510-5.630 (.350 (.65 (.00 (.10 (<LOD-1. PCP is absorbed rapidly and well by all exposure routes.01 (<LOD-1. has been restricted.18 (<LOD-1.350 (.350-. herbicide.350 (.64) 1. so it is relatively non-persistent.350-.350-.78) 1. PCP use in the U. Acute.350-.350-2.S.30) 1.37) .350) . Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.75) 2.91 (1. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350-.94 (1. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.350-2.500-2.350) < LOD .45-2.37 (. and metabolic acidosis were observed in CAS No. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.42) 696 680 521 696 603 951 Limit of detection (LOD. PCP cannot be used on wood in residential or agricultural buildings. Effects including hyperthermia.70) 2.350) < LOD .350 (. utility poles and fence posts). population from the National Health and Nutrition Examination Survey. 1979). water and sediments because of the large amounts that were produced and used historically.350) < LOD .350-2.60) 1. air. and animals.83 (2. < LOD means less than the limit of detection.00) 1.650) 1.350) < LOD .350 (.50) 1.990 (<LOD-2.5. mollusicide.350-2.76) 1.770 (. 1997).350) < LOD .990-2.08-3.350) < LOD .53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .58-2.30 (1.980 (.350-. 1976.00) 1.09) .350-.650 (. 40 Fourth National Report on Human Exposure to Environmental Chemicals .S.67) 1.350-.30) . After a single dose.350) < LOD .350 (. and dermal contact with PCP-treated products.54-2.65 (.350) < LOD .350 (.76) .30) 1.350 (.350) < LOD .90) 2.350-.53) size 1994 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .98 (1.47-5.350 (. 2002..350 (. hypertension.00) 2.350 (. After absorption.25 and 0.960) 1..350-1.10) 1.390 (. The parent compound and conjugates.10 (.350) < LOD .350-1.350-. PCP has been detected in soils. with repeated or chronic exposure.350-1.350) < LOD . and it is used primarily as a preservative for wood to be used outdoors (e. ingestion of contaminated food or water.48 (.90 (1.350-.480-2.350 (.94 (1.350-.350) < LOD . General population exposure to PCP may occur by inhalation of contaminated air.350-2.10) 1.32 (.850-2.350-1.890-1.62 (.390 (. Since 1984. Kohli et al.70) .860-2. PCP is distributed to most tissues and is not extensively metabolized.660 (.47-3.350) < LOD . 1986).30 (. Human exposure to PCP has become less common.350 (.350) < LOD . along with small amounts of tetrachlorohydroquinone and conjugates.33) .30 (.350 (. PCP is eliminated over a few days (Braun et al. algaecide and insecticide..10 (1.350 (.510-3. PCP is degraded by sunlight and metabolized rapidly by microorganisms. In the environment.

67 (1..40) 1.35-2. In NHANES 2001-2002 subsamples.11) 2.800) < LOD 1.700-2.e.250 (.25 (1.40) 1.06 (.06) 1. environmental levels) and health effects is available from the U.710-1.30-2. EPA has developed standards for PCP in drinking water and the environment.900-1.67 (1.19) 2. Pentachlorophenol is not mutagenic or teratogenic.57 (1.560) < LOD .35) 1.320) < LOD .52 (<LOD-1. Fourth National Report on Human Exposure to Environmental Chemicals 41 .99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * ..Fungicides adults and children severely exposed to PCP through ingestion.290-. 1995).92) 1.26 (1.330-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67 (1.30) 1.25 (1.18 (1.75) 1.84) 1..6 and 14.990 (.19) 2.epa.78) 1. 1989)... interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.83 (1.52 (<LOD-1.75 (<LOD-2.55) 1.420) < LOD .78) 1.09 (<LOD-2.gov/ toxpro2.910-1.73 (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.36) .500-1.310-.67-3.90) 1.270-.800-1.. More information about external exposure (i.25-2.780) < LOD .67-3.25-2.340-.79) 1.94-3.350) < LOD . In animals.500 (. 2003).08 and 5.21-2.850 (.40) 1. Survey Geometric mean (95% conf.82 (1.950-1.650) 90th 1.280) < LOD .08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. The U.67-2. EPA at: http://www. 2003).57 (. 1991).650 (.400 (.84-4. 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.510-. Death can result from seizures and cardiovascular collapse.260 (.16-1.950-1.29-3.370 (.51) 1.630 (.S. population from the National Health and Nutrition Examination Survey.440 (.290) < LOD .69 (1.56) 1. chronically administered high doses of PCP were hepatotoxic.40) 1.250 (.25-1.30) 1.320) < LOD . inhalation.470 (.830) < LOD .300 (.00) 1.35-2.16 (.760 (.19 (1.300 (. respectively) (Becker et al.00-1.580-.35) 1.430) < LOD .34 (.10-2.13 (.84 (1.270-.320) < LOD < LOD 75th . children in the 1980’s. 2004. van Raaij et al.380-.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .94 (1.52) 1.300 (.590-1. or skin absorption. 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.52 (1.cdc.510-. In a small sample of U.360-. respectively) (Seifert et al.95) 3.0 mg/L.S. IARC has determined that pentachlorophenol is possibly carcinogenic to humans. Among adults in the NHANES 1999-2000 subsample.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .590) < LOD .290-.220-.40-2.67 (1.570 (.650 (.82) 1.06-3.. 1989).360 (. and the FDA has established a standard for bottled water.94 (1.gov/ pesticides/ and from ATSDR at: http://www.560-.500-.EPA.310) < LOD ..780-1.490) < LOD .atsdr.26 (1.920 (.S.S.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 .560) < LOD . the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.S. carcinogenic.30 (.18) .21 (.10 (1. the 95th percentile of urinary PCP levels was about fiftyfold higher than that for 6-11 year olds in NHANES 2001-2002 (Hill et al. OSHA has established an occupational standard. 2000).220-. Biomonitoring Information In NHANES 1999-2000 the median urinary PCP levels among children aged 6-11 and 12-19 years were as much as thirteen times lower compared to a sample of German children aged 6-14 years in 1990-1992 (4.320 (.430-. 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.19) 2.610 (. and adversely affected thyroid function (U.25) 1.67 (1.950-1.240-.09-1.9 mg/L.48-2.730) < LOD .40) 1.html.00-1.

Needham LL. Pharmacokinetics of pentachlorophenol in man.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect.S. Seiwert M. Engel R. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Arch Environ Contam Toxicol 1989. Gregg M. Environ Health Perspect 1997. PCP: Human Risk Characterization [online]. et al.4:289296.inchem. 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. Toxicology 1991: 67(1):107-16. J Expo Anal Environ Epidemiol 2000. To-Figueras J. Schulz C. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Jones D. Rodamilans M. Dev Toxicol Environ Sci 1979. Fast DM. available at URL: http://www. Bailey SL.18:475-481. Pesticide residues in urine of adults living in the United States: reference range concentrations. urine. Phillips DL. Sala M. Smith SJ. To T. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Krause C. References Becker K. EPA). International Programme on Chemical Safety (IPCS). Shealy DB.S. 2002. Helm D. Barrot C.71:99108. Cline RE. Seiwert M. Needham LL. Available at URL: h t t p : / / w w w. Arch Environ Contam Toxicol 1989. Santiago-Silva M. Seifert B. Environ Res 1995. Environmental Protection Agency (U. Chenoweth MB. Schlatter C. Int J Hyg Environ Health 2003.105(1):78-83. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Braun WH. Hill RH Jr.18(4):469-474. hair. house dust. The metabolism of higher chlorinated benzene isomers. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. 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. Bragt PC. Becker K. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Schulz C. et al. U. drinking water and indoor air. Blau GE. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.10:552-65. htm. Hill RH. Baker S. Holler JS. 4/21/09 Kohli J. Hill RH Jr. Lindane. Safe A. Uhl S. 42 Fourth National Report on Human Exposure to Environmental Chemicals .54(3):203-208. van den Berg KJ. Seifert B. Can J Biochem 1976. Notten WR. 4/21/09 van Raaij JA. 11/30/2004. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.org/documents/jmpr/jmpmono/2002pr08. Otero R. Head SL. r e g u l a t i o n s . Kaus S.58:182-186. Schmid P. 206:15-24. et al. Arch Toxicol 1986.

364-.20 (1.17 (.508 (. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.490 (<LOD-. < LOD means less than the limit of detection.20-3. 2006). sodium ortho-phenylphenate (SOPP).690-1. it was used in home sanitizers for surfaces.00 (1.61) 2.770 (.30) < LOD .696) * .14 (<LOD-3. such as fruits and vegetables.470 (<LOD-.370-. or apply these chemicals may be more highly exposed than the general population. 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.890 (.90) .28 (.830 (.950) < LOD .760-2.40-7.490 (<LOD-.600) < LOD .402-.27 (.590-2.50-3. fungicides.34) 1. 1989).00 (1.624) * .10) 1.10-2.30) < LOD 1.10 (1.490 (<LOD-.90) 2.00) < LOD .88) 1. however.600-1.40 (.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .00) .740 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 1. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.600-1. and sanitizers.433-.600) < LOD .600) < LOD 75th .60 (1.780) < LOD .10-1..638) * . 2006).600) < LOD 1.80-3.3 and 0.10) .389-.836) * .970 (.500-2. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.22) 2.930 (..860) * 99-00 01-02 99-00 01-02 99-00 01-02 . interval) . In the past. Both chemicals degrade within hours to weeks in the environment (U.370-.22 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Survey Geometric mean (95% conf.20) < LOD 2.390-. Estimated human intakes have been below recommended intake limits (U.567 (.S. on ornamental plants and turfs.30-7.S.850 (. which may vary for some chemicals by year and by individual sample.840-1.890) 1.580-1.23) 695 680 520 695 603 953 Limit of detection (LOD. 2006).50) < LOD .670) 2.560-8.60 (1.50 (1.600-1. OPP is still used as a disinfectant fungicide for industrial applications.621) * . Cnubben et al.50) .880-2.520 (.03) 1. SOPP is applied topically to the crop and then rinsed off.28-3.550-1.20) 2.420 (<LOD-.20-2.466 (.349-.640) < LOD . EPA. Workers who manufacture.410-.76) 1. 90-43-7 General Information Ortho-phenylphenol (OPP.50) < LOD .EPA.40-5.00 (1.570 (.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .30) < LOD 90th 1.386-.85) 2. OPP is volatile.540-2.630) < LOD .493 (. in paints.490 (<LOD-. 2002.50-2.80 (2.20 (1. 1998.50 (1.90 (1. General population exposure can occur via dermal. OPP is considered to be moderately toxic after acute oral doses in animal studies.07 (.497 (.800-3.33 (. formulate.480-1.570 (.50 (1. Most agricultural food applications have been revoked.60-2.498 (.Fungicides ortho-Phenylphenol CAS No.710-2.770 (.50-4. 1998).636) * ..S.750-2.09) 2.645) * .790) 2.350-1.389-.00) .60-3.10) 1.40-5.30 (1.90 (1.552 (.610 (. but OPP and SOPP are still used on pears and citrus (U.610-1. are antimicrobial agents used as bacteriostats. Fourth National Report on Human Exposure to Environmental Chemicals 43 .450 (<LOD-. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.90) 1. inhalational.450 (<LOD-.3.820 (.496 (.50) < LOD . Timchalk et al.570-2.450 (<LOD-. population from the National Health and Nutrition Examination Survey.40-2.30) 1.00-2.90) .92 (. Both have been used in agriculture to control fungal and bacterial growth on stored crops.710) 3. Available evidence suggests that OPP does not accumulate in the body.20 (.85) size 1991 2529 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .570-1.60 (1.690) < LOD .490 (<LOD-. and as a wood preservative.02) 1. 2006).10) 2.EPA.S.570-.860 (. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.10 (1.10) . or 2-phenylphenol) and its water-soluble salt. whereas SOPP is not volatile and is more water soluble.20) < LOD 1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.10) .30-2.370-.00 (1.50) 1.509 (. and it has limited water solubility. leaving the chemical residue OPP.19 (.890 (.742) * .80) 1.

88-4.28 (2.410 (<LOD-.320 (<LOD-.EPA 2006).30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 . Detectable levels were seen in over half the U.00 (1.58) 2.46) < LOD 1.770-2.84 (1. Ito et al.09-6.940-2. 44 Fourth National Report on Human Exposure to Environmental Chemicals .52 (.301-.670) < LOD .06-4..11) 4.29) 1. or developmental toxicity was observed (Bomhard et al.910-1.91 (1.S.gov/pesticides/.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.910 (.560) < LOD 75th . Survey Geometric mean (95% conf.09-3.550 (.860 (. OPP was not found to be mutagenic.78 (2. Pathak and Roy.53) 1.33) 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 . 1999.93) . Additional information is available from U. 1986).. 1992. Murata et al.880-1.81) 1.59) . OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated. CDC.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.59) 1.75 (1.610) < LOD 1.32) 3. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect..353-.69 (1. but no neurologic.06 (1.750 (.510-. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.453 (.810) < LOD . 1993. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.550-.800-1. Zhao et al.40-13.690 (.08-1.EPA 2006). 2005).382 (. 1997.51-3.580) < LOD .900-1. Bomhard et al. 1999. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.61 (2.07) 2.990) < LOD .Fungicides anemia.93) 1.96 (1.420 (<LOD-..38) 2.361-. Kwok et al.480-.08) 1.950) < LOD .04-4.62) .20) < LOD 3.385 (.600-1.670 (. 2002.89 (1.17 (.25-6.44 (1.21) 1.96-4. 2000. or.S.514 (.780-14.750 (.17) 2.455-.33) .61 (1.96) 1.470) < LOD .970) 1.21 (.550) < LOD .403-.750-2.96 (1.08-2.93 (1..640-1.568) * .00 (.09 (1.02 (.380 (. Nakagawa et al. Brusick.4) 3.12) < LOD 1.620-1.840 (.EPA at: http:// www.248-.791) * .590) * . 1998.270-.01) 1.. interval) .38-3.24-2.670 (.26) 1.329-.291-.473) * .21-2.780 (.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.06-5. 1984.11) < LOD 90th 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.510 (<LOD-.620-1.93) .560-2. 2002).580-1.S.440 (.900) < LOD . 1984.11 (.311-. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.11-1.27) < LOD .31) < LOD .. U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.47) . U.343 (. Volunteers exposed to 0.97 (2.epa. 2002.86 (1.860 (.75 (1. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. less likely.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .410 (<LOD-. leading to production of two metabolites.32) 1.650-1..38) 1.64 (2.74 (1.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .18) 2.13) 1. In high dose animal studies. 2005.17 (.470 (<LOD-.43) 3.29) 1.28 (<LOD-4.S.980 (<LOD-1.500) < LOD .43 (1.420 (<LOD-.61 (. population from the National Health and Nutrition Examination Survey.S.24-2.12-2.508) * .33-2..496 (. reproductive.. and it has classified OPP as not classifiable with respect to human carcinogenicity. Biomonitoring Information Urinary OPP levels reflect recent exposure.570) < LOD 1.11 (.43-2.444 (.05-2. 2005). Smith et al. IARC has classified SOPP as a possible human carcinogen.0) 1.656) * .360 (<LOD-.43-2.980 (. by possible genotoxic mechanisms (Hagiwara et al.666) * .460-.810-1.484) * . 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.910 (<LOD-1.

Vogel JS. Toxicol Appl Pharmacol 1998. Bromig KH. EPA 739 R-06004. Ito N. Food Chem Toxicol 1984. Imaida K. Bormett GA. Moldeus P.EPA). Environ Mol Mutagen 2005. Murata M.nih. Leser KH. Roberts AL.22(10):809-814. Roy D. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Elliott GR. Bartels MJ. Bartels MJ. Fourth National Report on Human Exposure to Environmental Chemicals 45 .20(5):851-857. Toxicol Appl Pharmacol 1999. EPA). Third National Report on Human Exposure to Environmental Chemicals. Drugs. Moriya K. Fukushima S.35(2 Pt 1):198-208.S. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Narang A. Crit Rev Toxicol 2002. Available at URL: http://ntp. Office of Toxic Substances. van de Sandt JJ. March 1986. National Toxicology Program (NTP). J Agric Food Chem 2002. McNett DA. Hum Exp Toxicol 1998. Hirose M. 90-43-7) in Swiss CD-1 mice (dermal studies).(56):399-407. Christenson WR. Regul Toxicol Pharmacol 2002.pdf. Brusick D. Bartels MJ. 1989. Mutat Res 1993. et al. Cnubben NH. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol.S.45(5):460-481. Inoue S. Timchalk C. et al. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Hagiwara A. Centers for Disease Control and Prevention (CDC). Fukushima S. Pathak DN. Buchholz BA. Meuling WJ.Fungicides References Appel KE. Environmental Protection Agency (U. Nakagawa Y. Timchalk C. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Kawanishi S.S. Biochem Pharmacol 1992. Arch Toxicol 2000.pdf.17(8):411-417. Available at URL: http://www. Brzak KA.niehs. U. Brendler-Schwaab SY.. Atlanta (GA). Mendrala AL. Eadon G. U. St John MK.32(6):551-625. 2005. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol.S. Moore GA.150(2):402-413. 4/13/09 Onstot JD.gov/ntp/htdocs/LT_ rpts/tr301.epa. Gierthy J. Carcinogenesis 1999. Eastmond DA. Christenson WR. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Herbold BA. Freyberger A.703(12):97-104. The carcinogenicity of the biocide ortho-phenylphenol.gov/oppsrrd1/REDs/ phenylphenol_red. Zhao S. Richter M. 4/9/09. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Hagiwara A. Kwok ES. Bartels MJ. Hakkert BC.74(2):61-71.28(6):579594. Arnold LL. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Comparative metabolism of orthophenylphenol in mouse. Cano M. Selim S. Environmental Protection Agency (U. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Smith RA. Sangha G. Stanley JS. Shirai T.286(2):309-319. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Bomhard EM. Ito N.159(1):18-24. Sangha GK.43(7):14311437. Identification of SARA compounds in adipose tissue. Tayama S. rat and man. Shibata M. Xenobiotica 1998. IARC Sci Publ 1984.54(16):5731-5735. July 28. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Coelhan M. 2006. J Chromatogr B Biomed Sci Appl 1997. Glas K.50(11):3351-3358. EPA-560/5-89-003. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. J Agric Food Chem 2006. Turteltaub KW.

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

Urinary acetochlor mercapturate levels of 0. Jefferies et al.epa.gov/ pesticides/..S. EPA at: http://www. in some species and at doses above maximum tolerated doses.. 2005. 2006). Acetochlor has low acute toxicity.EPA. environmental levels) is available from U. a major pathway for acetochlor metabolism involves mercapturate conjugation. Hladik et al. U. and neurologic movement abnormalities (U. 1998). 1996). 2000. but other pathways occur. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2006). Plants can degrade acetochlor to 2-ethyl-6-methylaniline. Feng and Wratten. Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect. nasal epithelia. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. People exposed to acetochlor will excrete acetochlor mercapturate in their urine. mainly corn. and thyroid (U.S. 2-hydroxyethyl-6-methylaniline. however. including one that produces 2-methyl-6ethylaniline and its reactive metabolite.EPA 2000. NTP and IARC do not have ratings regarding human carcinogenicity. General population exposure to acetochlor may occur through diet or drinking water.e. 34256-82-1 General Information Acetochlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural crop land. 1989. However. Acetochlor is moderately toxic to fish and honey bees. and has been detected in watersheds of agricultural lands (Battaglin et al.S..EPA considers acetochlor likely to be carcinogenic in humans.EPA. 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. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies. 2007).Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure..5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al. the latter which may account for some observed effects (Coleman et al. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid. Fourth National Report on Human Exposure to Environmental Chemicals 47 . 1994. 2005). 2005)..0 μg/L (Curwin et al.. which are often more prevalent in the environment..S. In animals. and hydroxymethyl ethyl aniline (U.S.. this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. Acetochlor is microbiologically degraded. renal injury. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8. 2000. Additional information about external exposure (i. Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. CAS No.. Acetochlor is not mutagenic. but it has produced testicular atrophy. 2000. Estimated human intakes of acetochlor have been below recommended limits (U. Davison et al. animals have demonstrated tumors of the lung. Kolpin et al. 2006). 2000).. and it is unlikely to be genotoxic at relevant doses (Ashby et al. It is absorbed by plants and inhibits plant protein synthesis.S.EPA. remains in soils for up to 3 months. 2006).

see Data Analysis section) for Survey year 01-02 is 0. 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. 48 Fourth National Report on Human Exposure to Environmental Chemicals . 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.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. which may vary for some chemicals by year and by individual sample. < 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 2501 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 576 820 1105 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1178 1323 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 678 673 952 Limit of detection (LOD.S. Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1.S. population from the National Health and Nutrition Examination Survey.

Acetochlor (Harness) Pesticide Petition Filing 1/00. Casida JE.pdf. March 2006. Wilson AG. Hein MJ. Sci Total Environ 2000. imidazolinone. J Expo Anal Environ Epidemiol 2005. Hodgson E.S. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Green T. Kolpin DW. Barr JR.S. Deddens JA.html. J Agri Food Chem 1989. sulfonamide. Linhart SM. 2000. EPA). J Expo Sci Environ Epidemiol 2007.248(2-3):115-122. Environ Health Perspect 2000. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Linderman R. Olsson AO.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Occurrence of sulfonylurea.cornell. EPA 738-R-00-009.S. Davison KL. Camann DE. Andrews HF. and other herbicides in rivers.17(6):559-566. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. 5/30/06 U. Feil VJ. Environmental Protection Agency (U.cce. 5/30/06.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. EPA). Chem Res Toxicol 1998. Hladik ML.111(5):749-756.15(6):500-508. acetochlor. Third National Report on Human Exposure to Environmental Chemicals.39(17):6561-6574. pages 3682-3690. Furlong ET. Battaglin WA.24(10):1003-1012. Wratten SJ. Heederik D. Coleman S. Centers for Disease Control and Prevention (CDC). Barr DB. Rose RL. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Kier L. Curwin BD. Sci Total Environ 2000. Xenobiotica 1994. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Jefferies PR. U. Larsen GL. et al. Striley CA. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.S. Federal Register: January 24. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Environmental Protection Agency (U. epa. Dialkylquinonimines validated as in vivo metabolites of alachlor.Herbicides References Ashby J. Feng PCC. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Hum Exp Toxicol 1996. et al. Sanderson WT. Bravo R. Alavanja MC. Number 15. Roberts AL. Ward EM. Hsiao JJ. Thurman EM. et al. Tinwell H. Barr DB. 2005.S. Environ Health Perspect 2003. Hines CJ. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Whyatt RM. Comparative metabolism and elimination of acetanilide compounds by rat. Environ Sci Technol 2005.108(12):1151-1157. Burkhardt MR. Lefevre PA. Available at URL: http://www. Quistad GB. Peter CJ. Reynolds SJ.11(4):353359. reservoirs and ground water in the Midwestern United States. 1998.EPA): http://pmep. Available at URL(non U.37(4):10881093. Kinney PL. Atlanta (GA).248(2-3):123-133. Volume 65. Barr DB. and metolachlor herbicides in rats. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry.15(9):702-735.

U. 1995. 1999. 2000. the latter may account for some observed effects (Davison et al.S. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Jefferies et al. 15972-60-8 General Information Alachlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural cropland. Biomonitoring 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.EPA. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. In animals. 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. 2003). mercapturate conjugates were predominant metabolites. 1996. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. 1997. Hines et al. IPCS. formulators. 1998.EPA.. WHO. but not likely at low doses.1 mg/L at various collection times (Sanderson et al.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. Alachlor and its degradates are leachable from agricultural soils and have been detected in watersheds of agricultural land including ground and surface waters (Battaglin et al. ranged from 0. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. 1995). 2003). WHO. 2005). hemosiderosis. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. 2003). EPA at: http://www.gov/pesticides/.S. In a study of applicators and workers exposed to alachlor... 1988. stomach. Alachlor has a soil half-life of a few weeks.S.. Hladik et al. Alachlor has low potential for acute toxicity.EPA considers alachlor to be a probable human carcinogen at high doses.EPA. USGS.6-diethylaniline and its reactive metabolite. U. 1999 and 2007. 50 Fourth National Report on Human Exposure to Environmental Chemicals .epa.Herbicides Alachlor CAS No. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. soybeans. peanuts and other crops. 1998. about 20-25% of the U.. In 1993-1995. but shows little bioaccumulation. 2005. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. whereas 60% of applicators had detectable amounts. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. and field workers. 1998.1 to 1. NTP and IARC do not have ratings regarding human carcinogenicity.S. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. 1998).S. 2003). mean values of urinary concentrations of alachlor metabolites.. and uveal degeneration. In animal studies. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. 1998). Estimated human intakes have been below recommended limits (U. 1994. General population exposure to alachlor may occur through consumption of contaminated food or drinking water.EPA. but has not shown developmental or reproductive toxicity in mammalian systems (U. but another metabolic pathway can produce 2. (2003) showed that 2. Because it can be absorbed through skin.EPA. 2000. Hill et al. It is absorbed by plants and inhibits plant protein synthesis. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. the dermal exposure route is potentially significant for applicators. as measured through conversion to deethylamine. Tessier and Clark. U. 1989. Kolpin et al. Feng and Wratten. corn cropland was treated with alachlor.S. including corn.S. Since the late 1980s alachlor use has been declining. Alachlor itself is not considered mutagenic. In chronic animal testing.S. 1996). WHO.. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates.. and on non-crop land for general weed control. Additional information about is available from U. alachlor has demonstrated hepatotoxicity. 1998).. WHO.

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

S. Xenobiotica 1994. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Hum Exp Toxicol. 2003. 2/27/09 U. Sci Total Environ 2000. Roberts AL.S. WHO/ FAO Data Sheets on Pesticides. Centers for Disease Control and Prevention (CDC). Peter CJ. Biagini RE. MacKenzie B.43(9):2504-2512.usgs. 2007. Bull Environ Contam Toxicol 1996. Available at URL: http://www. Hines CJ. Feil VJ.47(6):503-517. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Heydens WF. Dialkylquinonimines validated as in vivo metabolites of alachlor. Geological Survey (USGS). Sacramento. J Ag Food Chem 1995. U. et al.gov/oppsrrd1/ REDs/0063. 2/27/09 Jefferies PR. Wratten SJ. Occurrence of sulfonylurea.S. EPA). Erratum in: Life Sci 1989. Casida JE. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.56(6):853-859. Brown MA. Wilson AG. Geological Survey (USGS).395(2-3):159-171. Quistad GB. 86.11(4):353359. World Health Organization (WHO). Barr JR. Hladik ML.org/documents/pds/pds/pest86_e. Alachlor in Drinking-water. Shealy DB. California.Herbicides References Battaglin WA.111(5):749-756. Supplemental Technical Information (available on-line only). Circular 1291. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. 1992-2001. Life Sci 1988.37(4):10881093. Available at URL: http:// www. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.44(18):1325. Mutat Res.epa. 1999. and metolachlor herbicides in rats. Furlong ET. Thake DC. No. 1998. Environ Sci Technol 2005. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Striley CA. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Kolpin DW. Barr DB. Brown KK. Whyatt RM. Am Ind Hyg Assoc J 1995. December 1998. Ann Occup Hyg 2003. 98-4245 (by Barbash JE.S. Hines CJ. Sci Total Environ 2000. Comparative metabolism and elimination of acetanilide compounds by rat. Biagini R. acetochlor. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Thurman EM. Hill AB. Reregistration Eligibility Decision (RED) Alachlor. Kier LD.248(2-3):123-133. 4/2/09 U.htm. and other herbicides in rivers. Hsiao JJ. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.pdf. reservoirs and ground water in the Midwestern United States. Andrews HF.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Linhart SM. revised February 15. Geneva. Kolpin DW.24(10):1003-1012. 1996. Kimmel EC. Tessier DM.56(9):883-889.248(2-3):115-122. Larsen GL. Clark JM. Burkhardt MR. 2005. Available at URL: http://water. Martens MA. Available at URL: http://www. Deddens JA. Sanderson WT. Lau H. Casida JE. sulfonamide. World Health Organization.43(25):2087-94. Kinney PL. EPA 738R-98-020. ALACHLOR. Davison KL. Environmental Protection Agency (U. 1999. Hull RD.pdf. Casida JE. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). Feng PCC. Tolos W. March 2006. Shoemaker DA. Quistad GB. Jefferies PR.int/water_sanitation_health/dwq/chemicals/en/alachlor. 1997. J Agri Food Chem 1989. Hill RH Jr.inchem.18(6):363-391. DNA adduct formation by alachlor metabolites.php. et al. Camann DE. Henningsen G. who. International Programme on Chemical Safety (IPCS). Thelin GP. Background document for development of WHO Guidelines for Drinking-water Quality. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Environ Health Perspect 2003. Gilliom RJ). Chem Res Toxicol 1998. Driskell WJ. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. imidazolinone.39(17):6561-6574.

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

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

Wetzel LT. Gammon DW. Toxicol Sci 2000.. Goldman JM. 1996. Stuart AA.atsdr. Schmid J.15(6):500-508. Ferrell JM. In small studies of Maryland residents in 19951996 (MacIntosh et al... Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 .. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. In a small number of field workers.115(8):1254-1260.58(2):366-376. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Environ Health Perspect 2001. Laws SC. Hein MJ. Toxicol Sci 2003. Wetzel LT. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides.53(2):297-307. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Stoker TE. Extrom PC.30(2):244-247. Shoemaker DA. 2001 [online].inchem. 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. Toxicol Sci 2000. Saiz SG. Lucas AD. Tapia J. et al. Noriega N.. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Eldridge JC. Lioy PJ. Perry et al. Cooper RL. Atlanta (GA). Hermaphroditic. et al. Maroni M. Hines CJ. References Adgate JL. Deddens JA. Breckenridge CB. WHO/ FAO Data Sheets on Pesticides. 2003. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. 1993). Ferrell JM. Mendoza M. et al. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Freeman NC. Cooper RL. Biagini RE. Stevens JT. Simpkins JW.61(4):331-355. Proc Natl Acad Sci USA 2002. In a study of 60 farm worker children. J Expo Anal Environ Epidemiol 2005.. Biological monitoring of human exposure to atrazine. Bersani M. Bradway DE. Geneva. Pfeifer KF. Stoker TE.99(8):5476-5480. et al.109(6):583-590.gov/toxprofiles/tp153. Pest Manag Sci 2005. 2005). Goodrow MH. Heederik D. Toxicological profile for atrazine. Striley CA. Barr DB. atrazine was detected in only four children (Arcury et al. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Grzywacz JG. Reynolds SJ.47(6):503-517. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. 2005. 82.76(1):190-200. Curwin BD. Stoker TE. Toxicol Lett 1993. Barbieri F. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure.64(9):672-678. Third National Report on Human Exposure to Environmental Chemicals. Collins A. Fleenor-Heyser DG. Steroids 1999. Jones AD. Barr DB. ATRAZINE. Sanborn JR. Environ Health Perspect 2007. 2000). Eberly LE.cdc. A risk assessment of atrazine use in California: human health and ecological aspects. Sanderson WT. Tyrey L. Brown KK. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http:// www. Ann Occup Hyg 2003.html. Eldridge JC. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Seiber JN. Available at URL: http://www. Cooper RL. Centers for Disease Control and Prevention (CDC). World Health Organization. Clayton CA. et al. The geometric mean of urinary atrazine mercapturate was 1. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. 2005). diamino-S-chlorotriazine and hydroxyatrazine. J Toxicol Environ Health 1994. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Gillis JH. 3/11/09 Arcury TA.43(2):155-167. Blewett C. Agency for Toxic Substances and Disease Registry (ATSDR). Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Aldous CN. McElroy WK. J Toxicol Environ Health 1994. Ferioli A. Catenacci G.org/documents/pds/pds/pest82_e. 2001). Gillis JH. 3/11/09 Laws SC. J Agric Food Chem 1982.69(2):217-222. et al. In the NHANES 2001-2002 subsample. International Programme on Chemical Safety (IPCS). Hayes TB. Moseman RF.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Carr WC Jr.htm. Cottica D. 2007)..43(2):155-167. Barr DB. Quandt SA. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Vonk A. Lee M. No. levels of atrazine mercapturate were generally not detectable (CDC. Chen H. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.

3/11/09 U. Hammerstrom KA.S.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Laws SC. Christiani D. Osborne DW. The Quality of Our Nation’s Waters. Crit Rev Toxicol 1997. 1992-2001.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. A longitudinal investigation of selected pesticide metabolites in urine.pdf. EPA Office of Pesticide Programs. Environmental Protection Agency (U. Breckenridge CB. Chem Res Toxicol 1993.195(1):23-34. J Toxicol Environ Health A 1999.S. Interim Reregistration Eligibility Decision For Atrazine. Sanderson JT. Toxicol Sci 2002. Fenton SE. Cooper RL. J Expo Anal Environ Epidemiol 1999. Stoker TE. Guidici DL. Available at URL: http://www. Circular 1291.epa. Available at URL: http://water.S. Urinary biomarkers of atrazine exposure among farm pesticide applicators. 2003b. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Pesticides in the Nation’s Streams and Ground Water. Wood C.10(7):479. Lansbergen GW. A review of epidemiologic studies of triazine herbicides and cancer. Wetzel L.67(2):198-206. Kastl PE.php.9(5):494-501. Case No. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Tortorelli J. Washington (DC). 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats.S. U. Available at URL: http://www. Guidici DL. Perry M. Toxicol Appl Pharmacol 2002. Ann Epidemiol 2000. Toxicol Sci 2000.27(6):599612.gov/oppsrrd1/REDs/ atrazine_ired. Supplemental Technical Information (available on-line only). Environmental Protection Agency (U. Office of Prevention. May 2003a. Timchalk C. Needham LL. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat.S. Toxicology 1990. van den Berg M.56(2):69-109. Langvardt PW. Dagenhart D. Stoker TE. A risk characterization for atrazine: oncogenicity profile.usgs. Singzoni B. Geological Survey (USGS). March 2006.Herbicides development of a biomarker of exposure. Cooper RL.pdf. revised February 15. Pesticides and Toxic Substances. Environmental Fate and Effects Division. EPA). Sathiakumar N. EPA). Stevens JT. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. 6/1/09 U. Dryzga MD. White paper on potential developmental effects of atrazine on amphibians.58(1):50-59. Toxicol Appl Pharmacol 2004. 2007. Laws SC.61(1):27-40.6(1):107-116. Delzell E.182(1):44-54. Ryan PB. Boerma J. Rayner JL. 0062.epa. MacIntosh DL.

490) < LOD < LOD < LOD .49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . and aquatic environments. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.250 (<LOD-. General population exposure to 2.370-.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al. As much as 62 million pounds of 2.10 (<LOD-1. by direct contact with agricultural and residential areas after applications. headache.230-.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .80) 1.4-D) controls broadleaf weeds in residential. 1974. agricultural. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.S. < LOD means less than the limit of detection.4-D is rapidly absorbed via oral and inhalation routes..310 (..400) < LOD . in 2001 (U.560-1.66) < LOD 1. hypotension.4-D has low acute toxicity.20 (<LOD-1.410) < LOD .10) < LOD 1. MCPA. It is rarely detected in ground waters (USGS. myotonia.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.210 (<LOD-.330 (.S.43) 1. it acts as a plant growth hormone. which may vary for some chemicals by year and by individual sample. renal and hepatic injury.740 (.21) 1.930 (.13) < LOD .560-.910) < LOD . 2.4-D may occur during residential applications. 1977).27 (.. Similar to other chlorophenoxy herbicides.690 (.48) < LOD 1.610 (.890) < LOD .00-2. these herbicides can enhance plant growth. population from the National Health and Nutrition Examination Survey.690 (. Survey Geometric mean (95% conf.30 (<LOD-2.40) 1.4-Dichlorophenoxyacetic Acid CAS No.02-1.730 (.960-1.EPA.760 (. and delayed Urinary 2.550-1.Herbicides 2.4-D have been below recommended intake limits (U.EPA in 1948.22) < LOD .2. 2.952 and 0. 2. with a half-life of several days to several weeks. 1989.03) 695 659 520 668 589 892 Limit of detection (LOD.250 (<LOD-.810-1. Fourth National Report on Human Exposure to Environmental Chemicals 57 .4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.210-. Kohli et al.27 (1. 4-D.10 (<LOD-1.910) 1.690-1.310) < LOD .230 (<LOD-.420-. 94-75-7 General Information Widely used throughout the United States.S.37) size 1977 2413 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD .890 (. 2004).4-D were used in the U.420) < LOD . Human health effects from 2.70) 1. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.690 (. 2007).24 (. It was first registered with U. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.930-1.08) < LOD .07 (.350) < LOD < LOD < LOD .16) < LOD . 2005).51 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and by consuming food or drinking water contaminated with 2.60) 1.4-dichlorophenoxyacetic acid (2.05-2.610-.20 (.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and mecoprop). Once absorbed.670-1. It is poorly bound in soils. Recent estimates of chronic intakes of 2.4-D can be applied either as an aqueous salt or as oil-soluble esters.680-1. 2.S. the chlorophenoxy herbicide 2. It is not well absorbed through the skin.S. dizziness. At low levels. Sauerhoff et al.55 (1.540-. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.EPA.660) 1.490 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.320) 90th . but at higher levels they are herbicidal. abdominal pain.260 (<LOD-.32 (1.27-2.440-1. nausea.4-D or exposed for prolonged periods.

thyroid.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . 1996.S.13 (.EPA at: http://www. 2005)..890) < LOD 1.560-.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.610-. 2005.920) < LOD 1. 2005.Herbicides neuropathy (Bradberry et al.epa. 1985. Hill et al.850) < LOD . 1980.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. myotonia..14 (. 1994).780) .16) 1.580-. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.820-1.05) . Biomonitoring Information Urinary levels of 2.930-1.340 (. IPCS. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.410) 90th .410) < LOD < LOD < LOD ..17 (. 1995). and evidence of histological injury to the kidneys.660) < LOD . In previous samples of the U.720 (.670 (. eyes. 1989). population from the National Health and Nutrition Examination Survey..440 (. 2001. Epidemiological studies have reported associations of several types of cancer. other exposures. developmental.S. 58 Fourth National Report on Human Exposure to Environmental Chemicals . Average post-application urinary levels of 2.680) < LOD . 2005). IOM. 2005. The acid and salt forms of 2.S. Pearce and McLean.EPA.08 (. Kolmodin-Hedman and Erne.480 (. adrenals and gonads (NTP. 1996.670 (. 2002.4-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 .EPA 2005). 2005).780-1.520-. Survey Geometric mean (95% conf.19) . 1992).S. population (Hill et al. U. liver. Additional information is available from U. Acute high doses administered to laboratory animals produced ataxia.640 (.670 (<LOD-1.410 (<LOD-.380 (<LOD-.470) < LOD . 2.. Post-application levels in farmers and home gardeners were dependent on Urinary 2.790) < LOD ..26) size 1977 2412 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD . 2004).32 (<LOD-2.810-1.08 (.7. or teratogenic effects in chronic rodent studies (Charles et al...390) < LOD < LOD < LOD .610-. It is unclear whether these associations are related to the chlorophenoxy herbicides.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.890-1. and of adults and children (Baker et al.4-D levels were detectable in less than a quarter of the individuals studied. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.340-.990-1. 2.560-.270-. urinary 2.4-D are eye irritants.590 (<LOD-1.35) < LOD . 2002.620-.S.41 (1.08 (. Frank et al.56) .gov/pesticides/.790) 1.660 (.24) 1. Kutz et al.. CDC. U. 2000).380) < LOD .380-. or to contaminants in the herbicide formulations (specifically 2.380 (<LOD-.350 (<LOD-. 2005).810-1. IPCS.490 (.4-D production plant workers and a few forestry workers spraying 2.S.EPA.330-.73) .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. 2003. U.S.270 (<LOD-. 2006.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. 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. 1996.570) < LOD ..3.27-1.39) < LOD 1.780 (. 2005. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.550-.590 (<LOD-1.410) < LOD 1.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. 1995. Knopp et al. IPCS. U.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. in small samples of children (Hill et al.EPA.4-D reflect recent exposure. 2.740 (.980) < LOD 1.13 (.700 (.

Head SL. Updated March 7. van Ravenzwaay B.4-dichlorophenoxyacetic acid and its forms. Atlanta (GA). Washington (DC): National Academies Press. Acquavella JF. Third National Report on Human Exposure to Environmental Chemicals. J Expo Anal Environ Epidemiol 2005 Nov. Beeson MD. Solomon KR. Centers for Disease Control and Prevention (CDC). Hanley TR Jr. Mandel et al. Assessment of exposure to 2.10(6 Pt 2):789-798.4-Dichlorophenoxyacetic Acid).4-D): exposure and urinary excretion.4-D will result in an adverse health effect. Kohli JD.S. 2. 2003. 3/17/09 Institute of Medicine (IOM). Ritter L.4. Reynolds SJ. Bus JS. In farm families. Mandel JS. Xenobiotica 1974.71(2):99-108. Gregg M.inchem. Pesticide residues in urine of adults living in the United States: reference range concentrations. Gupta BN. Philbert MA. Barr DB.4-D. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.4-D). Shealy DB.37(2):277-291. Occup Environ Med 1994. 2005.4:318-321. Fast DM. Cook BT.4-dichlorophenoxyacetic acid in man. Environ Res 1995. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Arch Environ Contam Toxicol 1989. Estimation of occupational exposure to phenoxy acids (2. National Toxicology Program (NTP). and the use of protective clothing or equipment (Arbuckle et al. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Biomonitoring studies of 2. Finding a measurable amount of 2. 2005). Stephenson GR.4-D were highest in the farmers who applied the 2.4:427-435.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.32(4):233-257. general population.4-D and 2.nap. Arch Environ Contam Toxicol 1985. 2005. References Arbuckle TE. J Toxicol Environ Health 1992.Herbicides the time since application. Carter-Pokras OD. Harris SA.31 Suppl 1:90-97. Bailey SL. Kutz FW.htm. To T. the number of acres to which it was applied (Curwin et al. J Environ Sci Health B 1992. Available at URL: http:// www. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. TOX-63 Peroxisone Project (2. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Frank R. et al.18(4):469-474. Arch Toxicol Suppl 1980. Hill RH Jr. Barr DB. Alexander BH. Beasley VR. 2006. Honeycutt R. Scand J Work Environ Health 2005. Needham LL. Erne K. Dichlorophenoxyacetic acid.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Dhar MM.4-D) epidemiology and toxicology.nih.27(1):23-38. the amount of pesticide applied. Harris et al. Survival and Growth Curves from NTP Toxicity Studies. 2005). Baker S.4-D in urine does not mean that the level of the 2.4-dichlorophenoxyacetic acid (2.gov/index.31(2):121-125. Toxicol Sci 2001.. Selected pesticide residues and metabolites in urine from a survey of the U. et al. Driskell WJ..4-dichlorophenoxyacetic acid (2. Biomonitoring of herbicides in Ontario farm applicators. Pesticides residues in food: 1996 evaluations Part II Toxicology.4 dichlorophenoxyacetic acid (2. 3/17/09 Knopp D. Sircar KP.niehs. Brody D. Vet Hum Toxicol 1989.org/documents/jmpr/jmpmono/v96pr04. Tandon JS. Curwin BD. Smith SJ.15(6):500-508. TOX-63: TOXICITY REPORT CURVES.4:97-100. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Scand J Work Environ Health 2005. Sanderson WT. Baker BA. Ripley BD. Sirons G J.php?record_id=10603. Needham LL. Baker SE. Garabrant DH. Campbell RA. Hill RH Jr. Kolmodin-Hedman B. Developmental toxicity studies in rats and rabbits on 2. et al. Biomonitoring for farm families in the farm family exposure study. 2005 Charles JM. Cole DC.51(3):152-159. Review of 2. Arnold EK.4-D than levels found in the general population.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. Available at URL: http:// www. Hein MJ. Tables. Wilson RD. Crit Rev Toxicol 2002. Available at URL: http://ntp. Murphy RS. 1992). Khanna RN. J Expo Anal Environ Epidemiol 2000. Chapman P. geometric mean urinary levels of 2.5-T). International Programme on Chemical Safety-INCHEM (IPCS).31 Suppl 1:98-104. Holler JS. Board on Health Promotion and Disease Prevention.. 914.60(1):121-131. Absorption and excretion of 2. Exposure of homeowners and bystanders to 2. Forestry workers involved in aerial application of 2.edu/catalog. Heederik D. Veterans and Agent Orange: update 2002. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.4-.

Circular 1291.2000 and 2001 market estimates. revised February 15. March 2006.S. Geological Survey (USGS).htm.8:3-1U. 60 Fourth National Report on Human Exposure to Environmental Chemicals .pdf. Gehring PJ.S. Pesticides in the Nation’s Streams and Ground Water. 2.4-D RED Facts.epa. 2004. Pesticide industry sales and usage . Available at URL: http://water.S. Available at URL: http://www.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. S. 4/2/09 U. The fate of 2.Herbicides Sauerhoff MW. June 2005. Environmental Protection Agency (U.EPA). The Quality of Our Nation’s Waters. EPA 738 F-05-002.php.gov/oppsrrd1/ REDs/factsheets/24d_fs.usgs. 1992-2001. Blau GE.EPA). 3/17/09 U. May. Toxicology 1977.S. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Supplemental Technical Information (available on-line only). Environmental Protection Agency (U. Braun WH. 2007.4-D) following oral administration to man.S. Office of Prevention Pesticides and Toxic Substances. 3/17/09.4-dichlorophenoxyacetic acid (2. Available at URL: http://www.epa. Washington (DC): U.EPA.

and field workers may have significant exposures via this route. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al.S. Estimated human intakes have been below recommended limits (U. Davison et al. 2005). EPA at: http://www. whereas 60% of applicators had detectable amounts. Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Salivation. It is absorbed by plants and inhibits plant protein synthesis.S. 2005). 2003). Fourth National Report on Human Exposure to Environmental Chemicals 61 .. though the 95th percentile for males was 0. Biomonitoring Information CAS No..Herbicides Metolachlor available from U. Jefferies et al.. Occasionally in the past. and convulsions were observed at lethal doses in animal studies. People exposed to metolachlor will excrete metolachlor mercapturate in their urine. 2003). WHO. and it was not mutagenic in mammalian cells (U.S. lacrimation. Feng and Wratten. Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. 1998). metolachlor levels in water have exceeded lifetime human health advisory levels (U. Hines et al. USGS.EPA. In animals. metolachlor was quickly absorbed after dermal or oral doses.S. 2000.S. 2000. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment. U..S. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine. 2003). 1995. 51218-45-2 General Information Metolachlor is a chloroacetanilide type herbicide that is applied for preemergent control of grasses and broadleaf weeds on agricultural crop land. 1994. WHO. formulators. Kolpin et al. Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect..gov/pesticides/. NTP and IARC do not have ratings regarding human carcinogenicity.. (2003) showed that 2. Metolachlor has low potential for acute toxicity (U. mercapturate conjugates were the predominant metabolites. sorghum and other crops. Gilliom. 1989. EPA.EPA considers metolachlor to be a possible human carcinogen. 2007. 1995). 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. Metolachlor did not show developmental or reproductive toxicity in chronic animal studies. and eliminated in urine and feces over two to three days (WHO. Metolachlor is well absorbed dermally.epa.. Hladik et al. 1995).200 μg/L (CDC. 1999. including corn. 1995). but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. in both ground and surface waters (Battaglin et al.EPA. 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. The geometric mean metolachlor mercapturate was 4. 2005. 2007. In animal studies. and on non-crop land for general weed control. General population exposure may occur through the consumption of contaminated food or drinking water. so applicators. soybeans.EPA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 831 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.440 (<LOD-.2.S.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S. Survey Geometric mean (95% conf. 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.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 62 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.240) 679 701 957 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.670 (<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 . < LOD means less than the limit of detection.

Striley CA.ESTfeature_gilliom. Feng PCC. 3/26/09 U. Heederik D. Burkhardt MR. 1998. Feil VJ. Available at URL: http://water.15(6):500-508. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Metolachlor in Drinkingwater. Ann Occup Hyg 2003.S.108(12):1151-1157.gov/nawqa/pnsp/pubs/files/051507. Hein MJ. imidazolinone. Hladik ML. Larsen GL. 1992-2001.pdf. acetochlor. Supplemental Technical Information (available on-line only).37(4):10881093. Camann DE. Roberts AL. Sci Total Environ 2000. Circular 1291. Hsiao JJ. Background document for development of WHO Guidelines for Drinking-water Quality. Hodgson E. Thelin GP. Centers for Disease Control and Prevention (CDC). et al.who. Rose RL. J Expo Anal Environ Epidemiol 2005. EPA). Sacramento. Kolpin DW. Ward EM. Alavanja MC.24(10):1003-1012.S. 4/2/09 U. Chem Res Toxicol 1998. Sci Total Environ 2000. Kolpin DW.gov/nawqa/ pnsp/pubs/wrir984245/text. Barr JR. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.pdf 3/30/09 Hines CJ. World Health Organization (WHO). Available at URL: http://www.11(4):353359. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. sulfonamide. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Furlong ET. Deddens JA. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.S. Atlanta (GA). Thurman EM. et al. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Reynolds SJ. March 2006. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 .usgs.php.Herbicides References Battaglin WA. Gilliom RJ).39(17):6561-6574. R. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. J Agri Food Chem 1989. 2005. Pesticides in U.pdf. Environ Sci Technol 2007. Environmental Protection Agency (U.int/water_sanitation_health/dwq/chemicals/ metolachlor.gov/oppsrrd1/ REDs/0001. Geological Survey (USGS). Reregistration Eligibility Decision (RED) Metolachlor. U. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Barr DB. Available at URL: http://water. Brown KK. Environ Health Perspect 2003. reservoirs and ground water in the Midwestern United States. Coleman S. streams and groundwater.248(2-3):123-133.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. 2003. Linhart SM. usgs. Comparative metabolism and elimination of acetanilide compounds by rat. Gillion. Sanderson WT.111(5):749-756.html. Environ Health Perspect 2000. Xenobiotica 1994.S. Shoemaker DA. 2007. Peter CJ. Jefferies PR.S. Curwin BD. Occurrence of sulfonylurea. 6/1/09 Whyatt RM. Environ Sci Technol 2005. 1999. Linderman R. Wratten SJ. EPA 738R-95-006. 98-4245 (by Barbash JE. California. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Kinney PL. and other herbicides in rivers. Biagini RE.248(2-3):115-122. Geological Survey (USGS). Barr DB. April 1995. revised February 15. and metolachlor herbicides in rats.epa. Third National Report on Human Exposure to Environmental Chemicals. Dialkylquinonimines validated as in vivo metabolites of alachlor. Andrews HF. Casida JE.usgs.47(6):503-517.41:3409-3414. Available at URL: http://www. Available at URL: http://water. Davison KL. Quistad GB.

Ester forms of 2..4.4. but higher levels are herbicidal. 1989.4. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. Once absorbed into the body. and concern about contamination with 2.4. Epidemiological studies have reported associations of several types of cancer.5-T degrades to 2. hypotension.5T is rapidly absorbed via oral and inhalation routes. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-T (Holson et al.1.5-T in soil varies with conditions. Human health effects from 2.4.4.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2..g. and delayed neuropathy (Bradberry et al.4. < LOD means less than the limit of detection. 2. Kohli et al.5-trichlorophenol and other degradates. Agent Orange).4. 2.5-T is eliminated mostly unchanged in the urine. myotonia. 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. Chlorophenoxy herbicides act as plant growth hormones. which may vary for some chemicals by year and by individual sample. dizziness.5-T use as a herbicide in 1985.3. 1992. Mohammad and St. 2.5-Trichlorophenoxyacetic Acid CAS No. Omer.4-D were used as defoliants in the Vietnam War (e. abdominal pain. Given the commercial unavailability of 2. nausea. 1992).5-T. population from the National Health and Nutrition Examination Survey. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.2 and 0. Nelson et al.5-T was once applied as either an aqueous salt or as an oil-soluble ester..4. The half-life of 2.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2..4.. 93-76-5 General Information 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. ranging from several weeks to many months.Herbicides 2. renal and hepatic injury.4. 1986. the general population is unlikely to be exposed to it.5-T and 2..4.4.S.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 64 Fourth National Report on Human Exposure to Environmental Chemicals . it is not well absorbed through the skin.4. At low levels.4. headache. Although 2. 2004). Survey Geometric mean (95% conf.4. 2. with an elimination half-life of approximately 19 hours (Arnold et al. these herbicides can enhance plant growth.7.5-T has been rarely detected in ground waters (USGS. 1974).5-Trichlorophenoxyacetic acid (2.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2007).

7.Herbicides or contaminated herbicides. 2. Finding a measurable amount of 2.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2.5-T does not mean that the level will result in an adverse health effect.4. It is unclear whether these associations are related to the chlorophenoxy herbicides.4.S.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2005). Biomonitoring Information Urinary levels of 2.5-T also were below the limit of detection (Kutz et al. in which urinary levels of 2.4. Biomonitoring studies on 2.EPA at: http://www. 2003.4.5-T than levels found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.5-T itself is not mutagenic.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. 2005. urinary levels of 2. similar to results of NHANES II (19761980).gov/pesticides/.4. Urinary 2. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. U. or to contaminants in the herbicide formulations (specifically 2.EPA. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.epa.3. Additional information is available from U. 1980).S. IPCS. other exposures. Fourth National Report on Human Exposure to Environmental Chemicals 65 . 2002.4. Mean urinary levels of 2.5-T were generally below the limit of detection. Survey Geometric mean (95% conf.4. 1992).5-T reflect recent exposure. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.S. IOM.4.. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. Pearce and McLean. 2004). 1996.

et al. Board on Health Promotion and Disease Prevention.pdf. Fundam Appl Toxicol 1992. Toxicol Rev 2004.19(2):298-306.4. Vet Hum Toxicol 1989.inchem.htm. Khanna RN. Selected pesticide residues and metabolites in urine from a survey of the U.4-dichlorophenoxyacetic acid (2.31 Suppl 1:1825.org/documents/jmpr/jmpmono/v96pr04.5-trichlorophenoxyacetic acid (2.Herbicides References Arnold EK. Poisoning due to chlorophenoxy herbicides. Available at URL: http://www. Gaines TB.37(2):277-91.epa.4. 2. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Absorption and excretion of 2. discussion 5-7.23(2):65-73. et al. Dhar MM. Holson JF. Available at URL: http:// www.4-D/2. Nelson CJ.4. Garabrant DH. Holson JF. Veterans and Agent Orange: update 2002. Crit Rev Toxicol 2002. 2004. 2003. McCallum WF. Kutz FW. Arch Int Pharmacodyn Ther 1974. Sheehan DM.2000 and 2001 market estimates.8(5):551-60. Dichlorophenoxyacetic acid.EPA).S. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Behavioral and developmental effects in rats following in utero exposure to 2. Scand J Work Environ Health 2005. Estimation of occupational exposure to phenoxy acids (2.5-T). 210:250-255.S. Developmental toxicity of 2. 914.5-trichlorophenoxy acetic acid in man. Washington (DC): National Academies Press. Neurobehav Toxicol Teratol 1986. Brody D. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Nelson CJ. Mohammad FK.4-.4. I.19(2):286-297. Vale JA.5-trichlorophenoxyacetic acid (2. Philbert MA. Atlanta (GA). general population. Centers for Disease Control and Prevention (CDC). Murphy RS.S. Fundam Appl Toxicol 1992.4:318-21.32(4):233-257. Tandon JS. Multireplicated dose-response studies with technical and analytical grades of 2. McLean D. 2005. Gupta BN. Arch Toxicol Suppl 1980.4-D) epidemiology and toxicology.5-T). 3/17/09 Kohli JD.edu/catalog.4.5-T in four-way outcross mice. Sircar KP. Gaylor DW. Kolmodin-Hedman B. S. gov/oppbead1/pestsales/01pestsales/market_estimates2001.5-T).nap.php?record_id=10603. International Programme on Chemical Safety-INCHEM (IPCS). May. Gaines TB. Review of 2.5-t mixture. Developmental toxicity of 2. Proudfoot AT. Office of Prevention Pesticides and Toxic Substances. 3/17/09 Institute of Medicine (IOM). St Omer VE. Environmental Protection Agency (U. Cook BT.4. Carter-Pokras OD.4. Agricultural exposures and non-Hodgkin’s lymphoma. Beasley VR. Pesticides residues in food: 1996 evaluations Part II Toxicology. Wolff GL. Washington (DC): U. Available at URL: http:// www. U. LaBorde JB.EPA. Pesticide industry sales and usage . 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .4. Bradberry SM. Third National Report on Human Exposure to Environmental Chemicals. II.4-D and 2. LaBorde JB.31(2):121-125. Pearce N. J Toxicol Environ Health 1992. Erne K.

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

Carbamate Insecticides

Carbofuran

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 827 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1340

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

* * * * * *

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

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

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

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

696 680 521 696 603 953

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

68

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 826 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1339

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

* * * * * *

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

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

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

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

696 680 521 695 603 953

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

Fourth National Report on Human Exposure to Environmental Chemicals

69

Carbamate Insecticides

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

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Carbamate Insecticides

Propoxur

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

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

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Carbamate Insecticides

Urinary 2-Isopropoxyphenol
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2503

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 820 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1325

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

* * * * * *

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

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

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

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

664 677 500 696 585 931

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

Urinary 2-Isopropoxyphenol (creatinine corrected)
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2502

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 819 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1324

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

* * * * * *

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

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

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

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

664 677 500 695 585 931

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

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Carbamate Insecticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

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

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

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

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

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

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

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

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

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

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Organochlorine Pesticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Aldrin

CAS No. 309-00-02

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

Dieldrin

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

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 2275 1946

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

years 01-02 03-04

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

756 588 1519 1358

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

1057 946 1218 1000

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

* * * * * *

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

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

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

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

559 456 512 485 1045 881

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

Fourth National Report on Human Exposure to Environmental Chemicals

77

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

7) 15.100-.6 (15.160) .112-.054-.9 (12.0) 21.077 (.073-.139 (.190) .0 (15.5 and 7.6) 9.9 (13.2) 15.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.8-25.075) < LOD .8 (11.083-.059 (.098 (.2) 14.40-9.058) < LOD .00 (8.110) .30 (8.080-.0 (10.170) .8-24.S.070-.70 (7.80-10.117) < LOD .130) .1-16.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.4) 539 456 484 487 980 885 Limits of detection (LOD.3 (19.180) .090-.130) .138) .120-.2) 11.080 (.2-15.053 (<LOD-.160 (.9-22.120) .1) 14.242) .110 (.8 (9.6 (14.102 (.070 (<LOD-.120 (.147 (.4) 20.149) .110) .1-24.049-.80-9.5 (<LOD-11.120 (.1) 20.060) .3 (18.113 (.9 (13.109-.50) 15.1 (13.5) 19. 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 .190) .064 (.4-18.1) 10.109 (.9 (12.8) 15.6) 19.0-25.069) < LOD < LOD .9 (14.124) .130) .3-21.140 (.3 (14.130 (.1-19. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90) 90th 15.130-.8.110-.5-17.070) .8) < LOD 8. which may vary for some chemicals by year and by individual sample.8-17.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.50 (8.1) < LOD 9.5 (16. see Data Analysis section) for survey years 01-02 and 03-04 are 10.7 (15.089 (.116) .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. Survey years 01-02 03-04 Geometric mean (95% conf.096-.054-.112) 95th .177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .1) 13.103 (.064) 90th .4) 21.090 (<LOD-.0-21.101) .077-.80 (<LOD-10.7 (<LOD-15.00-14.048 (<LOD-.100 (.S.080) . 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.150 (.3 (18.086-.103 (.130-.138 (.7 (14.120 (.7-22.6-24. 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 9.110 (.088-.084-.6) 16.0) < LOD 9.5-15.6 (15.40-10.090-.1) 15.8) 14.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .4) 19.090-. < LOD means less than the limit of detection.100-.9-23.150 (.0) 19.5) 15.062-.4) < LOD < LOD 16.110 (.0 (11.056-.4 (12.147) 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 .139 (.8-17.180) .1) 15.062 (.1-18.054-.2) 12.109-.108-.4) 14. Survey years 01-02 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.1 (18.093) .8-19.4 (12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9-38.5-17.140-.062 (.100) .063-.055 (. population from the National Health and Nutrition Examination Survey.6-24.140) .10 (<LOD-16.0 (10.7-19.100-.160 (. Fourth National Report on Human Exposure to Environmental Chemicals 79 .3 (13.4-17.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.8 (18.158) .100) . which may vary for some chemicals by year and by individual sample.090 (.130-.4) 95th 20.30 (8.6-33.5) 21.60-10.

4/21/09 Bates MN. PA. Available at URL: http://www. References Agency for Toxic Substances and Disease Registry (ATSDR). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. either singly or in combination. Cancer Epidemiol Biomarkers Prev 2000. Ellis H. Int Arch Occup Environ Health 1994. Revised Feb.27:405-421. Grandjean P. Hartvig HB. Sanchez-Ramos J. New York. Pesticides in the Nation’s Stream and Ground Water. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Handbook of Pesticide Toxicology.atsdr. Part A 2000. J Occup Environ Med 2005. Psychopharmacology (Berl) 1987.cdc. Inc. Eds. Schulte P. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. 2 Classes of Pesticides. Jr. 15. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Smith AG. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. 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. Mann D.org/documents/ehc/ ehc/ehc91.cfsan. Soto AM. Corrigan FM. Mumtaz MM. Olea N. Daniel SE. 6/1/09 Ward EM. Cox.47:1059-1087. Andersen A. 731-915. Environ Health Perspect 1995.26:701-719. No:429-436. Needham LL. Vol. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Chapin RE. Food and Drug Administration (FDA). Available at URL: http://www. 1989. Facca A. Shore RF. Roy ML. Kanthasamy AG. Patterson DG Jr. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Teta MJ. Anantharam V. Tully DB. J Toxicol Environ Health. Frey JM.usgs. McIntosh LJ. International Programme on Chemical Safety (IPCS).64-65 Spec. Mink PJ. toxicology. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. et al. Song S. VT. Organochlorine insecticides in substantia nigra in Parkinson’s disease.html. Toxicological profile for aldrin/dieldrin [online]. and epidemiology in the United States.9:1357-1367. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Grajewski B. Effect of occupational exposure to aldrin on urinary D-glucaric acid.gov/ circ/2005/1291/.54:1431-1443. In Hayes WJ. Patterson DG Jr. Organochlorine exposure and risk of breast cancer. 1991. Brock JW. J Toxicol Environ Health 1989. 4/21/09 Jorgenson JL.inchem. Reprod Toxicol 2000.gov/~dms/ pesrpts. Demographic and seasonal influences on human serum pesticide residue levels. August 2008. and lymphocyte sister chromatid exchange. pp. United States Geological Survey (USGS).109(Supp1):113-139. Li AA. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Priestly BG. Basit A. plasma dieldrin. Buckland SJ.htm. Turner W.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). et al. 2007 [online]. Chemosphere 2004. September 2002. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Sonnenschein C. Fernandez MG.352:1816-1820. Chung KL. Garrett N. Ginsburg KS.91(1):122-126. 4/21/09 Hoyer AP. Kanthasamy A. Stehr-Green.150:263-271.html. Serrano FO. Jorgensen T. 1992-2001. Toxicol Lett 1992. Available at URL: http://pubs.14:95-102.gov/toxprofiles/ tp1. Available at URL: http://www. 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.103(Suppl 7):113-122. Environmental Health Criteria 91.fda. are nonestrogenic in transfected HeLa cells. Exp Neurol 1998.59:229-234. Aldrin and Dieldrin [online]. Environ Health Perspect 2001. Finley B. Six high-priority organochlorine pesticides. Lancet 1998. Carlson JN.66(4):229-234. Rosellini RA. Neurotoxicol 2005. Narahashi T. Jr and Laws ER. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Kitzazwa M. Wienburg CL. bioaccumulation. David VL. Edwards JW. Academic Press. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Chlorinated Hydrocarbon Insecticides.

6-53.1) 16.0-12. Fourth National Report on Human Exposure to Environmental Chemicals 81 . 2007).5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9-40. 57-74-9 Heptachlor CAS No.5.3) 37.4 (30.5-40. buildings.5) 10.1 (25.7-25.2-49.5 (41.6-18.2) < LOD 11.1-50.4) < LOD 11. and dairy products are the usual sources of exposure to these chemicals in the general population. which may vary for some chemicals by year and by individual sample.0 (20.6 (9. and 7.0) 21.4-45.2 (36.8) 53.9 (11.0) 75th 20.S.5) 38.9-21. and 03-04 are 14. 1994.0-67.6-24.7) 19. 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.6 (16.5-38.2 (41.2 (37.5) < LOD < LOD 9.69-10.2 (28. from the early 1950’s until the mid-1980’s.8-61.8-43.10-18.4-40.1-51.6) 48. Survey Geometric mean (95% conf.7 (42.4-21. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.1 (<LOD-12.2 (39.37 (8. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.8) 52.7 (34.2) 37.9) 37.6 (43.8 (40.2) * 12.1 (<LOD-12.0) 31.0-18.6-45.89-10.9 (18.5) 44.8 (42.6) 11.9) 23.9-42.4 (<LOD-12.3) 18.2 (10.2-26. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.2-56.8-33. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.7 (32.2-28. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20-11.8 (18.9 (11.9 (26.0 (37.2) 36.4 (10.4 (22.3 (28.7 (19.4) 22.3 (27. population from the National Health and Nutrition Examination Survey.3 (11.20-10.0) 41.3) 41.9 (17.3-32.8-73.1) 30.5-47.3 (25.9) 23.8) 44.0) 20. As a result of the manufacturing process.2-49.1-25.0) 27.7) 28.1-65.70 (<LOD-10.7-39.9 (29.6) 48. fish.9) 17.3 (26.5) 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 * * * * 11.5 (33.Organochlorine Pesticides Chlordane CAS No.1) < LOD < LOD < LOD < LOD < LOD 8. 10. respectively.4 (31.5.8-23.1) 30.1) * 11.5-32.5 (34.7) 9.30-11. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues..5) 21.36-11. Chlordane is not currently produced or used in the U.0-25.1 (11.5) 56.6) 39.8 (17.4-14.5-41.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.4) 39.7 (17.6) 8.7 (<LOD-13.7) 31. 2007).20 (<LOD-11.3-45.6) 9.S.3) 10.5-65.7-56.10 (8.63 (8.2) 22.5) 37.8-42.0-61.9 (31.6 (25.6-12.3 (<LOD-19.9) 11.9 (15.6) 9.90 (8.5) 9.6) 36.3 (21.4) 37.5 (31.8-31.9-38. 1994).7 (43.9-21.6-24.9) 47. Until 1988.2) < LOD 11.7 (34.74 (<LOD-10.7-14.0) 37.3) 10.8-20.1 (44.S. see Data Analysis section) for Survey years 99-00.0 (<LOD-12.3 (9.8) 52. 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.4 (30.4) 18.9 (36.9) 39.1) 22.5 (<LOD-12.0 (26.3-43.2-21.6) 49.7-12.9) 10.7 (10.9 (15.3 (20. Technical grade chlordane had contained 7% trans-nonachlor. in addition to trace amounts of numerous other related compounds (ATSDR.8.6) 20.1-19.9) 13.8 (10.3) 18.2) 46.4-51.8-33. heptachlor use has been limited to treatment of fire ants near power transformers.5-42.1 (27.1 (15. the technical grade product of each chemical contains 10%-20% of the other chemical.82-11.5-43.4) < LOD < LOD < LOD 23.8) 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. chlordane was used to kill termites and other insects on agricultural crops.3-45.5-44.7-70.0 (32.0-13.1 (<LOD-12.2 (21.8 (17.2) 33.1) * 11.6) 23.8-32.7) 35.6) < LOD 11.3-49.0-33. foods high in fat such as meat.1-15.0 (16.9 (26. Consequently.1) 90th 34.7) 19.4) 12. and in soil.9 (21.7) 42.8 (10.10-11.9) 36.7 (<LOD-32.2) 34.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.9) 11.5-13.6 (9.1-25. < LOD means less than the limit of detection. lawns.1 (20.2 (9.4) 29.5 (8.4 (35.1 (40. Since 1992.3-24. 01-02.5) < LOD < LOD < LOD < LOD 13.1 (17.1 (16.8) 27.9) 31.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.

