2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

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4'.3.5.gov/exposurereport/chemical_selection.4.4.5'-Hexabromodiphenyl ether (BDE 153) 2.5'-Tetrachlorobiphenyl (PCB 44) 2.2'.4’.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.2'.4.What’s New in this Report What’s New in this Report In this Fourth Report.5’.4.6-Heptabromodiphenyl ether (BDE 183) 2.2'3.2'.2-Dichloroethene Dichloromethane (Methylene chloride) 1. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.2'.4.5'.4. The process for selection is described at http://www.4'-Tribromodiphenyl ether (BDE 28) 2.4.cdc.2'.2'.4.4.2.2'.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.3.4'.2'4.1.2-Dichloropropane 2.2-Trichloroethane Trichloroethene (Trichloroethylene) m.1-Trichloroethane (Methyl chloroform) 1.4'-Tetrabromodiphenyl ether (BDE 47) 2.3-Dichlorobenzene (m-Dichlorobenzene) 1.2-Dichlorobenzene (o-Dichlorobenzene) 1.3.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.5.5-Pentabromodiphenyl ether (BDE 99) 2. Paradichlorobenzene) 1.3.6.4'.5.4. Table 1.4’. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.1.4'.2’.5. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.5'-Tetrachlorobiphenyl (PCB 49) 2. 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 (2.4'.4-Dichlorobenzene (p-Dichlorobenzene.4.1-Dichloroethane 1.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .1-Dichloroethene (Vinylidene chloride) cis-1.4-Tribromodiphenyl ether (BDE 17) 2.4.2'.4'-Pentabromodiphenyl ether (BDE 85) 2.4'-Tetrabromodiphenyl ether (BDE 66) 2.3-Tetramethylbutyl] phenol) Triclosan (2.3’.html.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.1.2-Dichloroethane (Ethylene dichloride) 1.3'.1.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.2'.6'-Hexabromodiphenyl ether (BDE 154) 2.2-Dichloroethene trans-1.6-Pentabromodiphenyl ether (BDE 100) 2.

and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. the presence of an interference) that produced results of inadequate quality.g.. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period. Data for other pesticides are included only for 1999-2000 and 2001-2002.. five results that all have the value 90. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. Percentiles for all three NHANES survey periods (1999-2000.5-dichlorophenol for the 1999-2002 survey periods. 2003-2004) have been re-computed by use of this improved procedure.g. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. urinary 2.4-dichlorophenol and 2.1). and these data will be included in the next release of the Report.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. Details of this procedure are provided in Appendix A. Explanations for each change are provided in Appendix B. 2001-2002. Fourth National Report on Human Exposure to Environmental Chemicals 3 .

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

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

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

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

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

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

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

2 (75.4) 100 (89. acrylamide has produced upper airway irritation following inhalation of high levels.9) 58. glycidamide.7-60. pulp and paper production. the main source of exposure is from the diet. interval) 61.6-65.9 (60. Tareke et al. Estimated intakes in children are about twice that of adults (DiNovi and Howard.2 (58. Fennell et al.1) 101 (95. FAO/WHO.7-64. see Data Analysis section) for Survey year 03-04 is 3.2-77.2-93.6-61.6) 71.4 (51. 2002).S. 2005).7 (63.1) 46. Elimination occurs mainly in the urine as mercapturic acid conjugates.3) 63. 2005). and well below doses known to cause nerve damage or carcinogenicity in animals.9-105) 86.4) 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 54.0 μg/kg for adults (FAO/ WHO.6 (56. EPA..0 (67. EPA reference dose of 0.1-64.5-85.6) 50.S. 2006. Recently.3 (55.5 (79. and in some cosmetics.5 (74.0) 85.4-60.9 (54.4 (54.1) 53.1 (73.6 (81.Acrylamide Acrylamide CAS No.8 (52.1-57.9-52. and binding agents.0) 57.2) 57. or to glutathione conjugates (Calleman et al. Natural substances in the food are converted to acrylamide.3) 86. and an average daily intake is estimated as 0. 2004).7 (65. 2005).. gels.0.6 (51.3-71. smoking.1-64. In humans.2-118) 98. In the general population.5 (44.7) 54. mineral processing. 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) 96.8-55. ocular and dermal irritation from direct contact with acrylamide containing materials.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.3-2. Survey Geometric mean (95% conf.3 (53.0-108) 152 (139-175) 126 (111-142) 108 (86. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.7) 73. drinking water. are heated at temperatures used for frying and baking.2 μg/kg/day (U.0-66. (NTP-CERHR.6-108) 61. Since acrylamide has limited volatility and high water solubility. as an absorbent in disposable diapers.2-91.6-104) 82.7) 96.1 (83. widely distributed in tissues. in some sealing grouts. acrylamide is synthesized and used in the production of polyacrylamide polymer. population from the National Health and Nutrition Examination Survey. and cosmetics (NTP-CERHR. FDA.0-58. 2004. People may be exposed to acrylamide from foods.7) 75th 79.2) 57. and is either metabolized to the reactive epoxide. Commercially.0 (69. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.0 (57. 1994). Fourth National Report on Human Exposure to Environmental Chemicals 11 . 1990.5 (52.2-67.9) 63.4-83. such as potatoes and some grains.7-64.1 (88.3) 70.7) 58.8 (81.2-59. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. These estimated intakes are hundreds of times lower than occupational exposures.1 (52. but can covalently bind to form adducts with proteins. and from dermal contact with products that contain residual acrylamide.9) 75. In 1997.S.9 (69.4-60. 2005.9) 57.8-57.5) 66.5-80.1 (47. Acrylamide is not thought to accumulate in the body at environmental doses.5) 58.0-49.4 (53.4 (59. in permanent press fabrics.6-75.4) 57. 2006). 217 million pounds of acrylamide were produced commercially in the U.2 (62.S.. Polyacrylamides are useful water-compatible polymers used in water treatment.1) 55.8 (91.S. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. it was discovered that acrylamide is formed when starch-rich foods.4) 57. but are generally above the U. 2005). soil conditioners.4-89. Animal studies indicate that acrylamide is well absorbed.6) 73.0 (53. 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).1) 62.1-61.8 (57.4 (54.9-61.2-70.7 (58.6) 90.6-66. and in the synthesis or compounding of dye materials. EPA.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 61.7 (55.4-76.

2005.5 (42.. 2005). 2005. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.. most non-smokers had levels less than about 100 pmol/gram hemoglobin.4-98.0 (52.6 (90. Schettgen et al. and other sites) (FAO/WHO. 1997. 2005.2 (63.1-62.who. dominant lethality).8 (51.5-92. population from the National Health and Nutrition Examination Survey.pdf. 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. respectively) are markers of integrated acrylamide exposure over the preceding few months. male germinal cell injury.1-56.. 2005.6 (66.9) 65.3-78.. NTP-CERHR. 2005). Vesper 2005) and smoking (Bergmark.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. 2005.5 (83.2-68..9-62. 2004)..9) 59.3) 59.5 (59. Vesper et al. Animal studies have shown that acrylamide can cause nerve damage (neuropathy). 2003. 2005. altered gene expression in testicular tissues (Yang et al. Survey Geometric mean (95% conf.8-49.4-103) 79.7 (87. 2006.0. 2006). 2005.8-48.7-62. EPA. thyroid.9 (57. AHA levels have been shown to increase with dietary intake (Hagmar et al.. 2005.1) 60. uterine. reproductive effects (reduced litter size.5-64. and neuronal DNA reactivity (Doerge et al.9) 87.1 (56. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.2-91.5) 75th 85. fetal death. Puppel et al.3 (56.2 (72. presynaptic nerve terminal binding (LoPachin.0 (80... U. 2008).1-70...4-59.9-64.4 (81. glycidamide (NTP-CERHR.9-138) 143 (130-159) 96. Schettgen et al.8 (44. 2005). 2006) have been demonstrated after acrylamide dosing.1 (70.0 (70.1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.S. 2005) and sperm DNA adducts (Xie et al.1 (82. 2002. 1997.0-103) 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 64.0) 118 (103-126) 121 (112-134) 113 (94.S.1 (66. 2005. 2005) have been demonstrated in animals.2) 55.. adrenal.7 (84.9-77.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71. Puppel et al. Klaunig et al.S.6-62. 2005).4) 53. scrotal. Maniere et al. After exposure ceases.S... 2005. Acrylamide is clastogenic and can produce dominant lethal mutations.2 (56. 2009).4 (90.. 12 Fourth National Report on Human Exposure to Environmental Chemicals .7) 74. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.4 (56.0-62.5-66.0-93.0 (75.3-101) 95.9 (58.int/ ipcs/food/jecfa/summaries/summary_report_64_final.2) 65.4 (51.7-86. 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. Additional information is available from U.8-61.7) 61.6-64.4) 83. although different analytic methods can affect results.4) 46. 2002. 2008).6-90.7 (57. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U..Acrylamide occupational exposures.4 (57.2-90.. U.9-78.8) 60.7 (61. EPA at: http://www. Mucci et al.4-65. probably through its epoxide metabolite.1) 62.4 (61.8) 45. In addition.2) 87..9-76. and cancer (mammary. interval) 59. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.5 (56. 2005. Rice. see Data Analysis section) for Survey year 03-04 is 4.5-94.1) 56. 2006).5) 71. Glycidamide has been shown to react with DNA (Doerge et al. EPA.3) 59. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. Hagmar et al.5) 87. IARC classifies acrylamide as probably carcinogenic to humans.epa. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.3) 59.7) 90.9) 75. Axonal degeneration.9 (81. 2004.3) 85.1 (57.7-64..0) 94. 2001)..1-60.7) 60.

Calleman CJ. April 13-15. Hagmar et al. Wu Y. Rome. Magnusson AL. gov/~dms/acrydata. Haugen M. Maniere I.Acrylamide In occupational settings. Yang JS. Available at URL: http://www. smokers and nonsmokers. 2005. [Epub ahead of print] Dybing E. 2004. Perez et al. et al. Metabolism and hemoglobin adduct formation of acrylamide in humans. 1993. Farmer PB. Calleman CJ. Summer SCJ. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Granath F. 2/3/09 Perez HL. and Research Strategies. Aprea P. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Paulsen JE. Food and Drug Administration (FDA). 8-17 February 2005. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. References Bergmark E. Kautiainen A. Tornqvist M. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. 2009 Jan 8. 64th Meeting: Summary and Conclusions (FAO/WHO).561:21-37. Rosen I. Uncertainties. Tornqvist M. Hagmar L.Toxicol Appl Pharmacol 1994.nih. Fennell TR. Chem Res Toxicol 1997 Jan. Adv Exp Med Biol 2005. Calleman CJ. Bergmark E. Cheong HK. 1999). Fennell TR. NIH Publication No. Beland FA. Acrylamide neurotoxicity: neurological. Kamendulis LM. et al. Andersen M. Mutat Res 2005. morphological and molecular endpoints in animal models. He F. Costa LG. Survey data on acrylamide in food: individual food products. smoking habits and gender.120(1):45-54. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Snyder RW.who. 2001.43:365–410.fda. National Toxicology Program.. Osterman-Golkar S. Scand J Work Environ Health 2001. 2004 Acrylamide in Food Workshop: Update Scientific Issues. CFSAN/Office of Plant and Dairy Foods. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . et al. et al. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Bruze M. Axmon A. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. The Updated Exposure Assessment for Acrylamide.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Mutat Res 2005. AHA levels correlated with a neurologic symptom index and specific physiologic measures in an occupational setting and correlated better with clinical signs and symptoms than urinary excretion of the mercapturic acid metabolite (Calleman et al. 2001). Toxicol Appl Pharmacol 1993.niehs. Adv Exp Med Biol 2005. DiNovi M and Howard D.580(1-2):119-129.126(2):361-371.. 2/3/09 Klaunig JE.10(1):78-84.cfsan. Malmberg B. Nordander C. J Agric Food Chem 2008. Churchwell MI. Available at URL: http://www. et al. Guffroy M. 1994).pdf. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. 054472. Laurentie M. Alexander J. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Mechanisms of acrylamide induced rodent carcinogenesis. da Costa GG. July. Spicer R. Mutat Res 2005. 6013-6019. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Twaddle NC.561:49-62. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Toxicol 2005. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). 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. Food Chem. In another study.html#u1004. Chicago. Tian G. 2006. February. Wilson KM. 2/3/09 Hagmar L. Paulsson B. Joint FAO/WHO Expert Committee on Food Additives. Zhang S. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Toxicol Sci. Bergmark E. Costa LG.580(1-2):131-141. Duale N.27(4):219-226.85:447-459. Mucci LA.. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin.gov/chemicals/ acrylamide/Acrylamide_Monograph. Illinois. Bergmark E. He F.56. Churchwell MI. Becher G.3:406-412. Doerge DR. McDaniel LP. Chem Res Toxicol 1990. Burgess J. Bridson WE.580(1-2):157-165.. LoPachin RM. Human exposure and internal dose assessments of acrylamide in food. Toxicol Sci 2005. Wirfalt E.pdf.. 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. Available at URL: http://cerhr. Bjellaas T. Italy. Godard T. Acrylamide intake through diet and human cancer risk. Doerge DR. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose.

Rice JM. 2/3/09. Xie Q. Drexler H. U. Office of Pollution Prevention and Toxics.epa. Toxicol Lett 2002. revised 1/3/06. Washington (DC). Angerer J. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. U. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Licea-Perez H. Available at URL: http://www. Liu K. EPA). Tornqvist M. Int J Hyg Environ Health 2004.580(1-2):3-20. Choi JH. Rapid Commun Mass Spectrom 2006. Ospina M.gov/chemfact/s_acryla. Han CH. Hemoglobin adducts of ethylene oxide.163(2):101-8. EPA).206(1):9-14. Vesper HW.580(1-2):71-80.Acrylamide glycidamide by gas chromatography-mass spectrometry. Reprod Toxicol 2005. Tjaden Z.htm. Lee SH. Benetou V. Ding X. Environmental Protection Agency (U. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. 1994.561:89-96. Jin Y. Smith A. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Schettgen T.56(15):6046-53. Toxicol Lett 2006. Ospina M. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Schettgen T.50(17):4998-5006. Tjønneland A. J Agric Food Chem 2008. Meyers T. Yang HJ. Int J Hyg Environ Health 2003. Letzel S.S. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Drexler H.274(1):59-68. Chae C. Drexler H.gov/iris/subst/0286. Environmental Protection Agency (U. Vesper HW. et al. Agudo A. Angerer J. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. propylene oxide. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Broding HC. Tareke E. Anal Biochem 1999. Rydberg P. Eriksson S. Fueller F. The carcinogenicity of acrylamide. Gray JG. Lee MH.epa. Angerer J.S. 14 Fourth National Report on Human Exposure to Environmental Chemicals .S. Weiss T. Available at URL: http://www. Rossbach B. Fu D.20(6):959-64.19(4):527-34. Chemical Summary for Acrylamide. J Agric Food Chem 2002. Liu Y. Mutat Res 2005 Feb 7. 2/3/09 Vesper HW. Integrated Risk Information System (IRIS). Adv Exp Med Biol 2005. Toxicological effects of acrylamide on rat testicular gene expression profile. Han DU. Marko D. Meyers T. Acrylamide. et al. Sun H. Schettgen T. Myers GL. Analysis of acrylamide. Hallmans G.134(1-3):65-70. Mutat Res 2005. Puppel N. Kutting B. Karlsson P. Ingham L.207(6):531-9. September.txt. Slimani N.S. a carcinogen formed in heated foodstuffs.

570 (.160) .370-.11) .050) .052 (<LOD-.060-.05 ng/mL. and 03-04 are 0. and 0.164 (.480-.42-4.88 (.S.S.139) * .533-. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.12) 1.060 (. ear problems.23 (.110 (.106-.153-.057-.96) 2.110 (.190-. Children exposed to ETS are at increased risk for sudden infant death syndrome.53-4.12 (2.81-2.120-.110 (.94) 1.040-.310-1. acute respiratory infections.180) .510 (.040-.234) .080-. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.66-3.900-1.89) 1.302) .506 (.120 (.950 (.770) .20-2..053 (<LOD-.050 (.077) .30) * .198) * .076-.05.063) .187) .50-1. Cigarettes contain about 1.230) .086 (.55-2.312) .99) 2.840) 3.150) .280 (. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.16) .05) 1.620 (.65 (1.02) 1.094) . see Data Analysis section) for Survey years 99-00.84-3.44 (1.142-.23 (1.540-.310) 90th 1.058 (.070) 75th .131 (.308 (.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .87-3.115-.060-.140 (.01 (1.600-1.120 (.050 (<LOD-.00) 1.96-4.167 (.Cotinine Cotinine CAS No.45) 1.75) 1.70-2.44) 2.068) . stroke.09-3.060 (<LOD-.62) 2.310-1.920 (.35 (2.690 (.047-.087 (.111-.120-.240 (.190-.17 (. 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.120 (. < LOD means less than the limit of detection.38-2.77 (1.726) .820) .201) .950-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350 (. maternal exposure during pregnancy can result in lower birth weight.14) .50-4.400-.220) .050 (<LOD-.19-2.63-2.20 (1.080-.066-.088-. 2004).997-3.77 (1. DHHS.17) . ** In the 2001-2002 survey period.570-1.050-.96 (1.130 (.410) .79) 3.660) .080-.130) .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.44 (2.059-.990 (.066) .060) .740-1.19) .580) .54) 1.104-.740-1.160 (. and exacerbated asthma (U.061) < LOD .160 (.068) .320) .040 (.23-2.015.180) .110-. DHHS.20) 1.860 (.428-.12-4.071 (.S.193) . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.76 (1.93) .83-2.145) .09-3.163 (.30) 2.090-.216 (.043-.30) 2.160-.120 (.34 (1.070) .23 (2.070-.062 (.077) . emphysema.12 (1.48-3. respectively. 2006).49) 1.124 (. and various other disorders (U.015 ng/mL.66 (1.580 (.080-.01) 3.030-.40) . cardiovascular disease. acute respiratory illness.39) 3.20 (.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 .54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .18-3.20) .63 (2.050 (<LOD-.22) 2.02) 1.21-1.080) < LOD .197) .57) 2.040 (.66) 1.48-2.144 (.43 (1.77 (2.180 (.70) 2.110 (.960-1.220-.310) .44) 2.47-3.070 (<LOD-.95) 1. 2004).520 (.060 (<LOD-.190-.50) 3.39 (1.137-.480-1. 83% of measurements had an LOD of 0.430-1.19) 1.071) .060 (.084) .53 (1.350-.62 (2.49) 1.160 (.630 (.050) .17 (1.200) 1. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.175 (.42 (1.164 (.68 (1.00) .180) .140 (.990) .02 (.260) 1.230 (. 1998).14-1.15) 2.625) .68) .850 (.5% nicotine by weight (Kozlowski et al.790) .220) . population from the National Health and Nutrition Examination Survey.470-.059-.080 (.21-1.066 (.110 (.213) .99) 2.54 (1.350-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. Survey Geometric mean (95% conf.140-.54 (1.32-2.054 (.450-.140-.110) .28-1.800 (. 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.78) 2.620-1. Fourth National Report on Human Exposure to Environmental Chemicals 15 .120) .080) < LOD < LOD .180 (.052 (<LOD-.33-2.210 (.21 (.300) .090-.50 (1.580-1.020-.770) .030-.630 (.087-.32-2.090-.110-.60-2.04 (1.621-1.930 (.770-1.92 (1.148-.060-.073) < LOD .110-.180) .730 (.154-.910-1.260-1. and 17% had an LOD of 0.126) .188) .32) 1.88 (1.55 (1.670) .630 (.087) < LOD < LOD .108) * .540 (.505 (.68) 2.150) .075 (.09-2.070) .120 (.089) Age group 3-11 years 99-00 01-02** 03-04 .360) .080 (.030-.030 (.100-.85 (1.26-1.500 (.28) .050-.15 (2.180) .160) .047-.163) .110) .040 (.137 (.14) .710 (. which may vary for some chemicals by year and by individual sample.050 (<LOD-.

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

Kira S.cdc. Absorption and metabolism of nicotine from cigarettes. Mowery PD. 4/13/09 International Agency for Research on Cancer. International Agency for Research on Cancer. IARC Monogr Eval Carcinog Risks Hum. Fong I. et al. Herrera B. 1988-1991. Giovino G. June. U. Metabolism and disposition kinetics of nicotine. Pechacek TF. Smoking and Tobacco Control Monograph 10 [online]. Kozlowski LT. DHHS).fr/ENG/Monographs/ allmonos90. Jacob III P. Pirkle JL. Dollery CT. Giovino GA.S Department of Health and Human Services (U. Perez-Stable EJ. National Toxicology Program (NTP). 1999.57(1):79115. Pirkle JL.S Department of Health and Human Services (U. Schober SE. Environ Health Perspect 2006.php. Nicotine metabolism and intake in black and white smokers.56:483-493. Available at URL: http://monographs. Department of Heath and Human Services. Pollack HA. 11th ed. Am J Public Health 2004. Maurer KR. Curtin LR. 2004. Tobacco Smoke and Involuntary Smoking. Atlanta (GA): 2005.114(6):853-858.gov/eid/rmca/critdocs/ criteriadoc/33.niehs. JAMA 1996.iarc. Vol 38. 4/13/09 National Cancer Institute (NCI). 1988-1991. Pickett MA. [online]. 1999-2002. JAMA 1998. Houseman TH. Tob Control 2006. Vol 83. Third National Report on Human Exposure to Environmental Chemicals. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Respiratory nicotine absorption in non-smoking females during passive smoking. U. Modin G. cigarette smokers: the Third National Health and Nutrition Examination Survey. In Report on Carcinogens. Coordinating Center for Health Promotion. Summary of Data Reported and Evaluation [online] 1986. available at URL: http://mtn.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. 4/13/09 U. Office on Smoking and Health [online] 2006. Centers for Disease Control and Prevention. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Centers for Disease Control and Prevention. Available at URL: http://ntp.S. Strauss WJ. DHHS). IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Warner K.gov/library/ secondhandsmoke/.18:188-204. Benowitz NL. Int Arch Occup Environ Health 1991. et al.S. Jacob P. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children.S. Benowitz NL. Trends in the exposure of nonsmokers in the U. BMJ 1975.nih. Herrera B.php. 4/13/09 Iwase A.4:313-316. Mehta NY. U. Sosnoff CS.275:1233-1240.S. Etzel RA.7:369-375. Lewis PJ. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Exposure of the U. Summary of Data Reported and Evaluation [online] 2004.291(3):1196-1203.15:302-307.94(2):314-320. Cotinine as a biomarker of environmental tobacco smoke exposure. Available at URL: http:// cancercontrol.pdf. Jacob P III. Caraballo R. Jarvis MJ. Tobacco Smoke. Epidemiol Rev 1996. and the United States. Bernert JT. Sweeney CT. 4/13/09 Centers for Disease Control and Prevention (CDC).gov/ntp/roc/eleventh/profiles/ s176toba. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.S. Tob Control 1998. 1991. Benowitz NL.S.280:152-156. Caudill SP. Aiba M. Department of Heath and Human Services.280:135-140. Flegal KM. Bernert JT. Hukkanen J. IARC Monogr Eval Carcinog Risks Hum. Coordinating Center for Health Promotion. Vogler GP. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Schwartz SS. Pechacek TF. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Richter PA. Benowitz NL.fr/ENG/Monographs/allmonos90. George CF.niosh. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Brody DJ.gov/tcrb/monographs/10/. Clin Pharmacol Ther 1994. population to secondhand smoke: 1988-2002. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. 4/13/09 Perez-Stable EJ. J Pharmacol Exp Ther 1999. Available at URL: http://www.cancer. the United Kingdom.pdf. Pharmacol Rev 2005. National Institute for Occupational Safety and Hygiene (NIOSH). iarc. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary.surgeongeneral. Brody DJ.63:139-43.S. Benowitz NL. Tobacco related exposures. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . References Armitage AK. Turner DM. Racial/ethnic differences in serum cotinine levels among adult U. Centers for Disease Control. National Center for Chronic Disease Prevention and Health Promotion. JAMA 1998. Soliman S. Jacob P III. Ethnic differences in N-glucuronidation of nicotine and cotinine. Available at URL: http://monographs.

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

140) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .N.180 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .130-. (U.140) < LOD . which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.gov/pesticides/.180 (.S.130-.170 (. 2002).140) < LOD .120-. < LOD means less than the limit of detection. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.epa. Sudakin and Trevathan.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 1995.210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD ..110 (.240) < LOD .N-Diethyl-meta-toluamide (DEET) N. One survey detected DEET in 74% of sampled streams in the U. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.130 (.110-.250) < LOD . DEET can be applied to clothing and the skin to repel biting insects.560) < LOD . About 3-8% of dermally applied DEET is absorbed. Fourth National Report on Human Exposure to Environmental Chemicals 19 .210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .100-.S.S. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.N-Diethyl-meta-toluamide (DEET) CAS No.110 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.100-.100-. including seizures and encephalopathy. EPA.110 (<LOD-. and it has not been rated by IARC or NTP with respect to human carcinogenicity.130-.170 (.220 (.140 (. (Kolpin et al. 134-62-3 General Information N.100-.140) < LOD .EPA at: http://www. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. 2003).100-. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. Neurological effects in humans.100 (<LOD-.190) < LOD . DEET is not genotoxic.140-.1.130 (. After absorption.449 and 0.180) < LOD .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 . 2002). Survey Geometric mean (95% conf. DEET is not a developmental or reproductive toxicant in animals (U.S.130-. There are over 225 insect repellents brands containing DEET.110 (. have been reported as result of self-poisoning by ingestion or excessive dermal application. Urinary N. Its use is recommended for prevention of several vector-borne diseases..S.520) < LOD .180 (. DEET is also used in combination with dermal sun screens (U.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.110 (<LOD-.120-.100-. population from the National Health and Nutrition Examination Survey. Additional information is available from U.130) < LOD .110 (.110-. and they range in concentration from 4% to 100%.S.130) < LOD . 1998).EPA.130 (. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. 1998).210 (.270) 688 678 518 700 598 956 Limit of detection (LOD. 2005).160) < LOD . DEET has low acute toxicity. DEET is not registered for use on agricultural commodities.. 2003). Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.150) < LOD .EPA.

S.580) 964 1191 1013 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .250) < LOD .170-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD ..240-. 2007).150-.150) < LOD .270) < LOD .N.240) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.330 (.250-.350) < LOD .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 .280-1.270-.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.330 (.410-..370-.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 .370) < LOD .550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Urinary N. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .480 (.320 (.350-.350) < LOD . representative subsamples from NHANES 2001-2002.230-.230-.190 (. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.93) < LOD .S.410 (.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al. population from the National Health and Nutrition Examination Survey.190 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.200 (.190 (<LOD-.390-. 2005).N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.410 (.500 (. Urinary DEET levels as high as 5.140-. In this survey period.270 (.440) < LOD .280 (. 1992).490) < LOD .630) < LOD .290-. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.640 (.320) < LOD .270 (<LOD-.130 (<LOD-. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al. 20 Fourth National Report on Human Exposure to Environmental Chemicals .250 (.300 (.190-.230) < LOD . 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. Survey Geometric mean (95% conf.

Hartnagel RE Jr. Smallwood AW.S.gov/oppsrrd1/REDs/0002red.epa. Tapia J. Environmental Protection Agency (U. Trevathan WR.EPA). Toxicity and Exposure Assessment in Children’s Health.pdf. Third National Report on Human Exposure to Environmental Chemicals.N. J Anal Toxicol 1992. September 1998. 2005 Kolpin DW. Chemical Summary. Atlanta (GA). 1993-1997. Centers for Disease Control and Prevention (CDC). J Toxicol Clin Toxicol 2003. Grzywacz JG. Environ Health Perspect 2007. Reregistration Eligibility Decision (RED): DEET. Zaugg SD. Lowry LK. et al. Washington (DC): U. Gabriel KL.25:95-100. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 .gov/teach/chem_summ/ DEET_summary. 4/9/09 U. 2005. pp. Fundam Appl Toxicol 1995.N-Diethyl-meta-toluamide (DEET) References Arcury TA. Available at URL: http://www.S. DEET: a review and update of safety and risk in the general population. DeBord KE. and other organic wastewater contaminants in U. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Barber LB. Barr DB. Environ Sci Technol 2002. Human exposures to N. U.S.S. Osimitz TG. Veltri JC. Bell JW. Furlong ET. metabolism. streams. hormones. 1-118. Schoenig GP.epa. Available at URL: http://www. and excretion of N. Pharmaceuticals.EPA).N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers.16(1):10-13.N-diethyl-mtoluamide following dermal application to human volunteers. Environmental Protection Agency (U. pdf. Int J Toxicol 2002.36(6):1202-1211. Sudakin DL.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. Page BC.EPA. U. EPA. Selim S. Meyer MT. Quandt SA. Absorption. Thurman EM. Diethyltoluamide (DEET).2:341352.41(6):831-839. 1999-2000: a national reconnaissance.S.S. EPA 738-R98-010.S. N.115(8):1254-1260. Chen H.

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

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

Jang JY.147(6 Suppl):S56-69.113(8):926-33. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure.Environmental Phenols Volkel W. An observational study of the potential exposures of preschool children to pentachlorophenol. Welshons WV. Kawamoto T. Nagel SC. Csanady GA. Colnot T. Biological monitoring of bisphenol a in a Korean population. Arch Environ Contam Toxicol 2003. III. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Food Chem Toxicol 2002. Endocrinology 2006. Large effects from small exposures. Wilson NK.40(7):905-12. Yang M. Hughes C. Vom Saal FS. Kim SY.15:12811287. and nonylphenol at home and daycare. vom Saal FS. Environ Res 2007. Lordo RA. Filser JG. Chang SS. Chuang JC. Dekant W. bisphenol-A. Environ Health Perspect 2005. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Witorsch RJ. Lee SM. et al. Morgan MK. Chem Res Toxicol 2002. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature.103(1):9-20. Sheldon LS.44(4):546-51. Fourth National Report on Human Exposure to Environmental Chemicals 33 .

1996). 1995.. < LOD means less than the limit of detection.600-1. through sewage.30 (1.200-. 2002). Bian et al. which may vary for some chemicals by year and by individual sample..10) 2. streams in 30 states (Kolpin et al. which are anionic surfactants used in detergents. and from contact with some personal care products and detergents.300-.30 (1.60-3.50-2.20-2.268-.30 (1. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). 2003.60) 1.900 (. have demonstrated estrogenic effects particularly when injected at high doses in animals. Katsuda et al.1.60) .10 (1.274-.30) 2.00 (1.. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.900 (.400 (.40) 1. and to alkylphenoxycarboxylates.3.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.30-2. to shorter chain alkylphenol ethoxylates.389 (.60-3.10-2.50 (1. 2000.600-1.600) .20-2.5% of 139 U.20-2..S.00) 1229 1288 03-04 03-04 03-04 * .30) 90th 1.600) . Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.600-1.50) 1.600) 1.477) .. 2002). including 4-tert-octylphenol.40) 2.000 tons of alkylphenol ethoxylates were produced annually worldwide. altered neonatal sexual development.Environmental Phenols 4-tert-Octylphenol CAS No.70 (1.300 (<LOD-.50) .2.20-2. and emulsifiers. 34 Fourth National Report on Human Exposure to Environmental Chemicals . altered estrus cycles and reproductive outcomes. Disposition in humans has not been studied sufficiently. fish) and drinking water. see Data Analysis section) for Survey year 03-04 is 0. Indoor and to a lesser extent. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. In 1999-2000.600) .500) .50) 1.80) 2.40) * 03-04 03-04 03-04 .40 (1.70 (1. Urinary 4-tert-Octylphenol (4-[1. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.900 (.600-1.g. In rats.g.50-3. industrial cleaners. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. did not bioaccumulate.700-1.300 (<LOD-.80 (1.60-3.60-3.60) 613 652 1092 Limit of detection (LOD. Less frequently.. Saito et al. 140-66-9 General Information 4-tert-Octyphenol. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. During the 1980s and 1990s.S. population from the National Health and Nutrition Examination Survey.20) 1.600-1.20) 314 715 1488 03-04 03-04 * * . 2004).40) 1.90) 2.10 (. 4-octylphenol monoethoxylate was detected in 43. The alkylphenols can bioaccumulate in some fish. an alkylphenol.500) 75th . 2000.200-.299-. impaired steroidogenesis.20-2.90) 2. 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.30) 1.50) .800-1. testicular atrophy. and impaired spermatogenesis (e.500 (. The alkylphenol ethoxylates enter the environment through human use of products containing them.507) * < LOD . textiles.500-1.20) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th . 1997.900 (.500-1.. Laws et al.900 (.80 (1.30 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. over 500. Blake and Boockfor.300 (<LOD-.20 (1.30 (. and some of their degradation products are toxic to aquatic life.300 (<LOD-. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. pesticides.20) 2.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.60-3. the various alkylphenols have also been used as emulsifiers and modifiers in paints. and the polyethoxy chain may consist of up to 50 ethoxy units.600-1.357 (..50) 1.400 (.00 (. In the 1990s.60-3.500) . and through manufacturing waste streams (Warhurst.20-2.80 (1. Ying et al. Several alkylphenols.10) 1.497) * .400) 1.70 (1. is used to manufacture alkylphenol ethoxylates. 2006. leading to inhalation as another potential exposure route (Rudel et al.40) 2. and some personal care products.10 (.300 (<LOD-. orally administered 4-tert-octylphenol was well absorbed.70 (1. and was quickly eliminated from the blood (Certa et al.500) .369 (.00 (.400 (. Survey Geometric mean (95% conf.300-.

890-2.31 (1.380 (<LOD-.630-1. Nagao et al.59) 1. Calafat et al.43) 1.640-1. 2000.54) * 03-04 03-04 03-04 .00) 1.11) 1. 4-tert-Octylphenol is not considered directly genotoxic. at lower or environmentally relevant doses (Blake et al. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.740 (..610) .53-3.20 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.450) 1..620-1.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.910 (.160-.18-4.25) 90th 1.60 (1. Tyl et al. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.31-2.3.00) 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 .500-1.410 (.25-2. 1999).73) 2. Kawaguchi et al.05-2.270-.85 (1.470) 75th . representative subsample of NHANES 2003-2004.50 (2. 2005.78) 3.17 (.860 (.62 (1.S.550-1.435 (.41) . 2004. or their corresponding ethoxylates with respect to human carcinogenicity.33 (2.730-1.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.620) . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..68) 2.269 (.207-. Survey Geometric mean (95% conf.43) 1.00) 2.40 (1.170-.540-1.199-.68-2.260 (<LOD-.320 (<LOD-.62) ..03 (1.570) .36-3.470-1. 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.81 (1. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect.560) .460 (. Fourth National Report on Human Exposure to Environmental Chemicals 35 ..64 (. 2001).1. Urinary 4-tert-Octylphenol (4-[1.450) .850 (.00) 2.76 (2.00 (.08) 1.02-4.65-3.06 (2.276 (.470-1.43-3.349) * < LOD .71) 2..770 (.25) 2. 2003.400) .337-.370 (<LOD-.11) 2.03 (1.530) .420) .300 (<LOD-. It is unclear if estrogenic or other effects occur in animals through oral dosing.62 (1. nonylphenol.740 (.78 (1.00 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.280-.11-2.67-2.10-2. 2004).59 (1.29) 2. 2001. population from the National Health and Nutrition Examination Survey. IARC and NTP have not rated octylphenol.14) 314 713 1487 03-04 03-04 * * .270 (. Sweeney et al.03-6.384) * .Environmental Phenols Myllymaki et al. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.40-4.33) 3.S.270 (.78) 1228 1286 03-04 03-04 03-04 * .96-4. Yoshida et al.15) 1.22) . In a small number of adult Japanese volunteers.