071 (.410) . OSHA has established occupational exposure criteria.140 (.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.126 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .130-. 2007).320) . Survey Geometric mean (95% conf.450) . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.280-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.070 (<LOD-.100 (.300 (. 1991).115 (.130-. Le Marchand et al. dermal.340) .047 (<LOD-.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .150-.056 (.180) .240) .280) .055-.170) .S. 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.189 (.286 (.231) .140 (. Shindell and Ulrich..290 (.310) .370 (.230 (.150 (.170) .062) < LOD .230) .350) .210 (.310) .130 (. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.280-.130-. Rogan.091) .170-.290-.080) .230-.148-.300-.510) . 82 Fourth National Report on Human Exposure to Environmental Chemicals .200-.069 (<LOD-.287) .061-.070-.180-.290-.077) .320 (.180) .242-.210-.110-..146) .260-.280 (.253-. neonatal mortality.073) < LOD < LOD < LOD < LOD .112 (. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.053-.063 (.204 (. which may vary for some chemicals by year and by individual sample.170) .207 (. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.S.140-.130) .269 (. Elimination of all these chemicals from the body occurs over months to years.068) . Acute.070 (<LOD-.258-.270 (.070) .070-.115-.130-.223) . 1981).300) . characterized by seizures and paralysis. 2007.190-.320 (.280-.066 (.140-.067 (.300) .310 (.070 (<LOD-. and breast milk is a major excretion route in lactating women.083 (.320 (. population from the National Health and Nutrition Examination Survey.260 (.066-.130) .065-.075 (.104-.092) .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .068) 75th .077) .200-.300) .058-.077) .200-. 1977a.066 (<LOD-.100-. which is also persistent in the body (ATSDR. and heptachlor epoxide in foods and bottled water.260 (.058-.170) .246-.190-.203-.120-. 1986). EPA has established environmental criteria for chlordane and heptachlor. 1986). and inhalation exposure.058 (.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 * * * * .070 (.150) .090) .079) .050 (<LOD-.350 (. IARC.240-.150 (.280 (.302) . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.370 (.430) .076) < LOD .146) < LOD < LOD .440) .148) . Takahashi et al.370 (.126) .090) .074-.290-.210 (.049 (<LOD-.130-.120 (..245-.053-.230-.350 (.150 (.063 (. FDA established allowable residues of chlordane.348) .104) .373) .320 (.106-.063) ..120-.200 (.208 (.100-. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.140 (.199-.119 (.100 (<LOD-.050-.Organochlorine Pesticides (Dallaire et al. 1991.315 (.250 (.110 (<LOD-.180-.080 (.079) < LOD < LOD < LOD .250-.130 (. The major metabolite of heptachlor is heptachlor epoxide.270 (.340) .060 (<LOD-.220-. to heptachlor.136) .216-.087-. heptachlor.057) * . 2001.240 (.225 (.070) < LOD < LOD < LOD < LOD < LOD .220-. and the U.063 (.160) .133) 90th . and alterations in immune function of offspring.077) . 2006).290) .128 (.090-. chronic doses of heptachlor have produced liver enlargement and injury.108-. In laboratory animal studies.070 (<LOD-.400) .258 (. 2002.168-.310) .064) < LOD .270 (.380) .160) .149 (. 1977b.360) .057-. The U.310-. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.286 (.073 (.083) .068-.227) < LOD . Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.400) .430) .450) .207) .082 (.160) .080) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240-.330 (. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.165-.063 (.S. 1996.140 (.190-.160 (.230 (.290) . Smith.271 (.066-.230-.250 (.048-.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .320) .220 (.130 (.189-.260 (.063) * . Chlordane and heptachlor are absorbed after oral.300) .560) .070-.057 (.170) .140) .080) .213) * .080 (.063-.120-.

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

interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.6 (13.2 (18.0 (11.3) 27.5) 19.3-18.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.7 (13.20 (<LOD-9.6 (12.4 (<LOD-54.8) 13.8) 15.1-38.6-17.8-24.8-46.8) 21.3) 23. and 03-04 are 14.5 (<LOD-21.90 (<LOD-9.0-16.6 (16.2 (<LOD-25.8-24.4 (11.2) 26.40) 15.8) 13.3) 18.8) 19.5) 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 7.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1 (16.S.8) 19.50) < LOD < LOD < LOD 17.3) 18.6) 14.6.9 (15.4 (15. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 21. 10.8-23.8 (13.7 (16.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.7 (10.0) 13.8) 14.3) 16.9 (12.7-25.8) 20.0 (15.4) 18.1-15.8-24.7-18.0-19.8.5 (<LOD-32.0) 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) 10.9-16.4 (11.5 (11.4 (<LOD-19.6) < LOD < LOD < LOD 27.3 (13.2) 15.9-25.3 (<LOD-25.9) * * * 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 8.0-54.7-19.1) 23.5) < LOD 14.8) 16. < LOD means less than the limit of detection.9-29.2-27. and 7.3) 22.6) 22.9-23.2 (<LOD-62.8 (18.2-16.1-29.6 (8.2) 13.2) 20.8 (18.6 (11.10-13.5.0-17.5 (11.6) 13.0-17.6-21.1) 20.9-29.6 (<LOD-27.8 (15. population from the National Health and Nutrition Examination Survey.5 (10.1) 13.8 (13.8) 14.5 (18. see Data Analysis section) for Survey years 99-00.3) 18.1 (19. 84 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample.9) 15.2-17.6 (14. 01-02.2-27. respectively.8 (<LOD-23.2 (<LOD-16.6 (16.1-16.

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

1-16.8 (42.9 (19.5 (44.6-88.5 (15.6-54.2-18.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.7-29.5-111) 68.7-32.6 (<LOD-14.8 (26.5-36.0) 75th 31.3) 18.8-67.8) 80.5-17.8 (16.2 (26.8) 47.3 (14.4-62.6-20.3) 16.8 (13.7 (74.6) 82.0 (62.5) 14.3-30.3) 36.5) 90th 55.3 (56.0 (48.9 (15.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.5.1) 32.6) 10.2) 59.2-88.9 (29.3-58. and 7.1 (17.9-69.9-20.8 (28.6) 25. 10.4 (28.3) 18.2) 19.1 (22.1-34.7 (30.7-34.6) 54.4) 55.2 (7.1-55.0 (15.5) 78.7) 35.3 (58.0 (19.3-32.3) 32.2-18.7-160) 86.3-50.4) 59.9) 51.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.9 (15.1-18.8-77.2-17.6-66.8-90.4) 107 (84.9 (28.8 (17.2 (64.0-23.6) 56.5) 14.1) 16.8 (26.9 (47.7) 15.6 (57.1) 17.4-36.7) 78.3) 25.1) 17.0 (16.7 (11.7-17.9-40.86-13.2 (60.0-38.4) 48.8-110) 59.7 (59.3-39.3-57.2 (14. see Data Analysis section) for Survey years 99-00.5) 20.7 (13.4) 16.0-93.9) 14.5-87.0) 13.0-20.7) 78.7) 14.6-22.2) < LOD 10.6 (56.0-24.6) 84.4-18.0) 18.7 (16.9-65.8-16.6-19.9-22.9) 51.5 (25.0) 19.6 (50.1) 17.0-22.1-20.6 (52.9 (51.8-79.0-23.3) 19.7-18.7-77.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.8-19.6 (12.8-129) 74.9 (51.7 (28.7) 28.8-19.7-20.0-37.9 (66.4-67.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.4-35.4 (67.1) 17.70 (<LOD-12.4) 19.3 (45.5) 36.7-21.7-38.9 (<LOD-14. which may vary for some chemicals by year and by individual sample.7-35. population from the National Health and Nutrition Examination Survey.8) 19. respectively.0 (60.1) 18.8) 51.3 (17.2 (14.3 (14.2 (59.9-36.9 (16.8 (<LOD-20.7 (18. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 78.9) < LOD < LOD < LOD 20.3) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.0 (42.2-23.9-45.1-22.2) 30.4) 20.6 (32.0) < LOD < LOD 8.7-22.2-21.3-86.3) 32.1-34. and 03-04 are 14.1 (41.8 (49.3) 30.9-35.1-28.8 (15.3) 15.5) 19. < LOD means less than the limit of detection.S.8 (11.7-113) 68.1-126) 67.0 (42.0-93.5) 26.1) 14.2 (25.9) 14.7) 17.10 (<LOD-11.0-68.9-58.5) 9. 86 Fourth National Report on Human Exposure to Environmental Chemicals .6 (15.2 (36.5-95.5) 48.8 (71.8 (45.3-21.6) 34.3 (16.1-51.6) 13.8 (28.4 (12.5-69.4 (16.2 (19.3 (49.8.1) 62.0 (29.6) 56.2) 34.8 (30.1 (10.7) 73.5) 35.0 (13.5) 30.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.0) 33.2) 39.5 (45.2-37.9 (36.0-59.0 (16.0-113) 68.8 (12.0-143) 112 (68.4 (11.8 (28.2) 20.9-64.2-16.4-23.7 (59.4-22.1) 18.1) 17.7-23.2) 17.8-21.1 (47.3) 30.0) 49. 01-02.3-74.8-41.9-89.6-82.5.5) 22.4 (30.8 (13.1) 31.8-16.2 (27.1) 17.5-19.6 (16.7) 56.8-90.0-123) 74.1-16.8 (26.7 (35.0 (13.0) 40.1) 30.5) 77.5 (13.2 (15.0 (14.5 (15.7) 59.1) 78.1) 17.4 (45.8 (19.6 (56.7) 52.9-65.6) 60.1 (65. interval) 18.5-20.1 (48.4-52.0 (15.

400 (.081 (.100 (.600) .300) .440-.120) .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .600 (.220 (.520 (.090-.141) .210-.099-.120-.371) . which may vary for some chemicals by year and by individual sample.210) .096) .480) .310 (.559) .130) .095-.240) .079-.106 (.960) .104 (.120) .301-.20) . interval) .420 (.470-.234) .270-.290-.409-.360-.400) .190-.288 (.460) .160-.470 (.410-.390-.120-.430-.177-.590) .081-.240) .090 (<LOD-.105 (.840) .690) .116-.125) .S.125 (.150) .112 (.180-.202 (.061-.460-.640 (.120 (.340-.220 (.190-.210-.930) .760 (.090-.310-.055 (<LOD-.160 (.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.112 (.130) .180-.190-.082) .060-.414 (.272-.078 (.510 (. Fourth National Report on Human Exposure to Environmental Chemicals 87 .110 (.096-.122) .089 (.370 (.367) .310-.111-.573 (.114) .397-.680) .091) .220 (.070 (.080-.250) .230 (.130) .540) .430-.310-.103 (.116 (.343 (.071 (<LOD-.186 (.109 (.090-.110) .330 (.220 (.500) .430-.171-.400 (.093-.080) .104-.220 (.317 (.135 (.120 (.127) < LOD < LOD .210 (.220) .405) .680 (.060 (<LOD-.092 (.090 (.520 (.360-.079-.110 (.310) .470 (.130) .180-.420) .260) .240) .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 .080 (.220 (.113) < LOD .113) .286-.191 (.130) .093-.280) .094 (.120-.098 (.098) .590 (.830) .126) .310-.130 (.085-.103 (.080-.220 (.220 (.380 (.120) .690) .100 (.490-.110 (.651) . Survey Geometric mean (95% conf.630) .100-.106 (.108) .119) < LOD < LOD < LOD .350-.093-.161-.131) .510-.054-.410-1.355 (.098-.069) .111 (.080-.205 (.300-.370 (.590 (. population from the National Health and Nutrition Examination Survey.232) .320-.242) .140) .580 (.470 (.400-.210 (.183 (.186-.285-.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.085-.173-.684) .497-.120 (.390) .150) .565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .580 (.085-.450) .141) .350 (.116) .190-.068-.047-.250) .340-.461 (.550 (.327 (.078-.390 (.092 (.120) .190-.580 (.129) .091-.100-.390 (.330-.490 (.630) .128 (.440) .237) .134) .170 (.060) .800) .110 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.158-.390 (.340) .108) 75th .084-.117) .520) .100-.090-.490) .122) .087 (.458 (.062 (.460) .320-.288-.069-.830) .240-.093) .417 (.097) .080-.330-.400-.090) .395) .161) .130) .110 (.109 (.237) .395-.100-.099-.130 (.260) .041 (<LOD-.090-.210) .124) .279-.210 (.110 (.390) .211) 90th .594) .108 (.210) .324 (.240 (.490 (.145-.098 (.250) .106 (.096-.565) .119) Selected percentiles ( 95% confidence interval) Sample 95th .630) .090-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .110-.190-.390 (.470-.130) .

heptachlor. Wohlleb JC. 2 Classes of Pesticides. Environ Health Perspect 2002.259(3):374-377. Dewailly E. International Agency for Research on Cancer (IARC). Distribution of polychlorinated biphenyls. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Environ Health Perspect 2002.inchem.gov/ntp/ htdocs/LT_rpts/tr009. Covaci A. Toxicological profile for heptachlor and heptachlor epoxide [online]. Organochlorine exposures and breast cancer risk in New York City women.org/documents/iarc/ vol79/79-12.110(8):835-838. August 2007. 731-915. Odland JO. Jaraczewska K. Available at URL: http://www. May 1994. Stehr-Green P. 1986. 6/1/09 National Toxicology Program (NTP). 79.110:617-624.atsdr. Poland. Toxicological profile for chlordane [online]. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii.gov/ntp/ htdocs/LT_rpts/tr008. Available at URL: http://www. Kolonel LN. 1991 pp. et al. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Berkowitz GS. Vol. Bleiweiss IJ. J Occup Med 1986. Bull Environ Contam Toxicol 1981:27:506-511.150:981-990. Chlordane and heptachlor [online]. Hansen JC. 1963-1967.org/ documents/cicads/cicads/cicad70. Eds.org/site/foundation/ research/projects2. Chashchin V. 1979-1980. Available at URL: http://ntp.html. Senie R. 9/25/07 International Programme in Chemical Safety (IPCS).gov/toxprofiles/tp31.cdc. 2006.niehs. Saidein D. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Wolff MS. Granath F. Vol. Bjerselius R. Sci Tot Environ 2006.nih. International Agency for Research on Cancer (IARC) .8:1-123. Available at URL: http://www. Concise International Chemical Assessment Document 70 Heptachlor [online]. 6/1/09 Rogan WJ. Wong L.330:55-70. Dendle WH. maternal serum and milk from Wielkopolska region. Glynn AW. Takei G. New York.28:497501. Tartter P. Mortality of workers employed in the manufacture of chlordane: an update. Willman E. Organochloride pesticide residues in human milk in Hawaii. Hawaii Med J 1991. Hertz-Picciotto I. Academic Press. Chlorinated Hydrocarbon Insecticides.html.atsdr. 4/21/09 Dallaire F. Lawrence River (Quebec. A Report to the Hawaii Heptachlor Research and Education Foundation. Lulek J. KalubaSkotarczak A. Voorspoels S. Ayotte P.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Arch Pediatr Adolesc Med 1996. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Available at URL: http://www. Van Oostdam JC.htm.html. Atuma S. 2001.pdf. Head SL.pdf. Pollutants in breast milk. Circumpolar maternal blood contaminant survey. Environ Res 2000. LeMarchand L. Arch Environ Health. Available at URL: http://ntp. Barker J. Royce W. 1993. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Bioassay of chlordane for possible carcinogenicity. 1994-1997 organochlorine compounds.50(3):108-118.inchem. Brower S. et al.84:151-161. Smith AG. Drews K.Summaries & Evaluations. Gilman A. Keller JA. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. 4/21/09 Baker DB. National Toxicology Program (NTP). Handbook of Pesticide Toxicology. Inc. Environ Health Perspect 2003. Jr and Laws ER. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Sci Total Environ 2004. Bioassay of heptachlor for possible carcinogenicity. Shindell S and Ulrich S.111:349355. 4/21/09 James RA.372:20-31. Takahashi W. Loo S. Charles MJ. Darnerud PO.htm. Muckle G. Jr.9:1-109. et al.41:145–148. Baker DB.cdc.niehs.nih. gov/toxprofiles/tp12. In Hayes WJ. Organochlorines in Swedish women: determinants of serum concentrations. Aune M. Canada). Dewailly E. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Siegel BZ. et al. Available at URL: http://www. JAMA 1988. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Laliberte C.

particularly meat.5 (14. DDT is converted to DDE and several other metabolites.6 (31.7) 12.3) 22.2-bis(p-chlorophenyl) ethane (DDD). including 1.8-23. population from the National Health and Nutrition Examination Survey.1 (23.9) 14. 17.0-35.6 (22.8) 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9) 29. and 7.0 (10. Fourth National Report on Human Exposure to Environmental Chemicals 89 .8. particularly for endemic vector and malaria control.70 (8. < LOD means less than the limit of detection.1 (<LOD-39.2) 30. and water. continues to be the primary source of DDT exposure. and trace amounts of several related compounds.9 (<LOD-20. DDT was used at one time as a treatment for head and body lice.7.9) < LOD < LOD 9.6-33.1-71.0 (21.3-236) 24.1’-dichloro-(2.8-17.5) < LOD < LOD 9.9) 17.0 (18.p’-DDT (15%-21%).3) 21. air.0-15. DDT is converted in the environment to other more stable chemical forms.3 (<LOD-31. 1991). In the general U.0-27.8-26. It was produced and used in the U.1) 31.p’-DDT (65%-80%).0 (18. It is still used in some countries.2 (<LOD-40.0-37. DDT and DDE can cross the placenta. 1988).4. although DDT and DDE intakes have decreased over time (FDA.9 (10.9 (10.2) < LOD < LOD 9.5-54. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. In the body.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 12.5) 25. sediments.2) 155 (59.0) 26.3) 21.8-39. Gunderson.9 (10. depending on conditions.4) < LOD 17.1-27.10 (<LOD-12.6 (9.5) 23.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. food.5 (15.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.8) 36. which is a mixture containing p. and dairy products.0) 40.90 (<LOD-12.S. These chemicals are highly persistent in soil.0-53.3-16.9-28. which may vary for some chemicals by year and by individual sample.2-65.8) 15. inhalation. 1991). Both Serum p.7) < LOD 18.6 (25. see Data Analysis section) for Survey years 99-00.5-36. and 03-04 are 20. respectively. 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. o.5 (23. after World War II until 1972. Smith. Survey Geometric mean (95% conf.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 2008.5 (23.0) 20. 2002. Only a small proportion of DDT is metabolized and excreted (Smith.10-13.9 (21. DDT usually refers to the technical product.0-155) 83. The biodegradation half-life of DDT in soil varies from 2 to 15 years. when virtually all use of it was banned. DDT can be absorbed after ingestion.2 (11. or dermal exposure. population.7 (15.S. fish.3-590) 293 (104-541) 48.7) 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 10.4) < LOD < LOD < LOD 61.7 (19. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.1’-(2.7-16.00 (<LOD-10. 01-02.S.1 (33.50-11.8) 30.3 (27. resulting in fetal exposure. p.0) 19.2-95.3) 28.9-34. as well as in plant and animal tissues.3 (<LOD-21.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.6 (<LOD-25.4 (23.p’-DDD (4% or less).2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. Food imported from countries that still use DDT may contain the chemical or its residues.

Animal studies reported reduced fertility.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * . Calle et al. In laboratory animals...01) .200 (. Longnecker et al..180) . overt signs of acute human toxicity include vomiting. population from the National Health and Nutrition Examination Survey.054-.095) < LOD . 1995.203) ..098-. and leukemia have also been inconclusive (ADSDR. dioxins and furans).. 2001).Organochlorine Pesticides chemicals are excreted in breast milk.330-4.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.313 (.120-. Beard.180-.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.084 (. 2006). 2002.S. polychlorinated biphenyls.190 (.150-.112 (.087 (. accidental exposures.170 (.170-. 2002. reproductive organ abnormalities. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. other organochlorines. 2006).146 (. A workplace standard for DDT has been established by Serum p. DDT may bind to estrogen receptors (Chen et al.260) .106) < LOD < LOD .051 (<LOD-. 1996).106) .530) .p’-DDE can produce anti-androgenic effects (Gray et al.160-.140) .170) . Reproductive effects in humans affecting birth weight.189-.190-1. have not been consistently demonstrated (Beard.00) .105-. and duration of lactation.130-. and altered behavior after neonatal exposure (Eriksson and Talts.180) . 2004.108 (. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.130 (<LOD-.068-.g. fertility. 2002. 2001).065-.059-. and o.250-1. 2006).220) . Gray et al.62 (.. which may vary for some chemicals by year and by individual sample. 2006. In high dose. Survey Geometric mean (95% conf.p’-DDD and p.143) < LOD < LOD .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 .290) . Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.114-.048 (<LOD-.097) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .078 (.061) < LOD < LOD < LOD . Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.130 (<LOD-. Jusko et al. 2006. Snedeker.201 (.240) .071-. 90 Fourth National Report on Human Exposure to Environmental Chemicals .250 (. premature delivery.26) 1. Studies of DDT exposure and pancreatic cancer. 2001).086 (. 1956)..079) < LOD < LOD . Hayes et al.071 (..150 (<LOD-.240 (. tremor.150 (<LOD-.146 (.530 (.190 (. Jusko et al.120 (<LOD-.230) .180 (.150) .420) . 1998).069) .220) . 2000. 2001).106-..400 (.343) < LOD .080-. resulting in exposure to nursing infants (Rogan.132-.34) .150-. lung cancer.078-.064 (.074-..180 (. Gladen and Rogan. 2002.107) 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.230) .570-4. Mariussen and Fonnum.140-.00 (..128 (. 2006. and seizures.400) .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 . Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.627) .063 (<LOD-. 1997). 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.075) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .130 (<LOD-.142 (.

Heudorf et al. and 03-04 are 18. compared to levels observed in this Report (Anderson et al... Stehr-Green.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. mean serum levels of DDT and DDE in the U. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. 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. 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. respectively.atsdr.6. 8. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. 2002. 01-02. 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. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.epa. Survey Geometric mean (95% conf.gov/ pestcides/ and from ATSDR at: http://www. Declining DDE levels over time have also been observed in the German population.e.7-119) 113 (100-140) 93.html. Fourth National Report on Human Exposure to Environmental Chemicals 91 . for males and females in the NHANES 19992000 subsample (Pavuk et al.gov/ toxpro2. Since the 1970’s.S. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. 1989). 2004).. 1991). respectively. 2003.6 (81.8... Compared to females in the NHANES 1999-2000 subsample. population declined by about fivefold to tenfold. 2005). and 7. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person.cdc. 2002. Smith. Biomonitoring Information DDE persists in the body longer than DDT.S. In a population-based sample of men and women from eastern Slovakia.3. More information about external exposure (i. 2004). environmental levels) and health effects is available from the U. population from the National Health and Nutrition Examination Survey.p’-DDT) as a possible human carcinogen. 2003). IARC classifies DDT (p.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. see Data Analysis section) for Survey years 99-00. Link et al. 1998.Organochlorine Pesticides OSHA and a guidance established by ACGIH... EPA at: http://www. In general..S.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. NTP considers DDT as being reasonably anticipated to be a human carcinogen.

48 (6.59 (1.81) 11.4 (8.p’-DDT.68) 2.85-10.21) 3.64) 3.25-14.1) 12.13) 4.04-1.90) 22.30-1.25-16.6) 11.07) 1.36-1.27) 3.52 (1.96) 1.385-.12-1.18-3.11-1.41-12.25) 1.52-6.59 (4.600) .5) 7.965-1.14-1.03-4.01-11.30 (1.66) 1.7-20.66-4.6 (9.01-1.2 (9.69 (. population from the National Health and Nutrition Examination Survey.58) 1.6 (7.66) 4.9) 5. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.46-2.6 (17.53) 7.26-2.65) 1.40 (3. serum levels of o.50 (2.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al. 309 versus 268 ng/g lipid.49 (1.27-1.6 (8.01-15.57 (3.51) 1.71) 12.61-2.6) 8.97 (3.76 (2.34) 2.63 (6.46 (1.32 (1.85-4.646) .10) 2.4-19.07 (5.92 (3.1 (9.5) 22.51 (1.00 (.635) 1.p’-DDT (Stehr-Green.31 (1.39-1.57-3.24) 1.796 (.39 (3.36) 3.59 (1.34-3.21) 90th 7.71) 32.75 (4.54) 8.8 (14.64-2.32-9.51-15.04 (6.18) 1.16-1.81 (1.10) .6) 12.49 (1.02-8.6) 13. 2001-2002 and 2003-2004 subsamples.37-16.75) 2..41 (1.37 (1.46 (1.40-4.43 (5.430-.83 (1.820-1.24-17.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.87 (5.54 (1. 2005).20 (.48-4.49) 8.Organochlorine Pesticides nearby agriculture (Botella et al. Survey Geometric mean (95% conf.78 (4. o.39-2.9) 7.80) 1.6) 9.51-49.6) 9.76) 1.06) 1.520 (.68 (2.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .18-1.56-2.7-19.34) 6.9-38. Finding a measurable amount of p.63 (1.76-3.26-10.12 (.70) 1.590 (.p’-DDT were below the limits of detection.860 ng/L) and DDE (about 14.77 (1.3 (8. 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.26) 3.39) 1.32-1.25 (1.92) 1.11 (2.7-48.19) 4.01-5.25) 8.2 (19.02) 1.2) 26.37-1. High mean levels of whole blood DDT (about 3.561 (.02 (2.01-11.15-4.71 (6.91-2.32-1. Serum p.488-.19-14. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.66) 3.7) 16.84-3.57 (1.730) .77 (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 3.36 (3.63-15.57-2.80) 3.58) 75th 3.66-17.99) 1.43-4.51) 3.84 (3.72) 1.51-8.40-8.25 (.55 (2.6) 9.7) 13.1) 7.61 (1.22) .557) 1.57-13. 2004).726) ..63 (1.3) 10.24 (1.2-32.36-2.30 (1. 1991).419-.72) 1.22-1. less than one percent had detectable serum levels of o.91 (6. or p.01) 1. interval) 1.56) 2.43-8. considerably higher than levels in this Report (Smith.14-9.00-1.32 (1.52 (3.6) 9.680-1.8 (9.82 (1.75) 6.62-6.4) 9..35) 1.75) 1.81-18.47) 3.0) 2.37-10.60-13.68-4.36-11.28) 1.2 (6.0 (9.80) 1.70-3.00) 7.456 (.3) 13.59) 6.01-1.500-.49 (6. 1971).03-1. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.69) 4.9-17.2) 19.4 (12.31-2.10-1.611-1.88 (2.97-4.09-1.4) 14.8-90.80 (2.75 (8.8 (13. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.50-17.5) 5.26 (1.13 (1.30-1.45 (1.7) 9. 1989).87-16.57 (1.17-3.963-1.79) 4.57) 2.22 (7.88-35.18-4.45 (1.07) 1.82) 1. 2004).623 (.32) 1.1) 40.71 (5.17 (3.90-8.76) 1.4) 13.S.10-5.8 (13.14 (1.38 (1.06) 3.56-3. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.92 (3.59) 3.5) 16.38 (1.05) 1.890-1.91-3.516 (.9 (15.9 (26.14) 2.1 (8.55-9.p’-DDT.3) 16.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.43-4.0 (12.23 (7.53 (2.37-4.16 (2.33-1.870 (.5) 10.96) .00 (6.7 (8.8) 15.91) 3.54-7.3-43.40-4.18-1.34 (7.34-11.31-12.93 (7.85 (1.0) 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 .81-5.53-15.69 (2.53) 1.65 (1.66-2.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.01) 1.81 (7. In the NHANES 1999-2000.47 (1.13-2.534-.58) 1.3 (9.12 (6.44) 1.69) 8.05 (3.14) 2.56-6.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.29 (1.994-2. In a subsample of NHANES II (19761980) participants.18 (6.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.2 (9.69 (1..66) 1.

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

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

Organochlorines and breast cancer risk. Lepom P. Botella B. Hanrahan L. Klebanoff MA. August 2008. 4/21/09 Anderson HA. et al. Environ Health Perspect 2004.358:110-114. Biochem Pharmacol 1997. Int J Hyg Environ Health 2002. Garrett N. Epidemiology 2006. Paepke O. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Notides AC. et al. Needham LL. September 2002. Klebanoff MA. Savitz DA. Bjerselius R. Krause C. Hediger ML. Swanson MK. Frumkin H.97(2):178192. Longnecker MP. Katz SH. Rivas A. Glynn AW. and other chemicals. Baker RJ. Int J Hyg Environ Health 2003. Burse VW. Granath F. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Klebanoff MA. India. Gabrio T.72:261265. Cerrillo I. Eriksson P. et al. Herrman T.54:1431-1443. Parks L.112(17):1761-1767. CA Cancer J Clin 2002. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Zaidi SS. Hurd C. Effects of environmental antiandrogens on reproductive development in experimental animals. Olea-Serrano MF. Vorojeikina DP. Am J Epidemiol 2002. Bates MN.106(5):279-289. Cueto C. selected elements. Maternal DDT exposures in relation to fetal and 5-year growth. Maternal serum level of 1. Chemosphere 2004. Seiwert M. Davis MD.53(8):1161-1172. Olea N. Aune M. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Becker K. Talts U.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism.71(6):1200-1209.58:1185-1201. The Great Lakes Consortium. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.96:34-40. Ellis H. Crespo J. Zoellner I. Henley SJ. Needham LL. HCH. Zhou H. Organochlorines in Swedish women: determinants of serum concentrations. Patterson DG Jr.111:349355. Durham WF.7(3):248-264. Bhatnagar VK. Environ Health Perspect 1998. Link B. FDA total diet study. Sci Tot Environ 2006. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Schulz C. dichlorodiphenyldichloroethylene.. et al. Longnecker MP. DDT and human health. Rogan WJ. Brock JW.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). hypospadias. Drexler H. 4/21/09 Gladen BC.cfsan. Lancet 2001.21(1-2)37-48. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Bloom MS. Exposure of women to organochlorine pesticides in Southern Spain. Greenfield TA. Gray KA. Gladen BC. Jr.155(4):313-322. et al. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT).html. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Toxicological profile for DDT. April 1982 to 1984. Jr. Lambright C. Environ Res 2004.cdc. Gray LE Jr. Needham LL.17(6):692-700. Arnold SF. Environ Res 2005.52:301-309.205:297-308.gov/ toxprofiles/tp35. hexachlorobenzene. Brock JW. Willman EJ. Olson J. et al. and polythelia among male offspring. Available at URL: http://www. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Environ Health Perspect 2003. Wolf CJ. Koepsell TD. Chemosphere 2005.html. Saiyed HN. et al. lindane (g-HCH). Chen CW. DDE and shortened duration of lactation in a northern Mexican town. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Available at URL: http://www.atsdr.206:485-491. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Atuma S.85:504508. Hum Reprod Updat 2001. Neurotoxicol 2000. Moysich KB. Zhou H. Vena JE. Barr DB. Gunderson EL. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Darnerud PO.162:890-897. Buckland SJ. DDE. Piechotowski I. Biomonitoring of persistent organochlorine pesticides. and DDD [online]. Kashyap R. Olson JR. JAMA 1956. et al. Beard J. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Bull Environ Contam Toxicol 2004. Kaus S. Furr J. et al. Food and Drug Administration (FDA). Hayes WJ. Heudorf U. Profiles of ortho-polychlorinated biphenyl congeners. J Assoc Off Anal Chem 1988. Jusko TA. Levels of DDT. and dichloro(diphenyl)ethylene (DDE). Am J Public Health 1995.gov/~dms/ pesrpts. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Kulkarni PK. dietary intakes of pesticides. Calle EE.fda. Thun MJ.1-dichloro2. Charles MJ. Ostby J. and HCB residues in human blood in Ahmedabad.355:7889. Angerer J. Falk C.

et al.20(2):186-193. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Neurochemical targets and behavioral effects of organohalogen compounds: an update. Chemosphere 2004. Inc. Jr. Smith AG.54:1509-520. 731-915. Lubet R. Radomski JL.Organochlorine Pesticides Mariussen E. Thomas PE. children and newborn infants. Reddy AB. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults.53:455-477. New York. Nims R. Deichmann WB. Fox S. Demographic and seasonal influences on human serum pesticide residue levels. In Hayes WJ. Comparative pharmacodynamics of CYP2B induction by DDT. Academic Press. J Toxicol Environ Health Part A 1998. Chovancova J. and DDD in male rat liver and cultured rat hepatocytes. Stehr-Green. 2 Classes of Pesticides. Pollutants in breast milk. Pesticides and breast cancer risk: a review of DDT. Eds.109:35-47.36:253-589. Arch Pediatr Adolesc Med 1996. Toxicol Appl Pharmacol 1971.150:981-990. Snedeker SM.27:405-421. Cerhan JR. Lynch CF. Chlorinated Hydrocarbon Insecticides. et al. and dieldrin. Jr and Laws ER. Schecter A. Handbook of Pesticide Toxicology. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. DDE. Astolfi E. Rey AA. Fonnum F. Pavuk M. Vol. Rogan WJ. DDE. 1991 pp. Crit Rev Toxicol 2006. Environ Health Perspect 2001. Petrik J. Jones CR. J Toxicol Environ Health 1989. PA.

.10 (<LOD-5.20 (<LOD-5. endrin has been detected with declining frequency in U. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. and inflammation (Smith.S. Because it is metabolized so rapidly. In the body. 72-20-8 General Information Endrin.8.. All uses of the pesticide in the U. and occasionally at low levels in sediment and surface waters. total diet surveys (FDA. inhalation or dermal exposure routes.10 (<LOD-5. endrin is converted rapidly to its major metabolite. unless the dose is high and the exposure is very recent. population from the National Health and Nutrition Examination Survey... 1992). 1987). Hepatic effects of endrin exposure have included necrosis. a stereoisomer of dieldrin. Ketoendrin is a major photodegradation product (IPCS. manufactured. Survey Geometric mean (95% conf. have been cancelled by the U. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. At high doses. 1991). 1992. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.40 (<LOD-6. 1992). rodenticide and avicide. Smith. 2008). Kavlock et al.40-5. 1996.Organochlorine Pesticides Endrin CAS No.09 and 7.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD.50) < LOD 5. Endrin was used as an insecticide.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. Endrin is absorbed rapidly after ingestion. Endrin does not accumulate in body tissues (IPCS. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. Serum Endrin (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. 1979. or from contact with contaminated soils and sediments in areas where endrin was applied.S. 1991). General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. or discarded. 1981).20 (<LOD-5.70) < 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. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.50) < LOD < LOD < LOD 5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.30 (<LOD-6. endrin usually is not detected in serum of exposed individuals. is no longer manufactured in the U.30) < LOD 5.S. which may vary for some chemicals by year and by individual sample.40) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5.60 (5. fatty infiltration. An epidemic of acute endrin poisoning. EPA. unlike aldrin and dieldrin. Fourth National Report on Human Exposure to Environmental Chemicals 97 . Over time. endrin can persist for years. Endrin has been detected in soils. 1992). IPCS. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals.S. Depending on soil conditions. anti-12hydroxyendrin. Endrin was not widely used as a termiticide. < LOD means less than the limit of detection. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al.S. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.

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.S. with the highest value 6.Organochlorine Pesticides The U. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples.020 (<LOD-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. interval) Selected percentiles ( 95% confidence interval) Sample 95th .020 (<LOD-.24 ng/mL (about 6. Workplace exposure standards for endrin have been established by OSHA.020 (<LOD-.e. which may vary for some chemicals by year and by individual sample.020) < LOD < LOD < LOD . 2004). 2000).020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level. 98 Fourth National Report on Human Exposure to Environmental Chemicals .24 ng/g of serum) (Botella et al.020 (<LOD-. serum levels of endrin were below the limit of detection.020-. IARC has determined that endrin is not classifiable with regard to human carcinogenicity. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Information about external exposure (i. population from the National Health and Nutrition Examination Survey..cdc.gov/toxpro2. 2004.020 (.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 . endrin was detected in 9% of serum samples. environmental levels) and health effects of endrin is available from ATSDR at: http://www.atsdr. In a small study of Spanish women hospitalized for elective surgery.020) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.020) < LOD 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-.html. EPA has established environmental standards for endrin. and the FDA monitors foods for pesticide residues.. Survey Geometric mean (95% conf.S.020 (<LOD-.020) < LOD . This finding is consistent with other general population studies (Bates et al. Ward et al.. Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect.

21:141-150. Hanisch RC. Available at URL: http://www. Endrin [online]. Fetotoxic effects of prenatal exposure in rats and mice. Garrett N. Roy ML. Ellis H. 1992.cfsan. Sokal D.atsdr. Rivas A.13:155-165. Fourth National Report on Human Exposure to Environmental Chemicals 99 .inchem. New York. Gray J. Kavlock RJ. Toxicological profile for endrin [online]. et al. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. et al. et al.9:1357-136. No:429-436. Olea N. Chlorinated Hydrocarbon Insecticides. 731-915. Ward EM. Cerrillo I. Toxicol Lett 1992.79(6):928-934. Crespo J.gov/toxprofiles/tp89. Ginsburg KS. Grajewski B. Academic Press. Inc. Chernoff H. In Hayes WJ.cdc. Olea-Serrano MF. et al. Liddle J. Buckland SJ. Cancer Epidemiol Biomarkers Prev 2000. Whitehouse DA. Patterson DG Jr. Exposure of women to organochlorine pesticides in Southern Spain.htm. Perinatal toxicity of endrin in rodents. 2 Classes of Pesticides. Botella B. August 2008. 4/21/09 Bates MN. Available at URL: http://www. Rab MA. 4/21/09 International Programme on Chemical Safety (IPCS). Toxicology 1979. Handbook of Pesticide Toxicology. Jr and Laws ER. Chemosphere 2004. Patterson DG Jr. Jr. Perinatal toxicity of endrin in rodents. Vol. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Rowley DL. Turner W. Smith AG.gov/~dms/ pesrpts. Gray LE.64-65 Spec. Toxicology 1981. Gray JA. Narahashi T.fda.96:34-40. Andersen A. Fetotoxic effects of prenatal exposure in hamsters. Burse VW. I. Rogers E.html. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Schulte P.html. Pediatrics 1987. Hanisch RC. Environ Res 2004. Gray LE. August 1996. Frey JM. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. II. Hardjotanojo W. pp. Food and Drug Administration (FDA). Available at URL: http://www. Environmental Health Criteria 130.org/documents/ehc/ehc/ ehc130. Saleem M.54:1431-1443. 1991.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Eds. Convulsions caused by endrin poisoning in Pakistan. Chernoff N. Needham LL. 4/21/09 Kavlock RJ. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.

0 (25.9-32.3) < LOD < LOD 29.8) < LOD < LOD 27.7 (19.7-22. EPA cancelled its use in 1984.S.8-15.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.8. 01-02.5-15.3) < LOD < LOD 20.6) < LOD < LOD 26.5 (13.3 (22.1 (14.3-20.2 (14.6-19.4-15.0-16. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28. 100 Fourth National Report on Human Exposure to Environmental Chemicals . and 03-04 are 118.0 (18.5-TCP) and 2.6-32. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.4) < LOD < LOD 33. 2. primarily as a fungicide and seed treatment until the U.S.4) < LOD < LOD 22.2) < LOD < LOD 29.1 (13.4.S. or game taken from areas with HCB contamination.9) < LOD < LOD 16. and elimination occurs by renal and fecal routes.7-15.9) < LOD < LOD 19.7-26.0) < LOD < LOD 15. 1997).9 (25.1) < LOD < LOD 15.4 (18.0 (18.4 (11.9) < LOD < LOD 28. 2005).2) < LOD < LOD 13. HCB has been detected in fewer foods since the 1980s (FDA.1-20. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications. Therefore.9-24.3) 24.0-19.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.9) < LOD < LOD 20.4 (22. Gunderson.4. HCB is slowly metabolized.2-31.5-18.6) < LOD < LOD 26. 2002).7-30.4-16.3 (22.5-14.2-15.7-29. wildfowl.9) < LOD < LOD 15. population from the National Health and Nutrition Examination Survey.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.9-15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.1) * * 15.7 (27.2 (14. and accumulates in fatty tissues where it persists for years. 2008.0.7) < LOD < LOD 24.3 (16.4) < LOD < LOD 18.7-21.1 (14.7) * * 14.5-15.7 (15.6-trichlorophenol (2.7-16..5) < LOD < LOD 18.4. The FDA dietary surveys have shown that over time.6) < LOD < LOD 25. breast milk is an additional route of elimination in nursing women.1 (17. air. and 7.0 (14. < LOD means less than the limit of detection. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides. HCB is well absorbed after oral administration.2-15.9 (23.4.0) < LOD < LOD 15.Organochlorine Pesticides Hexachlorobenzene CAS No.8 (22.6-44. Although it is not manufactured as an end-product in the U.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13. and sediment (Barber et al.3 (20.5-33.9 (14. and foods with a high fat content.3-26.6-33.S. respectively.5 (14. distributes widely throughout the body. The general population may be exposed to HCB through diet.3-22.0) < LOD < LOD 24.5-14.3) * * 15.6) < LOD < LOD 24.0) * * 15.7 (15.9-20. and has been detected in soil.9-17.2 (13. which may vary for some chemicals by year and by individual sample. 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.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. 1988).6-26.8 (15.5-trichlorophenol (2.2 (17.6 (24.1-16.6-TCP) (To-Figueras et al.9) < LOD < LOD 20. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U. Survey Geometric mean (95% conf.9) 19.6 (23. water.4) < LOD < LOD 14.9-30.4) < LOD < LOD 23.6) < LOD < LOD 14.. Urinary metabolites include pentachlorophenol (PCP).0-25.6 (21.5 (13. see Data Analysis section) for Survey years 99-00.3 (14.4) < LOD < LOD 19. 31.2 (24.4 (18.0-28. 1976).8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. particularly by consuming fish.7-16.3 (12.4.9 (25.8 (26...

140 (.111-. HCB interferes with normal heme synthesis.099) < LOD < LOD .169-.125 (. very high.088-. thyromegaly.118) < LOD < LOD .111) < LOD < LOD .175) < LOD < LOD .159-.088-.120 (.123 (.114-.155) < LOD < LOD . and many died before 2 years of age (Peters et al. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.157-.092-.079 (.147 (.163 (.095) < LOD < LOD 75th < LOD < LOD 90th * * .085) * * .gov/toxpro2.090 (.121 (.082-. Biomonitoring Information Serum concentrations reflect the body burden of HCB.123 (.109) * * .072-.090 (.e. arthritis. which may vary for some chemicals by year and by individual sample. EPA has established a drinking water standard.095) * * .107-.176) < LOD < LOD .173) < LOD < LOD .115 (. were seen in an epidemic of poisoning in Turkey that occurred from 1955 to 1959 when HCB-treated seed grain was diverted for bread production.095 (.178-.179 (. environmental levels) and health effects is available from the U.094 (. immunologic abnormalities.083) < LOD < LOD . and weakness.S.090 (.176-.186 (.126) .223) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * .081 (.062-. and the FDA has established a bottled water standard for HCB.gov/pesticides/ and from ATSDR at: http://www.141) < LOD < LOD .218) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.073-. With chronic exposure.099) < LOD < LOD . Schmid.098 (. and liver and thyroid cancers (ATSDR.100) < LOD < LOD .148-.167 (.088-.102 (. Fourth National Report on Human Exposure to Environmental Chemicals 101 .156 (. This condition.089-.203) < LOD < LOD . reproductive and developmental toxicities.163-.171 (. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.129) < 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. EPA at: http://www.. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD . anorexia.163) < LOD < LOD . Infants were exposed transplacentally and through breast milk.085-. ACGIH has developed workplace exposure limits for HCB.epa.107) < LOD < LOD . acute doses produce central nervous system depression and seizures.086) < LOD < LOD .091-.092 (.127-.S.064 (.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .182 (.157 (.atsdr.160 (.143-.203) < LOD < LOD . 1982.118-.123 (.069) < LOD < LOD .132) < LOD < LOD .190 (.114-.092 (.087 (.191 (.135-. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity. as well as hypertrichosis.060-.065 (.130) < LOD < LOD .258) < LOD < LOD .078 (.090-.095-.196) < LOD < LOD .095 (.152) < LOD < LOD .097) .html.113-.S.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD . The U. Chronic feeding studies in animals have demonstrated kidney injury.147-.104 (.118-. population from the National Health and Nutrition Examination Survey.086-. In humans. IARC classifies hexachlorobenzene as possibly carcinogenic to humans. 2002).145-. More information about external exposure (i.092 (.145-. 1960).097 (.094) < LOD < LOD .Organochlorine Pesticides chemical.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 * * .089-.102) < LOD < LOD .077-.099) < LOD < LOD .174-. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.086-.081-.069) * * . Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.225 (.097) < LOD < LOD ..cdc.122) < LOD < LOD .

Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. dietary intakes of pesticides. Lackmann GM. respectively. Hexachlorobenzene in the global environment: emissions.110(8):835-838.. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Bryan GT. Biomonitoring of persistent organochlorine pesticides. Bertram HP. 2003). Safe A. FDA total diet study. more HCB levels were quantified. et al. trends and processes. Zoellner I. Herrman T. Bradman A.39(12):744-749. Lackmann. References Agency for Toxic Substances and Disease Registry (ATSDR). however. but overall. Dallaire F. Cripps DJ. Laliberte C. Holland NT. Fenster L. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Lackman. Otero R.. The metabolism of higher chlorinated benzene isomers.58:1185-1201. Aune M. 2005). levels. Schulz C. Paepke O.cdc. Jones D.gov/~dms/ pesrpts. Seiwert M. Ozalla D. Environ Health Perspect 2002. J Exp Sci Environ Epidemiol 2007.77:173182. Gocmen A. 2002. Dogramaci I. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect.. Darnerud PO. Piechotowski I.. Granath F.71(6):1200-1209. and the geometric mean concentration of HCB in whole blood was 0.9% of participants had quantifiable levels (Stehr-Green. Biol Neonate 2002..44 mg/L.81(2):82-85.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. van Wijk D. Link B. distribution. Sci Tot Environ 2005. 2002. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Chemosphere 2005. Sala M. April 1982 to 1984.111:349355. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Gunderson EL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Muller C.fda. Barr DB.17:388–399. 1989).gov/ toxprofiles/tp90. 2002. Arch Neurol 1982. Available at URL: http://www. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Food and Drug Administration (FDA). et al. Dewailly E. 2005). Int J Hyg Environ Health 2002. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Krause C. Environ Health Perspect 2003. HCB levels were directly related to age. Gabrio T. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Kemper FH. Lawrence River (Quebec. Ayotte P.205:297-308. Sweetman AJ. 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. Herrero C. Santiago-Silva M. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. In the 1976-1980 NHANES subsample. et al. and other chemicals. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Bjerselius R. selected elements. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. 4/21/09 Glynn AW. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area.html. IARC Sci Publ 1986. 1999). et al. In Spain. Glynn et al. 2002).atsdr. 2006). Atuma S.54(3):203-208. Kaus S.349:144. In a representative sample of the 1998 German adult population. 2005. Over the past two decades. Canada).. 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. Peters HA.cfsan. Available at URL: http://www.. Bradman et al. Jones KC. only 4. September 2002.html. Kohli J.. Arch Dermatol 1999. Muckle G. Toxicological profile for hexachlorobenzene update [online]. Schwartz JM. Reference values updated. Link et al. As a result of the lower limit of detection in NHANES 2003-2004. Eskenazi B. Lecha M. August 2008. Bertram et al. J Assoc Off Anal Chem 1988.. HCB detection in serum also was proportional to age. Can J Biochem 1976.. Becker K. Organochlorines in Swedish women: determinants of serum concentrations.. 2002) and among children (Link et al. 4/21/09 Barber JL. 1986. Lepom P. 2002.135(4):400404.

27:405-421. Cutaneous porphyria in Turkey. J Toxicol Environ Health 1989. N Engl J Med 1960. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. To-Figueras J. et al. PA. Fourth National Report on Human Exposure to Environmental Chemicals 103 . Otero R. Demographic and seasonal influences on human serum pesticide residue levels.105(1):78-83.263:397-398. Stehr-Green. Sala M. Rodamilans M.Organochlorine Pesticides Schmid R. Environ Health Perspect 1997. Barrot C. Santiago-Silva M.

6-62. exists in several isomeric forms.66-12.36.6) 653 758 589 1240 1533 1370 20 years and older 10.60-13.4) 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.S.8) < LOD 10.3-56.7 (53.5) 14.7) 56. The other isomers can be formed during the synthesis of lindane.0-21.9-24. < LOD means less than the limit of detection.0 (19.3) 25. EPA cancelled agricultural uses of lindane (ATSDR.5) 22.2) 9.7) 32.70 (6.5) 67.2 (31.6) 36. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.7-96.3 (42. including alpha. As pesticide applications of HCH were increasingly restricted or eliminated.7 (62.8.5) 40.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.3-38.0) 17.9-81.0 (14.1) 71.0-20.9) 45.2 (34.8 (21.4) < LOD < LOD < LOD 46.61-12. and sediment as a result of historic production and use.3 (13.0 (<LOD-12.2-42. 2005).1 (11.30-11. see Data Analysis section) for survey years 99-00. The gamma isomer.8-87. the U.6) 18.1-15. **In survey period 2001-2002.3 (42.76.70-19. containing about 64% alpha and 10%-15% gamma isomers.9) 15.7) 10.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.4 (11. General population Serum beta-Hexachlorocyclohexane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.5528.0 (35.1) 13.7 (25.0 (37.9) 81.6 (22.7) 18.5) 11.8-16. water.4 (16.3) 34.8) 7.4-45.1-16.9 (9. interval) 9. 608-73-1 beta-Hexachlorocyclohexane CAS No.8) 95th 68.8 (10. particularly alpha and gamma have been detected widely in air.80 (<LOD-14.1 (30.4) 51.5 (37.3 (26.46-11.3) 14. However. and 7.8-19.43 (<LOD-9. environmental levels declined.7) 27.7-96.9-21.4 (12.3 (62.1 (12.8 (17.5 (8.6-42.Organochlorine Pesticides Hexachlorocyclohexane CAS No.2-52.9-14. HCH isomers.1) 31.9-178) 48.9-51. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.1 (9.9 (62.8) 12.1) 12.0) 71.6 (10.2 (29.7-166) 70.7 (<LOD-16. 01-02. commonly known as lindane.4 (8.0-70.2-98. soil.0 (33.7) 97.6-37.8-199) 134 (85.6-18.1 (21.7-69. which may vary for some chemicals by year and by individual sample. and delta.3) 37.7 (13.7-69.4) 10.5) 90th 42.1 (18.0) 35.4) 11.0) 41.8-54.5 (43.2) 13.0) 8.4) 44.5) 16.1 (16.4-111) 84.5 (14.6-14.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.6) 50.9-56.6-20.6) 35.3-85.1) 12.2) 36. 58-89-9 General Information Hexachlorocyclohexane (HCH).2 (50.9 (40.7-26.8 (64.9 (50.6) 16. 319-85-7 gamma-Hexachlorocyclohexane CAS No.5 (16.2-67.6 (17.5) 29.6 (33. so they can accumulate in fatty tissues of animals. respectively.8) * * * * * * 15. and 03-04 are 9.4 (50.9) 17. beta.8 (9.2-17.8) 27.0-70.9 (32. 104 Fourth National Report on Human Exposure to Environmental Chemicals .1-32.S.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19. See the section “What’s New” at the beginning of this Report for details.2-46.7) 10. It is no longer produced or sold in the U.68 (<LOD-10.4-50.5-29.2) 62.1-37. 2005).2-22.04-10.2-20.2) 142 (99.70-12. Technical grade HCH is a mixture of all four isomers.70 (8.1 (27.7 (29.6-135) 69.5 (11. gamma.8) 39. population from the National Health and Nutrition Examination Survey.0) 7.7) 23. formerly referred to as benzene hexachloride.90-8.20-16.8-68. Lindane has a half-life of about two weeks in soils and water.4) 27.6-89.0-23.4) 901 1067 952 992 1224 1007 Females 11.50) 8.2-55.2 (9. In 2006.1-36.0-34.1-27.8) 52.8 (23. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.7-20. HCH isomers are lipophilic.87 (9. 6.1 (9.4 (52.4) < LOD 9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.56-12.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.4) 21.6 (40.8 (32.90) 7.6 (16.9 (11.0 (8.1-32.3) 51. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.7 (30.2 (18.2-87.5 (24.6) 47. and have been used either as fungicides or to synthesize other chemicals.S.1-49.90-8.9 (30.4-73.0-111) 70.9 (26.7 (35. each result has been multiplied by 1.6-47.80 (6.5-123) 49.8 (33.7) 73.89 (<LOD-9.2 (48.

070 (.220) .073-. interval) . Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways..092 (.S.412 (.056-.083) .070-.083 (.620-1.090 (. 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.310) . and seizures.372 (.150) .150) .050 (.234 (.125) < LOD < LOD < LOD .150-.040-.120-.090 (.814) . which may vary for some chemicals by year and by individual sample.330-.058 (<LOD-.191-.118 (.080 (.250 (.442 (.710) .096) .057-.064) .244-.056-.360) .070) . HCH crosses the placenta and is also excreted in breast milk (Radomski et al. 1977).050 (. 1971.S.190-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.460) .160 (.130) .560) .090 (.124-. tremors.070 (.290) .050) .480 (.110) .050 (<LOD-.910 (. ataxia.077) < LOD .068-.175 (.051-.01 (. and FDA has established a bottled water standard and food residue tolerances for lindane. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans. The U. hepatic enzyme induction. population from the National Health and Nutrition Examination Survey. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.180-.460 (.360-.048 (<LOD-.410 (.290) .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 .057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .290 (.404) .080) * * * * * * .078 (.060) .080-.305) .160-. **In survey period 2001-2002.260) .100) .382-.661) 901 1067 952 992 1224 1007 Females .100-.501) . OSHA and ACGIH have established workplace standards and guidelines. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity. or dermal exposure.139 (.089) .220-.100-.230-.080) .050-. EPA has established a drinking water standard. The beta isomer accumulates in fatty tissues and is metabolized more slowly.510) .120) .250-.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD . Distribution is mainly to fatty tissues.281 (.131-.250) .120-.340-.330 (. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1983).240-.290 (.250 (.089-.120) .072 (.470 (.140 (. respectively..080-.216 (..210-.690) . Fourth National Report on Human Exposure to Environmental Chemicals 105 .051 (<LOD-.173-.170-.091) .S.140) .150 (.390-.050-.140) .308-.059-.580-1.297-.050-.140) .480 (.067 (.319) .310 (.390 (.5528.200-.146-. and nephropathy developed (IPCS.110) .470) .120 (.221-.118-.069) .103-.098 (.05) .410-. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.167 (.200-.360 (.294-.410) .100) .070-.450 (.290 (.191-.222 (.174) . the serum half-life was about 20 hours among children (Ginsburg et al.320 (. See the section “What’s New” at the beginning of this Report for details. After dermal application of lindane 1% lotion. ingestion.620) .086) < LOD < LOD < LOD < LOD < LOD < LOD . 1996.200 (.260) . paresthesias.250 (.450) . 1981).144 (.110-.350) .050-.067) . 2002).420-.240 (.062 (.280-.280-.120 (. U.700) .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.110) .170-.400) .080-.057-. When animals were chronically fed lindane at high doses.120 (.587) 653 758 589 1240 1533 1370 20 years and older .450-.370-.077) < LOD . resulting in a half-life of about seven years. each result has been multiplied by 1.32) .350 (. HCH isomers are absorbed after inhalation. 1986).570 (.064 (.090-.600) .210 (...380 (.065 (. Rogan.254) 95th .410) .130-.Organochlorine Pesticides exposure to HCH is through the diet.210 (.065 (.190) .070-. enlarged livers.190) .100-.37) 1.100 (.100 (.220 (.331 (. Saxena et al.160) .340) . 2008.214) .103) 90th .840) . Workers who directly handled HCH have complained of headache.050 (<LOD-.120-. from 6% of samples in 1982-1984 to 2% in 1994 (FDA. probably by blocking inhibitory neurotransmitters in the central nervous system.062 (.057 (<LOD-.580 (.680) .047-.080 (.220-.300-.081-. and memory loss (Nigam et al.210) .310) .521 (.250-.130 (.260-.270 (.119) . for lindane.103 (.287 (.190-1. Gunderson 1988).400) .560 (.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .480) . Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.

1998). Survey Geometric mean (95% conf.. < LOD means less than the limit of detection.cdc.. 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. 2005.. aged 9-11 years. the maximum and 95th percentile beta-HCH values. 2001-2002. 2002). In NHANES 1999-2000. 1991. older age. Kutz et al. Becker et al. 2004) and India (Bhatnagar et al.. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. environmental levels) and health effects is available from the U. 1971.e.gov/pesticides/ and from ATSDR at: http:// www.S. In populationbased studies of New Zealand adults and German adults and children. 2005. 2004).gov/toxpro2..8. Additional factors associated with higher beta-HCH levels include rural residence. Kutz et al. respectively.. EPA at: http://www. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. and 2003-2004. 2004. serum levels of lindane were generally below the limits of detection. 10.5. male sex. see Data Analysis section) for Survey years 99-00. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. respectively.S. Biomonitoring Information Because of its longer half-life. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al.5. More information about external exposure (i. were similar to the 95th percentiles in this Report. 106 Fourth National Report on Human Exposure to Environmental Chemicals .html. 01-02... and a diet that includes meat (Becker et al..Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. Radomski et al. 1989). In recent years. and 7. which may vary for some chemicals by year and by individual sample. and 03-04 are 14. 1991. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. In an earlier (1996-1997) sample of German children. Bates et al. 1998. Sturgeon et al. the 95th percentile of betaHCH levels was twofold to threefold higher than the 95th percentile of 12-19 year olds in the comparable NHANES Serum gamma-Hexachlorocyclohexane (Lindane) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.atsdr.epa. Link et al.. 1989. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. Stehr-Green. Stehr-Green.. population from the National Health and Nutrition Examination Survey. 2002.

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

9(4):417-424. Astolfi E.52(1):59-67. Chemosphere 2005. Needham LL. et al.atsdr. Kaus S.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Falk C. India. Zaidi SS. Int Arch Occup Environ Health 1983. 4/21/09 Ginsburg CM. dietary intakes of pesticides. Granath F. et al.html. Bates MN. Rivas A.120:1-82. PA. Available at URL: http://www. Needham LL. Visweswariah K. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Rev Environ Contam Toxicol 1991. Olson J. Saxena MC. Metabolism of gammahexachlorocyclohexane in man. gov/toxprofiles/tp43. Int Arch Occup Environ Health 1986. Potischman N. HCH.57(4):315-320. August 2005. Burse VW. Karnik AB. Bottimore DP. Available at URL: http://www. The Great Lakes Consortium. Levels of DDT. Biomonitoring of persistent organochlorine pesticides. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.48:127-134. Herrman T. Saiyed HN. Toxicological profile for hexachlorocyclohexanes update [online]. Aune M. April 1982 to 1984. International Programme on Chemical Safety (IPCS). PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.91:998-1000. J Pediatr 1977. Arch Pediatr Adolesc Med 1996. Rey AA. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Cerrillo I. Becker K.106(5):279-289. Piechotowski I.cfsan. Paepke O. Angerer J. Deichmann WB. Radomski JL. Atuma S. and HCB residues in human blood in Ahmedabad. Siddiqui MKJ. FDA total diet study. org/documents/jmpr/jmpmono/2002pr08. Krishna Murti CR. Ellis H.54:1431-1443.150:981-990.20(2):186-193. and other chemicals. Environ Res 2004. Majumder SK. Int J Hyg Environ Health 2002. Crespo J. Botella B. et al. Pollutants in breast milk. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. selected elements. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults.gov/~dms/pesrpts. VI. Rogan WJ. Zoellner I.inchem. Bhatnagar VK. Lowry W. Olea N. Glynn AW. Seiwert M.27:405-421. 4/21/09 Anderson HA. Bull Environ Contam Toxicol 2004. Maass R. Buckland SJ. Hanrahan L. 2002. Environ Health Perspect 1998. Heinrich R. Darnerud PO. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Bjerselius R. et al. Patterson DG Jr. Stehr-Green. available at URL: http://www.205:297-308. Bai KM. Krause C. J Toxicol Environ Health 1989. Garrett N. Gunderson EL. Sturgeon SR. Arch Toxicol 1981.fda.cdc. Wood PH. August 2008. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Environ Health Perspect 2003.72:261265. Kashyap R. et al. Occupational exposure to hexachlorocyclohexane.71(6):1200-1209. Kutty D.58:1185-1201. Brock JW. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Chemosphere 2004. Nigam SK. Reisch JS. Kulkarni PK. Schulz C. children and newborn infants. Lepom P. J Assoc Off Anal Chem 1988. Gabrio T. Link B. Rothman N. Brinton LA. Bhargava AK. Placental transfer of pesticides in humans. Raju GS. Toxicol Appl Pharmacol 1971.htm. Demographic and seasonal influences on human serum pesticide residue levels. Lindane. et al. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Olea-Serrano MF. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Cancer Causes and Control 1998.96:34-4Food and Drug Administration (FDA). Organochlorines in Swedish women: determinants of serum concentrations. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.html.111:349355. et al. Absorption of lindane (g benzene hexachloride) in infants and children. Needham LL. 4/21/09 Kutz FW. Exposure of women to organochlorine pesticides in Southern Spain.

0-374) 11.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. and 03-04 are 14. Mirex binds strongly to soil. it is a highly persistent chemical in the environment.S.5-291) 11. or pesticide application. Occupational exposure is limited to workers at sites where mirex contamination is present. 10.6) 9. 1991).6 (<LOD-23. 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.5. Mirex is not metabolized in the body.0 (<LOD-108) < LOD < LOD 50.3) 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 13.70-24.5 (<LOD-42.2) 51.1 (13.40 (<LOD-13.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.90-29. since 1977.3-225) 15.7 (<LOD-47.6-305) 15.6. especially those from persons living in the southeastern U. respectively. In studies conducted in the 1970’s and 1980’s.70 (<LOD-15.6 (<LOD-108) 9. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. Mirex can cross the placenta and be excreted in breast milk. after which it is widely distributed in the body and stored in fat. aquatic organisms..0 (12.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.3 (15. see Data Analysis section) for Survey years 99-00.1 (<LOD-65.8 (12. 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.2 (7.S.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.S.5-425) 40. Formerly.S. disposal.2-230) 13. animals.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. 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. 2385-85-5 General Information Mirex has not been produced or used in the U.1 (8.3 (15.. < LOD means less than the limit of detection. 1985. Mirex is absorbed through the skin and from the gastrointestinal tract. Fourth National Report on Human Exposure to Environmental Chemicals 109 .10-37.8. Mirex has been detected in air.6) < LOD < LOD < LOD < LOD 71.5-82.S.7) 8. mirex was detected in human adipose samples. 1995).6 (<LOD-31.4) < LOD 15. soil.4) < LOD 63. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. population from the National Health and Nutrition Examination Survey.4 (8. and foods.Organochlorine Pesticides Mirex CAS No. where it was applied directly to soil and by aerial spraying. sediments.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4-230) 18. Some states and the U. Survey Geometric mean (95% conf. water. resulting in exposure to newborns and nursing infants.5 (9.8 (<LOD-73. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.5 (<LOD-115) 153 (30.7 (12.0 (14. (Kutz et al.10 (<LOD-15. 01-02. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.8) < LOD 15.7) < LOD 66. where it has a half-life of 12 years. and 7.70-40.

268) < LOD .170) < LOD . 1989).256 (. More information about external exposure (i.106) < LOD . 7.053-.102) < LOD < LOD < LOD < LOD . Finding a measurable amount of mirex in serum does not mean that the level of mirex causes an adverse health Serum Mirex (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Biomonitoring Information In the NHANES 1999-2000.450 (.e.atsdr. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 2001-2002. 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.635) < LOD . In addition. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.080-1.108 (.S.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 . population from the National Health and Nutrition Examination Survey.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 .090-1.gov/toxpro2.Organochlorine Pesticides exposures are unknown.430 (. 110 Fourth National Report on Human Exposure to Environmental Chemicals . and 2003-2004 subsamples.079 (<LOD-.510) < LOD < LOD .077 (<LOD-.8.470) .73) .070-1.140 (<LOD-.7 ng/g of lipid.100 (<LOD-. which may vary for some chemicals by year and by individual sample. Laboratory animals fed high doses developed liver enlargement and liver tumors.080-1.S.37) .090 (<LOD-.. Fishermen in New York who consumed Great Lakes sport fish had median levels of lipid-adjusted serum mirex that were lower than the 95th percentile value among males the NHANES 2001-2002 subsample (Bloom et al.470) . and 4.79) . 2005). In samples obtained between 1994 and 1997. serum mirex levels were generally below the limits of detection (Stehr-Green. Survey Geometric mean (95% conf.090 (<LOD-. reproductive toxicity included decreased fertility and testicular damage.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .062-.690) .470 (.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 . 1991).html.064 (<LOD-. The geometric mean mirex levels of the Inuit mothers were 8.090-1.089-.02) .093 (.170-3.052-.410 (. 1995.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .090-1. Smith. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.220) .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. as well as in a subsample of NHANES II (1976-1980) participants.110 (<LOD-.055-.059 (<LOD-. IARC classifies mirex as possibly carcinogenic to humans. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.450) 1.cdc.100 (<LOD-. The U.054 (<LOD-.08 (.610) < LOD < LOD < LOD < LOD ..106 (. 2004).310 (.92) .41) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . environmental levels) and health effects is available from the ATSDR at: http://www.220 (<LOD-.79) . Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than nonInuit mother from other Arctic regions.370 (. EPA has established environmental standards for mirex.112 (.090 (<LOD-.

Swanson MK.120:1-82. J Toxicol Environ Health 1985. Vena JE. Kutz FW. Stroup CR.27:405-421. Watts DL. In Hayes WJ. Vol. Profiles of ortho-polychlorinated biphenyl congeners. Sci Total Environ 2004. Chashchin V. Wood PH. Available at URL: http://www. Hansen JC. Toxicological profile for mirex and chlordecone [online]. Demographic and seasonal influences on human serum pesticide residue levels. Inc. New York. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.html. Leininger CC. Chlorinated Hydrocarbon Insecticides.gov/toxprofiles/ tp66. Gilman A. hexachlorobenzene. 4/21/09 Bloom MS. 731-915. The human body burden of mirex in the southeastern United States. Odland JO. Moysich KB. Eds. Bottimore DP. 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. et al. PA. Kutz FW.15:385-394. et al. Olson JR. Academic Press. 2 Classes of Pesticides. Fourth National Report on Human Exposure to Environmental Chemicals 111 .330:55-70. Strassman SC. August 1995. References Agency for Toxic Substances and Disease Registry (ATSDR). Circumpolar maternal blood contaminant survey. Rev Environ Contam Toxicol 1991.cdc. Environ Res 2005.atsdr. J Toxicol Environ Health 1989.97(2):178192. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Carra JS. 1991 pp. Dewailly E. Smith AG. Handbook of Pesticide Toxicology. Stehr-Green. Jr and Laws ER. Van Oostdam JC. 1994-1997 organochlorine compounds. Jr. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study.Organochlorine Pesticides effect. dichlorodiphenyldichloroethylene.

recent sampling of U. population from the National Health and Nutrition Examination Survey.40) < LOD 1.03) 9. 1976).30-27.00-3.0 (8.0) 5.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.30-3.60-18.40-18.0) < LOD 21. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16. other organochlorines.5TCP and 2.50 (2.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . Both chemicals have been detected in air. soils.S.40 (.20-36.40 (2.6-TCP were used as intermediates in the production of certain pesticides.00 (3. Such workers would probably Urinary 2. and polychlorinated benzenes (Kohil et al.80 (2.0 (4.72) < LOD 1.40 (2. Exposure to trichlorophenols also may result from metabolism of lindane. surface water.0 (3.0) < LOD 5.30 (.30) < LOD 4. including hexachlorobenzene and hexachlorocyclohexanes. which may vary for some chemicals by year and by individual sample. 2.50-25.4.5-trichlorophenol.6-Trichlorophenol CAS No.57 (<LOD-15. 2.40 (2.6-TCP in any of the samples (U. Formation of 2.S.42 (<LOD-12. 1999).4. EPA. 2006).5-trichlorophenol (2.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.60 (.50 (1.71 (<LOD-8.20-71.9 (<LOD-121) 9.4.4.S.4. 1999). Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.80 (1.31 (<LOD-9.27) 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 1.0 (4.20) < LOD 90th 5.940-3.50 (. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. * 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.0) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Trichlorophenols are no longer manufactured commercially.00 (2.50-63. 95-95-4 2.20) < LOD 5.42 (<LOD-8.71 (<LOD-8.9. 112 Fourth National Report on Human Exposure to Environmental Chemicals .60-8. 2.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.0) 14.0) < LOD 11.40 (1.4.80) < LOD 1.4.950 (<LOD-1.900-2.40) < LOD 6. 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.63) 18.0) 2. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.80-41.00-3.30-27.Organochlorine Pesticides 2. Survey Geometric mean (95% conf. public drinking water systems did not detect 2. Historically. however.0) 2.30) < LOD < LOD < LOD < LOD < LOD 1.8) 21. are metabolites of several organochlorine chemicals.7) 24.0) 2.6-TCP).0) < LOD 5. may occur by inhalation or dermal routes.0 (3. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.3.0) 2.0) 2.4.40 (2.20 (4.0 (5.0) < LOD 5.980-3.10-3.30-11.4. Occupational exposures.60) < LOD 8.40) < LOD 4.00-8.5-Trichlorophenol CAS No.20) < LOD 1.50) < LOD 1.40-11.19 (<LOD-6.7.9 and 0.90-33.30-40. hexachlorobenzene.920-3.4. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.5-TCP) and 2.30-44.4.980-3.60 (4.40 (.4.50-16.0 (4.40 (1.0) < LOD 11.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.30-27. and sediments.60 (2.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.27) 696 661 521 696 603 939 Limit of detection (LOD. usually at herbicide production or waste incineration facilities..6-trichlorophenol (2.

1995) and up to 19 times higher than the 95th percentile value of 1. in addition to dioxins.55 (4.31) < LOD 2.980 (<LOD-1.62-20. Laboratory animals chronically fed high doses of 2.4.Organochlorine Pesticides be exposed to mixtures of chlorophenols. However.69 (2.16) < LOD 90th 5.1) 2..36 (1..8) 4.24-11.13-13. 1995) were similar. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.57 (<LOD-7. as being possibly carcinogenic to humans.4.73 (<LOD-8.4. the 95th percentile urinary 2. the 95th percentile urinary 2.4.27-17. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.4.78) < LOD 1.5) < LOD 12. Radon et al..83-12.atsdr.02) < LOD 7.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.82 (<LOD-32. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.5-TCP.69-18. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al. 2003)..6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.05-8. Neither 2.4.67 (1.60-3.68 (<LOD-8.6) 4.44 (.4.17) 9.37) 16.6-TCP.00-19.16 (.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. 1989).50) < LOD 2.24) < LOD 5.4.html.02-3. The 95th percentiles for 2.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).6-TCP levels at the 95th percentile were up to eight times higher than 3. More information about external exposure (i.53-3.67 (1.32) < LOD 4.24) < LOD 1. Survey Geometric mean (95% conf.. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.920-2.3 mg/L reported in German adults aged 18-69 years (Becker et al. Among 6-11 year old children in NHANES 1999-2000. Urinary 2.78-19.9 (5.79-4. 2003).9) 12. 7.80 (1.24 (3. and other chlorinated compounds.4.05-17.820-2.90 (4. which includes trichlorophenols.46 (1.5-TCP nor 2.11) 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. At lower doses. leukemias. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.47-8.95 (3.8 (5.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * ..4) < LOD 3.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.4) < LOD 3.15) < LOD 2. IARC classifies combined exposures to polychlorophenols.5) 11.88-16..0) 7.64 (4. 2003.44 (1.57 (<LOD-7.4.00) < LOD 4.2 (2.4) 5. 1989).6-TCP as reasonably anticipated to be a human carcinogen.53-3.78 (3.gov/toxpro2.7 (4. urinary 2.cdc. furans.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.19-4.3 (5. environmental levels) and health effects is available from ATSDR at: http://www.4.68-4.6-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.19-12.43) < LOD 12.2) < LOD 5. 2004). Fourth National Report on Human Exposure to Environmental Chemicals 113 ..81 (<LOD-9.74) 11.33) < LOD < LOD < LOD < LOD < LOD 2.. population from the National Health and Nutrition Examination Survey.1 (<LOD-58.00-29.6-TCP had increased rates of hepatic tumors.57 (3. Human health effects from 2.75 (<LOD-6. animals showed hepatocellular abnormalities. NTP classifies 2.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.29 (1.5-TCP and limited for 2.75 (3.0 mg/L.2) 2.4.4.4 (6.6) 4.8) < LOD 9.20-6.24) < LOD 6.5-TCP or 2.37-11.e.86 (3.43 (2.49 (1.6) 4. and lymphomas.28-25. In the same 2-6 year old children.93-11.

00-4.76) 3. 2003).0-18.0 (9.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.4 (17.0-68.0) 14. population from the National Health and Nutrition Examination Survey.36-5.60-3.6-TCP (0.6-22.60-21.4 (9.7) 33.0 (4.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.0 (14.01-6.45 (2.40) 4.6-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. Finding a measurable amount of 2.67) 4.30-2..49 (6.45 (5.20 (3.98-7. Survey Geometric mean (95% conf.52 (2. Urinary 2.8-24.0 (7.1-25.70) 5.6-TCP in urine does not mean that the level of 2.5-TCP or 2.0) 14.59-6.40) 2.4.0 (6.0 (14.0 (8.2 (14.0 and 1. for males in NHANES 19992002 (Agramunt et al.48-26.10-2.0 (8.80 (2.0 (20.6 mg/g creatinine) and 2.57 (<LOD-2. Mean values of 2.5-TCP or 2.89 (3.60 (3.3 (11.40-4.45-9.53) 2.09) 15.70) 5.95) 3.9) 13. Urinary 2.06) * 2.23) 2.4.44) 75th 4. 1991).6 (12.40) 3.0) 10.65) 15.95 (4.0) 10.70-6.3-17.31 (3.. < LOD means less than the limit of detection.5-TCP and 2.26 (2.40 (2.80-20.0 (6.9) 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 2.3) 20.6TCP causes an adverse health effect.40-7.6 (11.87-14.70-6.54) 6.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2. the median urinary 2. similar to the limit of detection for this Report (Anderson et al.4-17.0) 19. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.50-5.4.4.0) 19.20-23.80-7.31) * 2.0) 13.78 (2.09-7.6-TCP exposure and health effects.98-11.6TCP values.0) 6.40-2.90 (3.99) 6.6-TCP level.80 (2.36 mg/g creatinine.91-4.63) 90th 15.5-TCP level of 0.10) 2. which may vary for some chemicals by year and by individual sample.0) 17.0) 7.70-3.65 (5.47 (3.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.5-TCP or 2.20-3.85 (2.0 (16.36 (1.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.72-10.69 (3. In harbor workers exposed to chlorophenol-contaminated river silt.4.0 (13.6-17.78 (2.40-14.3) 23.4.8-13.70) 1.4.32-4.58-3.79 (5.8) 18.4.0-41.0-43.92 (2.08 (2.30) 4.51-12.4.07 (<LOD-3.4.7-16.4 (8.04) 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 2.0 (11.60-37.0 (15.2) 12. 2004).90-8.00 (1.90) 2.32) * 3.9 (13.60) 6.55-3.40-2.10-3.9 (11.0) 13.50 (2. 1998).4.32) 3.90 (4. Biomonitoring data will also help scientists plan and conduct research about 2.0) 11.S.67-12.80) 1.0) 9.5-TCP (0.40) 2.0 (12.. 0.4.0 (6.0 (20.0) 9.60) < LOD 5. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.0) 15.6-19.0) 7.85) * 3..3) 37.7) 21.74 (2.30-33.5-TCP and 2.3.74-3.30-11.8 (9.6) 26. 114 Fourth National Report on Human Exposure to Environmental Chemicals .70 (2.52-3.56 (3.73-9.0) 13. interval) 2.4.0) 17.1 (8.0-38.2-0.24 (2.0 (14.0-54.66 (8.18-3.84) 2.7 (9.10) 6.6) 21.45) < LOD 11. was about six times lower than the median urinary levels for males in this Report (Radon et al.4.60 (3.4 (10.00-21.68 (<LOD-2.7 (13.35-3.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.02) 2.00 (2.7-3.7 mg/L.10 (5.95-6.0) 12.5-46.23-2.58 (1.0-50.4.53) 4.1 (10.5 mg/g creatinine) were similar to the limit of detection for 2.0) 11.40-32.25-11.12) 2.80-6.23) 3. respectively.59) 4.46-3.80 (3.3-26.14 (2.5-TCP or 2.4.28) 24.80-25.3 (11.9) 694 677 519 696 602 931 Limit of detection (LOD.28) * 2.20-6.33-4.40 (2.0-38.00 (4.70) 3.60 (2.4.20 (3.89-6.5-TCP and to the median 2.0 (15. Biomonitoring studies on levels of 2.8-15.75 (8.2) 25.0-44.1) 16.70 (2.30-2.4.20) 4.0-37.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.0) 13.4.8) 32.10-3.6-TCP than are found in the general population. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.

5) 12.19-5.05 (3.88) 4.88) * 2.4 (12.54 (2.6 (10.6) 12.5) 11.38 (2.50 (2.4) 8.6-31.58 (4.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.Organochlorine Pesticides Urinary 2.1-21.38) 22.78 (2.9 (9.25 (3.42 (2.75) 75th 4.4) 4.99-2.7) 6.32 (2.04-16.4) 9.25-2.20-2.0 (11.25-15.92) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.06) 4.6 (12.73) 5.13-6.5) 9.65) 18.0) 10.83-5.09-3.32-19.47-5.87-7.02 (1.0) 8.8) 21.56) < LOD 11.02) 3.5 (7.17) 2.4 (11.5) 8.9-34.51-21.63) * 4.21-11.0 (6.87-6.06-2.6 (6.3) 8.18-2.91 (3.98 (1.43 (2.5-28.18-4.05 (6. Fourth National Report on Human Exposure to Environmental Chemicals 115 .65) 2.5) 11.51) 18.87 (3.8) 11.52 (3.49) 4.8) 12.6 (9.67-17.13 (1.68) 2.9) 8.56 (7.72) 32.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.59 (2.6 (22.91 (7.06) 11.3 (9.22 (<LOD-2.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.10 (6.33 (1.94-13.10) 4.60-2.23) 4.22-2.6 (9.41 (3.8 (7.28-4.23 (1.14-13.25-17.38 (4.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.33 (7.29-4.88-7.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.15 (1.40 (2.9) 7.S.71 (3.77-4.66-4.43 (<LOD-2.63-13.41-6.24 (1.90) 2.56-5.87) 2.73-22.22 (3.53) 4.26 (6.50-8.76) 1.68) 2.04-2.63-15.70-9.62-15.8) 19.88) 4.2 (12.29-4.63) 4. population from the National Health and Nutrition Examination Survey.81-9.6) 13.4.5 (10.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.35 (3.76) 4.88 (2.9-29.46-14.63 (2.2 (13.96) < LOD 4. Survey Geometric mean (95% conf.7) 25.1) 11.8 (8.01 (3.38-5.17-4.00 (3.76-8.76) 2.83-6.53) * 2.22-9.2 (7.89-2.10-9.17) 13.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.29 (6.65-21.3-37.65-2.33) * 2.82-2.30-2.9-64.43-7.91-2.72-16.82 (8.48-2.6 (5.16-10.83 (3.89) 10.9) 19. interval) 2.0 (9.53-11.11) 10.9) 8.1) 14.7 (14.78) 2.42) 2.81) 2.1-32.53 (3.87) * 2.27-9.26-13.14-2.2 (8.49-3.60 (4.22 (1.08-2.52) 2.5 (8.88) 5.40 (7.82 (3.9 (9.51 (2.52) 2.82) 2.2) 19.55-2.83-6.77) 2.90 (1.44 (3.1 (13.52 (5.7-36.88) 1.33-2.1 (8.95-2.9-32.00) 4.78) 90th 12.00 (2.15 (6.6) 8.79-17.98) 10.63 (<LOD-2.00) 4.3-23.25 (3.

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

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

but are regarded as markers of exposure to organophosphorus insecticides. 1981. 2006). and OSHA have developed criteria on allowable levels of these chemicals in foods.. Franklin et al. Urinary levels of dialkyl phosphate metabolites vary with the type of field application.gov/pesticides/ and from ATSDR at: http://www. atsdr. 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.. U.. 1998. 1995. paralysis.epa.S. Franklin et al. FDA. agricultural workers. 1987. six urinary dialkyl phosphate metabolites of organophosphorus insecticides are measured in this Report and other research studies: dimethylphosphate (DMP). Rosenstock et al. the presence of one or more dialkyl phosphate metabolites without additional information cannot be linked to exposure to a specific organophosphorus insecticide. 1997.. Krieger and Dinoff.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites cholinesterase activity in the blood of pesticide applicators as part of monitoring exposure to organophosphorus insecticides. studies (Bouvier et al.S..S. children have slightly higher levels than adults. In some of these occupational studies. chlorpyrifos is metabolized to both diethylphosphate and diethythiophosphate. 1995. For example. Measurements of dialkyl phosphates in urine have been used to document exposure of farmers. Farahat et al. Measurement of these metabolites reflects recent exposure. Aprea et al. Diet influences the measured levels of urinary dialkyl phosphates. and diethyldithiophosphate (DEDTP). 1996. and therefore.e. 2003.. 2005). 2005). pest-control workers. 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. In these studies and the NHANES subsamples. Rothlein et al. and the workplace. 2005). USDA.. 2002. 1998). Pilkington et al. subjects ingesting “organicallygrown” foods were shown to have lower levels of urinary dialkyl phosphates than subjects eating a conventional diet (Curl et al... 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. In nationally representative subsamples of the U. PeirisJohn et al. 2002.. have shown possible subtle or subclinical neurological effects. For example. 1998a and 1998b.gov/toxpro2... without inhibition of acetylcholinesterase). 2003)... as well as mechanistically-related neurodevelopmental and reproductive effects (Astroff et al. Rodnitzky et al. 2000. predominantly in the previous few days. EPA. 1997. 2004. and demonstrate substantial variability when measured Fourth National Report on Human Exposure to Environmental Chemicals . Jamal et al. Mild to severe peripheral neuropathies and residual deficits in neurocognitive functioning can persist following acute poisonings (London et al. Takamiya. and others to organophosphorus insecticides (Davies and Peterson. though in general.html.. EPA at: http:// www. Maizlish et al.. 2004)... 2001. population from NHANES 1999-2000 and 2001-2002 (CDC. Prendergast et al. Biomonitoring Information Urinary dialkyl phosphate levels reflect recent exposure. Engel et al.. 1992. 1988). Few animal studies have addressed the potential for low environmental doses to produce non-cholinergic effects (i. Heudorf and Angerer. 2003.. but not all. 1991. Acute symptoms include nausea. seasonal use of the parent insecticide.. Also. Curl et al. and seizures. Fiedler et al. cholinergic effects.. About 75% of registered organophosphorus insecticides are metabolized in the body to measurable dialkyl phosphate metabolites. dimethylthiophosphate (DMTP).. Each of the six urinary dialkyl phosphate metabolites can be produced from the metabolism of more than one organophosphorus insecticide. Generally. weakness. vomiting. Young et al. the presence in a person’s urine may reflect exposure to the metabolite itself. 2000.. The table shows the six urinary metabolites and the parent organophosphorus insecticides responsible for these metabolites. Chronic exposures studied in farmers and insecticide applicators. dimethyldithiophosphate (DMDTP). Savage et al. 1981).. 2001. diethylthiophosphate (DETP). Saieva et al. Stephens et al. Stokes et al. reported levels of urinary dialkyl phosphates may exceed levels seen in the general population by up to fiftyfold. Animal studies at high doses generally demonstrate the effects of inhibition of acetylcholinesterase mentioned above for acute poisoning in humans. Daniell et al. Therefore. 2006.. 1994)... The U. The dialkyl phosphate metabolites do not inhibit acetylcholinesterase and are not considered toxic. Dialkyl phosphates may also occur in the environment as a result of degradation of organophosphorus insecticides 118 (Lu et al. 1998.. Additional information about insecticides is available from U. worker levels are only moderately higher.. diethylphosphate (DEP). 2006. 1975.S. 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. who have neither past acute poisoning or significant reduction in blood cholinesterase activity.. 1997. Rothlein et al. though various study results are inconsistent (Albers et al. the environment.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. which may reflect changes in exposure. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. collection timing. and these higher levels were associated with a few subtle neurobehavioral test results (Rothlein et al. 2005).. 2003). 2005. median urinary levels of DMTP and DMDTP were more than twentyfold higher than median levels in the U... estimates of dose or intake calculated from urinary dialkyl phosphate levels in studies of pregnant women in one agricultural community (Castorina et al. 2005. and elimination kinetics (Kissel et al. 2006. 2003) generally did not exceed doses considered to be safe. Lambert et al.S. representative subsamples from NHANES 1999-2000 and 2001-2002 (CDC. 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. In a study of farm workers. population as calculated from urinary dialkyl phosphate measurements were below environmental dose estimates based on multiple routes of exposure (Duggan et al.. 2006). except for one study in which DMTP levels were up to fourteenfold higher depending on the season and the type of crop application (Lambert et al. Also.. Petchuay et al.S. population (CDC.. Bradman et al. 2002. 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. 2003) and in another study of workers exposed on reentry to treated orchards (Fenske et al.. Koch et al. 2005).Organophosphorus Insecticides: Dialkyl Phosphate Metabolites over multiple times of day and over multiple days. Fourth National Report on Human Exposure to Environmental Chemicals 119 .S.. 2006). Information is limited with regard to associations between levels of urinary dialkyl phosphates and any health effects. Estimates of dose or intake for the general U... 2005). 2005).. 2005) than those presented in U. 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.

55-6.80) 2.1-23.10) < LOD .03 (.0) 10.955 (.717-1.2) 16.5-17.8) 19.26-6.830 (<LOD-3.2) 471 576 308 664 822 701 814 1122 922 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.0 (4.56 (6.0) 11.290 (<LOD-1.71 (2.17-3.53) 4.89) 9.57-7.52) * * 1.0) 10.0 (8.5 (8.20-4.0) 11.35-12.61) 4.1) 10.80 (2.00-12.20 (.15) 14.00 (4.08-15.60) .0) 11.46) 10.44 (2.19) 9.39 (3.00) 3.1-17.2-20.0-27.40-11.16 (2. interval) 1.56 (1.90-5.757-2.74 (8.05-7.0) 7.00-27.0) 10.0) 12.7) 11.0) 20.40-14.32) 1.97) 8.82-12.10 (.750-1.23-5.21) 9.0 (12.44-38.38-5.4 (7.2 (7.0 (7.50-5.4) 18.20 (2.0 (8.2.2) 14.00 (1.1 (10.72) 5.0 (8.5 (11.11 (.67) 3.2 (7.0 (5.80) 2.0) 15.2 (14.1 (9.6) 7.8) 7.620-1.34-3.98-12.82) 10.79-7.50 (2.10 (.28) 1.43-12.00-27.0) 11.60-25.8) 7.9) 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 1.579-1.99 (5.0) 5.5) 20. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.56 (4.37 (3.4 (9.90 (1. and 03-04 are 0.70) .32 (.40-5.34-7.70-14.0) 6.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.80-4.70) < LOD < LOD 1.9 (8.981 (.2 (7.22 (.00-12.12) 4.530 (<LOD-2.3) 17. which may vary for some chemicals by year and by individual sample.20 (.50 (.5-16.80) 4.8) 11.02) 4.70-11.80-24.7 (12.10 (2.42) .0) 6.758-1.27-3. < LOD means less than the limit of detection.S.840-1.670-1.0) 6.970-2.0 (6.91) 4.0 (7.623-1.80) .01) * * 1.94) 3.8 (9.0-28.00 (5.55-8.35-11.86 (1.2 (9.61 (3.73) * * .4 (9.780) < LOD 3.8-32.98-5.39 (8.0 (7.50 (4.2) 16.600 (<LOD-1.9-18.94) * * . see Data Analysis section) for Survey years 99-00.30 (2.20 (.54 (3.40-19.30-4.9) 14.76 (2.490-2.2 (9.95) 5.47) 5.85 (3.40-1.60 (1.00) 3.1) 13.81) 1.40-16.10-7.12-19.80) . 01-02.700-1.0) 10.58 (5.3) 16.740-2.599-1.20 (.8 (14.66) * * 1.2) 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 1.33 (5.71-9.70) < LOD < LOD 75th 3. population from the National Health and Nutrition Examination Survey.0) 9.83 (5.26-8.50-36.63) 1.36-4.860-2.70-23.13 (2.21 (. respectively.70 (4.27-15.0) 5.70 (2.5) 15.51) 2.30-6.08-2.4) 17.60-11.74 (8.80) 11.0 (6.1) 95th 13.890 (<LOD-2.30 (4.0) 5.60 (5.3-15.810-1.0 (9.70-19.10) < LOD < LOD 4.13-2.86-15.93-24.04) < LOD 1.81) 11.52) 6.2 (11.2 (14.2.81) 11.08 (<LOD-2.30 (2.48-7.4 (7.0) 10.56-13.8 (8.80) 3.80 (4.16) 4.20-7.13 (2.47) * * 1.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.3) 14.80-22.954 (.33-18.90) 3.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.60-18.6) 18.35-16.68-7.97) 90th 7.58 (2.15-12.58 (3.290 (<LOD-. 120 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.00-19.0 (7.40 (.9) 8.42-3.02-5.52-11.20-30. and 0.79 (5.10 (2.96-3.60) < LOD < LOD 4. 0.26 (5.8 (12.29) * * 1.07-10.00-7.4) 20.44-3.1.50) 2.80) 2.14) * * .90-4.7 (14.93 (4.90) 2.45 (2.0 (9.

61-13.84) 7.56) 7.37-3.31-14.60) * * .7 (8.66 (2.960 (.53 (6.07 (.574-1.45-11.0) 7.61-29.23) 4.3) 15.44 (2.57) 4.440 (<LOD-2.28 (5.53-11.1 (10.75) 14.570-1.01-2.83) 8.02 (2.98) .780 (<LOD-1.7) 672 678 472 509 695 577 595 948 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.06-2.32-12.5) 11.60) 2.03 (2.69) 4.29) * * .85 (6.1) 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 1.62-5.43 (.549-1.88 (5.5) 8.66 (1.56) .38 (1.5) 7.92-5.90-8.5-32.78 (2.60-9.94 (4.9 (5.03-6.30 (1.7) 471 576 308 664 821 699 814 1122 921 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .47) * * .47 (1.6 (10.34 (6.8) 16.883 (.82-6.8 (10.28-9.87-5.710 (<LOD-1.95) 2.94-10.75 (7.80 (7.15-10.94-23.1 (6.02-14.42 (3.87 (1.23 (4.820 (.2) 8.89) * * 1.5) 7.10-13.40-3.54-11.6) 9.8) 8.53) 9.5-13.2 (8.34 (6.960 (<LOD-2.6 (9.1-15.13) 4.6) 13.6) 11.11-6.8) 6.8) 7.37) 9.7) 18.09-11.00 (4.98) 9.608-1.88-10.37 (4.39 (2.560-1.40-5.67) 4.76) < LOD .5 (4.19 (4.50) 7.533-1.94-9.69-10.35) < LOD < LOD 3.94-22.71-2.79-9.36) * * 1.58) * * 1.21-23.98) .54-2.818 (.73 (1.14 (3.890 (<LOD-1.2 (6.00-19.924 (.93-9.42) 12.66 (5.92-2.41) .84 (5.5) 12.9) 11.890 (<LOD-1.2 (10.633-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5-20.77 (6.88-15.98-5.66-15.45-5.870-2.67) 1.773-1.3) 5.30) 2.2) 13.46-5.41) Selected percentiles ( 95% confidence interval) Total * * 50th .80 (6.75 (3.7 (9.79-3.45-5.40) 4.09 (.43 (3.1) 4.6) 8.750 (<LOD-1.830-1.03 (7.72) 11.10 (3.40-28.18 (.35 (1. Fourth National Report on Human Exposure to Environmental Chemicals 121 .95 (3.28) 10.51-5.52) 4.S.4 (4.650-1.75-7.00) 8.02 (7.28 (4. population from the National Health and Nutrition Examination Survey.510-1.74) 90th 7.29 (2.87 (3.790 (.1 (7.37-5.61 (1.94 (2.57 (6.40) < LOD < LOD 75th 2.1 (9.89-3.25) 6.920 (.500-1.38) .860 (.932 (.28 (2.4) 4.56) 4.31 (3.9-28.0 (8.56-13.27) < LOD 2.04 (1.71) 10.9) 12.7) 5.0) 6.88) 2.05 (.25) < LOD .76-4.47 (3.3) 12.9 (9.996 (.34) * * .3) 16.54-4.66-34.81-5.540-1.74) 4.05 (1.00-13.5-16.46) 2.41-12.2) 7.83 (7.47) 2.00 (4.4) 13.3) 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 1.47 (3.69 (4.04-6.4) 4.57 (4.57-10.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.09) 2.98 (3.34) < LOD < LOD .8) 12.430-1.54-15.20-8.02-2.4 (9.1 (11.1) 4.2) 5.2) 9.75) 2.61 (1.2) 5.62) .93) 9.900 (.7) 12.82-26.98-22.40 (3.9) 16.82-14.40-14.24-3.55-20.68) < LOD < LOD 3.69) 2.54) .68-4.9 (9.80 (2.1 (8.566-1.90-5.67-19.26) * * .00-17. interval) .620-1.05) .855 (.43) 2.64-5.81 (1.37 (5.2) 95th 12.85) 2.82-14.7 (10.03) 2.93-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 9.03) 2.40-12.

80) .81-6.70-8.9 (12.00-4.31) 1.5-26.30) 3.0 (15.70 (1.90 (6.8-20.27 (3.0 (10.0) 11.7) 14.70-9.90-15.40 (2. 122 Fourth National Report on Human Exposure to Environmental Chemicals .2 (7.27) .0) 9.0 (9.90 (6.70 (8.8) 8.27) 4.7) 15.42 (1.22 (6.5) 21.34-10.75 (3.9) 95th 14.20-8.5 (8.8-20.62-17.75 (2.1 (10.40) < LOD < LOD 75th 2.67-10.89) 2.35 (6.66-13.78) 5.58 (1.00) 8.6) 14.0 (14.50-4.7) 16.90-15. and 03-04 are 0.790 (<LOD-1.90-9.80-4.17 (7.0) 12.0) 13.30) 3.70-5.30) < LOD < LOD 4.50) 5.01 (2.S.16-1.50-5.00 (.0) 6.31-7.64) 10.00-18.7) 22.80-14.80) 5.0-24.20) 3.34-5.80-6.00-4.3) 14.95-9.47-6.59-3.34-3.98-9.10-15.6) 18.96) 3.6-41.4) 7.15-6.90-31. and 0.67) 3.90) 4.80) .97-4.3) 8.90 (1.0) 23.33-11.580-2.84-4.52 (6.740 (<LOD-1.61-32.670 (<LOD-1.67) 4.5) 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 * * * * * * .60) < LOD < LOD 2. see Data Analysis section) for Survey years 99-00.51) < LOD 1.00-16.66) 4.4-17.18) * * * * * * * * 1. which may vary for some chemicals by year and by individual sample.910 (<LOD-2.22-12.80-8.70) 2.2) 14.3 (9.99 (3.88) 3.24-5.31-12.1 (10.4) 11.0) 13.89 (2.6 (10.29-4.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0) 14.41) 3.34 (6.00-9.0 (10.3 (9.8) 9.7-19.00) 3.80-3.72) 2.3) 10.90 (5.20-18.86-10.15-2.0-19.46-4.3) 20.20) 3.12 (4.80-21.1) 11.6) 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 * * * 1.63-14.73) 7.90) 8.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5. respectively.22) 8.0) 9.20 (<LOD-2.970 (<LOD-2.60 (6. 01-02.4 (10.680 (<LOD-1.06 (2.27) 9.0-24.77-14.9) 10.3 (12.8-17.90 (2.30) 8.1-23.0 (5.25 (2.39 (5.0) 7.4 (14.28 (7.0) 14.9) 9.39-13.82) 8.6-19.30) < LOD < LOD .35) 4.58.0-29.74) * * * * * 1.40 (2.27 (7.6) 11.3 (6.20) .650-1.41-5.0 (8.9) 16.6 (10.37) 2.8 (12. 0.4 (10.9-14.80-12.0) 12.7) 10. < LOD means less than the limit of detection.90 (2.46-28.7 (11. population from the National Health and Nutrition Examination Survey.18 (3.11-6.3) 22.45 (3.90 (6.2 (9.7-21.80 (5.9-15.5 (8.95 (5.0 (7.00) < LOD .80 (2.10 (.9-17.00) 7.96) 90th 7.0) 18.90 (6.5.0 (9.8 (12.80 (2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .22 (6.8-21.6) 14.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3 (11.670 (<LOD-1.20-4.60 (2.00-18.7 (10.9 (7.0 (13.5 (9.35-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.90 (2.61 (3.00) 3.50) 3.24 (2.14 (6.0) 19.10) 6.10-10.77-3.0) 12.29) < LOD < LOD < LOD < LOD 3.04 (3.92) 9.88) 10.49-4.70-9.92-17.10 (<LOD-1.10-4.0-33. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.670 (<LOD-1.3 (7.670 (<LOD-1.0) 11.60 (5.95 (2.50) .37 (3.53 (3.

7) 14.1 (8.32) 2.21) * * * * * 1.30) 2.94-14.6 (13.48 (2.30) 7.71) < LOD < LOD 2.64-11.7-19.25-9.16-14.23-3.780-1.920 (<LOD-1.36 (2.27) 1.68) .4) 16.78 (6.78) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.83 (6.4) 9.3-15.7) 9.54 (7.29-2.8) 14.79-6.1) 20.27) 5.810 (<LOD-1.99 (4.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .82-11.4-16.54-5.21-21.63 (6.70-2.94 (5.38-13.9-17.97) < LOD .0 (10.00) 2.01-5.39-17.83 (7.59-3.89-3.4 (11.09-11.5 (11.88 (1.4-15.78-10.1) 13.42) 7.07 (5.33) 3.00 (<LOD-1.03) 3.89) 5.2) 8.86) 9.9 (9.1 (19.620 (<LOD-.11 (5.51-10.55 (2.28 (1.06) .77 (2.74-19.89 (3.75-3.33-10.3-21.79-9.6-19.70-35.1 (13.3) 12.940) < LOD < LOD 1.7 (11.8 (10.16 (3.38 (2.93 (6.07) 2.74-4.2) 10.7 (8.6 (13.4) 15.2) 16.0 (13.51-7.3) 8.5 (9.3-17.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.07) 2.38 (.S.77) 3.00 (2.0) 14.5) 8.7) 14.41 (7.99) 2.2) 12.4-16.2) 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. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .93-10.6) 6.00 (5.86 (3.6 (11.00 (3.20-3.32-8.6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.91-9.38) 1.590 (<LOD-.973 (.88-7.92) 3.81 (7.04) 9.71 (1.27) < LOD .28) 6.18) 2.05-3.530-1.3 (7.73 (5. population from the National Health and Nutrition Examination Survey.93 (2.9 (9.34) < LOD < LOD < LOD < LOD 3.5 (15.6 (11.91) 3.52-3.3) 9.67 (1.2-30.2 (9.12 (7.69-11.54) 9.5 (10.2) 12.0 (11.5) 22.92 (5.37-5.00 (7.45) 6.80) 3.12) < LOD < LOD 4.82-8.06 (<LOD-1.44-6.11-3.67 (7.950) .68-10.29 (5.29) 3.4) 6.3) 6.89-13.7) 15.0-21.55) .87 (3. Fourth National Report on Human Exposure to Environmental Chemicals 123 .50 (6.55) 16.3-17.89-3.4-18.34-18.07-3.42-19.2) 12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.38 (1.8 (8.2-15.2) 15.97-4.03 (6.09-11.42) 8.9-25.61 (2.9) 19.30-5.890-2.47-9.50-17.00 (<LOD-1.30) 8.95) 3.6) 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 * * * .53-8.690 (.77 (2.7-23.89 (2.4) 7.72) 4.5) 10.63 (2.43 (2.0 (8.93 (<LOD-2.8) 11.5) 13.28-12.95) 90th 8.850 (<LOD-1.29 (2.7) 12.760 (<LOD-1.15) < LOD < LOD 75th 2.72-4.4) 7.4) 7.25 (4.2) 19.02-4.85-17.0-19.78 (4.68-4.75-3.7 (10.6) 12.1) 10.5 (8.8) 16.5-17.6) 14.6 (12.68-19.03 (2.27-13.58 (4.89-10.37) 3.86-3.2 (9.9 (9.85-8.19) 3.6) 7.9) 16.6 (10.6) 13.95 (2.27) * * * * * * * * 1.00) 8.96-11.45) 3.910 (<LOD-1.3-34.7 (10.14 (2.15 (1.6) 95th 16.96-10.

22 (1.10) 1.90-4.69-4. and 03-04 are 0.570) * .570 (<LOD-.73-5.37-2.19-1.2.04) .670) .550 (.303-.990-1.720-1.50-2.800 (.20 (1.740 (.83) 2.500 (<LOD-.449 (.01-1.50 (1.30 (1.359-.22-3. respectively.70-7.680-1.90) 2.00) 2.89) .201-.49) .30) 2. population from the National Health and Nutrition Examination Survey.618) * .63 (1.58 (1.353-.34) 2.760 (.33-2.31) 2.35) 1.1.75 (2.11-3.570-1.20) 3.80) 3.350-.425 (.690-.39) 2.50 (1.20 (2.05-2.31-3.930-1.949) .13) 2.83 (2.580-.50-2.20-2.95-5.40 (1.30 (.80) 3.80) 2.27 (2.17) 1.740 (.455 (.55 (3.18 (1.20-2.10) 1.585) * * .97 (2.41-5.30 (.87-3.03) 1.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.970) .600-1.160 (<LOD-.80) 3.77-2.390-.59-6.700) .14-1.910-1.11-3.45-4.42-2.350-.22-8.960) 1.76 (1.880 (.10-1.850) < LOD .22-2.570 (.70-2.90) 2.260 (<LOD-.759) * .740-1. which may vary for some chemicals by year and by individual sample.83 (2.910 (.89) 471 575 296 664 822 690 814 1122 919 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .880) < LOD 75th .46) 1.710 (.47 (1.34) 2.336-.600-.29) 1.450 (<LOD-.00-4.68-5.80) 5.690 (.65 (2.80 (2.00 (1.17-4.45 (1.10) 1.46 (2.29-2.70 (1.780) .60 (2.90 (1.48 (2.398-.00) 1.80) 2.74-5.930 (.S.05-3.50) 1.73 (1.16) 2.30) 4.20) 2.960) .930) < LOD .89-6.86) 3.620-1.94 (2.780 (.380-.940) < LOD .510 (.570 (<LOD-.22-3.48 (1.453 (.790 (.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.810) .960) .960-1.657) * * .720 (.20 (1.26 (2.90) 3.32) 3.820 (.61 (1.57 (2. 124 Fourth National Report on Human Exposure to Environmental Chemicals .26) .592) * .490 (<LOD-.210 (<LOD-.980) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.73 (2.10) 3.587) * * .04) 1.79) .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 * .01-3.750-1.40 (1.382-.650-.78) .50 (1.60-4.98-3.710 (.16-3.15) 2.690) .680-1. < LOD means less than the limit of detection.77 (1.570 (.09 (.31) 95th 2.820 (.960 (.750) 1.08 (2. 01-02.549 (.32-1.388-.59-2.60) 2.74) 3.30-3.30 (.380-.690-1.20) 1.950) 90th 1.83) 1.20-1.86 (1.30) 1.45 (1.25-1.23-3.27 (3.20 (1.45 (2.592) * 50th .91) 2.14 (1.340-.580-1.280-.390-.76-6.830 (.30-1.49) 2.32 (1.46-3.54 (2.17) 1.60) 3.970) 1.64 (1.94 (3.550 (.80 (1.50 (1.30-3.560-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.597) * .50 (1.01) .380) . and 0. 0. interval) Selected percentiles ( 95% confidence interval) Total * .700) .600 (<LOD-.467 (.54) .459 (.21) 3.10-1.730) .930) 1.94) .20-3.83) .46 (1.440-.505 (.08 (2.860) < LOD < LOD .20) 3.720-1.880) < LOD .47) 2.98 (2.57 (1.18 (.70 (1.20) 1.98) .240 (<LOD-.400) .41 (2.590-.910) 1.749 (.09.96-3.710) .460-.30) 4.592-.840 (. see Data Analysis section) for Survey years 99-00.95) 2.89) 1.38) 1.79) .20) 2.70 (1.510 (<LOD-.96-5.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .740-.88) 1.584) .13) .95 (2.343 (.00-2.75-2.457 (.780 (.540 (.36-4.16) 1.31-3.54-2.15) 2.

09) .77 (3.39) 2. interval) Selected percentiles ( 95% confidence interval) Total * .32) 1.82) 2.05-4.07) 1.320-.49 (1.690) < LOD < LOD .550-.14 (2.66) .80) 2.590) * 50th .44) 2.00 (3.990-1.22-3.688) * .16-2.60) 1.370-.400-1.55-3.06-2.17) 2.710 (.368) * .870 (.830 (.820) 1.11-2.22-2.700 (.43) 2.84-6.38 (1.08-2.30-2.20-2.742) * * .81) 2.510 (.70 (2.310 (<LOD-.17) 2.20) 1.22) .04) 95th 2.67) .470) .00-3.720-1.640 (.393 (.760) .67 (1.39 (1.38 (2.800) < LOD .750 (.790) .70 (3.06) 4.550) .830) 90th 1.41 (.04-1.78) 3.580) .75-3.250 (<LOD-.285-.00-1.350) .980-1.22) 1. population from the National Health and Nutrition Examination Survey.82 (2.71) .50) 1.11 (.76) 1.08-3.08-3.61) 2.820) .05 (1.460 (.540-.490 (.71) 2.77-4.270-.31-1.08) 2.23 (.870) .32 (.335-.460) .11) 1.23) 2.850) 1.24) 4.08 (.22) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07-3.07) 1.94) .47-4.53) .97) 1.520 (.32) 5.560-.77-3.42 (.515) * * .88) .640 (.348-.790 (.560-.480-1. Fourth National Report on Human Exposure to Environmental Chemicals 125 .32-1.80) 471 575 296 664 821 689 814 1122 918 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .05) < LOD .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 * .75) 6.44-2.50 (1.04-5.400) .33) .47 (1.67) 1.645) .710 (.29-4.136-.97 (1.630) * .61 (3.38-3.43) 1.25-3.97) 672 678 478 509 694 552 595 948 744 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.08-3.300 (<LOD-.10) 2.750 (.318-.300-.55 (1.57-4.71 (1.67-3.42-8.403) .940-1.66 (2.90) 2.64 (2.520-.560 (.740) < LOD 1.33 (1.453 (.08-3.448 (.61-3.63 (1.42-6.380) .79 (1.535 (.75 (2.57-2.380-1.72-4.69 (3.23) 3.60) .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.52 (1.372 (.98) 1.64 (2.13 (1.800-1.08-2.32) 2.73-3.92-8.57 (3.485) * * .730) .580 (.597) * .72 (2.47 (1.08 (2.930-1.43) 2.509 (.591 (.87 (2.16) 1.840) 1.02-6.43 (1.57 (1.460-1.740) .760) < LOD 75th .180 (<LOD-.739) * .390-1.700 (.02-3.19 (1.330-.72) 1.99) 1.840) 1.97 (1.05) 1.36) 3.22-3.840) .480) .720 (.07) 5.52) 3.310 (<LOD-.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 * .234 (.61-3.580-.377-.03-2.60 (2.65) 2.60 (1.07 (.03-1.412-.510 (.470 (<LOD-.440-1.23) 2.390) .550-.710 (.30) 3.910) < LOD .79) 1.97) 2.62 (2.550-1.75 (1.270-.250 (<LOD-.230 (<LOD-.670 (.380-.58-6.45 (1.69 (1.444-.73 (2.42) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.700 (.660-.58 (1.20-7.17-2.510-.89 (1.58) 3.08) 1.640 (.18-2.72 (1.16-1.89-3.45 (2.88 (1.95) 1.950-2.500-.920) .270 (<LOD-.330 (<LOD-.590 (.67 (1.34 (1.91 (1.552 (.92) 3.23) 1.530 (.22 (2.310-.680 (.62 (1.280 (<LOD-.07-2.320-.84 (2.28 (1.590-1.471-.880) 1.99) 2.92 (1.305 (.900) 1.253-.08-2.S.05-2.447 (.07) 1.02-3.49-4.

0) 3.2 (12.8 (12.90-8.23-2.00 (.29) 2.44-7.78) 9.41) 1.1) 38.3 (14.0) 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 2.25-3.70) 1.0 (38.3) 38.6-45.2 (19.5-20.16) 2.50-2.41 (1.0-92. and 03-04 are 0.1 (26.5 (24.0) 4.7 (12.0) 16.0 (6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.35-6.1) 140 (46.83 (1.9 (19.9 (27.0 (38.23-2.8) 41.21 (4.76 (2.0) 17.20) 1.3 (12.4.0) 28.2-47.52 (4.40) < LOD 2.11) 2.3 (23. see Data Analysis section) for Survey years 99-00.13 (1.0-47.29-9.0) 6. and 0.40) < LOD 1.93-3.0) 18.88) 3.5-45.19-2.8 (12.64-3.1-40.0 (38.8-24.0-43.48-2.30 (. 126 Fourth National Report on Human Exposure to Environmental Chemicals .71-2.0 (13.1) 38.19) 2.0 (38.6) 52.9) 48.11 (4.02 (2.12) 1.0-53.10 (7.74-2.96) 5.0 (38.0 (7.18) 14.48-2.610 (<LOD-1.2-39.1-20.660-2.0-69.8 (26. respectively.0-50.4) 38.29-4.44) 3.0) 3.6 (9.81-2.7) 47.83 (3.36-2.48) 5. < LOD means less than the limit of detection.18.0-52.9-51.1 (10.21 (3.63-6.46 (.53) 40.0-31.4) 19.43-7.71 (4.06) * 2.50 (2.6-27.66-5.04-8. population from the National Health and Nutrition Examination Survey.0) 15.41) 1.6-54.7 (12.0) 19.1 (11.16) * 1.7-22.0 (38.600-2.14) 5.7 (28.0-29.1-46.64-8.0-110) 42.0) 42.59 (1.91 (4.2) 16.0-110) 34.05) 1.78 (1.4 (19.80-2.0 (33.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 8.23) 9.21 (1.0-58.59 (1.45) 2.12 (3.90) 11.85) * 2.99 (2.0-53.0) 32.13 (1.1 (25.3) 28.88) 1.10 (1.2-27.46-6.5-74.54 (1.10-4.98) * 2.0 (21.92-5.6-22.05) * 2.5-27.0) 3.0-230) 35.1) 95th 48.17-2.58-2.31-6.8-21.27-6.0) 3.3 (24.9 (19.470 (<LOD-1.70) 1.20 (2.97) 6.87-7.8) 62.50-20.0) 20.32 (2.85 (1.58) 16.86 (1.67 (1.9) 17.98 (1.4-76.53) 1.5) 30.60 (2.40-4.70 (7.2-62.79 (1.0-260) 34.1-19.30) 11.80) 1.70) 5.0 (38.5) 69.40-16.70 (1.3 (10.46-2.50-5.79-2.00 (.41) 5.9-21.20-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.61-2.10) 39.41-4.75-14.45) 2.13) 12.70 (.0-41.04) 3.83-2.9 (23.42) 1.72 (1.77 (1.71) 5.0 (8.92) * 2.57-2.57-2.69) 2.0 (17.0 (40.0 (24.90 (1.1 (25.10-13.95 (5. 01-02.94 (1.05-3.S.61 (1.0-39. which may vary for some chemicals by year and by individual sample.0-62. interval) 1.9 (10.9) 38.10) .33 (5.0 (20.80) < LOD 1.7-41.0 (8.0) 15.0-41.44) 2.0) 13.0) 16.10 (1.0) 5.86-3.26) 75th 11.07-5.83-2.830-3.0 (20.10 (1.0) 4.79 (2.9) 18.2-33.1-25.690-3.30-14.2-80.70-17.0-49.8) 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 1.3) 33.4-22.90 (1.76 (2.0 (37.2) 31.0) 31. 0.8) 32.0-39.5.0 (8.50-17.54 (3.18) 6.50-7.0 (26.7) 20.60) < LOD 1.0) 4.04 (<LOD-2.80-18.3 (12.1-47.30) 4.80) 90th 38.530-4.0 (32.0-41.1) 18.10 (1.8 (22.40) 50th 2.0) 45.06 (1.49-2.26 (.6 (26.8) 39.53) * 2.82 (1.2-26.4 (15.0 (11.6 (15.2-27.70-6.4 (10.6 (11.830-4.53 (1.70 (1.81-3.0) 20.77) 38.0) 28.0 (25.18) 20.44) Selected percentiles ( 95% confidence interval) Total * 2.0 (19.5-40.1 (22.80) .0-62.65 (4.09 (4.3) 26.3) 31.0) 17.0) 33.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.0) 30.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00-24.0-58.

0 (19.29-5.9-37.0 (23.23-1.83) .23) 37.80-8.69-18.46-5.61 (1.60) 4.870-3.9) 54.38-1.37-2.40-7.6 (24.70 (1.28) 1.31) 2.64 (1.2 (21.02 (.03) 1.0) 10.54-2.1) 25.6) 7.44) 9.12) 3.58-2.2-28.2) 41.1) 36.99-4.6-38.88 (1.55 (2.4) 3.2) 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 1.51) .2 (8.76-2.7 (18.8) 11.18) 3.4-34.9-52.02) * 1.16 (1.88 (1.34) * 1.0) 3.41 (2.72) 2.00) 1.79-17.96) 2.6) 112 (40.0 (14.14 (.40 (5.3-22.1) 25.28 (1.71 (1.95 (2.0) 952 1187 945 996 1330 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.6-32.88 (4.9) 3.32-3.00) 6.3) 13.0 (17.91-2.19) 5.7 (18.07) 9.1 (50.7-47.899-2.60 (.08 (1.07-2. interval) 1.71-2.8-45.70-4.1-60.19) 5.16-2.7-109) 22.2) 13.68 (1.2) 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.6) 3.22-3.67-3.46) 1.54-15.2) 33.6 (27.22 (.2) 13. population from the National Health and Nutrition Examination Survey.51) < LOD 1.06) 75th 9.2 (15.32 (3.4 (5.8) 23.6 (7.0) 47.4) 14.5 (15.1 (33.5 (41.7-20.30) 28.75 (1.94-20.00-16.6) 11.33) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.83 (.0 (25.5-190) 30.S.67 (1.9) 24.95) 90th 32.1) 13.5 (15.36) 10.0 (6.25-3.1) 52.37 (1.9-95.33) < LOD 1.67-16.35) .890-4.0) 48.03-2.5) 27.2-38.7 (11.5 (34.1 (34.75) * 1.670-1.7 (24.48 (4.75 (1.94) 19.4 (25.06) 1.00 (4.0 (32.0) 25.1) 27.3 (8.47 (1.16 (1.9-18.6-51.21 (4.1) 13.15 (.3 (10.7) 15.8) 15.23) < LOD 2.27-3.8) 31.50-5.43) * 2.9 (10.7-37.35) 1.5 (13.66 (1.3-19.47 (3.40 (2.5 (8.06) 1.680-4.7) 26.82) 1.80 (1.4) 12.9-36.8 (7.57 (6.2) 36.27) 50th 2.22-2.8-34.7) 61.3-42.3 (10.33-5.6) 19.9 (26.8) 32.26-2.9 (19.14-8.0-71.50 (2.58-17.2-47.5-36.66) 8.62) 4.88 (4.2 (22.59-15.53) 1.11-2.2-70.1 (25.56) 1.93) 5.35 (2.07-2.19-6.4 (19.43-12. Fourth National Report on Human Exposure to Environmental Chemicals 127 .84-13.870-3.2 (9.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.47-17.0 (23.86) * 3.4-71.9) 24.96-16.36-13.9 (39.27 (6.69-5.20) Selected percentiles ( 95% confidence interval) Total * 1.9 (13.36 (4.52-4.6) 3.16 (1.52 (1.20-5.46-6.1) 27.7 (10.95-16.0 (39.63-5.40-4.71) 8.7-38.860 (<LOD-1.79 (2.24 (1.1) 17.94) 1.86) * 2.6-49.59-2.38-5.930 (<LOD-1.27) 10.90 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.18) * 2.7) 95th 51.5) 70.08) 1.5 (6.9 (7.4-21.06-1.56 (2.1-63.0) 13.8-37.1-22.0) 30.82 (2.38) 5.22 (2.7-19.7-43.1 (39.95-16.5-43.67 (1.750 (<LOD-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) 34.19-14.8-26.7) 66.66 (1.870-3.4 (11.45-1.3-27.02) 1.91 (6.5-97.1) 15.2) 4.61-22.5 (17.45 (1.7) 23.68) 47.9) 12.3 (20.57) 4.8) 3.97 (1.6 (11.01 (.59-2.61-2.6) 23.48) 1.12 (1.18-1.4) 12.0-40.26-4.4-67.4 (12.09 (5.2-34.11) < LOD 1.4 (9.3 (9.4 (25.8-43.3) 28.4-39.75-6.43-2.9) 3.0-70.17-3.888-1.0-118) 29.4 (21.46-22.9-41.62 (2.1 (12.19 (1.33) 1.39 (1.2 (16.17) 2.38 (3.7) 30.

090 (<LOD-.410) < LOD < LOD < LOD < LOD .700-1.400-.00) .870 (.490 (.470-1.460 (.510-1.15) .990 (.730) .380-.110-.870 (.450 (.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.290) < LOD < LOD < LOD < LOD .540) Sample size 1949 2516 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .140-.10) .099-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.830) < LOD .290 (<LOD-.370-.610 (.390 (.160) .610 (.230-.05.090 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .090 (<LOD-.580) 471 576 310 664 822 717 814 1118 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .370-.550) .770 (.190 (.117 (.740) < LOD .100 (.850) < LOD .171) * * . 128 Fourth National Report on Human Exposure to Environmental Chemicals .180) .60) 1. 0.450 (.700-1.440-1.1.130) .32) .870) < LOD .10) .570) .162) * * * * * .30) .350) < LOD < LOD < LOD < LOD .770) < LOD 95th .820 (.080 (<LOD-.870 (.42) .640-1.540) .640) .1.680 (.540 (<LOD-.130-.03) .410-.310 (.830 (.42) .140-.930 (.380-. respectively.850 (.650 (.630 (.450 (.760) < LOD .820 (.260 (.680-1.140) .690-1.290) < LOD < LOD < LOD < LOD 90th .640) .650) .410-1.160) .530-.780) < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) .650) .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 .58) .610-.650-1.090 (<LOD-.310 (.120-.050-.130-.420-.130) .36) .680-1.10 (.120-.300-.310-.630 (.540) .080 (<LOD-.S.850 (.13) .640 (.310) < LOD < LOD < LOD < LOD .860-1.320-.610-1.360-.220 (.360-.330-.120 (<LOD-.300-1.680) .230) .720 (.240 (<LOD-.840) .130-.830 (.310) < LOD < LOD < LOD < LOD .40) .940 (.870 (.320 (.10) .470 (.730-.350) . population from the National Health and Nutrition Examination Survey.220 (<LOD-.30) .130 (.560 (.210 (.990) .600 (.090 (<LOD-.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks . see Data Analysis section) for Survey years 99-00.380-.200) < LOD < LOD .560 (. 01-02.090 (<LOD-.720-1.390) < LOD < LOD .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.190 (.860) .280) < LOD < LOD < LOD < LOD .150) .150 (<LOD-. < LOD means less than the limit of detection.650-1.660 (.840) . and 03-04 are 0.20) .700-1.410-.430 (. and 0.870 (.190 (.990) .084-.700-1.620 (.430-.170-. which may vary for some chemicals by year and by individual sample.270 (.140-.830) .160-.900 (.210 (.460-.12 (.720) .

730) .140-.260-.410 (.580 (.170 (.580) .300-.610-1.330-.300-.60) .360-.600-1.29 (.03) .14) 1.170) < LOD < LOD .210 (.200 (.360-.380-.270 (.650-1.490-1.250-.S.58) 1.230) < LOD < LOD < LOD < LOD .110) .110) .740 (.270) < LOD < LOD < LOD < LOD .330-.730 (.02-1.740) < LOD 1.990) .940) .080 (.880-1.03 (.380-.670 (.730) .500-1.570-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.760) .870) .730) .460 (.230-.810 (.380-1.280) < LOD < LOD < LOD < LOD .070 (<LOD-.670-1.220) < LOD < LOD < LOD < LOD .540) .050 (<LOD-.190-.200 (.084-.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 * * * * * * .161) * * .400 (<LOD-.290) < LOD < LOD < LOD < LOD 90th .550 (.38) 1.390-.100-.070 (<LOD-.340-.310) < LOD < LOD < LOD < LOD .230 (<LOD-.140-.470 (<LOD-.710-1.700 (.03 (.86) .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 * * * * * * * * * .057-.86) .24 (.110-.330-.410) < LOD < LOD .360) < LOD < LOD < LOD < LOD .116 (.720 (.080) .02) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.140-.400) .570 (.600) .140) .380-.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.440-1.700-1.750) < LOD 95th .540 (.110) .880 (.500 (<LOD-.640-1.570-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .410-.12) < LOD .01 (.060-.111) * * * * * .780) < LOD 1.410) .700 (.850 (.090 (<LOD-.190 (.660-1.67) .03 (.150-.330 (.070 (<LOD-.550 (.580 (.120) .390-. population from the National Health and Nutrition Examination Survey.720 (.78) .370 (<LOD-.650) < LOD .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.180-.510-.410 (.860-2.780 (.800-1.100 (<LOD-.960) .440 (.670 (.070 (<LOD-.450) .320 (<LOD-.220 (.380 (.410-.580) < LOD .09) .970) .700) .520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .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 .540 (.24) .120) .66) 1.090 (.360 (.140-.140-.860 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .260) .520-.500) .450 (.62) 1.940) .190 (.560 (.080 (<LOD-.36 (1.20) 1.890 (.580-1.240-.170 (.990) .19 (.43) .300 (.110) .860 (.330 (.00) < LOD .

800-4.0-38.20) < LOD < LOD < LOD < LOD < LOD 1.960 (.07 (3.90-9.850) 16.94-3.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.60) .20 (1.0 (5.0 (17.11) 13.730 (.30 (.90) .94-8.0 (6.90-20.0 (5.0) 4.30 (1.67 (1. see Data Analysis section) for Survey years 99-00.67 (2.74) 5.20-4.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.49) 17.47 (3.68) 2. and 03-04 are 0.750-2. < LOD means less than the limit of detection.0-40.55-4.40 (1.66) 4.87) 12.83-3.960 (<LOD-1.0 (17.30 (1.3) 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 * * * * * * * * * .35) 11.0) 2.36-3.480-.610 (.28) .40-7.86) 4.00-17.21-3.40-8.74 (3.6) 5.40 (1.49 (1.36-3.53) 20.07 (3.1.32-9.23-6.30-7.01) 5.10-9.00) 1.48) 13.0 (3.880) 5.15) 19.30 (1. which may vary for some chemicals by year and by individual sample.0 (17.28) 1.30) 95th 19.360-1.0) 5.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.03 (.370-.740 (.0) 5.45 (2.20-4.59-5.510-.97) 20.640 (.0) 4.30 (2.800) 90th 13.07) 1.87) 5.13 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60) 1.46 (1.99 (1.910) 2.691 (.0 (17.40-20.05 (3.900 (.30-6.11) .0 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.62) 471 575 306 664 821 699 814 1122 925 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .10 (3.39) .14) .840-3.0-38.21) 3.0 (7.67) .0-44.1.10-3.88-3.00) .640 (.620-1.90-28.38-3.90-37.50) 2.63 (3.10 (.40-4.11 (1.0) 2.97) 20.0) 2.61 (1.50) .42) 2.00 (.80 (4.250 (<LOD-.53 (2.90 (2.51-8.42) .12-1.0) 3.0 (4.52 (1.31) .55-8. population from the National Health and Nutrition Examination Survey.70-50.05-3.35-10. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.94 (1.S.610) < LOD < LOD < LOD < LOD < LOD 2.40) 2.83-3.90 (1.190-1. 130 Fourth National Report on Human Exposure to Environmental Chemicals .890 (.380-.35) 5.00-17. 0.00) .870) < LOD < LOD .14-5.0-39.26 (2.0 (17.800) 17.52) 5.20 (1.99) 19.260-.30-3.28-9.15) 14.29-10.690 (.0) 7.18) 1.400-1.350-.00 (1.0 (5.90) .07-3.63) 32.330 (<LOD-1.0-40.170-1.70-30.0) 5.0) 5.0) 2.600 (.85-3.07-3.720) 2.840 (<LOD-1.0) 4.40) 1.62-8.37) .10-3.32 (1.70-3.750-1.48 (2.16) Sample size 1949 2518 1930 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .0) 4.12) * * * * * * * * .580 (.08.33 (4.20-17.840 (.96 (1.49 (1.53-7. 01-02.24-7.70-17.0 (13.110 (<LOD-.14) 2.0 (16.05 (2.590 (.65) 1.080-1.76 (1.52 (1.07 (1.770 (<LOD-1.0 (4.82-4.51 (2.0-38.30) .99) 11.43-4.350-.70) 2.830 (.0) 2.90) .31-10.83) 2.210-1.10 (3.0 (5. respectively.770) 2. and 0.70-7.425-1.39 (2.0) 2.0) 2.

10) 2.13 (2.41 (4.260-.22) 2. Fourth National Report on Human Exposure to Environmental Chemicals 131 .430) 1.91) 2.02 (1.88 (2.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.660) < LOD < LOD .56) .62-17.7) 6.73 (4.07-21.03) 2.800-2.96-25.31) .14 (1.270 (<LOD-.22-27.1 (7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.32-6.370) < LOD < LOD < LOD < LOD < LOD 1. population from the National Health and Nutrition Examination Survey.9) 5.85 (1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.71 (.04-16.370 (.57-40.40 (.8) 7.08) .36 (.840-3.57) 8.500 (.560 (.31-7.1) 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 * * * * * * .92 (2.67) 2.81-17.64) 30.474-1.330-1.820) .820 (.80) 3.370-1.320-1.75) 5.28-6.830 (.00-19.85-3.23-7.97) .88) 17.71 (2.48-7.45 (1.48 (4.29 (4.0 (4.7 (12.5 (8.88-3.41) 18.5) 7.79 (.2 (8.53) .44-11.98 (4.61) 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 .27 (2.67 (2.630-1.47-10.55) 21.5 (11.07 (2.0) 4.62 (1.340-.1) 2.940-4.51-4.50) .25-38.5) 2.06 (.260-.77 (.43) .03) 16.15) 9.30 (4.11-5.540 (.52 (.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.860-2.930) .540-1.5 (9.8) 2.620-3.04 (1.31-18.340 (.51-44.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.10 (2.8-33.47-10.730-3.25 (1.57 (.190-1.38 (2.9) 6.8 (20.890 (.40-12.17 (1.3) 2.6) 952 1187 934 997 1330 993 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .01 (1.7) 3.790 (.12 (4.2-38.90-6.60 (1.32) 9.49-2.02) .8) 4.02 (.05) .360 (.580) 16.700) < LOD < LOD < LOD < LOD < LOD 1.5-40.47) 5.7) 5.39) 20.340-.96-8.650 (.67-6.390-.44) .31) .69) 2.14-6.670 (.970-3.850-3.33 (3.740-1.50) 11.33-4.09-3.270-.18) 95th 21.7 (6.91-4.310-.960 (.10-3.56) 2.790) 11.33-3.25-9.96) 2.580 (.590) 2.4) 2.17) 5.650) 90th 10.S.33-5.50 (2.1 (5.7) 4.48-42.74 (2.710 (<LOD-1.56 (1.3) 3.67) 1.64-4.580-1.69-7.470 (.700) 6.830-3.600 (<LOD-1.240-.65 (2.430 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.690-5.150 (<LOD-.580) 1.8) 7.66-47.86) .35 (.57) 1.12-4.18) * * * * * * * * .11) .4-34.37) 4.55 (3.00) .780-4.40) 1.33 (1.21-3.55) 21.5) 2.250 (<LOD-.83-11.29-4.89 (2.50 (4.0 (9.450 (.770) .86 (3.40-2.83 (4.53) 27.8) 2.18) 1.84) 9.9 (11.340-.47) .82-11.88 (.4 (4.02-4.748 (.24) 3.80 (.8) 1.59 (1.

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An epidemiological study of the relations between exposure to organophosphate pesticides and indices of chronic peripheral neuropathy and neuropsychological abnormalities in sheep farmers and dippers. Tumino R. Lewis JA. Environmental Protection Agency (U. Arch Environ Contam Toxicol 2000. van der Hoek W. Thompson ML.12(2):134-141.44(4):352-357. Jamal GA. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand.30(2):98-103. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Effects of long-term organophosphate exposures on neurological symptoms. Mounce LM.52(10):648-653. Available at URL: http://books. et al.26(2):199-209. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Rohlman D. Neuropsychological effects of long-term exposure to organophosphates in sheep dip.2000 and 2001 market estimates. Samuels S. Rodnitzky RL. Eskenazi B. Lancet 1995. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Wickremasinghe AR.345(8958):11351139. Saieva C. Irish RM. Scand J Work Environ Health 1998. Rothlein J. Pesticides in the Diets of Infants and Children. Buchanan D. et al. Rothlein J. Rosenstock L. Vitayavirasak B. Buccafusco JJ. Lancet. Dinoff TM. McConnell R. Santana J.113(4):504-508.S. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Lambert WE. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Effects of chronic.pdf. Stokes L. EPA). Malathion deposition. EPA. London L. Washington (DC). Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). 4/7/09 Young JG. and cholinesterase status of date dusters and harvesters in California. Neurotoxicology 2005. Keefe TJ. U. Visuthismajarn P. Salvini S.edu/ openbook. metabolite clearance. Office of Prevention Pesticides and Toxic Substances.epa. Lu C. discrimination. J Toxicol Environ Health A 2005. 1/12/09 Peiris-John RJ. Gladstone EA. Int J Occup Environ Health 2006. National Academy of Sciences. Hansen S. Masala G. Stephens R. O’Malley M. Stark A. Pesticide industry sales and usage . Petchuay C.84(5):731-736. Arch Environ Health 1975. 1991.24(1):18-29. Chronic central nervous system effects of acute organophosphate pesticide intoxication.52(2):190-195. Jenkins B. low-level organophosphate exposure on delayed recall. Am J Ind Med 1987. Berry H. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. J Occup Environ Med 2002. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Pedersen L. Bradman A. Marshall E. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Caltabiano LM. The Pesticide Health Effects Study Group. Am J Public Health 1994.S. Neurotoxicol Teratol 1998.114(5):691-696. Environ Health Perspect 2005. Chrislip D. Frasca G. Levy LS. vibration sense and tremor among South African farm workers. Aprea C. Bull Environ Contam Toxicol 1994. 2004. Steenland K. Pilkington A. et al. Beach J.nap. Heaton RK. et al. Robson MG. 1993 [online]. Ames RG. Hore P.38(4):546-563. McCauley L. Neurotoxicity among pesticide applicators exposed to organophosphates. Myers JE. Environ Health Perspect 2006. Keifer M.43(1):38-45. Available at URL: http://www. Takamiya K. Narang A. A behavioral evaluation of pest control workers with short-term. Burcar PJ.12(2):153-172.338(8761):223-227. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Kidd M. Claypoole K. Seiber J. Occup Environ Med 2001. et al. Muniz J. Arch Environ Health 1988.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Barr DB. Savage EP. Phillips J. Calvert IA. Lasarev M.68(3):209-227 Maizlish N. Scherer J. Occup Environ Med 1995. Muniz J. Nell V.php?record_id=2126&page=1. National Research Council (NRC). Ruberu DK. Daniell WE.58(11):702710. S. Smit LA. Washington (DC): U. Prendergast MA. and spatial learning in monkeys and rats.332(1-3):71-80. Weerasekera G. Lasarev M. Spurgeon A. Russo J. Bravo R. Schenker M.20(2):115-22. low-level exposure to the organophosphate diazinon. Gillham R. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Terry AV Jr. May. Weisskopf C. Chronic neurological sequelae to organophosphate pesticide poisoning. Johnson C. Sci Total Environ 2004.

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

90 (3.24-3.20) 10.77-6. and dust.90 (1.51-2.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.70 (1.60-2.30 (2.60-3.40 (5. air.29-1.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.40-10..22) 2.S.00) 3.74 (1.0) 12.44-5.22 (1.83) 1.19-3.7) 8.60-3.84) 1.50-4.EPA. population from the National Health and Nutrition Examination Survey.50 (1.26) 7.47-9.04-10. Survey Geometric mean (95% conf.44-2. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.0) 9.37) 5.5.51) 1.20-2.05-5.4-15.97) 2.95 (4.80) 2.0 (7.8) 10.20-4. and sprayed to kill mosquitoes.59-2. Exposure can also result from contact with contaminated surfaces. dermal.77-15.40) 9.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.50 (1.50-4.01) 1.0 (7.52-2.10 (4.0) 12.40) 2.00) 2.57 (2.90 (1.20-16.63 (1. staying bound to soil particles. Approximately 21-24 million pounds per year were used domestically from 1987-1998.79-2.0 (7.90-8. interval) 1. It also has been applied directly on animals to kill mites.52-12. and on plants for days to several weeks.74-9.6) 7. 2002).10-17.3) 8.02) 1.50-14. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.28-3.3 (8.10 (3. 5598-13-0 General Information The chemical 3.32-1.62-2.76 (1.3 (10.30-2.90-4.20) 2.29) 90th 7.89 (2. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.1) 5.70) 1.7) 9.20 (2. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.4.4 (9.94 (4. 2005).64) 3.0) 12.37 (1.66-4.60) 5.21) 3.81-2.24-1.90 (2.97-7.0 (10.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.0) 7.39-2.03) 1.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.80-8.4 and 0.0) 8.50 (2.99-4.16) 2.10) 2.28) 2. 2921-88-2 Chlorpyrifos-methyl CAS No.EPA.0 (9.46-2.25) 1.39) 4.0) 8.80) 4.27 (7.17 (1.0 (13. in 142 urban homes and preschools in North Carolina.60 (5.61-7.97) 7. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.7-23.30) 5.9 (10.09 (3.0) 10. 1999.45 (1.10) 6.53 (1.92 (1.91 (1.50-5.47) 1.80 (1.15 (1.20-3.72-4.87-6.67 (1. and is infrequently detected in ground water (IPCS.43-2.96) 3.9 (7.30 (4.40-13.13-3.2 (10.90) 3.and post-construction structural applications for termite control were to be phased out by 2005 (U.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 1.31-2.47-11. 2007).61 (1. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration. pre.0) 15.30-11.90-7.66-15.47 (4.04-10.30-5.30) 4.9) 11.0) 14.89-2.70-15.86) 4.0 (7.90-2.47-13.80-10.50 (2. Estimated intakes from diet and water have not exceeded recommended intake limits. USGS.50-2. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.43-2.35) 1. chlorpyrifos was no longer registered for indoor residential uses in the United States.13 (1.20) 4.8) 9.70-5. 2002).S. It has low leachability.00-24.61) 75th 3.0) 11.97) 2.97) 4.5-24.76 (1.7) 13.59) 2.71 (2.4 (8.00-8.9 (9.80) 12.50-2.5 (8.9-18.20) 2.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.000 pounds are used per year.51 (1.30 (2. and inhalation routes.25) 3.31-2.8-15.40-26. applied to structures to kill termites.35) 2.19 (1.0-28.60-4.00) 1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.40-2. For instance.9) 697 660 521 701 602 947 Limit of detection (LOD.90 (6.09 (2. After 2001.88 (1.30-9.70 (1.63 (2.63 (8.05) 1.70-16.80 (7. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.20 (4.40 (5.68 (7.78 (7.38 (3.0 (7.98-15. Approximately 80.70-17.4 (10.0) 18.60 (2.67 (2.44 (3. 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.71 (1.55-5.95) 7.77) 1. The general population may be exposed to chlorpyrifos via oral.70-11.10 (5.37 (4.1-16.72) 2.0) 12.50 (2.02 (7.20-11.91) 16.20-14.32) 2.0) 6.5) 7.50-8.30-1.60 (4.02 (1.34) 1.80) 1. Chlorpyrifos is Urinary 3.0) 10.3 (11.67 (2.0) 10.77 (1.90) 7. but can be detected in streams receiving runoff from application sites.S.5.30) 4.10 (1.68-2.40 (6.36 (4. Fourth National Report on Human Exposure to Environmental Chemicals 135 .30-12.71 (6.0) 12.