37(20):4543-53. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Barber LB. Arch Toxicol 1996.71(1-2):112-122. Tyl RW. Environ Sci Technol 2002. Reprod Toxicol 2001. Yoshida M. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. hormones. Song L. Phthalates.Environmental Phenols References Bian Q. An environmental assessment of alkylphenol ethoxylates and alkylphenols.foe. Kawaguchi M. Ye X. prolactin. Chen J.44(8):1355-1361. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Reidy JA. Two-generation reproduction study with para-tert-octylphenol in rats. pesticides. Izumi S. Regul Toxicol Pharmacol 1999. Wang X. Boockfor FR. Indoor air pollution by alkylphenols in Tokyo. Taya K. Carey SA. and testosterone.18(1):43-51. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats.pdf. alkylphenols. Fedtke N. McCoy GL.S. Raychoudhury SS. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. 2003. 1995.54(1):154-167. Katsuda S. Indoor Air 2004. Marr MC. Sweeney T. Available at URL: http:// www. Certa H. Seto H.co. Biol Reprod 1997. 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. testis size. polybrominated diphenyl ethers. and other endocrine-disrupting compounds in indoor air and dust. bisphenol A and methoxychlor in rats. Toxicol Appl Pharmacol 2000.165(3):217-226. Takai N. Spengler JD. Toxicol Lett 2001.36(6):1202-1211. Estrogenic activity of octylphenol. Brooks AN. Paranko J. Anal Chim Acta 486:41-50. Wong LY. Needham LL. Toppari J. Roche JF. Environ Health Perspect 2008. Takenaka A. and sertoli cell number. Nair-Menon JU. Haavisto TE. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Taya K.121(1):21-33. Nakagomi M. Myers CB.uk/resource/reports/ethoxylates_alkylphenols. Qian J. Brine DR.799(1):119-125. Maekawa A. Reprod Toxicol 2004. Katsuda S. Millette CF. Ono H. Saito I.S. Myllymaki SA. Makino T. Environ Sci Technol 2003. Warhurst AM. Ferrell JM. Okada F.141(7):2667-2673. et al. Kawaguchi M. Blake CA. Meyer MT. Onuki A. Inoue K.28(3):215-226. Ito R. Endocrinology 2000. Karjalainen M. Calafat AM. Saito Y. et al. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Fail PA.folliclestimulating hormone. Xu L. Yoshimura S. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Thurman EM. Pharmaceuticals. Maekawa A. Camann DE. Food Chem Toxicol 2006. streams. Exposure of the U. Nagao T. Watanabe G. et al. Bodman GJ. Zaugg SD. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Nicol L. Furlong ET. Horie M. Toxicol Appl Pharmacol 2005. Seely JC. Toxicol Sci 2000. Muller AM. Rudel RA. Yoshimura Y. Laws SC.15(6):683-692.207(1):59-68. Kolpin DW. nonylphenol. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Kookana R. and other organic wastewater contaminants in U. Brody JG. et al.14(5):325-332. Usumi K. Boockfor FR.30(2 Pt 1):81-95.57(2):255-266. 2/4/09 Ying GG. 1999-2000: a national reconnaissance. Bolt HM. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review.116(1):39-44. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Cooper RL. Wiegand HJ. Sakui N. Watanabe G. Yoshida M. Williams B. Environ Int 2002. Blake CA. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Korn LR. Inoue K.

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

8-60.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13. population from the National Health and Nutrition Examination Survey.6-111) 33.0 (34.22-10.3-31.2 (27.30-14.1) 13.5-14. population from the National Health and Nutrition Examination Survey.93 (7.5) 11.9 (8.4) 7.5 (11. interval) 12.6-15.6 (30.1 (8.72-13.6-37.48 (8.4) 317 (231-433) 144 (96.2 (25.11-11.10-9.1) 9.21 (6.40-11.54 (8.7 (28.7) 292 (151-432) 132 (78.6-20.29-12.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60 (8.80 (5.8 (21.32-14.0 (11.8-112) 30.18 (5.0-19.7 (11.4 (38.9) 8.20-13.3-35.9 (11.1) 50.4) 75th 43.2 (11. Survey Geometric mean (95% conf. Urinary Triclosan (2.S.0 (26.20-10.6) 90th 212 (172-241) 03-04 03-04 03-04 9.1) 7.20 (7.82 (8.2) 13.94 (7.1) 14.50-10.6) 10. see Data Analysis section) for Survey year 03-04 is 2.40-17.5) 20.4.8-85.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.3) 47.4) 90th 249 (188-304) 03-04 03-04 03-04 8.1) 11.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.6-14.6) 31.1 (15.9 (50.8) 14.9) 75th 47.2-58.3 (11.1 (45.2 (10.3 (9.4-19.70-16.2 (13.4-18.8-127) 37.7) 123 (36.6 (10.3-67.Environmental Phenols Urinary Triclosan (2.3.8-63.0-213) 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 .00-8.86-12.9) 7.60 (6.0-15.7 (14.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.1) 9.45 (5.4 (12.2 (37.9-61.9-236) 193 (90.8) 7.2-14.5) 13.38-18.S.2) 12.89-11.4) 25.55 (4.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6 (9.4 (11.4 (32.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.4) 51.8) 116 (39.3) 6.90-10. Survey Geometric mean (95% conf.5) 66.1) 9.3-15.1) 9. interval) 13.0-15.6-65.8) 9.4.6-14.00 (4.3 (26.48-10.7 (39.2-46.4) 73.0 (8.20 (7.6 (12.7 (9.0 (36.0) 49.10) 84.20-11.5-86.1-39.0) 65.2-58.7) 10.74 (5.43-13.9 (33.92-12.6) 12.16 (6.2) 9.3) 10.45-10.9) 32.4) 357 (225-456) 203 (87.3 (8.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.6) 39.1) 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 9.45-13.0) 9.0-73.50) 10.

Williams FM. Katsura E. Br J Clin Pharmacol 1987. Kanetoshi A. Wigmore H. et al. The oral retention and antiplaque efficacy of triclosan in human volunteers. Bennett ER. Calafat AM. Osachoff H. Okui T. Biol Pharm Bull 2005.38(4):361370.24(3):209-218. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps.Environmental Phenols References Aiello AE.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. 4. IMS Ind Med Surg 1969. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Bodey GP.50(1-5):153-156. Bhargava HN. Readman JW. Hirano M. Lyman FL. Windham G. Pharmacokinetics of triclosan following oral ingestion in humans. Gomez MJ. Chemosphere 2007. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Urinary concentrations of triclosan in the U. Benson WH. et al. Larson EL. and other organic wastewater contaminants in U. Moss T. Erratum in: Aquat Toxicol 2007. 4’-trichloro-2’-hydroxydiphenyl ether. et al.69(20):1861-1873. hormones. Sandborgh-Englund G. Nagao Y. Watanabe N. Mar Environ Res 2000.38(2):64-71. Percutaneous penetration and dermal metabolism of triclosan (2.524:241-247.83(1):84.17(5):637-644. Ekstrand J. Ogawa H. Kaneshima H. Furia T. Pilot study of urinary biomarkers of phytoestrogens. and phenols in girls.S. Adolfsson-Erici M. streams. Meyer MT. Reidy JA. Chelimo C. Gunderson MP. Skirrow RC. Thurman EM.45 Suppl 2:S137-S147. Hong HC.66:1052-1056. Furlong ET. Arch Environ Contam Toxicol 1988. Matsumura N. Environ Health Perspect 2007. Evidence of 2. Kolpin DW. Aguera A. J Invest Dermatol 1976.36(6):1202-1211. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Howes D. Ferrer I. Photolytic degradation of triclosan in freshwater and seawater. Gilbert RJ.67(4):532-537. population: 2003-2004. Leonard PA. J Toxicol Environ Health A 2006.23(5):579-583. Am J Infect Control 1996. Zaugg SD.4. Needham LL.S. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Mezcua M. Aranami K. Ebersole R. Ye X. Veldhoen N. Pharmaceuticals. Fernandez-Alba AR. Foran CM. 1999-2000: a national reconnaissance. Clapson DJ. Teitelbaum SL. Toxicology of 2.7/2.4’-trichloro-2’hydroxydiphenyl ether).80(3):217-227.28(9):1748-1751. Levy SB. Food Chem Toxicol 2000. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Triclosan: applications and safety. Williams PE. Ishibashi H.. Wolff MS. Britton JA. et al. Environ Health Perspect 2008. Hernando MD. phthalates. Wong LY. Shiratsuchi H.116(3):303-307.115:116-121. Pinney SM. Aquat Toxicol 2006. Barber LB. Environ Sci Technol 2002. Odham G. Anal Chim Acta 1004.

350) < LOD .660 (.25 and 0. In the environment. General population exposure to PCP may occur by inhalation of contaminated air.350) < LOD . which may vary for some chemicals by year and by individual sample.350 (.350-. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.. ingestion of contaminated food or water.350-1.630 (.90) 2.09) .00) 2.37) .33-2. and dermal contact with PCP-treated products. 1976. with repeated or chronic exposure.94 (1. PCP is absorbed rapidly and well by all exposure routes.23 (.350-.91 (1. along with small amounts of tetrachlorohydroquinone and conjugates.94 (1.. To-Figueras et al.350) < LOD .60) 1. 40 Fourth National Report on Human Exposure to Environmental Chemicals . 2002.90 (1.350 (.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 . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.30) 1.350) < LOD .770 (.350-.S.350-. PCP is degraded by sunlight and metabolized rapidly by microorganisms.58-2. Since 1984.350 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350-.350) < LOD . PCP is eliminated over a few days (Braun et al.530) 1.350) < LOD .480-2.350 (.650 (.18 (<LOD-1.350-.350-1.350 (.00) 1.350) < LOD . 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.98 (1. plants.500-2.g. air. bactericide.350-. utility poles and fence posts).80) .47-5.960) 1. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60) 1.350-.350-.350) < LOD .350) < LOD < LOD 75th . 1997).350-1.890-1.5. and animals..65 (.04) 1.47-3. Acute.350 (.10) 1.70) 2.10) 1.S. are eliminated in the urine.350 (. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.33) .350-. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.350) < LOD . hypertension.350-2. The parent compound and conjugates. After a single dose. PCP is distributed to most tissues and is not extensively metabolized.350-2.350-2.350) < LOD . herbicide.680-1.990-2.30 (.51) 1.350) 90th .350) < LOD .350) < LOD .350-.980 (.390 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30) 1. 1979).42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 1986).510-3. the elimination half-life may be a week or more (Uhl et al.350-2. PCP has been detected in soils.350-.45-2.350 (.76) 1.390 (.50) 1. so it is relatively non-persistent.350 (. < LOD means less than the limit of detection.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. Survey Geometric mean (95% conf.650) 1.890 (.10 (<LOD-1.64) 1.350-1. PCP cannot be used on wood in residential or agricultural buildings. algaecide and insecticide.70) . and possibly of lindane (IPCS. Human exposure to PCP has become less common.58-2.350-.62 (.350-.350) < LOD .53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * . has been restricted.37 (.350 (. PCP use in the U. mollusicide.990 (<LOD-2. Kohli et al.30 (1.350 (.10 (1.30 (. After absorption.350-. other polychlorinated benzenes..850-2.10 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350 (.67) 1.40 (.350-.350-.42) 696 680 521 696 603 951 Limit of detection (LOD.350 (.350-. and it is used primarily as a preservative for wood to be used outdoors (e.350) < LOD .00 (.83 (2.350 (.350 (.350 (. and metabolic acidosis were observed in CAS No.350-2.78) 1.00) 1.350) < LOD . population from the National Health and Nutrition Examination Survey.350 (.350 (.90) 1.48 (.350 (.30) .76) .350-. Effects including hyperthermia. water and sediments because of the large amounts that were produced and used historically.65 (.590-1.75) 2.350) < LOD .350-.350) ..350-.350 (.32 (.54-2.01 (<LOD-1.510-5.350-.08-3.73 (1.48-2.860-2.

30 (.490) < LOD .250 (.650 (.25-1.06 (.69 (1.25) 1.610 (.440 (.35) 1.730) < LOD .94-3.epa.630 (.25 (1.290-.10-2. In a small sample of U.430-.55) 1.34 (. 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..79) 1.40-2.16 (.S.240-.94 (1.850 (.gov/ toxpro2.. Survey Geometric mean (95% conf.48-2.780-1.67-3. and adversely affected thyroid function (U. Death can result from seizures and cardiovascular collapse.25 (1.310) < LOD .920 (. 2003).52) 1. 1989).430) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67 (1. Pentachlorophenol is not mutagenic or teratogenic.95) 3.270-.290) < LOD .18 (1. 2004.360 (.78) 1.560-.35-2..30) 1.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 1991).67 (1.40) 1.09 (<LOD-2.18) .800-1.950-1. 1995). the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.16-1.21 (.0 mg/L.320 (.6 and 14.760 (.atsdr.830) < LOD .19) 2. population from the National Health and Nutrition Examination Survey.S.83 (1.29-3..25-2. 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.400 (.51) 1.320) < LOD .09-1.67 (1. children in the 1980’s.260 (. EPA has developed standards for PCP in drinking water and the environment.82) 1.340-.280) < LOD .320) < LOD < LOD 75th . 2000). In NHANES 2001-2002 subsamples. chronically administered high doses of PCP were hepatotoxic. 2003).08 and 5.56) 1. In animals.270-.220-.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 .36) .420) < LOD ..52 (<LOD-1.500-.57 (1.220-.75 (<LOD-2.19) 2.73 (1.780) < LOD ... 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.e. The U.500-1.html. Fourth National Report on Human Exposure to Environmental Chemicals 41 .40) 1.13 (.84 (1.310-. respectively) (Becker et al.380-.10 (1.910-1.82 (1.470 (.360-.52 (1.500 (.S.21-2. inhalation.52 (<LOD-1.570 (.990 (.EPA.26 (1.gov/ pesticides/ and from ATSDR at: http://www.320) < LOD . Among adults in the NHANES 1999-2000 subsample.950-1.250 (. 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.06) 1.11) 2.510-. 1989).590) < LOD .00-1.26 (1.370 (.67 (1. EPA at: http://www.900-1.300 (. 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.cdc.57 (.S. 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.650) 90th 1.40) 1.30) 1. carcinogenic. respectively) (Seifert et al.00) 1.40) 1.700-2..90) 1.800) < LOD 1.19 (1.710-1. van Raaij et al.67-3. and the FDA has established a standard for bottled water.650 (.84) 1.40) 1.560) < LOD .9 mg/L. environmental levels) and health effects is available from the U.92) 1. or skin absorption.560) < LOD .94 (1.19) 2.290-.590-1.30-2.300 (.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.84-4. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .67-2.S.350) < LOD .78) 1.00-1.950-1.35-2.510-.Fungicides adults and children severely exposed to PCP through ingestion.580-.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . OSHA has established an occupational standard. More information about external exposure (i.330-.25-2.06-3.67 (1.300 (.35) 1.75) 1.

11/30/2004. Pesticide residues in urine of adults living in the United States: reference range concentrations. g o v / f d m s p u b l i c / c o m p o n e n t / main?main=DocketDetail&d=EPA-HQ-OPP-2004-0402. Arch Environ Contam Toxicol 1989. Becker K. Shealy DB.S. Kaus S.inchem. 2002. Smith SJ. Dev Toxicol Environ Sci 1979. Seiwert M. Lindane. Krause C. Blau GE. house dust. Hill RH. Schulz C. International Programme on Chemical Safety (IPCS).18(4):469-474. van den Berg KJ. PCP: Human Risk Characterization [online]. r e g u l a t i o n s . Cline RE. et al. Int J Hyg Environ Health 2003. References Becker K. hair. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Toxicology 1991: 67(1):107-16.S. Braun WH. urine.54(3):203-208. Pharmacokinetics of pentachlorophenol in man. To T. Bragt PC. Chenoweth MB.org/documents/jmpr/jmpmono/2002pr08. Environ Health Perspect 1997. Notten WR. Rodamilans M. drinking water and indoor air. Helm D. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Arch Environ Contam Toxicol 1989. The metabolism of higher chlorinated benzene isomers. Safe A.4:289296. Santiago-Silva M. Seifert B. Gregg M. Holler JS. Otero R. Can J Biochem 1976. 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.71:99108. Uhl S.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. 4/21/09 Kohli J. Environmental Protection Agency (U. Fast DM.58:182-186. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Phillips DL. Hill RH Jr. J Expo Anal Environ Epidemiol 2000. Arch Toxicol 1986. Needham LL. Barrot C. Sala M. Environ Res 1995. Hill RH Jr. htm. Needham LL. Schmid P. et al. Seifert B. 206:15-24. available at URL: http://www. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Seiwert M. U. Jones D. 42 Fourth National Report on Human Exposure to Environmental Chemicals . et al. To-Figueras J. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.10:552-65. Baker S. Schulz C. Available at URL: h t t p : / / w w w.18:475-481. Bailey SL. Head SL. Engel R. 4/21/09 van Raaij JA. EPA).105(1):78-83. Schlatter C.

632) Selected percentiles ( 95% confidence interval) Sample 95th 2.30) < LOD .60-2..20-2.17 (.770 (.20) < LOD 2.40-7.509 (.S. and sanitizers. on ornamental plants and turfs. or 2-phenylphenol) and its water-soluble salt.850 (.350-1.40-2.610-1.50 (1.450 (<LOD-.470 (<LOD-.490 (<LOD-.386-.40 (.690-1.690) < LOD .890) 1.50-4.590-2.S.10 (1. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al. Available evidence suggests that OPP does not accumulate in the body.621) * .638) * . 2006).800-3. OPP is volatile.670) 2.40-5.00 (1.50) 1. fungicides.640) < LOD .30-2.600) < LOD .80) 1. 2006).10) 2.490 (<LOD-.624) * .3 and 0.496 (.567 (.402-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.570-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.830 (.645) * .840-1. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.10 (1.490 (<LOD-.860) * 99-00 01-02 99-00 01-02 99-00 01-02 . SOPP is applied topically to the crop and then rinsed off.433-.00) . inhalational.710) 3.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 . OPP is still used as a disinfectant fungicide for industrial applications.600-1.80-3.552 (.34) 1. 2006).02) 1.10) 1.30) 1.600-1. 90-43-7 General Information Ortho-phenylphenol (OPP.22) 2.890 (.07 (.466 (. interval) .60-3.09) 2. it was used in home sanitizers for surfaces.28 (.Fungicides ortho-Phenylphenol CAS No.630) < LOD .EPA.508 (.750-2.600) < LOD .90 (1.20 (1.760-2.520 (. Workers who manufacture. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.970 (.636) * .50-3.00) .10-1. leaving the chemical residue OPP.710-2. Both have been used in agriculture to control fungal and bacterial growth on stored crops. Both chemicals degrade within hours to weeks in the environment (U.364-.80 (2. population from the National Health and Nutrition Examination Survey.10) .550-1. Fourth National Report on Human Exposure to Environmental Chemicals 43 .880-2. however.00-2.S.410-. 2002.950) < LOD .28-3.500-2.10) . In the past.450 (<LOD-. or apply these chemicals may be more highly exposed than the general population.27 (.S.600) < LOD 75th . are antimicrobial agents used as bacteriostats.480-1.. which may vary for some chemicals by year and by individual sample.370-. sodium ortho-phenylphenate (SOPP).390-.60 (1.80) 1.770 (.610 (.890 (.570 (.570-1. formulate.742) * . but OPP and SOPP are still used on pears and citrus (U.50) .497 (.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .600-1.820 (.60 (1. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.EPA.370-. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.50 (1.10-2. in paints.570-2.03) 1.50) < LOD .33 (. Timchalk et al.10) . Estimated human intakes have been below recommended intake limits (U.20) < LOD 1. Survey Geometric mean (95% conf. and it has limited water solubility.389-.19 (.90) .600) < LOD 1. whereas SOPP is not volatile and is more water soluble.00 (1.3.493 (. 1989).450 (<LOD-.420 (<LOD-. and as a wood preservative. 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.10) 1.00 (1.490 (<LOD-. 1998). such as fruits and vegetables.490 (<LOD-.20 (..61) 2.370-.20-3.90) 2. Cnubben et al.30 (1.30) < LOD 90th 1.740 (.20) 2.50) < LOD .560-8.90 (1.90) .50-2.389-.76) 1.40-5.22 (.60 (1. OPP is considered to be moderately toxic after acute oral doses in animal studies.88) 1.50 (1.85) 2.00 (1.20 (1.90) 1.790) 2.570 (.780) < LOD . 1998. EPA.580-1. Most agricultural food applications have been revoked. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.498 (. General population exposure can occur via dermal.92 (.696) * .836) * .00) < LOD .540-2.30-7.50) < LOD .30) < LOD 1.860 (.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 . 2006).930 (.349-. < LOD means less than the limit of detection.14 (<LOD-3.23) 695 680 520 695 603 953 Limit of detection (LOD.

01) 1.06-5.EPA 2006).580) < LOD . 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...970) 1.860 (.38) 2.670) < LOD . Ito et al.940-2.47) . 2005).78 (2.64 (2.32) 3. 2002.44 (1.640-1.32) 1. Volunteers exposed to 0. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.650-1.403-.93) .770-2.31) < LOD .670 (. In high dose animal studies.52 (.980 (<LOD-1.38) 1. or.17 (. Additional information is available from U.51-3. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.59) 1.600-1. Smith et al. 1984.460-.75 (1.21-2.11 (.550-.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.20) < LOD 3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..514 (. Pathak and Roy.248-.96) 1.S.81) 1.27) < LOD .484) * .33) .29) 1. but no neurologic. 1984.11) < LOD 90th 1.43-2. 2002.510-.455-. 2000.910 (<LOD-1. Murata et al.11 (.473) * .620-1.11) 4.690 (.08-1.06-4.43-2.361-.18) 2.96-4.13) 1..810-1.09-3.270-.12-2.800-1.05-2.69 (1.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .560-2.24-2.96 (1. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.4) 3. OPP was not found to be mutagenic.670 (. 1998.46) < LOD 1.500) < LOD .496 (.17 (.453 (.40-13. 1986).360 (<LOD-.86 (1.420 (<LOD-.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.88-4.420 (<LOD-.440 (.568) * .28 (2.900) < LOD .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 .320 (<LOD-. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.410 (<LOD-.EPA 2006).780 (. and it has classified OPP as not classifiable with respect to human carcinogenicity. reproductive.97 (2. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC. U.93) .11-1.580-1.880-1.28 (<LOD-4. Zhao et al. CDC. Detectable levels were seen in over half the U.S.810) < LOD .570) < LOD 1.590) * . or developmental toxicity was observed (Bomhard et al.860 (. 2005.02 (.53) 1.666) * .61 (1. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.840 (. 2005).75 (1.343 (.09 (1.353-. by possible genotoxic mechanisms (Hagiwara et al.gov/pesticides/. 1999.62) .470) < LOD .21) 1.74 (1..558) Selected percentiles ( 95% confidence interval) Sample 95th 2.791) * .750 (.61 (2.560) < LOD 75th .950) < LOD .93) 1. Nakagawa et al. 1997.990) < LOD . 1999.61 (.S.S.06 (1. leading to production of two metabolites.910-1.43) 3. Brusick. 2002).29) 1.17) * 99-00 01-02 99-00 01-02 99-00 01-02 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.26) 1.04-4.17) 2.291-.84 (1.444 (.58) 2.620-1..43 (1.329-.900-1.S..09-6.550) < LOD .91 (1. interval) .08) 1.382 (.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .38-3. U.980 (.96 (1.0) 1.750-2.00 (.750 (.08-2.311-.Fungicides anemia. Biomonitoring Information Urinary OPP levels reflect recent exposure. Kwok et al.25-6.510 (<LOD-.93 (1.508) * .380 (. 1992.656) * .24-2.480-.385 (. 44 Fourth National Report on Human Exposure to Environmental Chemicals .610) < LOD 1.epa.470 (<LOD-.301-.410 (<LOD-.780-14.550 (.910 (.07) 2.89 (1.21 (. IARC has classified SOPP as a possible human carcinogen. Survey Geometric mean (95% conf..33-2. less likely. 1993.59) .00 (1. Bomhard et al.12) < LOD 1.EPA at: http:// www.. population from the National Health and Nutrition Examination Survey.

Office of Toxic Substances. Inoue S. Imaida K. J Agric Food Chem 2006. 2005.S. Atlanta (GA).niehs. Shirai T.43(7):14311437. Arch Toxicol 2000.35(2 Pt 1):198-208.20(5):851-857. Bomhard EM. Moore GA. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Brzak KA. Hirose M. Drugs. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes.S. Buchholz BA. Hagiwara A. Regul Toxicol Pharmacol 2002. Herbold BA.50(11):3351-3358. Toxicol Appl Pharmacol 1998. Environmental Protection Agency (U. National Toxicology Program (NTP). et al. Timchalk C. Environ Mol Mutagen 2005. Turteltaub KW. Richter M.S. Kwok ES.(56):399-407. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Nakagawa Y. Arnold LL. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Environmental Protection Agency (U. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Eadon G.159(1):18-24.22(10):809-814. July 28.28(6):579594. EPA 739 R-06004.54(16):5731-5735. Coelhan M. Zhao S. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Centers for Disease Control and Prevention (CDC). Mendrala AL. Bartels MJ. Timchalk C. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. EPA-560/5-89-003. Roberts AL. Hagiwara A. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Ito N. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. St John MK. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Gierthy J. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. J Agric Food Chem 2002. Cnubben NH. Bartels MJ. Kawanishi S. Fukushima S. Fukushima S.gov/oppsrrd1/REDs/ phenylphenol_red. Christenson WR. Meuling WJ.epa.S. Elliott GR.. McNett DA. Vogel JS. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Food Chem Toxicol 1984. Murata M. Toxicol Appl Pharmacol 1999. Freyberger A. Available at URL: http://www. 4/13/09 Onstot JD. Moldeus P.Fungicides References Appel KE. March 1986. Bromig KH.gov/ntp/htdocs/LT_ rpts/tr301. U. Brusick D. EPA).nih. Ito N. Smith RA.74(2):61-71. Brendler-Schwaab SY. Narang A. Glas K. 2006.150(2):402-413. Third National Report on Human Exposure to Environmental Chemicals. van de Sandt JJ. 90-43-7) in Swiss CD-1 mice (dermal studies).32(6):551-625. U.286(2):309-319. Bartels MJ. Moriya K. Pathak DN. Sangha GK. Identification of SARA compounds in adipose tissue.17(8):411-417. Selim S. J Chromatogr B Biomed Sci Appl 1997. Christenson WR. Hakkert BC.45(5):460-481. Mutat Res 1993. Shibata M. Biochem Pharmacol 1992. Comparative metabolism of orthophenylphenol in mouse. IARC Sci Publ 1984. Sangha G. Hum Exp Toxicol 1998. Tayama S. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries.pdf.703(12):97-104. Leser KH. 1989. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). et al. The carcinogenicity of the biocide ortho-phenylphenol. rat and man. Xenobiotica 1998. Stanley JS. Available at URL: http://ntp. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Roy D. Cano M. Bormett GA.pdf. Bartels MJ. Carcinogenesis 1999.EPA). 4/9/09. Eastmond DA. Crit Rev Toxicol 2002.

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

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

48 Fourth National Report on Human Exposure to Environmental Chemicals . < LOD means less than the limit of detection. Survey Geometric mean (95% conf.S.S. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2500 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 576 819 1105 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1178 1322 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 678 672 952 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor 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. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2501 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 576 820 1105 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1178 1323 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 678 673 952 Limit of detection (LOD. see Data Analysis section) for Survey year 01-02 is 0.

March 2006. EPA). Hodgson E. Larsen GL. Ward EM. Environ Sci Technol 2005. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Casida JE. Volume 65. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. reservoirs and ground water in the Midwestern United States. Barr DB. Fourth National Report on Human Exposure to Environmental Chemicals 49 .gov/oppsrrd1/reregistration/REDs/acetochlor_tred.pdf. Reynolds SJ. et al. and metolachlor herbicides in rats. Kier L. U. J Expo Sci Environ Epidemiol 2007.S. Number 15. Heederik D. Sanderson WT. Comparative metabolism and elimination of acetanilide compounds by rat. Whyatt RM. et al.108(12):1151-1157. Bravo R.11(4):353359. Deddens JA.248(2-3):115-122. Linderman R. Sci Total Environ 2000. 5/30/06. 5/30/06 U. Occurrence of sulfonylurea. imidazolinone. EPA). Jefferies PR.cce.S. Hladik ML. Hines CJ. Peter CJ. Curwin BD. et al. Chem Res Toxicol 1998. Hsiao JJ.248(2-3):123-133. Federal Register: January 24. Thurman EM. Wilson AG. Alavanja MC. Burkhardt MR. EPA 738-R-00-009.15(6):500-508. epa.S.15(9):702-735. Kolpin DW. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Lefevre PA. Environ Health Perspect 2000. J Agri Food Chem 1989. Xenobiotica 1994. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Environ Health Perspect 2003. Linhart SM. Centers for Disease Control and Prevention (CDC). Dialkylquinonimines validated as in vivo metabolites of alachlor.37(4):10881093. Rose RL. Kinney PL. Battaglin WA.Herbicides References Ashby J. Feng PCC. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Camann DE.111(5):749-756.html.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Barr DB.39(17):6561-6574. Third National Report on Human Exposure to Environmental Chemicals.S. Acetochlor (Harness) Pesticide Petition Filing 1/00. Andrews HF. sulfonamide. Hein MJ. 2000.24(10):1003-1012. Barr DB. pages 3682-3690. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.S. Environmental Protection Agency (U. J Expo Anal Environ Epidemiol 2005. Available at URL: http://www.cornell. Wratten SJ. Environmental Protection Agency (U. Tinwell H. Atlanta (GA). Coleman S.17(6):559-566. Quistad GB. 2005. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Davison KL. Roberts AL. Green T. Olsson AO. Furlong ET. acetochlor. Striley CA. Feil VJ. Hum Exp Toxicol 1996. and other herbicides in rivers. Sci Total Environ 2000. 1998.EPA): http://pmep. Available at URL(non U. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Barr JR.

Herbicides Alachlor CAS No.. NTP and IARC do not have ratings regarding human carcinogenicity.EPA. WHO.S. 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. 2005). whereas 60% of applicators had detectable amounts. Tessier and Clark. 2000. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. In animal studies.S.... 1996.S. but shows little bioaccumulation.. In animals. IPCS. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al.epa.. Feng and Wratten.. Additional information about is available from U. the dermal exposure route is potentially significant for applicators. mercapturate conjugates were predominant metabolites. Because it can be absorbed through skin. and uveal degeneration. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. USGS. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. Hladik et al. It is absorbed by plants and inhibits plant protein synthesis. Hines et al. Estimated human intakes have been below recommended limits (U. mean values of urinary concentrations of alachlor metabolites. 1999 and 2007.6-diethylaniline and its reactive metabolite. ranged from 0. and field workers. (2003) showed that 2. 1998. U.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. U..S. soybeans. In chronic animal testing. alachlor has demonstrated hepatotoxicity. 2003).S. hemosiderosis.1 mg/L at various collection times (Sanderson et al. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. 2005. 2003). In 1993-1995. Since the late 1980s alachlor use has been declining. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Hill et al.EPA. In a study of applicators and workers exposed to alachlor.1 to 1..S. 1997. 1995).EPA. 2003). Kolpin et al.EPA. 1996). and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. 50 Fourth National Report on Human Exposure to Environmental Chemicals . the latter may account for some observed effects (Davison et al.S. formulators. WHO. Alachlor has low potential for acute toxicity. as measured through conversion to deethylamine. but not likely at low doses. peanuts and other crops. and on non-crop land for general weed control. including corn..EPA. 2003). WHO. Alachlor itself is not considered mutagenic. 1998. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. U. 2000. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. but another metabolic pathway can produce 2. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. Jefferies et al. 1998). Biomonitoring studies on levels of alachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of alachlor than are found in the general population. Alachlor has a soil half-life of a few weeks. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC.gov/pesticides/. 1989. WHO. corn cropland was treated with alachlor. 1998).EPA considers alachlor to be a probable human carcinogen at high doses. but has not shown developmental or reproductive toxicity in mammalian systems (U.S. EPA at: http://www. 1996. stomach. about 20-25% of the U. 1998. 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. 1988. 1994. 1995. U. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1999. 1998). though positive genotoxic results are reported for several metabolites of alachlor (Brown et al.

S. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 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. Urinary Alachlor mercapturate (creatinine corrected) Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. Survey Geometric mean (95% conf. * 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 51 .18. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 99-00 is 1. population from the National Health and Nutrition Examination Survey.Herbicides Urinary Alachlor mercapturate Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < LOD means less than the limit of detection. 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.

Jefferies PR. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Driskell WJ.24(10):1003-1012.11(4):353359. Comparative metabolism and elimination of acetanilide compounds by rat. Geological Survey (USGS). Clark JM. Sanderson WT. World Health Organization (WHO).Herbicides References Battaglin WA. Life Sci 1988. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor.43(9):2504-2512. California. and other herbicides in rivers. reservoirs and ground water in the Midwestern United States. Thake DC. Feil VJ. Tessier DM. Hladik ML. Alachlor in Drinking-water. Brown MA.S. Sci Total Environ 2000. Tolos W. Erratum in: Life Sci 1989. Feng PCC.47(6):503-517. Third National Report on Human Exposure to Environmental Chemicals. et al. sulfonamide. Chem Res Toxicol 1998. Kolpin DW. 1992-2001. Xenobiotica 1994. Biagini R. Quistad GB. 1999. Hill AB. Geneva. International Programme on Chemical Safety (IPCS). 2003. imidazolinone. March 2006. Furlong ET. Casida JE. EPA 738R-98-020. Camann DE. 2005.pdf. ALACHLOR. Background document for development of WHO Guidelines for Drinking-water Quality. Barr JR. Available at URL: http://www. Am Ind Hyg Assoc J 1995. Thurman EM. Centers for Disease Control and Prevention (CDC). Biagini RE.S. J Ag Food Chem 1995. WHO/ FAO Data Sheets on Pesticides. Environmental Protection Agency (U. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. 1998. Occurrence of sulfonylurea. Casida JE. Reregistration Eligibility Decision (RED) Alachlor. Lau H.111(5):749-756.org/documents/pds/pds/pest86_e. Kinney PL. U.39(17):6561-6574. et al. Heydens WF. acetochlor. Quistad GB. Linhart SM. 4/2/09 U. December 1998. who. Larsen GL. Supplemental Technical Information (available on-line only). Shoemaker DA. Hsiao JJ. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Environ Health Perspect 2003. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Striley CA. Casida JE. EPA). Whyatt RM. Hines CJ. Geological Survey (USGS).int/water_sanitation_health/dwq/chemicals/en/alachlor. World Health Organization.php.gov/oppsrrd1/ REDs/0063.18(6):363-391. Hill RH Jr. Available at URL: http://water. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Gilliom RJ). Brown KK.usgs. Shealy DB.inchem. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.S. Ann Occup Hyg 2003. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Hines CJ.37(4):10881093.56(9):883-889. revised February 15. Environ Sci Technol 2005. Deddens JA. J Agri Food Chem 1989. 2/27/09 Jefferies PR. Mutat Res. Hum Exp Toxicol.pdf. Wratten SJ.S.395(2-3):159-171. Burkhardt MR. Atlanta (GA). Roberts AL. Sacramento. Hull RD. 1996. DNA adduct formation by alachlor metabolites. Available at URL: http://www.44(18):1325. Kier LD. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Thelin GP. 98-4245 (by Barbash JE.56(6):853-859.248(2-3):115-122. 86. No. 2/27/09 U.248(2-3):123-133. Henningsen G. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Dialkylquinonimines validated as in vivo metabolites of alachlor.epa. Wilson AG. Bull Environ Contam Toxicol 1996. Kimmel EC. Peter CJ. 1997. 1999. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Available at URL: http:// www. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Circular 1291. MacKenzie B. Barr DB. Davison KL. Kolpin DW. and metolachlor herbicides in rats. Sci Total Environ 2000. 2007.43(25):2087-94. Martens MA.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.htm. Andrews HF. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.