00-8.57) 2. Ricceri et al. cholinergic effects.64-7.23) 14.42-2. Once absorbed.97-3..53-5.05-4.46 (2.6-Trichloro-2-pyridinol (creatinine corrected) Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.81 (3.97) 3.48 (1.07) 1.97 (3.EPA.22) 1.44 (6.76 (2. Urinary 3.58) 5.22-6. TCPy is more persistent in the environment than chlorpyrifos itself (U.42 (5.47-2.71 (1.85 (3.44-6.81) 2.75) 6. paralysis.77) 1. resulting in excess acetylcholine at nerve terminals..21-1. In pesticide applicators. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.72-2.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1. 2006b).48 (2.92-2.3 (7. 2005.05-1.93 (2.82 (2.06 (1.54) 5.11 (2.60 (1.83) 1.1 (10.64 (1.92 (1.22 (4.46 (1.90-9.28) 2.09 (1.20 (2.80-6. Slotkin et al.93) 2.69 (1. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.33 (5.88 (1.29 (3.01) 3.44 (5.95 (3.11-9.63-2.12-3.06-4.1-21. 2006...33-7.1 (7.94-12. 2006.17-4.56) 2.58-5. TCPy can also occur in the environment from the breakdown of the parent compounds.55 (4.56) 5.19) 3.09-3.98 (7.91) 2. 2006a.27-7.97 (2.93 (4. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.33 (.16) 6. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).99) 1.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals ..05) 3.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.42 (6. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis. and other metabolites.91) 10.91) 1.27-1.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.91 (4.49 (1.73 (1.68) 6.93 (1.39 (2. Metabolic hydrolysis leads to the formation of TCPy.85) 4.19-1.0) 6.88-8.11 (2.11) 7.88 (1.9 (12..66 (1. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.06 (5.08) 6.33) 2.72) 2.25-12.84-6.39) 6.66-11. and seizures.30-4.35) 2.8) 9.2) 6.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.83-2.88) 6.24-24.59) 3.02 (5. 2002).96) 3.75 (1. neurotransmission.31) 1.51 (1.71) 3. Betancourt et al.31-4.34-1.24) 5.24-1.66) 1.5 (6.85-4.91 (3.940-1.47 (5.45 (1.49-2.97) 3. Survey Geometric mean (95% conf.83-11.99-8.50 (4.12) 1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.19-2.07) 5.88-10.91) 1.40) 1.56 (4.05-8.30-1.85) 1.39 (4.65-11. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.63 (5.80-11.2 (7.62-7.47 (1.21-6.55) 1.03) 1.88-8.38) 3.86 (1.0) 12.15 (4.52 (5.0) 10.25-11.70-4. Roy et al.82-4. Based on animal data and human cholinesterase monitoring during occupational exposure.87-3.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.62) 1.S.76 (3. 2005.98 (6.57-2. interval) 1.58 (1.68) 1.23-1.57) 9.4) 4.5) 5.09-1. weakness.24-5.64-2. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.91-4. 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.41 (1.44 (1. 2005.3) 9.16 (4..3) 8.09-2.65-15.63 (4..59-2.6) 10.45-1.37 (1.39-1.49-2.3) size 1994 2508 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.00) 1.28) 2. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.14-8.01) 3.47 (1.93) 5.89) 4.05-3. and producing acute symptoms such as nausea.02) 7..35) 1.17-4.86 (1.24-4.92) 3.82 (3.82) 8.74) 1.57-2.53 (2.6) 9.7) 7.58 (1. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.56 (1.43-10.36) 1. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.56-2. 2000).22 (6.0) 16. population from the National Health and Nutrition Examination Survey.31-1.55 (1.60-3.24) 75th 2.80) 3. Howard et al.35-1.43 (4. vomiting.86 (3. Thus.80-4.49-2.S.20-1.95 (1. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.32) 1.91-13.85 (2.00 (7.62) 90th 5.79-13.72) 1.5.44 (5.1-38.3) 8.00-13.94-14.24 (1.01) 1.19) 6.58) 1.25-1.78 (1.33 (1.88-9.58 (4.54 (2.26-14.44 (1.12-1.14) 1. 1984).

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

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. Pesticide residues in urine of adults living in the United States: reference range concentrations. Lein PJ. Ricceri L. Environmental Health Criteria 198. U. Lu C. Levin ED. Seidler FJ. Acquavella JF. Angerer J.114(2):260-263. Pellizzari E. Toxicol Appl Pharmacol 1984. Head SL. Slotkin TA. Jones PA. Morgan MK. Eskenazi B. Toxicol Sci 2006. Rauh V. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites.15(3):271-281. et al. Seidler FJ. Environ Health Perspect 2006. Seidler FJ. Chapman P. Bravo R. J Expo Anal Environ Epidemiol 2005. 1992. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. A longitudinal investigation of selected pesticide metabolites in urine. International Programme on Chemical Safety-INCHEM (IPCS). Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures.93(1):105-113. Freeman N. Sheldon LS. Tsai WY. et al. Bravo R. Adgate JL. Herrick RF. et al. Chrislip DW. Edwards RD. Baker BA. Fortuna S. Bradman A.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. et al. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Hammerstrom KA. Kinney P.htm. National Toxicology Program (NTP). Sharma V. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.73:8-15. Wartenberg D. Baker S.71:99108. Tate CA. Zhang J. Mandel JS. Alexander BH. Environ Health Perspect 2003.207(2):112-124. Barr DB. Ryan L.155(1):71-80.S.10(4):327-340. Scand J Work Environ Health 2005.114(10):1542-1546. February 5.niehs. 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Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Chlorpyrifos: pharmacokinetics in human volunteers. Executive summary of safety and toxicity information. Weltzien E. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population.nih. Roy TS. et al. Hore P. Ryde IT. Shealy DB.51(1):53-65. Freeman N. Freshour NL. Rick DL. Barr DB. Irish R. Environ Health Perspect 2006a. Croghan CW. Bailey SL.5. Hardt J.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC).9(5):494-501. Yang D. Gregg M. Interim registration eligibility decision for chlorpyrifos. gov/ntpweb/index. Chlorpyrifos. Environ Health Perspect 2004.5. Hill RH Jr.inchem. Third National Report on Human Exposure to Environmental Chemicals. Jewell NP. Honeycutt R.113(2):211-219. 4/7/09 Koch HM. Toxicol Appl Pharmacol 2005.6-trichloro 2-pyridinol in their everyday environments. Chuang JC. Urinary pesticide concentrations among children.114(5):746-751. Environ Health Perspect 2006b. Levin ED. Steenland K.S. Robson M. Bucelli R. Heederik D.204(2-3):175-180. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Kromhout H. Toepel K.

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

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

270) < LOD 659 701 920 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.S. Fourth National Report on Human Exposure to Environmental Chemicals 141 . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .210) < LOD < LOD 567 815 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1312 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.S.670 (<LOD-1.2.200 (<LOD-.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 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. Survey Geometric mean (95% conf. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 01-02 is 0.27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 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 .200 (<LOD-. which may vary for some chemicals by year and by individual sample.380 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

Human exposure to diazinon from dietary sources is expected to be low due to its limited applications to food crops and due to its rapid degradation.EPA. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. 2007). and other metabolites. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. aerial. an organophosphorus insecticide that is used to control insects on nuts.7. in some pest strips. Diazinon is not well-absorbed through the skin. and forage crops.S. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. fruits.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. < LOD means less than the limit of detection. but is rapidly absorbed orally (IPCS.S. since 2004. Inhalational and dermal routes of exposure can be significant for pesticide applicators.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD.S. Prior to 2000. seed and foliar applications are planned to be phased out (U.45 (<LOD-3. which may vary for some chemicals by year and by individual sample. It is also used for cattle ear tag applications to control flies and ticks and. 2004). phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. Most granular formulations. Estimated intakes from diet and water do not exceed recommended intake limits (U. 2004). in the past. 1998. and particularly when it was ingested in granular form.11) < LOD < LOD < LOD < LOD 454 580 632 829 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. diazinon produced wild bird kills before use restrictions were in place. It is toxic to birds. Once absorbed. but these uses have been phased out. Survey Geometric mean (95% conf. as inferred Urinary 2-Isopropyl-4-methyl-6-hydroxypyrimidine Metabolite of Diazinon Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Before these restrictions. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1998). vegetable. USGS.49 (<LOD-2. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. Fourth National Report on Human Exposure to Environmental Chemicals 143 . diazinon cannot be sold for residential use. population from the National Health and Nutrition Examination Survey.2 and 0. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine.EPA. 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. diazinon was widely used in residential and garden application.

EPA at: http://www. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. cholinergic effects. diazinon does not accumulate in tissues (IPCS. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate.epa. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants. and seizures. animal carcinogen. 1992). in the 2001-2002 subsample (CDC. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. population from the National Health and Nutrition Examination Survey. Thus.49 μg/L.EPA considers diazinon unlikely to be carcinogenic in humans. Intoxications in humans from intentional overdose... In addition to being a human metabolite of diazinon. The U. subsamples of NHANES 1999-2000 and 20012002. Seifert and Pewnim. respectively (Baker et al. 2003). 2000.76 (<LOD-3. Survey Geometric mean (95% conf. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. teratogen. In two nonrandom samples of United States adults and children.. and indoor applications have been documented. resulting in excess acetylcholine at nerve terminals. paralysis.html and from U. 1998). 144 Fourth National Report on Human Exposure to Environmental Chemicals . 1986 Rajendra et al. 2002). 1998). agricultural.S.cdc. Diazinon has moderate acute toxicity in animal studies. weakness.S. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. 1986.. 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.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.72 (<LOD-4. vomiting. At high doses. Diazinon is not considered to be a mutagen.45 and 1.S.e.S. In animals. and producing acute symptoms such as nausea. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. respectively.gov/toxpro2.gov/pesticides/. environmental levels) and health effects is available from ATSDR at: http://www. Additional information about external exposure (i. 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. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al.atsdr.. or reproductive toxicant (IPCS. In the U. Olsson et al..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.

Noisel N. Beeson MD. Environmental Health Criteria 198.epa. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. et al. Oloffs PC. In a small number of men visiting fertility clinics in Missouri and Minnesota. Needham LL. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Liu F.pdf. Banister E. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Centers for Disease Control and Prevention (CDC). Diazinon. Available at URL: http://www. Diazinon. May 2004.111(12):1478-1484. Toxicol Lett 2002. Available at URL: http://www. Barr DB. Biochem Pharmacol 1992. Effect of sublethal levels of diazinon: histopathology of liver. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.Organophosphorus Insecticides: Specific Metabolites 2005).10(6 Pt 2):789-798. Environ Health Perspect 2003.org/documents/ehc/ehc/ehc198. revised February 15. Bouchard M. Bravo R. Third National Report on Human Exposure to Environmental Chemicals. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Anal Bioanal Chem 2003. 1/14/09 U. Mason HJ. References Anthony J. Barr DB. Redmon JB.50(5):505-515. 2007 [online]. Rajendra W. In 54 Canadian greenhouse workers. Fenske RA. Nguyen JV. Banister EW.114(2):260-263. Jones K. 1992-2001. Seifert J. Semen quality in relation to biomarkers of pesticide exposure. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Baker SE.gov/ oppsrrd1/REDs/diazinon_ired. 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. Irish R.37(4):501-507. U. International Programme on Chemical Safety-INCHEM (IPCS). Pesticides in the Nation’s Streams and Ground Water.. Oloffs PC.44(11):2243-2250. Drug Chem Toxicol 1986. Ann Occup Hyg 2006. 4/7/09 Lu C.inchem. Sadowski MA. Geological Survey (USGS).gov/circ/2005/1291/.S. Swan SH. Dumas P. In 23 children. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers.usgs.9(2):117-131. Environmental Protection Agency (U. Bull Environ Contam Toxicol 1986. Atlanta (GA). Driskell WJ.376(6):808-815. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses.134(1-3):105-113. Interim reregistration eligibility decision (IRED. EPA).S. 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. 2006). Pewnim T. Barr DB. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.S. Olsson AO. 2005. Available at URL: http://pubs. The Quality of Our Nation’s Waters. Toepel K. Barr DB. Carrier G. Swan et al.. J Expo Anal Environ Epidemiol 2000. Garfitt SJ. 2006). EPA 738-R-04-006. 1998. Cocker J. Study for Future Families Research Group. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 .htm. Drobnis EZ. Brunet RC. Environ Health Perspect 2006. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. March 2006. Kruse RL.

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

..S.5 and 5. Fourth National Report on Human Exposure to Environmental Chemicals 147 . 1993.. EPA at: http://www. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. 2000).gov/pesticides/.html and from U.S. 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.74 (<LOD-5.atsdr..gov/toxpro2.EPA. representative subsample from NHANES 19992000 (Adgate.. but cholinesterase activity was not affected. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. 2005). Survey Geometric mean (95% conf.epa. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003). 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. population from the National Health and Nutrition Examination Survey.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. and it is not considered an animal teratogen or a reproductive toxicant. 1990)..cdc. Additional information about external exposure (i. Malathion itself has not been considered genotoxic (U. IARC considers malathion not classifiable as a human carcinogen. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. Giri et al.EPA. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al.S. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al.. 2006). Thomas et al. environmental levels) and health effects is available from ATSDR at: http://www. Of 382 pregnant women living in an agricultural community. Toxicity from unprotected bystander exposure during applications is rare (U. 2004).. Pluth et al. A study of agricultural workers reported preshift urinary levels of malathion dicarboxylic acid that were twofold to eightfold higher than detection limits in the NHANES 1999-2000 subsample (Krieger and Dinoff. 2006). 1999). 1999.e.. 2001. 1996. Flessel et al. A study of 13 children from an agricultural region of Washington State reported median levels that were below the detection limit in the NHANES 1999-2000 subsample (Kissel et al. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect.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. CDC.. 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. 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. Lu et al. but isomalathion. 2002.S. 1987. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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..S. 2005.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. 2005). Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. 2006). Human studies of single oral doses between 0.

Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Griffith W. Barr DB. Toepel K. Gosselin NH. Jewell NP. Blasiak J. Nicklas JA.22(1):7-17. Thomas D. Needham LL.epa. J Expo Anal Environ Epidemiol 2005. Dumoulin MJ. and cholinesterase status of date dusters and harvesters in California. Environ Health Perspect 2006. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Bradman A. Petitti D. Am J Epidemiol 1990.514(1-2):223231.pdf. U. Malathion deposition. Trzeciak A. Flessel P. metabolite clearance. Environ Health Perspect 2004. J Expo Anal Environ Epidemiol 1999. Available at URL: http://pubs.usgs. Centers for Disease Control and Prevention (CDC).S.445(2):275-283. Harley K. March 2006. Rappaport E. Goldhaber M.77:1009-1010. Giri A. MacIntosh DL. Bravo R.15(2):164-171. Pluth JM. Samuel O. Cancer Res 1996. Barr DB. Mutat Res 1999.73(1):182-94.org/documents/jmpr/jmpmono/v2003pr06. Barr DB.56(10):2393-2399. 2007 [online]. et al. EPA). Carrier G. Hertz-Picciotto I. Lu C. Toxicol Sci 2003 May. Swan SH. Dinoff TM. Neutra R. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Irish R. Hooper K. Grether JK. Prasad SB. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Weltzien E. 1992-2001. Lioy PJ. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Giri S.gov/circ/2005/1291/. Environ Health Perspect 2001. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Brunet RC. Mutat Res 2002. Ryan PB. htm. Eskenazi B. Available at URL: http://www.S. Barr DB. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Kedan G. Curl CL. Sharma GD. et al. Reregistration eligibility decision (RED) Malathion. Third National Report on Human Exposure to Environmental Chemicals. Eberly LE. Environ Mol Mutagen 1993. Jaloszynski P. Genetic toxicity of malathion: a review. EPA 738-R06-030. Fenske RA.114(2):260-263. Clayton CA. Quintana PJ. Reproductive outcome in women exposed to malathion. Am J Public Health 1987. Malathion (addendum). Available at URL: http://www. O’Neill JP. Atlanta (GA).inchem. Erratum in: Toxicol Sci 2003 Aug. Freeman NC.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Geological Survey (USGS). Albertini RJ. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Pesticides in the Nation’s Streams and Ground Water. Environmental Protection Agency (U.74(2):following table of contents. Krieger RI. Szyfter K. revised February 15. Harris JA. Hammerstrom KA. Bouchard M.38(4):546-553.109(6):583-590. Arch Environ Contam Toxicol 2000. 4/7/09 Kissel JC. Lu C. International Programme on Chemical Safety-INCHEM (IPCS). Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. The Quality of Our Nation’s Waters. July 2006.gov/oppsrrd1/REDs/ malathion_red. A longitudinal investigation of selected pesticide metabolites in urine.132(4):794-795. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues.9(5):494-501.112(10):1116-1124. 2005. 6/1/09 U.S. et al.

85 (2.00) 3.50) 2.50 (1.57) 1.33) 2. all registered uses were voluntarily cancelled (U. 1977).32-1.11) 2.298-00-0 Ethyl Parathion CAS No.80 (2.940 (<LOD-2.30-16.70-6. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. In the 1990s.10) 4.37-4. Fourth National Report on Human Exposure to Environmental Chemicals 149 .30-5.69) 4.79) 4.00 (2.700 (<LOD-. 2007).0) 3.92-2.30 (1. more slowly absorbed through the skin. Many previous registered agricultural uses of methyl parathion have been cancelled (U.80) 2.70-3.40-4.50) 3.300-. 2006).0) 4. It had been applied to cotton.02-6.15-3.70) 2.50-14.28 (1.50 (2.0) 2.92) 5.37) 2.57-4.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .70) 2.46 (3.90 (1.01-4.36-1.16) < LOD 1. Survey Geometric mean (95% conf.40-4. and has a short half-life in soils and on plants.32-1. and of the chemical nitrobenzene.74) 5.50 (1.47) 2. and oral routes can occur in pesticide and agricultural workers (Muttray et al.32-3.10 (<LOD-6. which may vary for some chemicals by year and by individual sample.20-5. Ethyl parathion.58) 3.0) 3.10) 22.00) 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. first registered in 1948.28-4. ethyl parathion. binds tightly to soils resulting in low leachability.27) 2. Once absorbed.71 (3.S.90-11.60-24. < LOD means less than the limit of detection. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .21 (2.910) < LOD .45) 5.26 (1.21-1.40-3. was once a restricted-use insecticide with limited applications on certain agricultural crops. on cereal grains.EPA. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. Methyl parathion is not registered for residential use in the United States.20 (<LOD-2.60-19. Morgan et al. population from the National Health and Nutrition Examination Survey.09-1.40 (1.50 (2.30 (2.40) 4.60-36. Methyl Parathion.01) 4. and eliminated rapidly from the body after absorption (Kramer et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .10-1.10 (3. fish.0) 3.30-3.60-5. methyl parathion was rapidly absorbed after ingestion. but by 2003.61) < LOD 1.910) < LOD < LOD < LOD 1. In animal studies.40) 1.60) 1.32 (1..69 (2.05) 4.20) 5.37-4. 2003).0) 3.0) 3.60 (4.50 (1.89 (2.28 (1.33 (1. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.49 (1. with limited applications in agriculture.40) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.01) 695 660 518 679 603 941 Limit of detection (LOD. Both are toxic to birds. Methyl parathion has low water solubility.S.70 (3.1.18-3.910) < LOD < LOD .70 (2.770 (. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.70-6. 2002..990-1. Estimated intakes from diet and drinking water have been below recommended limits. pulmonary.70 (2.850) < LOD .860 (<LOD-1.70-3.34 (3..Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.80 (2.45 (1.44) 2.50 (1.62 (1.8 and 0.730 (<LOD-. Given its limited use.10-11.37-2.00 (2. and aquatic invertebrates.67) < LOD 1.70) 2. 2000).48) 90th 2.10 (3.61) < LOD 1.72 (3.80 (1.67 (1.66 (2.70-6.90-9.790 (<LOD-.70 (2.91-3.71 (2.22-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. peak domestic use was as high as 5-6 million pounds per year. Increased risk of exposure via dermal.13-1.S. Methyl parathion use is highly restricted.0 (3.50) 1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50) 3.41-4.20 (2.11-4. and to a lesser extent.19 (.50-9.12) < LOD < LOD 1.EPA.70 (<LOD-3.

01 (. Jaga and Dharmani.870) < LOD .840 (. 1991).cdc.7) 3.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .84) 3. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.950) < LOD .1) 2. 2006.23) 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 . gov/pesticides/. 2006. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. does not inhibit acetylcholinesterase enzymes.67 (3.21-21.930 (.83 (1.830-1.55) 2.680 (<LOD-1.89 (2. 1995.S.61) 4.20) . 2004). cholinergic effects.EPA considers methyl parathion unlikely to be carcinogenic to humans.16-4. Lores et al.15) 3.91) 1.07 (1.60 (1.730-1.35-3.S.530) < LOD < LOD < LOD .97 (<LOD-4. weakness.67-2. Karanth and Pope et al. ethyl parathion.79 (1.07) 2.3) 2.26 (1..25) 1. 2005.690-1. Recent in vitro and in vivo animal studies suggest that parathion may have additional neuronal and glial cell effects at lower doses (Guizzetti et al.15-10.29 (2. Parathion and methyl parathion have high acute toxicity in animal testing. EPA at: http://www.epa.13-12. Thus. vomiting. but lists ethyl parathion as a possible human carcinogen.71) 1.73 (1.01-3.970 (.33-3. accidental exposure.57) 6.. 1978.57-2.78-2.500) < LOD < LOD . In addition to being a metabolite of methyl and ethyl parathion.10 (1. Additional information about external exposure (i.2) 2.04 (2.80 (1. methyl parathion.96 (1.html and from U.S.72-2.97-10. 1995).94-47.82 (2.76-14..01 (2.04) 1.57-7.. 2003.790-1. 150 Fourth National Report on Human Exposure to Environmental Chemicals .39) 1.20) 3.13) 4.97 (2. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.26) 17. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.82) < LOD . The metabolite. 1990. Methyl parathion is not considered genotoxic.39 (1.33-6.940 (<LOD-1.00 (1.640) < LOD < LOD 1.Organophosphorus Insecticides: Specific Metabolites Metabolites”).95) 1.850-1.70) 3.23) 1.400 (<LOD-. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.89 (2.59 (1.71 (1.930 (.. U.88 (1.79) 1. and unintentional acute or chronic high-level occupational exposure (Hill et al.14-3.77-7.970 (.78) 2. paralysis.44-3.08) < LOD .790-.2) 2..370 (<LOD-. gov/toxpro2.00 (1.38-3.37-1.10) 90th 2. resulting in excess acetylcholine at nerve terminals.86 (2. population from the National Health and Nutrition Examination Survey.78-2.00) 2.20 (3.44-3. Methyl Parathion.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .9) 1. and producing acute symptoms such as nausea.30) 3.30-1.11-4.60-2.56-2. Orsorio et al.17-4.98-7. 2004). Survey Geometric mean (95% conf. In large doses.880 (.80 (1. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.430 (.35-3. teratogenic.96 (1.41-2.94-4.48-4.980 (.33-3.08-3. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene. Slotkin et al.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .31-3.87 (1.05) 4.92 (2.08 (1.88) 1.21) 1.55 (<LOD-3. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. environmental levels) and health effects is available from ATSDR at: http://www..45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.29) 2.78 (2. and seizures.720 (<LOD-.11) 1.31) < LOD .93 (2.09) 2.4 (3. paranitrophenol.310-.720-1.60) 2.. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.540) < LOD .800-1. and other metabolites.440 (<LOD-. WHO. At high animal doses of methyl parathion.90 (1.17) .43) 4.91 (1. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.29) 1.e.atsdr.25 (2. Zurich et al.

110 Suppl 6:1085-1091. Shealy DB. Laboratory investigation of a poisoning epidemic in Sierra Leone. 2005). McCann KG. Slach EF. Barr JR. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Lores EM. Harley K..org/documents/jmpr/jmpmono/v95pr14. Dharmani C. CDC. J Biomed Sci 2002. Jewell NP. McCann et al. a range of values several hundred times higher than levels found in the U.. 2005). Arch Environ Contam Toxicol 1977. Costa LG. Environ Health Perspect 2002.S. Role of individual susceptibility in risk assessment of pesticides. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Curl CL. References Barr DB.. Baker SE. et al. Alley CC. Pharmacokinetics of methyl parathion: a comparison following single intravenous. 1995). Centers for Disease Control and Prevention (CDC). Runkle KD.. Pesticide workers may have much higher levels following pesticide applications.15(2):164-171. Turner WE. Environ Res 1995. Needham LL. 2005. Lewalter J. Parathion-Methyl (addendum). Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Hill RH Jr. Eskenazi B.25(5):599-606. Kramer RE. 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. Karanth S. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Moseman RF. Gregg M.. 2002. 1999).inchem. Baker S. et al. Occup Environ Med 1999. et al. Morgan DP. Ashley DL. Methyl parathion: an organophosphate insecticide not quite forgotten. Atlanta (GA). end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Griffith W. 2002). Pope C. Neurotoxicol Teratol 2003. J Expo Anal Environ Epidemiol 2005. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Arch Environ Health 1978. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Moomey CM. Toxicology 2005.. 2005. Bradman A. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Hill RH Jr. Clark JM. et al. Biomonitoring studies of para-nitrophenol can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of parathion than are found in the general population.9:311-320. Bradway DE. Hetzler HL. 2002. J Anal Toxicol 1990. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Head SL. Environ Health Perspect 2004. 4/7/09 Jaga K. and levels were similar or slightly lower that those in a small convenience sample of the U.71:99108. Weltzien E.6(2-3):159-173. Hill et al. Environ Health Perspect 2002. ACGIH recommends a BEI of 0.110 Suppl 6:1075-1078. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. 2004). Lu C. Chicago area methyl parathion response.14(4):213-216. Third National Report on Human Exposure to Environmental Chemicals. general population (CDC. Giordano G. Head SL. In a study of workers who handle parathion.112(10):1116-1124. 2005.5 mg (500 µg)/g creatinine for workers at the end of shift.htm. 1995. Guizzetti M. DiPietro E. and many residents were symptomatic (Barr et al.215(3):182-190. Wellman SE.S. Hryhorczuk DO. Pesticide residues in urine of adults living in the United States: reference range concentrations.56(7):449553. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. oral or dermal administration. Barr DB. population (Olsson et al. Barr DB. Available at URL: http:// www. Rockhold RW. Barr DB.. Cline RE. Leng G. International Programme on Chemical Safety-INCHEM (IPCS).21(1):5767. Kedan G. Baker RC. 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. Bailey SL. McClure PC. Kissel JC. et al. Rev Environ Health 2006. Lin LI.33(5):270-276. 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. Rubin et al. Pathak S.

Osorio AM. Kieszak S. Toxicol Lett 2006.int/water_sanitation_health/dwq/chemicals/ methylparathion.Organophosphorus Insecticides: Specific Metabolites Muttray A.04/106. May 2003. Interim reregistration eligibility decision (IRED) for Methyl Parathion. pdf. R. Environ Health Perspect 2002. Tate CA. Ryde IT.114(10):1542-1546.who. Hill RH Jr.D. Schilter B. Environmental Protection Agency (U. Costa LG. Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition.gov/oppsrrd1/REDs/factsheets/0155fct. Environ Health Perspect 2006. Nguyen JV. Sadowski MA. et al.epa.epa. 1/12/07 U. Case No. 0153.110 Suppl 6:1047-1051.376(6):808-815. Methyl parathion in drinking water. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos.usgs.S. Available at URL: http://pubs. Hill G. 2007 [online].pdf. 1992-2001. Esteban E. Ethyl parathion.S. Barr DB. U. September 2000. Toxicol Appl Pharmacol 2004.S. 1995-1996. Levin ED.E. External and internal exposure of wine growers spraying methyl parathion. Yacovac R. Ames RG. 5/19/09 Zurich MG. Monnet-Tschudi F. Am J Ind Med 1991. The Quality of Our Nation’s Waters.201(2):97-104. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Rosenberg J.20(4):533-546. March 2006. Backer G. 6/1/09 World Health Organization (WHO). revised February 15. Slotkin TA. Available at URL: http://www. Seidler FJ. Mengle DC. Dunlop B. Ohio.S. Facts. Geological Survey (USGS). Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Environmental Protection Agency (U. Letzel S.162(2-3):219-224. 1/14/09 U. Olsson AO.pdf.gov/circ/2005/1291/. EPA). Available at URL: http://www. Anal Bioanal Chem 2003. Honegger P. Jung D. Investigation of a fatality among parathion applicators in California. EPA). Rubin C.S. gov/oppsrrd1/REDs/methylparathion_ired. Available at URL: http://www. WHO/SDE/WSH/03. 2004. Pesticides in the Nation’s Streams and Ground Water. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. EPA-738-FOO-009.

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

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.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .27) .740 (.500 (.210-1.470 (. population from the National Health and Nutrition Examination Survey.250 (<LOD-.55) .820) < LOD < LOD .680 (<LOD-. which may vary for some chemicals by year and by individual sample.2. Survey Geometric mean (95% conf.210 (<LOD-.780 (.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .770) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .950) < LOD < LOD 1.840 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 154 Fourth National Report on Human Exposure to Environmental Chemicals .15) < LOD .Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.780 (.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .07) .S.580-1. see Data Analysis section) for Survey year 01-02 is 0.700-.670 (<LOD-1. Survey Geometric mean (95% conf.17 (.300-1.200-.94) .850 (.760 (<LOD-.21) < LOD .210-.64) .460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.610 (<LOD-1.840) 669 687 929 Limit of detection (LOD. < LOD means less than the limit of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.430 (<LOD-.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .S. interval) Selected percentiles ( 95% confidence interval) Sample 95th .740-1. population from the National Health and Nutrition Examination Survey.31) .410 (<LOD-1.780 (<LOD-1.780 (<LOD-1.

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

Outside the U. Pyrethroid pesticides have low volatility. Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown.2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. In agriculture. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers.. Unmetabolized pyrethroids have been measured in breast milk. 2003. animal facilities. Soderlund et al. 2002. by either ester hydrolysis or hydroxylation. but pyrethroids are highly toxic to fish and some aquatic invertebrates. which are natural chemicals found in chrysanthemum flowers. About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U. Compared with other classes of insecticides such as organochlorines. Soderlund et al.S. Woollen et al. Adverse effects from large doses are related to the action of pyrethroids on the nervous system. pyrethroids are rapidly metabolized. Pyrethroids are not well absorbed through the skin (ATSDR. EPA. cypermethrin.S. The table shows the urinary pyrethroid metabolites measured in this Report. 2006a. This class of pesticides has low toxicity in birds and mammals. Certain pyrethroid insecticides (such as permethrin. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. pyrethroid pesticides have less acute toxicity in animals and people.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals . Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. they are not persistent in the environment due to their rapid degradation within days to several months.2-Dibromovinyl)-2. 2002). After absorption from inhalation or ingestion. and then eliminated over several days in urine and bile (Kuhn et al.. They are also applied on livestock to control insects. warehouses. solvent oils. so usage is restricted near water (U. 2006b). followed by conjugation. and synergists. 2005). bind to soils. Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. 2003. Estimated intakes from diet and drinking water are below recommended limits. 1992). deltamethrin has been used for indoor protection against mosquitoes that carry malaria. They are ranked as having moderate acute oral toxicity. 1992).2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations. organophosphorus. where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al. 2005. 1999. The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. Generally. agricultural fields. but may be poorly transferred across the placenta (ATSDR. and sumithrin) are also registered for use in mosquito-control programs in the United States.. 2007)... 2002). Possible other additional actions on neuroreceptors Pyrethroid Insecticides Metabolites in this Report Pyrethroid (CAS number) Cyfluthrin (68359-37-5) Cypermethrin (52315-07-8) Cyfluthrin (68359-37-5) and Permethrin (52645-53-1) Deltamethrin (52918-63-5) Cyhalothrin (68359-37-5) Cypermethrin (52315-07-8) Deltamethrin (52918-63-5) Fenpropathrin (39515-41-8) Permethrin (52645-53-1) Tralomethrin (66841-25-6) Urinary metabolite (CAS number) 4-Fluoro-3-phenoxybenzoic acid (77279-89-1) cis-3-(2. and are rarely detected in ground waters (USGS. in some situations replacing the use of DDT. resmethrin. cyfluthrin.EPA.S.2-Dichlorovinyl)-2.. such as piperonyl butoxide. or carbamate pesticides. and greenhouses. 1997.. Leng et al. WHO.. Woollen et al. and deltamethrin have been used frequently on cotton. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides.Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins. There are about 30 different pyrethroid pesticides in use.2-Dichlorovinyl)-2.

2006. Zhao RC. Biochem Biophys Res Commun 1998. 2003.35(2 Pt 1):227-237. References Agency for Toxic Substances and Disease Registry (ATSDR). IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity.. Hu et al. Kunimatsu et al. salivation.. et al.cdc. Levsen K. Toxicol Appl Pharmacol 2006. 2006). 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. McCarthy AR. Int J Hyg Environ Health 2002. 1999. Kim TS. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Idel H. fenvalerate. Garey J.23(6):665-673. Generally. Kang IH.gov/toxprofiles/ tp155. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Kim et al. tremor. Bull Environ Contam Toxicol 1999. Hu JY. Neurosci Lett 2001. et al. Elwan et al. Spinosa HS. Wolff MS.27(4):609-614. Sugiri D. Lazarini et al. 2003. J Reprod Dev 2004.html. Xenobiotica 1997. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Leng G. and permethrin) in the Hershberger and uterotrophic assays. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Chen JH.gov/pesticides/ and from ATSDR at: http://www. Regul Toxicol Pharmacol 2002. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Ose K.. Salzgeber SA. 2002. 2004. Varoli FM. Moniz AC. on immature and adult mice: changes in behavioral and muscarinic receptor variables. et al. Moniz et al. Toxicol Appl Pharmacol 1991. WHO. Eriksson P. Lewalter J. Neurotoxic effects of two different pyrethroids. and seizures (ATSDR. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Agrawal AK. 2003. Lee SJ. Cruz-Casallas PE..atsdr. Soderlund et al. Go et al. epa. Ray et al. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Leng G.atsdr. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Pogo BG. Abell AD. 2005).8(1):18-21.html. In California. Wang SL.. Sunami O. Kuhn K. September 2003. Bernardi MM.. 2005). Yang J. Toxicological profile for pyrethrins and pyrethroids. bioallethrin and deltamethrin. 2002). Eriksson and Fredriksson. Leng A. 2006. 1998. motor activity. Kim IY. Seth PK. J Environ Monit 2006. Additional information about pesticides is available from U. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects.1/15/09 Aziz MH. Leng G. choreoathetosis..251(3):855-859. Kuhn KH. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Yamada T.gov/toxpro2. 2001.108(1):78-85. Song L. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Florio JC. Thomson BM. McCarthy et al. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides.. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Wolff MS. cdc. 2002). Environ Health Perspect 1999.. 2001. Elwan MA.205(6):459-472. Neurotoxicol Teratol 2005.8(1):197-202. neurochemical changes in cholinergic. Pyrethroid pesticide-induced alterations in dopamine transporter function. Available from URL: http://www.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. 1991. Shukla Y. Garey and Wolff. EPA at: http://www. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. 2005). Fredriksson A. dopaminergic... Bernardi MM. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Pauluhn J. Wieseler B. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Kunimatsu T. Shafer. Shin JH. Richardson JR. Okuno Y. In developing rodents. Ranft U. Neurotoxicol Teratol 2001. et al. hypersensitivity.107(3):173-177.S. Lemonica IP. Garey J.. Go V. 2003..50(2):245-255. Shaw IC. Adhami VM.211(3):188-197. Guillot TS. Miller GW. and striatal dopamine levels in male and female rats. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Estrogenicity of pyrethroid insecticide metabolites. Idel H. 2005).62:101-108.300(3):161-165. Kim HS. Kamita Y. Berger-Preiss E. Lazarini CA. 2000. Caudle WM. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR.27(12):1273-1283.

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

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

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

Fourth National Report on Human Exposure to Environmental Chemicals 161 . Survey Geometric mean (95% conf.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid (creatinine corrected) Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. 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.

Berger-Preiss E. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Hadnagy W. J Expo Anal Environ Epidemiol 2003.186:57-72. Angerer J.Pyrethroid Pesticides References Baker SE.209(3):293-299.209(3):221-233. Leng G. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. 2005. Heudorf U. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. et al. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Third National Report on Human Exposure to Environmental Chemicals. Idel H. Williams RL. Angerer J. Ball M. Int J Hyg Environ Health 2006. Human exposure to indoor residential cyfluthrin residues during a structured activity program.77(1):67-72. Barr DB. Schulz C. Krieger RI. Becker K. Spencer J. Hoppe HW. Rev Environ Contam Toxicol 2006. Arch Environ Contam Toxicol 2004. Int J Hyg Environ Health 2006.46(3):281-288. Kolossa-Gehring M. Int Arch Occup Environ Health 2004. Olsson AO. Pyrethroid illnesses in California. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Atlanta (GA). Angerer J. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.109(3):213-217. Heudorf U. Butte W. Ranft U. Sugiri D.206(2):85-92. O’Malley M. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.13(2):112-119. 19962002. Drexler H. Centers for Disease Control and Prevention (CDC). Seiwert M. Angerer J. Environ Health Perspect 2001. Bernard CE. Int J Hyg Environ Health 2003. Heudorf U.

Fourth National Report on Human Exposure to Environmental Chemicals 163 .202 (.670-2.44 (.920) 1. Biomonitoring Information Urinary levels of cis.790) .200) < LOD < LOD < LOD .220-.180 (.870) 1.280 (.170 (. Cyfluthrin.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .310) .120-.960 (.210) .500 (.330 (.68 (.07 (.150 (.11) .24) 1.400-.880 (.380-.700) .890 (.160 (<LOD-.1 and 0.300 (.630) .520) .250-.120-.490-1. The chemical trans-3(2.32) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. cis-3-(2.270 (.240) .270-.740) 1.490-.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .600 (.650-1.200) .1. trans-permethrin.S.340) .490-. but it can also reflect exposure to cis-3-(2.68) .770-1. Similarly. Survey Geometric mean (95% conf.460-1.630 (.550) .680 (.710) . Kuhn et al. but can also reflect exposure to trans-3(2.270 (.470 (.15) .200-.110-.710-1.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. more of the trans-metabolite than Urinary cis-3-(2. the presence of trans-3-(2.780) .120-.or trans-3-(2.230) .850 (.510 (. Kuhn et al.490-1.210-.2-dichlorovinyl)-2.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .630) .380) .510 (.2-dichlorovinyl)-2.35) 1.68) . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.770) .220-.43) .28) 671 680 518 701 591 957 Limit of detection (LOD. trans-cypermethrin. 52315-07-8 CAS No.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.260 (.2-dichlorovinyl)- CAS No.410) .300 (.470-1.420-.220-..430-. 1985.250 (.740 (.300-. which may vary for some chemicals by year and by individual sample.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. 1999). population from the National Health and Nutrition Examination Survey.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.380-.510 (.200-.50) .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 .110-..690) .730 (.270 (. transcypermethrin and trans-cyfluthrin.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.500 (.240) . < LOD means less than the limit of detection.12 (.900 (.262) * * * < LOD < LOD .2-dichlorovinyl)-2.790 (. 1999).580) 1.340) .580-1.640 (.68359-37-5 Cypermethrin Permethrin CAS No.730 (.890 (.790-1.370-. 1985.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.670 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.35) .740-1.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.600-1.790-1.155-.110-.21) .300-.210) 90th .330) .630-.08) . Generally.680-3.220) .730 (.340-. and trans-cyfluthrin.380-.77 (.220-.160 (.54) .140 (.670-1.80) .600) .200) .530 (.160 (.570 (.820 (.440 (.370 (.53) .110 (<LOD-.and trans-isomers. In the body.910-5.2-Dichlorovinyl)-2. ciscypermethrin and cis-cyfluthrin.47 (.200-.670-1.610) .380 (. cis-permethrin.140 (<LOD-.350) .410) .13 (.460-.570-. cis-cypermethrin.460 (. The presence of cis-3-(2.950-2.610) .2-dichlorovinyl)2.740-2.2dichlorovinyl)-2.280-.200 (.180) .120-. and ciscyfluthrin. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.

2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.11) 1.390-. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.230-.340) .550) .59) .250-.200-.600 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.280-.2-dichlorovinyl)-2. 2005). 2006). post- Urinary cis-3-(2.920 (.470-1.800 (. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al. 2006) and 1177 urban adults and children (Heudorf et al.560) 1.420 (.290) . though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al. 2003).880) .360-1.130-. In a study of urban residents in Germany (Berger-Preiss et al.300-.530 (.450-.570) ..67 (.250) .Pyrethroid Pesticides 2.810 (.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.370-. In a study of volunteers.270) .400 (.240 (<LOD-.840 (.200-.350) .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 .S..560) .320-. urinary trans-3-(2.440-..200) .590) .550) .11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .400-1.530 (.150-.750 (.410) .270 (.450-1.37) .270) . 2006.170 (.24) . 2004).370-. Cyfluthrin.03) 1. 2003).320) . Studies in Germany of 396 children and adolescents (Becker et al.540 (.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .12-2.160 (<LOD-. Survey Geometric mean (95% conf.59 (1.230-.190 (.300) . 2005).and trans-3(2.430-1..260) .290) .33 (.80) .210-.750-1.250-.270-. the median and 95th percentile of urinary levels of cis-3-(2.230-..780 (.. 2002).230 (.190) . 2006. population from the National Health and Nutrition Examination Survey.138 (.550-1.690-1.150-.2dichlorovinyl)-2.260 (.120 (.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . 2002).550 (.2-dichlorovinyl)-2. representative NHANES 2001-2002 subsample (CDC. 2004.11) .840 (.200 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.180-.290-.380-.640 (.540 (.510-1.450 (.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.080-.580) .640-. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.S.440 (.380 (.280 (.140-.11) ..260 (.640-1.170 (. 2005) In a small group of indoor pest-control operators.300 (.. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.104-.380) .370-.2-dimethylcyclopropane carboxylic acid did not increase.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.710-3. 2006). urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.680-1. 2001.2-dichlorovinyl)-2.260-.710 (.290 (.150-.11 (.640-1.780) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.182) * * * < LOD < LOD .680 (.890 (.250) 90th .700-2. Lu et al.49) .59) ...390 (.2dichlorovinyl)-2.350 (.21) .220 (.250) .680-1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin. 2005).220) .33) .2-dichlorovinyl)-2.250 (<LOD-.29 (.260 (. Schettgen et al. median urinary levels of trans-3-(2.300) .2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.220 (.430-.2-Dichlorovinyl)-2.31) .340-.830) . 164 Fourth National Report on Human Exposure to Environmental Chemicals .67) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. Other studies have provided evidence that urinary levels of cis.500 (.550-1. 2005).540) . In these volunteers.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al..580-1.390-.190) .180 (.440 (.250-.590 (.640) 1.and trans-3-(2.170) < LOD < LOD < LOD .12 (.440-.340) . In the same residents.300 (.430 (. 2001) showed urinary levels of cis.890) .900 (.700) .700) .

77 (1.08) 1.480-.520-.97-11.400 (<LOD-.76-4.5) 2.63) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.25-3.490-1.780 (.970 (.56) 2.25 (1.07 (1.580 (.760) .810-1.43) 2.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.940 (.62 (1.68) 1.01) 4.27 (1.2-dichlorovinyl)-2.920-1.39 (1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.10) 2.89 (2.560 (.66) 691 680 518 690 595 954 Limit of detection (LOD.610) 1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.09 (.860) .60) .700) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500-.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.40 (1.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .20 (.14-6.76-3.530) .16) 1.42) 1.680-1.Pyrethroid Pesticides application median urinary levels of summed cis.35) 1.620) < LOD 2.20 (.710 (. Finding a measurable amount of cis.68) 1.68-2.55-5.560 (.41-14.4.50 (1.800-1.410-.7) 2.17 (.730) .670) .460-.01 (1. however.410 (<LOD-.68) 2.63) 1.66) .69 (1.470 (<LOD-.440 (<LOD-.400-.08-6. Urinary trans-3-(2.11-2. population from the National Health and Nutrition Examination Survey.60-4.48) 4. trans-Cypermethrin.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.59 (1.85) 4.87 (1.49-5.77) 2.91 (1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.81) 2.S. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.11-1.90) 1.14-2.37 (1.560 (.95) 3. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.56 (1.23 (.17 (.03-1. Biomonitoring studies on urinary levels of cisor trans-3-(2.19) 1.54) 4. Fourth National Report on Human Exposure to Environmental Chemicals 165 .670) .68-3.470 (.550 (.39-5.07-3.500) .850-1.or trans-3-(2.84 (1.910-1.70) size 1976 2525 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .22 (1.08-4.and trans-3-(2.12-6.64-4.20 (.56 (1.23) 2.410-.41 (1.17-1.94 (1.2-Dichlorovinyl)-2. 2005).69) 1.49-3.26 (. 2005). The maximum post-application urinary levels.95) 2.54 (1.820) .19 (3.55-3.520) .19 (2.840-1.910-1.490 (<LOD-.700-1.460-.570) 90th 1.60) 1.13) .420 (<LOD-.2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.750) .500 (.410 (<LOD-.4 and 0.55-4.660) 1.28 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.2-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.2dichlorovinyl)-2.49-3.77) 1.830-1.03-1.42 (2.28 (1.56) 2.14) 1.

720 (<LOD-.15 (1.08 (.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 .470-.750) .37 (1.48-2.89) 2.13) 1.880 (.22) 1.700 (.87 (1.15) 2.41) 1.08 (. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.15) 3.970 (.80) 1.68) 3.47-2.00) 1.29) 1.60) 2.64 (1.33-2.57) 3.530 (<LOD-.91 (1.07-2.00 (1.470 (.930-1.770) < LOD 2.670) .60) 2. population from the National Health and Nutrition Examination Survey.580 (.47 (1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .00) 1.45 (1.34-4.22-2.61) 1.580) .30-3.720-1.13) .820-2.65) 1.98 (1.15-3.00) 5.33 (1.45-2.07) 2.81 (2.700 (.70 (.87-3.780) .2-Dichlorovinyl)-2.07-3.44) 2.640) .74) 2.780) 90th 1.22-1.87) 1.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.410-.02-1.35 (1.60 (1.47-2.500-.42) 1.20-2.540) .57 (1.40-2.850) .55 (2. Survey Geometric mean (95% conf.28) 2.900 (<LOD-1.15-3.56 (1.3) 2. 166 Fourth National Report on Human Exposure to Environmental Chemicals .31 (2.570-.740) .88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.30-6.56-2.91-11.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .520 (<LOD-.19 (1.75 (1.31 (.850) 1.56-5.800-1.530 (.700-.760 (.87-8.720-1.48 (1.91) 1.74) .570 (.86 (2.850-3.660) .570 (<LOD-.27-2.560 (.55 (2.07) 2.800-1.780 (<LOD-.55 (2.35) 1.31) 1.39) 1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin. trans-Cypermethrin.67 (2.27-2.15-3.Pyrethroid Pesticides Urinary trans-3-(2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.610-.11) .33-1.36 (1.00-5.07-1.880-1.26 (1.39 (1.16 (1.880 (<LOD-1.34-3.36) 2.19) .12 (.42 (.730) .440-.87) 1.65 (2.12-1.S.480-.20 (1.

Angerer J. Int Arch Occup Environ Health 2004. Leng G. Angerer J. Heudorf U. Idel H. Heudorf U. 2005. Permethrin and its two metabolite residues in seven agricultural crops. Butte W. Idel H. Hoppe HW. Int J Hyg Environ Health 2006.77(1):67-72. Leng G. Ball M. Hadnagy W. Schettgen T. Schulz C. Leng G. Hardt J. Kuhn K. Angerer J. Berger-Preiss E.114(9):14191423. Angerer J. Bravo R. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Lu C. 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 2002. Heudorf U. Ranft U.109(3):213-217.209(3):293-299. Wieseler B. Idel H. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.76(7):492-498. Angerer J. Sugiri D. Int J Hyg Environ Health 2006. Sugiri D.205(6):459-472. Ranft U. Pearson M. Third National Report on Human Exposure to Environmental Chemicals.62:101-108.206(2):85-92. Levsen K. George DA. Int Arch Occup Environ Health 2003. J AOAC 1985. Drexler H. Drexler H. Atlanta (GA). GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Heudorf U. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. et al. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Angerer J.134(1-3):141-145.Pyrethroid Pesticides References Becker K. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Environ Health Perspect 2001. Bull Environ Contam Toxicol 1999. Biological monitoring of workers after the application of insecticidal pyrethroids.209(3):221-233. Centers for Disease Control and Prevention (CDC). Int J Hyg Environ Health 2003. Bartell S. Kolossa-Gehring M.68(6):1160-1163. Barr DB. Seiwert M. Environ Health Perspect 2006. Berger-Preiss E. Fourth National Report on Human Exposure to Environmental Chemicals 167 .

deltamethrin has been used against mosquitoes that carry malaria. Following residential spraying with deltamethrin for malaria protection in Mexico.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.2-dimethylcyclopropane carboxylic acid of 0..S.2-dibromovinyl)-2. 52918-63-5 General Information Cis-3-(2... Outside the U. 2005).2-dibromovinyl)2.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dibromovinyl)-2.2-dibromovinyl)-2. 2001.5 μg/L) than the detection limit (0.2-dibromovinyl)-2. Deltamethrin can degrade to cis-3(2.2-dibromovinyl)-2.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. 2001) showed that urinary levels of cis-3-(2.2dimethylcyclopropane carboxylic acid formed in the environment. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Urinary levels for adults and children in these studies were similar (Heudorf et al. In the NHANES 2001-2002 subsample. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.2-dibromovinyl)-2. 2006) and 1177 urban adults and children (Heudorf et al.3-0.2-dibromovinyl)-2.Pyrethroid Pesticides Deltamethrin CAS No.2-dibromovinyl)-2. 2005).. Thus.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. (2004) reported a geometric mean concentration of cis-3(2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS. 2005). in detection of cis-3-(2. urinary levels of cis-3-(2. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population. 1990). Biomonitoring Information Urinary levels of cis-3-(2.39 µg/L. in some situations replacing the use of DDT. 2004).. Studies in Germany of 396 children and adolescents (Becker et al. mean peak urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. Finding a measurable amount of cis-3-(2..2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2-dibromovinyl)-2. Baker et al. 168 Fourth National Report on Human Exposure to Environmental Chemicals .

Pyrethroid Pesticides Urinary cis-3-(2. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.2-Dibromovinyl)-2.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 and 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Fourth National Report on Human Exposure to Environmental Chemicals 169 .2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1. 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. Survey Geometric mean (95% conf.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2-Dibromovinyl)-2. 170 Fourth National Report on Human Exposure to Environmental Chemicals .S.Pyrethroid Pesticides Urinary cis-3-(2. 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.

Environmental Health Criteria 97.109(3):213-217. Hoppe HW. Angerer J. Lopez-Guzman OD.209(3):293-299. Heudorf U. Centers for Disease Control and Prevention (CDC). 5/26/09 Ortiz-Perez MD. Environ Health Perspect 2001. Angerer J. International Programme On Chemical Safety (IPCS). Schulz C.org/documents/ehc/ehc/ ehc97. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Heudorf U. toxicokinetics. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. 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. Kolossa-Gehring M. Heudorf U. Seiwert M. et al. Environ Health Perspect 2005.209(3):221-233.77(1):67-72. 2005. Drexler H. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Butte W. [online] 1990. and genotoxicity in exposed children. Deltamethrin. Int J Hyg Environ Health 2006.htm.inchem. Ball M. Int J Hyg Environ Health 2006. Int Arch Occup Environ Health 2004. Grimaldo M. Available at URL: http://www.Pyrethroid Pesticides References Becker K.113(6):782-786. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Angerer J. Angerer J. Batres LE. Carranza C. Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals. Torres-Dosal A. et al.

(2004) reported geometric mean levels of 3-phenoxybenzoic acid that were approximately sixfold higher than levels for adults in the NHANES 2001-2002 subsample (CDC. 2005). Becker et al. A study of 396 German children (Becker et al. 2006. Following residential spraying with deltamethrin for malaria protection in Mexico. 2002. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Saieva et al.52315-07-8 CAS No. 2006). 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. 2005).S..Pyrethroid Pesticides Cyhalothrin CAS No. mean peak urinary levels of 3-phenoxybenzoic acid in children increased at least sixtyfold over non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (OrtizPerez et al. In a small group of indoor pest-control operators. 2003). In the New York City study. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. 52645-53-1 Tralomethrin CAS No. Fenpropathrin Permethrin CAS No. 2005). 2005). the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. 2003. Baker et al. 2005). representative NHANES 2001-2002 subsample (CDC. 2003.. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides.. 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. Hardt and Angerer. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.... CDC.. Biomonitoring studies of 3-phenoxybenzoic acid provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of pyrethroids than levels found in the general population. 68359-37-5 Cypermethrin Deltamethrin CAS No. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. 52918-63-5 use and house dust levels (Lu et al. 39515-41-8 CAS No. Urinary levels of 3-phenoxybenzoic acid in children were found to be related to residential pesticide 172 Fourth National Report on Human Exposure to Environmental Chemicals . CDC. 2005. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. 2005). 2004). 2005). Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. 2005. CDC.. Thus. 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. In one study of 145 urban residents in 80 private homes in Germany. 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. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng 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.

46) 2.41-2.53-3.311 (.710 (.44) 5.510-.35 (1.470-.33 (1.320 (.90) 1.48-2.267 (.240 (.220-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin. interval) .25-1.86 (1.25-7.41-3.27-2.16) 1.64) 697 680 524 701 603 957 Limit of detection (LOD.266-.62) 5.260 (.260 (.355) .46) .30) 3.8) 3.25-4.16-1.260-.780) 4.507 (.560-1.71 (1.314) .250 (.320) .190-.290 (.250-.76 (1.265-.750-1.300 (.78) 1.277-.810) 1.190-.28) 1.81 (1.63 (3.160-.1) 3.226-.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 .321 (.352-.250 (.200-.62-6.30 (.05) 1.200-.940) 1.427) .590 (.590-.820) .35) 2.340) .04) .830-2.240 (.33 (2.50 (2.600 (.35 (2.27-11.353 (.52-5. Deltamethrin.72 (1.35) 1.54) 1.530-.233-.34 (2.276-.490-.328 (.32 (1.227-.34-6.570-.325 (.36) 1.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.510-.374) 99-00 01-02 99-00 01-02 99-00 01-02 .190-.340) 75th .360) .89-71.238-.18 (1.1) 3.300 (.45 (2.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .39) 2.700-1.336 (.850) .270 (.297 (. population from the National Health and Nutrition Examination Survey.700 (.56-5.13) .740 (.49-2. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.75 (1.430-.550-.21 (2.292 (.48-2.1.92-3.246-. Fourth National Report on Human Exposure to Environmental Chemicals 173 .800) 1.13 (.320) .26-2.33) .428-. Survey Geometric mean (95% conf.320) .26) 2.38 (2.12) .1) 3.12) 4.210-.320) .330) .51-6.387) .315 (.34) 8.12 (.25 (2.271-.04-5.610) .18 (2.93 (1.730 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.292-.55 (1.49 (1.35) 2.53) 1.32-21.680 (.570-1.350-.1 and 0.230 (.03 (3.29-1.280 (.840-1.364) .340) 1.450 (.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .49-2.530-.314 (.42-2.390) .250 (.41 (1.362) .253-.190-.32 (2.210-.670 (.78 (1.454 (.60) .560-.69) 3.160-.52-4.586) .78) 6.25 (2.434) .230-.520 (.62-8.288-.69 (1.230 (.440) .760 (.330) .78) 1.200-.01 (1.73) 1.27-2.65-2.740 (.830) 90th 1.370) .640 (.601) .26) 2.420) .870 (.560-.63-3.260 (.820) .38 (2.270) .65 (1.180-.41) 3.800 (.630) .45-5.298 (.230-.02-6.750) .247-.373) .300 (.288 (.750) .300) .960 (.850) .369) .710 (.23 (2.30 (1.384) .230-.620-1.595) .S.49 (1.79) 3.14-6.490) .417 (.05) .273 (.51-3.650 (.295) .83-11.430-.43) 3.406) .990) .

253) .510 (.220 (.300-.240-.19 (2.490-.261-.860-1.335-.280 (.27) 1.534) .446) .88-5.560 (.35-3.700-1.73-4. Survey Geometric mean (95% conf.316 (.75-8.510 (.670) 3.229-.00) 1.49 (1.730-1.240 (.720 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.13 (.570) .480 (.150-.272) .37) 1.440-.15-2.240-.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .423 (.274 (.330) .04 (3.61-2.490 (.21 (1.63-3.35) .590-1.41) 1.321-.530-.350 (.240 (.270) .550 (.67) 1.400-.261 (.49-2.640 (.21-4.960-1.238-.810) 1.03-1.278) .190-.200-.44 (1.41-4.210 (.60) 1.250 (.43 (1.11 (.55 (1.63) 1.S.500) .290) .280-.49) 1.190 (.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .225-.590) .930) 1.329) .202-.40 (1.299-.250) .275 (.580 (.74) 3.210-. Deltamethrin.62) .11 (.240 (.378 (. interval) .460-.09) 3.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.44) 2.09 (.320) .10 (2.860 (.94 (1.91 (2.52 (1.630) .370 (.270) .220-.200-.210 (.51-7.09-2.04 (.280) .53 (1.246 (.84 (1.240-.17-1.216-.16-4.40) 2.07-5.230-.230) .48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.91) 9. population from the National Health and Nutrition Examination Survey.740) .72 (1.280) .270-.450 (.19-6.22 (1.677) .730) .36 (1.750-1.91) .173-.640 (.230-.550 (.55) 3.330) .00) 5.480-.410-.590) .380 (.310) .860-1.00) 1.234 (.200-.39) 1.670) .437) .226-.274-.80) 4.13-1.590) .73) 1.13-1.35 (1.64-5.309 (.43-64.54 (1.328) .460-.270 (.25) 2.271-.400) .490 (.224-.580) .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 .400-.380-.530-.95) 1.52) 2.200-.370-.96 (1.190-.264 (.0) 3.330 (.06-3.43 (2.90) 3.49) 3.550 (.610 (.390-.330) 75th .329) .43) 1.36-6.19) 2.227 (.730) .250 (.35) 1.540 (.323 (.17 (.311 (.440-.07) 2.760) .300-.372) .270 (.440-.312 (.280 (.840-1.09-2.401) .387) .930) .25-2.350) .03 (.48 (1.309) .290) .67 (1.240-.365) 99-00 01-02 99-00 01-02 99-00 01-02 .178-.510 (.362 (.720) 90th 1.02-1.83 (1.160-.83) 1.290-.25-5.32 (2.91-4.81 (1.60-4.357) .410) .280 (.37 (1.86 (1.650) .420-.272 (.05-3.330) 1.240 (.62) 1.67 (1.02 (2.

Lapinski R. Atlanta (GA). Hardt J. Third National Report on Human Exposure to Environmental Chemicals. Bravo R. Leng G. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Environ Health Perspect 2003. Carranza C. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Kolossa-Gehring M. Int J Hyg Environ Health 2002. Indoor pyrethroid exposure in homes with woollen textile floor coverings.113(6):782-786. Arch Environ Contam Toxicol 2004. Olsson AO. Deych E. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. et al.206(2):85-92. Grimaldo M.111(1):79-84.46(3):281-288. Int J Hyg Environ Health 2006. Berger-Preiss E. et al. Leng G. Hoppe HW. Berkowitz GS. et al. Seiwert M. Barr DB. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Bartell S. Fourth National Report on Human Exposure to Environmental Chemicals 175 . A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Obel J. Biological monitoring of workers after the application of insecticidal pyrethroids. Liu Z. urban cohort. Int J Hyg Environ Health 2003.Pyrethroid Pesticides References Baker SE. and genotoxicity in exposed children. Sugiri D.205(6):459-472. Centers for Disease Control and Prevention (CDC). Pearson M. Idel H. Lu C. Idel H. Lopez-Guzman OD. Angerer J. Environ Health Perspect 2005. Hadnagy W. Environ Health Perspect 2006. Godbold J.209(3):221-233.114(9):14191423. 2005. Angerer J. toxicokinetics. Berger-Preiss E. Levsen K. Int Arch Occup Environ Health 2003. Ortiz-Perez MD. Becker K. Ranft U. Batres LE.76(7):492-498. Barr DB. Ball M. Sugiri D. Torres-Dosal A. Exposure to indoor pesticides during pregnancy in a multiethnic. Ranft U.

220) 95th .099 (.090-.180) .270) .170-.120) .530) .120) .122 (.270 (.410) .112-.300-.130 (.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.120-. ceramics.230-.350) .070 (<LOD-.260 (.119) .160 (. respectively.140) .220-.100 (.250) .170-.210) .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 .190) .130 (.490) .160-.175 (.280 (.240 (. and 03-04 are 0.176 (.120 (.140) .178) .280-.180 (.350 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals .310 (.114) .350) .200-.320) Total .140) .145) Selected percentiles ( 95% confidence interval) 50th .330) .340) .300) .320 (.117-.240 (.310 (.310-.140) .105 (.04.370-.180 (.320-. Stibine is a metal hydride form of antimony used in the semiconductor industry.270 (.330-.184) .164-.400 (. solder. People are exposed to antimony primarily through food and.560) .200) .150-.197) .240-.460) .300 (.350) .290 (.350-.390) .157) .070-.125 (.190-.240) .190) .200 (.260) . storage batteries.210-.300) .130-.070 (<LOD-.04.142 (.190 (.130) < LOD . 01-02.400) . and glass. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.230-.440) .390 (.400 (.290-.220) .154) .109-.410-.240 (.132 (.150 (. 0.400-.090-.400 (.150 (.420) .150-. from air and drinking water.108 (. It is also used in paints. and pewter.150) .087-.360 (. fireworks.119-.170 (.310-.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 .250-.134 (.110-.120 (.100-.115-.350 (.120) .100-.120-. Dermal contact with soil.150-.146 (.210) .130-.470 (.210 (.130 (.120-.260 (.098-.150-.200 (.130 (.230-.250 (.133) * .180-.130 (.230-.160) .190) .120-. castings.430 (.132 (. and refuse incinerators that process or release antimony.240 (.200-.180-.154-.360) .110 (.110-.360) .161) .120-.150-.460 (.220) .710) .140-. interval) .190-. or other substances containing antimony is another means of exposure.330) .260-.350 (.370) .220-.120 (.120-.270-.410) .160 (. metal bearings.140 (.156-.600) .260-. enamels.154) .200) .250-.440 (. population from the National Health and Nutrition Examination Survey.150) .280) .250 (.270 (.190-.190 (.330) . ammunition. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Antimony enters the environment from natural sources and from its use in industry.170) .07.100 (.320 (.210) .131-.470) .180 (.130-.130 (.160) .190 (.130 (.290-.170-.250-. water.180-. and as a fire-retardant in textiles and plastics. The absorption.150 (.310 (.130) .220 (.200) .270 (.350-.400) .300) .230) .160) .120-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.220-.350 (.320-.220-.090 (. Workplace exposures can occur at smelters.145 (.230-.280-.110-.120) .280) .180 (.500) .240-.330 (.190-.126-.140 (.134-.080-.230 (.210) .210 (.200-.140) .S.130-.310) .200 (.148-.220-.430 (.200) .310 (.260) .570) .320) .117-.207) .190) .260) .190 (. 7440-36-0 General Information Antimony is found in ores or other minerals.470) .140 (.130) .103) .230 (. coal-fired plants.120 (.130) . and excretion of antimony vary depending on its oxidation state.135) * .150) 90th .300-.080) .250-.350) .390-.270) .360-.120 (.170-.360 (.350-.310) .220-.320-.490 (.230 (.190-.180 (.330 (.130-.280 (.137) .210) .390-.230) .169 (.136) * .180) .400) .180-. and +5.200 (.230) .340 (.390) .280) .240 (.180-.280-. Antimony can exist in one of four valences in its various chemical and physical forms: -3. distribution.440) .120-.330) . see Data Analysis section) for Survey years 99-00.160 (.143 (.120-.140) .128 (.160-.350 (.137) . < LOD means less than the limit of detection.140 (.095-.280-.128 (. +3.093 (.095 (.170-.200 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 0.160-.080 (<LOD-.141-.160) .390-.200 (.200-.144) . 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.115) .190) .460 (. which may vary for some chemicals by year and by individual sample.280-.079-.108-.110-.158 (.130-.280) .220) .330-.330 (.180 (.126 (. It is used in metal alloys.160) .460 (.390) .088-.390) .320-.150) .090 (<LOD-.210-.260 (.340 (. to a lesser extent.123 (.250 (.136-.170 (.300 (.100) .090) 75th . sheet and pipe metal. and 0.130 (.160) .220 (.080) .430 (.110) .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 .Metals Antimony CAS No.130-.190 (.300-.500) .160-.510) .