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

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

et al. In a small number of field workers.30(2):244-247. Atlanta (GA). Tapia J. 2000). Ferrell JM. Noriega N. 1993). The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Stoker TE. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Hayes TB. Brown KK. levels of atrazine mercapturate were generally not detectable (CDC.. Biagini RE. Aldous CN. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Fleenor-Heyser DG. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Deddens JA. Stuart AA.cdc. Breckenridge CB. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. 1996. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). J Toxicol Environ Health 1994. 2007). Bersani M. Biological monitoring of human exposure to atrazine. International Programme on Chemical Safety (IPCS).53(2):297-307. Catenacci G. 3/11/09 Arcury TA. diamino-S-chlorotriazine and hydroxyatrazine. 2003. Available at URL: http:// www. Eberly LE. Striley CA. et al.html. et al. 3/11/09 Laws SC. McElroy WK. Sanborn JR.58(2):366-376. References Adgate JL. 2005).. A risk assessment of atrazine use in California: human health and ecological aspects. Vonk A. Sanderson WT. Barbieri F. Barr DB. Wetzel LT. J Toxicol Environ Health 1994. et al. Centers for Disease Control and Prevention (CDC). Cooper RL. Reynolds SJ.. Stoker TE. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Hein MJ. In the NHANES 2001-2002 subsample. 2001 [online]. Freeman NC. atrazine was detected in only four children (Arcury et al. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Tyrey L. Quandt SA. Saiz SG. Mendoza M. 2005. Chen H. Collins A. Lucas AD. et al. Lee M. Geneva.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Cottica D. No. Jones AD. Extrom PC. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Proc Natl Acad Sci USA 2002. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect.gov/toxprofiles/tp153. Bradway DE. Shoemaker DA. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Ferrell JM. Blewett C. Gammon DW.43(2):155-167. Cooper RL. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Hines CJ. Third National Report on Human Exposure to Environmental Chemicals. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.47(6):503-517. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.69(2):217-222. Perry et al. Laws SC. Ferioli A. WHO/ FAO Data Sheets on Pesticides. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Wetzel LT. 82. Gillis JH.org/documents/pds/pds/pest82_e. In small studies of Maryland residents in 19951996 (MacIntosh et al. Eldridge JC. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Pfeifer KF. Pest Manag Sci 2005. Hermaphroditic. Toxicol Sci 2000. Barr DB. Schmid J.. ATRAZINE. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Seiber JN.76(1):190-200.109(6):583-590. 2005).115(8):1254-1260. 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 2000.43(2):155-167. Toxicol Sci 2003. Barr DB.61(4):331-355. Agency for Toxic Substances and Disease Registry (ATSDR). Cooper RL. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Grzywacz JG. Moseman RF. Ann Occup Hyg 2003. Toxicol Lett 1993.15(6):500-508. Carr WC Jr. J Agric Food Chem 1982.. 2001). Stoker TE. Simpkins JW. Available at URL: http://www. Heederik D. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Lioy PJ. Stevens JT. Eldridge JC.64(9):672-678. Clayton CA. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Curwin BD..htm. Environ Health Perspect 2007.99(8):5476-5480. Goodrow MH.atsdr. Maroni M.inchem. Gillis JH. Toxicological profile for atrazine. et al. In a study of 60 farm worker children.. Goldman JM. J Expo Anal Environ Epidemiol 2005. The geometric mean of urinary atrazine mercapturate was 1. Environ Health Perspect 2001. World Health Organization. Steroids 1999.

Timchalk C. Hammerstrom KA. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Toxicol Sci 2000.182(1):44-54. EPA Office of Pesticide Programs. Langvardt PW. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Toxicol Appl Pharmacol 2004.S. EPA).67(2):198-206. 0062. Boerma J. Environmental Protection Agency (U. Sathiakumar N. 1992-2001.56(2):69-109. A longitudinal investigation of selected pesticide metabolites in urine. Guidici DL.S. Laws SC. Wetzel L. The Quality of Our Nation’s Waters. Pesticides and Toxic Substances. Christiani D. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. J Toxicol Environ Health A 1999.27(6):599612. Toxicology 1990. Guidici DL.S. MacIntosh DL. 2007. Available at URL: http://www.php. Perry M. Ryan PB. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Ann Epidemiol 2000.epa. Breckenridge CB. Laws SC. EPA).pdf. Environmental Protection Agency (U. Stoker TE. White paper on potential developmental effects of atrazine on amphibians.10(7):479. Pesticides in the Nation’s Streams and Ground Water. Cooper RL.S. Case No. A review of epidemiologic studies of triazine herbicides and cancer. May 2003a.pdf. 3/11/09 U. Stoker TE. A risk characterization for atrazine: oncogenicity profile. Interim Reregistration Eligibility Decision For Atrazine.epa. Geological Survey (USGS). Chem Res Toxicol 1993. Sanderson JT. Needham LL. Supplemental Technical Information (available on-line only). Delzell E. Circular 1291. Toxicol Sci 2002. Rayner JL.61(1):27-40. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .gov/oppsrrd1/REDs/ atrazine_ired. Stevens JT. Available at URL: http://www. Washington (DC). Fenton SE. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function.58(1):50-59. 2003b.Herbicides development of a biomarker of exposure.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.6(1):107-116. Cooper RL.usgs. Tortorelli J. Toxicol Appl Pharmacol 2002. Environmental Fate and Effects Division. Osborne DW.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Office of Prevention. Singzoni B. Dryzga MD. Wood C.195(1):23-34. March 2006.S. J Expo Anal Environ Epidemiol 1999. 6/1/09 U. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. U. Available at URL: http://water.9(5):494-501. Lansbergen GW. van den Berg M. Crit Rev Toxicol 1997. revised February 15. Dagenhart D. Kastl PE.

2. but at higher levels they are herbicidal.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .250 (<LOD-.27 (1. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms. by direct contact with agricultural and residential areas after applications.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al. 1977). 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.960-1.13) < LOD . and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. headache.210 (<LOD-.20 (<LOD-1. 2007).48) < LOD 1. It is rarely detected in ground waters (USGS.4-D may occur during residential applications.890) < LOD . Once absorbed. < LOD means less than the limit of detection.30 (<LOD-2. General population exposure to 2.420) < LOD ..310 (.210-.27 (.230-. At low levels.24 (.740 (.952 and 0.330 (.490 (.02-1.10 (<LOD-1.370-.410) < LOD . and delayed Urinary 2.610-.05-2.S.4-D has low acute toxicity. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.70) 1. Human health effects from 2. Survey Geometric mean (95% conf.4-D were used in the U. Recent estimates of chronic intakes of 2. dizziness. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.760 (.540-.550-1.51 (1. it acts as a plant growth hormone.55 (1. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. 1989.910) 1.930 (.930-1.00-2. 2.690 (.690 (.230 (<LOD-.730 (. 2005). 1974.350) < LOD < LOD < LOD . abdominal pain.670-1..4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. with a half-life of several days to several weeks.07 (.S. It was first registered with U.4-D can be applied either as an aqueous salt or as oil-soluble esters.08) < LOD . renal and hepatic injury.21) 1.27-2.10) < LOD 1.4-Dichlorophenoxyacetic Acid CAS No. myotonia. Kohli et al. Sauerhoff et al.60) 1.910) < LOD .690-1.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .. 94-75-7 General Information Widely used throughout the United States.250 (<LOD-.20 (.420-. 2. As much as 62 million pounds of 2.4-D) controls broadleaf weeds in residential.37) size 1977 2413 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 57 . It is poorly bound in soils. these herbicides can enhance plant growth. MCPA.80) 1.32 (1. and aquatic environments.22) < LOD .690 (.560-. and by consuming food or drinking water contaminated with 2. which may vary for some chemicals by year and by individual sample.4-dichlorophenoxyacetic acid (2.610 (.4-D or exposed for prolonged periods. agricultural.40) 1.10 (<LOD-1.16) < LOD .910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400) < LOD . population from the National Health and Nutrition Examination Survey.320) 90th .S.EPA in 1948.660) 1. It is not well absorbed through the skin.680-1.S.440-1. 2.66) < LOD 1.490) < LOD < LOD < LOD .810-1.43) 1. Similar to other chlorophenoxy herbicides.4-D is rapidly absorbed via oral and inhalation routes.560-1.4-D have been below recommended intake limits (U. the chlorophenoxy herbicide 2.Herbicides 2.260 (<LOD-.EPA.890 (.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. hypotension. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. and mecoprop). nausea.EPA.03) 695 659 520 668 589 892 Limit of detection (LOD. 4-D. 2004). in 2001 (U.310) < LOD .

40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.980) < LOD 1. 1995. in small samples of children (Hill et al. 2005. 1985.380) < LOD . and of adults and children (Baker et al. CDC..8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.850) < LOD . The acid and salt forms of 2.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. IPCS. or to contaminants in the herbicide formulations (specifically 2.S. 2005).590 (<LOD-1.24) 1. Survey Geometric mean (95% conf. 1989).56) . with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.810-1.790) 1.S.890-1.410) 90th . 2005).930-1.660 (.820-1. Biomonitoring Information Urinary levels of 2..EPA 2005). developmental. 2006. 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. It is unclear whether these associations are related to the chlorophenoxy herbicides.520-.39) < LOD 1.16) 1.S.08 (. eyes.14 (.990-1.410) < LOD 1.470) < LOD .920) < LOD 1. 2. liver. or teratogenic effects in chronic rodent studies (Charles et al.S.610-.560-.270-. 2004).390) < LOD < LOD < LOD .570) < LOD .S.19) ..380-.330-.720 (.340 (. urinary 2.340-. U. Acute high doses administered to laboratory animals produced ataxia. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.890) < LOD 1. 58 Fourth National Report on Human Exposure to Environmental Chemicals .S.410) < LOD < LOD < LOD . 2005). Knopp et al.380 (<LOD-. other exposures. and evidence of histological injury to the kidneys.13 (.4-D levels were detectable in less than a quarter of the individuals studied. thyroid.790) < LOD .7. In previous samples of the U. 2002. 2005.350 (<LOD-.550-.EPA. Kutz et al.epa..670 (.05) . Post-application levels in farmers and home gardeners were dependent on Urinary 2. Hill et al.740 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. myotonia.13 (.4-D does not have significant reproductive. 2005).. 2003.640 (.780 (. 2005.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. U. U. Additional information is available from U. 1995).4-D are eye irritants..490 (. Pearce and McLean.Herbicides neuropathy (Bradberry et al.560-.EPA.680) < LOD .29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .660) < LOD .480 (. Average post-application urinary levels of 2. adrenals and gonads (NTP. 2002. 1994). 1996.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD ..620-.4-D production plant workers and a few forestry workers spraying 2.73) .590 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380 (<LOD-.EPA. U.780) . IOM.440 (.41 (1.17 (. 2000).35) < LOD . 2.08 (. population from the National Health and Nutrition Examination Survey.08 (.810-1. IPCS.. 1992).780-1.610-. 2001.270 (<LOD-. 1996.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.4-D reflect recent exposure.670 (<LOD-1.26) 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 . 2005.4-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.3. population (Hill et al. 1996.700 (.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert..S.670 (. Epidemiological studies have reported associations of several types of cancer. IPCS.580-.. Kolmodin-Hedman and Erne. Frank et al. 1980.32 (<LOD-2.27-1.EPA at: http://www. 2.410 (<LOD-.gov/pesticides/.

Khanna RN.gov/index. Heederik D.4-. the number of acres to which it was applied (Curwin et al. Hanley TR Jr. Holler JS.4-D were highest in the farmers who applied the 2. Atlanta (GA). Kutz FW. the amount of pesticide applied. In farm families. Beasley VR. 2003. Fast DM.org/documents/jmpr/jmpmono/v96pr04. Bus JS. Solomon KR.51(3):152-159. International Programme on Chemical Safety-INCHEM (IPCS).4:427-435. 3/17/09 Institute of Medicine (IOM). Forestry workers involved in aerial application of 2. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Hill RH Jr. and the use of protective clothing or equipment (Arbuckle et al. Ripley BD.5-T).. Hill RH Jr.Herbicides the time since application. 2005). Beeson MD.4-D in urine does not mean that the level of the 2. Tandon JS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Murphy RS. Vet Hum Toxicol 1989. et al. Philbert MA. Erne K. Sanderson WT.4-D. Baker S. J Toxicol Environ Health 1992. Needham LL. geometric mean urinary levels of 2. Pesticides residues in food: 1996 evaluations Part II Toxicology. Mandel et al. Updated March 7. Campbell RA. Cook BT. Wilson RD. Survival and Growth Curves from NTP Toxicity Studies.. Biomonitoring studies of 2. Acquavella JF. Arch Environ Contam Toxicol 1989. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.71(2):99-108.31(2):121-125. Third National Report on Human Exposure to Environmental Chemicals. References Arbuckle TE. TOX-63 Peroxisone Project (2. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Sirons G J. Smith SJ. Sircar KP. 2006. Scand J Work Environ Health 2005. Head SL. J Expo Anal Environ Epidemiol 2005 Nov.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Harris SA. Hein MJ.4-D) epidemiology and toxicology. Selected pesticide residues and metabolites in urine from a survey of the U.S. Honeycutt R. Alexander BH. Needham LL.nih.31 Suppl 1:90-97. Crit Rev Toxicol 2002. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Cole DC.4-D and 2.htm. Garabrant DH. 1992).. Scand J Work Environ Health 2005. Arch Environ Contam Toxicol 1985. van Ravenzwaay B. Available at URL: http:// www.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. Centers for Disease Control and Prevention (CDC). Biomonitoring of herbicides in Ontario farm applicators.15(6):500-508. general population.4-D than levels found in the general population. Reynolds SJ. J Environ Sci Health B 1992. Arnold EK. Barr DB. Brody D. Xenobiotica 1974.31 Suppl 1:98-104. Occup Environ Med 1994.4-D will result in an adverse health effect. Mandel JS. Dichlorophenoxyacetic acid. Pesticide residues in urine of adults living in the United States: reference range concentrations. Shealy DB.4.. Gregg M.32(4):233-257. Toxicol Sci 2001.4-Dichlorophenoxyacetic Acid). Ritter L. et al. Absorption and excretion of 2. Review of 2.nap. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Stephenson GR. National Toxicology Program (NTP).inchem. Kohli JD. Developmental toxicity studies in rats and rabbits on 2.niehs. Board on Health Promotion and Disease Prevention. TOX-63: TOXICITY REPORT CURVES. Barr DB. Chapman P.4-dichlorophenoxyacetic acid in man.4-dichlorophenoxyacetic acid and its forms.18(4):469-474. 2005. Carter-Pokras OD. 914.4-D). Curwin BD.27(1):23-38. Baker BA. Gupta BN. Estimation of occupational exposure to phenoxy acids (2. Tables.4:97-100. Environ Res 1995. Finding a measurable amount of 2. Kolmodin-Hedman B.php?record_id=10603. Exposure of homeowners and bystanders to 2. Baker SE. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. J Expo Anal Environ Epidemiol 2000. Veterans and Agent Orange: update 2002. Dhar MM. 2005 Charles JM. Frank R. 3/17/09 Knopp D.37(2):277-291. 2005). 2.60(1):121-131. Bailey SL. Harris et al. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. To T. Driskell WJ.10(6 Pt 2):789-798. Washington (DC): National Academies Press. Biomonitoring for farm families in the farm family exposure study.4:318-321.4-D): exposure and urinary excretion.4 dichlorophenoxyacetic acid (2. Available at URL: http://ntp. et al. Available at URL: http:// www.edu/catalog. 2005. Arch Toxicol Suppl 1980. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .4-dichlorophenoxyacetic acid (2.4-dichlorophenoxyacetic acid (2. Assessment of exposure to 2.

2.EPA). EPA 738 F-05-002. June 2005. Office of Prevention Pesticides and Toxic Substances. revised February 15.EPA.4-D RED Facts. 3/17/09. 60 Fourth National Report on Human Exposure to Environmental Chemicals . 2004.S. 2007.gov/oppsrrd1/ REDs/factsheets/24d_fs. Geological Survey (USGS). Environmental Protection Agency (U.8:3-1U. May. S.usgs. 1992-2001. Supplemental Technical Information (available on-line only). The fate of 2.4-dichlorophenoxyacetic acid (2.htm. The Quality of Our Nation’s Waters.4-D) following oral administration to man. Blau GE. 4/2/09 U. Environmental Protection Agency (U.S. gov/oppbead1/pestsales/01pestsales/market_estimates2001.S. Toxicology 1977. Available at URL: http://water. Gehring PJ. Pesticide industry sales and usage . Braun WH.php.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Available at URL: http://www. March 2006.2000 and 2001 market estimates. Washington (DC): U. 3/17/09 U. Available at URL: http://www.EPA).epa. Circular 1291.pdf. Pesticides in the Nation’s Streams and Ground Water.Herbicides Sauerhoff MW.epa.S.S.

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

Survey Geometric mean (95% conf.670 (<LOD-. population from the National Health and Nutrition Examination Survey.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .440 (<LOD-.S.S. * 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 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-. 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 . Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. < LOD means less than the limit of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.2. see Data Analysis section) for Survey year 01-02 is 0.740) 679 700 957 < 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. Survey Geometric mean (95% conf.200 (<LOD-.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 62 Fourth National Report on Human Exposure to Environmental Chemicals .240) 679 701 957 Limit of detection (LOD.

Background document for development of WHO Guidelines for Drinking-water Quality. and metolachlor herbicides in rats. Available at URL: http://www. Thurman EM.int/water_sanitation_health/dwq/chemicals/ metolachlor. Larsen GL. EPA). 4/2/09 U. 1998. Wratten SJ. Andrews HF.gov/nawqa/ pnsp/pubs/wrir984245/text. Barr DB.usgs. Reynolds SJ. Metolachlor in Drinkingwater. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Circular 1291. Striley CA.Herbicides References Battaglin WA. Camann DE. Alavanja MC. R. Shoemaker DA. J Agri Food Chem 1989. Feng PCC. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Sci Total Environ 2000.41:3409-3414. Gilliom RJ). Burkhardt MR. Xenobiotica 1994. Kolpin DW. Kinney PL. April 1995. Pesticides in U.php.24(10):1003-1012. Environ Sci Technol 2005. World Health Organization (WHO). 1999. Kolpin DW. Available at URL: http://water. et al. Hodgson E. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.ESTfeature_gilliom. Available at URL: http://www. Sanderson WT. J Expo Anal Environ Epidemiol 2005. reservoirs and ground water in the Midwestern United States.108(12):1151-1157. Ward EM. Coleman S. Centers for Disease Control and Prevention (CDC). 2003. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Chem Res Toxicol 1998. Biagini RE. Ann Occup Hyg 2003.15(6):500-508. March 2006. 2007.pdf 3/30/09 Hines CJ. and other herbicides in rivers. Sacramento. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Heederik D. Reregistration Eligibility Decision (RED) Metolachlor. Thelin GP.47(6):503-517. usgs. Environ Health Perspect 2003. 2005. Available at URL: http://water. 1992-2001.S.S. Peter CJ. Supplemental Technical Information (available on-line only).111(5):749-756. Brown KK. Gillion. Hein MJ. Hladik ML.S.gov/nawqa/pnsp/pubs/files/051507.11(4):353359. Third National Report on Human Exposure to Environmental Chemicals.gov/oppsrrd1/ REDs/0001.248(2-3):123-133. Linderman R. Roberts AL. California.pdf. 6/1/09 Whyatt RM. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.usgs. Barr DB. Hsiao JJ. Geological Survey (USGS). streams and groundwater.248(2-3):115-122. sulfonamide.S.39(17):6561-6574. Furlong ET. Environ Sci Technol 2007. Environmental Protection Agency (U. Available at URL: http://water.S. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Davison KL. et al. Curwin BD.epa. Atlanta (GA). Comparative metabolism and elimination of acetanilide compounds by rat. 98-4245 (by Barbash JE. revised February 15. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 .gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Barr JR. Quistad GB. Environ Health Perspect 2000. Linhart SM. imidazolinone.37(4):10881093. Dialkylquinonimines validated as in vivo metabolites of alachlor. Jefferies PR.who.pdf.html. Occurrence of sulfonylurea. 3/26/09 U. Deddens JA. Geological Survey (USGS). Casida JE. EPA 738R-95-006. Sci Total Environ 2000. acetochlor. Rose RL. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Feil VJ. U.

see Data Analysis section) for Survey years 99-00 and 01-02 are 1.1. 1989. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. and concern about contamination with 2. the general population is unlikely to be exposed to it.3. 2007). 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. 2004). it is not well absorbed through the skin.5-T and 2.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. dizziness.5-T degrades to 2. 1986. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 1992).4.4. hypotension.4. which may vary for some chemicals by year and by individual sample. Human health effects from 2..5T is rapidly absorbed via oral and inhalation routes. 1992. Survey Geometric mean (95% conf.5-Trichlorophenoxyacetic Acid CAS No. At low levels.2 and 0.4. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.5-trichlorophenol and other degradates. but higher levels are herbicidal. with an elimination half-life of approximately 19 hours (Arnold et al. Kohli et al. Mohammad and St.g.4. Epidemiological studies have reported associations of several types of cancer. Once absorbed into the body..4. abdominal pain. Chlorophenoxy herbicides act as plant growth hormones.7.4.5-T use as a herbicide in 1985.5-T.5-Trichlorophenoxyacetic acid (2.4.4-D were used as defoliants in the Vietnam War (e.5-T is eliminated mostly unchanged in the urine.5-T was once applied as either an aqueous salt or as an oil-soluble ester. nausea. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2.4. 93-76-5 General Information 2. Ester forms of 2.. 64 Fourth National Report on Human Exposure to Environmental Chemicals . < LOD means less than the limit of detection. 1974). myotonia.. The half-life of 2.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. population from the National Health and Nutrition Examination Survey.4.S. Nelson et al.4. these herbicides can enhance plant growth.5-T in soil varies with conditions. Although 2.4.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. renal and hepatic injury. and delayed neuropathy (Bradberry et al. 2.4. Given the commercial unavailability of 2.5-T (Holson et al.. ranging from several weeks to many months.4. Agent Orange). 2.Herbicides 2. Omer.4. headache. 2.4.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2.5-T has been rarely detected in ground waters (USGS. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.

7. or to contaminants in the herbicide formulations (specifically 2. Additional information is available from U. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. Survey Geometric mean (95% conf. urinary levels of 2. 2002. 2005. similar to results of NHANES II (19761980).5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2005).5-T does not mean that the level will result in an adverse health effect. * 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 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.4. 1992). 1980).gov/pesticides/.Herbicides or contaminated herbicides. Biomonitoring studies on 2.4.4. Mean urinary levels of 2.5-T itself is not mutagenic. 2003.EPA.4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. 2.4.EPA at: http://www. other exposures.5-T than levels found in the general population.S. 2004). Fourth National Report on Human Exposure to Environmental Chemicals 65 .4. Biomonitoring Information Urinary levels of 2..S. It is unclear whether these associations are related to the chlorophenoxy herbicides. 1996.4. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. in which urinary levels of 2.epa.3. population from the National Health and Nutrition Examination Survey. U. IPCS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary 2. Pearce and McLean.5-T were generally below the limit of detection.4.4.5-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. IOM. Finding a measurable amount of 2.5-T reflect recent exposure.S.5-T also were below the limit of detection (Kutz et al.

LaBorde JB. U.pdf. Pesticides residues in food: 1996 evaluations Part II Toxicology.4:318-21. Developmental toxicity of 2. 2004. Arch Toxicol Suppl 1980.4-D/2.epa. Sircar KP.23(2):65-73. Pesticide industry sales and usage . S. Tandon JS. St Omer VE.5-t mixture. 3/17/09 Institute of Medicine (IOM). Selected pesticide residues and metabolites in urine from a survey of the U. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .inchem.4-D) epidemiology and toxicology. May. Veterans and Agent Orange: update 2002. Wolff GL. 210:250-255. general population.4.37(2):277-91.19(2):298-306.4. Poisoning due to chlorophenoxy herbicides.S. Proudfoot AT.S. Dichlorophenoxyacetic acid.htm. Vale JA. et al.32(4):233-257. Holson JF. 3/17/09 Kohli JD.php?record_id=10603. Toxicol Rev 2004. Mohammad FK. Khanna RN. 2. Available at URL: http:// www. International Programme on Chemical Safety-INCHEM (IPCS). Bradberry SM.org/documents/jmpr/jmpmono/v96pr04. II.5-T). Review of 2. Kutz FW. Gaines TB.4-. 2005.4-dichlorophenoxyacetic acid (2. Philbert MA.5-trichlorophenoxyacetic acid (2. Erne K. Scand J Work Environ Health 2005. Fundam Appl Toxicol 1992. Brody D. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Gaylor DW. Pearce N. I. Environmental Protection Agency (U. Beasley VR.8(5):551-60.5-trichlorophenoxyacetic acid (2. Nelson CJ.31(2):121-125. McLean D.5-T). Garabrant DH. Centers for Disease Control and Prevention (CDC). Dhar MM. Gupta BN. Kolmodin-Hedman B. Holson JF. Multireplicated dose-response studies with technical and analytical grades of 2. Arch Int Pharmacodyn Ther 1974. et al. Estimation of occupational exposure to phenoxy acids (2.4-D and 2.31 Suppl 1:1825. Gaines TB. Washington (DC): U. Nelson CJ. 2003. Carter-Pokras OD.EPA. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.2000 and 2001 market estimates.4. Atlanta (GA). McCallum WF. Developmental toxicity of 2.4.4. discussion 5-7.S. Agricultural exposures and non-Hodgkin’s lymphoma. Behavioral and developmental effects in rats following in utero exposure to 2. LaBorde JB.4. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http:// www. Neurobehav Toxicol Teratol 1986. Board on Health Promotion and Disease Prevention. Washington (DC): National Academies Press. Murphy RS. Available at URL: http://www. Absorption and excretion of 2.19(2):286-297. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice.EPA).5-T in four-way outcross mice. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.4. Fundam Appl Toxicol 1992. 914. Vet Hum Toxicol 1989.nap. J Toxicol Environ Health 1992.edu/catalog.5-trichlorophenoxy acetic acid in man. Cook BT.5-T).4. Sheehan DM. Office of Prevention Pesticides and Toxic Substances. Crit Rev Toxicol 2002.Herbicides References Arnold EK.

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

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

dieldrin at higher doses caused irritability. population from the National Health and Nutrition Examination Survey. but no estrogenic effect was noted in a study that used cultured cells (Tully et al. 2004). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.html.. nausea. 1995).. and the FDA monitors foods for pesticide residues. both aldrin and dieldrin caused liver enlargement and liver tumors. IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity.cdc. In a study of pesticide applicators with occupational exposure to aldrin. When fed to experimental animals. in which only 10.6% of the subsample had dieldrin levels above the limit of detection (Stehr-Green 1989).atsdr. 2000).. 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). Epidemiologic and animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al. OSHA has established workplace exposure standards for aldrin and dieldrin. Survey Geometric mean (95% conf. 1987). tremors.Organochlorine Pesticides twitching. 2005).. serum aldrin levels were below the limit of detection. 2000). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 2275 1946 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 756 588 1519 1358 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1057 946 1218 1000 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 559 456 512 485 1045 881 < LOD means less than the limit of detection for the lipid adjusted serum level. environmental levels) and health effects is available from ATSDR at: http://www. which may vary for some chemicals by year and by individual sample.gov/toxpro2. the median serum dieldrin level was generally similar to the 90th percentile for females in this Report (Ward et al. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples.e. and occasionally. 2000. EPA has established environmental standards for aldrin and dieldrin. Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al. Kanthasamy et al...S. The U.S. seizures (Smith. similar to results in a subsample of NHANES II (19761980) (Stehr-Green. 2004). 78 Fourth National Report on Human Exposure to Environmental Chemicals . Information about external exposure (i.. 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... 1989). Li et al. 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... 1998). Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al. 1998) and behavioral changes (Carlson and Rosellini. the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al. 2005. 1991). In samples obtained between 1973 and 1991 from Norwegian women. 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. vomiting. and seizures. When dieldrin was fed to pregnant rodents.

090-.053 (<LOD-. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.190) .5-17.S.0 (10.090-.4) 14.103 (.7 (<LOD-15.8 (9.124) .138) .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 8.9 (14.070) .3 (19.3 (18.6-24.2) 14.9 (13.5) 21.3 (14.0-25.056-.8-24.089 (.10 (<LOD-16.1) 15.138 (.101) .100-.120-.130-.00 (8.077 (.120 (.093) .120 (.6-24.110 (.054-.1-19.110) .140) .9 (12.00-14.8-17.130-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.139 (.109-.060) .062-.70 (7.083-.112) 95th .30 (8.084-.1 (18.063-. Survey years 01-02 03-04 Geometric mean (95% conf.3-21.100-.054-.5 and 7.160) .6 (15.1) 15.048 (<LOD-.5-17.40-9.055 (.100 (.0 (10.4 (12.130) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 19.090 (. see Data Analysis section) for survey years 01-02 and 03-04 are 10.077-.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .062 (.120) .60-10.4-17.80 (<LOD-10.150 (.7) 15.0) < LOD 9.130) .2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.50 (8.2) 11.069) < LOD < LOD . which may vary for some chemicals by year and by individual sample.8-19.058) < LOD .2-15.116) .7 (14.4 (12.4) 539 456 484 487 980 885 Limits of detection (LOD.30 (8.9-23.1-16.9-38.8) 14.2) 15.90) 90th 15.9 (12.100) .8 (11.112-.110 (.S.070-.1) < LOD 9.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.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 .140-.088-.109 (.9 (13.102 (.5 (16.7-19.1 (13.6) 9. Survey years 01-02 03-04 Geometric mean (95% conf.110-.80-10.170) .180) .090-.0 (15.6 (15.103 (.6) 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 .090 (<LOD-.100-.8.5) 19.6) 16.147 (.064) 90th .0) 21.096-.130 (.049-. 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.8-25.110 (.080-.1-18.139 (.4) 95th 20.080) .0-21.062 (. 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 9.1-24.110) .075) < LOD .6-33.8) < LOD 8.8 (18.130-.1) 10.242) .177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .086-.3 (18.120 (.158) .109-.5) 15. population from the National Health and Nutrition Examination Survey.160 (.180) . Fourth National Report on Human Exposure to Environmental Chemicals 79 .098 (.1) 13.1) 20.059 (.3 (13.070 (<LOD-.9-22.7 (15.117) < LOD .80-9.40-10.160 (.50) 15.0) 19.073-.5 (<LOD-11.4) 21.054-.4-18.8-17. which may vary for some chemicals by year and by individual sample.5-15.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.149) .080 (.0 (11.1) 14.108-.4) 20.2) 12.150 (.130) .4) < LOD < LOD 16.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.8) 15.190) .6 (14.7-22.140 (.113 (.100) .064 (.

1991. Ellis H. Shore RF. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. PA. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants.103(Suppl 7):113-122. Psychopharmacology (Berl) 1987. Needham LL. Patterson DG Jr.gov/toxprofiles/ tp1. 2 Classes of Pesticides. 731-915. Chapin RE. Kanthasamy A.64-65 Spec. Daniel SE. Fernandez MG. Environ Health Perspect 2001. New York. Roy ML.html. Hartvig HB. Turner W. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. September 2002. Chlorinated Hydrocarbon Insecticides. August 2008. Available at URL: http://www. 2007 [online]. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Patterson DG Jr.9:1357-1367. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. VT.352:1816-1820. bioaccumulation. Olea N. plasma dieldrin.atsdr. are nonestrogenic in transfected HeLa cells. Six high-priority organochlorine pesticides. Finley B. Available at URL: http://www.cdc. Chung KL. No:429-436. Buckland SJ. Environmental Health Criteria 91. either singly or in combination. Smith AG. Organochlorine exposure and risk of breast cancer. Cancer Epidemiol Biomarkers Prev 2000. References Agency for Toxic Substances and Disease Registry (ATSDR). Frey JM.fda. Academic Press. Environ Health Perspect 1995. Revised Feb. Neurotoxicol 2005. toxicology.150:263-271. Narahashi T. Reprod Toxicol 2000. Kanthasamy AG. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Sonnenschein C. 4/21/09 Bates MN. Jr. Demographic and seasonal influences on human serum pesticide residue levels. Tully DB.org/documents/ehc/ ehc/ehc91. Mink PJ.gov/ circ/2005/1291/. Cox. Int Arch Occup Environ Health 1994. Mumtaz MM.html. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Mann D.htm. Kitzazwa M. Li AA. Garrett N. Basit A. 6/1/09 Ward EM. Schulte P. Exp Neurol 1998. Part A 2000. Ginsburg KS.26:701-719. and epidemiology in the United States. Brock JW.cfsan. Sanchez-Ramos J. Song S. J Toxicol Environ Health. Available at URL: http://pubs. Jorgensen T. Food and Drug Administration (FDA).54:1431-1443.91(1):122-126. 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. 1992-2001. Edwards JW. J Toxicol Environ Health 1989.47:1059-1087. J Occup Environ Med 2005. Handbook of Pesticide Toxicology. et al. Grandjean P. Inc. Jr and Laws ER.usgs. pp. 15. Priestly BG. Soto AM.gov/~dms/ pesrpts. Rosellini RA. 4/21/09 Jorgenson JL. and lymphocyte sister chromatid exchange. 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. Pesticides in the Nation’s Stream and Ground Water. Toxicol Lett 1992. Corrigan FM. In Hayes WJ. Eds. Stehr-Green. Grajewski B. Andersen A. Teta MJ. United States Geological Survey (USGS). Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. McIntosh LJ. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. 4/21/09 Hoyer AP. Vol.14:95-102. Anantharam V. Facca A.66(4):229-234.109(Supp1):113-139. Serrano FO. Available at URL: http://www. Aldrin and Dieldrin [online]. 1989. Toxicological profile for aldrin/dieldrin [online]. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Chemosphere 2004.27:405-421. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. David VL. Lancet 1998. Wienburg CL. Carlson JN.inchem. et al. Effect of occupational exposure to aldrin on urinary D-glucaric acid. International Programme on Chemical Safety (IPCS). Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994).59:229-234.

7) 42.1 (<LOD-12.5 (8.6-45.2 (41. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.0) 41.6-53.7-56.0) 21.3 (11.2-49.4-21.9 (17.4-51.4) 39.6) 20.1-65. 2007).0) 37.1) 30.8-33.9) 39.5 (34.0 (37. which results in exposure to the fetus and nursing infant Serum Oxychlordane (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.0-18.37 (8. which may vary for some chemicals by year and by individual sample.S.3) 10.2) 34.5.1 (16.0-13.8-33.9) 11. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.2 (9.1 (15.9) 23.74 (<LOD-10.2) 36.1-25.5) 44.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.5) 56.5-47. Technical grade chlordane had contained 7% trans-nonachlor. and 03-04 are 14.4 (35.8-23.2-49.7) 35.8 (10.8-43.8) 52.9 (21.8 (42.1) < LOD < LOD < LOD < LOD < LOD 8.1 (<LOD-12.7 (<LOD-13.5-41.6 (9. 1994).3) 18.2) < LOD 11.5 (<LOD-12.4) 18.6 (25.6 (9.1 (40. in addition to trace amounts of numerous other related compounds (ATSDR.4 (31.6) 39.6) 9. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.9 (29.1) * 11.3-49. Chlordane is not currently produced or used in the U.3-43. < LOD means less than the limit of detection.9 (11.10 (8. population from the National Health and Nutrition Examination Survey.89-10.4) < LOD 11.4) < LOD < LOD < LOD 23.5) 21.1 (<LOD-12.3 (25.8-20.7 (19.20 (<LOD-11.1) 22.20-10.5) 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 * * * * 11.2 (39.S.4) 12.5-38.8-31.1-50. lawns. 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. the technical grade product of each chemical contains 10%-20% of the other chemical.0 (20.69-10.8 (40.1) * 11.6) 49.2-56.4-45.8-73.2 (36.2) 46.8 (10.1 (25. 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.63 (8.6-12.30-11. Consequently.4) 37.Organochlorine Pesticides Chlordane CAS No.8-61.4-40.2-21.3) 41.9 (36.3) 18.1-19.5) 9.7 (32.9 (18.5-32.0 (16.9) 47.0 (<LOD-12.9) 23.3 (28.0-25.4) 29.8) 44. chlordane was used to kill termites and other insects on agricultural crops.7) 31.6) 23. Since 1992.2 (10.4 (30.5 (33. foods high in fat such as meat.5-42.5-43.3-24.70 (<LOD-10.9) 31.7) 9.6) 11.3-45.7-39.3 (21. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues. Survey Geometric mean (95% conf.4-14. and dairy products are the usual sources of exposure to these chemicals in the general population.8 (17.7-12.8) 18.9 (31.5) < LOD < LOD 9.1 (20.0-12.8) 53.5) 10.7 (43.6) 8.0-67. 2007).3 (27. heptachlor use has been limited to treatment of fire ants near power transformers.1 (27.5 (41.9) 37.0) 75th 20.7) 28.6) 48.1-51.8 (17.1-25.1) 16.0 (32.5) 38.7 (42.5-44.4 (<LOD-12.2) 37.3) 37.6) 9.3 (<LOD-19.7-25.9-21.S.82-11.8) 52.6) < LOD 11.1) 30. and in soil.3 (9.5-13.1 (44. fish. Fourth National Report on Human Exposure to Environmental Chemicals 81 .5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6) 36. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7) 19.1) 90th 34.9 (15.9-40.9) 36.8-42.9-21.9 (26. buildings.7 (10.7-14. 10.0-33.2) 22.5) < LOD < LOD < LOD < LOD 13.2) < LOD 11.0) 27.9 (15. see Data Analysis section) for Survey years 99-00.8.36-11.5.2 (28.3 (20.10-18.4 (30.5) 37.8) 27.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11. 01-02.9 (11.10-11.6-24.5-65.3-32.2-26.0) 20.0 (26.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.6-18.9) 11.4 (22.9 (26.1-15.7 (34.6 (16.0-61.2) 33.9) 10. from the early 1950’s until the mid-1980’s. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U. Until 1988.2-28.1 (17.6) 48.6-24.7-70.9-42. and 7.3-45. 1994.5 (31.90 (8.3) 10. As a result of the manufacturing process.8-32.7 (17.7 (<LOD-32..7) 19.2 (37. respectively.9) 17.3 (26.9-38.6 (43.4 (10.9) 13.8 (18.7 (34.1 (11.5-40.2) * 12.2 (21.0) 31.20-11. 57-74-9 Heptachlor CAS No.4) 22.

066 (<LOD-. which may vary for some chemicals by year and by individual sample.280-.076) < LOD . 1986).133) 90th .146) .286 (.200-.062) < LOD .270 (.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .S. Elimination of all these chemicals from the body occurs over months to years.200-.063 (. Takahashi et al.077) .149 (.130-.061-.300 (.070 (<LOD-.130 (.270 (. and the U.370 (.320 (.231) . The major metabolite of heptachlor is heptachlor epoxide.115-. chronic doses of heptachlor have produced liver enlargement and injury.250-.190-.340) . 1981).348) .067 (.049 (<LOD-.148-.140 (. 1977b. 2007. In laboratory animal studies.104) ..071 (.063 (.057-.290-.310 (. and alterations in immune function of offspring.053-.340) .200 (.320 (. 2001.063 (.189 (. Survey Geometric mean (95% conf.080) .220 (. 82 Fourth National Report on Human Exposure to Environmental Chemicals .380) .077) .290 (.073 (. 1991).079) .090) .150 (.100-.070) . 2007).077) . Smith.300) .280) .180) . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.300) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .070 (.315 (.056 (.148) .126) . Le Marchand et al. 1991.280-.207 (.100 (.068-.250 (.320) .130-.150) .200-. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.120-.S.091) . Shindell and Ulrich. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.430) .287) .160) .130-.242-.320 (.110-.070 (<LOD-.240) .260 (.087-.165-.400) .077) . FDA established allowable residues of chlordane.080 (.270 (. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.065-.310-. 2006). interval) Selected percentiles ( 95% confidence interval) Sample 95th .280-.227) < LOD .053-. and inhalation exposure.136) .350 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.050 (<LOD-..106-.240-.060 (<LOD-.260 (.240-.100 (<LOD-.246-.370 (.410) .230 (.063) * .360) . OSHA has established occupational exposure criteria.269 (.170-.253-.290) .210 (. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.083 (.310) .104-.290) .090) .350 (.066-..080) . IARC.112 (.430) .350) .260-.047 (<LOD-.120-.220-. which is also persistent in the body (ATSDR.064) < LOD .140 (.140 (.090-.286 (.230-.050-.S.066 (.120 (.160) .092) .213) * . and breast milk is a major excretion route in lactating women.079) < LOD < LOD < LOD . EPA has established environmental criteria for chlordane and heptachlor. population from the National Health and Nutrition Examination Survey.290-.058 (. to heptachlor.140) .128 (.230) . Acute.250 (.074-.560) .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. neonatal mortality.126 (.204 (.258-.280 (.140-.083) . 2002.048-. 1986).258 (.220-.055-.120-.063 (.058-.450) .115 (.230-.075 (. Chlordane and heptachlor are absorbed after oral.082 (.170) . The U.170) .440) .370 (.130-.300) .170) .302) .290-.070-.271 (. 1977a. 1996.110 (<LOD-.146) < LOD < LOD . Rogan.300) .070-.068) 75th .203-.180) .057 (.150 (.280 (.450) .210-.170) .Organochlorine Pesticides (Dallaire et al.063-.063) . and heptachlor epoxide in foods and bottled water.108-.310) .069 (<LOD-.210 (.373) .130 (.207) .320 (.066-.130 (. dermal.070 (<LOD-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.058-.208 (.180-.225 (.168-. heptachlor.150-.245-.189-. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.080) . 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. characterized by seizures and paralysis.216-.160 (.320) .140 (.199-.170) .070) < LOD < LOD < LOD < LOD < LOD . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.070-.230 (.190-.230-.180-.070 (<LOD-.310) .190-.150 (.130-.160) .400) .130) .100-.119 (.300-.260 (.240 (.223) .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 * * * * .130) .057) * .068) .330 (.140-.080 (.510) .073) < LOD < LOD < LOD < LOD ..

than the 90th percentile values of NHANES 1999-2000 (Baker.org/documents/cicads/cicads/cicad70. Biomonitoring studies on levels of oxychlordane.html. or heptachlor epoxide in serum does not mean that the level of oxychlordane. 1993). trans-nonachlor. the mean serum heptachlor epoxide and oxychlordane levels were more than twice as high.. Biomonitoring Information Serum oxychlordane and trans-nonachlor levels in NHANES 1999-2000. resulting in human exposure to heptachlor epoxide that was excreted into the milk. A recent assessment of heptachlor is available at: http://www. Biomonitoring data can also help Fourth National Report on Human Exposure to Environmental Chemicals 83 .. In serum samples obtained in between 1994 and1997 from Inuit women in different Arctic countries.cdc. 2006).. mean serum heptachlor epoxide and oxychlordane levels were about sevenfold and threefold higher. inchem. respectively. 2000).. than the 90th percentile values of NHANES 1999-2000 (Stehr-Green et al. from ATSDR at: http://www. and 2003-2004 subsamples were comparable to levels measured in Swedish women from 1996-1997 (Glynn et al. A small sample of Polish women had mean levels of oxychlordane and trans-nonachlor that were about fivefold lower than in females in the NHANES 20012002 subsample (Jaraczweska et al. Two episodes (one each in Arkansas and Hawaii) of inadvertent heptachlor contamination of dairy cattle feed occurred in the early-to-mid 1980’s. environmental levels) and scientists plan and conduct research on exposure and health health effects of chlordane and heptachlor is available effects.. and heptachlor epoxide provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of heptachlor and chlordane than are found in the general population. 2001-2002. 2003). In the Hawaii episode. 1988). transnonachlor. respectively. Finding a measurable amount of oxychlordane.gov/toxpro2. 2002). 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.atsdr. transnonachlor.Organochlorine Pesticides about external exposure (i.. or heptachlor epoxide causes an adverse health effect.e.. For the exposed persons drinking milk in the Arkansas episode.htm#ref. 2004). 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. 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.

3) 10.9-29.9 (12. Survey Geometric mean (95% conf.2 (<LOD-25.4 (11.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.2) 15.6 (16.6.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. which may vary for some chemicals by year and by individual sample.3) 16.4 (<LOD-19.10-13.0-19. population from the National Health and Nutrition Examination Survey.9 (15.1) 20.1) 13.8) 13.4) 21.8) 15.6) 14.7 (10.6) 13. see Data Analysis section) for Survey years 99-00.5 (18.2-27.8 (<LOD-23.8-24.8 (13.3) 22.3) 18.7-19.3-18.6 (<LOD-27.8-23.6-21.4 (<LOD-54.6 (14.2 (18.1-15.50) < LOD < LOD < LOD 17.1-16.4) 18.8 (15.3) 18.0-54.7-25.1) 23.9-23.8) 16.8.0-17.2) 20.2-16.3) 27.3 (13.0) 13.5.5) 19.7 (16.8-24.9) 15.4 (11. 84 Fourth National Report on Human Exposure to Environmental Chemicals .3 (<LOD-25.1 (16.1-29.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.8-46.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.2-27.8 (18.3) 18.6-17.5) < LOD 14.3) 23.40) 15.6) < LOD < LOD < LOD 27.7 (13.8) 21. < LOD means less than the limit of detection. respectively.20 (<LOD-9.0-17.6 (11.9-25.7-18.0 (11.1-38.2-17.8) 19.8-24.2 (<LOD-16.2) 26.4 (15.5 (11.6 (13.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.6 (8.1 (19.6 (12.2) 13.6) 22. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (<LOD-32.8) 14.8) 20.0-16.8 (13. 01-02.9-16.8) 14. 10.0 (15.S.5 (<LOD-21. and 7. and 03-04 are 14.0) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.5 (11.8) 19.2 (<LOD-62.6 (16.90 (<LOD-9.8 (18.9-29.5 (10.8) 13.

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

2-18.1) 62.6) 34.6 (57.3-74.1 (65.3) 19.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.2) 19.1) 32.0 (16.9 (66.5 (15.0) 49.1-28.2-23.9-64.5) 30.5 (15.8-16.4-35.7 (59.7-20.7-21.9-58.4-22.8-90.2 (60.4 (28.9 (51.0-23.8 (28.4 (16.7) 17.7 (30.0-24.9 (<LOD-14.6-88.6 (12.2-88.8) 19.8 (<LOD-20.5) 26.6-66.7) 35.5-111) 68.4) 48.1-16.2) 59.3 (14.5) 14.3) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.5-95.8.1) 17.8 (26.7 (74.9-65.1) 78.2) 20.1-20.2 (15.6) 56.1) 17.0 (16.5-87.2 (59.8 (13.2 (7.0) 18.0 (29.2 (27.1) 78.6) 25.3-39.4) 59.7 (35.8 (71. which may vary for some chemicals by year and by individual sample.3) 32.8-21.9 (29.0-37.6 (52.1) 31.1-22.2-17.8-67.6) 56.8 (28.6) 13.7-32.9) 51.0 (13.2-21.8 (26.7) 73.5) 22.8 (42.3-32.9) 14.0) 19.7 (16.9) < LOD < LOD < LOD 20.6-19.9-65.3-21.9 (15.7 (59.8-129) 74.4 (30.1 (10.5-69.5-17.2 (36.7-23.2) 17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3-50.0 (42.2-18.3 (56.1-34.2 (64.1-126) 67.4 (67.3) 32.7-22.4 (11.7-160) 86.5) 14.8-110) 59.9-35.2 (25.7 (11.0-123) 74.2-37.8 (45.6 (32.0-38.0 (48.7) 56.S.70 (<LOD-12.3 (58.2 (14.2 (26.8 (16.5-36.5) 35.6 (16.3) 30.9-20.2-16.7 (13.1 (47.7-17.8-19.0 (42.9-40.5) 48.0) 33. interval) 18.3-86.2) < LOD 10.1) 17.3) 15.1) 18.0-22.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.5 (44.5 (45.4) 19.1) 16.1 (48.9-22.0 (15.3) 18.0) < LOD < LOD 8.1) 18. see Data Analysis section) for Survey years 99-00.1 (41.8-77.8 (12.5) 78.7) 28.4) 20.8 (15.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.4 (45.5-20. 86 Fourth National Report on Human Exposure to Environmental Chemicals .4-23.0-20. 01-02.5) 20.0 (15. Survey Geometric mean (95% conf.0-23.7-77.6 (56.10 (<LOD-11.6 (15.6) 84.7) 59.7) 78.7) 15. and 03-04 are 14.0-93.6 (50.6) 10.6-82.9) 14.1-34.6-22.8 (30.1-51.3) 16.0) 40.8) 51.6) 82.0-93.8 (49.1) 17.3) 36.0 (60. and 7.6) 54.8-16.7) 78.1) 17.7-29. 10.7-35.5 (13.4) 55.4-52.2) 30.6 (56.4) 16.8 (26.9 (19.5) 77.5) 36.3 (16.0-68.4-36.9-89.9-69.5) 9.8 (13.7) 52.8-19.2) 39.9 (15.3-30.0 (14.8) 80.0) 75th 31.2) 34. population from the National Health and Nutrition Examination Survey.8) 47.1) 17.7 (28.5) 90th 55.0 (62.3 (45.7) 14.4) 107 (84.0-113) 68.9 (47.3) 25.0 (19.0-143) 112 (68.1) 14.8-41.9 (36.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.8 (28.1 (17.3 (14.3-57.8-90.6-54.9) 51.3-58.1) 17.9 (28.7-113) 68.8 (19.3) 18.7-34.9-45.6 (<LOD-14. < LOD means less than the limit of detection.8 (11.1-55.5.8 (17.9-36.5.3 (49.4-18.9 (16.7-38.2 (19.1) 30.4-67.3 (17.7 (18.2 (14.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.0) 13.5-19.4 (12. respectively.0-59.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.8-79.6-20.7-18.1-16.1 (22.4-62.6) 60.0 (13.1-18.9 (51.5) 19.5 (25.3) 30.86-13.

087 (.094 (.684) .110) .130) .096-.300-.205 (.120) .240) .390 (.232) .103 (.250) .600) .161) .117) .141) .242) .409-.400-.120-.460) .060-.126) .240) .131) .122) .417 (.099-.280) .141) .092 (.237) .600 (.330 (.110-.098) .095-.130 (.100 (.470 (. Fourth National Report on Human Exposure to Environmental Chemicals 87 .070 (.116-.177-.081-.590) .089 (.191 (.104 (.130) .134) .470 (.130) .330-.110 (.590 (.210 (.340) .324 (.120) .220 (.690) .092 (.145-.400 (.125) .110 (.220 (.310-.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.103 (.116 (.414 (.090) .084-.124) .405) .097) .113) < LOD .140) .100-.520) .220) .450) .800) .127) < LOD < LOD .630) .171-.081 (.360-. interval) .120-.520 (.237) .130) .080 (.460) .395-.310-.130) .109 (.240) .170 (.240-.272-.210-.085-.190-.510-.090-.120 (.760 (.210) .093-.096-.130) .580 (.285-.183 (.390-.440-.410-1.090 (.630) .190-.069-.840) .290-.106 (.160 (.128 (.085-.360-.420 (.210-.130 (.098-.310-.116) .069) .080-.180-.220 (.461 (.202 (.490 (.490 (.096) .680) .930) .430-.594) .100 (.180-.190-.111-.397-.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.340-.350 (.286-.078-.480) .190-.260) .558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .470-.460-.220 (.085-.108) 75th .106 (.210) .098 (.110 (.093-.458 (.470-.082) .371) .110 (.310 (.180-.330-.630) .690) .830) .108 (.119) < LOD < LOD < LOD .380 (.090-. Survey Geometric mean (95% conf.060 (<LOD-.060) .390 (.210 (.120) .390 (.400 (.400) .355 (.490) .093-.565) .080) .830) .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 .100-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .080-.680 (.370 (.120 (.300) .540) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) .230 (.090-.400-.129) .071 (<LOD-.054-.651) .105 (.112 (.395) .062 (.104-. which may vary for some chemicals by year and by individual sample.580 (.250) .390) .100-.068-.559) .186 (.161-.111 (.098 (.090-.090-.573 (.470 (.106 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .410-.080-.310-.119) Selected percentiles ( 95% confidence interval) Sample 95th .310) .440) .279-. population from the National Health and Nutrition Examination Survey.150) .327 (.108) .079-.270-.500) .390) .320-.220 (.160-.510 (.490-.078 (.091) .520 (.367) .288 (.220 (.420) .430-.047-.220 (.173-.135 (.158-.080-.250) .260) .340-.093) .120) .190-.210 (.350-.110 (.370 (.113) .055 (<LOD-.061-.640 (.186-.580 (.110 (.100-.430-.090 (<LOD-.130) .497-.190-.122) .210) .317 (.550 (.320-.090-.301-.091-.390 (.109 (.960) .288-.112 (.590 (.343 (.099-.150) .120 (.120-.079-.211) 90th .125 (.240 (.220 (.114) .234) .S.041 (<LOD-.

Saidein D.28:497501.atsdr. Poland. Jr.inchem.Summaries & Evaluations. Drews K. Toxicological profile for chlordane [online]. J Occup Med 1986.niehs. Available at URL: http://ntp. Berkowitz GS. Granath F.gov/ntp/ htdocs/LT_rpts/tr009. et al.cdc. New York. Takei G. Covaci A. Loo S.html.org/documents/iarc/ vol79/79-12.9:1-109. Wong L.110(8):835-838.niehs. Available at URL: http://www. Arch Environ Health. JAMA 1988. Bull Environ Contam Toxicol 1981:27:506-511. Smith AG. Brower S. Bjerselius R. Shindell S and Ulrich S. Environ Res 2000. International Agency for Research on Cancer (IARC). Voorspoels S. maternal serum and milk from Wielkopolska region. 6/1/09 National Toxicology Program (NTP).heptachlor.org/ documents/cicads/cicads/cicad70. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Odland JO. Handbook of Pesticide Toxicology. Muckle G.110:617-624. Academic Press. Eds. Bioassay of chlordane for possible carcinogenicity. 1986. Ayotte P. Wohlleb JC.84:151-161. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States.cdc.htm.inchem. Keller JA. Lulek J. Pollutants in breast milk. 6/1/09 Rogan WJ.50(3):108-118. A Report to the Hawaii Heptachlor Research and Education Foundation.372:20-31. Available at URL: http://www.330:55-70. International Agency for Research on Cancer (IARC) . Available at URL: http://ntp. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii.pdf. Environ Health Perspect 2002. Sci Tot Environ 2006. Takahashi W.150:981-990. Available at URL: http://www. Wolff MS.8:1-123. Jr and Laws ER. 2006. Organochloride pesticide residues in human milk in Hawaii. 2001.gov/toxprofiles/tp31. Environ Health Perspect 2003. 4/21/09 Baker DB. LeMarchand L.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Lawrence River (Quebec. Bleiweiss IJ. In Hayes WJ. 1994-1997 organochlorine compounds. Circumpolar maternal blood contaminant survey. August 2007. gov/toxprofiles/tp12. 1991 pp. Charles MJ. Toxicological profile for heptachlor and heptachlor epoxide [online]. Inc. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Laliberte C. Jaraczewska K. Kolonel LN. Barker J.pdf. Vol. KalubaSkotarczak A. Arch Pediatr Adolesc Med 1996.org/site/foundation/ research/projects2.htm. 731-915.41:145–148. et al. Bioassay of heptachlor for possible carcinogenicity. Head SL. Sci Total Environ 2004. Organochlorine exposures and breast cancer risk in New York City women. Hansen JC. Vol. Chlorinated Hydrocarbon Insecticides. Royce W. 9/25/07 International Programme in Chemical Safety (IPCS). Hawaii Med J 1991. Stehr-Green P. Atuma S. Van Oostdam JC. Canada). Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Aune M. Tartter P. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Hertz-Picciotto I. National Toxicology Program (NTP). et al. 1979-1980.259(3):374-377. Baker DB.nih. Distribution of polychlorinated biphenyls. 1963-1967. Senie R. Willman E. Gilman A. Available at URL: http://www. Darnerud PO. Glynn AW. Available at URL: http://www. Siegel BZ. Chlordane and heptachlor [online].html. Concise International Chemical Assessment Document 70 Heptachlor [online]. Dewailly E.gov/ntp/ htdocs/LT_rpts/tr008. 1993. 79. Dewailly E. et al. 2 Classes of Pesticides. 4/21/09 Dallaire F. Dendle WH. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. 88 Fourth National Report on Human Exposure to Environmental Chemicals .nih. Organochlorines in Swedish women: determinants of serum concentrations.html. Chashchin V.atsdr. 4/21/09 James RA. Environ Health Perspect 2002. Mortality of workers employed in the manufacture of chlordane: an update.111:349355. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. May 1994. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii.

fish. DDT was used at one time as a treatment for head and body lice.7 (19.6 (22.3) 28. particularly for endemic vector and malaria control.p’-DDT (65%-80%).2 (11. 2008.5) 23.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8) 30. as well as in plant and animal tissues.5 (23. population from the National Health and Nutrition Examination Survey. Both Serum p.0-27.1 (23.5) 25.6 (<LOD-25.3) 21. p.9) < LOD < LOD 9.0 (18.3) 21.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. or dermal exposure.9 (21.7) < LOD 18.0 (10.2) 30.0-155) 83. DDT is converted to DDE and several other metabolites. 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. Only a small proportion of DDT is metabolized and excreted (Smith.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.3-16. and water. < LOD means less than the limit of detection.0 (18. and dairy products.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. population. In the general U.9 (10. It is still used in some countries.9 (<LOD-20.1-27.9) 14.7-16.2 (<LOD-40.3 (27. which may vary for some chemicals by year and by individual sample.4) < LOD 17.0) 19.5-36.50-11.1 (<LOD-39. Food imported from countries that still use DDT may contain the chemical or its residues.8-39.2-65.2) 155 (59.8.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.5 (15. DDT is converted in the environment to other more stable chemical forms. The biodegradation half-life of DDT in soil varies from 2 to 15 years.3-590) 293 (104-541) 48. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7 (15.1 (33. after World War II until 1972.p’-DDD (4% or less).8) 15.9 (10.2-bis(p-chlorophenyl) ethane (DDD).S.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 10.0-15.90 (<LOD-12. It was produced and used in the U.8-17. inhalation.1’-(2.1’-dichloro-(2. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR. food.8) 36.6 (31.00 (<LOD-10.3) 22. These chemicals are highly persistent in soil.9) 17.9-34. Fourth National Report on Human Exposure to Environmental Chemicals 89 .6 (9. Survey Geometric mean (95% conf. particularly meat.1-71. 1991). which is a mixture containing p.0) 40.0) 26.5-54.2-95. 1991).9-28.0-37. and trace amounts of several related compounds.3-236) 24. resulting in fetal exposure.5 (23. continues to be the primary source of DDT exposure. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.5) < LOD < LOD 9.7) 12.6 (25.4.3 (<LOD-31. and 03-04 are 20.8) 799 1073 959 880 1232 1006 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.0) 20. Gunderson. air.70 (8.4) < LOD < LOD < LOD 61. 01-02. DDT usually refers to the technical product.8-26. DDT can be absorbed after ingestion.p’-DDT (15%-21%).8-23. although DDT and DDE intakes have decreased over time (FDA.5 (14.3 (<LOD-21. DDT and DDE can cross the placenta.7.0-53. depending on conditions. o.S.0 (21.4 (23. 17. when virtually all use of it was banned. 1988).S. including 1. 2002.9 (10.0-35. see Data Analysis section) for Survey years 99-00. sediments.9) 29. Smith.10 (<LOD-12. respectively.1) 31.2) < LOD < LOD 9.10-13. In the body.6-33. and 7.

tremor.400 (. Mariussen and Fonnum.. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. resulting in exposure to nursing infants (Rogan.098-.530 (. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.063 (<LOD-.080-. Jusko et al. 2001).190 (. 1956).132-. 2001).240) .p’-DDE can produce anti-androgenic effects (Gray et al. 2006.140) .180) . and seizures.106) . Jusko et al.g. and leukemia have also been inconclusive (ADSDR. 2006.064 (.170 (.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .143) < LOD < LOD .189-. 2001).190 (.. have not been consistently demonstrated (Beard.180 (.00) .250 (.Organochlorine Pesticides chemicals are excreted in breast milk. 2002.071-. Longnecker et al. 1997). Calle et al.079) < LOD < LOD . and duration of lactation. dioxins and furans). fertility. reproductive organ abnormalities. Survey Geometric mean (95% conf.130 (<LOD-.150-. In high dose. 2000.086 (.201 (. Reproductive effects in humans affecting birth weight. other organochlorines.078-.. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.400) .p’-DDD and p. Hayes et al.130 (<LOD-.107) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.330-4.26) 1.095) < LOD . Gray et al.S.62 (. Snedeker.150-.160-. 2002.054-.065-. DDT may bind to estrogen receptors (Chen et al.061) < LOD < LOD < LOD . 2006. 2002.170) .290) .130 (<LOD-.051 (<LOD-. lung cancer.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.071 (.420) .230) . A workplace standard for DDT has been established by Serum p.220) . and altered behavior after neonatal exposure (Eriksson and Talts. and o. 2001). premature delivery.180 (. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. 2006)..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 . 2006).570-4.059-. 2006).530) .105-.01) . Beard. interval) Selected percentiles ( 95% confidence interval) Sample 95th .078 (.180) .627) .146 (. polychlorinated biphenyls.069) .250-1. 2002. accidental exposures..084 (.114-.075) 1.140-..074-.068-. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.087 (.34) .180-. 1998).146 (.190-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..220) . overt signs of acute human toxicity include vomiting.142 (.200 (. Gladen and Rogan.343) < LOD .106-. which may vary for some chemicals by year and by individual sample.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 . 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. 90 Fourth National Report on Human Exposure to Environmental Chemicals .240 (.130-.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.. Studies of DDT exposure and pancreatic cancer.106) < LOD < LOD .230) .150) .00 (. In laboratory animals.. population from the National Health and Nutrition Examination Survey.203) . 1996).120 (<LOD-.120-. 2004..313 (. 1995.150 (<LOD-.112 (. Animal studies reported reduced fertility.150 (<LOD-.260) .048 (<LOD-.108 (.170-.128 (.

so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. EPA at: http://www. 2003). Link et al. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.. 2004). and 7. Fourth National Report on Human Exposure to Environmental Chemicals 91 . and 03-04 are 18. 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.6.6 (81.. 1989). IARC classifies DDT (p. Since the 1970’s. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. 1998. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. respectively. Heudorf et al. respectively.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. In general. Stehr-Green.3. 01-02. Declining DDE levels over time have also been observed in the German population.. 2003. compared to levels observed in this Report (Anderson et al. Smith. Survey Geometric mean (95% conf. 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..atsdr...cdc. see Data Analysis section) for Survey years 99-00. Median DDE levels among a population-based sample of Swedish women in 19961997 were similar to females in the NHANES 1999-2000 subsample (Glynn et al. 8.epa. More information about external exposure (i.gov/ toxpro2.html. 2002..gov/ pestcides/ and from ATSDR at: http://www. 2002. 2004). for males and females in the NHANES 19992000 subsample (Pavuk et al.. population declined by about fivefold to tenfold. environmental levels) and health effects is available from the U.S.p’-DDT) as a possible human carcinogen. 2005). mean serum levels of DDT and DDE in the U.Organochlorine Pesticides OSHA and a guidance established by ACGIH. Compared to females in the NHANES 1999-2000 subsample. 1991).S.e.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. population from the National Health and Nutrition Examination Survey.8. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.S. Biomonitoring Information DDE persists in the body longer than DDT.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.7-119) 113 (100-140) 93. In a population-based sample of men and women from eastern Slovakia.

91 (6.76 (2.45 (1.34) 6. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.31 (1.18-1.6 (7.26) 3.57) 2.2 (6.6) 9.81-5.516 (.30-1.87 (5.963-1.33-1.34) 2.39) 1.80) 1.81 (7.13) 4.1 (8. Finding a measurable amount of p.6) 11.63 (1.34-11.7 (8.6) 13.66) 4.22-1.646) .31-2.5) 5.00 (.49) 8.35) 1.55-9.18-1.81-18.40-4.623 (.680-1.62-6.50 (2.385-.43 (5.25) 8.6 (9. less than one percent had detectable serum levels of o.53-15.75 (8.51 (1..24 (1.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.26-10.46-2.9 (26.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.8-90.01-11.85 (1.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.88-35.01-1.55 (2.590 (.56-6. o.61-2.36-2.46 (1.32 (1.05 (3.1) 12. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.32-1.18-3.58) 1.32 (1.31-12.0 (12.01-1.78 (4.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.03-1.36-11.05) 1.49 (1.68 (2.75) 2.534-. In the NHANES 1999-2000.39-1.82) 1.72) 1.10) .71) 32.66) 3.10) 2.18 (6.50-17.91-2.49 (6.70) 1.0) 2.53) 7. 1971).69 (1.66-2.17-3.06) 1.52 (3.93 (7.456 (.10-1.88 (2.07) 1.7-20.26-2.488-.06) 3.51-49.37-4.635) 1..30-1.43-4.3) 16. 309 versus 268 ng/g lipid.79) 4.40-8.90) 22.21) 3.2 (19.9 (15.870 (.18) 1.12 (6.07) 1. Serum p.6) 9.965-1.72) 1.75 (4.3 (9.66-17.85-4.7-48.59 (4.7) 13.14-9. considerably higher than levels in this Report (Smith.59 (1.430-.66) 1.04-1. High mean levels of whole blood DDT (about 3.83 (1.3 (8.5) 16.14) 2.43-8.51-15.57 (1.58) 1. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE than are found in the general population.82 (1.25 (1.4 (12.59 (1.49 (1.9-17.69 (2.4-19. 1991).8 (13.9) 7. 2004).2) 19. In a subsample of NHANES II (19761980) participants.01) 1.97 (3.37 (1.5) 10.2 (9.36 (3.14 (1.20 (.91-3.0) 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 .92) 1.p’-DDT.68) 2.p’-DDT were below the limits of detection.69 (.03-4.91) 3..39-2. interval) 1.80) 3.51-8.17 (3.60-13.69) 8.726) .2-32.11 (2.00) 7.48 (6.51) 1. 2001-2002 and 2003-2004 subsamples.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.8) 15.37-10.47) 3.26 (1.46 (1.36) 3.00-1.92 (3.81 (1.1) 7.87-16.557) 1.6 (17.59) 6.25) 1. 2004).65) 1.41 (1.61 (1.37-1. 2005).53) 1.14) 2.18-4.419-.34 (7.04 (6.6 (8.28) 1.57-3.02 (2.58) 75th 3.92 (3.1) 40. 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.39 (3.57 (3.6) 8.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.6) 12.57 (1.10-5.71) 12.56) 2.0 (9.54 (1.19) 4.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .81) 11.43-4.77 (1.796 (.23 (7.32-1.63 (1.32) 1.p’-DDT.500-. serum levels of o.9) 5.8 (9. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.611-1. 1989).24) 1.3) 13.13-2.75) 1.65 (1.96) .66-4.85-10.520 (.19-14.56-2. or p.730) .11-1.600) .76-3.01-5.6) 9.01-11..64-2.09-1.27-1.22 (7.561 (.53 (2.52-6.25-16.4) 14.4) 13.40 (3.68-4.99) 1.5) 22.97-4.12-1.Organochlorine Pesticides nearby agriculture (Botella et al.51) 3.45 (1.00 (6.41-12.24-17.22) .76) 1.5) 7.48-4.16 (2.4) 9.02-8.77 (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 3.27) 3.6) 9.02) 1. Survey Geometric mean (95% conf.90-8.01-15.30 (1.38 (1.2) 26.p’-DDT (Stehr-Green. population from the National Health and Nutrition Examination Survey.32-9.8 (14.64) 3.57-2.66) 1.3-43.7) 9.96) 1.80) 1.56-3.69) 4.7-19.7) 16.30 (1.9-38.820-1.75) 6.37-16.8 (13.70-3.890-1.71 (5.71 (6.52 (1.1 (9.76) 1.25 (.4 (8.29 (1.63 (6.36-1.44) 1.3) 10.07 (5. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.80 (2.84 (3.994-2.12 (.2 (9.38 (1.15-4.13 (1.34-3.63-15.57-13.47 (1.54-7.01) 1.16-1.14-1.25-14.21) 90th 7.40-4.54) 8.S.860 ng/L) and DDE (about 14.59) 3.84-3.

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

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

html. Garrett N. Am J Epidemiol 2002.72:261265. Kashyap R.155(4):313-322. Becker K. Lepom P.gov/ toxprofiles/tp35. Available at URL: http://www. and DDD [online].54:1431-1443. and HCB residues in human blood in Ahmedabad. Organochlorines in Swedish women: determinants of serum concentrations. Barr DB. et al. Chen CW. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Thun MJ. dietary intakes of pesticides. Hurd C. India. Durham WF.206:485-491. et al. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. The effect of known repeated oral doses of chlorophenothane (DDT) in man. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Bloom MS. Botella B. Organochlorines and breast cancer risk. DDT and human health. Frumkin H. Cerrillo I. September 2002.96:34-40. et al. Jusko TA. Food and Drug Administration (FDA). Toxicological profile for DDT. et al.205:297-308. Levels of DDT.gov/~dms/ pesrpts. hexachlorobenzene. et al. Drexler H. Rogan WJ. and dichloro(diphenyl)ethylene (DDE). Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Arnold SF. Herrman T. Hanrahan L. Sci Tot Environ 2006. Olea N. Zhou H.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).fda. Davis MD.. Zhou H. Ostby J. Lancet 2001. August 2008. Environ Res 2004. Koepsell TD. and polythelia among male offspring. et al.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Int J Hyg Environ Health 2002. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Gray LE Jr. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Beard J. Hediger ML. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Chemosphere 2004. Environ Health Perspect 2004. Parks L. Olson JR. 4/21/09 Anderson HA. Effects of environmental antiandrogens on reproductive development in experimental animals. Maternal DDT exposures in relation to fetal and 5-year growth. Paepke O. Bhatnagar VK.358:110-114. Cueto C.52:301-309. Epidemiology 2006. Burse VW. Am J Public Health 1995. Hayes WJ. Swanson MK. Maternal serum level of 1. Savitz DA. Olson J. Aune M. Charles MJ. Gunderson EL.7(3):248-264. FDA Pesticide Program Residue Monitoring 1993-2006 [online].112(17):1761-1767. Katz SH. Vena JE. Talts U. Baker RJ. Fourth National Report on Human Exposure to Environmental Chemicals 95 .162:890-897. Bates MN. Ellis H. hypospadias. Klebanoff MA. Willman EJ. Kaus S. April 1982 to 1984. Environ Res 2005. Zoellner I. Crespo J.71(6):1200-1209. Schulz C. Buckland SJ. DDE and shortened duration of lactation in a northern Mexican town. Environ Health Perspect 2003.85:504508. Heudorf U. Notides AC. selected elements. Needham LL. Greenfield TA.cfsan. Patterson DG Jr.1-dichloro2. Needham LL. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Bull Environ Contam Toxicol 2004. Olea-Serrano MF.106(5):279-289. Biochem Pharmacol 1997. J Assoc Off Anal Chem 1988.53(8):1161-1172. et al. dichlorodiphenyldichloroethylene. Longnecker MP. Needham LL. Henley SJ.17(6):692-700. Biomonitoring of persistent organochlorine pesticides. Piechotowski I. Environ Health Perspect 1998. Exposure of women to organochlorine pesticides in Southern Spain. Vorojeikina DP. Neurotoxicol 2000. CA Cancer J Clin 2002. Moysich KB. Klebanoff MA. Glynn AW. Granath F. Rivas A. Brock JW.97(2):178192. Kulkarni PK. et al. FDA total diet study. Seiwert M.atsdr. DDE.58:1185-1201. Jr. Gladen BC. Calle EE. Gray KA. The Great Lakes Consortium.21(1-2)37-48. Gabrio T. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. 4/21/09 Gladen BC. Klebanoff MA. Profiles of ortho-polychlorinated biphenyl congeners. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Krause C. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Hum Reprod Updat 2001. Longnecker MP. Furr J. Link B. Eriksson P. Int J Hyg Environ Health 2003.cdc. Zaidi SS. and other chemicals.355:7889. Available at URL: http://www. Darnerud PO. Atuma S. Jr. HCH. Bjerselius R. Saiyed HN. Falk C. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.111:349355. Angerer J.html. Brock JW. Chemosphere 2005. JAMA 1956. et al. Lambright C. lindane (g-HCH). Wolf CJ.

96 Fourth National Report on Human Exposure to Environmental Chemicals . et al.Organochlorine Pesticides Mariussen E. Neurochemical targets and behavioral effects of organohalogen compounds: an update.36:253-589. PA. Lubet R. Handbook of Pesticide Toxicology. Demographic and seasonal influences on human serum pesticide residue levels. children and newborn infants.53:455-477. Pollutants in breast milk. J Toxicol Environ Health 1989. Rogan WJ. Petrik J. Comparative pharmacodynamics of CYP2B induction by DDT. Crit Rev Toxicol 2006. and dieldrin. et al. Jr and Laws ER. Environ Health Perspect 2001. Fox S. Nims R. Fonnum F. Lynch CF. DDE.150:981-990.54:1509-520. Astolfi E. Stehr-Green.20(2):186-193. Thomas PE. New York. Arch Pediatr Adolesc Med 1996. 1991 pp. Pavuk M. Schecter A. Vol. and DDD in male rat liver and cultured rat hepatocytes. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Radomski JL. Cerhan JR. Academic Press. Inc. Chovancova J. Chlorinated Hydrocarbon Insecticides. In Hayes WJ. Snedeker SM. Environmental exposure to PCBs and cancer incidence in eastern Slovakia.27:405-421. Deichmann WB. DDE. J Toxicol Environ Health Part A 1998. Rey AA. Toxicol Appl Pharmacol 1971. Smith AG. Eds. Pesticides and breast cancer risk: a review of DDT. Reddy AB.109:35-47. 731-915. 2 Classes of Pesticides. Jr. Jones CR. Chemosphere 2004.