117-.417) .146-.343 (.209 (.068 (.195 (.146-.130) . Histopathologic inflammatory and degenerative changes in the lung.414) .364 (.250) .391) .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 .130) .146) .195-.109-.171) .259 (.082) .30) .167 (.317) .121 (.178-.080 (<LOD-.192 (. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.338) .357-.235-.139 (.150-.175 (.256 (.238 (.199-. Ming-Hsin et al.318-.164-. Fourth National Report on Human Exposure to Environmental Chemicals 177 . 1995).485) .310) .230-.132) .268) .261) .100 (.143) 90th .310) .318-.373) .138) * .267-.122 (.173 (.108-. 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.214) .265 (.138-.250-.109 (.120 (.102-.338 (.107-.196 (.124-.129 (.320) .263 (.115-.163 (.267) . Inorganic antimony salts irritate the mucous membranes.119 (.173) . resulting in hemolysis with abdominal and back pain (Dernehl et al.145) .106-.149-.111 (.099-.352 (.178 (.310 (.115) .162-.317) .425) .144-. skin.S.138-.129) * .286 (.242-.185 (.076-.200-.140) < LOD .159-.298 (.181) .203) .092) . 1986).189 (.123 (.185 (.095-.109 (.320 (.069-.238) .263-.130) .096-.117-.176-.135) . and kidney have been demonstrated in high dose animal studies depending on the dose.081 (<LOD-.098-.288 (.220) .118 (..167 (.153-.108-.280 (.333-.333 (. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.391) .333) .173-.156-.333-.115-..245) .238) .163 (.266 (.124 (.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 .152) .112-.315) .188) .123) .333 (.250 (. 1954).213 (.143 (.161) ..106-.200-.471) .134) .333-1.140) .313-.185-.119-.421) .241-.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 .126-..236 (.317) . and ulcers (Werrin.179-.112 (.113) .300 (.205-.209) . 1973). 1962).191 (.217 (.182 (.204-.192-.149) .320-.176 (.085) .130 (.113-. population from the National Health and Nutrition Examination Survey.113-.092-.364 (.371 (.114 (. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.095-.255) .132 (.333 (.128-.248-.125-.075 (.225 (.114 (.103-.086) 75th .120 (.159-. species.143) Selected percentiles ( 95% confidence interval) 50th .429) .076-.193) .164 (.265-.250-.195-.107-.277 (.126) .097-.151) .281-.208 (.114 (.115 (.135) .480) . and route of exposure (Elinder and Friberg. interval) . 1988.207) .430) .138 (.120 (.267 (.087) .135 (.Metals than for trivalent compounds (Elinder and Friberg.203) .108 (.161) .405) . myocardium.156 (.225) .294) Total .380 (.320 (.074 (.320-..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.357) .160 (.278) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.127) .082) .147) .172-.352) .159-.417) .080 (.143) .278 (.107-.133) .200) .227-.250 (.081) .126 (.741) .228-.152) .116 (.247) .233 (.181) .105-. 1944).082 (<LOD-.230) 95th .135 (.135) .084) .061-.272) .098-.447 (.183) .071-.194-. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.186) .253-. Acute antimony poisoning may cause a metallic taste.308) .121) .209) .112 (.209-.150-.148-.154-.269 (.321) .108-. and eyes.500) .127) .089) .295 (.741 (.118 (.139 (. 1953).192) .233-.143) .727) .444) .129) .127) .125 (.129 (.127) .164) .253 (.167 (.068-.131) .228 (.103-.099-.115 (.444) .136) . 1958) and occupational exposures (Briegner et al.241-.137 (.300) .208-.200-. abdominal pain.117-.121 (.308-.255-.124-.098) .438) .115 (.471 (.131 (.385 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.167-.078 (. diarrhea. and gastrointestinal symptoms such as vomiting.120 (.122 (.176 (.276 (.248) .198) .187) .211) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.188-.226 (.250-.193 (.131-.153 (.229-.075 (.102-.222 (.338 (.250-.400 (.170 (.124) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.244-.300) .111-.224 (.148) * .429 (. 1986).333-.173 (.146-.069-.119-.271-.228 (.181) . liver.147-.206-.239-.127 (.086 (.233) .280-.104-.079 (<LOD-.104-.257) .148-.116-.077) .

and antimony in optoelectronic industry workers. Sabbioni E.atsdr. Shao-Chi C. and future strategies.76:432436. Luedersdorf R. Biological monitoring of exposures to aluminum. Chia-Yu H. Urinary antimony in infancy. and hydrogen sulfide.521-523. Friberg L. Hamilton EI. Nau CA. Chemotherapy for leishmaniasis: Biochemical mechanisms. Earlier measurements in general populations (Minoia et al. Bailly R. Vouk VB. External and internal antimony exposure in starter battery production. Dezateux et al. Roland H. Lauwerys R.64(2):182-185. New York: Elsevier. Pulmonary edema of environmental origin. Gebel TW. Dezateux C. J Trace Elem Med Biol 2002.10(3):560-586. even when exposure levels were below workplace air standards (Bailly et al. Iavicoli et al. Cordasco EM.. Kuo-Juie Y.. HH. Wade A. Cheng-Wei L. et al. Rev Infect Dis 1988. which may be due to methodologic. population. Chin Med J 1958. Iavicoli I. Industrial antimony poisoning. 1998) or compiled reference ranges (Hamilton et al. Kiberd B. or exposure differences.16: 33-39. J Clin Pathol 1998. Antimony trioxide is rated by IARC as a possible human carcinogen. Suchenwirth R.. Bolten C.. Matthews T. Piatnek DA.51:238-240. pp.. 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. Int Arch Occup Environ Health 1995. plasma and urine and a critical evaluation of reference values for the United Kingdom population. References Berman JD. Atlanta (GA).Metals to antimony have been established by OSHA and ACGIH.. Pietra R. Review of elements in blood. Ho C-K.158:165-190. Leinemann M. Cullen A.html. Biomonitoring of a worker population exposed to low antimony trioxide levels. 1998). Chest 1973. Biological assessment of exposure to antimony and lead in the glass-producing industry.. Environ Health Perspect 1998. Arsine. Wu M-T. J Occup Environ Med 2004. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Trace element reference values in tissues from inhabitants of the European community I. 1990. Third National Report on Human Exposure to Environmental Chemicals.59:469-474. Arch Dis Child 1997. 26-42. Industrial Medicine 1944. Int Arch Occup Environ Health 1987. Gallorini M. Delves HT. Skulsukai G. Dernehl CU.67:119-123. Yu H-S. Apostoli P. Element reference values in tissues from inhabitants of the European community. 2002. Briegner H. environmental levels) and health effects is available from ATSDR at: http://www. Handbook on the toxicology of metals. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Dunkelberg. 2nd ed.. Ju-Sun P. In: Friberg L..76(2):103-115. Elinder CG. Buchet JP. 1997). Van der Venne MT. and a drinking water standard has been established by the U. gallium.48:93-97. EPA.. eds. Ludersdorf et al. Delves HT. Ming-Hsin H. Stead FM. Konings J. 1986. Information about external exposure (i. Pozzoli L. Mahieu P. 20012002. Schacke G. Antimony in blood and urine of infants. et al. Costeloe K.13:361-362. 1991.106:33-39. Nordberg GF. VI. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. gov/toxpro2. 1994) have reported values slightly higher than those in this Report. Kentner et al. Kentner M.e. Chen J-R. Mayer P. respectively. and 2003-2004. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. et al.46:931-936. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Stone FD. 1995. Yang C-Y. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Petrucci F. 1998. Centers for Disease Control and Prevention (CDC). Minoia C. Semisch CW. indium. Schaller KH. Sci Total Environ 1994. Stasney J. 2005. 2004.. Carelli G. Paschal et al. Lenert G. Biomonitoring Information Levels of urinary antimony reflect recent exposure. stibine. Liao Y-H et al. arsenic. Sabbioni E. Fuchs A. Industrial Medicine and Surgery (Dec. Alimonti A.S. Liao Y-H. Weltle D. Stocks J. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals .cdc. Pilgrim L. 1987). Mayne P.. Caroli S. Antimony. O’Regan M. clinical efficacy.)1954. Br J Ind Med 1991. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al.

et al.Metals in urine. 27:38-45. Paschal DC. Ting BG.99-108.76(1):53-59.95:89-105. Environ Res 1998. Renes LE. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Trace metals in urine of United States residents: reference range concentrations. Chemical food poisoning. Jackson RJ. Antimony poisoning in industry. Sci Total Environ 1990. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Morrow JC. Werrin M. Sampson EJ. Pirkle JL. Industrial Hygiene and Occupational Medicine 1953. blood. and serum of Italian subjects.

4 (48.1) 15. such as arsenopyrite (FeAsS) and realgar (As4S4). Gallium. ocean and fresh waters.90-7.5) 41.0 (43.1) 7.7 (11. mental disorders.0 (15. aluminum.5) 66. Arsenic and its compounds have had many uses in the past and present as medicines.70-9.8) 33.7) 65. In nature. and produce. and arsenates (oxidation states of -3. General population exposure to inorganic arsenic can occur through consumption of drinking water and. copper arsenates.70) 8.7-95.12 (6.25-9. and.10) 10.3) 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. Various arsenic compounds were used in paint pigments and for tanning animal hides. Although it is still widely used in the United States. mostly for use in wood preservation (ATSDR.8) 7. Water sources contain mostly inorganic arsenate.20 (8.40) 7.3) 10. Since the 1940s. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. see Data Analysis section) for Survey year 03-04 is 0.8) 7. retaining walls.90 (5. cacodylic acid.02-8.5) 95th 65. Before the 20th century.90-8.80) 6. were used as treatments for syphilis.9-62. meats. arsenocholine. semiconductors.5 (14. or rarely as elemental metalloids (yellow.2-61.Metals Arsenic CAS No. 2005).34-9.4) 60.70 (6.5-41.90-14.0 (11.5 (23.10 (6.10-7.5 (40.6 (9.0-19.2-17. to a lesser extent.1 (38. and other metals.90-8.9-34.80-9.29 (8.4 (24.90 (7. Arsine (AsH3) is a reactive.19-9.S.9 (17.9 (8.6) 11.66-8. and play sets.8-77.57) Selected percentiles ( 95% confidence interval) 50th 7.4 (7. and foods.8) 29.6 (13.30) 17. Arsenic trioxide is approved to treat acute promyelocytic leukemia.97) 8. and as homicidal poisons.2-20. lead. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.0 (22.0-60. interval) 8. it is found in over 200 crystalline or mineral forms.6) 618 722 1074 Limit of detection (LOD.08 (5.5-19.1) 290 725 1542 03-04 03-04 9.50 (8.7-83. psoriasis.10-10.2 (51. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. and in lead-acid storage battery grids. solders.8) 17. and gray forms). from coal burning. gaseous hydride manufactured in small quantities for use in the semiconductor industry.8-61. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. +3 and +5). to a lesser extent. arsenic as elemental metalloids may be used in some ammunition.8) 30.4) 40. lead hydrogen arsenate.9) 21.00-9.4-65. Arsenic trioxide (As2O3.7) 90th 37.90-11.27) 9.12-10.6-35.50-14.3-111) 78.5 (34. black.4 (26.9) 68.90) 75th 16.000 metric tons annually.00 (6.4 (31. population from the National Health and Nutrition Examination Survey. In the last century. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.8 (48. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. referred to as inorganic arsenic compounds.2) 46. and indium arsenides are used in the semiconductor industry.34-10.74.30 (6. and arsenosugars. cancers. as alloy in metal bearings.84) 8. 2001). Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.90) 16.6-43.2 (41. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.3-15.1-18.6 (32.2 (13.1) 1281 1276 03-04 03-04 03-04 9.1-40. Survey years 03-04 Geometric mean (95% conf.3-19. though in some locations arsenite may be prevalent (WHO.84) 8.90 (7. Also.4) 13. pesticides.8) 34.5) 43. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.41 (7.30 (7.5-178) 46. and as a cosmetic to lighten complexion. arsenites.77) 6.9-46.5 (36.2 (12. particularly arsenic trioxide. 180 Fourth National Report on Human Exposure to Environmental Chemicals .6 (15.1 (32. sodium arsenite.2) 15.5-52. arsenic compounds. alloys. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. grain. trimethylarsine oxide.0 (14.13-8.2-93. the smelting of copper. The United States no longer produces arsenic from mining but imports about 22.7) 24.80 (5.6-141) 53. Arsenic is measurable in most soils.55 (7.

are used in enclosed ultraclean operations within the semiconductor industry.8 (12.0-38.44-11.S.8) 27.8 (20.4 (40.4 (11.93-9.23-7.0) 14.S.10-8.6 (35. 2001). EPA’s maximum contaminant level (Hughes.7 (11. 2001).g.2) 15. and folate status (Chen et al. age.35) 7.7-34. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. Tseng.04) 7. and arsenosugars.30-9.07-9.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .13) 8.93-8. arsenic does not show biomagnification in the food chain (WHO.0) 33.6 (10. organic arsenic can be converted back to methylated and inorganic arsenic. selenium. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.64 (7.3 (24.88) 7.41) 6.4 (12.7-188) 27. WHO.4 (26. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet. NRC. Smoking tobacco is also a source of inorganic arsenic.7-18. interval) 8..58-10.66-8.66 (7. Though modest bioconcentration occurs in some aquatic life. Arsenate is reduced in the body to arsenite (oxidation state +3).0-18. Steinmaus et al. Direct exposure to DMA and MMA may result from use of the two pesticides.2-15. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.38-10. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.20-9.61 (7.9) 53.. 2001.47-6.50 (6.99-9.8 (11.3 (27. EPA.7 (25. Survey years 03-04 Geometric mean (95% conf.1 (14.7-35.1) 6. U.31 (6.10-16. trimethylarsine oxide (TMAO). dust.6) 45.4-64. dose level. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.0 (31.33 (6. 2001). 2001).0) 1281 1276 03-04 03-04 03-04 8.9-56. 2001). 2001).3-53. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.7-17.51) 75th 14. 1988). 2006.6 (17. and some other seafood can contain organic forms of arsenic including arsenobetaine.4 (24.04 (5..5 (9.9) 13.3-41. so exposure to the general population is extremely limited.75 (5.2-46.0) 42.4) 32. 2007. shellfish.0-26.00 (6.25-9.01) 11.2) 90th 30. and contact with CCA-preserved wood structures. 2007.2) 40. Chowdhury et al.45) 5.47 (7.8-62.S.1) 7.01) 7.2 (12.3) 9.8 (21.76 (6.25 (6.86-17.06 (4. Extremely high groundwater arsenic levels. but is poorly absorbed dermally (WHO.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.59) Selected percentiles ( 95% confidence interval) 50th 7.33-10.88 (5.8-32.1) 58. gallium arsenide and indium arsenide. Fish.0-69.81-9. mine tailings).44) 6.1) 8.96) 12. 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.40) 8.1 (11. Gamble et al. population from the National Health and Nutrition Examination Survey. Inorganic forms of arsenic demonstrate high acute toxicity.75) 13.66-8.0) 26. as observed in Bangladesh where millions of people have been exposed. 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. arsenocholine. In aquatic sediments.4 (42.1) 24.3) 6.24 (7.0) 12.9 (45.5) 290 725 1542 03-04 03-04 8. cacodylic acid and monosodium methyl arsenate.7) 28.8) 22.. 2007.3-64. 2001). 2006.18 (5.5-120) 40.1-36.5) 17..47 (6.8 (27. 2001).6-17.12-10. In aquatic organisms.3-62. kelp.7 (9. though some reduction may occur in the gut prior to absorption. 2001.32 (5. Children may have additional exposures from ingestion of contaminated soils (e.5-17.28-7.7) 95th 50. After absorption. The semiconductor dopants.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 8.11 (5. inorganic arsenic is widely distributed within the body.4) 54. have caused clinical arsenic poisoning. WHO.8-75.0 (17. 2003.

respectively. Chronic arsenic exposure in humans is considered to be a cause of skin.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. substitution in phosphate metabolism.EPA.10 (<LOD-1. and endothelial injury (Kumagai and Sumi. and by uncoupling oxidative phosphorylation (NRC. Chile). 2004). and diarrhea. 2001). With chronic exposure. gluconeogenesis. and hyperpigmentation of the skin (NRC. The U. including inhibition of numerous enzymes. Bredfeldt et al. 2004). Although arsenate is reduced in the body to arsenite. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells.20 (<LOD-1. increased oxidative stress.50) 621 725 1078 Limit of detection (LOD. NRC.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Such actions may lead to decreased energy production. 2001).50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. vomiting. lung. 2001). Studies of arsenic at levels typical of U.. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. 1998.EPA has established drinking water.g.10 (<LOD-1. WHO. 2007. can cause peripheral sensorimotor neuropathies. 2006.. 2006. 2001).S. noncirrhotic portal hypertension.10 (<LOD-1.20 (<LOD-1.0. Chronic elevated arsenic intakes have been associated with diabetes. and DNA repair inhibition (Cohen et al. Acutely. U. hematocytopenias. and altered gene expression. 2006) or when exposure occurs in smokers (Chen et al. Cohen et al.50) 1. population from the National Health and Nutrition Examination Survey. apoptosis.60) 1..30) 1.. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al.g.. Bangladesh. hypertension.. including drinking water sources with elevated arsenic levels (e.20 (<LOD-1. which may vary for some chemicals by year and by individual sample. fatty acid oxidation. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al.60) 1. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. hyperkeratosis.80) 1. Chronic human intake of arsenic at less than acutely toxic doses. Taiwan. < LOD means less than the limit of detection. WHO. food residue. drinking water have not been associated with increased cancer rates (Schoen et al. 2004.. hepatotoxicity. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. WHO.S. Raml et al.. 2000. WHO. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. 2001). see Data Analysis section) for Survey year 03-04 is 1. Survey years 03-04 Geometric mean (95% conf. 182 Fourth National Report on Human Exposure to Environmental Chemicals . and bladder cancer (IARC. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e.S... Arsenic has many actions demonstrated in cellular studies.10 (<LOD-1. and production of glutathione may be affected as well.S. but additional or confirmatory research is needed (Kapaj et al. which can lead to dehydration and shock.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. 2006. NRC. 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. some of these effects may take years to develop. peripheral vascular disease. 2001. leading to a decrease in adenosine triphosphate energy production. cell transformations. renal failure. 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. arsenic trioxide) includes hemorrhagic gastritis with nausea. 2001). Cellular glucose uptake. Cardiac arrhythmias.10 (<LOD-1. and childhood neurodevelopmental effects in observational human studies. 2007). The organic forms of arsenic occurring in seafood have little known toxicity. and it also will inhibit succinate dehydrogenase.. 2007. cytotoxicity. interference in signal transduction pathways. 2001.20 (<LOD-1.. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose.

gov/toxpro2. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al.. 2000. 2006. Josyula et al. 1999). population (Rubin et al..33 (<LOD-3. population from the National Health and Nutrition Examination Survey. In a Nevada town where groundwater levels were naturally elevated.. median urinary total arsenic levels in 4052 adults varied with seafood intake.00) 1. Compared with this Report... arsenic has been fetotoxic and teratogenic. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 1999..e. although urinary arsenic levels were not associated with CCA contact (Shalat et al. Pellizzari and Clayton.S.atsdr. Shalat et al. 2004. Survey years 03-04 Geometric mean (95% conf. Meza et al. 2001).. Vahter et al. In the German Environmental Survey III of 1998. 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..75 (<LOD-2..89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.. Caldwell et al.. 2007.18 (<LOD-3.. 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. 2001). the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.. Caldwell et al. Consequently. 2006).75 (<LOD-2. 2006. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.Metals compounds.html. 2008. 1998. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens.41) 3... Pellizzari and Clayton. 2004. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. 2000).. 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. Pellizzari and Clayton 2006).18) 3. 1999..S. 2007. had decreased since the prior 1990– 1992 survey. Additional information about external exposure (i. and the FDA has established a bottled drinking water standard..33 (<LOD-3. Several studies have shown that urinary arsenic levels are not correlated with low levels of arsenic measured in house dust or in washings taken from hands (Hysong et al. Offergelt et al. environmental levels) and health effects is available from ATSDR at: http://www.. 2006). Shalat et al. Levels of total urinary arsenic in the U.. 1992. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. Valenzuela et al. and were about two-fold lower than those for the U.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. DMA produced bladder cancer in some chronic rat studies (Cohen et al.61 (<LOD-3. 1986). 2006).. 2008).50) 1. Calderon et al.80 (<LOD-4.S.69 (<LOD-3..04 (<LOD-3. 2008). population in NHANES 2003–2004 (Schulz et al. 2001). WHO. but generally only at maternally toxic doses (WHO.cdc.S. 2006.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. In animal studies. Though CCA-treated wood contains several thousand times more arsenic than untreated wood.19) 3. 2003. 2006).

and TMAO were detected in only 7.. 4.30) 10.31-1..48-2. WHO.800 (..10 (4. DMA and MMA.10) 8.30 (2. 2000.60-3. 2005.6.700-1.5) 621 725 1078 Limit of detection (LOD.4.8-40. 2008.90-7.70 (5.00-1. These associations are stronger at higher urinary levels. and other factors such as nutrition. Tseng et al.g.19 (. population from the National Health and Nutrition Examination Survey. and two methylated metabolic products.20 (1. arsenite.68) . with DMA.. arsenocholine.70-21. 1.80 (4.80-5.. 1985.80 (.3 (21. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.45 (1.50) .800-1.20-25.. Total arsenic measured in the urine includes all species of inorganic and organic arsenic. 2007). when seafood organic arsenic is subtracted).20) 7.40-6. 2008). Pellizzari and Clayton. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.20-190) 31. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.3-39. Some noncancer effects of arsenic (e..3) 1284 1284 03-04 03-04 03-04 1. MMA. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.3% of a representative sample of the U.5 (26. population (Ahsan et al.10) 4.60) 1. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. Individually measurable species resulting from inorganic arsenic exposure are arsenate.6-44. In most human studies. Aposhian et al.3 (9..900 (. 2008).900-1.62) 2..70-21.8) 35.S.. In the residents of a Chilean town who consumed water with high levels of arsenic. and TMAO.7) 13.9-23..5) 29. For residents of Inner Mongolia. 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.6 (11. see Data Analysis section) for Survey year 03-04 is 0. 2008). Caldwell et al.S.80 (3.600 (.28) 1.00) 3.S.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 * * 1.4-35.6 (25.70) 6.7-22.9 (7.Metals other areas of the world (Ahsan et al.00 (.83) Selected percentiles ( 95% confidence interval) 50th 1. interval) 1.74 (1.93) 1.3) 95th 35.5) 32. 2000.66 (1. population (Sun et al.30 (1.00-4. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (27.50) 90th 16. < LOD means less than the limit of detection.7) 15. 2007) with higher levels of arsenic in the drinking water. 2001.2-38.37 (1.S. population showed a higher contribution of arsenobetaine (Caldwell et al. 1990. After recent seafood ingestion.7 (21.20) 3.17-1. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.1-51.4 (16.8. 1996.70 (3..700-1.1-94. 2005. geometric mean levels were about 70-fold higher than for the U. methylation capacity.7 (13.40) 75th 5. 2008. vasospasm. arsenite.4) 31.. 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. Also. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.400-.20 (2. Chowdhury et al. 2000.0-23..800-4.50) . 2006).80) 1.8-50. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic. The higher percentiles of total urinary arsenic levels in the U.5) 292 728 1548 03-04 03-04 1.871-1.5 (14.05) < LOD .2 (6.00 (1.1-25. When seafood intake is avoided.20 (.30) 2.0 (26. in NHEXAS 1995–1996. China.90-29.. arsenobetaine.6 (13. 2003).40-7.50-6.S.3) 35.1) 45. 2001).29 (1. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine. 2008).800 (... arsenocholine.20-3. Arsenate.55 (1. respectively. Measurable organic arsenic species in this Report are three biologically generated environmental forms.2-35.500-1.1) 18. Valenzuela et al.9 (6. Caceres et al. In the late 1980s. Sun et al.8 (12.20) 18.. Caldwell et al.0) 29. 184 Fourth National Report on Human Exposure to Environmental Chemicals .20 (4. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.11-1.43-1. Survey years 03-04 Geometric mean (95% conf. Blom et al. and 0. Caldwell et al.e. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. population in the NHANES 2003–2004 subsample. dermal keratosis.8 (17.00-6. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.0) 4.800) 1.4) 23.9) 13. 2005. and duration of exposure are also considered important.40) 5.6...00-12.

833-1.50-15. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.55) 1.81 (4.62-6.14 (1.7) 17.43) 75th 5.05) 1.6-32.43) 14.2 (4.28) 1.00 (1.67) 1..30) 1.51-2.29-14.0-36.80) .88) 2. 1998.64-29.4 (24.76-27.05 (.91) 90th 16.10 (.9 μg/L.612-1.61-6. 2001).4-82. WHO. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.9) 14.29 (4. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.65 (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. 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.82) 4. not to imply a safety level for general population exposure.2 (13.4) 292 728 1548 03-04 03-04 1.73-6.901-2.40 (1.7) 30.2 (12.83) 8.5 (18.30-1.00 (3..3) 95th 29.Metals as with DMA.6-29.44 (1. Sun et al.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.3 (10.79 (1.78 (3. 2007).938-1.78-5.1-36. 2008).25-7.88 (5.70) 5.4 (11.93 (1.39-3.4) 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 * * 1.36) 2. 1986. Information about the biological exposure indices is provided here for comparison.S.5) 17. In recent years.5 (18.0 (9. which is below the ACGIH BEI (Caldwell et al.47 (1. 2003. 2006.638) 1.1) 26. 2008).58 (3.2 (12..6 (9. population from the National Health and Nutrition Examination Survey.15-4. 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.5) 26.531 (. Offergelt et al.18-1.6 (6.91 (4.82) Selected percentiles ( 95% confidence interval) 50th 1.32-7.909-1.16 (.37-2.4-28.53 (..1 (26.400-.67) 4...9 (25.19-2. Survey years 03-04 Geometric mean (95% conf.3 (10.8) 29. 1992.47 (2.5-20.9 (13.50-7. Fourth National Report on Human Exposure to Environmental Chemicals 185 .45) 1. Caldwell et al.12) < LOD .25 (. 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.83) 2. 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.S.40) 1.3) 1284 1284 03-04 03-04 03-04 1.51) 5.21) 5.11 (.72) 12.6) 19.15-1. interval) 1.786-1.4) 32. population for the sum of inorganic related species was 18.4) 13..68 (1.80-153) 17.1-18.7) 9.959-1.9) 32. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2001).0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.877 (.9-18.3-24.6-46.13-39. The 95th percentile of the U.15-1.54 (1. Vahter et al.4-21.

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

00 (<LOD-2.S.08 (<LOD-4.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. which may vary for some chemicals by year and by individual sample.S. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Survey years 03-04 Geometric mean (95% conf. Survey years 03-04 Geometric mean (95% conf.80) < LOD 621 725 1078 Limit of detection (LOD.2. Fourth National Report on Human Exposure to Environmental Chemicals 187 .Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (<LOD-3.40 (<LOD-1.44) 2.00) 1.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.76) < 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 3.95 (<LOD-2. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. 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 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (<LOD-1.

00 (3.91) 75th 5.92) 3.22) 4.33) 3.3 (8.32-10.9 (7.39-3.0 (11.0) 9.6) 1284 1284 03-04 03-04 03-04 4.55 (2.67) 9.0) 14.00 (3.82) 3.0-18. Survey years 03-04 Geometric mean (95% conf.1 (8.80 (4.65-8.0-16.79 (3.0 (12.8) 7.00 (4.45) 3.44) 5.89 (3.7-16.00-3.0 (13.0) 11.14) 3.7) 13.48 (2.00 (5.0 (10.00-13.0-17.09 (7.10) 6.92-12.08 (2.00-7.80) 7.13-4.0 (8.49-4.11 (3.73) 6.84-8.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.81 (5.17-4.20-4.00-10.0) 13.69 (3.34) 3.0-25.71 (3.11) 4.00-15.6) 292 728 1548 03-04 03-04 3.00-3.0) 10.00-15.67) 8.00) 9.85 (3.00 (3. population from the National Health and Nutrition Examination Survey.00-8.30) 3.0) 9.45) 8.86-7.5) 95th 13.69-3.0) 13.0) 95th 16.78) 4.00) 3.7) 1284 1284 03-04 03-04 03-04 4.00-11.38 (3.15) 4.84-18.28) 2.00) 6.14) Selected percentiles ( 95% confidence interval) 50th 3.00 (5.00-11.16-11.3 (7.86-21.50 (4.16 (4.1-18.82-5.5 (11.74 (2.18 (6.0) 16.00) 4.94) 3.34-4.0 (9.27 (3.82-9.70-4.7 (10.03-6.00-12.00-7.0) 9.05) 5.80-5.S.0-19.00-4.03 (3.80-6.16 (2.00 (5.71 (4.20-12.34 (3.00-4.24-4.24) 3.97-3.00) 6.45 (8.9) 13.00-4.86 (2.6 (9.06) 5.32 (8.0) 16.00) 6.00) 3.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.29-4.0) 11.60-3.00 (3.0 (14.0 (9.0) 17.00-7.62) 4.70) 5.70-12.S.50-15.00-4.00 (7.12 (3.05) 10.61-16.17 (2.95-3.71-4.9 (11.0 (10.59 (6.6-18.60-6.3 (8.98) 4.71) 3.19) Selected percentiles ( 95% confidence interval) 50th 3.70-3.0) 12.31) 4.00) 7.0 (13.20) 11.70 (3.95 (4.00) 5. interval) 3.0-12.00-11.00 (5.69-6.00 (6.69 (3.27 (2.27-5.7) 12.44 (2.9) 12.48 (3.0 (12.00-22.34 (3.80-3.94-3.32 (4.1-22.12-4.00) 4.9) 5.42) 3.73 (3. Survey years 03-04 Geometric mean (95% conf. interval) 3.00) 12.49) 10.37 (2.57-5.34-4.2) 10.0-16.00-4.00) 90th 11.31-4.00 (6.1-15.60-4.00 (6.0 (9.8) 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. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic 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.95-4.33-4.50-5.25 (4.0) 292 728 1548 03-04 03-04 4.00 (5.80) 2.52) 3.0-17.00 (3.0 (8.00-4.78 (4.61-11.8) 7.46 (4.0 (10.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .90 (3.27-2.00-7.00-12.0 (10.00) 75th 6.90) 5.90) 2.00-15.17-6.57 (3.77 (3.00 (3.74) 90th 9.4 (7.30 (7.9) 11.00-9. see Data Analysis section) for Survey year 03-04 is 1.0) 17.0) 621 725 1078 Limit of detection (LOD.05) 3.65-6.88 (4.95-6.10) 3.00) 6.5) 12.60-7.72 (4.37 (3.7.00-5.00 (7.

00 (<LOD-1.88 (1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.70-2.10) 95th 2.00) 1.00) 2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.70-3.07-3.70-2.10 (1.853-1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.20-3.58) 2.20 (1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00-2.50 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.96-2.71-2.45) 3. population from the National Health and Nutrition Examination Survey.90) 2.05-1.80) 1. Survey years 03-04 Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.90 (1. population from the National Health and Nutrition Examination Survey.S.00) 1.20 (1. which may vary for some chemicals by year and by individual sample.40 (1.61) 2.00-2.40) 2.14-1.22) 3.80-2.86 (2.10-1.11-1.30) 1.80) 1.00 (1.40 (2.60 (1.30) 90th 1.50-2.88 (1.30 (1.79) 2.30-1.80 (2.9.50) 621 725 1077 Limit of detection (LOD.S.36) 1.30 (1.16 (2.17) 2.30 (1.70-2.60) 2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .60-2.53 (1.86) 2.46-2.985) 1.82-2.10-1.23) 1.20 (1.62) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-3.43-3.60) 2.00-1.00 (<LOD-1.70-2.40-2.28 (1.30 (2.00-1.81) 1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.80 (1.73-2.80 (1.22 (1.40-3.40) 1.20) 2.50 (1.34) 2.31-3.00 (2.40) 1. see Data Analysis section) for Survey year 03-04 is 0.20 (1.20 (1.54) 90th 2.33 (1.30-1.10 (.50) 1.18-1.86 (2.53-2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.816 (<LOD-.33 (1.30-2.31 (1.28 (1.77) 1.20-1.90) 1.30) 2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.84-3.60 (2.57) 95th 2.80-2.40-3.20 (1. < LOD means less than the limit of detection.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70) 2.10 (<LOD-1.50 (1.37 (1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.50 (2.90) 2.80 (1.85) 1.46 (1.61-3.93) .36 (1.10) 2.80 (1.10 (1.88-2.00-4.00 (2.63 (<LOD-1.00) 1.90 (2.07) 2.85) 2.60) 1.40-2.18-1.30) 1.07 (1.82-2.15-1.52 (2. Survey years 03-04 Geometric mean (95% conf.10 (.00) 2.900-1.35-3.86) 3.

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

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Certain foods.87-7.70-2.78) 1.00 (2.54 (2.20 (4.82) 1. are high in barium (Genter.95-6.01-7.70) 1. 01-02.78) 1.42 (1.11 (3.93 (4.77-3.80 (1.76-2.51) 1.49) 2.05% of the earth’s crust.70-8.01 (4.39) 1.87 (6.54-1. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.97 (1.77 (3.18 (6.95 (4.53) 2. soluble forms of barium.61 (5.48) 1.61 (1.63) 1.30 (2.21 (1.70-5.1) 9.73-5. In nature.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 2.80) 1.65-8.75-3.50 (1.34 (1.g.80 (1.20-5.66 (4. see Data Analysis section) for Survey years 99-00. Barium salts have also been available as rodenticides.35-1.62 (1. Workers employed by industries that make or use barium compounds can be exposed to barium dust. depilatories.64 (1.81-2.19-1. In single dose animal studies.35-1.04-6. Barium compounds are used by the oil and gas industries to make drilling muds.49) 4.16) 5.63) Total 1.80 (2.61 (3.71-9.60) 4.10) 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 1.54 (6. and 0.43 (5.90) 1.59-11.54) 1.40 (1.11-1. population from the National Health and Nutrition Examination Survey.00) 4.50-1.52 (4.65-1.48-4.26) 2. fireworks.03 (1.74-2.20) 2.66) Selected percentiles ( 95% confidence interval) 50th 1.30-2. Some barium salts are freely soluble in water.38) 8.8 (6.90-2.14-1. bricks.59) 3.80-7.70-3.91 (2.30-3.37-8.88) 7.73 (6.06-1.76-3.63 (2. barium sulfate and barium carbonate).80-5.99 (4. 0.50 (1.4) 7.00) 1.49) 8.12.54-1.35 (2.57-7.15-11.20 (1.S.35 (3.86) 6.65 (5.67) 6.44 (1.10-5.78-2.56 (6.8) 5.07 (2.72) 75th 3.64-3.71) 1.65-5.10) 3.27 (1.12) 7.21-2.29-1. tiles.34 (1.27) 2.19) 2.46-1. it combines with other chemicals such as sulfur or carbon and oxygen.73 (5.37 (4.61 (1.50 (4.50 (2. rubber.60) 1.60-3.72) 4.70) 7.50 (4.25-1.31.61 (2.63) 1.71 (2.34 (2.50 (1.88 (5.76) 1.63 (1.91) 2.52 (1.90-9.31 (2.47) 4.80-2.60) 3.48) 1.09 (1.60-6.93-2.30-1.38 (1.36 (1.50) 4.28) 90th 5.96-2.65) 1.43) 6.00) 6.74) 3.60-6.00 (1.22-1.50 (3.37-1.21 (1.10 (3.34) 2.43 (1.86 (4.35) 5.87-3.32) 8.61-8.54) 2.43 (1.49-1.30 (5.44-5. and food.20-1. Small amounts of barium can be released into the air during mining and other industrial processes.70 (5.40 (1.41-1.00) 1.50 (6.18-1.36 (4.40 (5. such as brazil nuts.Metals Barium CAS No.28-1.50-6.62) 1. glass.44-2.40) 3.88) 1.50-6.09 (2.30) 5.32-7.82-6. interval) 1.90 (1.00-3.30-1.14 (6.12 (2.54) 1.63 (5.35-4.36-1.90 (4.10) 5.12) 6.86 (4.33 (1.60-2.87 (5.15 (2.56 (2.15-1.49 (1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70) 4.15 (6.20-6.25 (1.26-7.73) 3.87-9.50) 2.24 (4.51) 7.30 (3.55-7.30-2. and 03-04 are 0.48-4.24-1.18) 3.12 (2.60 (2.85) 1.71) 2.70-2.56 (1.08-8.46) 1.22-1. Barium compounds are also used commercially in paint.86-5.20-8.94-6.20-8.27 (1.51) 2.46) 1.55-3.62) 1.69 (1.10-4.40) 7. 2001).90) 4.30 (1.40 (1. respectively.11 (3.11 (2.05-2.40-13.91) 6.12.80) 7.87) 7.75) 2.30) 8.50) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.22) 6.72) 1.39 (1.38) 2.70) 1. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).25-11.53) 1.8) 9.35 (1.24-1.9) 5.60-10.81-3.26-1.99-5.50 (1.2) 6. Fourth National Report on Human Exposure to Environmental Chemicals 193 .00-76.37) 1.50 (1.92) 2.02 (7.57) 3.20-8. water.70) 3.70 (1. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and ceramics.80-3.30) 2. 7440-39-3 Medically.50-1.80) 6.16 (1.71) 95th 6.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.39-1.32-1.38 (1.20-1.76-7.30-5.20-1.39 (1. such as barium chloride.10 (2.29) 5.47-1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.4) 9.14-6.77) 1.00-8.85) 1.98) 1.74-3.93-8.06-2.43) 2.20 (3.30) 4.60) 1.37) 5.86-4.80 (1.73) 1.88) 4.29-5.87-14.21-8.45) 7.80 (2.62 (1.82) 2.20-1.50 (4.54-8. whereas others are practically insoluble (e.90 (6.47-1.84) 5.15 (1.40 (4.56) 4.50) 2.41-3.17-1.40 (5.78-3.30 (5.65) 3.4) 6.57 (5.80 (5.70-6.40) 7.36-1.81-2.26) 5.39) 4.56) 1.36) 5.76 (3.41) 1.65) 1.49-9.68 (1.10 (4.51 (1.30) 5.70) 5.53-5.12-1..63 (8.40 (5.45 (1.08 (6.31-2.50 (5.49) 11.60 (1.15-1.30) 5.90) 2.48 (6.56 (1.90) 2.04-2.85 (2.30) 3.90-13. The general population can be exposed to low amounts of barium in air.15) 5.

68) 3.27-3.72 (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 1.66 (1.0) 6.52) 2.39) 4.55) .24-6.86 (2.30 (1.26) 4.20 (1.34 (1.59) 1.75) 2.38) 1.96) 4.22-1.16) 11.91) 2.48 (1.44-2.56-3.57-5.33) 6.74 (5.5) 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 1.77) 1.00 (3.88 (6.03-1.29-4.37-1.49-1.3) 6.34-3.04) 5.921 (.45) 1.46) 3.96 (4.00-1.12) 2.32 (1.45-1.20) 4.44-2.27) 7.11) .26-1.84-2.32) 2.51) 6. 1985.23-5.76-3.81-6.57-7.97 (4.54 (2.29 (3.42) 1.53-21.77) 1.68-3.41 (2.78 (2.59) 1. The health effects of exposure to barium compounds depend on the dose. 1989).47) 4.64) 7.47 (5.56 (1.74) 1.22-2.26-4.49-1.27) 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 .38 (1.24 (3. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.69 (5.703-1.28) 5.50) 1.87) 1.85-5.43-6.62 (2.31-1.33-4.02) 4.3 (6.19-1.50 (4.68 (2. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.62 (4.89) 90th 4.58) 1..75) 1.24-11.99) 1.00 (2.26-1.63-4.2 (3.51) 4.48) 2.69-9.11-2.97-3.47) 10.05-1.08-2.10) 3. paralysis.41) 4.58) 4.76) 2.46-22.38) 4.33) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00) 4.54) 1.77) 5.71 (5.20-1.56) Selected percentiles ( 95% confidence interval) 50th 1. 1990).55-6.59-7.47) 1.33-1.20-8.52-10.31 (4.24-3.39-1.99 (2.51 (1.96) 4.01 (5.20-2.52-4.28-7.41 (1.58) 75th 2.31-1.25-11.96) 4.Metals was eliminated primarily in feces and to a lesser extent.39 (3.03) 3.38-5.50) 2.777-1.21 (1.29 (1.40 (1.81-7.06) 2. 2001).79-5.30) 2.36-2.67-6.86) 5.4 (5.76) 2.36 (3.2) 5.2) 6.45 (1.832-1.65 (5. and cardiac dysrhythmias.09) 6.04) 1.35-1.39-5. Symptoms following acute high dose include perioral paresthesias.77) Total 1.36 (3.16 (1.41 (1.10 (6.36-1.8) 4.40 (1. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.29) 1.38-7.92) 2.31) 5.49 (1.76 (2.01 (4.60 (1.27 (2.58-6.57) 2.73) 2.82) 1.77) 1.28-1.57 (6.63) 1.34-1.891 (.96 (4.37 (1.68 (3.53) .83) 3.47-8.55 (1.45 (3.72) 6. Insoluble barium salts.32) 2.40-1.41) 5.51 (1.881 (.16-1.45-6.36-1.24 (5.68-3.38-1.35-1.74) 1. weakness.26-1.77-5..22-1.60 (2.22-4.33 (1.35-3.56 (1.25 (1.47 (2.754-1. Chronic exposures to natural low levels of barium in drinking water have not produced general health effects or evidence of cardiovascular risk (Brenniman and Levy. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4) 5.23-1.59 (1.36 (5.58 (4.76) 1.76 (4. Toxicity from soluble barium salts is rare.75) 1.96-6.84-5.33 (1. chemical form. Wones et al.97 (5.50) 1.70) 1.75) 2.43) 1.19-1.19-2.97) 1. Chronic high doses in animals resulted in kidney damage (McCauley et al. hypertension.40 (1.27-1.55 (1.68) 1.44 (1.0) 5.38 (4.47) 1. 1994.89 (2.39 (2.39-1. 1986).24-6.92 (4.00-7.00) 4. NTP.49 (1.79) 1.00 (5.64 (1.60 (1.64 (1. vomiting.32 (2.72) 4.51) 4.01) 1.24) 3.30 (1.97-4.18 (1. interval) 1. in urine.38) 1.90-2.34-5.19-1.10-2.31 (1.S.39 (2. water solubility.55 (4.81-6.55 (5.91 (3.86-7.24-1.38 (1.48-3.32 (1.04 (2.96) 7.75-22. are not absorbed when administered. and route of exposure.61 (4.59 (1.83) 2.80) 4. Barium is not rated for human carcinogenicity.91-2.37) 2.39 (2.915 (.48 (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 2.76 (3.80) 3.60 (5.51 (3.84) 2.55-5.54) 2.13-3.15-4.02 (3.88 (2.56) 4.48 (1.52 (3. population from the National Health and Nutrition Examination Survey.46) 1.11) .29-7.28-11.880-1.45) 95th 6.64 (1.62) 2.13-2.06) .03-1..64 (1.34) 1.0) 7.52) 1.36 (1.29-4.28-6.00) 1.42) 1.23-2.710-1.24-1.84 (3.57-10.29-3.37-2.75-3. Following intravenous injection in animals.963 (.64) 7.91 (3.49-1.26-1.80-6.70) 4.36 (1.52) 7.18 (1.98 (2. 1984.03) 2.73-4.73-2.46 (2.82) 1.51-3.53 (2. Perry et al.10-1. a benign condition that may occur among barite ore miners.48-5.00) 6.02-5.29-1.25) 4.60 (2.02) . such as those used in medical radiographic procedures.37 (1.45-8.38 (4.61) 2.68 (3.00 (3. diarrhea.54 (1.48-1.39-10.03) 1.59) 2.33 (5. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.70) 10. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.42 (4.46) 2.65 (2.99 (4.58 (2.14-2.905 (.45-1.08-1.28 (1.10) 6.62 (1.31-1.

pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. 2000) to levels in NHANES 1999-2000 and 2001-2002. et al.gov/ntp/htdocs/LT_rpts/tr432. Frohman. Wones RG.. Fourth National Report on Human Exposure to Environmental Chemicals 195 . Trace metals in urine of United States residents: reference range concentrations. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. Levy. Pozzoli L.S. Costa R. Pietra R. and radium In: Bingham A. Gallorini M. Douglas BH. Perry HM. Powell C. 84-94. Vouk VB. Perry EF. Nordberg GF. Apostoli P. barium. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Biomonitoring Information Levels of urinary barium reflect recent exposure. et al. Stadler BL. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. Magnesium. Calabrese EJ. 1994. Sci Total Environ 1990. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Genter MB. Reeves AL.95:89-105. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no.. ed. Epidemiological study of barium in Illinois drinking water supplies. 1986.html?charset=iso-88591&url=http%3A//ntp. 4/8/09 Paschal DC.. Atlanta (GA). McCauley PT. 2001. 1992).gov/toxpro2. Sampson EJ. 1998). Princeton (NJ): Princeton Scientific Publications. strontium. In: Calabrese EJ. Environ Res 1998. et al. 1985. pp. et al..nih. Princeton NJ: Princeton Scientific Publications.html. the welders had no obvious adverse clinical effects (Zschiesche et al. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). Zschiesche W. Handbook on the Toxicology of Metals. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Sabbioni E. 1984. Barium. Environ Health Perspect 1990. and serum of Italian subjects. Advances in modern toxicology.. Centers for Disease Control and Prevention (CDC). Pirkle JL.85:355-359. Exposure to soluble barium compounds: an interventional study in arc welders.. and 2003-2004 (CDC. Jackson RJ. Available at URL: http://ntp. Comparison of representative ranges based on U. environmental levels) and health effects is available from ATSDR at: http://www. 2001-2002.. Int Arch Occup Environ Health 1992.296(1-2):71-90. p.S.niehs. NTP.cdc. Morrow JC. New York: Elsevier. 221-252 Komaromy-Hiller G.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Ting BG. PS.. Laurie RD.e. Kopp SJ. patient population and literature reference intervals for urinary trace elements. Patty’s toxicology.64(1):13-23. Minoia et al. 2005. References Brenniman GR. Jr.197210. 2nd Ed. Trace element reference values in tissues from inhabitants of the European community I. p.28(3):373-388. eds. Weltle D. National Toxicology Program (NTP). blood. 1989. Minoia C. Information about external exposure (i. Vol 2: Specific Metals. LA.atsdr.76(1):53-59. EPA. In: Inorganics in drinking water and cardiovascular disease. Clin Chim Acta 2000. Cohressen B. and a drinking water standard has been established by U. 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. p. New York: John Wiley & Sons. Howerton K.niehs. In Friberg L. 5th ed. Paschal et al. Third National Report on Human Exposure to Environmental Chemicals.gov:8080/cs. ed. Investigations into the effect of drinking water barium on rats. A study of 46 elements in urine. 231-249. J Toxicol Environ Health. Inc. calcium.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. 1990. Lack of effect of drinking water barium on cardiovascular risk factor. 2005. eds. Ash KO. [online].nih. Schaller KH.

are mined for commercial recovery of beryllium.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. x-ray machines.140 (<LOD-.150) < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and dental bridges. near some hazardous waste sites.13. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. Beryllium compounds are commercially mined. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. aircraft. and 03-04 are 0. and refined beryllium is used in mirrors and special metal alloys for the automobile.Metals Beryllium CAS No. computer. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. coal. the lightest of all metals.130 (<LOD-. or drinking water containing the metal. 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. eating food. 01-02. Low-level beryllium exposure in the general population can occur through breathing air. and from breathing tobacco smoke. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.13. In medicine.S. In studies of laboratory animals.130 (<LOD-. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. 196 Fourth National Report on Human Exposure to Environmental Chemicals . soil. beryllium is used in instruments. nuclear. electrical. Exposure to beryllium occurs mostly in the workplace. and machine-parts industries. respectively. bertrandite and beryl. and can be found in mineral rocks. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 7440-41-7 General Information Pure beryllium is a hard gray metal. see Data Analysis section) for Survey years 99-00. Two types of minerals. < LOD means less than the limit of detection. 0.13. and 0.170) < 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 . which may vary for some chemicals by year and by individual sample.

Fourth National Report on Human Exposure to Environmental Chemicals 197 . Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2003. 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 . Skin exposure can result in delayed hypersensitivity reactions. 2002). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. NTP considers beryllium to be a known human carcinogen. 1990).Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. 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.S. and drinking water and environmental standards have been established by U.333) < LOD < LOD < LOD < LOD 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. respectively.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 .281 (<LOD-.346 (<LOD-. which produces pneumonitis.231 (<LOD-. Maier. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. IARC has classified beryllium as a human carcinogen. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH.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. S. Chronic beryllium disease. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. based upon excess lung and central nervous system cancers in studies of workers. EPA. population from the National Health and Nutrition Examination Survey. including contact dermatitis and subcutaneous nodules. or berylliosis.

Centers for Disease Control and Prevention (CDC). References Apostoli P. Pozzoli L. Am J Epidemiol 2003. Int Arch Occup Environ Health 2001.gov/toxpro2. Sabbioni E.org/documents/ehc/ehc/ ehc106.S.Metals (i. Minoia et al.95:89-105. Comparison of representative ranges based on U. Environ Res 1998. and the 95th percentile for males in NHANES 2001-2002. 106. Apostoli P.e. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. and serum of Italian subjects. McCanlies EC. 0. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. et al. Trace element reference values in tissues from inhabitants of the European community I. Howerton K. Sci Total Environ 1994.74:162-166. Sabbioni E. 20012002.13 μg/L. less than 0. Pietra R. Schaller KH. HLA-DPB1 and chronic beryllium disease: a HuGE review. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Review of elements in blood. Kriess K. Morrow JC. Hamilton EI. population were generally undetectable in NHANES 1999-2000. Pirkle JL. and 2003-2004. Andrew M. it is likely that urinary beryllium levels in the U.296(1-2):71-90.S. Paschal DC. Given these results.. 2001).inchem.e.76(1):53-59. 1990.12 to 0. environmental levels) and health effects is available from ATSDR at: http://www. Sampson EJ.23:827-839. Ash KO. Clin Chim Acta 2000. Available at URL: http://www. patient population and literature reference intervals for urinary trace elements. 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..htm. et al. Weston A. Atlanta (GA) 2005. 1998). Clin Chest Med 2002.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Element reference values in tissues from inhabitants of the European community. VI. Beryllium [online]. 1990. Van der Venne MT. Gallorini M. Levels of beryllium in urine for the U.1 μg/L). Maier L. Costa R. A study of 46 elements in urine. population are lower than levels in workers. Hamilton et al. Trace metals in urine of United States residents: reference range concentrations.atsdr. Sci Total Environ 1990. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Ting BG.html. which approximate this Report’s limit of detection. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. 2000. and the fact that most NHANES participant levels were undetectable. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. 198 Fourth National Report on Human Exposure to Environmental Chemicals .15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. 3/27/08 Komaromy-Hiller G. Environmental Health Criteria.. Third National Report on Human Exposure to Environmental Chemicals. Paschal et al. International Programme on Chemical Safety (IPCS). Jackson RJ.cdc.S. blood. They reported urinary beryllium levels ranging from 0.. In other studies. Minoia C.158:165-190. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Genetic and exposure risks for chronic beryllium disease.157:388-398.

400) .500-.00 (.700 (.400 (.10 (1.400) .50 (1.00 (.20) 1.800 (.500) .300-.20) 1.300 (.600-1.366) * * .00-1.600 (.00 (.60 (1. and incineration of municipal waste materials.300-.700) .70) 1.400 (.500) .700-1. population from the National Health and Nutrition Examination Survey.40 (1.400) < LOD .70) 1.216-.500-.40) 1. and 03-04 are 0.S.900 (.300 (.300) .400) < LOD < LOD < LOD .400-.300) .460) .10 (1.300) .600) .900-1.20) 1.00 (.600 (.3.309-.00 (1.300 (.400 (.300-.304 (.900-1.367-.700) .500 (.400 (.40 (1.40 (1.S.3.359-.300 (.344) .300) . or copper smelters (U.400 (.40-1.10) 1.400-.500) .400 (.382 (.50-1. Since 2001.20-1.40 (1.421 (. 7440-43-9 General Information Cadmium is a soft.200 (<LOD-.600-.00 (.400-.200-.00 (.398) < LOD < LOD < LOD < LOD < LOD < LOD .300-.30) 1.300-.500-.70) 1.400-.300 (<LOD-.20-1.500-.20) 1.700-1.420 (.300 (.600 (.800-1.300) .600) 1. 0.400) .700) 1.60) Total * .200-.500 (.00) .10 (1.300 (<LOD-.400) .500-.304-.50-1.900-1.400 (.20-1.200) . < LOD means less than the limit of detection.300-.400-.300) .386-.500 (.20-1.10 (1. Cadmium also may be emitted into the air from zinc.255) .40-1.300 (.300) .50) 1.500-. as zinc sulfide) and to a lesser extent.313 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.235 (.800-1.900-1.00-1.200 (.600) . 01-02.600 (. and 0.300-.300-.700) .400 (.400 (.300) . respectively. see Data Analysis section) for Survey years 99-00.400-.300 (.40 (1. and nonferrous alloys.500-.00 (1.500) .800 (.424) * .333 (.500-.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. malleable.40 (1.00 (.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 * * * * * * .300-.20) 1.600) .10 (1.60) 1.300-.500-.300) .60 (1.400) .900-1.300 (<LOD-.500-.300) 1.700-1. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.80) 1.500-.20) .368-.400 (.300-.500 (.600-.60) 1.200-.513) .400-.300) 75th .20) 95th 1.337) .900-1.500-.376-.468 (.326 (.20-1.200 (.600 (.500-.20-1.14.300-.300-.427) * .300-.600 (. The predominant commercial use of cadmium is in battery manufacturing.500) .600) .300) .900-1.20 (. coatings and plating.400) .600-.50) 1.900-1.00) .300-.600 (.300-.20) 1.500-.800) .700) .400-.600 (.30) .60 (1.403) .395 (.500) .60 (1.300 (.00-1.400 (. during refining of lead and copper from sulfide ore.300 (.90) 1.10) 1.449) Selected percentiles ( 95% confidence interval) 50th .300-.800) 1.30-1.00 (.50 (1.400) .80 (1.700) .200-.300-.361-.500) .600) 90th 1.600 (.10) 1.00 (.425 (.50) 1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.10 (1.30-1.gov/minerals/pubs/commodity/cadmium).400) .30-1.10) 1.304 (.20) .600) .900-1.70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 . interval) .50 (1.00-1.300-.300 (.400) < LOD .289-.400) .300 (<LOD-. EPA.296-.10) 1. which may vary for some chemicals by year and by individual sample.393 (. plastic stabilizers.70) 1.300-.600 (.600 (.300 (.300-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.400 (.300-.400 (.50-1.600 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .30) 1. lead.600) .600) .90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .400 (.200-.200 (.20 (1. Other uses include pigment production.400) < LOD .266-.10) 1.452) .500 (.400-.400) .400-.400-.50 (1.275-.40) 1.500 (.283 (.500-.300 (.500 (.00 (.900 (.331) .00-1.500 (.10 (1.412 (.426-.00-1.600 (.Metals Cadmium CAS No.30-1.20) 1.400) .10 (.378-.usgs.700) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.600) .500-.80) 1.40 (1.200 (<LOD-.378 (.600 (.30) 1.400) .30-1.400) .500-.00-1.300) .20-1.470) * .00-1. U.700) .400) .600) .60-1.10) 1.300) .400 (.60) 1.362-.60 (1.441) * .20) 1.300 (.10) 1.400 (.S.500-.700) . cadmium use has declined in response to environmental concerns (http:// minerals.30 (1.800) .300) .500 (.403 (.400 (.900-1.50-1.200) .00-1.

136) .078 (.336) .219 (.38) ..445 (.530 (.813 (.157-.148) .192-. rice.919) .32 (1.17 (.167-.06.28 (1. 2003.475 (.169-.06-1.820) 1.243-.390 (.100-.714-1.394-.216 (.087-.466 (.261-.277 (. Cadmium absorption may be increased with iron deficiency (Berglund et al.220) .04 (.539) .067-.848 (. wheat.S.972 (.730-.195-. ingestion through food is the largest source of exposure.20 (1.20 (1.190-.272-.193-. Kikuchi et al.479) .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 .19) 1. Diamond et al.500) .875 (.990) .717-.255) .450 (.189-.208-.980-1.980 (. 1999.980) .890-1.22 (1.229-.160) .886) . cadmium accumulates in the liver and kidneys where it is bound to metallothionein.623) .820-1.210) .150) .52 (1.886-1.387) .270 (.077 (.890 (.880) .306 (.51 (1. and 0.279 (. including many food crops such as cereal grains.270 (.081) .15 (.810-1.191-.855-1.918-1. Horiguchi et al.766 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th . an inducible metal binding protein..34) 1. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.354) .790 (. 2003).327 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .38) .231) .150-.238-.20 (1.839 (.302 (.204 (.36) 1.190-. and various seeds.229) .38) 1.551 (.326) . population from the National Health and Nutrition Examination Survey.24) 1.330-.135-. and 03-04 are 0.700-.633 (.263) . Renal tubular and glomerular damage. For nonsmokers who are not exposed to cadmium in the workplace.289-.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.705-.295) .38) 1. 200 Fourth National Report on Human Exposure to Environmental Chemicals .067-.15) 1.191-.493-.211 (.06) .530) .989-1.265 (.283 (.800-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.240-.713) .226) . 2003).733) .240) .090) .092 (.285-.892 (.20-1.257) .436-.57) 1.01) .875) .177-.210 (.284) .13-1.351-.430) .430-. With chronic exposure.360) .03) .220 (.282 (.440 (.12 (.980) .700-.790 (.183-.452 (.109 (.210 (.456-.540) .300 (.25) 1.255) .426 (. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.080 (..640) .763-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.393-.060-.607) .214-. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al..210) .151-.191 (. 0.173) .545 (..963-1.20) 1.170-.247) .13) .253-.260-.17) .230 (.210 (.892-1.686-. copper) and protein.260 (.13 (.114-.412) .203) .519) .470-.232) .322 (.170-.519) .135 (. 2004a.01-1.490) 1.210 (.400-. potatoes.120 (.445 (.160) .190-.498-. interval) .423-.753-.200 (.372) .836-1.077 (.299) .366-.440 (.310 (.237-. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.115-.260-.15) .280 (.25 (1.520-.202-.121 (.977) .** Survey Geometric mean (95% conf.200 (. Cadmium in soil is absorbed by plants.221) ..061 (<LOD-.06.220-.175 (. whose body burdens of cadmium can be approximately twice that of nonsmokers.192-. 01-02.440-.450 (.189-.221 (.06-1.233) .843-1.390-.210 (.160-.160 (.222) .175 (.220-.184-.559 (.179-.22 (.281 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.589 (.193 (.550 (.246) .211-.313) .41 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.458 (. Cadmium is absorbed via inhalation and ingestion.229) . zinc.233) .01 (.388-.255) .507) .061-.817 (.462 (.065-.261-.820 (.178-. respectively.06.858 (.273 (.199 (.134) .201 (.83) 1. calcium.17 (.251) .366-.818 (.110-. 2003).206) .390-.366) .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 . drinking water is a source for cadmium intake.48 (1.200-.510-.232 (.219 (.206 (.596) .300) .492 (.17 (.316 (.290-.109-.320) .207-.181 (.551) .28) 1.47) 1.148-.101) .Metals 2000).447 (.482) .249) .308) .234 (.092) .223 (.128 (.680 (.265) .241) .112-. see Data Analysis section) for Survey years 99-00.219 (.230) .235) .239 (.72) 1.310) .194-.090) .198) .107-. 1994).220) Selected percentiles ( 95% confidence interval) Sample 95th 1.157) .633-1.362) .200-.12-1.940-1.480) .748-1.238) .339) .130 (.860) 1.980-1.381-.262) .733-.580) .249-.870) .126) .455 (.329 (.09-1.153-.202 (.741-1.500) 90th .800 (.400-.140 (.10 (1.196-.806) .481) .141 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers.817 (.209 (.82) 1.490) .257-.170 (.203 (. however.74) 1.187 (.960 (.171-.02-1.28-1.350 (.700-.230) 75th .165-.43) 1. To a lesser extent.180 (.227 (.960) 1.07-1.610) .30-1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.510) .476-.04 (. 2001).189) .433-.

667) .192) .833-1. 2002.181 (.516-.614) .227-.545) .245 (.162 (.431) .316) .335 (.111-.476) .096) .171-.387 (.813-.927-1.140-.826-1.07) .336-.267 (.289) .856) . However.647-.472) .219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .191) .163 (.075 (<LOD-. 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.252 (.876-1.242) .085 (. population from the National Health and Nutrition Examination Survey.631) .293-.289) .190 (..094) .329 (.404) .106) .071 (.220 (.663 (.708-1.233 (.051-.757) ..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.00 (. most often a result of occupational exposure (Roels et al.107) . 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.225) .296 (.176 (.321) .184) .168-.144-.645-.146-.687 (.865 (.211 (.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 .491-.199-. Noonan et al. 2004).147-.940-1.10) 1.754) .985 (.157-.696-.288-. 1999).686 (.190 (.166 (.551) .268 (.086 (..154 (.176 (.210 (.941 (.884) . 2003. 2002.229) .215 (. Jarup et al.630-.537-.075-.216-.308) .350) .806-1.440) .198) .38) .414 (.131-.181-.077-.063-.693 (.531 (.562-.691-.182) .084-.687-.112) .161-.487 (.197-.135) .196 (.718 (.364) .470) .827) .500-.712 (.209) . 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.083-.209) Selected percentiles ( 95% confidence interval) Sample 95th ..170 (.830-1.147-.690-.297) .113-.163) .250) .484 (.470) .325 (.084 (.716) .518) .432 (.795) 1.221-.404 (.234 (.650-.156-.802 (.690-.175-.13) .150-.674-1.14) 310 368 287 648 762 724 1299 1559 1532 12-19 years 20 years and older 99-00 01-02 03-04 Gender Males 99-00 01-02 03-04 .340) .184-.414-.818) .757 (.784) .148 (.202 (..104) .906) ..533) .159 (.232) .07 (.856 (.206-.874-1.234) .282 (. 1996.962) .212 (.281) . can result from high dose chronic exposure.261-. 1999).247-.300-.783) .263 (.05) 1.261) .426-. Fourth National Report on Human Exposure to Environmental Chemicals 201 .255-.446) .267 (.767 (.S.091 (.098) .122 (.170-.234-.783 (.311) .813-1.423-.288 (. At lower environmental exposures.421 (.238-.221 (. Horiguchi et al.137 (.278) .238) .136-.303) .02 (.617 (.137-..156 (.281) .187) .126 (.931 (.173-.653) .104) .222-.183) .228-.440) .074-.767) .218) .438-.940 (.235) .274) 1.178) .415) .398-.06 (.725-1.185) . Kidney dysfunction that led to osteoporosis was associated with very high urine cadmium levels in residents of an area of China where extensive environmental cadmium pollution occurred (Jin et al.140-.292) .183 (.168 (.157-.123-.09 (.288) .223) .444-.700 (.253) .270 (.449) .418-.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.143-.207-..253 (.256-.690 (.818) .559-.266-.097) .316 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.091 (.490 (.219 (.078 (.716-.308 (.181) .091) .154-.381-.433-.130-. 1999).194-.591 (.143) .283 (.917 (.208-.850) .769 (.387-.201-.123-.507-.873 (.423 (.917) .078-.338 (.178-.224 (.17) .093 (.200 (.666-.143-.441-.263-.067-.391-.085-.909-1.158-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.204-.261 (.168-.219 (.205 (.950) .850) .232) .826-1.740 (.722-.185 (.239-.16) .719 (.479 (. During the 1950’s and 1960’s.08) .830) .090 (.191 (. Most studies of relatively low level environmental exposure to cadmium have demonstrated associations between higher urine or blood cadmium levels and an increased prevalence of various biomarkers of renal tubular effects (Alfven et al.225) .159 (.536 (.241) .00 (.560-.678-.668-.100 (. Staessen et al.919 (.382) .247-.343-.240) .688-.541) .501 (. 2004b).352) ..101) .412 (.318 (.729 (.678 (.727-.177) .** Survey Geometric mean (95% conf.174-.210) .779 (.191-.207) .304) .04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th . two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.473 (. 2000.187-.998) .388-.273 (.438) 90th ..839) .175 (.607) .16) 1.929) .622 (.182) .189-.136-.199 (. Olsson et al. 2002.979 (.304-.181 (.210 (.377-.331 (.792 (.434 (.700) .266) .418) .173 (.382-.280 (.156) .226) 75th . interval) .247-.538) .184-.208 (.147 (.240) .789 (.175 (.182) .12) 1.481 (.828) .236-.

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

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. Available at URL: http://www. Tsukahara T. Kumagai N. et al. Machida M. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Chiappino G. Komaromy-Hiller G.13(11):1627-1631. Kundiev YT. Occup Med 1996. Occup Environ Med 2000. Seifert B. et al. possibly better than b2microglobulin. et al. Ye T. Seiwert M. Holguin F.59:497]. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Mannino DM. et al. Schulz C. Mascagni P. 2005. et al. Lukyanova EM. Becker K. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. References Akesson A. ShkiryakNizhnyk AZ. Consonni D.148(1-2):11-20. patient population and literature reference intervals for urinary trace elements. Vahter M. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Ezaki T. Sasaki S. Anthropometric. Toxicol Lett 2004. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers.46:372-374. Furuki K. Atlanta (GA).205:297-308. Lancet 1988. Taylor AJ. Savage-Brown A.1(8587):663-667. Fukui Y.296(1-2):71-90. Persson B. J Occup Health 2003. Bernard A. Nerbrand C. Ash KO. Venables KM.59:194-8. Takebayashi T. 4/8/09 Alfven T. Pickering CA. Vahter M. Sanz P. Zhu G. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Lepom P. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Berglund M.354:1508– 1513. Gadea E. Fernandez MA. Olfactory function in workers exposed to moderate airborne cadmium levels.S. Horiguchi H.cdc. Stock AL. Tsukahara T. 196:114-123. Carlsson MD. Int Arch Occup Environ Health 2003. Lidfeldt J. Nomiyama T.102:83-89. Oguma E. Centers for Disease Control and Prevention (CDC). Lundh T.24:717-724. Miyamoto K. et al. Jarup L. Serra J. et al. Palomar M. Thayer WC. Davison AG. Environ Res 2006.66(Pt A):2141-2164. Environ Health Perspect 1994. Alfven T. Jin T. 1999 [online]. Jones RL. Nordberg G. Mucha A. Bo M. Krause C. et al. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Int J Hyg Environ Health 2002. 206:15-24. Toxicol Appl Pharmacol 2004a. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Okamoto S. Nermell B. Friedman LS.76:186-196. Furuki K. Int J Hyg Environ Health 2003. Akesson A.gov/toxprofiles/tp5. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Neurotoxicology 2003. et al. Thorax 2004. Lancet 1999. Bellerup P. Horiguchi H. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Miyamoto K. Sasaki S. Fatal chemical pneumonitis due to cadmium fumes. Environ Res 2004b. Comparison of representative ranges based on U. Buchet JP. Kaus S.000 women in the Japanese general population: a nationwide large-scale survey. Environ Health Perspect 2005. et al. Machida M. Greves HM. Environ Health Perspect 2002. 102:10581066. Jarup L.96:353-359. Cadmium fume inhalation and emphysema. Ikeda Y. Kikuchi Y. Darbyshire J. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Moriguchi J. Ukai H. iron deficiency.html.57:668-672. J Toxicol Environ Health 2003. Costa R.110:699-702. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Agency for Toxic Substances and Disease Registry (ATSDR). diabetes mellitus. Bregante G. Lison D. Chislovska NV. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Hotz P.atsdr. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Schulz C. Toffoletto F. Uemura T.S. Comprehensive study of the effects of age. Wang H. Oguma E. Third National Report on Human Exposure to Environmental Chemicals. Moriguchi J. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Lauwerys R. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers.95:20–31. Fukui Y. Grubb A. Ezaki T. Howerton K. Seiwert M. Ikeda Y. Dekio F. Environ Res 2004. Kaus S. Elinder CG.45:43-52. Toxicological profile for cadmium update. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Diamond GL. population. et al. Clin Chim Acta 2000. Choudhury H. Becker K. Fayers PM. environmental. Hellstrom L.

pp. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Nakagawa H. Lybarger JA. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. et al. Gangemi S. Tanebe K. Liu QF. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Sarasua SM. Roels HA. Environ Health Perspect 2002. Wilhelm M. New York: Plenum Press.110:1185-1190. Hoet P. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women.110:151-155. Zhang YL.84 (Section A):4455. In: Clarkson TW. Roels H. Cadmium carcinogenesis. Environ Res 2000. Friberg L. Biological monitoring of cadmium. Int J Hyg Environ Health 2006. Ginucchio G. Environmental exposure to cadmium. Merlino MV. EPA). Honda R. Nakagawa H. Zhu HD. dietary intake. Vangronsveld J. Occup Environ Med 2002. Oskarsson A. lead. Skerfving S. et al. iron status. Olsson IM.3:26-41. Mueller PW. lead. lead. Time trends in burdens of cadmium. Minciullo PL. Tanebe K. forearm bone density. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Cadmium in blood and urine – impact of sex. Emelianov D. Suwazono Y. Nishijo M. Environ Res 2006. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk.59(1):22-25.21(3-4):251-262.gov/ttn/atw/ hlthef/cadmium. Stelitano A. Buchet JP. Staessen J.Metals Nishijo M. 2001. age. Thijs L. Nakagawa H. Toyama. Lundh T. cadmium. Lundh T.epa. 151-168. Saito S. Lancet 1999. eds. Sager PR. Honda R. Revised 2000 [online]. Fan YG. Campagna D. Nordberg GF. Tawara K. Gallmans G. 2004. Mutat Res 2003. Nordberg GF. Revised and new reference values for arsenic. Bruiglia S. Arch Environ Health.59:394-397. Nogawa K. Lison D. or cadmium in controlling occupational and environmental risks of nephrotoxicity. and former smoking – association of renal effects. Lijnen P. Environ Health Perspect 2002.S. Salpietro CD. and mercury in the population of northern Sweden. Available at URL: www. Noonan CW. et al.100:330-338. Cadmium compounds. Biological monitoring of toxic metals. Hazard Summary. Schwenk M. Ren Fail 1999.209:301305.html. Kobayashi E. et al. United States Environmental Protection Agency (U. 2000.39:2507-2515. Zhao YC.353:1140-1144.30(5):395-399. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Staessen JA. Kathman SJ. Schultz C. et al. Bergdahl IA. Bensryd I. Wennberg M. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Kido T. created 1992. Stegmayr B. Usefulness of biomarkers of exposure to inorganic mercury. Jansson J-H. Relationship between newborn size and mother’s blood cadmium levels. J Environ Sci Health B 2004. Roels HA. Okubo Y. Wang JX. and risk of fractures: prospective population study. Nordberg M. et al.533(12):107-120. J Perinat Med 2002. Lauwerys R. Ottosson H. 4/8/09 Waalkes MP. Kuznetsova T. J Cardiovasc Risk 1996. Japan.