Depending on soil conditions.30 (<LOD-6.S. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. inhalation or dermal exposure routes. endrin has been detected with declining frequency in U. Ketoendrin is a major photodegradation product (IPCS.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. Fourth National Report on Human Exposure to Environmental Chemicals 97 .50) < LOD < LOD < LOD 5. Survey Geometric mean (95% conf. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.40-5.10 (<LOD-5.. Endrin was not widely used as a termiticide. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.Organochlorine Pesticides Endrin CAS No. Endrin is absorbed rapidly after ingestion. 2008). < LOD means less than the limit of detection..S. 1987). or discarded. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. At high doses. unlike aldrin and dieldrin. which may vary for some chemicals by year and by individual sample. EPA. manufactured.20 (<LOD-5. 72-20-8 General Information Endrin. 1991).8. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.S. and inflammation (Smith. 1992). 1981). endrin usually is not detected in serum of exposed individuals. In the body. 1979. population from the National Health and Nutrition Examination Survey. An epidemic of acute endrin poisoning. IPCS. a stereoisomer of dieldrin.30) < 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.S..09 and 7. All uses of the pesticide in the U. Endrin has been detected in soils.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. rodenticide and avicide. endrin is converted rapidly to its major metabolite. total diet surveys (FDA.S. anti-12hydroxyendrin. endrin can persist for years. have been cancelled by the U. Hepatic effects of endrin exposure have included necrosis. 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. is no longer manufactured in the U. unless the dose is high and the exposure is very recent. and occasionally at low levels in sediment and surface waters. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1991). Because it is metabolized so rapidly. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. fatty infiltration. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. 1992). 1996.50) < LOD 5. 1992.20 (<LOD-5. or from contact with contaminated soils and sediments in areas where endrin was applied. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. 1992).60 (5. Endrin was used as an insecticide.40 (<LOD-6.40) < 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.. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. Smith.10 (<LOD-5. Endrin does not accumulate in body tissues (IPCS. Kavlock et al. Over time.

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

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

4) < LOD < LOD 23.3 (20.5-14.0-25.6-TCP) (To-Figueras et al.3 (16.S.2 (14.4-15.6-44. and has been detected in soil.4) < LOD < LOD 19.1) * * 15.9) 19.6) < LOD < LOD 26.2-31.6) < LOD < LOD 24.4) < LOD < LOD 33.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13..8) < LOD < LOD 27.4) < LOD < LOD 14.1 (13. 1997).0) * * 15.S.4) < LOD < LOD 22.8 (26.7-16.5-14.5-33. measuring HCB in serum is a specific indicator of exposure to the parent Serum Hexachlorobenzene (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.4 (18.5 (13.0) < LOD < LOD 24.. and accumulates in fatty tissues where it persists for years.2-15.5-15.4..4 (18. Although it is not manufactured as an end-product in the U. 2005).9) < LOD < LOD 15.4 (11.2 (14.5) < LOD < LOD 18. population from the National Health and Nutrition Examination Survey.4.9-32. 2.8-15.3 (22.5 (13.6-32. respectively.9) < LOD < LOD 20. EPA cancelled its use in 1984.0) < LOD < LOD 15.7 (15.7-30. The FDA dietary surveys have shown that over time.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 * * 16.7 (15.2-15.4.1 (14.2 (24. 1976).3) * * 15.. HCB is well absorbed after oral administration.2) < LOD < LOD 13. and foods with a high fat content. HCB is slowly metabolized. or game taken from areas with HCB contamination.4.1-20.6-19.6-trichlorophenol (2.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.5-trichlorophenol (2. Therefore.0-16.7-26. which may vary for some chemicals by year and by individual sample.0 (14.0. and 03-04 are 118.8 (22.7-21.6-26. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.6 (24. particularly by consuming fish.8.3 (14.9-20. primarily as a fungicide and seed treatment until the U.0 (25.2) < LOD < LOD 29.9 (25. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.1-16. and elimination occurs by renal and fecal routes.6 (21.0) < LOD < LOD 15. wildfowl.9-30. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28. see Data Analysis section) for Survey years 99-00. The general population may be exposed to HCB through diet.9) < LOD < LOD 19. distributes widely throughout the body.9 (25.9) < LOD < LOD 28.6 (23.S. air. and 7.9) < LOD < LOD 20. 31.0 (18.6) < LOD < LOD 25.6-33.4) < LOD < LOD 18.4. breast milk is an additional route of elimination in nursing women.S. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.9-24. water.9) < LOD < LOD 16. < LOD means less than the limit of detection.8 (15. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.7) < LOD < LOD 24.3) < LOD < LOD 20. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.1 (17. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.7) * * 14.7-15.Organochlorine Pesticides Hexachlorobenzene CAS No. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.5-15.7-22.7-29. 2002).3-20.2 (13.1 (14.3) < LOD < LOD 29.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.9 (23.0-28.4-16.5 (14.5-TCP) and 2.9 (14.3 (12.3-26. and sediment (Barber et al.1) < LOD < LOD 15.7-16.6) < LOD < LOD 26.2 (17. 1988).6) < LOD < LOD 14.0 (18. 100 Fourth National Report on Human Exposure to Environmental Chemicals . 2008.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 01-02.9-15.7 (27. Gunderson. Urinary metabolites include pentachlorophenol (PCP).3) 24.9-17.3-22.7 (19.4 (22. HCB has been detected in fewer foods since the 1980s (FDA.3 (22.0-19.5-18.

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

4/21/09 Barber JL. Int J Hyg Environ Health 2002. Muckle G.349:144. respectively. 2006). 2002. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Schulz C. Canada). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Otero R. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. and other chemicals. Ayotte P.44 mg/L. Lackmann GM. Atuma S.. Bertram et al. Dogramaci I. Paepke O.html. Arch Dermatol 1999. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Gunderson EL. J Assoc Off Anal Chem 1988. Lackman.fda. Jones D.111:349355. Bryan GT. 1999). Herrero C. As a result of the lower limit of detection in NHANES 2003-2004.atsdr.. J Exp Sci Environ Epidemiol 2007. Glynn et al. Becker K. Aune M.205:297-308. Environ Health Perspect 2002. Hexachlorobenzene in the global environment: emissions. Bjerselius R. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.. 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..cfsan. HCB levels were directly related to age.cdc. Herrman T. IARC Sci Publ 1986. Kemper FH. trends and processes. Gabrio T. Barr DB. Food and Drug Administration (FDA). 2002.81(2):82-85. Fenster L. and the geometric mean concentration of HCB in whole blood was 0. Bertram HP. Muller C. Kohli J. Bradman A.. Bradman et al.39(12):744-749. Schwartz JM. et al. April 1982 to 1984. HCB detection in serum also was proportional to age. Toxicological profile for hexachlorobenzene update [online]. Arch Neurol 1982. et al. August 2008. Peters HA.html.gov/ toxprofiles/tp90. selected elements. dietary intakes of pesticides..58:1185-1201. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect.gov/~dms/ pesrpts. Dewailly E.71(6):1200-1209. Lepom P. 1986. van Wijk D. Gocmen A. distribution. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Lackmann. 4/21/09 Glynn AW. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Lawrence River (Quebec. Organochlorines in Swedish women: determinants of serum concentrations.54(3):203-208. 2005). 2002). Reference values updated. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Kaus S. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Can J Biochem 1976. Dallaire F. FDA Pesticide Program Residue Monitoring 1993-2006 [online].. Laliberte C. Safe A. Sala M. only 4. FDA total diet study. Santiago-Silva M. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. et al. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. et al. Granath F. Ozalla D. Biomonitoring of persistent organochlorine pesticides. 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. Krause C. 1989). Zoellner I. 2002) and among children (Link et al. Holland NT. Biol Neonate 2002.. however. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. The metabolism of higher chlorinated benzene isomers. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Sweetman AJ.. Chemosphere 2005.110(8):835-838. Environ Health Perspect 2003. 2002. Piechotowski I.. In the 1976-1980 NHANES subsample. Cripps DJ. Link et al. Darnerud PO. Available at URL: http://www. September 2002. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. References Agency for Toxic Substances and Disease Registry (ATSDR). but overall. levels. Link B. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. 2005. Lecha M. In a representative sample of the 1998 German adult population. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.135(4):400404.9% of participants had quantifiable levels (Stehr-Green. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. more HCB levels were quantified. In Spain. Over the past two decades. Sci Tot Environ 2005.. Eskenazi B.17:388–399.77:173182. Jones KC. 2002. Seiwert M. 2005). Available at URL: http://www. 2003).

Rodamilans M. Fourth National Report on Human Exposure to Environmental Chemicals 103 . Otero R.Organochlorine Pesticides Schmid R. To-Figueras J.27:405-421. Demographic and seasonal influences on human serum pesticide residue levels.263:397-398. Barrot C. Cutaneous porphyria in Turkey. PA. et al. Santiago-Silva M.105(1):78-83. 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. Environ Health Perspect 1997. Sala M. Stehr-Green.

6) 36.70 (6. soil.7-26.5) 40. so they can accumulate in fatty tissues of animals.76.8) 7.20-16.90) 7.1-32.6-47.8 (9. beta.1 (9.9) 81.0-21.6) 35.2-17.9) 15.5) 67.3-56.2-98. formerly referred to as benzene hexachloride.4-45.4) < LOD 9.6-20.70-12.0 (8.5 (11.90-8.4 (16. 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. and delta.43 (<LOD-9.0) 41.0-23. population from the National Health and Nutrition Examination Survey.9-51.3 (26. The other isomers can be formed during the synthesis of lindane.2-42.9 (32.8) 12.7-96.0 (19.1-49.8 (33.9-56.7 (35.3 (42.8 (32.4 (11.9 (62.7) 73.8-16.8. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf. 104 Fourth National Report on Human Exposure to Environmental Chemicals .50) 8.2-22. and sediment as a result of historic production and use.9-81. commonly known as lindane.0 (37.S.4) 51. 2005). EPA cancelled agricultural uses of lindane (ATSDR.7 (62. < LOD means less than the limit of detection.7) 27.5 (43.2) 142 (99.0-111) 70.5) 14.2 (50. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice. interval) 9. It is no longer produced or sold in the U. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.2-87.6) 50.0-70.0 (35.6-37.6-62. respectively.2 (34.7-20.90-8.6-135) 69.1-37.4-50.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.7 (29.3-85.5528.4 (12.8 (21.4 (50.5) 11.70-19.0) 7.1 (27.2) 9.6) 47.36.2) 36.7) 18.5) 29. As pesticide applications of HCH were increasingly restricted or eliminated.7-69.4) 901 1067 952 992 1224 1007 Females 11.7 (13.1 (11.6) 16.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.5 (14.4) 21. HCH isomers.7 (<LOD-16.1-36.9) 45.9 (11.4) 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (16. containing about 64% alpha and 10%-15% gamma isomers.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.3) 34.7-69.9-24.7 (30. HCH isomers are lipophilic. In 2006.1 (30. 58-89-9 General Information Hexachlorocyclohexane (HCH).8 (10. Lindane has a half-life of about two weeks in soils and water.7) 23.7) 56.1) 13. The gamma isomer.5-123) 49.6) 653 758 589 1240 1533 1370 20 years and older 10.1-16. 6.6-42.3-38.70 (8.4 (8.8-68.5) 90th 42.9) 17.1) 31.1-27.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.66-12.2 (48.4) 10.7 (53.S. and 7.1) 12.2-20.2-52.0-34.1 (21. 319-85-7 gamma-Hexachlorocyclohexane CAS No.6-14. **In survey period 2001-2002.68 (<LOD-10.9 (50.4) 27. 608-73-1 beta-Hexachlorocyclohexane CAS No. exists in several isomeric forms. see Data Analysis section) for survey years 99-00.5 (37.2 (9.1-15.7 (25.0 (<LOD-12.3) 14.6 (10.9 (26.1) 71.2 (31.8 (64.6 (33.0) 35.2-46.8 (17.8) * * * * * * 15. 01-02. and 03-04 are 9.Organochlorine Pesticides Hexachlorocyclohexane CAS No.8 (23.4-111) 84.0 (33.56-12.6-18.8) 52. which may vary for some chemicals by year and by individual sample.9 (30.1 (18. including alpha.8) < LOD 10.4-73.0 (14.46-11.7-96.0) 17. See the section “What’s New” at the beginning of this Report for details.9 (40. However.8) 39.3) 25.8-54.0) 71. environmental levels declined.89 (<LOD-9. the U.1-32.5) 16.3 (13.6) 18.1) 12.3 (62.80 (6. and have been used either as fungicides or to synthesize other chemicals.4) 11.8) 27. each result has been multiplied by 1.1 (12. particularly alpha and gamma have been detected widely in air.8-19.6-89.6 (22.2 (18.5 (24.7) 32. water.S.9-178) 48.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.2 (29.7) 10.6 (40.1 (9.9-14.2) 62.0-20.8-199) 134 (85.80 (<LOD-14.6 (16.3) 51.60-13.87 (9.2) 13.9 (9. Technical grade HCH is a mixture of all four isomers.9-21.7-166) 70.5-29.61-12.0) 8.3 (42.1 (16. gamma.2-55.8-87.7) 97.4) 44.2-67.6 (17. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.7) 10.5 (8. 2005).4 (52.30-11.5) 22.3) 37.04-10.4) < LOD < LOD < LOD 46.8) 95th 68.0-70.

S.140) .244-.254) 95th . and nephropathy developed (IPCS. 1971.080 (.103) 90th .098 (.065 (. 1996.260-.100 (.37) 1.290 (.120 (.070 (. Rogan. each result has been multiplied by 1.290 (.078 (. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.250) . resulting in a half-life of about seven years.510) .210 (.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .089) . 1986).200-.250 (.062 (.100) .308-.372 (. 2002).270 (. **In survey period 2001-2002.050-.140) .191-.250-.587) 653 758 589 1240 1533 1370 20 years and older .167 (.065 (.410) .690) .130) .077) < LOD .240-.331 (. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.360) .310 (.140 (.560 (.150 (. 1981). U.040-.062 (.081-.190) .340) .840) .661) 901 1067 952 992 1224 1007 Females .170-.146-.S.240 (.220-. for lindane.080-.210) .560) .210 (.100-.120-.330-. 1983). which may vary for some chemicals by year and by individual sample.064) .680) .32) . and FDA has established a bottled water standard and food residue tolerances for lindane. Gunderson 1988).100-.090 (.190) .100 (.Organochlorine Pesticides exposure to HCH is through the diet.200 (.442 (.096) .501) .910 (.410-. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.300-.5528.294-.058 (<LOD-. tremors.080-.290) .160-.450 (.069) .140) .404) .370-.050 (.190-.310) .214) .222 (.047-.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 .. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.320 (.070-.190-1.234 (. HCH isomers are absorbed after inhalation.118-.330 (..170-.073-.125) < LOD < LOD < LOD .160) . paresthesias. OSHA and ACGIH have established workplace standards and guidelines.118 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.210-.382-. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.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.280-.083) .119) .090 (.290 (.01 (. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.480 (.221-.083 (.050 (. The beta isomer accumulates in fatty tissues and is metabolized more slowly.130-.144 (. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.050-.580-1.310) . When animals were chronically fed lindane at high doses.057 (<LOD-.05) .480) .050 (<LOD-. ataxia.059-.139 (. The U.051-.420-.400) .100-.120) .297-.068-.070 (. or dermal exposure.814) .380 (.220-.350 (.110-. hepatic enzyme induction.470) .390 (. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.103 (.050 (<LOD-.230-.080 (.067 (.080) * * * * * * .070-.521 (.250 (.216 (.580 (.110) .070-.064 (.174) .090 (.175 (.250-.131-.390-.092 (. enlarged livers.340-. Saxena et al. 2008.700) .080-. Fourth National Report on Human Exposure to Environmental Chemicals 105 .S. Distribution is mainly to fatty tissues. After dermal application of lindane 1% lotion.319) .160 (.480 (.710) .057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .287 (.150) . EPA has established a drinking water standard.056-. and seizures.067) .070) .110) .150) . respectively. and memory loss (Nigam et al.305) .050-.050) .103-.. population from the National Health and Nutrition Examination Survey.191-.620) .120-.410 (.080) .089-.360 (.072 (. interval) .260) .220 (.057-.220) .051 (<LOD-.620-1..110) .350) . See the section “What’s New” at the beginning of this Report for details.048 (<LOD-. 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.180-.060) . the serum half-life was about 20 hours among children (Ginsburg et al.120) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .412 (.450-..130 (.600) .077) < LOD .090-.360-. Workers who directly handled HCH have complained of headache. 1977).460) .124-.281 (.057-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.260) .150-.173-.050-.100) .091) .460 (.450) .400) .086) < LOD < LOD < LOD < LOD < LOD < LOD .470 (.200-.290) .280-.056-.410) .570 (.120 (.120 (. ingestion.120-.250 (. probably by blocking inhibitory neurotransmitters in the central nervous system.

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

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

72:261265. Botella B. Siddiqui MKJ. 4/21/09 Anderson HA. Bai KM. Toxicol Appl Pharmacol 1971. et al. Lowry W. available at URL: http://www.52(1):59-67. Piechotowski I. Deichmann WB. Burse VW. Toxicological profile for hexachlorocyclohexanes update [online]. Patterson DG Jr. April 1982 to 1984. Bottimore DP. Levels of DDT. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Granath F. Crespo J. Organochlorines in Swedish women: determinants of serum concentrations. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Bhatnagar VK. Herrman T. Schulz C. et al. Falk C. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Chemosphere 2004.91:998-1000. Gabrio T. Becker K.54:1431-1443. Astolfi E. Rev Environ Contam Toxicol 1991. children and newborn infants.58:1185-1201.111:349355.html. Occupational exposure to hexachlorocyclohexane. Krause C.fda. Darnerud PO. 2002. Visweswariah K. Zoellner I. Bjerselius R. PA. Lepom P. Radomski JL. August 2008.57(4):315-320. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Needham LL.120:1-82. Environ Res 2004. Int Arch Occup Environ Health 1983. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Zaidi SS. et al. org/documents/jmpr/jmpmono/2002pr08. Stehr-Green. Bull Environ Contam Toxicol 2004. Exposure of women to organochlorine pesticides in Southern Spain. Nigam SK. Lindane. Buckland SJ. Olea-Serrano MF. Rogan WJ.71(6):1200-1209. August 2005. Brock JW.150:981-990. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. selected elements. and HCB residues in human blood in Ahmedabad. and other chemicals. Kutty D. Paepke O.48:127-134. Needham LL. Environ Health Perspect 1998. Link B. Bates MN.9(4):417-424.atsdr. Krishna Murti CR. Int J Hyg Environ Health 2002. Rey AA. et al. India. Demographic and seasonal influences on human serum pesticide residue levels.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.htm. J Pediatr 1977.cdc. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Available at URL: http://www. Placental transfer of pesticides in humans. Arch Pediatr Adolesc Med 1996.gov/~dms/pesrpts. Available at URL: http://www. Metabolism of gammahexachlorocyclohexane in man. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. The Great Lakes Consortium. Garrett N. Olson J. Absorption of lindane (g benzene hexachloride) in infants and children. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Kulkarni PK. Needham LL. Environ Health Perspect 2003. J Assoc Off Anal Chem 1988. Wood PH.html. Reisch JS.27:405-421. 4/21/09 Ginsburg CM.106(5):279-289. Maass R. et al. International Programme on Chemical Safety (IPCS). Potischman N. Raju GS. Glynn AW. Heinrich R. Sturgeon SR. VI. Hanrahan L. Saiyed HN. HCH. Gunderson EL.96:34-4Food and Drug Administration (FDA). dietary intakes of pesticides. Arch Toxicol 1981.inchem. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Saxena MC. Kaus S.cfsan. Angerer J. Biomonitoring of persistent organochlorine pesticides. Bhargava AK. Pollutants in breast milk. Cerrillo I. J Toxicol Environ Health 1989. Ellis H. et al. Majumder SK. Olea N. Rivas A. Cancer Causes and Control 1998. 4/21/09 Kutz FW. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Int Arch Occup Environ Health 1986. Chemosphere 2005. Karnik AB. Atuma S. FDA total diet study.20(2):186-193. Rothman N.205:297-308. Kashyap R. et al. Brinton LA. gov/toxprofiles/tp43. Seiwert M. Aune M.

S.8. which may vary for some chemicals by year and by individual sample.70-40.0 (12. Formerly.S.6) < LOD < LOD < LOD < LOD 71.1 (8.70-24. and foods. animals.2 (7. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.70 (<LOD-15. resulting in exposure to newborns and nursing infants.3-225) 15.6) 9.4-230) 18.0 (14.3 (15. 2385-85-5 General Information Mirex has not been produced or used in the U.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. Mirex binds strongly to soil.4) < LOD 15. Mirex is absorbed through the skin and from the gastrointestinal tract.6. Mirex can cross the placenta and be excreted in breast milk. 1985.0-374) 11. sediments.10-37.2) 51. Mirex has been detected in air.40 (<LOD-13.5 (<LOD-42. since 1977. aquatic organisms.10 (<LOD-15.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.7 (12.0 (<LOD-108) < LOD < LOD 50.4) < LOD 63.5-291) 11. In studies conducted in the 1970’s and 1980’s.8) < LOD 15. 1995). respectively. where it has a half-life of 12 years. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. Occupational exposure is limited to workers at sites where mirex contamination is present.6 (<LOD-31.8 (12. after which it is widely distributed in the body and stored in fat.5 (<LOD-115) 153 (30. or pesticide application.6 (<LOD-108) 9.4 (8. especially those from persons living in the southeastern U. Fourth National Report on Human Exposure to Environmental Chemicals 109 .3 (15. it is a highly persistent chemical in the environment.S.Organochlorine Pesticides Mirex CAS No.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 01-02.7) 8.6 (<LOD-23.7 (<LOD-47. water. < LOD means less than the limit of detection.1 (13. disposal. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.. Mirex is not metabolized in the body. and 03-04 are 14. soil.90-29.8 (<LOD-73. (Kutz et al.5. Some states and the U.5 (9.3) 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 13.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. and 7.0) * * * 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. 1991).2-230) 13. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. 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.6-305) 15. see Data Analysis section) for Survey years 99-00. 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. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.5-82.7) < LOD 66.S. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. where it was applied directly to soil and by aerial spraying. 10..5-425) 40.S.1 (<LOD-65. mirex was detected in human adipose samples.

106 (.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 .055-.084) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .064 (<LOD-.080-1.080-1.102) < LOD < LOD < LOD < LOD .atsdr.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.610) < LOD < LOD < LOD < LOD . 2004).370 (. EPA has established environmental standards for mirex.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and 2003-2004 subsamples.052-.S.220 (<LOD-.08 (. and NTP classifies mirex as reasonably anticipated to be a human carcinogen. 2005).html. Survey Geometric mean (95% conf. Laboratory animals fed high doses developed liver enlargement and liver tumors.410 (.053-. population from the National Health and Nutrition Examination Survey.077 (<LOD-.S. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.310 (. 1989).140 (<LOD-.690) .054 (<LOD-. Smith.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 .090 (<LOD-.268) < LOD . serum mirex levels were generally below the limits of detection (Stehr-Green.470) .089-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .gov/toxpro2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. as well as in a subsample of NHANES II (1976-1980) participants.510) < LOD < LOD . More information about external exposure (i. In addition. 110 Fourth National Report on Human Exposure to Environmental Chemicals . In samples obtained between 1994 and 1997.256 (.110 (<LOD-.430 (. 1991).8.73) .450 (.059 (<LOD-.470) .79) . 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. 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.79) .112 (. IARC classifies mirex as possibly carcinogenic to humans.170) < LOD ..062-. 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.220) .635) < LOD .37) . 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.090 (<LOD-.450) 1.090-1.079 (<LOD-. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.070-1.41) . The U. Biomonitoring Information In the NHANES 1999-2000. environmental levels) and health effects is available from the ATSDR at: http://www. 1995.093 (. 7.. and 4. which may vary for some chemicals by year and by individual sample.106) < LOD .92) .7 ng/g of lipid.108 (. reproductive toxicity included decreased fertility and testicular damage.090-1.Organochlorine Pesticides exposures are unknown.090-1.e.170-3.100 (<LOD-. The geometric mean mirex levels of the Inuit mothers were 8. 2001-2002..02) .cdc.100 (<LOD-.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .470 (.090 (<LOD-.

PA. Gilman A. Jr. Demographic and seasonal influences on human serum pesticide residue levels. Jr and Laws ER. Strassman SC. Van Oostdam JC. 1991 pp. Smith AG. Kutz FW.html. The human body burden of mirex in the southeastern United States.15:385-394. Watts DL. hexachlorobenzene. Vena JE. Eds. Sci Total Environ 2004. dichlorodiphenyldichloroethylene. Circumpolar maternal blood contaminant survey. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Biomonitoring studies on levels of mirex provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of mirex than are found in the general population.27:405-421. 731-915. J Toxicol Environ Health 1985. Inc. Chashchin V.cdc. References Agency for Toxic Substances and Disease Registry (ATSDR). Handbook of Pesticide Toxicology. 1994-1997 organochlorine compounds. J Toxicol Environ Health 1989. Leininger CC. Dewailly E. et al. Bottimore DP. 2 Classes of Pesticides. Kutz FW. Moysich KB. Academic Press. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. August 1995. Stehr-Green. Rev Environ Contam Toxicol 1991.120:1-82. In Hayes WJ.97(2):178192. Carra JS. Environ Res 2005. Vol.atsdr.gov/toxprofiles/ tp66. Available at URL: http://www. Toxicological profile for mirex and chlordecone [online].330:55-70. Chlorinated Hydrocarbon Insecticides. Odland JO. Hansen JC. Profiles of ortho-polychlorinated biphenyl congeners. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Wood PH. et al. Swanson MK. New York. Olson JR. Stroup CR.Organochlorine Pesticides effect. 4/21/09 Bloom MS.

surface water.00 (3.31 (<LOD-9.4.80 (1.50-63. Exposure to trichlorophenols also may result from metabolism of lindane.5-Trichlorophenol CAS No.30-3.00-3.9.30) < LOD < LOD < LOD < LOD < LOD 1.50) < LOD 1.0) 2. Both chemicals have been detected in air.50-25.S.0) 5.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. 2.40 (1.0 (8.4.4.0) 2.0) < LOD 11.0) 2.60-18.71 (<LOD-8.0) < LOD 5.20) < LOD 90th 5.0) 2.60) < LOD 8.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds. recent sampling of U.4. 1999).3.4.9 and 0. 112 Fourth National Report on Human Exposure to Environmental Chemicals .90-33.30-11.5-trichlorophenol (2. Survey Geometric mean (95% conf.20) < LOD 1. 2006).63) 18.6-Trichlorophenol CAS No.71 (<LOD-8.5-TCP) and 2.60 (4.42 (<LOD-8.9 (<LOD-121) 9.30-44. 1999).0) < LOD 5.0) < LOD 5.30-27.20-36. Such workers would probably Urinary 2.6-TCP). 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.27) 696 661 521 696 603 939 Limit of detection (LOD. soils.20) < LOD 5.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2. may occur by inhalation or dermal routes. public drinking water systems did not detect 2.0 (4.. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. however.40 (1. other organochlorines. including hexachlorobenzene and hexachlorocyclohexanes. 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.19 (<LOD-6.57 (<LOD-15.40-18.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.5TCP and 2. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16. EPA. Trichlorophenols are no longer manufactured commercially.7.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .40 (.980-3.27) 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 (5.0 (3.8) 21.40) < LOD 6.50 (. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.40 (2.72) < LOD 1.30) < LOD 4.4. < LOD means less than the limit of detection.42 (<LOD-12.6-TCP in any of the samples (U. Formation of 2.4.920-3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.80) < LOD 1. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.940-3.60 (.4. are metabolites of several organochlorine chemicals.40 (.60-8.30-40.S.50 (1. and sediments.0 (3. 95-95-4 2. and polychlorinated benzenes (Kohil et al.40 (2.4.80-41.4.0) < LOD 11.40 (2.10-3. 2. hexachlorobenzene.900-2.40-11.40) < LOD 4.40) < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (4.50 (2.4. usually at herbicide production or waste incineration facilities.00-8. 1976).03) 9.20-71.S.30 (.5-trichlorophenol.980-3.0) < LOD 21.30-27. 2.4. Historically.0 (4.50-16.6-trichlorophenol (2.0) 2.30-27.00 (2.0) 14. which may vary for some chemicals by year and by individual sample.80 (2.Organochlorine Pesticides 2.00-3.0) 2. Occupational exposures.60 (2.40 (2.7) 24.6-TCP were used as intermediates in the production of certain pesticides.20 (4.950 (<LOD-1.

27-17.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.20-6.46 (1.2) 2.e.32) < LOD 4.83-12.44 (1.86 (3.6-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.1) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.68-4.atsdr.5-TCP and limited for 2.24) < LOD 6.4.24 (3.920-2. 1995) and up to 19 times higher than the 95th percentile value of 1.79-4. population from the National Health and Nutrition Examination Survey.24) < LOD 1.53-3.6-TCP levels at the 95th percentile were up to eight times higher than 3. furans.5) 11.5) < LOD 12.68 (<LOD-8. 1989).980 (<LOD-1.78-19.43) < LOD 12. 7.Organochlorine Pesticides be exposed to mixtures of chlorophenols.43 (2.67 (1. 2004). However.78) < LOD 1.3 mg/L reported in German adults aged 18-69 years (Becker et al. in addition to dioxins.31) < LOD 2.50) < LOD 2.02-3..5-TCP. 1989).16 (. and lymphomas..820-2.00) < LOD 4.29 (1..44 (.90 (4.5-TCP nor 2. Urinary 2.4.0 mg/L. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.4.78 (3.4. Laboratory animals chronically fed high doses of 2.6) 4.0) 7. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.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. 2003.4..15) < LOD 2.4 (6.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.7 (4..80 (1. urinary 2.02) < LOD 7.3 (5.37) 16.6) 4.cdc.24-11.00-29.8) 4.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. 2003).69 (2.6) 4.73 (<LOD-8. the 95th percentile urinary 2. Survey Geometric mean (95% conf.00-19.4) 5.4.05-17.28-25.69-18.6-TCP. as being possibly carcinogenic to humans.47-8.37-11. More information about external exposure (i.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). In the same 2-6 year old children..2 (2.6-TCP had increased rates of hepatic tumors. 1995) were similar.S.4) < LOD 3. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.gov/toxpro2.13-13.4. environmental levels) and health effects is available from ATSDR at: http://www. The 95th percentiles for 2.6-TCP as reasonably anticipated to be a human carcinogen.74) 11. IARC classifies combined exposures to polychlorophenols.64 (4. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al. leukemias.html.75 (<LOD-6..4.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.67 (1.4.17) 9.57 (<LOD-7.11) 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 2.16) < LOD 90th 5.88-16.36 (1.57 (<LOD-7. and other chlorinated compounds.93-11. Radon et al. At lower doses. the 95th percentile urinary 2.62-20. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al. which includes trichlorophenols.33) < LOD < LOD < LOD < LOD < LOD 2.8) < LOD 9.4.60-3.95 (3.9 (5.5-TCP or 2.53-3.19-12.4) < LOD 3.. Human health effects from 2.4.19-4.75 (3.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .9) 12.8 (5.82 (<LOD-32.1 (<LOD-58. 2003). animals showed hepatocellular abnormalities.49 (1.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. NTP classifies 2.24) < LOD 5. Fourth National Report on Human Exposure to Environmental Chemicals 113 .05-8. Neither 2.57 (3..81 (<LOD-9. Among 6-11 year old children in NHANES 1999-2000.55 (4.4.2) < LOD 5.

33-4.4 (8.4.53) 4.3) 23.4.47 (3.80) 1.74 (2.1 (10. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.44) 75th 4.0 (9.70-6.51-12.30-11.6TCP values.4.7) 21.70-6.20-3.10) 6.40-4.5 mg/g creatinine) were similar to the limit of detection for 2.40) 3.6 (11.90 (3.50 (2.14 (2.70) 3.8) 18.67-12.60-21.40-32.84) 2.0 (20.0-38.95 (4.S.76) 3.4 (17.0 (6.9 (13.69 (3. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. 2003).0) 13.40 (2.72-10.48-26.7 (13.1 (8.1) 16..23) 3.40 (2.55-3.45) < LOD 11.5-TCP or 2.95-6.28) 24.0 (16.0) 15.60) 6.75 (8.65 (5.0) 17.92 (2.3-26.32) 3.5-TCP (0.35-3.53) 2.89-6.0-50.0 (6.85 (2. was about six times lower than the median urinary levels for males in this Report (Radon et al..60-37.80 (2.4.4.98-7.70 (2.4.52 (2.9) 13.7) 33.80-25.30-2.36 (1.4.0 (8.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.6-TCP exposure and health effects.6-TCP (0.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.40-14.45 (5. In harbor workers exposed to chlorophenol-contaminated river silt.70 (2.79 (5.4.0 (11.20 (3. Urinary 2. population from the National Health and Nutrition Examination Survey.5-TCP or 2.0-41. 2004).59-6.9) 694 677 519 696 602 931 Limit of detection (LOD.00 (4.31 (3.4.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.60 (2.40) 2.0-37.5-TCP or 2.4.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.40-7.0-44.30) 4.6 mg/g creatinine) and 2.08 (2.78 (2.4.60 (3.4.20-6.45 (2.65) 15.4.0) 19.0) 13.90 (4.2 (14.5-TCP level of 0.5-TCP and 2.40-2.8) 32.00 (1.5-TCP and to the median 2.30-33.0) 9.90) 2.0-18.02) 2.20 (3. which may vary for some chemicals by year and by individual sample.23) 2.5-TCP or 2.6-19.8 (9.23-2.40) 2.3) 37.4.6 (12. 114 Fourth National Report on Human Exposure to Environmental Chemicals .12) 2.91-4.0) 10.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.25-11.80 (3.0) 17.0) 7.40) 4.0 (12.74-3.56 (3.0 (8.1-25. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.3 (11.0-43.68 (<LOD-2. interval) 2.4-17. Mean values of 2.52-3.0 (7.59) 4.00 (2.3) 20.7 mg/L.07 (<LOD-3.4.0-68.0) 13.80-20.20) 4.0 (15.78 (2.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.36-5..8-24.40-2.0) 12.6-TCP in urine does not mean that the level of 2.60) < LOD 5.0) 11.73-9.3-17.6-TCP than are found in the general population..5-TCP and 2.7 (9.4 (10.4 (9.24 (2.0) 14.70) 1.18-3.5-46.30-2. Biomonitoring studies on levels of 2.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.49 (6.57 (<LOD-2.70) 5.60-3.32) * 3.50-5.10-3.0) 7.6-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.63) 90th 15.10 (5.01-6.0-54.0 (13.06) * 2.00-4.66 (8.10-3.0) 11.89 (3.0 (6.36 mg/g creatinine.0 (20.98-11.2) 12. the median urinary 2.10-2.6-TCP level.10) 2.80 (2.0 (14.6) 21.4.0 (14.0) 9.32-4.0 (14.67) 4.00-21. 0. respectively.09-7.90-8.31) * 2.20-23.8-15. Biomonitoring data will also help scientists plan and conduct research about 2.54) 6.09) 15. 1991).0) 6.26 (2.0 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 19.46-3.6) 26. for males in NHANES 19992002 (Agramunt et al.80-7.80-6.7-16.6TCP causes an adverse health effect. Finding a measurable amount of 2.3.58 (1.99) 6.7-3.4.9 (11.0) 10.2-0.95) 3. 1998).45-9.4.0-38.60 (3.0) 14.3 (11.04) 2.70) 5.8-13.0 and 1. similar to the limit of detection for this Report (Anderson et al.9) size 1989 2503 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.28) * 2.4.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.85) * 3.87-14.0 (15.58-3.6-17.4.0) 13. Urinary 2.6-22.70-3.2) 25.

08-2.5) 11.22 (<LOD-2.44 (3.27-9.88 (2.18-4.81) 2.7) 6.5) 9. Survey Geometric mean (95% conf.22-9.88-7.43-7.76) 2.17-4.9 (9.82) 2. population from the National Health and Nutrition Examination Survey.53 (3.91-2.41 (3.16-10.56-5.50-8.1-21.71 (3.90) 2.3-23.06) 4.59 (2.48-2.87-6.63) * 4.21-11.1) 14.0) 8.00 (2.22-2.25 (3.4) 8.26 (6.9 (9.25-2.1-32.82 (8.77) 2.2) 19.77-4.04-16.96) < LOD 4.02) 3.65-21.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.2 (12.3) 8.30-2.70-9.15 (6.26-13.88) 1.23) 4.94-13.6 (9.99-2.02 (1.68) 2.63 (<LOD-2.75) 75th 4.9) 8.25 (3.32 (2.53) 4.23 (1.53-11.6) 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 2.0) 10.5-28.6) 8.78 (2.76) 1.29-4.9) 7.8) 21.87) 2.0 (11.56) < LOD 11.67-17.38 (2.5 (7.49-3.17) 2.66-4.13-6.09-3.05 (3.49) 4.78) 2.4 (11.4) 4.50 (2.25-15.8 (8.9) 8.56 (7.28-4.6 (9.81-9.98 (1.51 (2.88) * 2.7 (14.10 (6.29-4.58 (4.06) 11.Organochlorine Pesticides Urinary 2.88) 4.52 (5.6) 13.83-6.41-6.24 (1.7) 25.63) 4.42 (2.65) 2.63-15.33 (1.83-6.9-34.73-22.38-5.65-2.06-2.1 (13.79-17.43 (<LOD-2.91 (3.89) 10.25-17.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.15 (1.63 (2.9-32.87-7.6 (5.8) 12.54 (2.10-9.14-13.42) 2.53) * 2.88) 4.78) 90th 12.8) 11.38 (4.91 (7.17) 13.00) 4.43 (2.2 (8.20-2.22 (1.60-2.32-19.51) 18.88) 5.60 (4.8 (7.90 (1.35 (3.87) * 2.65) 18.6) 12.33) * 2.18-2.4) 9.00) 4.40 (2.62-15.38) 22.01 (3.00 (3.13 (1.3-37.1) 11.46-14.95-2.82-2.52 (3.52) 2.92) 4.83-5.4 (12.5 (8.9) 19.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6 (10.87 (3.63-13.33-2.76) 4.40 (7.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.68) 2.72) 32.98) 10.2 (7.6 (6.6 (22.2 (13.29 (6.22 (3.S.51-21.5) 12.1 (8.9-29.0 (6.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.14-2. Fourth National Report on Human Exposure to Environmental Chemicals 115 .6-31.6 (12.3 (9.47-5.8) 19.04-2.55-2.76-8.7-36.0 (9.73) 5.5 (10.5) 8.33 (7.72-16.19-5. interval) 2.89-2.52) 2.83 (3.9-64.05 (6.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) 4.11) 10.5) 11.82 (3.

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

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

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

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

0) 10.0) 20. 01-02.68-7.670-1.38-5.7 (14.23-5.970-2.76 (2.05-7.0 (7.39 (8.70) < LOD < LOD 1.0 (8.9) 14.55-8.80) 4.0) 11.0) 10.5) 20.10 (.9 (8.12-19.35-16.30 (4.8 (9.99 (5.33 (5.5-17.954 (.9) 8.40 (.4) 18.2-20.530 (<LOD-2.30 (2.79-7.60 (5.1-17.20 (.15) 14.29) * * 1.97) 90th 7.71-9.70 (2.82-12.0 (9.27-15.1) 10.90 (1.79 (5.16) 4.32 (.46) 10.48-7.5 (8.2.2 (9.89) 9.5) 15.58 (3.34-7.98-5.90-5.40-5.90-4.830 (<LOD-3.955 (.4 (7.81) 11.4) 20.2 (14.66) * * 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40-16.04) < LOD 1.2) 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) 10.2.45 (2.40-11.890 (<LOD-2.44 (2.14) * * .1) 95th 13.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.4 (9.579-1.80-22.757-2.50) 2.70 (4.80) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20-7.39 (3.7) 11.56 (6.34-3.0 (7.0 (6.2) 16.16 (2.30 (2.72) 5.8-32.17-3.13-2.S.83 (5.13 (2.70) .43-12.28) 1.5-16.0) 11.8) 19.40-1.21) 9.00-27.81) 11.0) 6.10 (.490-2.90) 3.8) 7.00-12.93 (4.10) < LOD < LOD 4.47) 5.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.40-19.56 (4. interval) 1.82) 10.2 (9.94) 3.63) 1.73) * * .07-10.90) 2.60-11.2 (7. 0.70-19.60-18.81) 1.8) 7.0 (8. < LOD means less than the limit of detection.10-7.4 (7.70-11.58 (2.85 (3.86 (1.0 (8.2) 16.0 (6.61) 4.10) < LOD .80) 3.3) 17.70-23.44-3. see Data Analysis section) for Survey years 99-00.10 (2.37 (3.3-15.70) < LOD < LOD 75th 3.2 (14.80) 11.6) 7.0) 7.2 (11.55-6.26-8.52) 6.08 (<LOD-2.30-6.26 (5.80) 2.08-2.623-1.9) 952 1187 928 997 1333 1003 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0-27.20-30.0) 11.0) 6.74 (8.44-38.599-1.52-11. respectively.0) 11.740-2.13 (2.00-12.60-25.02) 4.50 (.840-1.758-1.0) 15.0) 10.700-1.00 (1.3) 14.0) 5.8 (12.7 (12.1 (9.02-5.00) 3.35-11.1 (10.2 (7.10 (2.2 (7.9-18.11 (. and 03-04 are 0.20 (2.80 (2.67) 3.50-5.00) 3.0) 10.8 (14.780) < LOD 3.80) .717-1.80) 2.290 (<LOD-.80) 2. 120 Fourth National Report on Human Exposure to Environmental Chemicals .810-1.96-3.56-13.1-23.03 (.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 1.981 (.32) 1.56 (1.00-7.58 (5.2) 14.4 (9.97) 8.0-28.94) * * .51) 2.0) 6.42) .01) * * 1.620-1.5 (11.57-7.60) .12) 4.50 (4.80-4.26-6.08-15.20 (.36-4.86-15.93-24.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.61 (3.20-4.0) 5.42-3. population from the National Health and Nutrition Examination Survey.80-24.54 (3.750-1.00 (4.74 (8.35-12. which may vary for some chemicals by year and by individual sample.22 (.3) 16.98-12.50 (2.70-14.52) * * 1.860-2.60) < LOD < LOD 4.600 (<LOD-1.0) 5.91) 4.1) 13.290 (<LOD-1.20 (. and 0.0 (7.60 (1.50-36.0 (12.33-18.00-27.0 (5.1.21 (.6) 18.30-4.00-19.19) 9.4) 17.95) 5.8) 11.0 (7.47) * * 1.0) 9.0) 12.00 (5.0 (9.27-3.0 (4.71 (2.80 (4.53) 4.8 (8.15-12.40-14.20 (.

02-2.03) 2.830-1.88) 2.84 (5.61-29.9) 11.45-5.1 (10.04 (1.02-14.89) * * 1.40) < LOD < LOD 75th 2.51-5.3) 12.1 (8.11-6.35) < LOD < LOD 3.34) * * .1 (11.924 (.98) .4 (9.7 (8.56) 4.21-23.960 (<LOD-2.61 (1.960 (.54-15.28 (4.03) 2.19 (4.7 (10.01-2.0) 7.62) .92-5.29) * * .750 (<LOD-1.1) Sample size 1949 2519 1928 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.42) 12.1 (6.890 (<LOD-1.8 (10.540-1.67-19.83) 8.07 (.31-14.78 (2.3) 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 1.02 (2.47) * * .3) 15.94-9.34 (6.7) 12.37-3.37) 9.1) 4.883 (.10 (3.45-5.4 (4.77 (6.90-8.83 (7.1 (9.57) 4.2) 5.533-1.790 (.68-4.0 (8.5-20.1) 4.818 (.900 (.00 (4.2) 9.566-1.560-1.62-5.43 (3.4) 4.92-2.7) 18.05 (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 .76) < LOD .45-11.780 (<LOD-1.860 (.53-11.03-6.98 (3.1-15.57 (4.25) 6.41-12.02 (7.56) .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.18 (.82-14.9 (5.0) 6.57-10.870-2.66-34.54-2.6) 8.47 (3.574-1.633-1.20-8.28 (5.855 (.2) 7.40-28.15-10.67) 1.89-3.2 (6.73 (1.03 (2.80 (2.1 (7.32-12.94-23.31 (3.6 (9.82-6.46-5.5-32.37-5.84) 7.05 (.6) 13.61 (1.61-13.55-20.40-12.36) * * 1.81-5.81 (1.00 (4.69) 4.29 (2.69) 2.66 (1.53 (6.09) 2.14 (3.72) 11.932 (.44 (2.79-9.920 (.25) < LOD .60-9.38) .93) 9.54-4.26) * * .00-19.53) 9.60) 2.440 (<LOD-2.9-28.80 (6.60) * * .2 (10.82-26.46) 2.5) 11.608-1.430-1.94 (2.39 (2.42 (3.41) Selected percentiles ( 95% confidence interval) Total * * 50th .24-3.04-6.75-7.23) 4.10-13.43 (.549-1.510-1.75) 2.75) 14.6 (10.2) 5.09-11.87 (1.94-22.6) 9.75 (7.74) 90th 7.69-10.3) 16.7 (9.94 (4.996 (.8) 12.66 (2.2 (8.8) 8.27) < LOD 2.9 (9.5) 8.85) 2.37 (4.00-17.79-3.710 (<LOD-1.09 (.30) 2.37 (5.47 (3.87 (3.98-22.40) 4.47) 2.9 (9.05) .7) 5.38 (1.23 (4.03 (7.47 (1.98) .95) 2.56) 7.98-5.95 (3.40-5.28-9.5) 7.52) 4.54) .74) 4.98) 9.85 (6.2) 8.13) 4.88-10.94-10.5) 7.87-5.28) 10.66-15.34) < LOD < LOD .88 (5.820 (.67) 4.5-16.2) 95th 12.93-5. population from the National Health and Nutrition Examination Survey.50) 7.68) < LOD < LOD 3.40 (3.5) 12.80 (7.2) 13.90-5.8) 16.76-4.4) 4.82-14.28 (2.773-1.8) 7.34 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5-13.9) 12.6) 11.71-2.54-11.650-1.56-13.75 (3.69 (4.S.9) 16.40-3.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.57 (6.30 (1. Fourth National Report on Human Exposure to Environmental Chemicals 121 .500-1.00-13.43) 2.40-14.41) .93-9.66 (5.58) * * 1.890 (<LOD-1.8) 6.570-1.64-5.3) 5.88-15. interval) .620-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.06-2.5 (4.80) 9.4) 13.00) 8.35 (1.71) 10.

66-13.31) 1.50-5.80) .82) 8.6-41.18) * * * * * * * * 1.92-17.3 (6.9) 9.0 (9.80-4.0-19.0) 12.7) 10.22 (6.650-1.9-14.30) < LOD < LOD .67) 4.5-26.31-7.49-4.6) 18.7 (11.35 (6.25 (2.61-32. which may vary for some chemicals by year and by individual sample. and 03-04 are 0.3 (9.7) 15.98-9.59-3.20 (<LOD-2.00) 8.11-6.5) 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 * * * * * * . population from the National Health and Nutrition Examination Survey.9) 10.90 (6.970 (<LOD-2.34-5.0) 11.3 (11.5 (8. see Data Analysis section) for Survey years 99-00.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.6) 11.74) * * * * * 1.80) .35-3.2 (9.670 (<LOD-1.75 (2.6 (10.50) 5.22 (6.0) 14.S.8-20.670 (<LOD-1.00-9.50) .580-2.89) 2.61 (3.5) 21.790 (<LOD-1.41) 3.5 (8.00) 3.20-18.6 (10.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90-15.70-5.00-16.0 (5.9) 16. 0.60 (5.70-9.46-4.40 (2.04 (3.27) 4.34 (6.41-5.5.84-4.0) 18.88) 10.0) 12.20) .1) 11.9-17.70 (1.90 (2.70) 2.81-6.53 (3. respectively.7 (10.740 (<LOD-1.70-9.37) 2.88) 3.30) 8.0) 14.90 (5.86-10.40) < LOD < LOD 75th 2.34-3.99 (3.9 (12.18 (3.67) 3.80-14.90) 4.7) 14.39-13.910 (<LOD-2.0) 23.90 (6.77-3.4) 7.0-24.24 (2.70-8.5 (9.10 (<LOD-1.90-9.14 (6.8) 9.90 (6.00) 3.63-14.8 (12.6) 14.15-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2) 14. and 0.8 (12.22-12.58.97-4.31-12. < LOD means less than the limit of detection.6) 14.680 (<LOD-1.50) 3. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .40 (2.7-21.89 (2.27) .00-4.24-5.00-18.0 (8.0-33.96) 90th 7.29-4.20-8.12 (4.95 (2.00 (.4 (10.7) 16.66) 4.67-10.80-8.0 (14.80 (2.70 (8.0) 11.0-29.1 (10.10-4.0) 12.29) < LOD < LOD < LOD < LOD 3.45 (3.3) 22.3 (7.80 (5.00) 7.670 (<LOD-1.27 (3.80 (2.34-10.22) 8.90 (2. 01-02.670 (<LOD-1.0 (15.75 (3.0 (13.37 (3.30) < LOD < LOD 4.42 (1.80-6.90-31.10) 6.35) 4.80-12.7) 22.64) 10.3) 20.00-4.95-9.47-6.33-11.28 (7.4-17.20) 3.90 (2.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5.0) 6.9 (7.3 (12.30) 3.96) 3.92) 9.95 (5. 122 Fourth National Report on Human Exposure to Environmental Chemicals .73) 7.80) 5.46-28.58 (1.0-24.4 (14.9) 95th 14.3) 14.78) 5.3) 10.80-21.0) 9.10 (.8-21.62-17.80-3.17 (7.60 (2.60) < LOD < LOD 2.0) 9.0) 13.06 (2.0 (10.4) 11.1-23.00-18.3 (9.77-14.60 (6.27) 9.20) 3.72) 2.1 (10.90-15.0 (7.15-6.8) 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 1.10-15.52 (6.4 (10.2 (7.6-19.0) 7.0 (9.20-4.51) < LOD 1.8) 8.8-17.01 (2.9-15.90 (6.8-20.0) 13.39 (5.30) 3.0) 19.3) 8.90 (1.7-19.00) < LOD .90) 8.10-10.0 (10.27 (7.16-1.50-4.

87 (3.32-8.18) 2.28) 6.920 (<LOD-1.44-6.28-12.71 (1.58 (4.93-10.5) 22.68) .00 (5.00) 8.88 (1.5 (10.96-10.38 (.81 (7.72-4.6 (12.95 (2.36 (2.7-23.00) 2.9 (9.2) 10.15 (1.69-11.89-13.00 (<LOD-1.61 (2.27) 5.03) 3.77) 3.850 (<LOD-1.51-7.70-35.1) 10.59-3.93 (6.83 (7.68-4.4-15.95) 3.06) .92) 3. population from the National Health and Nutrition Examination Survey.5) 10.89 (3.91-9.01-5.25 (4.77 (2.07-3.27-13.63 (2.53-8.2 (9.7) 14.63 (6.00 (<LOD-1.86) 9.2-15.530-1.7 (10.93 (<LOD-2.590 (<LOD-.8) 16.02-4.88-7.3) 9.21) * * * * * 1.78 (4.4) 7.3) 6.4-16.11-3.54) 9.04) 9.79-9.70-2.1 (8.5 (15.78 (6.68-19.67 (7.14 (2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.42) 8.3 (7.45) 6.29) 3.74-19.78) 4.4) 16.89-3.55) 16.64-11.0 (11.45) 3.89-10.54-5.7) 14.0 (13.28 (1.09-11.8 (10.910 (<LOD-1.3) 8.8) 14.7) 9.27) 1.05-3.33-10.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .2) 16.3-15.3-17.8 (8.4) 7.51-10.2) 12.950) .6 (11.67 (1.25-9.2) 12.2) 19.5 (8.82-8.5) 13.07) 2.93 (2.2) 12.30) 8.92 (5.5) 8.12) < LOD < LOD 4.99 (4.4 (11.33) 3.96-11.73 (5.0-21.34) < LOD < LOD < LOD < LOD 3.68-10.9 (9.85-17.74-4.2-30.5 (11.91) 3.55 (2.1 (19.9-17.0-19.0 (8.23-3.S.07) 2.6 (10.77 (2.75-3.38) 1.38 (2.7) 12.95) 90th 8.79-6.6) 6.16-14.690 (.54 (7.72) 4.7-19.5 (9.6) 12.973 (.94-14.50 (6.89 (2.52-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.89-3.890-2.48 (2.99) 2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .20-3.71) < LOD < LOD 2.30) 7.37) 3.3-17.2) 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.2) 8.4) 6.86 (3.00 (7.97-4.41 (7.86-3.9) 16.760 (<LOD-1.85-8.27) < LOD .6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.6-19.94 (5.2) 15.810 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.82-11.75-3.00 (2.6) 14.42-19.3) 12.7 (10.7 (8.29 (5.55) .80) 3.3-21.9-25.78-10. Fourth National Report on Human Exposure to Environmental Chemicals 123 .7) 15.6 (13.47-9.21-21.6 (11.6) 7.50-17.27) * * * * * * * * 1.16 (3.07 (5.6 (13.4) 15.2 (9.37-5.30) 2.09-11.39-17.4-16.97) < LOD .5-17.6) 95th 16.3-34.1 (13.11 (5.6) 13.620 (<LOD-.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 * * * .4) 7.83 (6.03 (2.9) 19.38-13.4) 9.42) 7.03 (6.32) 2.0) 14.940) < LOD < LOD 1.15) < LOD < LOD 75th 2.00 (3.19) 3.12 (7.43 (2.8) 11.29-2.1) 20.34-18.780-1.7 (11.29 (2.4-18.38 (1.9 (9.06 (<LOD-1.1) 13.0 (10.89) 5.30-5.

31) 95th 2.79) .597) * .90) 2.910-1.57 (1.13) .160 (<LOD-.79) .48 (1.80) 3.690-.09.55 (3.16) 1.580-1.91) 2.74-5.700) .960-1. and 03-04 are 0.89) .41 (2.455 (.80 (1.46 (2.70-7.260 (<LOD-.64 (1.2.353-.930) < LOD .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.20) 3.960) 1.32-1.440-.37-2.08 (2.00) 1.94 (3.90-4.749 (.240 (<LOD-.76 (1.70 (1.490 (<LOD-.68-5.20-2.14-1.650-.570 (.720-1.18 (.30 (.980) 1.39) 2.820 (.20) 3.47) 2.48 (2.90 (1. see Data Analysis section) for Survey years 99-00.600-1.10) 1.83) 2.970) 1.780 (.350-.425 (.95-5.22-3.18 (1.10-1.22-2.04) 1.42-2.80) 2.80) 3.459 (.303-.27 (3.940) < LOD .60 (2.49) 2.930 (.30) 1.657) * * .26) .17) 1.96-5.10) 1.75-2.25-1.31-3.380-.11-3.740 (.585) * * .990-1.467 (.32) 3.35) 1.860) < LOD < LOD .96-3.930) 1.50 (1.450 (<LOD-.34) 2.80) 3.740 (.46-3.380-.970) .580-.400) .45-4.670) .77 (1.54 (2.50-2.830 (.30-3.30-3.89) 471 575 296 664 822 690 814 1122 919 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .690-1. respectively.41-5.50 (1.680-1.618) * . population from the National Health and Nutrition Examination Survey.800 (.840 (.592-.90) 3.592) * .949) .570 (.70-2.740-1.83 (2.13) 2.58 (1. 01-02.38) 1.83) .343 (.60) 3.880) < LOD 75th .1.74) 3.453 (.570) * . 0.20) 1.570-1.336-.05-2.59-6.80) 5.510 (<LOD-.97 (2.98) .457 (.29) 1.20-2.36-4.16) 2.700) .50 (1.73-5.600-.340-.690) .54-2.50-2.540 (.398-.950) 90th 1.70 (1.460-.549 (.740-.80 (2.89-6.960) .680-1. 124 Fourth National Report on Human Exposure to Environmental Chemicals .20 (2.86) 3.710 (.60-4.20-1.550 (.03) 1.01) .14 (1.94 (2.388-.65 (2.550 (.31) 2.880 (.59-2.98-3.69-4.10-1.17) 1.40 (1.05-3.587) * * .750-1.20 (1.22-8.00-2.50 (1.27 (2.16-3.449 (.390-.00 (1.80) 2.61 (1.390-.30) 2.83 (2.850) < LOD .87-3.17-4.95 (2.810) .40 (1.01-3.49) .720 (.57 (2.89) 1.70 (1.280-.45 (1.690 (.820 (. which may vary for some chemicals by year and by individual sample.500 (<LOD-.78) .880) < LOD .00) 2.S.930-1.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .15) 2.710 (.34) 2.88) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) 2.22-3.15) 2.570 (<LOD-.90) 2.32 (1.210 (<LOD-. < LOD means less than the limit of detection.63 (1.75 (2.04) .30) 4.359-.77-2.759) * . and 0.10) 3.30 (1.54) .960) .11-3.95) 2.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.08 (2.45 (1.31-3.47 (1.720-1.83) 1.560-.10) 1.46) 1.30 (.50) 1.910 (.201-.94) .01-1.23-3.380) .09 (.00-4.60) 2.600 (<LOD-.76-6.20) 2.584) .46 (1.20) 1.30-1. interval) Selected percentiles ( 95% confidence interval) Total * .780) .20 (1.510 (.73 (1.20 (1.78) Sample size 1949 2519 1905 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .592) * 50th .382-.73 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.26 (2.86 (1.750) 1.790 (.730) .760 (.780 (.590-.30 (.30) 4.570 (<LOD-.505 (.19-1.350-.22 (1.50 (1.20-3.98 (2.910) 1.45 (2.620-1.21) 3.710) .33-2.960 (.29-2.

180 (<LOD-.77-3.670 (.70 (3.136-.06-2.32 (.08) 1.92 (1.23) 2.10) 2.05-2.23) 1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.840) 1.800-1.880) 1.91 (1.38-3.81) 2.67 (1.940-1.04-1.460) .840) 1.350) .43) 2.08-2.75) 6.60) .850) 1.84 (2.380) . population from the National Health and Nutrition Examination Survey.950-2.320-.71) .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 * .20-7.79 (1.49-4.08 (.32-1.640 (.390-1.S.72-4.72 (2.447 (.870 (.710 (.08-2.47 (1.95) 1.02-6.69 (1.368) * .32) 5.97 (1.320-.13 (1.92-8.08-2.520 (.47 (1.52 (1.790 (.71) 2.55-3.460-1.08) 2.740) .32) 1.16) 1.930-1.99) 2.08-3.53) .11) 1.870) .730) .750 (.22) 1.700 (.710 (.830 (.90) 2.30) 3.44-2.05 (1.78) 3.84-6.52) 3.98) 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 * .72 (1.07-3.24) 4.55 (1.75 (2.270 (<LOD-.31-1.372 (.49 (1.990-1.75-3.02-3.73 (2.08-3.510 (.61-3.07) 1.393 (.560-.460 (.380-1.760) .88) .66) .820) .42) .760) < LOD 75th .590 (.06) 4.88 (1.76) 1.92) 3.330-.591 (.580-.412-.550-.57 (3.09) .07-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.08-3.39 (1.89-3.720-1.720 (.509 (.03-1.510-.910) < LOD .318-.64 (2.07) 1.485) * * .77-4.41 (.453 (.230 (<LOD-.550-.98) 1.448 (.270-.560-.330 (<LOD-.590) * 50th .45 (2.69 (3.377-.64 (2.38 (1.440-1.700 (.82) 2.39) 2.58 (1.75 (1.471-.470 (<LOD-.688) * .470) .17) 2.11-2.597) * .82 (2.42-6.820) 1.50 (1.530 (.590-1.47-4.08 (2.05-4.33) .22-3.67) .33 (1.61) 2.79) 1.57 (1.00 (3.580) .14 (2.00-1.97) 1.42 (.645) .63 (1.16-1.44) 2.310-.348-.57-2.980-1.66 (2.67-3.19 (1.920) .77 (3.04) 95th 2.630) * .790) .29-4.280 (<LOD-.23) 3.740) < LOD 1.444-.335-.30-2.490 (.480-1.640 (.60) 1.23 (.20) 1.300-.05) 1.11 (.390) .403) .58) 3.07 (.535 (.38 (2.310 (<LOD-.17-2.02-3.480) .739) * .253-.22-2.552 (.58-6.22) .380-.65) 2.34 (1.71 (1.700 (.310 (<LOD-.540-.23) 2.520-.270-.57-4.234 (.87 (2.05) < LOD .830) 90th 1.800) < LOD .580 (.04-5.22 (2.62 (2.43) 1.660-.60 (1.550) .510 (.22-3.72) Sample size 1949 2518 1903 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .08-3.22) 4.97) 2.97) 672 678 478 509 694 552 595 948 744 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Fourth National Report on Human Exposure to Environmental Chemicals 125 .560 (.32) 2.750 (.67 (1. interval) Selected percentiles ( 95% confidence interval) Total * .60 (2.742) * * .72) 1.03-2.400-1.70 (2.515) * * .300 (<LOD-.42-8.73-3.45 (1.07) 1.18-2.43) 2.80) 2.67) 1.97 (1.305 (.710 (.43 (1.640 (.25-3.50) 1.900) 1.28 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.370-.00-3.89 (1.20-2.61-3.690) < LOD < LOD .680 (.400) .99) 1.250 (<LOD-.250 (<LOD-.07) 5.36) 3.62 (1.500-.94) .285-.840) .550-1.61 (3.17) 2.16-2.

45) 2.3 (14.17-2.64-8.10-4.7-22.46-6.76 (2.6-27.40) 50th 2.9) 48.0) 28.0-49.52 (4.53) * 2.25-3.3 (23.41-4.0 (33.48-2.1-47.06 (1.71) 5.3) 28.0-53.98 (1.0) 18.5-40.0 (13.5) 69.0-52.74-2.50 (2.0 (26.23-2.6 (26.85) * 2.0 (17.60 (2.63-6.50-17.0) 3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.14) 5.0 (21.2) 16.92-5.30-14.70-6.00 (.80) < LOD 1.41) 5. see Data Analysis section) for Survey years 99-00.41) 1.90-8.95 (5.29-4.58) 16.0-41.5 (24.82 (1.7 (12.00 (.83 (3.10) .48) 5.10 (1.40) < LOD 2.1-25.18.70 (.4.0) 4.610 (<LOD-1.11) 2.1-40.9 (27.7) 47.21 (1.79-2.2 (19.0) 15.72 (1.6 (15.10 (1.2-26.6-54.2) 31.0 (6.5-20.50-2.S.0-41.76 (2.0-62.4-76.44) 3.79 (1.0) 13.1 (22.4) 19.04 (<LOD-2. 0.50-20.40) < LOD 1.0-31.77 (1.1) 95th 48.0-230) 35.0-53.99 (2.23) 9.78 (1.0-29.0-110) 42.78) 9.18) 14.0 (38.80) 1.70) 1.0 (38.8 (12.40-16.0) 3.0) 20.1 (10.10 (1.54 (3.0) 3.30 (.9 (19.00-24.8) 62.92) * 2.18) 6.0-69.4) 38.3 (10.18) 20.9) 18.1-20.87-7.70 (1.85 (1.36-2.530-4.86 (1.80-2.0 (24.0 (32.20-4.4 (19.70) 5.8 (12.0 (38.83-2.70 (7.0) 17.0) 20.10 (1.0) 15.6 (11.0) 3.0-50.59 (1.70 (1.8) 41.46-2.12 (3.0-110) 34.0) 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 2.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1 (11.9-21.0-62.43-7.19-2.0-58.50-5.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0 (38. respectively.0 (19.10) 39.30) 11.91 (4.470 (<LOD-1.0 (8.94 (1.04) 3.3 (24.8) 32.44) Selected percentiles ( 95% confidence interval) Total * 2.1) 38.0 (11.93-3.830-3.7 (28.27-6.1-19.44) 2.05) * 2.97) 6.86-3.02 (2.830-4.80) 90th 38.0 (37.3) 38.46 (.8 (26.29-9.0-41.2-47.13 (1.9 (23.79 (2.1) 140 (46.0 (20.2-33.5-74.58-2.57-2.8 (22.0 (38.1) 38.3) 31.0) 17.50-7.9) 38.64-3.5-45.48-2.80) .2-39.98) * 2.0-260) 34.0 (25.04-8.32 (2.1 (25.4 (15.20 (2.44-7.88) 3.05) 1.7) 20.9 (10.30) 4.0 (38.83-2.0) 33.3) 26.29) 2.05-3.33 (5.26) 75th 11.1) 18.59 (1.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.09 (4.5) 30.2-62.13) 12.41) 1.57-2.0) 4.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. 01-02.8-24.75-14.88) 1.8) 39.67 (1.0 (38.66-5.49-2.600-2.70) 1.6-22.70-17.41 (1.53) 1.40-4.35-6.90) 11.10-13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2 (12.21 (4.71-2.53) 40.8-21.61-2.0-58.6) 52.2-27.0) 28.69) 2.53 (1.12) 1.0-47.21 (3.16) 2. population from the National Health and Nutrition Examination Survey.0) 30.690-3.2-27.60) < LOD 1.5-27.4 (10. and 0.1 (25.80-18.0) 16.90 (1.0 (20. and 03-04 are 0.26 (.0) 32.0) 31.11 (4.06) * 2.0 (8.10 (7.96) 5.9-51.660-2.0) 19.7 (12.1 (26.0 (7.90 (1.4-22.1-46.3) 33.0-39.0-39.07-5.9 (19.23-2. < LOD means less than the limit of detection.71 (4.65 (4.20) 1.6-45.7-41.6 (9.3 (12.81-3.0 (40.0 (8.16) * 1.45) 2.54 (1.13 (1.0) 42.0-92.0) 8.2-80. which may vary for some chemicals by year and by individual sample.0-43.0) 16.42) 1.77) 38. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0) 4.81-2.61 (1.0) 45.3 (12.31-6.0) 5.83 (1.9) 17.19) 2.5. interval) 1.0) 6.

6 (11.54-15.46-6.14 (.20) Selected percentiles ( 95% confidence interval) Total * 1.59-2.0 (23.37-2.6-38.3 (10.40 (2.33) < LOD 1.2 (16.5 (13.16-2.7-20.5 (15.71-2.899-2.7 (10.23) 37.22-2.7) 66.6) 19.66) 8.2-70.7) 95th 51.80 (1.57) 4.86) * 3.26-4.22 (2.36 (4.99-4.00) 6.5-36.88 (4.1) 52.26-2.1) 17.12) 3.1) 25.7-38.7-43.2) 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 2.38) 5.15 (.41 (2.9 (26.67-3.4 (11.75 (1.0 (6.45-1.0) 47.8) 31.3 (9.0) 13.88 (1.07) 9.06) 1.0) 10.6) 11.5-97.2) 13.0) 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 1.22-3.62 (2.58-17.95 (2.79 (2.0 (19. Fourth National Report on Human Exposure to Environmental Chemicals 127 .94-20.43-12.3-42.3 (8.48 (4.2) 33.53) 1.11-2.40-7.0 (32.48) 1.36) 10.90 (. interval) 1.888-1.02) * 1.23-1.1) 13. population from the National Health and Nutrition Examination Survey.7) 15.750 (<LOD-1.3) 13.46-22.1) 36.60) 4.59-2.7) 34.91-2.9) 24.4-39.69-18.2) 13.5-43.17) 2.9 (39.47-17.9-52.63-5.0) 3.47 (3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.27) 10.70 (1.8) 23.7 (24.5) 27.33-5.75 (1.09 (5.27-3.6 (27.1 (39.2-47.50-5.8-43.7-19.00-16.8) 15.35) .1) 25.18-1.82 (2.1 (12.08) 1.08 (1.19) 5.07-2.2 (9.670-1.6) 23.2 (22.7) 30.7 (18.94) 1.79-17.40 (5.38-5.35) 1.33) 1.51) < LOD 1.0-70.51) .4) 12.3-19.06) 1.0 (23.4 (25.6-32.7) 23.11) < LOD 1.23) < LOD 2.9 (13.2) 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 1.03-2.44) 9.25-3.2) 4.38-1.860 (<LOD-1.7) 26.16 (1.06-1.19-6.0 (14.870-3.9-18.19-14.7-37.83) .30) 28.6 (24.45 (1.4 (9.88 (4.5 (8.9-37.4-71.5 (17.2-34.8-26.95-16.9-41.37 (1.4 (19.9) 54.0) 30.43) * 2.6 (7.4 (12.80-8.69-5.52 (1.02) 1.40-4.32-3.4) 3.95) 90th 32.S.5) 70.0-40.43-2.3 (20.6-51.8 (7.2-38.64 (1.2 (15.0-71.54-2.930 (<LOD-1.9) 24.0-118) 29.0 (39.7-47.1 (34.67 (1.890-4.9) 12.57 (6.0 (17.58-2.4) 14.28 (1.19 (1.1) 13.680-4.36-13.9) 3.88 (1.66 (1.72) 2.1) 15.3-22.68 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.16 (1.9 (10.1) 27.83 (.28) 1.1 (50.4) 12.0) 25.96) 2.5 (41.56 (2.9-36.2 (8.82) 1.1-63.17-3.20-5.60 (.47 (1.4-67.35 (2.62) 4.31) 2.18) 3.71) 8.7-109) 22.0 (25.27) 50th 2.5 (34.5 (6.9-95.66 (1.67-16.12 (1.6) 3.01 (.91 (6.9 (19.1) 27.9) 3.7) 61.19) 5.3 (10.61 (1.75-6.76-2.75) * 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.84-13.46-5.16 (1.1 (25.46) 1.6) 3.2 (21.96-16.7 (11.2) 41.52-4.22 (.5-190) 30.8-37.4 (21.9 (7.29-5.70-4.32 (3.34) * 1.2) 36.6) 7.00) 1.0) 48.50 (2.38 (3.4 (5.2-28.3-27.93) 5.67 (1.68) 47.8-34.02 (.55 (2.21 (4.8-45.56) 1.4 (25.6) 112 (40.6-49.1 (33.86) * 2.97 (1.00 (4.870-3.94) 19.1-22.95-16.06) 75th 9.870-3.24 (1.18) * 2.33) 2.61-2.1-60.07-2.61-22.8) 11.4-21.59-15.39 (1.3) 28.8) 3.4-34. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.27 (6.03) 1.8) 32.14-8.71 (1.7 (18.5 (15.

210 (.630 (.290) < LOD < LOD < LOD < LOD .620 (.190 (.390) < LOD < LOD .700-1.700) 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 .830 (.740) < LOD .380-.410) < LOD < LOD < LOD < LOD .610 (.870 (.120-.1.820 (.130-.270 (.840) .310-.720 (.40) .680-1.540) .450 (. respectively.570) .090 (<LOD-.130) .220 (<LOD-.770 (.090 (<LOD-.350) < LOD < LOD < LOD < LOD .13) .610 (.830) < LOD . population from the National Health and Nutrition Examination Survey.330-.170-.36) .05.470 (.140) .190 (.10 (.20) .00) .870 (.380-.990 (.540 (<LOD-.230-.1. and 0.084-.850) < LOD .150 (<LOD-.12 (.430 (.310) < LOD < LOD < LOD < LOD .730) .03) .130-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900 (.850 (.320-.760) < LOD . see Data Analysis section) for Survey years 99-00.650-1.440-1.640 (.099-.10) . 0.930 (.430-.140-.460 (.30) .080 (<LOD-.850 (. < LOD means less than the limit of detection.42) .700-1.310 (.130-.310) < LOD < LOD < LOD < LOD .830 (.240 (<LOD-.190 (.300-.370-.870 (.150) .100 (.540) .310 (.120 (<LOD-.360-.530-.720-1.260 (.680-1.650-1.410-.130 (. 01-02.32) .600 (.680) .560 (.640-1.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .090 (<LOD-.730-.S.171) * * .870) < LOD .140-.42) .320 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 * * * * * * * * * .090 (<LOD-.200) < LOD < LOD .290 (<LOD-.120-.990) .490 (.860) .160) .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.560 (.30) . which may vary for some chemicals by year and by individual sample.230) .380-.610-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.30) .10) .210 (. and 03-04 are 0.550) .370-.870 (.390 (.630 (.280) < LOD < LOD < LOD < LOD .160-.080 (<LOD-.660 (.990) .460-.10) .090 (<LOD-.290) < LOD < LOD < LOD < LOD 90th . 128 Fourth National Report on Human Exposure to Environmental Chemicals .770) < LOD 95th .700-1.160) .610-1.830) .60) 1.050-.110-.700-1.470-1.410-.180) .400-.870 (.940 (.640) .130) .650 (.450 (.420-.690-1.650) .360-.650) .58) .510-1.350) .450 (.140-.15) .780) < LOD 1.680 (.410-1.820 (.840) .220 (.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 * * * * * * .860-1.117 (.162) * * * * * .720) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .640) .300-1.090 (<LOD-.