00) 7.80 (4.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.4) 9.2) 12.45-8.40-11.50 (4.2-13.90) 5. Most human exposure to cesium occurs through the diet.12-11.73-5.20) 7.77-8.15-8.43 (5.47-8.80) 7.84) 8.50) 5.12 (4.57-5.0) 12.90) 4. For absorbed cesium salts.01) 7.2.08-5.81 (4.30-10.2-13. population from the National Health and Nutrition Examination Survey.54-11. and clay.50 (7.59-5.13 (7. Fourth National Report on Human Exposure to Environmental Chemicals 205 .89) 4.20 (6.62 (5.50 (6.74) Selected percentiles ( 95% confidence interval) 50th 4. Radioactive 137Cs has been used medically to treat cancer.81) 9.03 (4.87-7.04) 7.66 (7.59-5.8 (10.64) 5.37) 7.05-5.03-4.0) 12.8 (11.20 (4.09-5.70-8.40-5.90-10.60) 7.14 (4.40-5.43-8.3-15.70) 5.82-4. and 03-04 are 0.82) 5.56) 5.39) 7.23) 9.42-7.3-13.22 (4.50) 9.20-7.64-5.70 (6.49) 4.97 (7.32 (3.9) 11.55 (4.1-12.2-14.77 (9.80 (4.31-8.5) 10.74-5.71-5.71) 4.1 (10.60) 5.7 (11.60 (8.25-5.5 (8.05) 5.50 (4.89-5.84-9.49) 75th 7.3-13.13 (5.10 (8.40-11.8) 12.27-5.21 (4.59-5.96 (6.0) 11.99-6.42) 6.81-14.1) 11.63 (4. However.23-4.9) Total 4.30) 5.72-7.98 (7.S.6 (9.20-5.91-8.35 (4.08-5.24) 4.14.92-13.1 (9.35 (4.40 (4.77 (4.2-12.99) 7.4) 12. the body half-life is estimated to be 70-109 days based on 137Cs exposures.59 (5.80-10.13-8.16-6.0) 11.94) 4. and 0.07) 4.30-5.68 (7.6 (9.32-5.9) 12.4 (9.67 (4.49 (4.50 (4.27) 4.26) 4.8) 9.12) 5.83-4.1) 9.33-5. soil.7-14.25 (3.33 (5.08 (7. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.71-8.00) 6.56 (4.71 (8.09) 5.13 (8.5-14.34 (4.90-8.86-11.22-4.71 (4.4) 95th 11. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.02 (4.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.80-6.33 (6.00-8.61) 7. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.91 (7.72) 4.70 (4.3) 12.52-9.98 (7.7) 11.46) 7.40) 7.68) 9.20) 5.73-11.4) 10.84-5.2) 11.93 (4.04 (4.6 (11.8) 12.3 (8.Metals Cesium CAS No.9 (11.47-4.80-11.8 (10.62 (5.99) 9.0) 9.7 (9.8) 9.87 (4.70 (6.0-13.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4.70 (5.3) 10.60-6.26) 7.08 (6.81) 4.30 (6.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.71-9.84) 5. 0.1 (11.94-4.00-4.95 (3.00-9.35-5.56 (4.05-5.00-8.0-15.55 (7.3 (8.1-12.90) 9.27 (7.21) 90th 9.10 (6.86 (7.34) 9.53-11.3) 10.70-5.44 (8.94 (4.53 (6.00) 4.64) 5.55-11.2 (9.70 (8.4-13.52) 7.8) 11.90-10.59) 7.49 (5.62) 4. 01-02.40) 5.40) 5.14.0) 10. and as polymerization catalysts.4) 11.54) 4.60-7.86-12.9 (11.90-12.7 (10.97) 4.40-5.4 (10.9 (10.39-4.94 (4. scintillation counters.10-5.8-13.80 (4.0) 12.83) 6.5) 12.0 (10.16-6. photographic emulsions.76-6.6) 11.45-5.64 (4.90) 5.80-13.6 (9.0 (9.50-7.87 (4.29) 4. semiconductors.5-14.10-7. cesium hydroxide is corrosive and irritating at high concentrations.64) 4.32) 4. diarrhea.80-10.38) 5.80 (8.90-12.9 (11. although cesium was generally of low toxicity when given to animals.17 (6.64-10.81) 4. 2004).3) 9.9 (10.10 (6.36 (6.36 (3.05) 5.01-6.20-8.7) 10.69-6.10 (8.25) 4.1) 9. nausea.60-12.4) 12.5 (10.20) 8.30 (6.3) 10.84 (4.87 (4.10-9.17-6.8) 11. Whether cesium compounds are carcinogenic is unknown.70) 5.1) 10.99-11.4) 10.1) 11.1-13.88 (8.80-10. see Data Analysis section) for Survey years 99-00.00-10.26 (3.3) 10.12-5.60-5.70) 7.70 (8.99-11. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.63-4.61-6.2 (9.60) 7.2-13. Little is known about the health effects of this metal.9 (11. and high-power gas-ion devices.30) 7. interval) 4.29 (4.40-5.36) 3.80 (8.7 (9.7 (8.7 (9.70 (9.89) 5.6 (9.56-11.80 (8. respectively.7) 10.20) 4.08) 7.95) 5. infrared lamps.8) 12.60-6.9) 8.5) 9. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.07-11.77 (9.5-16.97-7.7 (10.60-7.95-4.6) 10.01-8.10-8.87) 5.5-13.4 (9.03 (4.6 (11.79 (4.74 (4.17) 4. and cardiac arrhythmia (ATSDR. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60 (7.37) 5.7 (10.90 (6.40-7.20-4.90 (4.42) 7.26-11.7) 11.63) 6.90) 7.00 (7.90-10.

50) 4.23 (7.95-12.51) 4.3 (8.51 (4.35) 3.40) 7.03) 5.01-8.82) 7.95) 8.27-4. Komaromy-Hiller et al.93-7.56) 4.24-4.30-4. population.15) 95th 8.42-4.05-3.91 (5.41 (5.09) 8.96) 4.90 (7.03-5.62) 5.10 (3.05) 6. 1990).26 (4.S.20-8.99) 4.27 (8.51 (4.39) 8.6) 6.07-4.74) 3.37-3.47) 6. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3) 9. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.91-9.16-8.63-6.77 (6.13-9.06 (3.26 (3.50) 4.1) 11.83-7.07) 8.43 (4.31 (4.44-5. Using clinically submitted specimens.76-9.46) 6. population from the National Health and Nutrition Examination Survey.38-7.77-5.41-4.67 (5.91 (5.12) 3.91-6.35 (3.02-4.29) 4.98 (6.36-6.08) 4. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.8) 10.3) 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 3.35 (4.54 (4.68) 6.74-11.00-5.0) Total 4.87 (5.60) 3.85) 5.91) 5.74 (5.95) 4.50 (6.66 (5.33 (5.50) 4.26-6.64) 5.99-4.40-5.46-4.47) 6.09) 4.98) 5.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.21-5.34 (5.27-6.16-8.15-11.11 (5.65 (6.87-4.2 (8.42-6.59) 4.56) 3.18) 8.86 (4.5) 9.0 (7.S.88-10.2) 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 3.53 (4.00 (8.81 (4.42-4.47 (4.05 (4.9) 10.04-5.7) 10.29) 4.77 (4.31 (4.19-6.6 (9.20-4.22 (3.64 (4.15 (7.41) 9.14) 4.71) 6.25) Selected percentiles ( 95% confidence interval) 50th 4.72 (4.00-8.12 (3.12-6.02 (5.37) 4.43 (3.10) 7.17 (6.93-9.39) 5.60-20.24-10.44-9.29-3.70) 6.04) 5.95 (5.08) 4.79-5.54 (4.11 (5.68 (4.30-4.14-7.03-6..14 (6.36-10.70) 7.95-6. interval) 4.04) 6.3-15.30 (4.41 (8.95 (3.94 (5.47) 7.90-8.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .33-8.97) 8.84-7.00-9.13-9.60 (5.28) 8.99 (3.08 (5.8) 6.10 (5.59-8.8) 5.68) 4.63 (4.92 (5.61 (7.20-4.96) 4.35-11.83-6.75 (7.33-3.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.22) 6. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5) 9.45 (4.27 (6.64-6.08) 3.S.98) 5.28 (4.47 (7.96-4.08-3.99-9.38-12.00-4.79) 9.66 (6.63 (7.48) 90th 7.31-6.38 (3.43 (8.13) 7.47) 4.19-3. Two small studies of European populations reported urinary cesium levels similar to U. 2005.99-9.5 (9.44 (4.66-6.30 (7.90-8.79 (5.52-5.75 (6.58-5.64 (8.91) 4.75-11.41 (4.31-4.84-9.56) 4.95) 10.44) 3.84-11.58) 3.98 (7.84-9.18 (7.06) 4.77 (7.08 (3.20) 5.78 (3.7-12.30 (3.61-3.46 (8.08-7.46-8.87) 5.84-7.21-3.49) 3.22-11.56-10.9 (9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf..74 (4.48) 7.94) 7.07 (5..72) 4.54 (3.64) 9.48-6.56 (4.73-4.79) 6.07) 8.43 (4.18-7. 2004). Minoia et al.88-4.89-4.78) 4.25) 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.3 (10.63) 6.51 (3.51 (3.91) 5.17) 9.14) 4.28 (5.85) 4. and were also roughly similar to those in this Report.41-7.24 (3. (2000) found urinary cesium levels that were slightly lower than those reported for the U.62-8.60 (3.71 (7. population results shown in this Report (Alimonti et al.55 (3.8 (9.50 (5.16-5.00-10.30) 10.85-4.77) 4.50) 8.13 (3.40) 6.7) 10.15-4.00-5.73 (3.55) 4.42 (5.38) 10.06 (5.17-4.54 (5.05) 3.68) 3.27 (6.50 (7.2 (8.18-6.06) 5.00) 6.58 (4.78) 4.60-10.78 (3.46 (7.35-7.14-6.36-3.72-5.96-4.03) 6.4) 10.05-3.83) 8.97-4.28) 7.5) 7.55-5.29-3.66 (5.41) 4.10-4.39 (5.09 (4.80) 6.17) 4.97-5.43) 8.57) 3.76-6.05-4.74) 75th 5.63-6.90-3.92) 3.43-11.44 (8.42 (4.43-6.3) 11.04-11.9 (10.3 (9.6 (9.64) 4.27) 4.96 (4.20-4.67 (6.16) 5.82-4.53) 3.29) 5.14-4.81 (4.70 (7.79) 4.45-6.58) 8.50-5.91-7.33 (5.21 (2.38 (3.67) 5.51 (7.65-4.0) 7.10 (3.63 (6.53) 6.53 (6.68-11.21-4.08 (6.30) 10.58 (6.65-3.2) 11.

Gallorini M. Howerton K. Voorhees RE. Mincione G. Assessment of urinary metals following exposure to a large vegetative fire. patient population and literature reference intervals for urinary trace elements. Wood CM. Mott JA.html. A study of 46 elements in urine.S. J Expo Anal Environ Epidemiol 2004. Sabbioni E. Clin Chim Acta 2000. Gatti A. Wolfe MI. Centers for Disease Control and Prevention (CDC). Available at URL: http://www. New Mexico. Forte G.Metals References Agency for Toxic Substances and Disease Registry (ATSDR).cdc. Costa R.atsdr. Pozzoli L. blood. 4/8/09 Alimonti A. Sewell CM. et al. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Apostoli P. et al. Comparison of representative ranges based on U.14:120-128. Atlanta (GA) 2005. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. Toxicological profile for cesium.gov/toxprofiles/tp157. antimony and tungsten. Ash KO.2004 [online]. Paschal D. Komaromy-Hiller G. Sci Total Environ 1990. Third National Report on Human Exposure to Environmental Chemicals. et al. Pietra R. Ronchi P. Minoia C. 2000. cesium.95:89-105. and serum of Italian subjects.296(1-2):71-90. Rapid Commun Mass Spectrom 2005.19:3131-3138. Spezia S. Trace element reference values in tissues from inhabitants of the European community I.

39) 1.33-1.316 (.26) 1.05 (.16) 1.460 (.340 (. Cobalt compounds are used as catalysts in producing oil and gas.48) 1.452 (.291-.52 (1.17 (1.550-.67) 1.530-. and magnetic recording media.13) 1.515 (.32) 1.410-.950 (.07.760 (.343 (.340) .790-. diamond-polishing wheels.690-.47 (1.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.800) .450-.940 (.300 (.670 (.386) .800-. industry is imported or obtained by recycling scrap metal that contains cobalt.950-1.373) .370) .650 (.04-1.32 (1.487) .380-.630 (.680 (.920-1.450) . Cobalt is used as a drying agent in paints.580 (.870 (.08) .760) .68 (1. large appliances.28-2.06 (.04-1.410-.360-.28 (1.680 (.530 (.610) .339 (.03 (.490-.33 (1.45 (1.610 (.73) 1.610-.81) 1.320 (.333-.19) .600) .36) 1.S.81) 1.520-.02-1.350-.333-.660) .07.24 (. see Data Analysis section) for Survey years 99-00.910-1.414) .390 (.940-1.790) .07-1.340-.540-.350-.740-.820 (. The cobalt used in U.334) .405-.690 (.431) .352 (.564) .330-.700) .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 .890-1. shiny.330 (.290-.25-1.890) .520 (.06-1.430 (.520 (.450-.26-2.56) 1.620-.65) 1.640) .360-.469-.950) .950-1.920) 1. 0.660-.17 (1.388-.470) .373-.313) .379 (.750 (.419) Selected percentiles ( 95% confidence interval) 50th . blue-colored pigments.03-1.32) 1.15 (1. Cobalt may be released into the systemic circulation of patients who receive joint prostheses that are Urinary Cobalt Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. It is emitted into the environment from burning coal and oil and car and truck exhaust.930-1.890-1.590 (.17-1.16 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.454 (.450) .580 (.550 (. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.28 (1.860 (.560 (.870-1.440-.940-1.73) 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 . seawater.32-2.15-1.12) 1.520 (.465) .367 (.430 (.430) .310 (.540) 1.519 (.520) .327-.620) .270-.22 (1.790 (.390 (.496) .740-.980-1.430) .950 (.850) .540-.470 (.410 (.500) .300-. and soil.710 (.398 (.620-.350 (.435 (.850-1. Cobalt compounds are also used in manufacturing battery electrodes.305-.850-1.810-.01-2.07-1. hard metal (alloys of cobalt and tungsten carbide).543) .348-.670-. steel-belted radial tires.640) .810) .398) .390-.570-.S.424) .570 (.42) 1.420) .830-1.03) .20 (1.650 (.280-.47) 1.570) .270-.590) . and in synthesizing polyester and other materials.16 (1.890-1.600-.420) .12) 1.640) .480 (.01-1.461 (.05 (. automobile airbags.50 (1.960-1.336-.700) .23) .331-.460 (. and inks.370 (.750 (.410 (.14-1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.26-1.670 (.03) 1.319) . 01-02.430 (.410-.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 .460) .64) 1.350) 75th .359 (.590-.880-1.520-.800-.37-1.17 (. Cobalt occurs naturally in airborne dust.390) .400-.660) .380-.29 (1.348-.08.740 (.730) 1.338-.404) .680) .377-.770) .00) . It is also a component of porcelain enamel applied to steel bathroom fixtures.850) 1.371 (.570) . interval) .53) 1.330) .540-.01 (.369 (.480-.410 (.316-.380 (.355-.480 (.99) 1.360-.870 (.520-.308-.750-.520 (.630-.14) .16) 1.394) .610) .03) 1.26) Total .16-1.285 (.06 (.502) .01 (.630 (.390 (.372) .570-.670 (.59 (1.460-. hard metal or in combination with other elements.44) 1.350-.399) .05) 1. and fertilizers.420 (.09) .510) 1. respectively.410 (.310-.540-.380 (.520) .294 (.380 (.550) 90th .28 (1.379 (.301 (.259-.900-1.04-1. varnishes.980) .92) 1.670-.460) .340) .16-1.427-.393-.900) .580 (.09 (.22-1.32 (1.21) 1.583) .590-.75 (1.22) 1.710) 1.370-.418 (.650-.03 (.48) 1.410) .50) 1.47) 1.890) 95th 1. and 03-04 are 0.750 (.581) .Metals Cobalt CAS No. and 0.08-1.370-. Usual human exposure is from food sources.09 (.417) .900-1.270-.23-2.24 (1.880 (.431) .900) .930 (.410) .04 (.490-.500 (.450) .450) .430-. population from the National Health and Nutrition Examination Survey.04) 1. 208 Fourth National Report on Human Exposure to Environmental Chemicals .520-.523) . and kitchenware.499 (.710) .46 (1.60 (1.463-.690-.600 (.460) .620-.16 (.416) .47 (1.530) .820 (.840) .374 (.810) .375 (.930) .900) .428-.434 (. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.07 (.364-.410 (.340-.370-.820 (.680) .

830 (.363) .467-.342-.04 (.736-.313-.728 (.313-.561) .317 (.289) .861-1.343 (.256-.435 (.842) .277-.36) 1.00 (.419) .508-.407 (.16) .740-1.279) .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 .513-.291 (.274-.442-.537 (.644 (.259-.337) .938) .328 (.352) ..378-.960 (.955) .393-.708) .500-.378 (.00 (.409) .328) .365) .09) 1.439) .630-. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.360) .471 (.591 (.547 (.11-1.554 (.381) . 1979).259) .337 (.362) .12-1.785) .394) .548 (.11-1.275-.329-.606 (. Exposure in the workplace may come from electroplating.324-.581) .348) .333 (.522) .361-.303-.257 (.777-.738 (.50 (1.301-.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 .963-1.582-.327-.949) .372) .376 (.728) .829-1.421) .457) . 2003).503-.838 (.333-.328 (.402 (.298 (.28) 1.251-.33) 1.463-.247 (.462) .00 (.824 (.361 (. or using diamond-polishing wheels that contain cobalt metal.857-1.257-.10) .368) .500-.826-1.703-.634-.449-.609) . population from the National Health and Nutrition Examination Survey.983) .660-.334) .552 (.290 (.737 (.304-.355) .83) 1.282-.234 (.700 (.438) .905) .781-1. 1972).400 (.433) . respectively.282 (.. an essential human nutrient.333-.286) .00 (.500 (.760-1.329 (.861 (.25 (.523 (.243-.16 (1.821-3.847) .331-.505) .15 (.983-1.73) 1.585) .895-1.608 (.937 (.03-1.679-.404-.23 (1.879-1.408 (.479-.479) .630-.407) .844 (.487-.368 (.929) .487-. using hard metal cutting tools.593) .640) .963) .600-.12 (.380-.384) .396) .29) .833-1.392 (.626-.378-.36) 1. 1972).963-1.27) 1.563-.616-.271 (. in the feces.560-.471-.669) .598 (.15) 1.19) .851 (.290 (.388 (.54) 1.365-.04-1.13) 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 .744) 1.667-1.468) .425) .297) .248-.475 (.543) .55) .534 (.872 (.02 (.306) 75th .469-.990) .850 (.391) Selected percentiles ( 95% confidence interval) 50th .35) 1.326-.829) . Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.275-.33) .280-.529 (.382-.14 (.952 (.562) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.689 (.515 (.694) .343-.304) .378-. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.49) 1.10) Total .313 (.753) 1..753-.248-.428-.429) 1.781) 95th 1.323) .495 (.667-1.895-1. cobalt is excreted predominantly in the urine.425-.353 (.25 (.313-.313-.632-.272-.733-1.457 (.444 (.29) 1.294-.821 (.595) .611) .804) 1. interval) .369 (.963) .358 (.237-.00) . Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.388 (..562) .774 (.434-.738 (.. 1994.60) 1.50) 1.352 (.638-1.60) 1.723 (.574-.534-.00-1.964 (.533 (. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.324) .310) .16 (.06 (.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 .03 (.50) 1.635 (.417 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).250) .361 (.313-.594) .346 (.757-1.335 (.44 (..476-.750) .683-.786-. refining or processing alloys.27) 1.362 (.938-1.297-.599) .457-.673-. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.268 (.29 (1.488) .707) .848 (.990-1.449) .481) 90th .333-.17) .955) . Smith et al.932-1.911-1.Metals fabricated from cobalt alloys (Lhotka et al.10 (. Cobalt is absorbed by oral and pulmonary routes.293 (.278 (.615) .662) .647) .319-.29 (1.368) .29 (1. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.850-1.302-.386 (.352 (.57) 1.792 (. and to a lesser extent.301) .513) .296-.S.353-.455 (.471-.279 (.513 (.691 (.426 (.975 (.700 (.281) .393 (.750-.727 (.273 (.309) .24) .611) .259 (.792-1.756 (.300) .10-1.452-.396) .16 (.339-.461) . with pulmonary clearance half-lives of from one to two years (Hedge et al.00) .327 (.550-.306 (.976 (. 1994).239-. Once absorbed and distributed in the body.900-1.316 (.278-.35) .290 (.542 (.417) .554 (.30 (1.362-.523 (.314 (.215-.349) .898 (. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.391 (.361-.387) .344-.435-. A portion of cobalt retained for long periods is concentrated in the liver.917) .296) .704-.

Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al.gov/toxpro2. Am J Med 1972. 2003. not to imply that the BEI is a safe level for general population exposure...e. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. Morgan WKC. Lisi. 1955). a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen.. Hailey JR. environmental levels) and health effects is available from ATSDR at: http://www.43(4):299-303. Atlanta (GA). Dunstan et al. 1997. Shirakawa et al. Inhalation toxicity and carcinogenicity studies of cobalt sulfate.. 1998). Sills RC.. Perkins DG. Information about the BEI is provided here for comparison. 2003). Centers for Disease Control and Prevention (CDC). 1988). Sci Total Environ 1994.. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. 2005. 1999). Daniel et al.. 2001).atsdr. “Hard metal” disease. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans.. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis. 1992). For workers exposed to cobalt in the air. Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. 210 2006.S. Urinary measurements mainly reflect recent exposure.Metals Toxic effects of cobalt have been encountered in workplace settings.. Rubin A. Bucher JR.. Cugell DW. 1990). Lauwerys and Hoet. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. Information about external exposure (i.. although substantial occupational exposures have produced elevated urinary levels for many weeks.cdc. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. Cobalt-beer cardiomyopathy. 2001.49:56-67.. has been associated with exposure to dusts that contain cobalt. 1993).53:395417. Grumbein SL. 2005. Blood and urinary concentrations as estimators of cobalt exposure. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al. 1994).gov/ exposurereport/. A clinical and pathological study of twenty-eight cases. et al. Cobalt was once added as a foaming agent to beer. Arch Environ Health 1988. 4/3/08 Christensen JM. 1994. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. Alexandersson R. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. Poulsen OM.. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. 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.. with mean levels that were about 15-20 times higher than in the general U. 1985. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al.. 2001. population (CDC. Iavicoli et al. 2006. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. White and Sabbioni. 2005 [online]. Linnainmaa and Kiilunen. 1998).. Haseman JK... 1988). Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect... 1997). References Alexander CS. 2003. MacDonald et al. 1972). Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al.S. A 1982-1992 surveillance programme on Danish pottery painters.cdc. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L.. population results in this Report (Kristiansen et al.50(13):95-104. Lison et al..html. Third National Report on Human Exposure to Environmental Chemicals. 1994. Toxicol Sci 1999. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. Thomassen et al. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Roycroft JR. Available at URL: http://www.. Swennen et al.. 1993). usually in combination with tungsten carbide (Cugell et al.. Krause et al. 1989). The respiratory Fourth National Report on Human Exposure to Environmental Chemicals .

28(5):1121-1128. Meyer zum Buschenfelde K-H. Tilley S. Lasfargues G.69(3):193-200. Health Phys 1972. Daniel J. Hoet P. Lison D. Clin Orthop Relat Res 2003. Swennen B. Lauwerys RB. Co-sensitivity between cobalt and other transition metals. Iavicoli I. Science 1988. Peltier A. 1985. De Boeck M. Bourne RB. J Bone Joint Surg Br 2005. Lung cancer risk in hard-metal workers. Salvatori S. Absorption and retention of cobalt in man by whole-body counting.87(5):628-631. a study of 13 elements in blood and urine of a United Kingdom population. Lauwerys R. Kriss JP. Long-term clearance of inhaled 60Co. Blunn G. Occup Environ Med 2001. and hard metal dust. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Zweymuller K. Kato M. Swennen B. Bozec C. and cobalt metals. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Oksa P. Goto S. Kristiansen J. Buchet JP. Arch Intern Med 1990. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Molders J.150.58(10):631-634. 3rd ed. Mutat Res 2003.406:282-296. Diepgen TL. Bacis M. Kiilunen M. Salama A. et al. Linnainmaa M.204:147-160. Cleland D.216:253-270. Biological monitoring of workers exposed to cobalt metal. Thabe H. Unwin P.50(9):835-842. Pisati G. Br J Ind Med 1993. Sci Total Environ 1994.21(2):189-195. Sabbioni E. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group.55(4):269-276. et al. Cannon SR. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Occupationallyinduced “isolated cobalt sensitization. Pradhan C. Am J Ind Med 2003. Schank M. Hammon E. X. J Occup Med 1992. Lhotka C. Cobalt and antimony: genotoxicity and carcinogenicity. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Moulin JJ. Cresti R. salt. Dunstan E. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Thakker DM.157:117121. Goto S. Shirakawa T. Sabbioni E.34:620-626. Edmonds CJ. Wild P.150(1-3):167-171. Hedge AG. Goldberg MA.95:29-37. Chess DG. Lison D. Zedda S. Iversen BS. Rorabeck CH. J Orthop Res 2003. Kirsch-Volders M. Romazini S. Sanghrajka AP.44:124-132. Robinson C. Fujimura N.88(4):443448. McCalden RW. Barnaby CF. Lison D. DeSantis V. Jarvis JQ. Steffan I. Christensen JM. Boca Raton (FL): Lewis Publishers.22:359367. et al.150:177-183. Linna A. Respiratory health of cobalt production workers. Leghissa P. Radulescu M. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Schaller KH. Int Arch Occup Environ Health 1997. Contact Dermatitis 2003. Alessandrelli M.48:172-173.Metals effects of cobalt. A report of two cases from mineral assay laboratories and a review of the literature. 2001. MacDonald SJ.” Contact Dermatitis 2001. Weyher I. Kusaka Y. et al. oxides. Bunn HF. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Buchet JP. Stanescu D. Heki S. Lauwerys R. Kuska Y. Laippala P. Am J Epidemiol 1998.45:246-247. Uitti J. Dunning SP. Sabbioni E. J Trace Elem Med Biol 2006. et al. Sci Total Environ 1994. Occup Environ Med 1994. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Ichikawa Y. et al. Vitali MT. The release of metals from metal-onmetal surface arthroplasty of the hip. Health Phys 1979. Epidemiological survey of workers exposed to cobalt oxides. Palmroos P. Thomassen H. Weber A. Dickel H. White MA.533:135-152. Kraus T. Ghat IS.148:241-248. Lisi P. Meier R. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Sci Total Environ 1997.(1-3):133-139. Gross RT. Outcome of occupational asthma due to cobalt hypersensitivity. Trace element reference values in tissues from inhabitants of the European Union. HoffmannB. Carnes WH.51(7):447450. Mosconi G. Int Arch Occup Environ Health.36:732-734. Angerer J. Cobalt cardiomyopathy. J Bone Joint Surg Br 2006. Hoher T. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis.20(1):25-31. Zhuber K. Ziaee H. Chest 1989. Sci Total Environ 1998. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. McMinn DJ.242:1412-1415. Smith T. Schramel P. Szekeres T. Roto P. Zobelein P. J Rheumatol 2001. cobalt salts. Falcone G. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium.

00-1. leaded glass.10) 1.70-5. brass.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.50 (2.50 (4.00) 3.50-3.50) 5.10 (2.30 (2.53) 1.56 (1.40) 2.50-5. metal alloys (e.60 (2.20) 3.30 (1.20) 1.60 (1.30 (1.60 (1.70) 4. such as lead phosphate and tetraethyl lead. ammunition.10-6.50-1.80 (2.80 (2.30 (2.20) 4.50-2.70 (3.90) 2.30 (1.60) 2.40) 4.10) 1.37 (1.91) 1.40) 1.70-2.22 (1.10) 4.70) 1.60) 2.80 (2.70) 2.20 (3.69 (1.50) 7.900 (.20 (2.55 (1.60 (2.60 (2.20-6.60 (4.10-2.800-1.20 (4.78 (1.00) 1.80) 1.70) 1.10 (4.80-4.20) 3.40-2.62-1.942 (.20 (2.00 (2.30 (2.60-4.90-4.60) 2.60-1.40) 3.70 (2.46 (1.50) 1.01 (1.25) 1.S.60-4.10-4.70 (1.66 (1.23 (1.70 (1.3.28.60 (3.50-5.60 (3.50-6.66) 1.55-1.20 (1.32-1.10 (1.70-1.90) 5.00) 4.986) .40-6.50 (1.50-1.52-1.90-3.20 (3. Lead was used in plumbing for centuries and may still be present.40 (1.60) 1.90) 2.31) 1.10) 3.50 (1. In the past.878-1.90-6.10 (2.20 (1.50) 1.80-3.00) 1.00-4.30-5.80 (1.30-1.60) 5.00) .10 (1.00) 2.50) 2.00) 1.60) 4.10-2.90) 3.70-2. Before the 1980’s.43) 1. population from the National Health and Nutrition Examination Survey.40-1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.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 2.36) 1.80) 2.60-6.60) 4.00) 4.90) 2.60 (1.30-1.20) .32-1.83 (1.70-6.40-3.50-4.80 (1.50) 75th 2.70-3.50 (2.70) 1.50) 4.00 (6.30-2.60) 1.10-6.50-1. dense.20-1.40 (3.48) 1.40-3.10-3. see Data Analysis section) for Survey years 99-00.70 (1.60-2.60) 2.93-2.90-4.50) 4.10) 2.87) 1.40-1.14-1.30) 95th 5. interval) 1.75-1.00 (4.51) 1.39) 1.10) 1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.50 (3.20 (1.00-4.90) 3.50-2.36-1.80-4.20 (3.10-2.900-1.30) 2.50) 2.900 (. 7439-92-1 General Information Elemental lead is a soft.14-1.69) 1.40-5. Since lead has been eliminated from gasoline.90 (3.00) 1.60) 3.20-4.95) 1.70-4.10) 2.20 (3.34-1.30 (4.40-6.90-2.80) 1.80) 1.71-1.43-1.80-3.70) 3.10-3.00-2.60-2.80) 1.60 (3.40 (5.10 (3.40 (4.90-2.90-4.25 (1. solders.70 (2.60-1.90 (2.20-2.30-2.40-2.30 (2. antique-molded or cast ornaments.20-1.30-2.45-1.55-1.10-2.20) 5.60 (1.10-4.40) 2. blue-gray metal that occurs naturally in soils and rocks.45 (1.90 (4.80) 1.00 (1.40) 5.50-3.20 (3.70-2.30-2.90) 1.75-2.10 (1.90 (3.60 (1.65 (1. Lead has a variety of uses in manufacturing: storage batteries.30) 1.40-1.70) 3.25 (1.40) 2. malleable.39-1.899-.50 (2.80 (4.75 (1.3.90-4.00) 6.Metals Lead CAS No.20) 2.90) 2.90 (2.52 (1.30 (3.50 (1.50 (4.50-2.80) 2.00) 2. and for radiation shielding.80-3.10-3.20 (3. the main source of lead exposure for the general U.10) 3.68-1.87 (1.70) 4.52-1.10-3.80-4.50-1.20-3.43) 1.37 (1. and 03-04 are 0.40 (2.70) 4.10-2.60-1.40 (1.77 (1.30 (1.51 (1.00) 2.00-1.60) 1.80 (4.70 (2.75) 1.80 (5.80 (1.30-4.81) 1.00 (1.10-1.20-3.80 (1.20-3.70) 1.60) 4.37-1.40-1.10-8.30) 2.80-2.90 (3.60-3.12-1.90-2.60) 5.30 (4.90) 1.00-4.60) 2.90) 2.30 (4.40) 1.S.10) 5.62) 1.60 (1.g.00 (5.90 (3.60 (2.60) 1.20) 4.60) 4. 0.20-2.30 (2.40-4.30 (2.10-1.20-3.69 (1.20) 3.00 (3.30) 5.30 (2.14-1.86) 1.40) 2.20) 3.60) 3.70) 4. plastics.40) 1.40 (1.946 (.60) 3.00-5.00-6.80) 2.90-2.50 (3.60) 3.80 (1.60 (2.10-2.40-1.49-1.30-1. 01-02.60) 1.50) 1.80) 3.40) Total 1.62 (1.70 (1.10-1.69) 1.80-3.70-1.90 (1.40 (1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.60 (3.20 (1.09) 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 2.50-1.70 (3. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.20 (3.72) Selected percentiles ( 95% confidence interval) 50th 1.00) 5.30-1.70) 3.96-2.00 (4.50 (1.40-3. respectively.30) 2.00) 2.70) 1.30-6.40-2.02) 1.30-1.43 (1.50) 5.70 (5.04-1. bronze).50-4.70-1.10 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60 (2.40 (2. ceramic glazes.19 (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. and 0.50-2.17) .60 (1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .50 (2.80 (1.80) 2.89) 1.40-1.60-1.43 (1.36-1.20 (1.80-5. Lead is most often mined from ores or recycled from scrap metal or batteries.80 (3.90 (3.20) 90th 3. Elemental lead can be combined with other elements to form inorganic and organic compounds.10) 3.90) 1.30-1.50) 3.00) 3.90 (1.80 (5.00) 1.50) 1.50 (2.

66 (2.40 (2.731 (.900-1.920 (.29 (2. Fourth National Report on Human Exposure to Environmental Chemicals 213 .850 (.718) .00-2.14-1.44-2.800 (.773) .745-.33-2..60 (1.20 (2.40-1.970-1.62) Total .50) 2.50) 2.70 (2.800 (.03-2.60-2.40 (2.90 (2.00 (1.03 (1.80) 2.600) .10 (1.23-4.72) 1.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.600-.23) .30-2.50 (1.556-.900) .40 (1.27 (1.600-.625-.13-3.35 (. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.708-.50 (2.506-.00) .40) 1.10-1.07 (.900 (.900) .40-5.822-1.50 (1.80) 1.604 (.04 (.10 (1. 0.20) .00) . and 0.20 (3.700) .90) 2.60-1.900 (.680) .10) .795 (.828) Selected percentiles ( 95% confidence interval) 50th .730 (.20 (1.80) 2.605) .1.00 (1. or after soluble lead compounds are ingested.729-.70) 1..526-.30) 1.90 (2.540-.960 (.82 (1.50-2.40 (1.14 (1.560-.12) 90th 2.90-2.78-2.900) .636 (.22) 1.41) 2.10-5.80) 1.00 (1.30 (1. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.80-2.20 (1. pewter utensils and drinking vessels.800 (.30) 1.20) 1.62-4.940 (.80-2.60 (1.66 (2.70) 1.52 (1. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.20 (2.86) 1.640 (.10-1.960-1.848 (.700-.S.00) .800-. interval) .27) 1.595-.50-2.579-.40) 1.40 (2.753 (.40-2.818) .900) .815 (.50-1.10 (1.591 (.40) 3. 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.90 (1.620 (.60) 2.642 (.20-2.40) 2.30) 1.30) 2.90-2.52-1.677 (.700 (.00-2.50) 3.10 (.00-2.40) 1.06) .700-.20) .30) 1.31 (1.20 (1.50-2.651) .579-. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.04) .04 (.700-1. lead-containing folk remedies and cosmetics.59) 1.50) 1.990) 1.572-.80) 2.680-.628) 1.833 (.10-1.70-3.1.40-1.02) 1.10 (1.30-5.60 (2.573 (.60-2.862) .710-.04-2.40) 2. In the blood.50-3.60-3.900-1.80 (1.589-. see Data Analysis section) for Survey years 99-00.70-2.07-1. and 03-04 are 0.60-3.52-1.990) 2.900) .616) .13) .90 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.90) 1.800) .738) .700-.30-1.800-.833-1.75) 4. bullet fragments retained in human tissue.50 (2.640-.82 (2. 01-02.86-2.535-.710-1.70 (2.30 (2.900-1.800) .691-.590 (.641-.910-.40 (1.90-3.40-1.660) .17 (1.10-3. lead-based painted surfaces undergoing renovation or demolition.40) 1.14 (1.20-1.20) .553-.701) .40) 1.86) 95th 2.800-1.700 (.90-2.86 (1.33 (2.91) 2.10-1.30) 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 1.637-. and contact with soil.785) .10) .78-2.40) 2.g.80) 2.70 (2. 2007.700-.840 (.600 (.40-1.695 (.00-1.900 (.04) 2. imported children’s trinkets and toys.30) 2.80) 2.680-.630 (.40-3.540 (.50 (2. lead-contaminated dust in indoor firing ranges.10-3.80 (1. respectively.613) . absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.00) 1.30-1.650) 1.21 (2.30) .00 (.625 (.800) .20-1.31-3.20) .800 (.73 (1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.80) 3.19 (1.20 (2.900) .24-1.931) .29) 2.70 (1.600) .10) 2.97) 4.766 (.500-.80-3.90) 2.90-3. Approximately half of the absorbed lead may be incorporated into bone.33. stained glass framing.20 (1.700) 1.30) 1.30-1.59-2. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.00) 2.810-1.90 (1.790 (.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 .570-.10) 2.80) 1.20-2.20) 1.800-1.600-.800) .757-. CDC.00 (2. battery and radiator manufacturing) and recreational sources.90) 2.20 (1. 2000).40) 2.671-.50) 1.Metals occupational (e.50) 1.49 (1.674) 1.564 (.70) 3.808 (.75) 3. However.11 (1.70) 1.90-4.40 (1.30-3.00-1.90-2.480-.60 (1.558 (.00-1. dust.955-1.20-1.915-1.986) .00) .70 (2.78-2.10) 1.70) 3.60 (1.700 (.749) . population from the National Health and Nutrition Examination Survey.20 (1.00) 2.90 (2.580-.30) 2.89) 2.600-.02 (.700-.600 (.610 (.10 (.820-1. older plumbing systems with leaded pipes or lead soldered connections.70) 2.920 (.688 (.10-3.900-1.620) 1.935) 1.960-1.40 (2.32 (1.40 (1.752 (.857) .800) .10-1.30-1.661-.64) 2.09) 1.80) 3.923 (.941) .659 (.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 1.30 (3.20) 1.600-.690) 75th 1.00 (1.700 (.80 (2.700 (. 1991). or water contaminated by mining or smelting operations.18-1.10 (.11) 2.700 (.

601-.72-2.71 (1.73-2.918-1.718) 1.541-.796-1.862-. based on prospective population studies. 2007).41-1.592-.731-.19-5.988 (.05 (1.917-1.03 (.55 (1.693 (.380-.679-.707 (.94 (1.698) .812-1.66 (1.98 (1.492-.14 (1.71-2. 1995.428) . with a half-life of years to decades.938 (.718) .04-3.15) 1.914-1.20) . 1993.608 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 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.70 (1.66 (1.677 (.988-1.61) 1.. CDC.383-.00 (1.938-1.992-1. Schwartz.37-1.58) 1.48 (1.07) .00 (1.34-1.496 (.08) .08-2.68 (1.27 (1.50-2.01) .657) 1.900 (.828) .39-1.12) 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 .639 (.898) .64) 2.22-1.28) 2.10) 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 .668-.02) 1.696 (.971 (.461) . with lesser amounts eliminated via the feces.702-. The skeleton acts as a storage depot.720 (.53-1.725) . zinc.98) 2.404 (. Large amounts of lead in the body can cause anemia.83 (2. hair.615 (.800-.677-. 1996).623 (.639 (.65 (1.667-.603 (.75 (2.44 (1. In 1991.10) 1.36-2. interval) .641 (.535) .11) 1.40-1.17 (.38 (2.667-.649 (.742) .03) . Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.11 (.09) 1.508) . 1993).97-18.882-1.72) .635 (.725) . population from the National Health and Nutrition Examination Survey.633 (.701 (.975-1.593 (.686) .73) 2.571-.03) .64-2.583-.47 (1.97 (1.621 (.551-.37-1.56 (1.460-.56) 3.61) 1.67-4.85 (1.607-.62-3. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.38 (2.400) .20) . 1991.838) .981-1.469 (.50) 1.561-.734) .06) .22) .88 (1.15) 1.59-3.587-.730) 1.655-.655) .648 (.712 (.89-5.26) 2.571-.703) .02-1.681-.609 (. Lead can cross the placenta and enter the developing fetal brain.85-2.28) . 2003.61) 1.12-1..662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.841-1.00) .18) .Metals 90% of the body lead burden in most adults.63) 1.62-2.638 (.765) .946-1. and paralysis.608-.375 (.07-1.870 (.28-1.44) 1.31) 1.701) .622 (.746) .588-.755 (. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.588-.918 (.43) 2.893) .77) 2.78-4.88) 1.0) 3.33) 1.50-1.933) .963-1.09-1.702) .957-1.753) .793-1.615 (. encephalopathy.639) .632 (.41) .710) .49 (1.579-.19) 1.682) .79) 2.03 (1.24 (1.66) 2.709 (.05-1.01 (.82) 1.700-.22) 1. scant amounts are lost through sweat.07 (.681-.74 (1.31 (1. O’Flaherty.617-.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 .35) 2. and through binding to ion channels and regulatory proteins.43 (2.676) .64 (1.20-3. Staessen et al. abdominal pain.18) 2.404 (.61) 3. BLLs and associated toxic effects differ in children and adults.708 (.851) .529-.436) .605-.03) 90th 1.644 (.659-.38 (2.43 (1.04) 2.03) 1.722 (.31 (2.739) .92) 2.997-1.50-2.45 (1.56-3.53) 1.920-1.87) 1.47) 1.962 (.639 (.97) 1.15-2.47 (2.887 (.83) 1.742) Selected percentiles ( 95% confidence interval) 50th .25-1.594-.11) .11 (.62) 2.569 (.655) 75th 1.677) .09-1.594-.52) 1. kidney injury.652 (. seizures.11-1.22-2.78 (2..10 (1.810 (.618 (.05 (.43-1.623 (.98-2.05-1.89-2.51) 1.51 (1.33 (1.586-.853-1.85) 1.03) 1.88-2. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.22) 1.06) 1.658 (.63) 4.408-.S.342-.23 (1.03) 2.88) 2.86 (1. Nash et al.763) .654) .33-1.29 (1.667) .97) 1.75-2.96 (1.55 (1.41 (1.645-.03-2.50-2.85-2.00 (1.15-2.17-1.79) 1. and nails (Leggett.679) 1.43) 1.31 (1.673) .781-1.683-.774 (.670) 1.33) 2. Approximately 70% of lead excretion occurs via the urine. The toxic effects of lead result from its interference with the physiologic actions of calcium.69 (1.03) 2.828-1.64) 95th 2.559-.404-.08) .722 (.10 (.11 (1.72-2.18 (1.625 (. through the inhibition of certain enzymes.645-. 1995).94-2.979 (.14) 1.926 (.721 (.990 (.03 (.03 (.06 (1.46 (1.31) 1. For instance.56-2.26) Total .52 (1.876-1.688) .790) .604-.61) 1.606-.25-1.18) 1.940 (.992-1.914 (.79 (1.15-3.11 (1.18) 1.06 (.46 (2. and iron.644) .671 (.510-.977) 1.603-. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.50 (1.612-.09-1.62-1.603-.88) 2.758) .00 (.65-2.933-1.432 (.44 (1.698) .720 (.702) . 2004.914 (.

0 µg/dL in females (Soldin et al.S. when the geometric mean BLL was 2.6%) were lower than those from NHANES 1991-1994.. 1994).. 2000).S. 1991. Schwartz et al. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. lead in women may be associated with hypertension during pregnancy. Bellinger 2005. Data submitted through state public health programs from 2006 showed that 1.7 µg/dL and 4.... Staessen et al. For example. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. and spontaneous abortion (Baghurst et al. Muntner et al.. particularly in the skeleton. EPA.3 million children tested had BLLs of 10 mg/dL or higher (http://www. and organic lead compounds not classifiable with respect to human carcinogenicity.. In NHANES 1999-2002 in children 1-5 years old. 2000).Metals µg/dL or higher as the level of concern in children.g.. 2002).. including minority race or ethnicity. may alter sperm morphology.000 adults.gov/toxpro2. 1999). 1995. Schwartz.07 µg/dL (Becker et al. In occupationally exposed adults. Payton et al. usually with BLLs greater than 40 mg/dL. higher than 100-200 µg/dL). 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. and peripheral neuropathy generally occurring at much higher levels (e.S. though there is greater individual variation in urine lead than in blood and greater potential for contamination. Both drinking water and ambient air standards for lead have been established by the U..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.5 per 100.cdc. 2005a). 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..9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1.4% of children had BLLs of 10µg/dL or higher (CDC. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR..xls). 1987. The U. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.S. CDC. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. 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.. 2005b).S.4% in NHANES 1999-2004.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. premature delivery. and decrease fertility (Alexander et al. Jones et al. adults in the 1999-2000 NHANES sample. Urine levels may reflect recently absorbed lead. NTP considers lead and its compounds reasonably anticipated to be human carcinogens.html.. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. Overall. Lanphear et al. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. Surveillance data reported by U.cdc. 2003. Pirkle et al. More recently. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al..6% in NHANES 1988-1991 to 1. with overt encephalopathy. BLLs reflect both recent intake and equilibration with stored lead in other tissues. 2002a).atsdr. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al.. However. reduce sperm count. 2006). 2003. IARC considers inorganic lead compounds probable human carcinogens. 1996. At low environmental exposures. 2009). Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH.75 µg/dL in U. respectively. 2003...2 µg/dL in males and 3. urban residence. 2007). residing in housing built before the 1950’s.. and low family income (CDC. Fourth National Report on Human Exposure to Environmental Chemicals 215 . A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. Korrick et al. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. which is an 84% decline. the geometric mean BLL was 3. seizures. 1996. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC.e. the prevalence rate has declined annually since 1994 (CDC. 1998). 2001). 2002. 1996. 2003). Telisman et al. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors.. 2005b. 1984. Borja-Aburto et al. Information about external exposure (i. adult residents. adults in the 19992000 NHANES sample (Apostoli et al. High dose occupational lead exposure. environmental levels) and health effects is available from ATSDR at: http://www.S. 1999).. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al. approximately 11. 2006)..21% of approximately 3.. both the geometric mean (1. almost double the geometric mean of 1.

Cory-Slechta DA.atsdr. Cox C.html. Available at URL: http://www. Becker K. van Netten C. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Jacobson SW. N Engl J Med 2003. Public Health Rep 2000.cdc. 1988-2004. Homa DM. Available at URL: http://www. Brody DJ.348:15171526. Age-specific kinetic model of lead metal in humans. Ganzi A. Hu H.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.55(32):876-879. 1999-2002. Ga. MMWR Morb Mortal Wkly Rep 2006. 4/14/09 Centers for Disease Control and Prevention (CDC). Acquisition and retention of lead by young children. CDC. Environ Res 2000. Birth Defects Research (Part A). Neurodevelopmental effects of postnatal lead exposure at very low levels. Wager C. Coresh J.htm. Caldwell KL. Rios C. Baj A. Adult blood lead epidemiology and surveillance—United States.89:330-335. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. JAMA 1996. Am J Epidemiol 1999. Ronchi L. Vupputyuri S.1542/peds:2007-3608. et al. Schulz C. Luukkonen R. Jacobson JL. Hänninen H. 4/14/09 Centers for Disease Control and Prevention (CDC). Robertson EF. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. IARC Monogr Eval Carcinog Risks Hum 2006. et al. Payton M. doi:10. Henderson CR. Aro A. 4/14/09 Centers for Disease Control and Prevention (CDC). Rojas LM. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Pirkle JL. Atlanta (GA). Cox C. Speizer FE. Third National Report on Human Exposure to Environmental Chemicals. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Bellinger D. Aug 2007 [online]. Kaufman JD. Scand J Work Environ Health 1984. Chiodo LM. et al. 2003-2004. Farias P.10:43-50.cdc. Blanco J. Ewers TG.cdc. 1991 [online]. Neurotoxicol Teratol 2004. Centers for Disease Control and Prevention (CDC).gov/toxprofiles/tp13. Lanphear BP.cdc. Korrick SA. Managing Elevated Blood Lead Levels Among Young Children. Sci Total Environ 2002. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Inorganic and Organic Lead Compounds.53:411-416. Manton WI. Sparrow D.cdc. Rotnitzky A. Stanek KL. Atlanta. Jones RL.gov/nceh/lead/publications/ books/plpyc/contents. JAMA 1996. Muntner P.htm. Teratogen update: lead and pregnancy. McMichael AJ. Kuehnemann TJ. Wigg NR. Hu H. Pediatrics 2009. 2005b. Rotnitzky A. Apostoli P. Hertz-Picciotto I. et al. Preventing Lead Poisoning in Young Children. Occup Environ Med 1996.113(4):1016-1022.gov/nceh/lead/ CaseManagement/caseManage_main. Vimpani FB. Angle CR.htm. MMWR Morb Mortal Wkly Rep 2005a. Korrick S. Canfield RL. Available from URL: http://www. Pediatrics 2004. Atlanta (GA). Checkoway H.275:1177-1181. Weiss ST. References Agency for Toxic Substances and Disease Registry (ATSDR). Leggett RW. Lanphear BP. Reese YR. Batuman V. The relationship of bone and blood lead to hypertension.54(20):513-516.8(3):395-401. 2005. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Bellinger D.115:521-529. Weiss ST. 4/14/09 Centers for Disease Control and Prevention (CDC). Toxicological profile for lead. Dietrich K. Available at URL: http://www. Mantere P.205:297-308. Blood lead reference values: the results of an Italian polycentric study.101(7):598-616. Lead. Environ Health Perspect 1993. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Kaus S. gov/mmwr/preview/mmwrhtml/mm5420a5. Hernberg S. et al.150(6):590-597. Baghurst PA. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Seiwert M. Neri A. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.73:409-420. Lead and hypertension in a sample of middle-aged women.26:359-371. Krause C. Blood lead levels measured prospectively and risk of spontaneous abortion. 2002 [online]. Bavazzano P.87:1-471.123:e376-e385. Semen quality of men employed at a lead smelter. Borja-Aburto VH.82:60-80.htm.275(15):1171-1176. Hunter DJ.287:1-11. Available at URL: http://www. Roberts RR. Auinger P. Meyer PA. Sparrow D. Int J Hyg Environ Health 2002. Muller CH. Hu H. Kim R. 4/14/09 Alexander BH. Neurotoxicol 1987. Lepom P.gov/mmwr/preview/mmwrhtml/ mm5532a2. Am J Public Health 1999. Blood lead levels—United States. Jusko TA.

Lead. Schulz D.104(1):60-66. et al. O’Flaherty EJ.Metals results from NHANES III. Gavella M. population to lead: 1991-1994. and copper in men. Hanak B. Stewar WF. Environ Health Perspect 1998. Exposure of the U. Payton M.9:303-327. Use of endogenous. cadmium. Hickman T. Kinetics of lead disposition in humans. blood pressure and cardiovascular disease in men. Rubin R. Blood lead concentrations in children: new ranges. Wilhelm M. Gunter EW. and hypertension in perimenopausal and postmenopausal women. Association of blood lead. J Hum Hypertens 1995. Flegal AR. Physiologically based models for bone-seeking elements. Semen quality and reproductive endocrine function in relation to biomarkers of lead. lead. Lee SS.108(1):45-53. Sparrow D. Revised and new reference values for arsenic. Lustberg M. Smith DR. stable lead isotopes to determine release of lead from the skeleton. blood pressure.106:745-750. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Staessen JA. Toxicol Appl Pharmacol 1993. Sherwin R. Magder L. Environ Health Perspect 1996.327:109-113. Blood lead. et al. Weiss ST. Am J Epidemiol 1994. Nash D. JAMA 2003. Amery A. Arch Environ Health 1995. Cvitkovic P. Kidney Int 2003. Pizent A. Roels H.209:301305. Schwenk M. Low-level lead exposure and renal function in the Normative Aging Study. cadmium. zinc.153(5):453464. Hu H. Low-level lead exposure and blood pressure. Kaufmann R. Hwang KY. Pirkle JL. Paschal DC. and tibia lead with neurobehavioral test scores in South Korean lead workers. Soldin OP. Lauwerys RR. Rocic B. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Telisman S. Jurasovic J. Schwartz BS.140:821-829. Osterloh JD. Int J Hyg Environ Health 2006. Lee GS. dimercaptosuccinic acidchelatable lead. Am J Epidemiol 2001. IV.S. Schwartz J. Brody DJ. Kaufmann RB.63:1044-1050. Lee BK. Environ Health Perspect 2000. Soldin SJ.289(12):1523-1531. 50:31-37. Clin Chim Acta 2003.118:16-29.

12) .60) 2085 2293 3478 Limit of detection (LOD.800 (.60-6.30) 4132 4241 03-04 03-04 03-04 . 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).90 (4.30 (2.300 (.700 (.800 (.00) 4.40-2.500-.472-.80) 1.418-.40 (3.00) 1. mercuric chloride).60) 1.70) 911 856 2081 4525 03-04 03-04 . The kinetics of the different forms of mercury vary considerably. Kingman et al.20-4..30-6. 2007).00-1. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.500) .00 (2.326 (.60-3.00 (.781 (. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.900) 1.700-. Also. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.300) .714-.00 (2. which can bioaccumulate in aquatic and terrestrial food chains. and dental amalgam. Atmospheric elemental mercury can be deposited on land and water.30-5.700) .40-2.50) 1.90 (1.900 (.600) 1.703-.20-4.574) .900) 1.90) 90th 3. phenylmercuric acetate) or topical antiseptics (e. see Data Analysis section) for Survey year 03-04 is 0. have often required public health intervention (Zeitz et al. predominantly from fish and other seafood.800 (. electrical lamps.30) 3.80 (1. Hursh et al.50) 5.2. inorganic. Accidental spills of elemental mercury.800-1. Some cosmetic skin creams from countries other than the U..80) 4.753-1.903) Selected percentiles ( 95% confidence interval) 50th .400 (.70 (1.797 (. an organic form of mercury. which create an episodic potential for volatization and inhalation of mercury vapor.40 (4..90 (1.g.50) 4.90) 95th 4.927) .700-.80 (1.. and organic forms. Other major uses include electrical equipment (e.Metals Mercury CAS No.30-2.S. thermometers. The ingestion of methyl mercury.40-1.20) 2. 1993). or oxygen.00 (1.700-. may contain inorganic mercury.40) 3.40-1.60 (2. Elemental mercury is a shiny. Poorly absorbed from the gastrointestinal tract.50-3.70-2.00 (.700-. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.70 (3.655-.30-4.886) .20 (2.900) 75th 1. synthetic organomercury compounds were once used in pharmaceutical applications. and mercury compounds are still used as preservatives (e. population from the National Health and Nutrition Examination Survey.30) 5. sphygmomanometers and barometers.979 (.00) 1. Survey years 03-04 Geometric mean (95% conf..700-.00 (.90-3. 2002).g.40 (3.877 (.40 (4. elemental mercury is absorbed mainly by inhaling volatilized vapor.800-1.814 (.80) 3.776 (. constitutes the main source of dietary mercury exposure in the general population.02) .60-6.30) 1... IARC.00) .500-.300-.70 (4. such as chlorine (e.50-1.g.484) .672) .00 (2. and mining and smelting..689-.30 (1.800-1.60-5.50-2.372) . In addition.. Woods et al. sulfur.S.60) 1.40) 1.900) . 218 Fourth National Report on Human Exposure to Environmental Chemicals . After elemental mercury is absorbed. with the highest concentrations occurring in the kidneys (Barregard et al. 1998. Apart from methyl mercury.00-5.g.500 (.400-.490 (. 1980.800-1.80 (1. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.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 .00) 3.919) . Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.50) 2. thimerosal. 1999 .400-. interval) .700) .60-2.419 (. solid-waste incineration.800-1.900) 1.30) 3.30) 1.70 (1. to form inorganic mercury compounds or salts.600 (. 1994.60 (1. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.800 (.500 (.563 (.10) .60 (1. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach. and is distributed to most tissues.90) 3.40-3.10-3.20-3. thermostats and switches).363-.860-1. merbromin).285-. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).00 (. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.80 (3.

300 (.02 (.35 (1. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.800 (.500-. 1992). 1969.700 (.700 (. 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 (1.10-1.200-.200-.60 (1. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al. a measure of accumulated dose (Cernichiari et al.500-.833 (. Sandborgh-Englund et al..40-2. 2005).. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al..300) .00 (2. thereafter.800-1. Miettinen et al.377) ..06-1..800 (.. 1973).300) .300 (.700 (.00-1..697-.30-6. Jonsson et al.50) 1.60) 1.80 (1. 2003).20) .29) .20) .50) 95th 2. 2004.60 (3.200-. Excretion occurs by renal and fecal routes. Myers et al. with most elimination occurring through in the feces (Sherlock et al.40) 1.60) 1.Metals the tissues to mercurous and mercuric inorganic forms. 1998).50) 1.14.700-.90) 2.800-1.20-3. 1994) and then undergoes slow dealkylation to inorganic mercury.30-4.40) 5.70-3.7) 4. National Health and Nutrition Examination Survey.20-11. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.10 (.00-6.70 (1.00 (3.73) 1.30-3.300) . McDowell et al.800 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.00) 4. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.900 (..700) 2.300) .27) .30) 1. Vimy et al. Geometric mean Survey years (95% conf. 1994.40-1.30 (1.80-3.50-2.800) 1.297-. Methyl mercury enters the brain and other tissues (Vahter et al.10) 1.60) 2..50) 2.10 (5.14 and 0.40-2.90 (4.00) 6. interval) Selected percentiles (95% confidence interval) 50th ..500 (.300) .00-2.S.60) 3.90 (3.299-.374) .40 (1.407) . 1996. Fourth National Report on Human Exposure to Environmental Chemicals 219 .10 (1.00) 1.10-3.00-3.300 (.10) .800) 75th . Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.268-.940) Race/ethnicity (females.80 (3. Blood concentrations decline initially with a rapid halflife of approximately 1-3 days followed by a slower half-life of approximately 1-3 weeks (Barregard et al.600) .30-6..343 (.800) 1.269-. Smith et al.30 (1. 1971).10) .377 (..90) 3.900 (. and a useful marker of exposure in epidemiologic studies (Grandjean et al. 1984. Methyl mercury is incorporated into growing hair.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 .10 (1. 1993). and the newborn’s levels decline gradually over several weeks (Bjornberg et al. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al. 1995.307 (.90) 5.00 (2.900 (.200-.944 (.70-5. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.824) 1.200 (.200 (.329 (. 2003)..726-1.30-2.700-1. 1992 and 1999.. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.400-.20 (2.30-5.500-1..20 (.871-1.3) 4.00) 2.60 (2.00) .40) 2.20-3. population.800-1.30) 1.700-.30 (.256-.90) 2.820 (.800) .70 (1.. 1996).30) 3. 1975.738-.265-.500-.60 (1.900-1.50-3.70-3.00-2. After exposure to elemental mercury.23) .919) .90 (1.70-6.70) 1. Smith and Farris.00 (2.541-.50 (2.80) 579 527 370 436 588 806 Limit of detection (LOD. 1999-2002.317 (.80) 1.00 (1. Suzuki et al.60 (3.600 (. 1993).00) 1.20) 1.90) 90th 1.60 (1.900-1.90 (1. 1998).318 (.50-12.664-1.40 (1.90 (4.369) 1.200-.00) 7.50) 3. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.10 (. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.395) . 1994).300 (.825-1.30-4. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 ..700-1.20-3.70) 4.10 (3.475) .500-.667 (.300) .70 (1.01) ..800) .30 (1. for both acute and chronic exposures. 1990). Vahter et al.70-5.00-2.0) 4.500 (.20-2.06 (.70) 4.50 (1..700 (.200-. 1991.. 1999).500-. 1992..30-11.600) .30-6.

DeRouen et al. population from the National Health and Nutrition Examination Survey.700) 2007 2240 3406 Limit of detection (LOD.500 (.600) . 2006. 1998. sensory impairments.500) . Rice.700 (.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .. short-term memory loss. see Data Analysis section) for Survey year 03-04 is 0.600 (. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. Smith et al.500-. fatigue. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. gingivitis. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.800) .500-. hypertension. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1995.600) . 1963). 1951.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD ..500-..600 (. 1996). 1983). and neurocognitive and behavioral disturbances. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. Sakamoto et al.600) . 2006.700) 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 . altered physical growth.. 1993).500-. particularly irritability.700) . Stern 2005.600-. 220 Fourth National Report on Human Exposure to Environmental Chemicals .600) . 2004).. 2002.700 (.Metals may be more efficient for inorganic mercury (Grandjean et al.500-.. Drexler and Schaller.500 (<LOD-.600) . depression. 1987).700-. pain in the extremities. 1995. Sakamoto et al.500 (. Rissanen et al. which may vary for some chemicals by year and by individual sample.600 (.600-. 2004.S. Overt poisoning from methyl mercury primarily affects the central nervous system. Smith et al. 2004. limb deformities.600 (. anorexia.700-.600) . 2000.. Factor-Litvak et al. hearing impairment. and pinkish discoloration of the hands and feet (Tunnessen et al.700 (..600) . Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.. 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.600 (. insomnia. Once absorbed. 2003). 2004). lower levels of prenatal exposure due to maternal seafood consumption have been associated with an increased risk for abnormal neurocognitive test results in children (NRC. dysarthria. typically after a latent period of weeks to months. 2000. 2005.500-. dysarthria. 2000). In recent epidemiologic studies.. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. and cerebral palsy (NRC.. 1970. Acute. Bellinger et al.. and progressive constriction of the visual fields.600 (.500-. 2005). The constellation of findings may include anorexia.. ataxia..500 (<LOD-. Survey Geometric mean (95% conf. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.800) .700 (.700 (.600 (.600) . Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.500-. causing parasthesias. and sleep disturbance (Bidstrup et al.600 (. < LOD means less than the limit of detection. Salonen et al. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.600) . Vupputuri et al..800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . Oskarsson et al.700-.. irritability. the existence of a causal relation is unresolved (Chan and Egeland.700 (.600-..600-. overt signs and symptoms of chronic inhalation may include tremor. Inorganic mercury exposure usually occurs by ingestion.42. maculopapular rash.. cerebellar ataxia.500-. At levels below those that cause acute lung injury.

67-3.07 (.480 (.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 ..440 (.405-.96 (1.29) 1.01 (.60 (1. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.420 (.. 1998).46) 3.534) .66) 3. population from the National Health and Nutrition Examination Survey. In NHANES 19992002.410-. particularly methyl mercury. Fourth National Report on Human Exposure to Environmental Chemicals 221 .447 (.382-..555) . total blood mercury geometric mean levels in females aged 16-49 years did not change. Kingman et al.. However.e. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. 1998).610-1..78-2.S. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.33 (2.430) .360 (.00 (. aged 18 to 69 years.60) 619 713 1066 Limit of detection (LOD.30) 3.76-4.97) 2.160-..63-2.46 µg/L for children. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.495 (. 2001.700 (. adult women in several ethnic subgroups (Hightower et al.840-1. et al.55 µg/L.90) 2. 2002). Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.700-1. 2006). range 40 years to 78 years) had an average total blood mercury concentration of 2. These distinctions can help interpret mercury blood levels in people.99-6.433 (.S.gov/toxprofiles.304) ..840) 1.430 (. the median concentration of blood mercury was 0.350-. environmental levels) and health effects is available from the U.14-2. Total blood mercury levels increase with greater fish consumption (Dewailly et al.313-. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.280-.290-.890 (. Sanzo et al. see Data Analysis section) for Survey year 03-04 is 0.360-.60-2.24) 1. Over the NHANES 1999-2006 survey periods.68 (2.330 (.8 years.77-2. Biomonitoring Information In the general population. Among the three racial/ethnic groups.31) 1266 1272 03-04 03-04 03-04 . 2001. 758 children.atsdr.34-3.16 (. Benes et al.00) 1. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.520) .476 (.9 years).54 (2.400 (. In Germany the geometric mean for blood mercury was 0.200 (.23) 2. 2004.330-.960 (. Survey years 03-04 Geometric mean (95% conf. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.epa.58 µg/L for 4645 adults. EPA at: http://www.88) 287 722 1529 03-04 03-04 ..413-.870-1. 2009).85-2.441 (.93 (1.840-1.12 (.340-.26 (1.65) 1. 2009). 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. 2003).480) 75th 1..460 (. EPA. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.52) 2.89) 3.330-.509) .05) 1.580) . 1997.Metals standard for inorganic mercury has been established by U.509) . IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity. From 1996 through 1998.408) ..420 (. During the same survey periods.530) . A cohort of 1127 U.254 (. average age 33 years.S.250) .442-. and increased slightly in non-Hispanic white children (Caldwell..16 (1.930-1..14.492) Selected percentiles ( 95% confidence interval) 50th .gov/mercury and from ATSDR at: http:// www.570) . Information about external exposure (i.18) 2.31) 2.14) 90th 2.360-.396-.460) .39-3. 2000).406-.08 (1.S. military veterans (mean age 52.940 (..61) 1.67-2.76-3. the total blood mercury concentration is due mostly to the dietary intake of organic forms.358 (. Mahaffey et al.03-4.05) 3.S.213-.78 µg/L for adults and 0.370) .24 (2.530) .42) 95th 3.cdc.96 (1.13-2.416 (..88 (1. interval) .463) .19 (2. Schober et al.870-1.88-3.770-1.09 (2.76-3.530-. average age 9.08 (1.20 (1. and the age-related changes differed across the groups (Caldwell et al. 1995. Grandjean et al.430 (.330-.549) . 2003).28) 1. who participated in a 1998 representative population survey (Becker et al.19 (1.23) . total blood mercury increased with age. slightly higher total blood mercury levels were found in U.