410 (.360 (.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 .140-.380-.02) .070 (<LOD-.370 (<LOD-.02-1.340-.070 (<LOD-.860-2.62) 1.670 (.390-.500 (<LOD-.230 (<LOD-.380-.450 (.540) .080 (.740 (.150-.330-.057-.580 (.03 (.060-.650) < LOD .640-1.410) < LOD < LOD .03) .190-.730) .190 (.360-.730) .570 (.190 (.400 (<LOD-.300-.800-1.720 (.110) .140-.320 (<LOD-.270) < LOD < LOD < LOD < LOD .870) .520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .03 (.070 (<LOD-.29 (.120) .960) .110) .500-1.300 (.38) 1.440-1.860 (.600) .700) .S.290) < LOD < LOD < LOD < LOD 90th .990) .01 (.710-1.550 (.300-.730) .240-.380-.880-1.090 (<LOD-.410 (.860 (.560 (.78) .310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.470 (<LOD-.570-1.66) 1.050 (<LOD-.730 (.19 (.260-.24) .280) < LOD < LOD < LOD < LOD .200 (.36 (1.230) < LOD < LOD < LOD < LOD .380 (.140) .990) .570-.58) 1. Fourth National Report on Human Exposure to Environmental Chemicals 129 .140-.360-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .720 (.740) < LOD 1.220 (.940) .550 (.500) .080 (<LOD-.080) .116 (.090 (.510-.270 (.220) < LOD < LOD < LOD < LOD . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.490-1.520-.450) .140-.00) < LOD .230-.330-.60) .250-.100 (<LOD-.700-1.110) .360) < LOD < LOD < LOD < LOD .700 (.410-.330 (.850 (.170 (.86) .200 (.14) 1. population from the National Health and Nutrition Examination Survey.110-.580 (.410-.390-.170 (.084-.700 (.161) * * .580) .260) .410) .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 * * * * * * .540 (.67) .970) .330 (.610-1.460 (.86) .110) .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 * * * * * * * * * .111) * * * * * .210 (.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.440 (.890 (.670-1.03 (.09) .170) < LOD < LOD .12) < LOD .580-1.20) 1.650-1.750) < LOD 95th .940) .660-1.140-.400) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.780 (.310) < LOD < LOD < LOD < LOD .070 (<LOD-.120) .180-.760) .43) .670 (.330-.600-1.810 (.780) < LOD 1.880 (.580) < LOD .24 (.540 (.380-1.100-.

51 (2.10-3.10 (.90) .31) .03 (.870) < LOD < LOD .30 (1.840-3.53 (2.190-1.05 (2.63 (3.62-8.0) 4.67 (1.42) .0 (3.850) 16.07 (3.67 (2.13 (3.0) 4.20-4.07-3.10 (3. 130 Fourth National Report on Human Exposure to Environmental Chemicals .99 (1.90-20.87) 5.730 (.250 (<LOD-.0) 5.370-.800) 90th 13.6) 5. 01-02.36-3.97) 20.0 (5.0) 5.70-17.360-1.74) 5.900 (.49) 17.480-.0 (4.99) 11.10-9.88-3.640 (.380-.86) 4.61 (1.39) .63) 32.28-9.3) 952 1187 935 997 1331 995 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .0) 5.590 (.50) .080-1.0 (5.51-8.0 (13.00 (1.30-3.24-7.770 (<LOD-1.83) 2.770) 2.14) .11) 13.36-3.48 (2.0-40.0) 2.0 (4.40) 1.0) 3. respectively.330 (<LOD-1.01) 5.21-3.20-4.90 (1.510-.400-1.90-9.70-3.30 (1.49 (1.S.07) 1.0 (17.640 (.53) 20.99) 19.890 (.47 (3. see Data Analysis section) for Survey years 99-00.750-2.07 (1.05-3.30 (2.07-3.425-1.26 (2.170-1. which may vary for some chemicals by year and by individual sample.0) 4.62) 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 * * * * * * .87) 12.60) 1.740 (.960 (.76 (1.16) 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 .20-17.0-38.0 (7.10-3.0) 2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.59-5.20 (1.30) .0) 7.55-4.90) .1.74 (3.18) 1.29-10.0 (17.840 (.70) 2.0) 2.94 (1.38-3.42) 2.800) 17.20) < LOD < LOD < LOD < LOD < LOD 1.66) 4.110 (<LOD-.40-7.90) .610) < LOD < LOD < LOD < LOD < LOD 2.15) 19.53-7.23-6.0 (16.0) 2.35-10.0-44.40-8.68) 2.40) 2.1.90-28.15) 14.94-3.800-4.67) .620-1.83-3.610 (.70-50.35) 5.0-38.31-10.14) 2. < LOD means less than the limit of detection.55-8.20 (1.21) 3.96 (1.52 (1.720) 2.0) 5.690 (.00) 1. and 03-04 are 0.691 (.83-3.28) .40-20.32 (1.00-17.12-1.52) 5.48) 13.11 (1.30-6.11) .210-1.82-4.70-30.350-.600 (.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.33 (4.0 (17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30-7.0) 2.32-9.40 (1.00) .0-40.840 (<LOD-1.830 (.90 (2.880) 5.00) .260-.0 (5. population from the National Health and Nutrition Examination Survey.30) 95th 19.910) 2.35) 11.960 (<LOD-1.10 (3.0 (6.30 (.580 (.350-.07 (3.40 (1.00-17.80 (4.0 (5. 0.05 (3.0-38.94-8.0) 2.750-1. and 0.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.49 (1.46 (1.0 (5.08.43-4.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.28) 1.45 (2.0) 4.60) .39 (2.0 (17.97) 20.30 (1.90-37.37) .85-3.0) 2.00 (.70-7.40-4.0 (17.12) * * * * * * * * .65) 1.52 (1.50) 2.14-5.0-39.

10-3.56 (1.07 (2.890 (.860-2.5) 2.4) 2.71 (.330-1.23-7.270-.90-6.12-4.25-38.57) 8.22) 2.83-11.85-3.700) 6.340-.9) 5.77 (.21-3.69-7.18) 1.57) 1.710 (<LOD-1.06 (.430 (<LOD-.41) 18.1) 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 * * * * * * .53) .850-3.790) 11.64-4. Fourth National Report on Human Exposure to Environmental Chemicals 131 .8-33.18) 95th 21.73 (4.33-5.32-6.56) .85 (1.340-.44) .540-1.33 (1.65 (2.57 (.81-17.47-10.830-3.770) .80) 3.6) 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 * * * * * * * * * .29 (4.840-3.14-6.31-18.8) 4.3) 3.43) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.8) 2.660) < LOD < LOD .7) 5.7 (12.82-11.580 (.1 (5.67 (2.820) .650) 90th 10.40-2.370 (.40 (.470 (.0 (9.5) 2.1 (7.240-.67) 1.260-.5) 7.84) 9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.52 (.96-25.66-47.7 (6.7) 6.690-5.57-40.820 (.55) 21.1) 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.53) 27.1) 2.260-.51-44.430) 1.88 (.71 (2.S.18) * * * * * * * * .41 (4.8 (20.48-7.190-1. population from the National Health and Nutrition Examination Survey.5 (9.9 (11.11-5.02 (.22-27.8) 1.24) 3.11) .28-6.9) 6.7) 3.2-38.7) 4.02-4.36 (.50 (2.91) 2.2 (8.10) 2.50) .67-6.79 (.38 (2.4 (4.62-17.91-4.09-3.44-11.748 (.5 (11.340-.98 (4.88-3.50) 11.32) 9.450 (.80 (.00) .960 (.780-4.930) .35 (.580-1.88) 17.61) 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 .360 (.40) 1.33 (3.8) 2.00-19.790 (.8) 7.700) < LOD < LOD < LOD < LOD < LOD 1.01 (1.0 (4.14 (1.620-3.55) 21.25-9.89 (2.62 (1.39) 20.580) 1.48 (4.31-7.31) .3) 2.33-3.150 (<LOD-.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.940-4.86) .86 (3.17) 5.830 (.390-.740-1.37) 4.96) 2.370-1.540 (.25 (1.49-2.75) 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60 (1.56) 2.650 (.47-10.13 (2.47) .0) 4.270 (<LOD-.500 (.74 (2.17 (1.600 (<LOD-1.07-21.590) 2.83 (4.370) < LOD < LOD < LOD < LOD < LOD 1.340 (.30 (4.31) .5 (8.4-34.92 (2.88 (2.580) 16.47) 5.04 (1.250 (<LOD-.29-4.64) 30.12 (4.67) 2.02 (1.48-42.27 (2.33-4.310-.51-4.970-3.730-3.800-2.8) 7.40-12.320-1.5-40.560 (.474-1.10 (2.59 (1.04-16.670 (.69) 2.55 (3.45 (1.630-1.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.15) 9.96-8.05) .50 (4.08) .03) 2.02) .03) 16.97) .

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Urinary excretion of alkylphosphates in the general population (Italy). Fenske RA. Third National Report on Human Exposure to Environmental Chemicals. Ann NY Acad Sci 1997. Freshwater KJ. Kissel JC. Angerer J.37(3):382-395. J Expo Sci Environ Epidemiol 2006. 2005. Daniell W. Kedan G. J Toxicol Environ Health 1981.177:37-41. Richardson RJ. Garabrant DH. Griffith W.837:257-268. et al. Abdel-Azis M. Curl CL. Anger WK. The effect of the 14-day agricultural restricted entry interval on azinphosmethyl exposures in a group of apple thinners in Washington State. Leffingwell JT. Checkoway H.111(3):377382. Environ Res 1992. Sartorelli E. Barr DB. Curl CL. Davis SW. Schweitzer SJ. Gillham RA. Am J Ind Med 2006.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites References Albers JW. Duggan A. Charnley G. The effects of occupational exposure to chlorpyrifos on the neurologic examination of central nervous system function: a prospective cohort study. Aprea C. Bravo R. Kipen H. 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Visuthismajarn P. Gladstone EA. Burcar PJ.52(10):648-653. Effects of chronic. Rothlein J. U. and spatial learning in monkeys and rats. Phillips J.338(8761):223-227. Arch Environ Contam Toxicol 2000. Pesticide industry sales and usage . Arch Environ Health 1975. Hansen S. Levy LS.12(2):134-141. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. van der Hoek W. 1993 [online]. Lu C. Environ Health Perspect 2006. Muniz J. Ruberu DK.26(2):199-209.345(8958):11351139. Schenker M.24(1):18-29. Savage EP. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Arch Environ Health 1988. 2004. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Masala G. Heaton RK. Rosenstock L. Neurotoxicity among pesticide applicators exposed to organophosphates. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Pilkington A.20(2):115-22. Stokes L. May. Bravo R. Johnson C. Salvini S. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Stark A.114(5):691-696. London L. Steenland K. 1/12/09 Peiris-John RJ. Bull Environ Contam Toxicol 1994. Nell V. et al. Dinoff TM. Lasarev M. Rodnitzky RL. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Rohlman D. Lasarev M. O’Malley M. Tumino R.43(1):38-45. Environ Health Perspect 2005. Chrislip D. Beach J. Occup Environ Med 1995. Occup Environ Med 2001.332(1-3):71-80. Narang A. Spurgeon A. S. Scand J Work Environ Health 1998.84(5):731-736. Russo J. Pedersen L. The Pesticide Health Effects Study Group. Berry H. Takamiya K. Neurotoxicology 2005. et al. Neurotoxicol Teratol 1998. Aprea C. Rothlein J. et al. Sci Total Environ 2004. Petchuay C. Eskenazi B. Terry AV Jr.epa.38(4):546-563. Lewis JA. A behavioral evaluation of pest control workers with short-term. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Buccafusco JJ. Frasca G.30(2):98-103.2000 and 2001 market estimates. Scherer J.S. Available at URL: http://books. Jenkins B. low-level exposure to the organophosphate diazinon. Pesticides in the Diets of Infants and Children. Lancet 1995.68(3):209-227 Maizlish N. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Buchanan D. Claypoole K. et al. McCauley L. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Gillham R. Lancet. Weerasekera G. Bradman A. Marshall E. J Toxicol Environ Health A 2005. et al. 1991.php?record_id=2126&page=1. Muniz J. National Research Council (NRC). Vitayavirasak B. Ames RG.S. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Environmental Protection Agency (U. Chronic neurological sequelae to organophosphate pesticide poisoning. Lambert WE.edu/ openbook. Weisskopf C. McConnell R. and cholinesterase status of date dusters and harvesters in California. low-level organophosphate exposure on delayed recall. Am J Public Health 1994. Int J Occup Environ Health 2006. Keifer M. EPA. Thompson ML. Samuels S. National Academy of Sciences. Robson MG. Barr DB.pdf.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Keefe TJ. Stephens R. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Kidd M. Santana J.12(2):153-172. Jamal GA. Hore P. Washington (DC). Malathion deposition. Wickremasinghe AR. Office of Prevention Pesticides and Toxic Substances. Mounce LM. Smit LA. Irish RM. Am J Ind Med 1987. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. vibration sense and tremor among South African farm workers. Saieva C. EPA).52(2):190-195. 4/7/09 Young JG. Caltabiano LM.nap. metabolite clearance. Prendergast MA. Calvert IA. Seiber J. Daniell WE. Washington (DC): U. Effects of long-term organophosphate exposures on neurological symptoms. J Occup Environ Med 2002. Available at URL: http://www.44(4):352-357. 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.113(4):504-508. Myers JE.58(11):702710. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. discrimination.

In addition to reflecting exposure to the parent insecticide. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report.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.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. For example. malathion is metabolized to malathion dicarboxylic acid. the level may reflect exposure to the environmental degradation products of these pesticides. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. parathion and methyl parathion are metabolized to para-nitrophenol.5. For general information about the organophosphorus class of insecticides. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides.

0) 14.96) 3.30-5.90-8.0) 12.22 (1.97-7.61 (1.0 (13.S.50 (2.20-4.00) 2.20-3.78 (7.000 pounds are used per year.90) 3.43-2.0) 11.0) 8.0-28.4-15.9) 11.47 (4.25) 3.8-15.57 (2.40 (5.88 (1.0 (7.10 (1. Survey Geometric mean (95% conf.1-16.47-9.47-13.36 (4. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al. 2921-88-2 Chlorpyrifos-methyl CAS No.67 (1.34) 1.90-7.S.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70) 1.51 (1.43-2.60 (5.50-8.4 (8.13-3.68-2.03) 99-00 01-02 99-00 01-02 99-00 01-02 2. Chlorpyrifos is Urinary 3.40-26. Chlorpyrifos is degraded in agricultural soils with a half-life of several months. and on plants for days to several weeks. 2005). Approximately 21-24 million pounds per year were used domestically from 1987-1998.72-4. Approximately 80.19-3.20-16.80 (1.5.30-1.70-15.8) 10. and sprayed to kill mosquitoes.67 (2. It also has been applied directly on animals to kill mites.50 (1.80 (7. For instance.70-5.04-10. The general population may be exposed to chlorpyrifos via oral. dermal.17 (1.and post-construction structural applications for termite control were to be phased out by 2005 (U.1) 5. but can be detected in streams receiving runoff from application sites.30) 4.97) 2.90) 7. Exposure can also result from contact with contaminated surfaces.70 (1.79-2.0) 12.60-3.80) 4.80) 2.00-24.40 (5.81-2.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.13 (1.0) 8.37 (4.0) 12.60) 5. USGS. chlorpyrifos was no longer registered for indoor residential uses in the United States. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.98-15.31-2.87-6.4 (10.66-15.27 (7.22) 2.9) 697 660 521 701 602 947 Limit of detection (LOD.71 (6.40-2.86) 4.4 and 0.9 (7. It has low leachability.00-8.0) 10.0) 10. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.30 (2.09 (3. Fourth National Report on Human Exposure to Environmental Chemicals 135 .7) 13.90 (6.47-11.60 (2.70-17.64) 3.02 (1.30-12.76 (1.50-2. After 2001.50-4.8) 9. applied to structures to kill termites.20-11.02 (7.77-15.30 (4.72) 2.74-9.0 (7.53 (1.3 (8.29) 90th 7.40) 2. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.92 (1.5.7) 8.80-8.3) 8.74 (1.10) 6.90-2..70 (1. staying bound to soil particles.19 (1.71 (1.28) 2.51) 1.63 (1.77-6.60 (4. pre.4 (9.95) 7.50 (1.97) 4.20-2.20-14. 2002). and dust.63 (2.44-2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.3 (11.5) 7.04-10. and is infrequently detected in ground water (IPCS.55-5.35) 1.97) 7.0) 6.66-4. 5598-13-0 General Information The chemical 3.15 (1. although some tolerances for specific food crops have been reduced in the past to avoid exceeding recommended intake limits for total dietary intake in special groups (U.35) 2.44-5.30) 5.61) 75th 3.61-7.77 (1.80) 12.31-2. 1999. 2007).70-16.0) 12.20 (4.37) 5.0) 18. population from the National Health and Nutrition Examination Survey.40-10.30 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.09 (2.7-23.30-11.05-5.59) 2.70-11.52-12.5-24.0) 7.60-3.50-4.5 (8.90 (3.40 (6.50-5.46-2.80-10.99-4. air.83) 1.40) 9.38 (3.0 (10.0 (7.90-4.10 (5.77) 1.S.01) 1.05) 1.32) 2.71 (2. 2002).97) 2.91) 16.95 (4.0) 9.20) 4.47) 1.02) 1.21) 3.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.EPA.4.30-9.50 (2.9 (10.89-2.0) 12.0) 10.0) 15.0 (7.10 (4.28-3.60-2.0 (9.10 (3.44 (3.62-2.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.30-2.37 (1.32-1.67 (2.60-4.51-2.50 (2.25) 1.26) 7.84) 1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.10) 2.16) 2.50-14.EPA.45 (1.39-2.0 (7.59-2. interval) 1.76 (1.20) 2.00) 3.20 (2.9 (9.94 (4.3 (10.29-1.24-1.9-18.00) 1.91 (1.39) 4.90 (2.90 (1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.7) 9.20) 2.90 (1. and inhalation routes.80) 1.24-3.20) 10.63 (8.68 (7.2 (10.40-13. in 142 urban homes and preschools in North Carolina. Estimated intakes from diet and water have not exceeded recommended intake limits.6) 7.10-17.89 (2.52-2.50-2.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.03) 1.30) 4.

3) 8. Roy et al.91) 2. weakness.6) 10.97 (3.48 (1.0) 12.30-4.24) 5.53-5.11 (2.22-6.17-4.28) 2.05) 3.42-2. 2002).91 (4.82 (3..38) 3.1-38.76 (3.3) 8..23) 14.82) 8.25-11.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.86 (1.3) 9. Slotkin et al.27-7.33 (.12-1.81) 2.24 (1.2 (7.43-10.93) 2. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.22 (4.65-11.59) 3. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies..59-2.85-4.74) 1.16) 6.43 (4.89) 4.39-1.47 (5.28) 2.83-2.57-2.94-12. Howard et al..84-6.19-1.63-2.45 (1.83) 1.2) 6.71 (1. 2006.31-1.31) 1.01) 1.22 (6.00 (7.19) 3.58 (4.30-1.75 (1.81 (3.62) 1.49-2.21-1.64 (1. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.86 (1.20-1.01) 99-00 01-02 99-00 01-02 99-00 01-02 3. Survey Geometric mean (95% conf.62-7..4) 4.09-1.09-3.72) 1.15 (4. In pesticide applicators.80) 3.S.39 (2.86 (3.95 (3.44 (1.56-2.63 (4.72) 2.33 (5.31-4.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .92 (1.25-1.60 (1.44-6.76 (2.44 (5.88-10.82-4.09-2.93 (2.29 (3.48 (2.05-4. cholinergic effects.00-8. 2000).33) 2.17-4.14-8. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.57) 9. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al. Thus.68) 1.47 (1.37 (1. Urinary 3.42 (5.94-14.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.940-1.19-2.58 (1.19) 6.77) 1.91) 10.05-8. The metabolite TCPy does not inhibit acetylcholinesterase enzymes. 2005.23-1. 2006a.62) 90th 5. and other metabolites.S.91-13.06-4.11) 7.56 (4. neurotransmission.88-8.09 (1.24-1.97) 3.80-4. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.12-3. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).90-9.75) 6.35-1. and seizures.51 (1. 1984). and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al. and producing acute symptoms such as nausea. 2005.46 (1.56) 2.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.73 (1.8) 9.97) 3.85) 1. 2005.26-14.97-3.07) 5. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.EPA. TCPy can also occur in the environment from the breakdown of the parent compounds.55) 1.93 (1.0) 6.53 (2.71) 3.33 (1.24-4.05-1.85 (2.35) 1.1-21.92) 3.66 (1.65-15.5) 5.57-2.02 (5.. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.47-2.6) 9.92-2. Once absorbed.16 (4.52 (5.46 (2.1 (10.98 (6.56) 5.99-8.00) 1.02) 7.91 (3..70-4.44 (1.91) 1.3 (7.7) 7.88 (1.78 (1.47 (1.22) 1.40) 1.95 (1.42 (6.44 (5.93) 5.07) 1.80-6.32) 1. resulting in excess acetylcholine at nerve terminals.88-8.3) 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 1.69 (1.58 (1.49-2.85) 4. Metabolic hydrolysis leads to the formation of TCPy. paralysis.24) 75th 2. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.08) 6.45-1.54) 5.58) 5.44 (6.49 (1.1 (7.58-5.60-3.01) 3.55 (1.21-6.14) 1.24-24.39) 6.24-5.06 (1.0) 16.0) 10.64-2.79-13.68) 6.57) 2.64-7.66-11.82 (2.87-3. Betancourt et al. Ricceri et al.80-11. 2006b).41 (1..85 (3.55 (4.03) 1. vomiting.88-9.54 (2.27-1.06 (5.36) 1.91) 1. population from the National Health and Nutrition Examination Survey.97 (2.83-11.98 (7.20 (2. TCPy is more persistent in the environment than chlorpyrifos itself (U.34-1.6-Trichloro-2-pyridinol (creatinine corrected) Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.49-2.25-12.56 (1.33-7.88) 6.5 (6.91-4. interval) 1.12) 1.39 (4.63 (5. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.11-9.11 (2.88 (1.58) 1. 2006. Based on animal data and human cholinesterase monitoring during occupational exposure.9 (12.72-2.66) 1.5.93 (4..99) 1.96) 3. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 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.05-3.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.35) 2.01) 3.00-13.50 (4.

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

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Interim registration eligibility decision for chlorpyrifos.15(3):271-281. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures.108(4):293-300. Tate CA. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Freshour NL. et al. Barr D. Striley C. Toxicol Appl Pharmacol 1984. Acquavella JF.10(4):327-340. Toxicol Appl Pharmacol 2005. Bennett DH. Herrick RF. Kinney P. Brain Res Dev Brain Res 2005. 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. Harley K. Toxicol Sci 2006.9(5):494-501. 2921-882.6-trichloro-2-pyridinol. Chlorpyrifos: pharmacokinetics in human volunteers. Ann Occup Hyg 2007. Executive summary of safety and toxicity information. Bucelli R. Eskenazi B.S. Environ Health Perspect 2005. 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J Expo Anal Environ Epidemiol 1999. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Zhang J. Ricceri L. Chlorpyrifos. Meeker JD. Ozkaynak H. J Expo Anal Environ Epidemiol 2005. A longitudinal investigation of selected pesticide metabolites in urine. et al.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Edwards RD.htm. Seidler FJ.114(2):260-263. MacIntosh DL. Pesticide residues in urine of adults living in the United States: reference range concentrations. Mandel JS. Available at URL: http://ntp.inchem. Yang D. Levin ED. Bravo R.114(5):746-751. Environ Health Perspect 2004. Lu C. Seidler FJ.6-trichloro 2-pyridinol in their everyday environments. Hore P. gov/ntpweb/index. chlorpyrifos. 1992. Curwin BD. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . 1999.73:8-15.113(2):211-219. et al.5.207(2):112-124. Sheldon LS. Shealy DB. et al. Scand J Work Environ Health 2005.nih. Environ Health Perspect 2003. Tsai WY. Environ Res 1995. Environmental Protection Agency (U. International Programme on Chemical Safety-INCHEM (IPCS). Bravo R. Lioy PJ. Hill RH Jr.

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

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

200 (<LOD-. Survey Geometric mean (95% conf.210) < LOD < LOD 567 815 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1312 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0. population from the National Health and Nutrition Examination Survey.380 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2. 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 . Fourth National Report on Human Exposure to Environmental Chemicals 141 .670 (<LOD-1. < LOD means less than the limit of detection. Survey Geometric mean (95% conf. 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 . Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.270) < LOD 659 701 920 Limit of detection (LOD.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. * 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. which may vary for some chemicals by year and by individual sample.

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

USGS. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. 2004).2 and 0.49 (<LOD-2. Most granular formulations. population from the National Health and Nutrition Examination Survey. aerial. < LOD means less than the limit of detection. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. 1998). see Data Analysis section) for Survey years 99-00 and 01-02 are 7. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. 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. It is also used for cattle ear tag applications to control flies and ticks and. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Estimated intakes from diet and water do not exceed recommended intake limits (U. an organophosphorus insecticide that is used to control insects on nuts. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). Once absorbed. and particularly when it was ingested in granular form. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. in the past.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. fruits. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. Survey Geometric mean (95% conf. but these uses have been phased out. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. in some pest strips. Before these restrictions. diazinon cannot be sold for residential use. Prior to 2000. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. which may vary for some chemicals by year and by individual sample. 2004). since 2004. vegetable.EPA. 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. and other metabolites. Inhalational and dermal routes of exposure can be significant for pesticide applicators. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. 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.45 (<LOD-3. and forage crops. diazinon produced wild bird kills before use restrictions were in place.S.11) < LOD < LOD < LOD < LOD 454 580 632 829 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. It is toxic to birds. seed and foliar applications are planned to be phased out (U. Fourth National Report on Human Exposure to Environmental Chemicals 143 .S.EPA. 2007). Diazinon is not well-absorbed through the skin. 1998.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. diazinon was widely used in residential and garden application. but is rapidly absorbed orally (IPCS.7.

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

2006). Redmon JB. Geological Survey (USGS). Oloffs PC. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Interim reregistration eligibility decision (IRED. Jones K. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses.. 2007 [online].. Available at URL: http://www. Seifert J. Olsson AO.usgs. Drobnis EZ. Atlanta (GA). Diazinon. U. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Barr DB. Available at URL: http://www. revised February 15. Environmental Health Criteria 198. 1/14/09 U. Biochem Pharmacol 1992. In 23 children. In 54 Canadian greenhouse workers.9(2):117-131.gov/circ/2005/1291/. Swan SH. Effect of sublethal levels of diazinon: histopathology of liver. Oloffs PC. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Toepel K.44(11):2243-2250.10(6 Pt 2):789-798. Carrier G. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Baker SE. Garfitt SJ. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Fenske RA. Needham LL. Diazinon. Drug Chem Toxicol 1986. Bull Environ Contam Toxicol 1986. Available at URL: http://pubs.50(5):505-515. Swan et al. Mason HJ. EPA 738-R-04-006. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Kruse RL. Driskell WJ. Cocker J. Banister EW. 1992-2001. Pesticides in the Nation’s Streams and Ground Water. 4/7/09 Lu C. Beeson MD.114(2):260-263. Dumas P. Irish R. 1998. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers.htm. In a small number of men visiting fertility clinics in Missouri and Minnesota.134(1-3):105-113. J Expo Anal Environ Epidemiol 2000. Toxicol Lett 2002.S.epa. Liu F. 2005. Barr DB. Bouchard M. Banister E. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Bravo R. 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. References Anthony J. 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.S. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. May 2004. Environ Health Perspect 2006. Semen quality in relation to biomarkers of pesticide exposure.S. Barr DB.376(6):808-815. Study for Future Families Research Group. Third National Report on Human Exposure to Environmental Chemicals.org/documents/ehc/ehc/ehc198. Noisel N. Brunet RC. Environmental Protection Agency (U. et al.inchem. EPA). 2006).pdf. Pewnim T. Ann Occup Hyg 2006. Barr DB.Organophosphorus Insecticides: Specific Metabolites 2005).gov/ oppsrrd1/REDs/diazinon_ired. Rajendra W. Environ Health Perspect 2003. The Quality of Our Nation’s Waters. Centers for Disease Control and Prevention (CDC). Nguyen JV.111(12):1478-1484. Sadowski MA. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.37(4):501-507. International Programme on Chemical Safety-INCHEM (IPCS). March 2006. Anal Bioanal Chem 2003.

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1990). 2002. 1999).Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. 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. Malathion itself has not been considered genotoxic (U. 2003).e. environmental levels) and health effects is available from ATSDR at: http://www. Pluth et al. Flessel et al. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid.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. IARC considers malathion not classifiable as a human carcinogen..S.. 2005). 2006). 2000). 30% had detectable levels of malathion dicarboxylic acid at a detection limit about tenfold lower than the detection limit in the NHANES 1999-2000 analyses (Eskenazi et al.epa. CDC. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC..EPA.5 and 5. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. Human studies of single oral doses between 0. 2005.gov/pesticides/.. 2006). 2006).74 (<LOD-5. Thomas et al. and it is not considered an animal teratogen or a reproductive toxicant. 1999. A study of 13 children from an agricultural region of Washington State reported median levels that were below the detection limit in the NHANES 1999-2000 subsample (Kissel et al. Of 382 pregnant women living in an agricultural community. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. 2001. 2004).S. Lu et al. but cholinesterase activity was not affected. 1987..html and from U. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al.. 1993.. 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.EPA.S. Urinary Malathion dicarboxylic acid (creatinine corrected) Metabolite of Malathion Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. 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..S. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. but isomalathion. Survey Geometric mean (95% conf..gov/toxpro2. 1996. Finding a measurable amount of malathion dicarboxylic 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 147 . 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. representative subsample from NHANES 19992000 (Adgate.atsdr. Toxicity from unprotected bystander exposure during applications is rare (U.cdc. Giri et al. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. Additional information about external exposure (i. EPA at: http://www. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. population from the National Health and Nutrition Examination Survey. 2005).0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS..S.

Mutat Res 2002.114(2):260-263.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Environ Health Perspect 2004. Lioy PJ. Trzeciak A. Eberly LE. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Available at URL: http://www. Bradman A. Hammerstrom KA. et al. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Available at URL: http://www. Barr DB. Jaloszynski P. 2007 [online]. Clayton CA. Swan SH. Nicklas JA. Curl CL.usgs. Pluth JM. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Krieger RI. Atlanta (GA). O’Neill JP. J Expo Anal Environ Epidemiol 1999. Giri A. The Quality of Our Nation’s Waters. Pesticides in the Nation’s Streams and Ground Water. Quintana PJ. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . et al.gov/oppsrrd1/REDs/ malathion_red. Irish R. Bouchard M.S. Albertini RJ. Barr DB.gov/circ/2005/1291/. Prasad SB.112(10):1116-1124. Harley K. July 2006. Sharma GD. Malathion deposition.inchem. Dumoulin MJ. Lu C. 4/7/09 Kissel JC.77:1009-1010. Brunet RC. 6/1/09 U.73(1):182-94. EPA). Weltzien E.S.132(4):794-795. Carrier G. Fenske RA. Gosselin NH. Szyfter K. Petitti D. Samuel O.514(1-2):223231. Neutra R. Mutat Res 1999. Lu C. Hertz-Picciotto I. EPA 738-R06-030.pdf. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Barr DB. Goldhaber M. A longitudinal investigation of selected pesticide metabolites in urine. Malathion (addendum). Erratum in: Toxicol Sci 2003 Aug. Centers for Disease Control and Prevention (CDC). Ryan PB. Harris JA.9(5):494-501. Environmental Protection Agency (U. Cancer Res 1996. Hooper K. Rappaport E. Bravo R. htm.22(1):7-17. revised February 15. Third National Report on Human Exposure to Environmental Chemicals. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Genetic toxicity of malathion: a review. and cholinesterase status of date dusters and harvesters in California. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Am J Public Health 1987. MacIntosh DL. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Reregistration eligibility decision (RED) Malathion. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Environ Mol Mutagen 1993.15(2):164-171.445(2):275-283. Toepel K. Environ Health Perspect 2006.74(2):following table of contents. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers.epa. Dinoff TM. Giri S.38(4):546-553. 2005. International Programme on Chemical Safety-INCHEM (IPCS). Blasiak J. Am J Epidemiol 1990. et al. Jewell NP. Flessel P.56(10):2393-2399. 1992-2001. Arch Environ Contam Toxicol 2000. U. Needham LL. Toxicol Sci 2003 May. Barr DB. Reproductive outcome in women exposed to malathion. Grether JK. J Expo Anal Environ Epidemiol 2005. Griffith W. Kedan G. Geological Survey (USGS). Thomas D. Freeman NC. March 2006. Eskenazi B. Available at URL: http://pubs.109(6):583-590. Environ Health Perspect 2001. metabolite clearance.org/documents/jmpr/jmpmono/v2003pr06.S.