88 (1.652) .587 (.333-.86) 95th 2.990) .79) 1.537) .785-1. interval) .13 (1.498) 75th .275) .404-.620-.391-. 2005).76 (1.400-.447 (..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. Langworth et al.464 (. population from the National Health and Nutrition Examination Survey.87 (1.365 (.46-2.485 (.67 (1. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine. Urinary mercury levels in recent German (Becker et al. 2006).443 (.S. In the study of U.65 (1.362 (.472-..11-2.40-1.619-.13-2.909 (.525 (. et al.09) 1.44) 1..21) 1.03) 2. 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.255 (. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al. Levels in U. DeRouen et al.Metals 2000).11) 2.S.62 (1.630) .455) .. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.16) 1.88-2.S. the urine mercury increased by approximately 0.246-.696 (.208-.32-2.11) 1.289) .35 (1. Information about the biological exposure indices is provided here for comparison.347) .391) .508 (.784) 1. 2002) adult population surveys were similar to those in a U.455-.385-.04-3.309-.. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects. Department of Health and Human Services noted that several studies have observed a modest.23-2.31 (1.18-1.01) 2.63) 1. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.196-.40 (1.400) .280-.463 (.969-1.476 (.480) .S.07) 1.00 (.06 (..30) 2.447-.88-2.77 (2..964-1.522-..358) .90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .384 (. 1988. 1998)..486) Selected percentiles ( 95% confidence interval) 50th . Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect. An expert-panel report recently prepared for the U.297 (.599) .667-1.306 (. and on average.566) ..301-.535) 1. 2002).00) 286 722 1529 03-04 03-04 .265-.1 µg/L.79 (1.61) 1.970 (.714-1. 2006. mean urinary mercury was 3.51-2.376-. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.25 (.455-. Survey years 03-04 Geometric mean (95% conf.56) 1266 1271 03-04 03-04 03-04 . 2009). Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.545 (.1 µg/L for each surface with a dental amalgam (Kingman et al.41-2.368) .67 (1.365 (. 1992).307-.392-.30) 1.54 (2. Czech (Benes et al.64-2.87) 2.417) .532 (. military veterans with dental amalgams.06 (.00) 90th 1. women of childbearing age have generally been much lower than these levels (CDC. et al.12-3.39) 1.343 (. 2003).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 .78-4.217 (.32 (1. reversible increase in urinary N-acetyl-glucosaminidase.276 (.225-.768 (.875-1.28 (. and Italian (Apostoli et al.S. not to imply a safety level for general population exposure. 2009). Urine mercury and the number of dental amalgams were correlated.687) .616) .800-1. a biomarker of perturbation in renal tubular function.

92) 3. Geometric mean Survey years (95% conf.580-.65-4.10-4.501-.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .32 (1.53-3.45) 2.03-2.41 (1.99) 1.909-1.92) 2. population.553-.410-.28 (1.45 (1.833) .846) .637) .930) .18 (3.84 (2.35 (1.565 (.809) .691) .23-1.502-.97 (1.48 (2.62 (4.84 (2. 1999-2002.14. Geometric mean (95% conf. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.664) . 1999-2002.850-1.62 (1.966) .03 (.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .45-2.65) 1.97) 2.03 (.89 (2.580 (.17) 95th 5.658 (.91-7.83-3.624-.710) 1.620 (.892) .05 (3. interval) Selected percentiles (95% confidence interval) Survey years 50th .42) 90th 2.450-.824) .99-2.81-6.14) 3. interval) Selected percentiles (95% confidence interval) 50th .57-4.522 (.S.46) 3.16-5. National Health and Nutrition Examination Survey.540-.721 (.790) .670) 75th 1.68) 3.610-.05 (2.43-1.719 (.656-.45) 2.47) 1.99 (3. population.95 (2.22-3.810) .21 (1.622-.09-1.31-1.744) 1.3) 5.21-3.27 (1.710 (.742-1.14-1.870) .639 (.03) 1.579-.14 and 0.30-2. 16-49 years) 99-00 01-02 .560 (.910) .657 (.772 (.636-.420-.72) 1.10-2.832-1.00 (2.04-1.59-5.54) 595 531 381 442 594 826 Limit of detection (LOD.81 (3.37 (1.04-10.45) 95th 3.606 (.41 (1.709) . National Health and Nutrition Examination Survey.46 (1.655 (.S.596 (.582-.615 (.76 (1.426-.23-1.39-3.97) 2.520-.30 (2.45-3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.25) 2.685 (.557-.76-5. 16-49 years) 99-00 01-02 .578-.69-3.Metals Urinary Mercury−Females Aged 16-49 Years Old.77) 2.24-1.13-4.30 (2.97) 2.00) 2.00 (3.616-.18) 3.56) 3.09-1.831) .15-1.98 (5.31 (1.508-.69 (1.520-.76) 2.32-3.723 (.47) 1.68 (3.56) 4.592 (.52) 3. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.62 (3.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.569-.600 (.27 (2.806) .46-4.699) 1.516 (.42-3.55-3.16) 5.686) .526-.665) .664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .387-.50 (1.79) 3.831) .650 (.14-2.56 (1.632 (.77) 1.740 (.24) 6.91 (2.87-4.68-3.07-5.42) 2.70 (2.540 (.15 (2.13 (2.37) 1.85) 4.30 (1.631-.55) 90th 3.475-.51) .774) .51 (3.92) 4.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.706 (. 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.32) 2.650) 1.07-2.22 (.605-.44) 3.21 (2.61-6.38) 4.27-1.760 (.560-.06 (.41-6.85-3.61) 1.799) .500-.99 (2.41 (2.650 (.709) 75th 1.50 (2.724 (.79) 1.710 (.50-4.94) 1.35) .07) 1.

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Mottet NK. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Leroux BG. Schober SE. Farris FF. Am Ind Hyg Assoc J 1970. Whittle K. 226 Fourth National Report on Human Exposure to Environmental Chemicals .124:221-229.110:129-132. Sandler DP. Turner MD. Jones RL. Public Health Nutr 2001. Lind B. Martin MD. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Stern AH. 1993-1998. Newton G. Azpiri MA. Dorronsoro M. Pediatrics 1987. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. The contribution of dental amalgam to urinary mercury excretion in children. Longnecker MP. Shen DD. Acrodynia: exposure to mercury from fluorescent light bulbs. Smith PJ. Toxicol Appl Pharmacol 1994. JAMA 2003.79:786789.4(5):981-988. Goldberg J. Leitao JG. Bernardo MF. 1999-2000. Smith JC. The kinetics of intravenously administered methyl mercury in man. Daniels JL. Allen PV.37:245-252. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Friberg L. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment.258(4 Pt 2):R939-945. Effects of occupational exposure to elemental mercury on short term memory. Environ Health Perspect 2007. Tunnessen WW. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish.2:117-131. et al. Suzuki T.98(1):133-142. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment.289(13):1667-1674. et al. Mooney TF. Blood mercury levels in US children and women of childbearing age.31:687-700. Kaye WE. Fisher HL. Toxicol Appl Pharmacol 1994. Burbacher T. Amiano P. Hislop D. Arch Environ Health 1993. Hongo T. Imai H. Environ Res 2005. The hair-organ relationship in mercury concentration in contemporary Japanese. Hall LL. Patil LS. Yoshinaga J. Amurrio A. Environ Health Perspect 2003. Toxicol Appl Pharmacol 1996. Environ Res 2005. Vahter M. Most B. Vimy MJ. DeRouen TA. Takahashi Y. Orr MF. Nakazawa M. et al.97(2):195-200. Am J Physiol 1990.Metals Sanzo JM.115(10):1527-1531. Smith AE. Zeitz P. Bolger PM. Effects of exposure to mercury in the manufacture of chlorine. Baser M. Smith RG. Sherlock J.40:413-419. Vorwald AJ. Sinks TH. McDowell M. Environ Health Perspect 2002. Vupputuri S. Aguinagalde FX.111(12):1465-1470. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000.48(4):221229. Woods JS. Langolf GD. Osterloh J. McMahon KJ. Smith JC. Guo S. Stern AH. Hum Toxicol 1984. Br J Ind Med 1983. Topping G. Methyl mercury pharmacokinetics in man: a reevaluation.128(2):25125-25126. Matsuo N. Lorscheider FL.

3 (84. Fourth National Report on Human Exposure to Environmental Chemicals 227 .0 (41. and paints. hydrogenation catalysts.9 (78.3 (73.1) 126 (106-147) 109 (94. In humans.5-52.3 (71.2-59.2-70.7-96.5) 80. aldehyde dehydrogenase.3-44.9-55.7) 77.7) 46.7) 45. interval) 45.1) 35.5-52. which exert homeostatic regulation over molybdenum balance. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.Metals Molybdenum or ore deposits.4 (79.1-44.0-77.7 (73.7 (58.8) 44.0) 60.0-38.3 (37.6-96.3) 65.4 (72.5-124) 108 (92.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.9 (34.5 (74.6 (55.7 (71.6-55.1-88. lubricants. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.7-41.7-60.2 (49.4) 45.1) 57.6-72.2 (69.1) 46.6-82.9-56.7-105) 69.3-75.0 (81.0-71.6) 93.7) 78.3 (46.2) 41.4) 52.0) 55.4) 49.1-48.4) 42.4-61.9 (33.6 (73. 2001.8-108) 87..3 (79.0) 54.4 (48. semiconductor and battery industries have begun to use molybdenum.0 (42.5 (81. Compounds of molybdenum are also used as corrosion inhibitors.7-84.7 (51. respectively.9 (44.0-56.2-42.4 (34.3 (55.7-68.4-82.6) 51.2 (38.0) 45.8.7) 51.1) 82.6 (40. inks.9 (52.5 (67.3-47.5) 85.8-106) 88.7-51. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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. At a daily oral molybdenum dose of 24 µg.0-100) 63.2) 52.9) 67. 1997).8-94.2-91.0 (48. 7439-98-7 General Information Elemental molybdenum is a silver-white.6 (40.8) 48.2) 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 (98.8) 40.0-65.2-59.4) 41.2) 79.7-39.3 (64.7 (44.3) 54.7 (45.7 (37.5 (41.5) 60.8 (82.1-52.5.5) 44.7-122) 93. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.6 (52.2 (40.1) 59.5 (43.2-79.2 (61.5-41. 2001).1 (71.6-58.5-66.0 (42.5 (48.2 (49.1 (34.8-49.6-62.5) 80.8 (42.3 (53.5 (49.4) 56.7-47.4-52.9-82. and 03-04 are 0.6 (43.3-115) 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. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.5 (41.9-109) 97.0 (46.2-37.7-73.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.8 (85.5-68.0 (43. see Data Analysis section) for survey years 99-00.0-101) 82.4) 76. 1996).7 (50.2 (63. and in pigments for ceramics.8) 75.7-91.8) 46.7-92.8 (67.S.7) 57.0) 84.9 (37.9) 34.1 (38.2) 40.6-111) 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 52.6) 53.2 (56.3) 41.2 (83.0-85.2-53.6-42.6) Selected percentiles ( 95% confidence interval) 50th 50. and xanthine oxidase (Kisker et al. chemical reagents in hospital laboratories.7) 86.5-91.4 (48.3 (38.5-65. urinary excretion over six days CAS No.8-46.3) 83.9-55.6) 71.0 (76.8) 39. WHO.1) 60.2) 48.9 (73.1-55.2 (55.2) 37.6) 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 (99.3) 85.3-91.7) 75th 84.0) 97.9-85.0) 62.9) 62.4 (80.9 (40. Excretion occurs predominantly via the kidneys. 01-02.1-52.0-110) 90.8. 0.1 (91. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.2) 53.3-108) 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 47.3) 47. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0-53.3) 37.3 (55.6 (55.1-59.6-46.3 (47.4-75.1-51. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.5-46.9 (32.1-63.7 (36.5) 47.9-83.8-90.7-50. population from the National Health and Nutrition Examination survey.7) 78. and 1.6) 71.0-62. More recently.0) 39.5 (37.

2-41.5-99.6) 39.7-52. population from the National Health and Nutrition Examination survey.0-120) 85.8) 71.7-43.5-44.8-65.0 (74.4 (40.8 (90.5 (34.3) 56.8-66.7-137) 129 (109-155) 112 (97.5-97. Biomonitoring Information Molybdenum is an essential element for health.5-50.1 (44.6) Selected percentiles ( 95% confidence interval) 50th 41.4-185) 106 (94.3) 64.5-119) 90.6-45.4) 89.2-96.7) 115 (93.4-66.0) 44.3-45.8-46..5 (80.1 (37.9 (79.8) 37.7) 112 (95.5-60.3) 43.3-43.7-93.9-68.4-76.1-100) 86.6 (57.8 (75.3-141) 109 (81.5-35. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.2) 39.4) 116 (101-126) 104 (88.0-46.1-39.5) 72.5-62.9) 92.4 (53.1-127) 90.3) 37.0-56.9 mg/kg/day and established a tolerable upper intake level of 0.6 (38.1-79.3-44.7-120) 87.8 (36.1-39.9 (39.0-41. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.8) 38.7 (30.4) 61.2 (50.3 (37.5 (54.9-45.2 (69.9) 79.7) 41.2) 38.7) 62.6-41.6 (71.9 (36.5 (65. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.6) 36.1) 101 (83. but available epidemiologic data are scant.2 (36.4 (56.2-49. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5 (37.3-59.9-87.0) 39.2-80.1 (54. EPA.0) 62.0 (80.5 (38.3-115) 98. at daily oral doses of 95 µg and 428 µg.5 (39.2 (37.5-69.0) 39. U.5-92.8-47.1 (40.3) 57.7-44.2 (40.9 (64.5) 63.4 (37.1 (39.5 (35.2 (40.7-40.8-67.4 (55.9) 41.5 (41.9 (40.2-47. and clinical or epidemiologic evidence of adverse effects is limited.3 (55.9 (35.7-62.4) 48. interval) 43.0-103) 103 (90.9-118) 91.0-46.1-38.1-112) 78.7 (66.9-40.6-88.8-42.4) 44.4) 47.2) 42.4 (67.2) 43.5-48.0 (58..7) 45.8) 38.5 (40.9-71.9 (64.7) 75th 63.1) 37.2 (73. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.2-46. 2001).5) 73.5 (41.3-68. 1961.4-39.3 (71.1 (33.9-45.3 (37.2) 42.2-96.4-107) 85.7) 42.2 (40.1-43.8) 61.0-133) 119 (88.1) 40.6 (59.3-46.2) 55.0) 33.5 (83.6-63.8 (56.0) 72.7-38.2-121) 107 (92.5 (50.6-76.9 (73.8) 62.3-52.03 mg/kg/day in humans (IOM. of the ingested dose (Turnlund et al.5-70.2) 37.2) 37. 1999).0) 36.1-34.3) 44.6) 43.4 (78. urinary excretion over six days rose to 50% and 67%.6 (42.4-106) 85.5 (35.9 (39.1 (49.5 (65. Molybdenum is generally considered to be of low human toxicity. 1993).2) 39.8) 79.S.4-41.6 (36.7) 53.3 (36.1 (38.0) 88.4) 122 (107-133) 109 (99.5 (40.5 (36.1) 37.3 (53.3 (51.4 (59.6) 39.1-41.1-45.2 (52. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.8-118) 81.5 (39.4) 58.3 (83.1-109) 89.3 (71.8-52.2 (43.9-42.7-100) 77.6-63.1-40.6-61.3) 41.9) 173 (130-243) 159 (129-170) 132 (107-158) 85. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.7) 57.3) 61.3 (36.9-41.9-61.5) 71.8 (57.1 (82.1 (30.2-65.4-120) 101 (84.2-40.1 (38.0 (35. Based on studies finding adverse reproductive effects in rats and mice.6 (36.S.3-102) 122 (116-147) 123 (109-139) 118 (101-134) 310 368 290 648 762 725 1299 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 40.6-78.8-84.5) 60.9-96.1-81.3) 40.2) 58.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.3-56.1) 43.1) 65.2-103) 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 42.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.8) 39.9) 31.6-61.5 (79..5 (59. respectively.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.Metals was 18% of the ingested dose.0) 38.5-45.9) 40. 1995).1) 56.7 (75.4 (44.9 (49.4-42.8) 45.4) 60.0-38.9-117) 57.4) 77. and urinary levels reflect intake from all sources. In industry.8 (37.4-118) 172 (131-195) 138 (120-163) 118 (106-134) 780 682 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites 228 Fourth National Report on Human Exposure to Environmental Chemicals .5-46.2 (33.0) 53.1-43.7 (77.3 (58.1-67.8-47. 1997).5 (37.6) 48.4) 40.1 (42.5 (78.9) 44.5) 90th 108 (97. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2 (57.

pp. Droste JHJ. silicon. Third National Report on Human Exposure to Environmental Chemicals. In: Trace elements in human nutrition and health.216:253-270. Available at URL: http://books. Christensen JM. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. manganese. Atlanta (GA). boron. Available at URL: http://ntp. vanadium. 420-441. 2001). Dietary reference intakes for vitamin A. 56:322-327. Minoia et al.15(2-3):149-154. Molybdenum 1993 [online]. nickel.Metals in urine for the U. EPA). Institute of Medicine (IOM).123(1):81-85. (DC): National Academy Press. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Peiffer GL. Turci R. Kisker C. Environmental Protection Agency (U. Minoia C. Yarovaya GA.66:233-267. Shmavonyan DM. Sabbioni E.nap. vitamin K.62(4):790-796.epa.gov/iris/ subst/0425. 1998).22(3):179-191. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. Weyler JJ.niehs. TR-462. References Centers for Disease Control and Prevention (CDC). Ann Rev Biochem 1997. 4/14/09 Iversen BS.htm. 4/14/09 White MA. Molybdenum in infancy: methodical investigation of urinary excretion. Schaub J. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. iron. Washington.S. Sci Total Environ 1998. iodine. and zinc: a report of the Panel on Micronutrients. 144-154. A study of 13 elements in blood and urine of a United Kingdom population. Vermeire PA. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Sabbioni E. excretion. Van Meerbeeck JP. et al. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Kristiansen J... 4/14/09 Sievers E.php?record_id=10026&page=420.S. chromium. Occupational risk factors of lung cancer: a hospital based case-control study. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Geneva: WHO. Food and Nutrition Board. Occup Environ Med 1999. Aprea C.. Rapid Comm Mass Spectrom 2002. Zhurnal Obshchey Biologii 1961. edu/openbook. World Health Organization (WHO). Available at URL: http://www. Schleyerbach U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. X. arsenic. copper. van Sprundel MP. White and Sabbioni. U. 2002. Koval’skiy GA. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Sciarra G. 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. White MA. Gatti A. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. 2005. J Trace Elem Med Biol 2001. National Toxicology Program (NTP). Molybdenum.nih. Keyes WR. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online].gov/index. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. 2001. 16:1313-1319. Schindelin H.S. Am J Clin Nutr 1995. Turnlund JR. Molybdenum absorption. Ronchi A. 1996. Fourth National Report on Human Exposure to Environmental Chemicals 229 . 2005). 1998. pp. Menne C. Analyst 1998. molybdenum. Trace element reference values in tissues from inhabitants of the European Union. Rees DC.

see Data Analysis section) for Survey years 99-00.Metals Platinum CAS No. 01-02. 0. 230 Fourth National Report on Human Exposure to Environmental Chemicals . and high catalytic activity. jewelry. 1998).04.. the ambient air concentrations of platinum associated with its use in automotive engine catalytic converters are estimated to be thousands of times lower than occupational exposure limits. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. and 03-04 are 0. and 0. and as drugs (e. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al.g. < 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. population from the National Health and Nutrition Examination Survey. thick-film circuits printed on ceramic substrates. however. cisplatin. 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. respectively. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. copper. Important properties of platinum are resistance to corrosion.04.07. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel.. Platinum compounds are used in electrodes. and iron. 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. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. carboplatin) in the treatment of cancer.S. dental alloys. 7440-06-4 General Information Platinum is a silver-gray. strength at high temperatures.

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

Br J Pharmacol 1969. Levels of platinum in urine for the U.123(3):451-454. Moore W Jr. Schierl R. Blanks R. Czerczak S.. 1997. Stilianakis NI. Cohrssen B. Occup Environ Med 2004. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Powell CH. Occup Environ Med 1998. and in blood and urine in the United Kingdom. Uptake of antineoplastic agents in pharmacy and hospital personnel. International Journal of Hygiene and Environmental Health 2003. Int J Hyg Environ Health 2004. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Thornton I. population were below the limit of detection (0.inchem. Environ Res 1975a. Urinary platinum levels associated with dental gold alloys. Several studies have shown that background concentrations in general populations were usually less than 0. 2003. Iavicoli I. Urinary excretion of platinum from platinum-industry workers.S. Ewers U.. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Saindelle A. Kaus S. 1991 [online]. Schierl. Analyst 1998. et al. International Programme on Chemical Safety (IPCS). Wilhelm M. Parrot JL. Schierl et al. et al. Arch Environ Health:1969. Part 1: monitoring of urinary concentrations. Ruff F: Platinum and platinosis. 5th ed. palladium.9:152-158. 2004) or less than 0. Seifert B. Angerer J.. Arch Environ Health 2001. Carelli G.. Rommelt H.56(3):283-286. Platinum concentrations in urban road dust and soil. Patty’s Toxicology. Environmental Health Criteria 125. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect.01 µg/L (Becker et al. 2003. Begerow J. pp. Influences on human internal exposure to environmental platinum. 2003). et al. which elevate urinary platinum by five to twelve-fold (Begerow et al.61(7):636-9. Gieler U. Ensslin AS. et al. Allergy and histamine release due to some platinum salts. Hauff K. Schulz C. Grimm CH. Herr CE. 3/31/08 Moore W Jr. 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. Kulka U. 1999. Kuster W.55(2):138-140. Pethran A. 289-380. 2004).10:63-71.org/documents/ehc/ehc/ehc125. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine.. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Fruhmann G. and platinum. Available at URL: http://www. rhodium.19:685-691. Crocker W. Biomonitoring Information Urinary platinum levels reflect recent exposure.. In: Bingham E. eds. Saindelle A. Senofonte O. Schierl R. Modest (ten-fold or less) elevations in urinary platinum concentrations were associated with handling of cisplatin and carboplatin by pharmacy and other hospital personnel (Ensslin et al. Platinum.04 µg/L) in this Report. Schierl R. 1998). Nowak D. 206:15-24. Neuendorf J. Hebert R. 1998). Ruff F: Histamine release by sodium cholorplatinate. Campbell K. Huber R. Pethran A. Turfeld M.70(3):205-208. Seiwert M. Boos KS.13(1):24-30... Herr et al. 2004. Biomonitoring of traffic police officers exposed to airborne platinum. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure.htm. Hysell D. Wilhelm et al. Bocca B. 2001). van de Weyer C. 2000.. Int Arch Occup Environ Health 2003. Fries HG. Hall L. Alimonti A. References Becker K. 232 Fourth National Report on Human Exposure to Environmental Chemicals .htm. Nickel.005 µg/L (Iavicoli et al.4(1):27-36. Pethran et al. Kavanagh P.35:313-321. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. palladium. Petrucci F. Kelly J. Int Arch Occup Environ Health 1997. ruthenium.Metals the International Programme on Chemical Safety at http:// www.. Schierl R.. Schulz C. Farago ME.76(1):5-10. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. J Expo Anal Environ Epidemiol 2003. New York: John Wiley & Sons.org/documents/ehc/ehc/ ehc125. and gold excretion of patients after insertion of noble-metal dental alloys.inchem. Duneman L:Long-term urinary platinum. 2003. Gromiec JP. Kazantzis G. Herr et al. Biomarkers 1999. osmium. Hysell D. Environ Health Perspect 1975b.207(1):69-73. Raab W. Jankofsky M.

430-.410-.190 (.340 (.300) .330-.330-.260-. thallium readily crosses the placenta and also distributes into breast milk.170 (.280) .200-.440 (.170) .290) .160-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion. 2005).340-.290) .170) .420-.200 (.390) .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.370 (.156) .490 (.180) 75th .410 (.280 (.183) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.190 (.520) .400) .290) 90th . In the United States.218) .170) .280-.290 (.02.340) .150-.360-.410 (. interval) .280-.470) .220 (.370-.310) .200) .190 (.162-.180 (.200) .440) .176 (.370 (.170-.480) .360 (.510 (.240) .300 (.480) .450 (.201 (.196) .181-. and 03-04 are 0.149 (.171 (.390) .400) .330-. see Data Analysis section) for Survey years 99-00.184 (.410-.230-.180 (.173) .230 (.420 (.250-.330) .520 (.180) .159 (.158) .340-.270) .147-.550 (.350-.630) .420) .500) .330) .320) .450 (.150-.270 (.250) .300 (.191 (.159 (.243) .270-. Human health effects from thallium at low environmental CAS No.02.360-.310 (.210 (.150-.180-.310 (.380 (.400-.330) .440) .240-.390-.520) .147-.165 (.410-.145-.440) .490) .137-.520) .320) .370-.280 (.201 (.390-.230-.240) .230) .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 .220) .560) .250-.190 (.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 .590) .153-.260 (.330) .360 (.370 (.135-.320-.400-.290 (.210-.390) .460) .300-.167 (.380 (.160-.470 (. In the past.420) .270-.200) .640) .220 (. respectively.500 (.410-.280) . however.470) .178) .146 (.140-.173-.380-.160 (.380-.410 (.180 (. From these and other sources.220-.133-.460-.154-. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.350-.430 (.187-.160 (.410) .260-.165) Sample size 2413 2653 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .260-.350) .370) .159 (.270-.450 (.690) .150-. the latter being the current major industrial consumer of thallium in this country.370 (.210) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .177) .200) ..200 (.250-.370-.450 (.200-.163) .350 (.400-.179-.220) .260-.280 (.192) Selected percentiles ( 95% confidence interval) 50th .240-.330-.215) .170-.350 (.300 (.290 (.148-.360-.270 (.200 (.160 (.250 (.150-.200 (.410 (.217 (. and 0.340-.440 (.218) .360) .156) .145-. 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.470 (.440 (.410 (.220) .185 (.250-.430 (.410 (.230) .182-. it has not been specifically mined or refined in the United States since 1984.250-.300) .290-.490) Total .172) .270 (.350-.250-.370) .196) .430 (.150-.280) .225) .460 (.420-.480) .155 (.400) .430) .290 (.320) .340-.170 (.240) .190 (. 0.370-.260) . 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.440-.170 (.134-.160 (.400 (.250-.440 (.420-.220) .Metals Thallium depilatory cosmetics.160-.200 (.330-.420) .390 (.160-.420) .450 (.420) .147-.197 (.350-.470) .500) .310-.390-. representing distribution into other tissues.400 (.250 (.400) 95th .400-.360-.02. In addition.320 (.300) .350) .190-. 01-02.260 (.160-.390) .190 (.270 (.360 (.173) .450) .230-.290) .S.350-.188) .239) .172 (.480) .200-.330-.430-.360 (.290-.490) .185-.202 (.206) .230) .430 (.400 (.370 (.450 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.450 (.220 (.420-.290 (.260 (.400 (.170-.420) .200) .167-.410-. thallium was obtained as a by-product of smelting other metals.167-.270) .310 (.220 (.360-.340) .217) .180-. population from the National Health and Nutrition Examination Survey.450 (.370 (.202) .160 (.300) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.220 (.144 (.157-.590) . Thallium disappears from the blood with a half-life of several days.400) .230) .172 (.490) .170-.390-.410-.390 (.220) .500) .480) .430-.220) .430) .170-.350-.400 (.200) .175) .420) .197-.250-.240-.170-.290) .200-.180-.145 (.180-.260-.210 (.510) .200 (.170-.400-.330-.370 (.290 (.270 (.156-.450 (.183) .380) .202 (.

S. Thallium produces toxicity by replacing intracellular potassium in the body.149) .235-.133-. Information about external exposure (i.147-.204) .Metals doses or at biomonitored levels from low environmental exposures are unknown.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 .194 (. Levels of thallium in urine for the U.368 (.169-.222 (.200-.424) .136 (.159 (.215) .348 (.226-.223 (.154 (.233) .167-.287-.177) .364 (.162 (.170) .135-.340-. Severe accidental thallium poisonings from ingesting of rat poisons that contained water-soluble thallium salt have occurred.192 (.159) .229-.140 (.166 (.380 (.282-.128-.293 (.217) .172) .321) .274-.176) .219) .213 (.227 (.307 (.191-.236) .304) .184-.158-.162) .173 (. EPA.306 (.313 (.278 (.272-.218 (.161 (.207-.243) .149-.278 (.424 (.269 (.458) .532) ..146 (. and death.333-.187-.214 (.271-.254-.306-.178 (.304) 95th .402) .S.152) .173) Selected percentiles ( 95% confidence interval) 50th .255 (.144-.164) .217-.337-.151-. Biomonitoring Information Urinary thallium levels reflect recent exposure.260-.313-.191-.369 (.389) .129-.238) .366) .150) .200-.155) .240) .325-.313 (.179) .148-.244 (.313-.122-.244-.234-.267-.166 (.156 (.184-.300) .235 (. arthralgias.171) .170-.188 (.171) .e.148 (.161) .153 (.176) .167-.145) .182 (.156) .333 (.258-.333) .212) .158) Sample size 2413 2652 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .217-.215-.286 (.156 (. Relatively high-dose intentional or accidental ingestion can result in gastrointestinal symptoms followed by multiorgan failure.387) .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 .231) .146 (.148-.145-.350 (.154 (. although additional mechanisms of action are possible.254 (.260 (.184-.389) .162) .230) .400-.146-.161 (.145-.297) .153 (.300-.292 (.157-.237-. and polyneuropathy.153-.198-.149 (.224 (.167 (.196 (.350) .343 (.138 (.html.200-.293) .146-.375 (.152) .156 (.300) .153-.319) .307) .131-.221 (.273-.147-.241) . population from the National Health and Nutrition Examination Survey.189) .155-.383) .148 (. neurologic injury.289) .137-.151) .142 (.211 (.143 (.169) .197-. IARC and NTP consider the evidence for the carcinogenicity of thallium as inadequate or unclassifiable.271-.144-.222 (.346) . respectively.198) .208-.160) 75th .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 .362) .155 (.286 (.203-.162-.192-.216 (.272 (.156 (.140-.167) .364 (.348) .250-.162-. environmental levels) and health effects is available from ATSDR at: http://www.143-.301-.167 (.370 (.180-.150) .168 (.185 (.346-.297 (.160-.330-.gov/toxpro2.200) .153 (.205 (.S.300 (.286) .206 (.226) .222) 90th .283 (.atsdr.173) .278) .328-.273 (.214) .160) .160 (.142 (.250-.412 (.146) .142-.135-.154 (. interval) .146-.324) . 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.289) .259) .600) .356) .278) .134-.318-.361 (.265-.143 (.198-.167) .304) .266-.291-.377) .469) .297 (.149-.176) . (ATSDR.377) .215 (.286 (.412 (.cdc.299-.164) .383 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.278-.170) .329) .221) .348-.237) .154 (.317) .248) .278) .326-.364) .196-.281-.304 (.238-.306-.207 (.280-.246-.143-.282 (.214-.222) . 1992) Workplace air standards and guidelines for external exposure are established by OSHA and ACGIH.349 (.280) .181) .207) .231-.328 (.176) .422) .171-.258 (.197) .141-.221) .233 (. Peripheral neuropathy and alopecia are well-documented effects of acute and chronic exposures.287 (.180) .200 (.271-.365) .462) .278-.456) .198-.153) .356-.338-.264 (.366 (.194 (.338 (.333-.286 (.204 (.143) .160) .286-.333-.286-.462) .155-. Chronic high-level exposures have been associated with weight loss.389-.263-.343 (.128 (.222-.342) .369) Total .140 (.148-.256 (.192-.153 (.214) .402) .161) .214 (.157) .378 (.250) .273-.317 (.148-.321 (.202 (.271-.304) .223) . and a drinking water standard has been established by U.153 (.162) .135-.159-.317 (.153) .312 (.167 (.387) .125-.211 (.146) .210 (.169 (.333) .157 (.458 (.333 (.158 (.167 (.269) .147-.145 (.229) .364) .179-.152) .119-.327) .208) .153-.323 (.133 (.208-.

et al. X.216:253-270. Schaller KH. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L.265 people living near a thallium-emitting cement plant in Germany. Cassot G.5 μg/L. Valentin H.35(1):4-9. Soddemann H. Boisson P. 2005. (1981) studied 1. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Investigation of a working population exposed to thallium. Atlanta (GA). 1998). 2005. Pietra R. blood. Radiat Prot Dosim. A study of 13 elements in blood and urine of a United Kingdom population. Pirkle JL. Int Arch Occup Environ Health 1981. Minoia C.. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Ting BG.gov/toxprofiles/tp54. Celier D. 1990. Trace element reference values in tissues from inhabitants of the European community I.Metals (CDC. 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. Trace metals in urine of United States residents: reference range concentrations. Toxicological profile for thallium. Schmidt M. Wiegand H. Sci Total Environ 1998.1 mg/m3 (Marcus. Environ Res 1998. Marcus RL. Brockhaus A. 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. 2005) and are shown with results from NHANES 2003-2004 in this Report. Raithel HJ. Manke G. Sabbioni E. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect.95:89-105. 1992 [online]. Investigations of thallium-exposed workers in cement factories. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Sabbioni E. Sci Total Environ 1990. 1985). Paschal DC. White MA. White and Sabbioni. Available at URL: http://www. Kramer U.. Fourth National Report on Human Exposure to Environmental Chemicals 235 . population) are thought to correspond to workplace exposures at the threshold limit value of 0. Jackson RJ. J Soc Occup Med 1985.113(1):47-53.cdc. Schaller et al. and serum of Italian subjects... References Agency for Toxic Substances and Disease Registry (ATSDR). Ewers U. Int Arch Occup Environ Health 1980. Buhlmeyer G. Brockhaus et al. 1981.47(3):223-231. with concentrations ranging up to 76. 1980. 7/15/09 Blanchardon E. Centers for Disease Control and Prevention. Challeton-de Vathaire C. Sampson EJ. 1998.48(4):375-389. Apostoli P. et al. Trace element reference values in tissues from inhabitants of the European Union. Pozzoli L. Martin J-C. Dolger R. Morrow JC.atsdr. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Third National Report on Human Exposure to Environmental Chemicals. et al. Gallorini M.76(1):53-59.html. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. A study of 46 elements in urine. Minoia et al. Paschal et al.S.

260 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.093) .160 (.180-.290-.170 (.158 (.460 (.076 (.420-.100) .110-.260-.180 (.350) .200 (.230) .073-.340-.130-.04. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.370) .460) .130) .090) .270 (.350) .430-.180) .170-.220) .370 (.170) .510-.087-.086 (.090-. and 0.250) .560) .107 (.088 (.090-.380) .690) .150 (.560 (.550) .130-.630) .320 (.050-.400-.066-.122) .160) .090-.430 (.082-.410 (.470-.04.110 (. Little information is available on the toxicity of tungsten.410-.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 . interval) .290 (.240-.430 (.113 (.250) .110) .080-.100) .400) .062 (.290) .135) .090-.140 (.280 (. 0.073-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.060 (.04.160 (. respectively.340-.470 (.560) .350 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.520) .100) .088) .190 (.104) .080 (.130-.151) .120 (.510 (.160-.620) .360) .100) Selected percentiles ( 95% confidence interval) 50th .830) .123-.300) .074-.120-.640 (.070-.620 (.190-.140-.180-.110 (.370-.240 (.100) .250) .060 (.230 (.140 (.116) .140) 90th .190 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.460 (.250-.670) .133) .150 (.110-.380 (.150 (.770 (.090 (.490 (.160 (.060-.300 (.068) .090-.480) Total .210 (.310-. which are used in rock drills and metal-cutting tools.060-.300 (.070 (.580) .400 (.069) .060 (.340-.190-.280 (. and for producing ferrotungsten.800) .260-.092 (.110 (.060-. 01-02.090) .071 (.080) .090-.530 (.220) .270-.400 (.790) .370 (.320-.250-.360-.170) .180-.110) .110-.160 (.300-.260) .190-.380-. population from the National Health and Nutrition Examination Survey.470) .120) .560) .060-.120-.100 (.330-.500) .350) . Tungsten is used mainly for producing hard metals.120) .090-.230-.250) .370 (.340) .550 (.073 (.111-.100 (.00) .Metals Tungsten CAS No.080 (.065-.113 (.100-.S.180 (.110 (.530 (.070) . and 03-04 are 0.073) .470 (.105 (.150-.320) .550) .120) . which is used in the steel industry.140 (.090 (.070 (.091) .620) .460) .070-.090) .210 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .080 (.180) .520) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.130) .050-.270-.065 (.280-.220 (.290-.070) .290-.400 (.400 (.101 (.113 (.430) 320 363 290 679 744 725 1339 1545 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .120-.260 (.130) .126) .210 (.380-.310-.132) .070) .53) .570 (.120-.430) .210) .160-.100-.100-.260-.440) .310 (.090-.570 (. see Data Analysis section) for Survey years 99-00. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).380 (.520) .082 (.450 (.250) .105) .230-.210-.500 (.360 (. Evidence is lacking for the carcinogenicity of tungsten.120-.450-.130) .310) .180) .300) 95th .800) .200) . filaments for incandescent lamps.270-.510-1.380-.650) .060-.080) .330 (.093 (.092 (. mainly as scheelite (CaWO4).078-.460 (.230-.080) .093-.330-.270 (.180) . Tungsten compounds are used as lubricating agents.070-.370-.430-.560) .420-.070-.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 .120) .095-.470) .490) .081 (.069-.060 (.120) .084) .204) .080-.350-1.060-.390) .170) .090) .390 (.150) .130-.140 (. bronzes in pigments.064-.230) .530 (.160-.160 (.120-.080 (.070-.140-.060 (.120) .060 (.170) .550) .096-.082) .100 (.062 (.076 (.058-.100 (.056-.330) .130) .080 (.113 (.082 (.109) .050-.310-.300 (.071-.250) .084 (.320 (.310-.170 (.100) .360 (.190-. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.087) .270-.077-.090 (.590) .050-.095-.230-.084-.220) . and as catalysts in the petroleum industry.320-.101-.210 (.200-.310-.950) .097-.500 (.360-.096 (.810) .380-.080-.056-.210 (.160-.070 (.330) .430 (.220-.160) .130 (.130 (.290) .070) .092) . Occupational exposure is from dusts released during grinding or drilling of hard metals.137 (.190) .110 (.270 (.180-.360 (.080) 75th .

222-.078 (.066 (.085 (.167-.253) 95th .079) .074-.255-.091 (.124-.069 (.331-.136-.157) .139-..199 (.198) .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.084) .100 (. population.412 (.065 (.253 (.060 (.061-.197) .158 (.098) .116 (.217-.245-.482 (.S.139) ..100) .197) .302-.154) .667) .072-.880) .459) .555 (.28) . Using neutron activation analysis to 2000.049-.150 (.086) .200-.462) .061-.082 (.554) .088) .170-.073 (.119-.108) .169 (.090-.069-.364 (.439 (.167) .077) .092) .206-.211 (.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 .240-.199 (.093-.094-.180-.072 (.143-.344-.079 (.153) .179-.301) .057-.255 (.106 (.317-.414) .302-.431) .079 (.208-.146 (.059 (.108-.071) .075-.(Kraus et al.150-.392) .727) .084 (.067 (.075 (.109-.122-.098 (.272-.086-.111 (.143 (.667 (.109 (.083 (.117 (.301) .152-. interval) .060-.090-.070 (.083) .136-.317) .329-.098-.138 (.080 (.161) .079) .294 (.215) . 1998).068 (.333 (.095) Selected percentiles ( 95% confidence interval) 50th .072-.265 (.329 (.222) .253-.095-.091) .077) .073 (.054-.216-.186 (.125) .059-.081 (.279 (.146 (.339 (.117) .074) 75th .431) .075) .169) .333 (.077-.426) .359 (.293 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.190) .080-.065 (.216 (.383 (.284) .148 (.216-.582) .214-. 2001).200-.070 (.S.079) .198-.201 (..136 (.078 (.081) .353 (.096) .217-.216 (.083-.081 (. 2003.084) .091 (.333) .258 (.087) .500) .078) . 1997).103-.139 (.121-.056-.203-.059-.073 (.091) .145 (.054-.151 (.359 (.071-.065-.063-.068-.060-.122 (.138 (.075-. similar to those in this Report (Schramel et al. measure urinary tungsten.058-.209-.120) .301) .300-.087 (.093) .285) .431) .278-.347 (.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 .164 (.267-.439) Total .144 (.436) .165) .066 (.153-.308) .083 (.059-.154) .179-. population (CDC.067-.215 (. population from the National Health and Nutrition Examination Survey.080 (.091) .057-.353 (. 2005).497 (.098-.073 (.074) .168 (.538) .094) .174) .116-.174 (. Patients with medically-inserted tungsten found at increased levels in drinking water.078) .078-.231-.261-.381) .158) .144-. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.797) .270 (.465) .158) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.237) .216-.205-.354-.071) .306) .201) .484 (.071) .107-.385 (.100) . and 2003-2004 (Paschal et al.130-.333) .105 (.065-.131-.258-.138) .099-.089 (.233-.063 (.436-1.354) .116) .086) .077-.085-.085) .181 (.286-.150-.167-.091) .155-.360 (.300 (.426) .275 (.120) .065-.069 (.056-.074-.283) .081-.300) .055-.823) .250 (.071 (.063 (.484) .176-.224) .333-.237) .237-.075) .299 (.136-.279 (.122-.146) .358) .333-.167) .339 (.098-.340 (.158) .267) .255 (.333 (.071 (.439 (.634 (.075 (.083) .386) .S.375) .064-.089) .063-.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 .326) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.148) .188-.231 (.094) .197 (.063-. 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.124 (.315-.250 (.333 (.300-.176-.064-.061-.067 (.250-.086) .104-.184 (.605) .197-.279 (.074 (.465) .136-.082) .126-.084 (.187) .218 (.287) .214) .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 .130 (. or exposure that a control group of non-metal workers had mean levels differences.088) .341 (.453) .053-.133) .062 (.105 (.119 (. 2001-2002.125 (.379 (.079) .082) .133) 90th .065) .739) .063-. Nicolaou et al.317 (.133) .452-. (1987) found possibly due to methodologic. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.308) .121 (. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.071 (.080-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.410-.

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

031 (.035) . and 234U.016-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.015 (.007-.009) .046 (.010) .013 (.022) . Fourth National Report on Human Exposure to Environmental Chemicals 239 .011) .040-.021 (.004.006-. Variable concentrations of uranium occur naturally in drinking water sources.008 (.007) .012 (.018 (.017) .073) .048 (.S.027 (.009) . or processing.053) .039-.010) .007 (.008) .021-.013-.279) .007 (.006 (.032 (.016 (.037-.038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .007-.012-.012-.008 (.049) .023-.026-.030 (.043) .060 (. including nuclear weapons.026) 95th .007) .039) .022-.026 (.048) .030-.007-.028 (.033 (.050) .012 (.007 (.006-.031 (.012) .067) .024 (.008 (.054) . in some ceramics.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 .010-.047 (.026 (. In workplaces that involve uranium mining.017) .009-.011-.023 (.030) .040) . human exposure occurs primarily by inhaling dust and other small particles.009-.007 (.010-.021) .035-.052 (.007) 75th .007) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.008 (.009) .005-. 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.004.031 (.009 (.007 (.009 (.029 (.013 (.009-.009 (.023-.045) .006-.007-.033 (.018) .008) .017-.012 (.007-.012-.010) . 0.015-.016) .015 (.012 (.014 (.009-.009-.009 (.012) .011-.088) .007-.036) .054-.006 (.016) .017-.027) .021) .056) .027) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.028-.011 (.056) .026) .040 (.013) 90th .033) .007-.013 (.009) .027-.007 (.011) .012) .007-.012) .024-.017) .008 (.044 (.008 (.023-.009-.009-.022-. Uranium has many commercial uses.009-.007 (.018) .069) .037 (.011-.014 (.010) .053 (.Metals Uranium CAS No.026 (.009 (.007-.009) * .037) .008-.020) . 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.046) . and as an aid in electron microscopy and photography.012 (.016) .017-.034-.008 (.009 (.009) .023) .007-.026) . Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).043 (.027-.006-.021 (.034) . milling.008 (.067) .015 (.017 (.008) .008-. and 0.038) .009) .019 (.006-.049) .007) .028 (.005-.010 (. Thus.011-.009-.007-.017) .046 (.018-.055 (.017 (.011) .040 (.013-.010-.006-.025-.023) .009) Selected percentiles ( 95% confidence interval) 50th .014 (.007-.007-.065) .006 (.023-.009) .010-.010-.063) .012-.040-.023) .019-.031 (.038 (.036-.013-.009) .006-.020-.042 (.007-.008 (.009) .006-.009) .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 .028-.046 (.006-. Since the 1990’s.010) * .006-.045) .041 (.065) . the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.010 (.017-.005.029-.010 (.051) .006-.013 (.008-.009) .72%).021) .010-.011-.023 (.027-.014 (.066) .020 (.008-.031-. interval) .012 (.007 (.013 (.017-.041 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.036 (.036-.011-.007) .007-.019-.114 (.008-.007 (.005-.008-.026-.013 (.006-.010 (.008 (.020-.015) . 01-02.037) .009) .019-.127) .007 (.037) Total .011-.009 (.039) .011) .034-.028 (.009-.005-.013 (.027) .008-.036 (. and 03-04 are 0.014 (.027 (.031 (.009 (.016-.007 (.011) .042) .024-. nuclear fuel.019-.008-.020) .064 (.008 (.010) * .050) .035) .008 (.030 (.005-.008 (.018) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.007-.046-.024-. see Data Analysis section) for Survey years 99-00.054) .017-.008) .011 (.006 (.008 (.021-. population from the National Health and Nutrition Examination Survey.021 (.018) .037) .006-.015) . 235U (about 0.010) .029-.008 (.033-.012-.036) .030 (.016-. respectively.016) .027) .010) .015 (.016) .010) .007-.012-.072) .020-.022-.009) .018 (.158) .016) .013) .009 (.010) .062) .008 (.027 (.017) .027 (.009 (.010 (.014 (.046 (.007-.011) .011) .020-.020-.022 (.040) .008 (.008) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.023 (.

009) . Radiation risks from exposure to natural uranium are very low.021) .006-.004-.011-.007 (.010) .030) .018-.033 (. After exposure to soluble uranium salts.006-.016-.024-.007 (.032) .006-.014 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.006-.011-.030-.027-.007 (.008) .005-.024 (.015-.008) .027-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.030 (.006-.016-.033 (.015 (.013 (.027 (.018 (.009-.013 (.029) .006-..026-.019 (.015 (.027-.044) .S.005-.010 (. 1992).013 (.050) .010 (.019 (.006-.023-.008) .034) .010-.013) .016) .005-.017) .013 (.008) .009) * .015-.043 (.007 (.008) .010-.008 (.024) .008-.011) .077) .. Depending upon the specific compound and solubility.024 (.034 (.013) .024-. 240 Fourth National Report on Human Exposure to Environmental Chemicals .007 (.017) .015-.007 (.006 (.031 (.028) .034 (.020) .030) .011-.010) .006-.020-.028 (.053) .028) .009) .080) .012) .014 (.040 (.011-.042-.015-. the shrapnel acts as a source of chronic.006-.011-.009) .007 (.020-.015) .005 (.013 (.007-.010 (.013) .015) .011-.008 (.015) .006-.051) .017) .013 (.007) .034 (.010) .270) .039) Total .009-.030 (.010) .042) .054) .007-.006-.008 (.009) .004-.016-.007 (.063) .007 (.006-.016-.012) .006) .011 (.035 (.033 (.008-.058) .039) .005-. 2005).007 (.007-.012 (.026 (.033 (.034-.051 (.013 (.005 (.008) .017-.009) Selected percentiles ( 95% confidence interval) 50th .009 (.006-.025-.007-.016) .006-. where limited absorption occurs (less than 5%).022 (.007 (.012-.029 (.018-. After long term or repeated exposure.009) .008-.009) .1%-6% of an ingested dose may be absorbed.006) .006 (.008 (. 2003).029 (.019 (.005 (. Inhaled uranium-containing particles are retained in the lungs. kidneys.007 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.058) .008-. which can occur occasionally from high occupational exposure.010) .011) * .007-.006 (.014-.011-.017-.022-. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.048) .006-.100 (.010-.011 (.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.005-.029) .017 (.017-.016) .009-.006-.024) .051) .016) .016) .020 (.024-.007-.010-.012 (.012 (.006 (.051) .009) . population from the National Health and Nutrition Examination Survey.027) .012) .013 (.053) .025-. After inhalation.016) .025-.011) .028) .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 .010-.005-..015 (.010-.008) .007 (.034 (.006 (.024) .009 (.009-.007 (. low level exposure.019-.034-.010) * .008 (.010-.045 (.019-.012 (.029) .021 (.024 (.020-.061) . liver.007 (.008 (.033) .006-. interval) .008 (.007 (. which represents distribution and excretion.021 (.047) .012-.007 (.010-.022) .013 (.016) .007 (.015) .009-.006-.010 (.019) .022 (.015-.006) .008) .010-.042) .041) .010-.030-.014-.017 (.029) .018) .008) .146) .008 (. with much slower elimination from bone.019-.013 (.006-.006) .032) .017-.074) .029 (.028 (.012 (.007 (.018-.008-.027) .024) .027-.056) .014) 90th .009-.018-.012 (.014) .012 (.007) .034 (.020 (.008) . Health effects from uranium exposure result from chemical toxicity to the kidney.039) .007-.019-.020 (.037 (.Metals impact.009) .007-. 0.006) .026 (.022 (.008 (.018-.006-.016 (.021-.006-.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 .067) .031-.035 (.007-.025 (.006 (.010) .019) .015 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.007-.059 (.026 (.007 (.006-.048) .011) .008) .019-.039) .021 (.027 (.020-.005 (.008-.022-.005-.022-. Uranium is eliminated in feces and urine.006-.027 (.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 .025) 95th .010 (.007) .013-.009 (.030 (.014-.011-.014) .010-.006-.009) .009 (.009) .016) .014) .050) .021 (. 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.028-.028) . In cases of retained DU shrapnel.008) 75th .026) .024) .009 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.025 (.009) .050 (.025-.011-.007 (.008 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.

41 (1). 1978). Breitenstein BD.110 to 45 μg/L (Ejnik et al. 1994. 2006). Hamilton et al. In the same study. soldiers evaluated before. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.e.. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. Horan P. 1992. Drinking water and other environmental standards have been established by U. soldiers who had been injured and had embedded DU shrapnel for as long as eight years.078 μg/L (ranging up to 5. 2006). in that the levels were below their respective detection limits (Byrne 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.. 1-49. McDiarmid et al. Karpas et al. 28 soldiers who may have been exposed to DU by inhalation. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Sci Total Environ 1991. 2006. 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.. 2003. Uranium content of blood. (Kurttio et al.gov/ toxpro2. McDiarmid M.S. Six workers in a depleted uranium program showed concentrations of 0. Thomas RG. Kent (England): Nuclear Technology Publishing. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure.61 μg/g creatinine. Hamilton MM. population. Pullat VR. Mil Med 2003. 2002.S. Atlanta (GA). In 17 U.html..S.. although slightly increased during and after deployment. Information about external exposure (i.011 μg/L (McDiarmid et al.162 μg/L) (Orloff et al.107:143-157. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. 2005. 2000). In a study of 105 persons exposed to natural uranium in well water. the median urinary uranium concentration was 2. 2006). Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. 2004). pp. Metivier H. Boyd P. Volf V.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. had a mean urinary uranium concentration of 0. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. Centers for Disease Control and Prevention (CDC). et al. (May et al.S. but in whom no shrapnel was embedded... Dietz LA. with emphasis on quality control. NRC. Radiation protection dosimetry. the geometric mean urinary uranium concentration was 0. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U.S. eds. Zimmerman I... EPA.066 μg/g creatinine (Gwiazda et al.78:143-146. 2004). Muggenburg BA. 1991.. and after deployment had geometric mean urinary uranium concentrations that were less than the NHANES 1999-2000 and 2001-2002 geometric means at all three time periods. 2000).. Durakovic A. Third National Report on Human Exposure to Environmental Chemicals.S. Stradling GN. 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. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population.65 μg/L). Tolmachev et al. Carmichael AJ. Komaromy-Hiller et al. ingestion.Metals injury associated with elevated urinary uranium levels (Kurttio et al.1992. 2006). Determining the normal concentration of uranium in urine and application of the data to its biokinetics. Benedik L. during. Health Phys 2000..cdc. Guidebook for the treatment of accidental internal radionuclide contamination of workers. 2004). or wound contamination. References Bhattacharyya MH. Vol.. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al.55 μg/L (median 0.168(8):600-605. Galletti. In: Gerber GB. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. A cohort of 46 U. the median urinary concentration was 0. 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.. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.1996... IARC and NTP have no ratings for uranium human carcinogenicity. The U.62:562-566. urinary levels of uranium were as high as 9. Dang HS. 2002). Byrne AR. and no consistent effects on multiple endpoints of kidney function were found. 2001-2002. Fourth National Report on Human Exposure to Environmental Chemicals 241 . Ejnik JW. and 2003-2004 (Dang et al.atsdr. environmental levels) and health effects is available from ATSDR at: http://www. Pillai KC. respectively. Squibb K. 2004). In two studies of a Finnish population with high natural uranium concentrations in their drinking water. Health Phys 1992..

Pirkle JL. Auvinen A. Hollriegl V.94:319-326. Paretzke HG. Health Phys 2006. Orloff KG.S. May LM. Wilson PD. Pinto V. Biologic monitoring for urinary uranium in Gulf War I veterans. Noguchi H. Kidney toxicity of ingested uranium from drinking water.47(6):972-982. Lorber A. Health Phys 1996. Kane R. Hamilton EI. Auvinen A. Int Arch Occup Environ Health 2006. Jarrett JM. Nuclear Regulatory Commission (NRC) Guide 8. Ash KO. patient population and literature reference intervals for urinary trace elements. July 1978. Marino R. Kuwabara J.296(1-2):71-90. Roiz J. D’Annibale L. et al. Howerton K. Gucer P. Saha H. Karpas Z. Roth P. Paschal DC.71(6):879-85.79(1):11-21. Makelainen I. Komaromy-Hiller G. McDiarmid M.22–Bioassay at uranium mills. Uranium daily intake and urinary excretion: a preliminary study in Italy. Kurttio P. Salonen L. Saha H. Clin Chim Acta 2000. Oberbroekling KJ. Wahl W. Environ Res 1999. Health Phys 2004. Human exposure to uranium in groundwater. concentration and daily excretion of uranium in urine of Japanese. NRC). Pekkanen J. Harmionen A. Oliver M. 242 Fourth National Report on Human Exposure to Environmental Chemicals .91(2):144-153. J Toxicol Environ Health A 2004. Ejnik J. et al. Scott K. Ting BG. Health Phys 2002. Review of elements in blood. Andrews WS. Am J Kidney Dis 2006. rapid. Squibb K. McDiarmid MA. Environ Res 2004. Military deployment human exposure assessment: urine total and isotopic uranium sampling results.158:165-190. Costa R. Tolmachev S. et al.67(8-10):697-714.82(4): 527-532. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Lewis BM.85:228-235. Cordero S. Health Phys 2004. Renal effects of uranium in drinking water. Engelhardt SM. Metcalf S. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo.S. Jackson RJ. Kalinsky V. Uranium and thorium in urine of United States residents: reference range concentrations. Bennett LG. Komulainen H. Gwiazda RH. Halicz L. Hancock RG. et al. McDiarmid MA. Inductively coupled plasma mass spectrometry as a simple. Kurttio P. Sampson EJ. Biokinetic modeling of uranium in man after injection and ingestion.86:12-18. Karpas Z. Van der Venne MT. VI. Radiat Environ Biophys 2005.87:51-56. Nuclear Regulatory Commission (U. Charp P. Englehardt SA.S. Heller J. Element reference values in tissues from inhabitants of the European community. Salonen L. et al.Metals Galletti M. Sci Total Environ 1994. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. U. et al. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Smith D.110(4):337-342. Environ Health Perspect 2002. Cremisini C. Health Phys 2003.S. Marko R. Li WB. U. Sabbioni E. Katorza E. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Ough EA.44:29-40. Oeh U. Washington (DC): NRC. Comparison of representative ranges based on U. Squibb K. Mistry K.81:45-51. Shelly T.

milk.90-12.0) 13.62 (3.0 (9.0-18.0) 13.0) 8.32 (3.0 (10.30-17.96 (3.0 (9.0 (12. potassium. interval) 3.26 (2.0-14.0-17.70-5.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.S.46) 3.51 (3.20 (4. 2005).40-5.18-3.20 (5.20) 3.60) 8.0 (11.0) 708 617 681 652 1228 1092 Limit of detection (LOD.03) 3.0 (9.81-16.70 (3.60) 3.0 (11.60 (4.10 (5.70 (3. 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 13.50-3.0) 15.0) 14.0 (9.35 (3.76) 4.90-11.40-11.10-11.Perchlorate Perchlorate (Urbansky.0 (11.10) 5. see Data Analysis section) for Survey years 01-02 and 03-04 are 0. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.0-29.05 (2.0) 19.74-3.0 (12.40 (4.30 (2. 1998).80-8.EPA.80-4. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7. certain catalytic metals.10-12.70-6.05 and 0.0 (8.80) 75th 6.50 (8.10-7.0 (8.50-11.80) 7.10) 3.76 (3.0 (8. leather tanning.0) 16.0-17.20-3.80 (7.20-4.40) 3.29-3.0 (12. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.g.40 (5.20-4.20-11.02 (3.0 (11.0) 10.0 (8.40 (8. laboratory analysis.11) 4.87-3.65) 3.40) 90th 10.10) 5.90-3.0 (13.20 (2.40) 3.0-17.0 (11.S.50) 5.0 (11.90-10. 2005).70 (3.0) 10.05.89-3.90) 6.90-9.0) 11. or ammonium salt.0) 12.0) 95th 14.40 (4.39-4. population from the National Health and Nutrition Examination Survey. Perchlorate was added to the U.30-7.40) 4.00) 7.0) 11.49-3.0) 13.66) 3.10) 12.0-20.50) 5.00-6.22 (2.00) 3.0) 15.0-18.20 (2.50 (5.80) 12. lettuce) can be the main sources of intake for humans (FDA.50) 11.40 (3.67-5.84) 14.0) 9.11) 3. 2002).20-12.93 (4.30 (5.30 (5. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.0-19.90 (5.70-9.10 (6.54 (3.0) 9.90 (3.31) 2.80-12.30-19.80 (6.20 (8.40-7.50) 6.0 (12.68) 4. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U. and reducing agents.0) 13. Drinking water.0) 9.16) 3.81) Selected percentiles ( 95% confidence interval) 50th 3.19 (3. 2007).60-7.10 (6.45-4.S.10 (2.0) 14.0 (9.09) 3.19-4.75 (3.60) 5.70-11.40 (5.30) 6. Other manufactured uses include fireworks. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.40-4.60-6. and limited applications in pharmaceutics.80-15.10-4.90-6.50 (3.00) 5.22-5.60 (4.80 (3.00-5.90-3.50-4.0-18.70) 3.0) 11.70-12.20) 7.70-7.50) 3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0) 9.0 (11.0) 14. and electroplating.75-3.0) 13.40 (5.10 (7.40) 6.40-13. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0-17. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.0) 13.93-3.60 (7. It is normally found and produced as the anion of a sodium.51 (3.80 (3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.01 (2.0) 8.40-4.00-6. In addition.20 (4.0 (11.80) 3.00) 3.70-3. but has strong oxidant properties in the presence of concentrated acids.0-17.80-4.38) 5.0) 10.. matches.5 hours and has a small estimated volume of distribution (Crump and Gibbs..00) 4.0-15.10-11.0 (11.70-3.0 (11.40-6. and certain plants with high water content (e.20) 4.0) 9.90 (2.44-4.0) 9.93-4.79 (2. Survey years 01-02 03-04 Geometric mean (95% conf.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.20 (7.90-9.0 (9.10) 3.40 (3.0-23.30 (2.21 (2.08-3. Inhibition of iodine uptake by competition for the sodium/iodide symporter in the thyroid can be estimated in humans by measuring radioiodine uptake CAS No. fabric dyeing.30-6.20 (6.0-15.90 (5.30-7.90 (5.90) 5.50-7.90 (4.40) 3.56) 3.07-4.30) 6.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.88) 3.40) 2.12) 3.0) 13.80-6.0 (9. Perchlorate is stable under most environmental and physiological conditions.0-17.47-4.0 (8.50-4.90-11.

30) 3.39-4.19-6.40 (3.20-3.0) 12. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.6) 20. 2005). 2005.89-3.86) 4. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.72 (3.80 (7.40) 5.12 (6.0) 708 616 680 648 1227 1080 2001-2002 performed on surplus samples (variable unavailable of NHANES website) 244 Fourth National Report on Human Exposure to Environmental Chemicals .g.44-6.22-6.60-5.22-4.25 (3.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.1-22.0 (9.90 (4.41-9.33 (7.10 (2.EPA.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses. Greer et al.35) 3.3) 11. congenital hypothyroidism is a condition for which nearly all newborn blood is screened. Lawrence et al.90 (2. 2005).25) 5.50) 9.1 (8.37-13.0-44.93-5.95 (2.7 (11.80-3..20-9. population from the National Health and Nutrition Examination Survey. NAS.90-15.50 (3.03 (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.39 (3.75) 3.02) 3..84) 2. Also.99 (5.46-4.0) 14.61 (5. thiocyanate.00-2.10) 3.3 (10.10) 13.50-9.S.S. 2001.0) 4.4) 13.0-19.60-11.61-5.00 (2.26) 4.10) 6.74) 7.98) 3.46-13.99-3.5 (13.20 (7.20-10.8 (11. women with urinary levels of iodine less than 100 micrograms per day..3) 8. Survey years 01-02 03-04 Geometric mean (95% conf.20) 8.60-3. medications).4 (11.93-5.91) 4.05 (4.46 (3. 2000).60 (3.S.97-5. 2005).42 (3.89 (2. and the presence of other substances known to affect thyroid function (e.53 (2.18-3.22 (2..80 (7.93-8.0 (8.35 (4. 2002)..70 (4.24-2.50) 95th 12. 2006. gender. up to 68% RUI has been demonstrated.0) 10.25) 5.15-12.30 (3.82 (5.30) 75th 5.66) 3.90-9.3-14.50-3.21 (2.80-3.90-11.90-2.51 (3.1-16.80 (4.87 (7.52-9.60) 3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.35 (2.00 (6. 1999.70-5.10) 4.04-3. nitrate. interval) 3.93) 3.93-7.76 (3.00-11. Lamm and Doemland.02-4.20) 3.87) 2. Steinmaus et al.59) 3.0) 11.40) 3.60) 8. levels and sufficient in most participants (Tellez et al.08 (3. perchlorate is negative in most genotoxic assays (U.0 (11.EPA..54 (2.0-14.90 (7. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.71 (5.96) 2.50 (6.50) 2.1-13.54 (3.0 (11.29) 2.S.30-10. 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.2) 8.44) 3.40-10.0) 9. 2003... Many factors may be important in consideration of perchlorate action on the thyroid: dose.77 (3.26 (3.83 (5.45-2.10 (1.5) 8.00) 3.32) 5.29-6.20 (3.10-3.0 (8.22-4.60-8.00) 9.39) 2.6-17.33-12.70-3.36 (8.08) 3.20 (2.30) 5.Perchlorate inhibition (RUI).10 (4.07 (2.0) 12.45) 3.87) 7.43) 6.00 (4. U.30 (6.50) 2.73) 3.52 (8. In the U.20-3.40 (7.37 (4.80) Selected percentiles ( 95% confidence interval) 50th 3.50) 5.60) 10.24 (4.0 (9.0) 12.87 (5.40) 17.10 (4.51-4.1-14.60-5.30) 90th 9.S.1 (11. 2007).61-10.20 (4.70 (2. dietary iodine intake.76-3..6) 12.0) 13. in a representative sample of U.S.40 (4. although iodine intake was higher than U.04-3.10-7.1) 8.0) 13. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.16-3.14 (2.64-3.S.4) 8.4 (10.60-15.50-5.20 (6.90-3.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.00-3. age. 2002.0-17.33-6..40 (3.60-8.87-3.0) 7.70-15.90-20.70) 2.50) 6.09 (7. Li et al. During gestation and infancy.19-10. 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.60-11.20-4.64) 5.30-5.70 (2.58) 2.12-2.0 (9.10 (6.30 (5.0 (10.67) 5.09) 3. However.81-3.3) 12.47) 2.0) 9.4 (11.0 (11. levels.56 (3.25) 5.90 (2. 2005. chronicity of exposure.34-3.70) 10. menopausal status. 2002.90) 5.0) 12.60-6.0) 6.0-14.30-5. 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.00) 4.70-4. 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.56-3.4 (8.4-16.2) 8.

Jackson WA... Rutherford GW.45(10):1116-1127. Doemland M.S. Valentin-Blasini L. Caldwell KL. May 2007. Li FX. most of the population is considered to be below the U. National Academy of Sciences (NAS). Osterloh JD.115(9):1333-1338. Lamm SH. Steinmaus C. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Blount et al. 2005).42(2):200-205. CFSAN/Office of Plant & Dairy Foods.html.11(3):295. Sesser DE.113(11):A732. Cross M. Food and Drug Administration (FDA). Also. J Occup Environ Med 2000. Richman K. Neonatal thyroxine level and perchlorate in drinking water. Available at URL: http://www. Braverman LE.html and from ATSDR at: http://www. Braverman LE. EPA reference dose (Blount et al. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Health Implications of Perchlorate Ingestion. Blount BC. Landingham CB. He X. 2005). Pleus RC. Braverman LE. Thyroid 2001. Pino S. Blount BC.. 2001-2002. Environ Health Perspect 2005.40(21):6608-6614. Li Z. Page Last Updated: 05/28/2009. Tellez RT. Lawrence JE. Valentin-Blasini L. Magnani B. Perchlorate in the United States. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Environ Health Perspect 2006. J Occup Environ Med 2003.EPA at: http://www. J Expo Sci Environ Epidemiol 2007. 2007). Barnard JC. Abarca CR.htm. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Analysis of relative source contributions to the food chain. Crump KS. (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. Howd R. Environ Sci Technol 2006. epa. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Gibbs JP. Crump KS. Environ Health Perspect 2007. 2005. Environ Health Perspect 2002. National Research Council of the National Academies.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. References Blount BC. J Clin Endocrinol Metab 2005. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Daaboul JJ. Dyke JV.cdc. Chacon PM. Buffler PA. Greer SE.gov/toxpro2. and environmental perchlorate exposure among residents of a Southern California community.fda. Additional information about exposure and health effects is available from the U. The effect of perchlorate. population.17(4):400-407. 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. Goodman G. Lawrence J. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect.90(2):700-706. Lamm SH. Deyhle GM. thiocyanate. Erratum in: J Occup Environ Med 2004. Miller MD. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Low dose perchlorate (3 mg daily) and thyroid function. Lamm SH. Thyroid 2000. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Byrd D. et al.S. newborn thyroid function. Erratum in: Environ Health Perspect 2005.S. Pino S. Perchlorate Exposure of the US Population. et al. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . and nitrate on thyroid function in workers exposed to perchlorate long-term. Kirk AB. Washington (DC): National Academy Press.113(8):10011008. Dasgupta PK.110(9):927-937. Primary congenital hypothyroidism. Lau EC. Lamm S. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. 6/2/09 Greer MA. Mauldin JP. 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.atsdr. et al.41(5):409-411. Pirkle JL.gov/safewater/ccl/perchlorate/perchlorate.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. 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. Pirkle JL. Benchmark calculations for perchlorate from three human cohorts.114(12):1865-1871. Osterloh JD. et al.10(8):659-663. Kelsh MA. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Skeels MR.46(5):509.

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

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

Unlike many organohalogen contaminant chemicals.. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. The PFCs often measured in human serum are listed in the table. including immunologic effects and tumor induction. 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.. Bookstaff et al..Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). C7). 1990). Some of the effects in animals may be mediated through peroxisomal proliferation. Prevedouros et al... growth retardation and delayed sexual maturation (Kennedy et al. Vanden Heuvel et al. EPA.. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. 2005. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. 1993).S. in part. 2005).S... Kannan et al. 2004. 2003a and 2004a)... 2005. and in human blood and semen (Calafat et al. in a wide variety of marine and land animals (Kannan et al. see Data Analysis section) for Survey year 03-04 is 0. or effects of other PFCs. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. U. Survey Geometric mean (95% conf. 2004. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 2006. C5.. 2002. and in offspring. there is limited information on the sources. the 8-2 telomer. It is unclear if environmentally degraded telomer products are a major source of other PFCs. Taniyasu et al. but still can have long residence times in the body.. PFOA is mostly excreted in the urine in animal studies. kidney. 2006a. 2007a).. 2000. PFOA has been reported to cause liver. 2003). which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.. endocrine and immune effects. hepatotoxicity. All sources of human exposure are uncertain.. Lau et al.. Tittlemier et al. In some cases. C6. Excepting PFOS and PFOA. heptadecafluoro-1-decanol. environmental fate.4. approximately 4.. but probably include dietary sources (Kannan et al. 1995. and β-oxidation of lipids (Kudo et al. The elimination half-life of PFOA in humans is roughly estimated to be 3. 2005).. 2003.8 years (Olsen et al. pancreas. by high protein binding in plasma and other proteins. human toxicokinetics. may metabolize or degrade to PFOA (Dinglasan et al. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins. 2004.5 years and for PFOS.. 2004. 2007).. 2005. 2004). For instance. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. peroxisomal proliferation.. PFCs have been identified in surface coastal and ocean waters (Yamashita et al. 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. < LOD means less than the limit of detection. thymus and spleen.e. 2003). 2004).. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. Olsen et al. Lau et al. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. 2005). the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. Guruge et al. Keller et al. 248 Fourth National Report on Human Exposure to Environmental Chemicals ..

1999.500) . 2007a.80) 640 1454 03-04 03-04 * * < LOD < LOD . hepatotoxicity.800) 1.700 (.108 times higher than background serum levels in humans (Butenoff et al.600-2.500 (<LOD-1. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.500) . 2003).00) ..900 (. PFOA. 2007a. 2005). the potential to estimate risks to humans from animal doses is uncertain. 2004).400 (<LOD-.10) . and humans.500-1. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Serum PFOS levels associated with toxicity in test animals were 310-1550 fold higher than 95 percent of the levels found in a study of adults (Olsen et al.400) .10) . U.500 (. population.700) . * 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 249 . animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.500) .800 (. In comparing three separate reports on adults.300 (<LOD-.400 (<LOD-. U. PFOA.800 (. Fei et al. At high but non-toxic maternal doses of PFOS. However. PFOS.500-1.500) 90th ..800) 1. perfluorohexanesulfonate (PFHxS). 2003a).S..300 (<LOD-. 2004a. Animal studies of PFOS have demonstrated weight loss. 1992. see Data Analysis section) for Survey year 03-04 is 0..00) . 2007)..900 (.500-1.800 (.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. 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. EPA..S.. development in offspring was stunted and hypothyroxinemia was observed.400-1. 2003. 2004b).. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.S. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. 2003.500-3. elderly and children.800 (. Olsen et al. Harada et al.400-.300-1.500-. 2003a. and changes in thyroid hormone concentrations (Grasty et al. and there was no clear evidence of excess all-cause or diseasespecific mortality. reproductive. 2004.10 (.20) .S. 2004). Thibodeaux et al.500) . 2007b).10) * 03-04 03-04 * * < LOD < LOD < LOD .900 (.00 (.300 (<LOD-.. monkeys. 2007. Kennedy et al.600 (. 2003). Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. 2003a). < LOD means less than the limit of detection. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. Olsen et al. thyroidal).400-. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years..400-1. Cook et al. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats..3. 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. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.40) . PFOS. In such studies.400-1....400-1. 2003a. 2003a. 2001. Olsen et al..600 (.500 (..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 . Lau et al.500-1. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. 2004. 2003. developmental and teratogenic effects were demonstrated in offspring. which may vary for some chemicals by year and by individual sample..400 (<LOD-. 2003).80) 485 538 962 Limit of detection (LOD. 2005).600 (.. At doses causing maternal toxicity. EPA.00) .400-1.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . 2007b.... possibly related to lung immaturity (Lau et al. or increased cancer rates (Alexander et al. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.50) .

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

Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.600 (.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .500) 485 538 962 Limit of detection (LOD.0. interval) Selected percentiles ( 95% confidence interval) Sample 95th . < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.S.600) < LOD .400 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 251 .3.500) 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 . population from the National Health and Nutrition Examination Survey.500-.400 (.300 (<LOD-. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.300-. see Data Analysis section) for Survey year 03-04 is 1.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S. see Data Analysis section) for Survey year 03-04 is 0. Survey Geometric mean (95% conf.400) .900) < LOD .Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500 (<LOD-.400 (<LOD-. 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.300 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

20-3.10-5.20 (1.00) 2.20-1.20) 2.50) 6.20 (6.73-2.20 (1.10) 1.10 (4.00 (1.87-2.80-3.60-3.00-8.800-1.86 (1.10 (.50 (4.80-4.40-3.70) 2.80-7.70 (2.984 (.721-1.10-9.50 (4.26) 2.80-12.90) 1.60) 2.00 (1.689 (.40) 2.50-3.08) 2.40 (1.30) 3.20 (1.80-6.70-6.90 (2.90 (1.10) 75th 1.861 (.72) 1.834-1.40) 1.90 (4.800 (.00) 1. Survey Geometric mean (95% conf.900-1.90 (4.54) .852 (.5) 5.10) 6.30-6.80 (1.62-2.30 (2.60 (1.50) 2.70) 2. interval) 1.40 (1.01 (1.80) 5.30) 3.44 (2.20 (1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.700-1.60 (6.50-10.00 (5.10) 4.80-4.90-19.03) 1.20) 485 538 962 Limit of detection (LOD.60-4.60-7.S.900-1.40) 640 1454 03-04 03-04 1.70-7.90 (1.60) 1.80-2.50-6.56-1.30 (1.30-12.10) 4.50 (1.10) 1.90) 90th 5.700 (.826-1.50 (1.816-1.6) 7.70) 1.42 (1.67-2.1.30 (2.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.90-10.50 (2.04) .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 1.00 (1.00) 3.40 (1.60-2.20-2.60-8.30) 3.30 (7.70 (1.70) 13.20) .40) 4.586-.80) 4.17-1.80 (1.00-7.40) .3 (9.80-7. see Data Analysis section) for Survey year 03-04 is 0.90 (1.60 (1.80-8.09 (.900 (.70-2.1) 485 538 962 Limit of detection (LOD.900-1.60) 3.90) 1.12) .00 (.20) 03-04 03-04 2.40) 1.10) 6.30 (3.30) .30) 03-04 03-04 .966 (.92 (1.80-3.27) 1.00 (1.90) 1.80) 1.40) 640 1454 03-04 03-04 2.10) 75th 3.600-.80-8.10 (.20-1.697-1.70-5.80-4.30-9.20) 1.30 (6.10) 1053 1041 03-04 03-04 03-04 .963 (.50 (1. Survey Geometric mean (95% conf.50 (6.10-9.10 (1.77-2.50-6.30 (1.90 (1.912-1.40 (1.20-1.30-2.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.90-2.90) 3.0) 1053 1041 03-04 03-04 03-04 1.80 (4.809) 1.00-1.80) 90th 2.70-10.900 (.30 (1.70) 3.00 (.20-1.00 (2.10) 5.3.00) 1.51) 1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.70) 1.835-1.17 (1.80) 3.00-6.50) 2.91) 2.20 (6.40-1.40 (2.72 (1.60-4. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.14 (.900) 1.60) 9.30 (1. see Data Analysis section) for Survey year 03-04 is 0.00-1.16) .10) 8.5) 8.60-2.10 (4.900-1.S.60-3.900-1.93 (1.40-1. interval) .05-2.60 (1.90) 8. 252 Fourth National Report on Human Exposure to Environmental Chemicals .60-2.0) 8.70-2.900-1.50 (6.50 (1.10 (. population from the National Health and Nutrition Examination Survey.20) 1.

00 (3. population from the National Health and Nutrition Examination Survey.20) 5.80 (7.99-3.90-4.11 (2.3 (17.30 (3.7 (35.40-6.27) 4.6-45.6) 18.90 (7. population from the National Health and Nutrition Examination Survey.3) 42.6) 62.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.60 (4.3 (44.80-9.40-17.65-4.20-9.90-12.4 (28.7 (43.5) 57.1-24.4) 56.60 (6.60 (5.1 (23.70 (5.70) 6.1-36.4.40 (6.2) 30.9) 22.7 (35.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.91) 3.80-12.1) 15.6 (19.4) 75th 30.37 (2.70-9. Survey Geometric mean (95% conf.7 (13.3 (35.0) 36.2-22.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.5 (28.70-10.95 (3.6) 9.60-6.5) 18.8 (45.50-4.50 (3.70 (3.5-62.5-23.0-20.40 (4.9) 27.0) 90th 41.3-61.5) 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 21.70-7.3-22.8-81. interval) 20.20) 7.60 (6.67-4.0) 21.0-70.1 (24.30-8.70 (5.40-10.0-66.20 (4.40-6.30) 6.5-33.1-35.30-5.9 (19.3) 28.00 (5.3) 485 538 962 Limit of detection (LOD.8-22.5 (28.90 (5.6 (35.8 (34.0) 23.1-25.2) 640 1454 03-04 03-04 4.8) 46.1-52.3) 41.8-22.2 (28.0) 21.0 (27.7-33.47-4.9-38.20 (4.70-5.5) 32. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.30) 7.9 (13.96 (3.60 (7.20) 5.2 (19.1 (19.70) 4. Survey Geometric mean (95% conf.2-57.60) 8.5) 9.9) 22.50) 4.6 (42.50 (4.1.10 (3.20) 7.18 (3.70-7.6) 1053 1041 03-04 03-04 03-04 3.60-13.7) 39.1-33.80 (6.20-5.89 (3.90-4.80) 8.6) 35.10-3.20) 10.4) 640 1454 03-04 03-04 23.07-4.3 (35.3 (28.20-4.7-53. see Data Analysis section) for Survey year 03-04 is 0.9-19.4 (19.30-3.30-6.30 (3.00) 3.82) 4.0) 485 538 962 Limit of detection (LOD.S.4-25.2) 30.6 (44.5) 1053 1041 03-04 03-04 03-04 14.10 (6.9 (17.21-3.40-14.8-35.90 (7.47 (4.9) 9.50-6.9-23.60-9.30 (5. see Data Analysis section) for Survey year 03-04 is 0.90 (7.60) 03-04 03-04 3.40) 90th 7.7 (43.2 (21. Fourth National Report on Human Exposure to Environmental Chemicals 253 .7-69.0-16.20) 4.4 (17.50) 7.50-13.4-17.0) 03-04 03-04 19.1) 57.2 (16.0) 43.4-42.5) 19.8) 32.2 (27.8-22.10) 5.85-4. interval) 3.2) 45.6) 42.5-21.8-78.6-24.6-50.4) 20.70) 3.9 (22.7-30.8) 27.7 (19.35) 3.53) 3.30-11.8 (37.0 (20.80-4.1) 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 4.7-23.79) 4.5) 7.8-30.S.6) 21.10 (3.5) 8.4) 21.6) 7.2 (18.84-3.40) 5.4 (23.7-49.90) 6.40) 3.60-14.80 (5.4 (19.40) 75th 5.60 (3.00 (5.80 (6.7 (7.

300 (.300) .200-. 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.300 (.300 (.S.300-.300 (.200-.300 (.300 (.200-.500) < LOD 485 538 962 Limit of detection (LOD.300 (.300) .500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300) .300 (.300 (. 254 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300 (.200-.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample.4. population from the National Health and Nutrition Examination Survey.200-. which may vary for some chemicals by year and by individual sample.200-.200 (<LOD-.300 (.500) . population from the National Health and Nutrition Examination Survey.300 (.300-.300) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (. Survey Geometric mean (95% conf.300) . < LOD means less than the limit of detection. see Data Analysis section) for Survey year 03-04 is 0. see Data Analysis section) for Survey year 03-04 is 0.400 (<LOD-.500) 485 538 962 Limit of detection (LOD.300) .200-.300 (.200-.500) .300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .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 . < 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.200-.200-.2.500) .300) .300-.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.300-.

900-1. Survey Geometric mean (95% conf.20 (1. Survey Geometric mean (95% conf.900-1.700 (<LOD-.50 (1.10 (1.900) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700) .10 (.60) 485 538 962 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th .600 (<LOD-1.10 (.10) .700 (<LOD-2.10-1.700) 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 .40) < LOD < LOD .900) 485 538 962 Limit of detection (LOD.800) . see Data Analysis section) for Survey year 03-04 is 0.600) .70) 1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.30) 1.10) .30) 1.300-2.800 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.400 (<LOD-.700) 1.700 (<LOD-.50 (1.10) 1. see Data Analysis section) for Survey year 03-04 is 0.40) 1.700 (<LOD-.10-1.00 (.10 (.900 (<LOD-1.300 (<LOD-1.30) .900-1. < LOD means less than the limit of detection.10-1.S.900) .900 (.900-1.500 (<LOD-.00 (.00 (.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 . Fourth National Report on Human Exposure to Environmental Chemicals 255 .S.900-1.00 (.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .30 (1.700 (<LOD-. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.300 (<LOD-.30 (1.20) 1.10-1.00-1. < LOD means less than the limit of detection.900-1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .60) 640 1454 03-04 03-04 * * < LOD < LOD .90) .600 (<LOD-1.900-1.20-1.80) 1.600 (<LOD-.700 (<LOD-.800) .80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .3. which may vary for some chemicals by year and by individual sample.30 (1.6.00) < LOD .80) 1.10-1.10) * 03-04 03-04 * * < LOD < LOD .700 (<LOD-.10) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700) 90th 1.400 (<LOD-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.600 (<LOD-1.

population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000.68(6):465-471. Olsen GW. Environ Sci Technol 2007a. Evans TJ. Environ Sci Technol 2004. Kannan K. Morikawa A. Toxicol Appl Pharmacol 1995. Polyfluoroalkyl chemicals in the U. Chem Biol Interact 2000. O’Connor JC. Bandai N.104(2):322-333.134(1):18-25. et al. Grey BE. Frame SR. Kannan K. Environ Sci Technol 2004. Yoshinaga T. Environ Health Perspect. Caudill SP. Occup Environ Med 2003. Needham LL. Environ Sci Technol 2005. Moore RW. Koizumi A. Cook JC. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Reidy JA.179:99-121. Rogers JM. Katakura M. Regul Toxicol Pharmacol 2004. Mandel JH. Loganathan BG. Butenhoff JL. Caudill SP.115(11):1596-1602.38(10):2857-2864. et al. Peterson RE. Cook JC. Kuklenyik Z. Halden RU. J Environ Monit 2005. Falandysz J. Cook JC. Environ Health Perspect 2007. Inoue K. Perfluorinated chemicals in selected residents of the American continent. Saito N. Liu RC. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Sasaki S. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Chlorinated. Laane RW. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Fei C. Characterization of risk for general population exposure to perfluorooctanoate. Hekster FM. Biegel LB. Kamiyama S. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Harada K. et al.S.1968--2003. Needham LL.S. in vivo. de Voogt P. Mohotti KM. Seneviratne HR. Kudo N. Fillmann G.115(11):1670-1676.41:2237-2242. Crit Rev Toxicol 2004. Moore JA. Frame SR. Chemosphere 2006b. Seacat AM. Fluorotelomer alcohol biodegradation yields poly.63:490496. Aguilar-Villalobos M. Day RD. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Olsen J. and ex vivo studies. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Harada K. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Mabury SA. Toxicol Sci 2001. Perkins RG. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Reidy JA.7(4):371-377. Kennedy GL Jr. et al. Mandel JS. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea.and perfluorinated acids. Mandel JH. Kuklenyik Z. et al. and perfluorinated contaminants in livers of polar bears from Alaska.46(2):141-147.39(1):80-84. Environ Res 2005.39(3):363-380.Perfluorochemicals References Alexander BH. Taniyasu S. Apelberg BJ. Reidy JA. Environ Sci Technol 2006a.40:21282134.113(2):209-217. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. brominated.60(10):722729. Rev Environ Contam Toxicol 2003. Environ Health Perspect 2007. Yoshinaga T. Calafat AM. Tully JS. Calafat AM. Olsen GW. Kumar KS. Holmstrom KE. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Yun SH. Calafat AM. Kuklenyik Z. McLaughlin JK. Lau CS. Gaylor DW. Guruge KS. Needham LL. Ingall GB. Reidy JA. Calafat AM. Environ Sci Technol 2005. Hurtt ME.34(4):351-384. The influence of time. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Environmental and toxicity effects of perfluoroalkylated substances. Yamashita N. Bignert A. Calafat AM. The toxicology of perfluorooctanoate.38(17):4489-4495. Ye Y. Arendt MD. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Herbstman JB.99(2):253-261. Grasty RC. Olsen GW. 2007b. Wijeratna S. Jarnberg U. Birth Defects Res B Dev Reprod Toxicol 2003. Hurtt ME.115(11):1677-1682. Wong LY.39(23):9101-9108. Biegel LB.60(1):44-55. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Kuklenyik Z. Dinglasan MJ. Rodricks J. Environ Sci Technol 2005. Yamashita N.Koizumi A. Edwards EA. Corsolini S. Kannan K. Needham LL. Keller JM. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth.39(23):9057-9063. Tarone RE. Inoue K. et al.124(2):119-132. J Occup Health 2004. Hurtt ME. Tully JS. O’Connor JC. Suzuki E. Taniyasu S. Watanabe T. Saito N. Toxicol Appl Pharmacol 1990. Butenhoff JL. Witter FR. et al. Toxicol Appl Pharmacol 1992. Bookstaff RC. Burris JM. Murray SM. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Kawashima Y.

Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. et al.perfluorohexanesulfonate.S. Ellefson ME. Reagen WK.) Tittlemier SA. Horii Y.82(1):359. Larson EB. Hanson RG. Cousins IT.epa. Olsen GW. Prevedouros K. Case MT. Seacat AM. Butenhoff JL.gov/opptintr/pfoa/pfoara. I: maternal and prenatal evaluations. Mandel JH. 2003a. Environ Health Perspect 2003a. Toxicol Appl Pharmacol 2004.68(1):249-264.37(12):2634-2639.198(2):231-241. Church TR. Kawashima Y. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. (Erratum in: Environ Health Perspect. Thomford PJ. Lau C. Hansen KJ. Olsen GW. U. perfluorooctanoate andother fluorochemicals in human blood. Biochim Biophys Acta 1993. Mair DC. Yamashita N.45(3):260-270. Hansen KJ. Olsen GW. van Belle G. 2007a. (Erratum in: Toxicol Sci 2004. Environ Health Perspect 2005. Hansen KJ.40(1):32-44. Gamo T. Lau C. Mandel JH. Burris JM. Buck RC. Chemosphere 2004a.51(8-12):658-668. Petrick G. J Occup Environ Med 1999. Rogers JM. Washington.54(11):1599-1611. Butenhoff JL.41(9):799-806. Rogers JM. Burris JM. Olsen GW. fish. Lundberg JK.55:3203-3210.26(1):47-51. et al. and perfluorooctanoate in retired fluorochemical production workers. Half-life of serum elimination of perfluoroo ctanesulfonate. Kannan K. II: postnatal evaluation. and food items prepared in their packaging. Environ Health Perspect. A global survey of perfluorinated acids in oceans. Richards JH. et al. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Seacat AM. Cao XL et al. Burris JM. The developmental toxicity of perfluoroalkyl acids and their derivatives.113(5):539-545. Mar Pollut Bull 2005.115(9):1298-1305. Korzeniowski SH. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Toxicol Sci 2002. htm.74(2):369-381. Environmental Protection Agency (U. Sterchele PF. Olsen GW. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Rogers JM. Horii Y. Hansen KJ. Available from URL: http://www. Burris JM. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. fish. Thibodeaux JR.. et al. Ehresman DJ. Fourth National Report on Human Exposure to Environmental Chemicals 257 . 1/15/06 Vanden Heuvel JP. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Lundberg JK. Hansen KJ. Environ Sci Technol 2003. Ehresman DJ. 2003. Taniyasu S. fate and transport of perfluorocarboxylates. Butenhoff JL. Chemosphere 2007b.74(2):382-392.111(16):1892-1901. Barbee BD. Burlew MM. Olsen GW.68:105–111. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Butenhoff JL. EPA).1177(2):183-190. Froehlich JW.2(1):53-76. Burris JM. Coordinate induction of acyl-CoA binding protein.S. Bronson R. Olsen GW. Environ Sci Technol 2006. Toxicol Sci 2003. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Olsen GW. Hanson RG. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat.111(16):1900) Olsen GW. Huang HY. et al.Perfluorochemicals Kudo N. birds. Mandel JH. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Thibodeaux JR. Moisey J. Zobel LR. Sources. Historical comparison of perfluorooctanesulfonate. and humans from Japan. fast foods. Butenhoff JL. Biol Pharm Bull 2003. Seymour C. et al. Yamashita N. Nesbit DJ. Taniyasu S. Kannan K. Butenhoff JL. Hanari N. Peterson RE. Grey BE. Grey BE. Stanton ME. J Occup Environ Med 2003b. Miller JP. Mandel JH. J Ag Food Chem 2007. Pepper K. Church TR. Toxicol Sci 2003. Helzlsouer KJ. J Children’s Health 2004b. Church TR. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water.

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

cdc. 2003. efficiency of intestinal absorption.. 1982). Castle L.Phthalates and metabolites have been tested. Mackay D. Hauser et al. 1986).. 2001. 2000b. In Staples CA (ed).805:49-56. Part Q: Phthalate Esters. 2005. Jongeneelen FJ. Lovekamp-Swan and Davis. High doses of di2-ethylhexyl phthalate (DEHP).. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. 2003. van der Broek PH. 1985. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. 2005). 2002).niehs. 2007). Cousins IT.. Drug Metab Rev 1989.html. References Agency for Toxic Substances and Disease Registry (ATSDR). Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. phthalates have been shown to induce peroxisomal proliferation in rodents. Schroeder JL. Evaluation of a recombinant yeast cell estrogen screening assay.. 2007. Dirven HA. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . at very high levels. 2004. and race/ethnicity (Silva et al. variation also occurs in the same person during repetitive monitoring (Fromme et al. 105:734-742. 2002). phthalates produced anti-androgenic effects by reducing testosterone production and. Springer. and Sertoli cell abnormalities in the male animals and.New York. 2002. Toxicological profile for di-n-butyl phthalate update [online].. Herbert AR. 2001. and extent of metabolite conjugation to glucuronide (Albro et al.3. 2004. but there are known species-related differences in the hydrolysis of diester phthalates. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. reducing estrogen production. Connor C.... Corbett JT. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. Toxicological profile for di(2-ethylhexyl)phthalate update [online].e. Available at URL: http://www. Scotter MJ. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. Hoppin et al.gov/toxpro2. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. Environ Health Perspect 1982. Coldham NG. 2000c. Peck and Albro. Food Addit Contam 2001. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. 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. Hauser et al.gov/ reports/index.. Needham LL. Massey RC.. McKee et al. The Handbook of Environmental Chemistry. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). 2004). at higher doses. dibutyl phthalate (DBP). testicular atrophy. 2004. which may be a pathway to the development of liver toxicity and cancers in these animals. Population estimates of concentrations of specific phthalate metabolites may differ by age. Silva MJ. Also. pp. 1982. Metabolism of di(2-ethylhexyl) phthalate. Anderson WA. Slakman AR.. 2000a. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Clark K. Jordan S. Matthews HB. 2004.atsdr. Calafat AM.atsdr. 2006).gov/ toxprofiles/tp9. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. 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. In animals. Information about external exposure (i.. gender. interactions with macromolecules and species differences in metabolism of DEHP. Albro PW and Lavenhar SR. Springall C. ovarian abnormalities in the female animals (Jarfelt et al.18(12):10681074. 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. However. J Chromatogr B 2004.45:19-25. 4/20/09 Albro PW. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www.21:13-34.. Sauer MJ. 227-262.html).cdc.. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels.html. Available at URL: http://www. Rhodes et al. Environ Health Perspect 1997. 2001).gov/toxprofiles/ tp135. NTP-CERHR.html. atsdr. Silvapathasundaram S. These differences may contribute to species-specific differences in toxicity (ATSDR.. Pharmacokinetics. 2006).cdc. Vol. Kessler et al.nih. McDonnell DP. Assessment of critical exposure pathways. Dave M.

Drexler H. Research Triangle Park (NC).gov/chemicals/ phthalates/dbp/dbp-eval. 2006 [online]. Yoshimura M. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride.103:582-587.26(8):1219-24. McKee RH. Ryan L. Hartle RW. Available at URL: http://cerhr. Research Triangle Park (NC). The estrogenic activity of phthalate esters in vitro. Mortensen GK. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Liss GM. Hauser R. 6/2/09 NTP-CERHR. Ryan L. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Toxicol Appl Pharmacol 2004. Koch HM.111(2):139-145.niehs. Mechanisms of phthalate ester toxicity in the female reproductive system. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Grote K. Hagmar L.64(8):555-560.105:802-811. Wang P. Calafat AM. Harris CA.25(2):293-302. Baird DD. Skakkebaek NE. Jarfelt K. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP).nih.nih. 6/2/09 Okubo T. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.382:10841092. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Davis BJ.195:142-153. Environ Health Perspect 1998. Reproducibility of urinary phthalate metabolites in first morning urine samples. Pan G. Bolte G. Tsukino H. Hass U. Numtip W. Dalgaard M. Meeker JD. Davis BJ. Richthoff J. Zhang S. Meeker JD. Giwercman A.210:21-33. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Angerer J. Kano K. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Reprod Toxicol 2005.html. Kessler W. Albro PW. Calafat AM. Skerfving S. NTP-CERHR. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. 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 . Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).nih. Research Triangle Park (NC). Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. 6/2/09 NTP-CERHR. Kano I.46(11):643-647.112(17):1740]. Stringer WT. 2000b [online]. White R. Environ Health Perspect 2004. Environ Health Perspect 2002. Sumpter JP. et al. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic.html. Silva MJ. Hum Reprod 2007.22(3):688-695. Chen Z. Jobling S. Silva MJ.16(4):487-493. Andersson A-M. Sumpter JP.niehs.gov/chemicals/dehp/dehp-eval. Scand J Work Environ Health 1985.110(5):515-518. Csanády G.11(5):381-387. Yokoyama Y. Chahoud I. Duty SM. 2000a [online]. Gans G. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Filser J.112(17):1734-1740. Nielsen J.106(1):23-26. Brock JW. Am Ind Hyg Assoc J 1985.niehs. Hoppin JA. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Ladefoged O. Rylander L.niehs. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Reynolds T. et al. 6/2/09 NTP-CERHR. Fromme H. Reprod Toxicol 2004.18(1):122. Main KM. Henttu P. et al. et al.html. Hauser R. Singh NP. Int J Hyg Environ Health 2007. Milligan SR. Borch J. Available at URL: http://cerhr. Available at URL: http://cerhr. Environ Health Perspect 2003. Brock JW. Butala JH. Environ Health Perspect 1997. Balasubramanian AV. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. David RM. Akesson B. Leffers H. Parker MG. consumer milk.Phthalates in human urine samples.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Park S. Hanaoka T. 2000c [online].nih. Park MG. Biol Pharm Bull 2003. Suzuki T. Lovekamp-Swan T.html. Int Arch Occup Environ Health 1993. Boehmer S. gov/chemicals/dehp/dehp-eval. Anal Bioanal Chem 2005. Silva MJ. Environ Health Perspect 1995. Available at URL: http://cerhr. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Epidemiol 2005. 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Environ Health Perspect 2004. Urinary levels of seven phthalate metabolites in the U.58:339349. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Batten PL. Toxicol Sci 2000. Ostby JS. 112(5):A270].46:282-293. Cunningham ML. Klinefelter GR. Fielden MR. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Wu ZF. Pratt IA. et al. Peters JM. Silva MJ. Environ Health Perspect 1982. Orton TC. Bratt H. Matthews JB.Phthalates phthalate (DEHP): a cross-sectional study in China. Meek MD. Barlow NJ. Environ Health Perspect 2006.36:459-479. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Jackson SJ. Lambright CR. Rusyn I. Albro PW. Toxicol Sci 1998. Environ Health Perspect 1986. et al. Rhodes C. Hodge CC.112(3):331-338. Abbott BD. Crit Rev Toxicol 2006. Fourth National Report on Human Exposure to Environmental Chemicals 261 .114(11):1643-1648. Clemons JH. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Malek NA. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat.65:299-308.45:11-17.S. et al. Caudill SP. Zacharewski TR. Parks LG. Reidy JA. Peck CC. Barr DB.

2) 66.8-121) 79.2-17.1) 31.1 (19.8 (10.8) 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 16.5-97.1) 32.3 (29.7-16. residents (Blount et al.5 (27.9-30.2-20.1) Selected percentiles ( 95% confidence interval) 50th 17.Phthalates Benzylbutyl Phthalate CAS No.3) 13.3-21.2 (25.5-35. and 03-04 are 0.7-16.8-76.6-92.9-87.1-16.8-14.7-13. High dose BzBP and its monoester metabolites.1-61.9-190) 86.0-55.8.3 (29. some personal care products.2-39.8) 24.6 (32. and 2003-2004 were generally similar those reported in U.3 (12. and diet is the major source for general population exposure.1-38.4) 14.4 (27.1) 67.6) 37.0) 24.5-145) 138 (106-241) 143 (127-179) 120 (99.6-18.1 (20.0 (12.4 (13.3-74.3) 23.4-127) 80.0 (15. 0.8-17.2) 78.4 (63.5-36.1 (14. car care products.1 (55.4) 129 (98.8 (86.9) 14. interval) 15.8) 63.1) 12.8 (30.4) 108 (96.7-15.8 (50.1-90.2) 15.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. can produce developmental and reproductive toxicity in rodents.7-17.0 (26.2-38.7 (82.4) 71.0 (20.8-35.2 (43. it can be released into the ambient air during use or disposal of the products.0-106) 58.9-14.6) 95th 103 (94.2 (10.3 (12.7) 40. and to a lesser extent.1-15.1) 29.8-13.5-84.2-115) 113 (91.4 (29.5-25.4 (10.S.0 (11.5 (67.7 (12.4) 51.2-183) 101 (78.9-16.2-31.6) 67.4) 80. Food crops take up BzBP.1 (10.8-72.2) 13.9 (22.6) 25. 2004.7 (70.1-214) 166 (116-191) 145 (110-213) 88.5-62.1 (13.5 (76.3-91.6-150) 94.4 (32.3-82.1) 76.9 (13.3) 94.8 (71.5) 82.5 (55.4 (68.7 (11.0) 34.5-40.0 (27.8) 14.9) 18.6 (21.5-33.0) 33.0) 16.8-48. NTPCERHR.0) 20.6) 13.1 (14.5) 30.6) 29.8 (53.2) 12.0-130) 101 (86.9) 13.3) 54. because it is not bound to products in which it is incorporated.8-14.0) 23.3-88.6) 14. 262 Fourth National Report on Human Exposure to Environmental Chemicals .5-18.5) 55.1-16.9) 43.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.9 (12.3 (54.2-40.3) 63.6 (41. including MBzP.1-35.3-161) 99.5) 27.2-19.3) 37.9) 49.7 (53.9 (16.6) 63.3 (33.9 (39.5 (47.1 (13.0 (14.2) 33.4 (48.6) 35.0 (43.8 (14. sealants.9) 11.3-125) Total 15.5) 65.3 (44.2 (47.8-16.4 (53.5) 15.8 (28.3 (22. see Data Analysis section) for Survey years 99-00.2) 22.6-92.6) 13.2-33.4-15.9) 12.9-49.9 (21.8-98.0 (33.1.6-43.3-130) 122 (88.4 (32.8) 33.2 (14.4) 38.7 (13.9 (28.8 (71. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.4) 75th 35.4) 12.6) 15.4 (53.5-41.5) 15.8 (38.6-132) 103 (84.6-39.8-16. vinyl tile.7-82.3.6 (13.3-75.7) 38.9-28.4-16.3) 15.7-14.8 (80.3-43.2 (11.3-27.7 (15.9 (12.7-35. population from the National Health and Nutrition Examination Survey.3) 13.6-116) 122 (102-142) 101 (85.1-15.0 (34.1) 13.6) 35.0) 90th 67.0 (23.4) 65.9 (11. BzBP can be released into the environment during its production and.7) 23.4) 81.9) 15.5 (13.6-72.3-12.1-43.3 (30.6 (12. and 0.7-172) 103 (74. 2000).6 (13.2 (19.4) 35. particularly male animals (McKee et al. 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.0-85.8 (12.5 (66.0 (30.6) 50.4-62. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6-79.7-16. 2000).0 (55.3 (12.S.8-17.4 (31.2) 14.2) 17.6 (13.4 (59.7 (80.5) 23.5) 16.3-18.5 (61.2-16.5-94.6) 14.4) 49.6) 16.4-25.4) 33.2) 69.4) 98.2) 32..2-116) 122 (102-143) 101 (84.5-36.6-29.4-24. 01-02.3-18.1-18.6 (13..9-47.0-26.8-41.0 (15. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.0) 70.8-133) 89. 2001-2002. respectively.6 (53.7-58.6) 24.9-62.1 (58.9-27.4-92.3-34.5 (57.2) 14.7-25.2 (19.8-18.8-64.6-17.1) 68.7-170) 169 (134-198) 152 (99.7-119) 99.8) 28.9 (70.2-155) 91.0 (30.4-120) 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 13.6-38.4 (10.8 (21.2-16.9) 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 39.3 (13.1-116) 122 (93.6 (66.1-39.1-120) 52.1) 14.5 (26.4) 35. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.1 (32.9) 14. IARC considers BzBP not classifiable with respect to human carcinogenicity.7 (51.5-14.0) 32.

5-16..9-104) 62.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.8-13.9 (15.6-20...6) 25.3 (15.5) 13.7) 25.6 (34.6) 12.8-13.0 (62. Urinary Mono-benzyl phthalate (MBzP) (creatinine corrected) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0-109) 65.0) 12.4) 60.1 (43.9-16.7 (14.5) 23.7 (13.0-53.3) 13.8) 68.6 (24.8-14.1 (21.0-48.9-13.4-18.7-12.6 (11.1-120) 77.7-90.7-14.5) 78.2-117) 95.8 (49.1 (14.9) 12. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.0 (67.8-85.3) 14.0-15.4 (11.2-51.0 (11.9-23.7 (11.3-73.4-99.0-51.7) 38.3) 18.7) 46.1-27..9-62.6) 53.5) 20.9-69.8-69. 2003).5-29. Hauser et al.8-14.7-31.4 (10.4 (60.5-76.4 (13.1-125) 86.0 (10.5-13.5-23.3) 37.3) 89..9 (9.1 (21.6-86.7 (19.3-38.0) 24.5 (11.8) 24.3 (39.1 (11.5-31.6-81.8-80.8) 108 (75.1 (9.7-123) 77.3-11.3 (12.4 (74.6 (30.7 (11.4-102) 70.1 (34. 2002.4) 25.5) 46.4 (34. Weuve et al.Phthalates York City (Adibi et al.5-38.9) 52.2) 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 12.4-93.1) 12.4) 21.7 (59.6-13.7 (23.3) 55.4-116) 73.1) 35.9 (10.7-29.1-14.6 (14.6) 73.9) 42.8 (50.8-42.5 (10.1 (18.4 (25.6-15.8) 53.95-14.2-15.5-99.7 (38.2) 11.0) 49.9 (29.8) 33.5-79.2) 32.6 (19.1 (19.2 (56. Hoppin et al.8) 71.6 (11. adolescents compared with adults.5 (42.2-26.4-90.5-57.0 (13.4) 17.1-12.1-58.2-15.9) 12.9 (51.9 (24.8) 56.8 (69.8) 16.3 (23.4) 44.4) 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 12.69-11.7-19.2) 67.4) 104 (89.0 (49.9 (12. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.2 (41.7) 19.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .7-14. in men attending a Boston infertility clinic (Duty et al.7 (11.7-69.4) 13.4 (46.6) 58.8 (12.3) 29.3-34. A small study of African-American women in Washington.6 (36.6-47.8-64.S. 2007).3) 14. In an annual sample of German university students. 2005.1) 39.0 (38.1 (25.73-12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4) 15.9-115) 57.1) 24.5 (49.1 (53.8) 34.5) 16.3) 12.0) 15.8 (46.3) 21.4-14.5 (12.4-60.8) 46.4 (26.8) 26.6 (51.4) 90th 50.4) 28.6-40.5-42.1) 17.9 (22.8-16. Limited studies in children younger than 2 years old have found median and geometric mean urine MBzP that were similar to children aged 6-11 years in the NHANES subsamples (Brock et al.7) 11.1 (21.4-27.6) 30. 2004).1-29.9 (10.5 (9.7-15.9 (55.5) 14.0 (12.7) 56. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.3-64.7 (54.0) 60.8-173) 195 (121-305) 229 (99.8-39.7-20.2-13.9 (24.2) 15.5 (35.8-13.4 (11.8 (10.8) 13.6 (22.3) 13.5-58.0 (41.8) 33.1-79. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC. 2002).0) 13. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.9) 12.9-83.2) 12.1 (23.4-14.4-19. 2003).1) 142 (99.2-21.8 (13.1 (41.9 (15.5) 17.3) 16.2-57.5-213) 49.. 2007).8 (57.7-61.8) 11.2-17.2) 11.4) 14.4 (21.6-99.0) 24.7-15.8-34.1 (46.9) Total 14.6) 75th 25.3 (38.4-23.4) 13.0 (12.3 (24. and in a small sample of German residents (Koch et al.4 (69.8-15.3-16. population from the National Health and Nutrition Examination Survey..1) 80.9) 64.. and females compared to males (Silva et al.9) 11.0 (33.6-12.9-13.3) 36.8-27.5) 10.4) 12.9) 100 (80.2-78.4 (12.8) 54.5-61.8) 80.9-28.4-142) 134 (116-176) 136 (85. interval) 14.5) 95th 77.6) 13.7 (21.9-40.2 (27. In NHANES 1999-2000.0-26.8 (64.3) 90.8) 15.3) 73.8 (30.2-12.4-42.2) 11.1) 23.4 (11. 2005).6) 38.4 (33.7-20.7-56.4) 50.5 (48.0-27.9 (39.2) 26.3) 13.0 (41.4 (63.9) 11.9) 24.4-15.7 (18.0-90.6) 12.8) 53.4-79.9 (12.7 (13.6 (57.3 (35.5 (10.7-397) 70.9 (43.6 (15.2-13.0) 11.8-60. 2004.6-26.1 (21.9 (54.7 (12. in young Swedish men (Jonsson et al.5 (56.3) 67.4-17.1 (15.3 (13..6 (11.7-19.9-14.1) 24.1) 27.5) 41.2 (69.1 (13.7 (55.1 (13.3 (60.0) Selected percentiles ( 95% confidence interval) 50th 13.5-26.7) 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 40.8 (11.2-49.4) 51.6-116) 74.6 (30.5-58.5-26. 2006).8-48.2 (40.1-35.1-12.8-15.

Poland. et al. Gans G. Baird DD. Singh NP. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Caudill SP. Reidy JA. Meeker JD. Perera FP. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://cerhr. Hagmar L. Epidemiol 2005. Koch HM. Ryan L. Environ Health Perspect 2000. Calafat AM. Angerer J. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Duty SM.111(14):1719-1722.93:177-185. Hu H. NTP-CERHR. Reprod Toxicol 2004.html. Caudill SP. Atlanta (GA).18(1):122. Weuve J. Phthalate monoesters levels in the urine of young children. 2000 [online]. et al. Silva MJ. et al. Caudill SP. Sanchez GN. Barr D. Ryan L. 112(5):A270].niehs. Needham LL. Environ Res 2003. Silva MJ. Sampson EJ. Camann DE. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Brock JW. Malek NA.nih.S. Reproducibility of urinary phthalate metabolites in first morning urine samples. Hum Reprod 2007. Chen Z. Jonsson BAG.114(9):1424-1431. Butala JH. Rossbach B. Green RA. Brock JW. Koch HM. Prenatal exposures to phthalates among women in New York City and Krakow. Helm D. Hoppin JA. McKee RH. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Barr DB. Environ Health Perspect 2004. Hodge CC. Wittassek M.110(5):515-518. Richthoff J.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Brock JW. Jedrychowski W. Drexler H. Urinary phthalate metabolites and biomarkers of reproductive function in young men.22(3):688-695.210(3-4):319-333. Davis BJ. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Levels of seven urinary phthalate metabolites in a human reference population. 2005. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Urinary levels of seven phthalate metabolites in the U.16(4):487-493. Jacek R. Eckard R. Hilborn ED. Wiesmuller GA. Dobler L. et al. Environ Health Perspect 2003. Int J Hyg Environ Health 2007.25(2):293-302. Centers for Disease Control and Prevention (CDC). Schettler T. Silva MJ. Silva MJ. Hauser R. Giwercman A. et al. Needham LL. Environ Health Perspect 2002. Pirkle JL. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.68:309-314.112(3):331-338. Research Triangle Park (NC). et al. Duty S.108(10):979-982. J Androl 2004. Bull Environ Contam Toxicol 2002.Phthalates References Adibi JJ. Environ Health Perspect 2006. Blount BC. Rylander L. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). 264 Fourth National Report on Human Exposure to Environmental Chemicals . 4/20/09 Silva MJ. Calafat AM. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. David RM. et al.

30-6.00) 4.90 (3.5) 23. 84-74-2 Di-isobutyl Phthalate CAS No.0) 9.S.30 (4.30) 5.10-9.46 (2. 2007)...20 (7.2 (8.4 (14.5) 14.28-5. residents (Blount et al.81 (3.60) 3.4 (20. 2005). about 65% to 80% of a dose is eliminated in urine within 24 hours.2) 5.50 (3.30-2. and insecticides.1 (13.30-3.6-14.40-12.10 (4.40) 5.6 (14.00 (7.4) 5. 2003).7) 18.50) 90th 12.0) 13. In addition. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.5-29.40 (3.3 (16.70-4. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.6-26.49-2.60 (5.7-20.6 (13.30-13.5) 22.0-14.0) 24.0-18.50) 18. 2001).80 (5.22 (3.30-7.11-3.7) 15.82-3.0 and 0.5 (17.97) 4.00) 6.3-18. 2000).33 (2.0) 20.6 (13.90-4.3.22) 3.68 (2.6 (11.46 (3.56 (5.40-3. Following oral administration of DBP to humans.20) 4.20) 7.55 (3. 2004.70) 5.07 (3.63) 3.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.5 (20. Koch et al.97-7.5) 18.20-9.0 (11.3 (11.50-2.84) 4.20-6.30) 6.44-2.10-2. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.67 (5.3 (19.46-5.10-9.90-4. and in a small sample of Japanese adults (Itoh et al.50 (6.5-24.80 (2.30-6.9) 15.00) 4.7 (16.90-7.0 (13.30) 10.8 (9.1 (8.3-24.5-16.02) 4.10) 3.7-31.72-3.6) 17. NTP-CERHR.0) 12.91) 4.6-20.8) 21.00) 7.3 (13.3-48.2-14.90 (4.6) 16.9) 10.6) 16.5 (10. 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.97) 2.1-25.5) 25.90) 12.10) 2.6 (29.50) 7.50) 2.0-38.1-17.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.8) 677 652 703 699 1216 1088 Limit of detection (LOD.3) 33.40-3.. DBP can produce reproductive toxicity in male rodents (McKee et al.10 (3.5 (27.3-20.6) 17.73 (2.9-14.00-11.3-43.40-4.7 (18.66) 2. interval) 2. Studies of children found age-related differences in urine MBP levels.80-5. Fourth National Report on Human Exposure to Environmental Chemicals 265 .8) 40.80 (5. CDC.20-12.4-27.48 (2..00-6. 2005).3-19. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.2-22.80) 75th 5.7) 4.90 (4.0 (19.1-12. 2005.50) 8.. Biomonitoring Information Median concentrations reported in the NHANES 19992000.7 (17. 2003).40-5.. 2000.20-12.10 (4. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.40 (2.10) 11.26 (2.40-4.3 (18. they have been referred to as monobutyl phthalate (MBP).5) 12.00-9.56 (3.40-9.70 (2. OSHA has established a workplace air standard for external exposure to DBP.1) 16.10) 8.40 (2.40-17.50) 5. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.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 2.7 (9.1) 25.3) 18. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.24-8.4) 12..30) 10.6) 12.7 (17.43) 6. in a small sample of pregnant women in New York City (Adibi et al.50-4.9-23.20 (6.71 (2.60 (2.4) 22.70) 3.0 (13.37) 6.90 (6.40 (7.5 (11.6) 26.3-30.30-11.6-34.00-4. Survey Geometric mean (95% conf.6 (10.30 (1. 2005).00 (5.10) 9. population from the National Health and Nutrition Examination Survey.70 (5.2 (12. Hauser et al.2 (11.5-16.20 (3.70-4.55) 2.17) 4.6) 10.80-5.1) 22.20-2. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.5) 18.80 (2.7 (7.5) 19.9 (16. 2004.2-33.9 (16.90-2.6 (14.85-6.60-6.60 (8.56) 3.3 (13.7-18.1-20.Phthalates Di-n-butyl Phthalate CAS No. in men attending a Boston infertility clinic (Duty et al.17 (2.60 (4.46) 2. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.3) 3.3 (16. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.6 (10.7) 14.50-6.6-18.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.00-6.73-5. mostly as MnBP (Anderson et al.19-3.0-25. When total DBP metabolites have been measured..96) 3.00) 10.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3. pharmaceutical coatings. and also in some printing inks.40 (6.6 (9.7) 7.59) 3.S.80 (3.50-10.30 (3..4-12. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.30) 2.70-8.7-31.56-4.

00-3.08-2.54 (4.1) 7.81 (6.2) 24.73 (5.74 (4.33 (2.0) 15.67-5.69) 4. 2005).56) 2.6 (10.9-26.82 (4.68) 3.56-4.7 (21.6) 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 2.31 (2.98 (2.57-4.1-25.9 (11..4) 23.03 (5.58-4.6 (8.62-12.1) 11. 2007).Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.55-6.91-6.04) 3.80) 7.46-11. Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.33) 3.53-3.34 (3.8 (9.20 (7.37) 3.65-11.99-4.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.3) 13.31) 2.4) 7. ranging from more than one-tenth the NHANES median (Itoh et al.20 (2. respectively.02-10.00-3.3) 16.02 (7.18) 3. samples from German university students had consistently higher median urine levels of MnBP and MiBP.6) 11. An analysis of NHANES 2001-2002 showed similar age.8-13.11 (5..20-3.25) 5.79-6. Weuve et al.66) 10.7) 3.27-12.1-15.6-19.. 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.15) 3. 2006).1) 15.07-5.7) 19.30) 2.54) 2.81) 9.96 (3.76-3.0 (10. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.00-7.95) 10. Finding a measurable amount of MnBP or MiBP in urine does not mean that these levels or the parent compound cause an adverse health effect.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.78) 9.29-8.18 (1.51) 15.1) 13.05) 2. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.81) 4.9-40..32 (7.3 (13.61-3.2-13.52 (2.4 (12. to about two to fourfold higher (Fromme et al.86-4.80 (3.69 (2. than adults in NHANES subsamples during the same time period.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.20-4.21 (5.44 (3.6 (15.13-6.76-3.47 (3.72-7.45) 3.38 (6.9 (15.53-4.78-8.69-7.59 (4.5 (11.5) 15.33 (3.14 (4.94 (5.46 (2.3) 13.39-3.81 (3.47-12.35) 3.0-18.30 (6..66) 2.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .36-7.11) 5.72) 5.64-7. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.78) 8.18-4.89-5.0 (8.84 (4.85 (2.01-2.80-3.86) 6.5 (9.21) 10.4-16.5) 13. 2007).7) 11.6 (8.99) 7.32 (3.62 (6.7 (11.26-2.2) 9.66) 4.38-10.4) 15.57 (3.10-5.9-16.75 (6.13 (2. the students’ median values for MiBP levels remained relatively unchanged.20-2.2) 8.68 (2.43) 3.39) 5.7-28.68) 5. 2004).6) 13.3) 28.1 (11.31) 2.22 (2.92 (7.93-6.95) 2.18-10.6 (12.28 (4. interval) 2..7 (13.20 (2.2-15.8-18.76 (3.0) 11.74-3.65-4.0) 7.42) 2.79 (4.76-15.17 (2. 2004).58-3.24) 3.and gender.83 (2..94-12.18 (4.1-12.64-7.43) 3.15-4.82) 4.43) 3.9) 12.97-2.9 (9.S.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.31 (7.04-5.46) 3.94) 6.89) 6.66 (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.28-13.65 (4.8 (10.2 (11.0 (12.51) 2.26 (2.47-5.56-15.11-2. 2005).1) 10.33-9.17) 90th 8.36-2.64-10.1) 4.6 (9.0) 3.88 (2.54 (2.03-11.00 (3.03-7. Over this time.89 (3.1 (10.79-8.75 (4.5-19. 2002.95-3.52-3.08) 75th 4.56) 5. Survey Geometric mean (95% conf.1-24.07 (2.51) 5.41 (2.8 (8.8-18. Between 1998 and 2003.84 (8.69) 6.53-5.8-36.04) 7.52) 3.7 (9.18) 4.09-2.3 (17.6-19.29-3. In an analysis of NHANES 1999-2000.3) 18.7) 10.32) 7.52-20.19 (2. population from the National Health and Nutrition Examination Survey.8) 10. while MnBP declined (Wittassek et al.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.57 (3. up to four and 13 fold.17-12.2 (10.

2 (17.3) 36. and 0.2-93.7-124) 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. interval) 24.6 (22.0-24.1 (58.1-22.2 (74.0) 117 (104-131) 112 (84.8) 75th 51.3-21.1-27.4 (36.3) 23.9) 46.5 (74.8-132) 95.5) 78.7-91.5) 20.4-31.7-34.5 (29.1-75.7-111) 64.7-92.5) 65.2 (58.6 (65.8-111) 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 23.6 (19.3-60.4-60.4) 52.8-119) 90.0-51.6) 35.8-22.9-101) 77.5-43.8) 58.8) 23.3 (42.0) 38.5-53.0) 120 (98.4-44.5 (28.9) 21.5-27.2-63.6) 46.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.1) 19.3-76.3 (56.2) 68.4-20.1 (41.1) 47.9-22. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.1-82.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4-25.6) 39.1-51.2) 42. population from the National Health and Nutrition Examination Survey.3-67.1 (17.3) 18. referred to as monobutyl phthalate (MBP).5) 21.1) 23. see Data Analysis section) for survey years 99-00.2) 20.9 (79.1 (19.9-87.0) 31.5-42.6) 21.2-21.3) 26.1-92.4 (23.6 (32.6-40.5-60.6-143) 127 (99.6-44.2 (19.5-47.5-121) 106 (94.2-32.2 (20.0) 27.2 (75.9) 18. 1.4) 20.6) 71.6) 17.2 (78. *In the 1999-2000 survey period.0 (17.5 (59.6-37.1 (16.1) 25.6-29.3) 24.0-32.6-20.0 (45.2) 90th 98.1 (21.1 (26. Fourth National Report on Human Exposure to Environmental Chemicals 267 .0 (78.1.4 (35.1) 17.1 (19.2-114) 73.1) 46.3) 40.1-24.6 (61.4 (19.1 (19.6) 80.7-26.8) 62.5) 17.9) 71.2) 26.0-19.9 (20.6-113) 108 (90.3 (51.0) 20.1) 23.5) 31.9 (17.5) 47.2-49.4 (38.0-58.7-121) 97.1 (36.8-42.6-24.1) 31.6 (90.7 (64.2-87.6-31.6 (44.2 (21.S.5) 34.8-123) 101 (90.2) 38.9-79.3-145) 85.6-49.2-56.7) 42.7-24.5) 37.4) 64.1 (18.3 (23.7-53. 01-02.1 (62.7) 28.1-80.2) 62.4 (25.3-40.7) 124 (98.7 (70.5) 85.1 (19.5-44.0 (72.0 (25.5-47.9-53.7) 52.7 (28.3 (36.7 (16.3 (17.2-159) 92.4 (35.7 (19.8 (57.7-34.2 (59.4-18.0-24.7-117) 118 (108-143) 93.0-26.8 (19.9) 26.7-127) 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 22.5) 26.4) 22.9 (17.9) 36.2 (21.6 (48.1 (34.4.7) 92.1) 30.1 (28.7-116) 95.3 (23.0) 84.7 (24. respectively.4 (21.1 (51.0-73.5) 24.1-20.3 (30.1 (31.0 (36.4-159) 107 (84.2 (18.3 (30.0 (23.7 (33.0) 21.6-36.9 (79.5) 19.2-23.5-117) 95.4 (35.3-24.7 (18.8) 19.7-106) 69.3-96.1-29.1 (54.4-42. and 03-04 are 0.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.5) 95.9-92.2 (79.0 (30.0 (20.6) 38.6 (55.9-28.3 (60.4-26.3-136) 137 (107-162) 119 (90.8-29.7 (38.5 (30.9-42.7-42. Survey Geometric mean (95% conf.2-24.6-29.3) 19.2 (25.7 (51.9.7-20.7 (43.0 (15.7) 74.9-114) 116 (97.1) 23.8) 48.9-22.5 (59.4 (71.5) 40.6-48.1) 36.3 (37.9) 75.2-22.6) 20.3) 21.8-25.4 (84.0 (18.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.7 (18.0 (31.1) 20.2) 32.0-19.9) 29.9-33.6 (26.3-85.5) 36.4 (72.0) 30.3-79.7 (22.8) 43.7-42.4 (35.5) 36.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.6-33.0-21.2-33.4) 59.6-69.6 (16.

5 (14.1) 44.6 (29.3 (28.3-40.9-36.9) 30.0 (50.6-16.6-53.0) 41.1-83.0 (16.3-71.6 (27.5-15.5-142) 81.8) 17.9 (56.6-92.7 (14.5-41.1 (32.0-75.1) 35.8) 19.1 (34.2) 21.2-21.8) 34.6 (74.5 (30.6-50.2-85.5-23.7-80.0-90.2-106) 64.8 (18.3-26.0-41.8) 34. interval) 22.4-65.6) 18.6-23.3) 19.6-44.3) 21.0-60.2 (19.4-103) 117 (83.0 (52.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.6) 14.0-92.9-56.5) 91.4) 19.6 (25.8 (33.1) 22.9) 24.1 (46.2) 59.4-72.3 (42.0 (18.0) 94.9) 52.7) 19.1) 17.9 (37.6) 34.5 (15.5) 84.9) 19. Survey Geometric mean (95% conf.6) 31.6-24.7 (60.0 (26.2 (83.9-38.2 (16.7 (57.3) 59.3 (17.1-21.9-100) 86.6-24.3-78.7-78.8 (22.7) 42.8 (16.5) 17.0-47.7-42.6-42.3 (71.9 (16.0 (27.9-26.0) 19.6-28.5-18.6) 64.3-17.6) 25.1-99.4 (53.0 (34.4 (18.6-44.4 (50.9 (73.8 (65.3-18.4 (17.0 (20.5) 90th 68.3 (21.2-48.8-43.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.6-19.3 (55.5) 21.4-164) 96.9) 62.6-119) 63.3 (24.3 (60.8) 22.7-51.8) 40.1 (29.7 (54.0) 53.7 (19.1-32.9 (58.6 (41.3) 33.4 (50.4-131) 81.1) 20.9 (20.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.3-106) 74.0) 59.5) 60.3-38.3) 17.9-105) 85.3-23.7 (73.6-155) 91.4-47.4 (23.3) 52.1-23.4 (20.6-26.2) 16.9) 28.9) 14.5-76.5-64.2-73.8 (17.5-70.9 (39.1) 50.3-39.2-61.4-61.1-18.1-99.7-21.1-62.2-22.8) 75th 38.9) 39.1) 37.1 (21.9-70.8-32.9) 91.9) 20.2-22.8) 17.4 (16.9 (35.4) 15.4) 62.0) 29.4 (37.0 (61.7 (27.5 (18.6 (61.8-24.8 (18.1-128) 97.8 (50.6) 38.9 (35.0 (15.5-21.4 (16.5 (81.7-20.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.7-19.3) 18.5) 82.7 (16.4) 53.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.0) 25.7-26.0 (69.9-34.9-84.0 (71.6) 24.8) 63.7) 36.7-28.3-21.8) 35.7 (12.6 (72.0) 28.3) 20.5-142) 89.9-68.7-23.9 (21.3 (76.3 (52.0 (19.4-76.1) 21.9 (30.2-16.6-27.2-179) 84.0-19.4 (19.3 (16.3-32.8) 30.9 (19.3 (19.7-19.2-86.5) 39.2 (35.5) 134 (93.4 (31.3 (17.9-14.2-28.8-23.1 (15.6) 37.1) 53.9 (30.3) 33.6) 65.4 (33.2-22.3 (48.1) 61. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.7-39.1 (56.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.3-21.3) 19.9) 49.0) 70.4 (13.4 (45.3 (69.6-22.7 (20.2-18.8) 13.4 (56.5 (18.0) 26.6) 23. 268 Fourth National Report on Human Exposure to Environmental Chemicals .S.5-22.2 (19.0-38.3) 35.9 (30.8 (25.7 (81.7 (43.9-49.8 (13.5-37.9 (64.0) 35.0) 108 (71.6) 24.4) 15.5-16.7 (60.0 (18.6) 39.4) 21.3-81.8) 17.2) 159 (102-263) 147 (93.4 (31.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.8) 20.4-34.4-24.6 (31.0) 81.6-74.6) 83.2) 74.4) 51.6 (17.1) 20.4) 16.8-24.6-32.8) 23.3 (52.6 (57.4 (47.2) 65.4 (68.6-128) 96.4) 20.1 (61.2) 31.4-135) 71.8 (18.3 (17.7) 20.2-27.8-235) 137 (108-198) 88.3-20.5-30. population from the National Health and Nutrition Examination Survey.4 (17.0-17.8) 28.1) 42.6 (25.6-23.8) 20.0) 75.4 (31.0) 55.6 (19.3-49.7-37.3 (46.2 (38.0 (43.5 (64.0-113) 104 (83.6-43.9-68.7 (28.0 (70.3) 67.

Environ Health Perspect 2000. Meeker JD. Weuve J. Perera FP. Blount BC. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Duty S. Hauser R. Prenatal exposures to phthalates among women in New York City and Krakow. Hum Reprod 2007. Caudill SP. Caudill SP. Scotter MJ. Int J Hyg Environ Health 2005.Phthalates References Adibi JJ. Caudill SP. Anderson WA.nih. Drexler H. Food Addit Contam 2001. Singh NP. Calafat AM. Reprod Toxicol 2004. Barr DB. et al. Richthoff J. Giwercman A. Calafat AM. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Hu H. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Masunaga S. Hodge CC. Castle L.210(3-4):319-33.25(2):293-302. Rossbach B. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Ryan L. Wittassek M. Eckard R. Environ Health Perspect 2006. Bull Environ Contam Toxicol 2002. Koch HM. Massey RC. Environ Res 2003. Barr D. Duty SM. et al. Ryan L. Camann DE. Centers for Disease Control and Prevention (CDC). NTP-CERHR. Schettler T. 4/20/09 Silva MJ. Needham LL. Silva MJ. Urinary phthalate metabolites and biomarkers of reproductive function in young men. McKee RH. Urinary levels of seven phthalate metabolites in the U. Koch HM. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Boehmer S. Springall C. Drexler H. Fromme H. Chen Z.gov/chemicals/ phthalates/dbp/dbp-eval. et al.S. et al. Phthalate monoesters levels in the urine of young children.114(9):1424-1431. 2005.93:177-185. Itoh H. Silva MJ. Dobler L. David RM. Atlanta (GA). Available at URL: http://cerhr. Jacek R. Brock JW. Sanchez GN. Brock JW. Hilborn ED. Int J Hyg Environ Health 2007. 2000 [online]. Hagmar L. Silva MJ. Environ Health Perspect 2003. Third National Report on Human Exposure to Environmental Chemicals. Green RA. Pirkle JL.208:237-245.16(4):487-493.html. 112(5):A270]. Epidemiol 2005. Poland. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. et al. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Koch HM. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP).210:21-33. Sampson EJ. et al. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Bolte G.18(12):10681074.68:309-314. Butala JH. Silva MJ.niehs. Angerer J.108(10)979-982. Environ Health Perspect 2004. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Helm D.112(3):331-338. et al. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Jedrychowski W. J Androl 2004. Levels of seven urinary phthalate metabolites in a human reference population. Jonsson BAG.22(3):688-695. Rylander L. Reidy JA. Angerer J. Needham LL. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.18(1):122. Wiesmuller GA. Malek NA. et al. Int J Hyg Environ Health 2007.111(14):1719-1722. Research Triangle Park (NC). Gans G. Yoshida K.

People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.500-.400) < LOD 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.00) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) < LOD < LOD .400 (<LOD-.600) .600) .200-.400) 1.500 (.300) < LOD .300) < LOD . only levels at or above the 90th percentile could be characterized.500 (.300 (.Phthalates Dicyclohexyl Phthalate CAS No. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.300 (. and polymers.400 (.500) 1.2.300 (.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 .70 (1.50) .400 (.300-.00-3.500) 1.00-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.400 (<LOD-.50) .200-.400-.400 (<LOD-.500 (.300 (.400) < LOD < LOD .500 (. see Data Analysis section) for Survey years 99-00.10 (<LOD-1.300-.400-.300-.10 (.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.300-.300 (.400-.300-.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .200 (<LOD-.10 (<LOD-1.400-.00 (<LOD-1.70 (1.200-.500) .900-1.500 (.400 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.200-. and polyvinyl chloride. Survey Geometric mean (95% conf.70) .10) .300 (. In this Report. polyvinyl acetate.S.700) .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.400 (. including nitrocellulose. respectively.200-.500) . 01-02.300 (<LOD-. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.500 (.300-. 270 Fourth National Report on Human Exposure to Environmental Chemicals .400 (<LOD-. and 0.70) .500) . 0.500) < LOD < LOD . < LOD means less than the limit of detection.9.00 (<LOD-1.300 (.90) .600) < LOD .500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (.500 (.400 (.600 (.300-. which may vary for some chemicals by year and by individual sample.600) . population from the National Health and Nutrition Examination Survey.20) .500 (.3.300-.400 (.200-.400-. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.500) 1.500) .500 (.600) .700) .80) . resins.600) .700) .500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. and 03-04 are 0.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00 (<LOD-1.400-.400-.10 (<LOD-2.500) < LOD 1.400) 1.

54) .610 (.170-.270) < LOD .830) 1.690-1.630 (<LOD-.500-.630 (<LOD-.670-1.12-1.74) .18) .10) .44) .54-6.910 (.590 (.11) .34) .690) < LOD 2.500 (.670 (<LOD-.410 (.530 (.910 (.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .560) 1.400-.950 (.250 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.Phthalates Urinary Mono-cyclohexyl phthalate (MCHP) (creatinine corrected) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.710) .420-.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 1.770-1.53) .310-.450 (.43 (1.17) .14 (<LOD-3.770) < LOD 2.00) .380-. Survey Geometric mean (95% conf.660) < LOD < LOD .500) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .470) 3.530) 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.620) < LOD .220 (<LOD-.910 (.790-1.500) 3.590 (<LOD-.690) < LOD < LOD .330 (.770-1.420-.510 (.880 (.33 (<LOD-3.360-.910 (.770-1.510-. population from the National Health and Nutrition Examination Survey.350-.260-.16 (<LOD-3.S.530-.660) .240-.740) < LOD < LOD .470 (.67 (1.370 (<LOD-.00 (<LOD-3.16) .690 (.310) < LOD .82 (1.450 (.940 (.420-.330 (.480 (.54 (<LOD-2.740) .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 .380 (.800-1.390 (.290-.33) .490) .530) 1.06) .53) .22 (<LOD-1.82) .770 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.06) . Fourth National Report on Human Exposure to Environmental Chemicals 271 .05) .400-.36-1.530-1.

and 03-04 are 1. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.Phthalates Diethyl Phthalate CAS No. soaps. see Data Analysis section) for Survey years 99-00. 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...4 (62.S. colognes. and also in men attending a Boston infertility clinic (Hauser et al. population from the National Health and Nutrition Examination Survey. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 2007). 01-02..3 (82. DC (Hoppin et al. and 0. 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.2. shampoos. 2002).3-103) 193 (141-256) 184 (148-227) 221 (165-294) 180 (140-221) 181 (152-212) 188 (158-219) 197 (129-249) 183 (142-217) 196 (170-241) 564 (419-818) 479 (387-651) 557 (432-695) 482 (390-590) 498 (441-567) 533 (471-629) 378 (290-730) 451 (315-636) 521 (295-571) 1510 (1050-2150) 1260 (983-1480) 1250 (973-1560) 1340 (1010-1660) 1350 (1060-1660) 1590 (1220-2070) 756 (379-1070) 808 (572-1090) 827 (542-1440) 3260 (1550-4420) 2070 (1470-3050) 2310 (1360-3310) 3480 (2230-4640) 2720 (2160-3670) 2980 (2250-3800) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 179 (149-215) 182 (157-211) 197 (173-224) 178 (154-206) 174 (153-198) 189 (160-225) 154 (119-197) 171 (139-199) 171 (148-201) 174 (138-210) 167 (139-194) 182 (138-219) 523 (372-650) 502 (419-603) 536 (449-654) 425 (350-508) 427 (387-498) 478 (392-564) 1440 (1020-2280) 1450 (1060-2110) 1520 (1210-2070) 988 (880-1230) 1050 (879-1310) 1260 (969-1640) 3500 (2130-4560) 3100 (2110-4390) 2910 (2210-3480) 2230 (1370-3880) 1860 (1490-2500) 2590 (1800-3420) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 181 (157-209) 226 (195-262) 267 (239-298) 322 (275-377) 352 (324-384) 357 (310-412) 152 (133-175) 158 (141-178) 167 (145-193) 174 (146-210) 220 (190-264) 249 (212-307) 306 (256-350) 357 (290-407) 306 (253-414) 134 (108-157) 147 (119-177) 148 (125-175) 441 (390-541) 530 (444-660) 597 (523-688) 789 (635-949) 853 (709-1090) 948 (769-1150) 367 (287-482) 413 (366-451) 418 (366-477) 1280 (851-1510) 1490 (1050-2110) 1640 (1320-2180) 1890 (1410-2270) 2160 (1620-2470) 2500 (1840-2980) 986 (798-1340) 1020 (905-1230) 1210 (954-1480) 1720 (1460-2130) 2630 (1540-4460) 3050 (2230-4300) 3610 (2130-4640) 3540 (2810-5070) 4370 (2780-5910) 2470 (1590-3880) 2320 (1560-2720) 2250 (1590-3290) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2-102) 95. 0. Biomonitoring Information MEP levels in the NHANES 1999-2000. particularly those containing fragrances. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.7 (70.7) 71. 2003) and African-American women in Washington.5) 81.3 (74. In contrast. respectively. deodorants. 2001-2002.4. Products that may contain DEP include perfumes.1-93. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9-92.1 (71. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. 272 Fourth National Report on Human Exposure to Environmental Chemicals . and hand lotions.8-111) 85.9. 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 91.9 (61. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.

Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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.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 .5-113) 122 (93. 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.S.6 (77. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (66.3-105) 87. Urinary Mono-ethyl phthalate (MEP) (creatinine corrected) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.9-110) 96. In an analysis of NHANES 1999-2000. the adjusted geometr