70 (2.00 (2.46 (3.27) 2.44) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. pulmonary.20-5.S.32-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.09-1.12) < LOD < LOD 1. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.0) 3.58) 3. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. 2003).30 (1.10 (3.61) < LOD 1.90-11.92-2.90-9.0) 3. In the 1990s.20 (<LOD-2.70 (2.50) 3..50 (1.0) 3.00 (2.69 (2.1.33) 2.57-4. and eliminated rapidly from the body after absorption (Kramer et al.20 (2.37-4.71 (3. on cereal grains.45) 5. Both are toxic to birds.01) 695 660 518 679 603 941 Limit of detection (LOD.74) 5.70-6.60 (4.10-11. Methyl parathion is not registered for residential use in the United States.01) 4.60-5.26 (1.71 (2.18-3.21 (2.S.910) < LOD .50 (1.EPA.770 (.40) 2.32-3.62 (1. Methyl Parathion. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. but by 2003.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.70) 2.21-1. Methyl parathion has low water solubility.37-4.50) 3. 2000).8 and 0.28 (1.10 (<LOD-6.05) 4.70) 2.850) < LOD .910) < LOD < LOD < LOD 1.00) 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 1.40) 1.80 (1. peak domestic use was as high as 5-6 million pounds per year.49 (1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80 (2.700 (<LOD-..32 (1.40 (1. Morgan et al. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.00) 3.91-3. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.40-4.67 (1.50) 2. Given its limited use.80) 2.85 (2.15-3.790 (<LOD-.0 (3.70-3.92) 5.70) 2. Fourth National Report on Human Exposure to Environmental Chemicals 149 .70 (<LOD-3.30-5. first registered in 1948.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Ethyl parathion.70-3.0) 4.60-36. binds tightly to soils resulting in low leachability.28 (1.30 (2. methyl parathion was rapidly absorbed after ingestion.40) 4.11) 2.S.50-9.02-6.910) < LOD < LOD . Once absorbed.860 (<LOD-1.79) 4.70-6. Increased risk of exposure via dermal.28-4. population from the National Health and Nutrition Examination Survey.70 (3.50 (2.. and to a lesser extent.22-3.0) 3. and oral routes can occur in pesticide and agricultural workers (Muttray et al.30-16.57) 1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.50 (1. 2007).20) 5.300-.EPA.50-14.70 (2. and aquatic invertebrates.10) 4.940 (<LOD-2.298-00-0 Ethyl Parathion CAS No.40-3.90 (1.40-4.60-19.730 (<LOD-. with limited applications in agriculture. 1977).37-2.01-4.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .61) < LOD 1. 2002.10) 22.60) 1.37) 2. Estimated intakes from diet and drinking water have been below recommended limits. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.34 (3.50 (2.10-1.45 (1.70-6. was once a restricted-use insecticide with limited applications on certain agricultural crops. all registered uses were voluntarily cancelled (U.30-3.19 (.47) 2. < LOD means less than the limit of detection.36-1.33 (1. fish.0) 3. Methyl parathion use is highly restricted.80 (2.0) 2. more slowly absorbed through the skin. 2006).69) 4.72 (3.13-1.10 (3. Survey Geometric mean (95% conf.32-1.50) 1.67) < LOD 1. and of the chemical nitrobenzene.66 (2. It had been applied to cotton. Many previous registered agricultural uses of methyl parathion have been cancelled (U.50 (1. In animal studies.60-24. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.48) 90th 2. and has a short half-life in soils and on plants.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .41-4.89 (2.11-4. which may vary for some chemicals by year and by individual sample. ethyl parathion.16) < LOD 1.990-1.

the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. Orsorio et al. Zurich et al. In addition to being a metabolite of methyl and ethyl parathion.870) < LOD .3) 2..13) 4. weakness.680 (<LOD-1..31) < LOD .930 (. 1978.html and from U.720-1.77-7. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.55 (<LOD-3.980 (.60-2.10 (1.540) < LOD .96 (1.44-3.89 (2.33-3.57-2.20) 3.07 (1. 2005. Methyl parathion is not considered genotoxic.84) 3.30) 3.78-2.970 (.09) 2. teratogenic. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.690-1.S.25) 1.15) 3.86 (2.310-.91) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.78-2.00) 2.440 (<LOD-. environmental levels) and health effects is available from ATSDR at: http://www.78) 2.89 (2.2) 2.94-4.S. Jaga and Dharmani.430 (.20 (3.82) < LOD . Slotkin et al. 2006. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.39) 1.33-3.25 (2.71) 1.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. In large doses.atsdr.00 (1. 1995).79 (1.67-2.00 (1.59 (1.96 (1. does not inhibit acetylcholinesterase enzymes.11-4.01 (2.01 (.7) 3.97-10. At high animal doses of methyl parathion. but lists ethyl parathion as a possible human carcinogen.48-4.44-3. and producing acute symptoms such as nausea.95) 1. vomiting. 2004).400 (<LOD-. ethyl parathion.88 (1.98-7.37-1. paranitrophenol.83 (1.840 (.88) 1.. gov/pesticides/.15-10....17-4. 1995. 150 Fourth National Report on Human Exposure to Environmental Chemicals . WHO..29) 1.79) 1.970 (.23) 1.80 (1.55) 2.41-2.60) 2.940 (<LOD-1. 1990.82 (2.930 (.56-2.530) < LOD < LOD < LOD . Lores et al.S.35-3.800-1. Additional information about external exposure (i.950) < LOD .39 (1. 2006.11) 1.640) < LOD < LOD 1. paralysis. and other metabolites. gov/toxpro2.97 (<LOD-4.29 (2.93 (2.67 (3. methyl parathion. The metabolite.01-3. EPA at: http://www.08-3..1) 2. 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.29) 2.2) 2.92 (2.35-3.57-7.80 (1.76-14. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.60 (1.94-47.97 (2.20) . cholinergic effects. U.26) 17.500) < LOD < LOD .87 (1.26 (1. Methyl Parathion. Karanth and Pope et al.04) 1. Parathion and methyl parathion have high acute toxicity in animal testing.830-1.72-2.850-1. and unintentional acute or chronic high-level occupational exposure (Hill et al.EPA considers methyl parathion unlikely to be carcinogenic to humans.cdc.10) 90th 2.73 (1.Organophosphorus Insecticides: Specific Metabolites Metabolites”). Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.61) 4. resulting in excess acetylcholine at nerve terminals. population from the National Health and Nutrition Examination Survey.370 (<LOD-.790-1.21-21.04 (2. 2004).78 (2.71 (1.08 (1.880 (.91 (1.90 (1.9) 1.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .38-3. 2003. Thus. 1991).13-12.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .4 (3. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.05) 4.31-3.43) 4. and seizures.e. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.epa.21) 1.14-3.730-1.720 (<LOD-.23) size 1989 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th .70) 3. Survey Geometric mean (95% conf. accidental exposure.16-4.57) 6.790-.33-6. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.08) < LOD .17) .30-1.07) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Laboratory investigation of a poisoning epidemic in Sierra Leone.110 Suppl 6:1085-1091. Needham LL. Giordano G. 2004).. Bailey SL.9:311-320.215(3):182-190.S.. 2005.15(2):164-171. Pharmacokinetics of methyl parathion: a comparison following single intravenous. International Programme on Chemical Safety-INCHEM (IPCS).110 Suppl 6:1075-1078. Head SL. Cline RE. ACGIH recommends a BEI of 0. Parathion-Methyl (addendum).112(10):1116-1124. In a study of workers who handle parathion. Lin LI. Atlanta (GA). Environ Health Perspect 2002. oral or dermal administration. Hetzler HL. Gregg M. Head SL. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al.. Harley K. Pathak S. Baker S. Griffith W. Moomey CM. J Expo Anal Environ Epidemiol 2005. population (Olsson et al. et al. 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. McClure PC. general population (CDC. Baker RC. Clark JM.71:99108. Turner WE. 2002. et al. 1995).S. et al. Hill RH Jr. Environ Health Perspect 2002. and levels were similar or slightly lower that those in a small convenience sample of the U.. Hryhorczuk DO. Alley CC.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Toxicology 2005. McCann KG. 2005. Karanth S. Arch Environ Health 1978. Leng G. Ashley DL. 1995.. Occup Environ Med 1999. Lu C.htm. a range of values several hundred times higher than levels found in the U. 2002). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http:// www. Guizzetti M. Dharmani C. Kissel JC. 4/7/09 Jaga K.21(1):5767.33(5):270-276. and many residents were symptomatic (Barr et al. Baker SE. Bradman A. Kramer RE.56(7):449553. Curl CL. Neurotoxicol Teratol 2003.25(5):599-606. 2002. Barr DB. J Biomed Sci 2002. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Chicago area methyl parathion response. Third National Report on Human Exposure to Environmental Chemicals. Hill et al. J Anal Toxicol 1990. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Centers for Disease Control and Prevention (CDC).. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects.6(2-3):159-173. CDC. Hill RH Jr. 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. Arch Environ Contam Toxicol 1977. References Barr DB. Biomonitoring studies of para-nitrophenol can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of parathion than are found in the general population. Lores EM. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. 1999). Fourth National Report on Human Exposure to Environmental Chemicals 151 . Jewell NP. Barr DB.14(4):213-216. Role of individual susceptibility in risk assessment of pesticides. Rubin et al. Costa LG. Eskenazi B. et al.org/documents/jmpr/jmpmono/v95pr14. Children and adults living in residences where methyl parathion was applied indoors had urinary levels of para-nitrophenol which were several hundred times higher than those in the NHANES 19992000 subsample. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Lewalter J. Environ Res 1995. Weltzien E. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Runkle KD. Bradway DE.5 mg (500 µg)/g creatinine for workers at the end of shift. Methyl parathion: an organophosphate insecticide not quite forgotten. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Barr JR. McCann et al. 2005. Slach EF. Rockhold RW. DiPietro E. Rev Environ Health 2006. 2005). Barr DB. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter.inchem. Environ Health Perspect 2004. Shealy DB. Moseman RF. Wellman SE. 2005). Pesticide workers may have much higher levels following pesticide applications. Pesticide residues in urine of adults living in the United States: reference range concentrations. Pope C. Morgan DP.. Kedan G. et al.

D. 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/methylparathion_ired. Osorio AM.S. 0153.110 Suppl 6:1047-1051.201(2):97-104. Olsson AO. Seidler FJ. Available at URL: http://www. U. Monnet-Tschudi F. Ethyl parathion. Kieszak S.pdf. Environmental Protection Agency (U. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Schilter B. Anal Bioanal Chem 2003. Environ Health Perspect 2006.04/106. Ohio.S. EPA).S.pdf. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos.epa. Honegger P.114(10):1542-1546. Rosenberg J. Investigation of a fatality among parathion applicators in California. Nguyen JV. Facts. External and internal exposure of wine growers spraying methyl parathion.epa. WHO/SDE/WSH/03. May 2003.E. 5/19/09 Zurich MG.usgs. Available at URL: http://www. 6/1/09 World Health Organization (WHO). Letzel S.162(2-3):219-224. 2004. Geological Survey (USGS). Yacovac R. Levin ED. 1/12/07 U.int/water_sanitation_health/dwq/chemicals/ methylparathion. Hill G. Pesticides in the Nation’s Streams and Ground Water. Slotkin TA. The Quality of Our Nation’s Waters. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. revised February 15. EPA-738-FOO-009. Jung D. 2007 [online]. EPA).gov/circ/2005/1291/. R.20(4):533-546. 1995-1996. Costa LG. 1/14/09 U.S. Toxicol Appl Pharmacol 2004. Case No. 1992-2001. Am J Ind Med 1991. Rubin C. March 2006.gov/oppsrrd1/REDs/factsheets/0155fct. 152 Fourth National Report on Human Exposure to Environmental Chemicals . 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. September 2000. Esteban E. Dunlop B. Barr DB. Environ Health Perspect 2002. Available at URL: http://pubs. Methyl parathion in drinking water. Backer G. pdf.S. et al. Mengle DC. Sadowski MA. Tate CA. Available at URL: http://www.Organophosphorus Insecticides: Specific Metabolites Muttray A.376(6):808-815. Ames RG. Ryde IT. Hill RH Jr.who. Toxicol Lett 2006.

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

410 (<LOD-1.770) 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 .27) .210-.760 (<LOD-.700-.250 (<LOD-.680 (<LOD-. population from the National Health and Nutrition Examination Survey.840) 669 687 929 Limit of detection (LOD.64) .S.55) . 154 Fourth National Report on Human Exposure to Environmental Chemicals . < LOD means less than the limit of detection. Survey Geometric mean (95% conf.950) < LOD < LOD 1.17 (.S.840 (.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . 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.31) . population from the National Health and Nutrition Examination Survey.500 (.21) < LOD .460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .470 (.740-1.07) .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.200-.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 .210 (<LOD-.850 (.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .430 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th . interval) Selected percentiles ( 95% confidence interval) Sample 95th .670 (<LOD-1.210-1.780 (<LOD-1.580-1.740 (. which may vary for some chemicals by year and by individual sample.700-1.820) < LOD < LOD .780 (.300-1.610 (<LOD-1.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.94) .15) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.780 (. see Data Analysis section) for Survey year 01-02 is 0.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .2.780 (<LOD-1.

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

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

Ose K. McCarthy et al. bioallethrin and deltamethrin... Garey J.S.atsdr.. salivation. References Agency for Toxic Substances and Disease Registry (ATSDR).205(6):459-472. 1991. 2003. WHO. Moniz et al. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. and permethrin) in the Hershberger and uterotrophic assays. et al.gov/toxpro2.108(1):78-85.8(1):197-202.atsdr. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Shaw IC. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Toxicological profile for pyrethrins and pyrethroids. Garey J.. 2002). Elwan MA.27(4):609-614. Richardson JR. fenvalerate. Zhao RC. Bernardi MM. 2006). Thomson BM. Int J Hyg Environ Health 2002. Ranft U. 2003. 2006. Idel H. 2005). In California. Moniz AC. et al. epa. Shafer. Kuhn K.gov/toxprofiles/ tp155. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Available from URL: http://www. Abell AD. Lazarini CA.html.. Shin JH. and seizures (ATSDR. et al. Fourth National Report on Human Exposure to Environmental Chemicals 157 . choreoathetosis. motor activity. Lewalter J. Sugiri D.23(6):665-673. Caudle WM. 2005). In developing rodents. Hu JY. Salzgeber SA. Yang J.. 2001. Neurosci Lett 2001.1/15/09 Aziz MH. Xenobiotica 1997. and striatal dopamine levels in male and female rats. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Idel H. Kim et al. Elwan et al. Go V. Seth PK. Agrawal AK. 2002).. Okuno Y. Toxicol Appl Pharmacol 2006. dopaminergic. Cruz-Casallas PE. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. 2005). Spinosa HS. Estrogenicity of pyrethroid insecticide metabolites. Kim TS. J Environ Monit 2006.. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Pogo BG.211(3):188-197. Lemonica IP. Guillot TS.62:101-108.cdc.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. hypersensitivity. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Garey and Wolff. Toxicol Appl Pharmacol 1991. 2003. Neurotoxic effects of two different pyrethroids. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Kim IY. Fredriksson A. 2004. September 2003..27(12):1273-1283.251(3):855-859.107(3):173-177. 1998. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Wolff MS. Soderlund et al. Bull Environ Contam Toxicol 1999. Biochem Biophys Res Commun 1998. cdc.. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Kunimatsu T. Kunimatsu et al. Wieseler B. Kuhn KH. Adhami VM. 2001. Leng G. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Eriksson and Fredriksson.. Wolff MS. Lee SJ. Florio JC.300(3):161-165.gov/pesticides/ and from ATSDR at: http://www. neurochemical changes in cholinergic. Leng G. 2006. Miller GW. Kamita Y. 2003. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Neurotoxicol Teratol 2005.. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Levsen K. et al. Varoli FM. Leng A. Chen JH. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Hu et al. Generally. Bernardi MM. Shukla Y. Neurotoxicol Teratol 2001.. Song L. 1999. Berger-Preiss E. Kim HS.50(2):245-255. Eriksson P. Pyrethroid pesticide-induced alterations in dopamine transporter function.8(1):18-21. Leng G. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. 2002. Regul Toxicol Pharmacol 2002. Sunami O. Environ Health Perspect 1999. EPA at: http://www. Pauluhn J. 2005). Kang IH. Lazarini et al.html. McCarthy AR. 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. J Reprod Dev 2004. Additional information about pesticides is available from U. Ray et al. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. tremor. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Go et al.35(2 Pt 1):227-237. 2000. Wang SL. Yamada T.

186:57-72.pdf.epa. pdf. Meyer DA. EPA). Rev Environ Contam Toxicol 2006.epa.gov/ circ/2005/1291/.171:3-59. J Toxicol Clin Toxicol 2000. Pyrethroid illnesses in California. Environ Health Perspect 2005.22(8):983-991. Pyrethroid insecticides: poisoning syndromes.usgs. resmethrin.S. Environmental Protection Agency (U. 2007. Clark JM.S. 5/26/09 U. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .38:95-101. Soderlund DM.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Crofton KM. Lesser JE. sumithrin synthetic pyrethroids for mosquito control. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). Permethrin. 1992–2001.who. 19962002.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes.113(2):123-136.Pyrethroid Pesticides Ray DE. Laird WJ.S. Pesticide and Evaluation Scheme.10. Forshaw PJ. Environmental Protection Agency (U. Available at URL: http://whqlibdoc.htm. June 2006a.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Geological Survey (USGS).S. EPA). March 2006. Available at URL: http://pubs.S. O’Malley M. Piccirillo VJ. June 2006b.S. Pesticides in the Nation’s Streams and Ground Water.epa. Reregistration Eligibility Decision for Cypermethrin. and therapy. Sheets LP.gov/oppsrrd1/REDs/cypermethrin_red. Sargent D. 5/26/09 U. Revised February 25. synergies. Available at URL: http://www. 5/26/09 U. Environmental Protection Agency (U. Marsh JR. Available at URL: http://www. Toxicology 2002. Xenobiotica 1992. 2005. EPA). World Health Organization (WHO). Mullin LS.S. Spencer J. April 2002. 5/26/09 Woollen BH. Available at URL: http://www. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Shafer TJ. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. Safety of pyrethroids for public health use. U. et al.htm.

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

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

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

Seiwert M. Pyrethroid illnesses in California. Heudorf U. Drexler H. Centers for Disease Control and Prevention (CDC). Idel H. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Angerer J. Int Arch Occup Environ Health 2004. Heudorf U.46(3):281-288. Heudorf U. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.209(3):293-299.13(2):112-119. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Angerer J.209(3):221-233. Hoppe HW. Ranft U. Third National Report on Human Exposure to Environmental Chemicals. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Ball M.206(2):85-92. Angerer J. et al.109(3):213-217. Human exposure to indoor residential cyfluthrin residues during a structured activity program. 2005. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Int J Hyg Environ Health 2003. Leng G. Angerer J. Int J Hyg Environ Health 2006. Int J Hyg Environ Health 2006. Krieger RI. Bernard CE. Olsson AO. Williams RL. Kolossa-Gehring M. Butte W. Arch Environ Contam Toxicol 2004. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Berger-Preiss E. Rev Environ Contam Toxicol 2006. J Expo Anal Environ Epidemiol 2003. Atlanta (GA). Spencer J. Hadnagy W. Environ Health Perspect 2001. Barr DB. 19962002. O’Malley M.77(1):67-72.186:57-72.Pyrethroid Pesticides References Baker SE. Becker K. Schulz C. Sugiri D.

670-1.140 (.2-dichlorovinyl)-2. which may vary for some chemicals by year and by individual sample.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.690) .1 and 0.35) 1.780) . trans-permethrin.870) 1.460-.300 (. In the body.890 (.280-.470 (.250 (.410) .670 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.2-dichlorovinyl)- CAS No.200-.200) . Generally. The chemical trans-3(2.32) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.820 (.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 . population from the National Health and Nutrition Examination Survey.310) .210) .2dichlorovinyl)-2.370 (. 1985.570 (. more of the trans-metabolite than Urinary cis-3-(2.850 (.. Fourth National Report on Human Exposure to Environmental Chemicals 163 .380 (.110-.740-2. and ciscyfluthrin.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .11) .530 (.600 (.140 (<LOD-.380) .600) .2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.950-2.350) .202 (.550) .380-.110 (<LOD-.740-1. the presence of trans-3-(2.960 (.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.270 (.670-1.220-.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.340) .300 (.220-.380-. but can also reflect exposure to trans-3(2..68) . The presence of cis-3-(2.580-1.and trans-isomers.790) .80) .510 (.670-2. and trans-cyfluthrin.68) .13 (.790 (.340-.410) .160 (<LOD-.770-1. cis-cypermethrin.2-Dichlorovinyl)-2.180) .08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .54) .2-dichlorovinyl)2.160 (. Similarly. Kuhn et al.380-.200-.28) 671 680 518 701 591 957 Limit of detection (LOD.120-.460-1.370-.220-.2-dichlorovinyl)-2.2-dichlorovinyl)-2.510 (.240) .770) .120-.890 (.or trans-3-(2.S.730 (.740) 1.300-.470-1.730 (.230) . transcypermethrin and trans-cyfluthrin.210) 90th .910-5.630 (. Survey Geometric mean (95% conf.400-.500 (.220-. Kuhn et al.490-.900 (.24) 1.1.510 (.490-.120-. 52315-07-8 CAS No.880 (.680-3.44 (.330 (.460 (.200-. trans-cypermethrin.630-.210-.50) .2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.53) .600-1.580) 1.500 (.180 (.630) .200 (.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.150 (.490-1.170 (. but it can also reflect exposure to cis-3-(2.710-1.330) .280 (.220) .650-1.680 (.160 (.730 (.790-1.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.700) .300-. Cyfluthrin.270 (. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.610) .110-.21) .790-1.110-.07 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.200) . 1999).430-.68 (.155-.240) .35) . ciscypermethrin and cis-cyfluthrin.68359-37-5 Cypermethrin Permethrin CAS No.250-.43) .440 (.520) .200) < LOD < LOD < LOD .77 (.270-.630) .420-.610) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.08) . cis-3-(2.15) .270 (. cis-permethrin. < LOD means less than the limit of detection.490-1.920) 1.710) . 1999).340) .120-.260 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.262) * * * < LOD < LOD .12 (.740 (. 1985.570-.640 (.2dichlorovinyl)-2.47 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Biomonitoring Information Urinary levels of cis.

220) . population from the National Health and Nutrition Examination Survey. the median and 95th percentile of urinary levels of cis-3-(2.230 (. 2002).33) .780) 1. 164 Fourth National Report on Human Exposure to Environmental Chemicals .2dichlorovinyl)-2. 2006). 2006.260 (.S.710-3.2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.59) .270) .540 (.250 (<LOD-.250-.750 (.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .920 (.540) .67) . In a study of urban residents in Germany (Berger-Preiss et al.380) . though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.150-.190) .12-2.S.290 (.500 (.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 . 2006.840 (.2-dichlorovinyl)-2.200-.21) .2-dimethylcyclopropane carboxylic acid did not increase.250-. 2005)..560) .300-.560) 1.270) .470-1.290) .240 (<LOD-.420 (.680-1.03) 1.350 (.200) .400-1.67 (. 2001) showed urinary levels of cis.290) ...260-. 2003)..230-.440-.80) . urinary trans-3-(2.780 (. 2005).2-dichlorovinyl)-2.550) .180-.450 (.and trans-3(2.190) .2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.11) ..200 (.710 (..580-1.130-.260) .Pyrethroid Pesticides 2.120 (.450-.540 (. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.450-1.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.320-.300) .430 (.530 (.300) .390-.550-1.880) . 2005). and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.800 (.590 (. Lu et al.260 (.12 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.11 (.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.580) .150-.700-2. In a study of volunteers.400 (.37) .440 (.510-1.640-1..340-.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.390-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.290-.210-. 2003).550-1.410) .570) . 2004. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.230-.260 (.840 (. median urinary levels of trans-3-(2.2-Dichlorovinyl)-2. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.440 (.680-1.59) .270-..810 (.750-1.350) .270 (.550 (.360-1. In these volunteers.440-. Survey Geometric mean (95% conf.150-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.138 (.700) . Studies in Germany of 396 children and adolescents (Becker et al. urinary levels of cis-3-(2.590) .2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.380 (.370-.640) 1.700) .250) 90th .11) .29 (.250-.370-. 2006).640-1. 2005).2dichlorovinyl)-2.2-dichlorovinyl)-2.640-.250) . 2004).300 (.140-.530 (.890) . Schettgen et al.640 (.49) . Cyfluthrin.830) .59 (1.080-.104-..320) .170) < LOD < LOD < LOD .340) .24) ..33 (.31) .180 (.380-.280 (.900 (.340) .2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.190 (.170 (. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al. representative NHANES 2001-2002 subsample (CDC. 2005) In a small group of indoor pest-control operators.280-. Other studies have provided evidence that urinary levels of cis.430-1.430-.370-. 2006) and 1177 urban adults and children (Heudorf et al.680 (.170 (.250) .550) . 2001.230-. post- Urinary cis-3-(2.300 (.690-1.890 (. In the same residents.and trans-3-(2.160 (<LOD-.220 (.182) * * * < LOD < LOD .390 (.200-.600 (.11) 1. 2002)..220 (.

730) .4 and 0.11-2.23 (.400-.94 (1.64-4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.7) 2.800-1.410-.22 (1.560 (.28 (2.560 (.69) 1.Pyrethroid Pesticides application median urinary levels of summed cis.48) 4.550 (.760) .560 (. Finding a measurable amount of cis.35) 1.90) 1. population from the National Health and Nutrition Examination Survey.700-1.20 (.56) 2.68-2.40 (1.16) 1.25 (1.12-6.580 (.520-. trans-Cypermethrin.60) 1.860) .780 (.84 (1.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.76-3.19) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.480-.23) 2.750) .08-6.840-1. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.410 (<LOD-. however.77) 2.07 (1.670) .11-1.680-1.68) 1.91 (1.49-3.77 (1.42 (2.55-4.95) 3.39 (1.54) 4.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .95) 2.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin. Survey Geometric mean (95% conf.4.66) .20 (.03-1. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.420 (<LOD-.43) 2.60-4.07-3. Fourth National Report on Human Exposure to Environmental Chemicals 165 .19 (3.26 (.410 (<LOD-.41-14.500-.2-dichlorovinyl)-2.S.37 (1.440 (<LOD-. which may vary for some chemicals by year and by individual sample.460-. The maximum post-application urinary levels.13) .68-3.59 (1. 2005).63) 1.41 (1.68) 1.39-5.920-1.81) 2.14-6.670) .27 (1.2-dichlorovinyl)-2.25-3.56 (1.87 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50 (1. Biomonitoring studies on urinary levels of cisor trans-3-(2.19 (2.410-.940 (.810-1.62 (1.850-1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.17 (.470 (<LOD-.03-1. Urinary trans-3-(2.66) 691 680 518 690 595 954 Limit of detection (LOD. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.490-1.10) 2.97-11.14) 1.490 (<LOD-.01) 4.08-4.or trans-3-(2.620) < LOD 2.76-4.2dichlorovinyl)-2.910-1.85) 4.and trans-3-(2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.89 (2.520) .570) 90th 1.54 (1.910-1.60) .77) 1.5) 2.68) 2.700) .530) .17-1.56 (1.28 (1.42) 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 .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.470 (.55-5.49-3.63) 1.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .20 (.660) 1.830-1.69 (1.970 (.01 (1.610) 1.49-5.14-2.09 (. 2005).500 (.55-3.460-.56) 2.710 (.820) .08) 1.500) .400 (<LOD-.2-Dichlorovinyl)-2.17 (.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.

780 (<LOD-.440-.33-2.930-1.74) 2.22) 1.15) 2.48 (1.75 (1.3) 2.00 (1.800-1.65) 1.610-.720-1.740) .16 (1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .26 (1. Survey Geometric mean (95% conf.11) .30-3.08 (.880 (.56 (1.700 (.37 (1.530 (.880 (<LOD-1.29) 1.47-2.68) 3.60) 2.91-11.13) 1.Pyrethroid Pesticides Urinary trans-3-(2.67 (2.07-1.57) 3. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.31 (.48-2.28) 2.07) 2.34-4.42 (.36 (1.470-.56-5. trans-Cypermethrin.850-3.74) .560 (.00) 1.00-5.15-3.39) 1.65 (2.820-2.S.57 (1.07-3.87) 1.780) .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 .70 (.91) 1.530 (<LOD-.750) .87) 1.40-2.850) 1.770) < LOD 2.27-2.08 (.500-.91 (1.89) 2.87-3.33 (1.700-.15-3.55 (2.13) .2-Dichlorovinyl)-2.39 (1.850) .470 (.44) 2.15-3.35 (1.42) 1.22-1.47 (1.34-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.56-2.31 (2.760 (.780) 90th 1.81 (2.580) .730) .410-.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.720 (<LOD-.87-8.570-.15) 3.700 (.20-2.02-1.570 (.800-1.880-1.36) 2.45 (1.00) 5.00) 1.540) .60) 2.33-1.12 (.41) 1.80) 1.580 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.98 (1.520 (<LOD-.61) 1.670) .55 (2.55 (2.47-2.60 (1.480-. population from the National Health and Nutrition Examination Survey.45-2.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.640) .570 (<LOD-.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . 166 Fourth National Report on Human Exposure to Environmental Chemicals .30-6.07-2.12-1.970 (.22-2.660) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (1.31) 1.86 (2.900 (<LOD-1.19) .07) 2.87 (1.720-1.64 (1.27-2.35) 1.15 (1.19 (1.

Biological monitoring of workers after the application of insecticidal pyrethroids. Leng G. Environ Health Perspect 2001. Int Arch Occup Environ Health 2003. Idel H. Idel H. J AOAC 1985. Kuhn K.206(2):85-92. Bartell S. George DA. Int J Hyg Environ Health 2006.209(3):293-299. Bravo R. Seiwert M. Schulz C. Sugiri D. Drexler H. Berger-Preiss E. Atlanta (GA). Ranft U. Environ Health Perspect 2006. Hadnagy W. Ball M. Barr DB. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Int J Hyg Environ Health 2006. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Third National Report on Human Exposure to Environmental Chemicals.109(3):213-217. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides.134(1-3):141-145. Angerer J. Angerer J. Ranft U. Butte W. Permethrin and its two metabolite residues in seven agricultural crops. Levsen K.209(3):221-233. Int Arch Occup Environ Health 2004.77(1):67-72. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002.114(9):14191423.Pyrethroid Pesticides References Becker K. Heudorf U. Angerer J. Schettgen T. Centers for Disease Control and Prevention (CDC). Heudorf U. Lu C. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Leng G. Hoppe HW. Hardt J. Leng G. 2005. Int J Hyg Environ Health 2003.62:101-108.76(7):492-498. Wieseler B. Kolossa-Gehring M. Bull Environ Contam Toxicol 1999. et al.68(6):1160-1163. Drexler H. Angerer J. Int J Hyg Environ Health 2002. Heudorf U. Angerer J. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Berger-Preiss E. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Idel H.205(6):459-472. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Pearson M. Heudorf U. Angerer J. Sugiri D. Indoor pyrethroid exposure in homes with woollen textile floor coverings.

.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. Outside the U..2-dibromovinyl)-2.Pyrethroid Pesticides Deltamethrin CAS No.2-dimethylcyclopropane carboxylic acid in the environment (IPCS. Biomonitoring Information Urinary levels of cis-3-(2. in some situations replacing the use of DDT.2dimethylcyclopropane carboxylic acid formed in the environment. 52918-63-5 General Information Cis-3-(2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. mean peak 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. Baker et al. Following residential spraying with deltamethrin for malaria protection in Mexico.2-dibromovinyl)-2.2-dibromovinyl)-2. 2001) showed that urinary levels of cis-3-(2. 2005).2-dibromovinyl)-2. In the NHANES 2001-2002 subsample..2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. in detection of cis-3-(2. 2004). (2004) reported a geometric mean concentration of cis-3(2.2-dibromovinyl)-2.2-dibromovinyl)-2.2-dibromovinyl)-2. In an analysis of 217 urine specimens from a nonrandom sample of United States residents..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. 2005).2-dibromovinyl)-2. Deltamethrin can degrade to cis-3(2.1 μg/L) for the NHANES 2001-2002 subsample (CDC. 168 Fourth National Report on Human Exposure to Environmental Chemicals . urinary levels of cis-3-(2. 1990). 2005).5 μg/L) than the detection limit (0.2-dimethylcyclopropane carboxylic acid of 0.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. deltamethrin has been used against mosquitoes that carry malaria.S. Finding a measurable amount of cis-3-(2.2-dibromovinyl)-2.39 µg/L.. 2006) and 1177 urban adults and children (Heudorf et al. Urinary levels for adults and children in these studies were similar (Heudorf et al.2-dibromovinyl)2.. 2001. Thus. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. Studies in Germany of 396 children and adolescents (Becker et al.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.3-0.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. which may vary for some chemicals by year and by individual sample.S.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.Pyrethroid Pesticides Urinary cis-3-(2. 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. population from the National Health and Nutrition Examination Survey.1 and 0.2-Dibromovinyl)-2. Fourth National Report on Human Exposure to Environmental Chemicals 169 .1. < LOD means less than the limit of detection.

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

Carranza C. Int Arch Occup Environ Health 2004.77(1):67-72. Third National Report on Human Exposure to Environmental Chemicals. 5/26/09 Ortiz-Perez MD. Angerer J. toxicokinetics. Ball M. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Heudorf U. Environ Health Perspect 2005. Centers for Disease Control and Prevention (CDC). Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. and genotoxicity in exposed children. 2005.org/documents/ehc/ehc/ ehc97. et al. Lopez-Guzman OD. Kolossa-Gehring M.inchem.113(6):782-786. International Programme On Chemical Safety (IPCS). Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Atlanta (GA). Seiwert M. Int J Hyg Environ Health 2006. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Hoppe HW. Schulz C.109(3):213-217. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Available at URL: http://www. Int J Hyg Environ Health 2006. Grimaldo M. Batres LE. Deltamethrin.209(3):221-233. [online] 1990. Butte W. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Angerer J. Heudorf U. Environ Health Perspect 2001. Torres-Dosal A.209(3):293-299.Pyrethroid Pesticides References Becker K. Heudorf U. Drexler H.htm. Angerer J. et al. Angerer J. Environmental Health Criteria 97.

In the New York City study. 2002. 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. 2005). 2003. CDC. Hardt and Angerer. 2005). 2004). In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Baker et al. A small sample of occupationally unexposed Italian residents had median levels of urinary 3-phenoxybenzoic acid that were about fourfold higher than for adults in the NHANES 2001-2002 subsample (CDC. 2005). Thus. 2005). a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. 52645-53-1 Tralomethrin 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. 2005). 2006) showed that urinary levels of 3-phenoxybenzoic acid at the 95th percentile were similar to levels at the 95th percentile for children in the U. 2006). Becker et al. 2006. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. 2005). 39515-41-8 CAS No. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above.52315-07-8 CAS No. In one study of 145 urban residents in 80 private homes in Germany.. (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. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. 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. In a small group of indoor pest-control operators... Biomonitoring studies of 3-phenoxybenzoic acid provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of pyrethroids than levels found in the general population. 2003). CDC... representative NHANES 2001-2002 subsample (CDC. 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... median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al.Pyrethroid Pesticides Cyhalothrin CAS No. Urinary levels of 3-phenoxybenzoic acid in children were found to be related to residential pesticide 172 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. 2005). Finding a measurable amount in urine does not mean that the level will result in an adverse health effect.. Fenpropathrin Permethrin CAS No. Saieva et al. CDC. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. A study of 396 German children (Becker et al. 52918-63-5 use and house dust levels (Lu et al. 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. Following residential spraying with deltamethrin for malaria protection in Mexico. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. 2003. 68359-37-5 Cypermethrin Deltamethrin CAS No.

810) 1.29-1.250 (.507 (.960 (.62) 5.364) .470-.311 (.850) .78 (1.190-.440) .1) 3.560-1.25) size 1998 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .25 (2.200-.79) 3.190-.290 (.32-21.560-.1) 3.39) 2.13) .05) 1.227-.420) .41 (1.200-.220-.233-.05) .01 (1.41-2.360) .1 and 0.266-.740 (.21 (2.25-7.595) .25-1.49-2.03 (3.314) .36) 1.740 (.86 (1.292 (.298 (.49 (1.S.820) .454 (.53-3.520 (.320) .30) 3.62-6.62-8.320) .265-.60) .45-5.51-6.55 (1.352-.710 (.288 (.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.680 (.940) 1.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.12 (.8) 3.428-.34) 8. interval) .240 (.43) 3.210-.230 (.27-2.300 (.30 (1.850) .730 (.374) 99-00 01-02 99-00 01-02 99-00 01-02 .340) 75th .23 (2.390) .590-.430-.325 (.240 (.46) .32 (2.750) .427) .81 (1.700 (.54) 1.16-1.71 (1.210-.550-.45 (2.26) 2.450 (.800) 1.292-.620-1.69 (1.230-.35 (1.34-6.670 (.250 (.800 (.1.570-1.27-2.26) 2.510-.530-.160-.270 (.434) .160-.280 (.75 (1.640 (.355) .267 (.190-.65-2.246-.53) 1.41) 3.490-.89-71.288-.330) . population from the National Health and Nutrition Examination Survey.230-. Fourth National Report on Human Exposure to Environmental Chemicals 173 .417 (.297 (.49-2.1) 3.18 (1.25-4.601) .321 (.760 (.12) 4.93 (1.190-.35) 2.630) .370) .63-3.90) 1.51-3.238-.04-5.52-4.64) 697 680 524 701 603 957 Limit of detection (LOD. Survey Geometric mean (95% conf.46) 2.315 (.490) .387) .590 (.260 (.180-.73) 1.990) .63 (3.25 (2.27-11.295) .320) .35 (2.38 (2.92-3.260 (.26-2.33 (2.32 (1.247-.830) 90th 1.586) .65 (1.406) .650 (.430-.820) .314 (.700-1.12) .41-3.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .320 (.510-.35) 2.48-2.78) 1.384) .350-.48-2.600 (.33) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.230 (.18 (2.840-1.300 (.56-5.300) . Deltamethrin. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.78) 1.83-11.260-.30 (.300 (.750-1.253-.13 (.72 (1.42-2.328 (.44) 5.200-.362) .38 (2.14-6.260 (.353 (.320) .250 (.230-.373) .750) .226-.369) .277-.69) 3.28) 1.710 (.610) .02-6.250-.330) .340) .530-.78) 6.780) 4.273 (.33 (1.336 (.35) 1.276-.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .04) .50 (2.830-2.16) 1.870 (.52-5.76 (1.270) .49 (1.271-.340) 1.570-.34 (2.560-.

750-1.300-.49) 1.246 (.264 (.299-.0) 3.280) .200-.150-.61-2.74) 3.350 (.480-.63) 1.610 (.52) 2.270 (.440-.460-.06-3.210 (.590) .590) .91) .15-2.280-.54 (1.446) .640 (.03-1.730) .190 (.580 (.510 (.16-4.00) 5.230-.311 (.328) .240 (.460-.740) .234 (.49 (1.410) .670) 3. Deltamethrin.227 (.09) 3.510 (.84 (1.83 (1.400-.36-6.490 (.09 (.40) 2.480 (. interval) .75-8.240-.22 (1.290-.72 (1.300-.423 (.202-.960-1.35) 1.330) 75th .25-2.290) .91 (2.95) 1.272) .63-3.35 (1.48 (1.540 (.372) .378 (.309) .630) .330 (.387) .440-.09-2. Survey Geometric mean (95% conf.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.225-.650) .410-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.560 (.200-.530-.41-4.570) .67) 1.62) 1.274 (.253) .720 (.55) 3.350) .226-.534) .550 (.380-.270 (.530-.25-5.19-6.240 (.04 (3.860-1.88) size 1998 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .930) .200-.09-2.840-1.390-.21-4.51-7.62) .330) 1.312 (.07) 2.67 (1.323 (.810) 1.S.270-.39) 1.90) 3.190-.274-.490-.13-1.35) .550 (.173-.02 (2.370 (.310) .304) Selected percentiles ( 95% confidence interval) Sample 95th 3.330) .240-.02-1.860-1.160-.230) .21 (1.43-64.261-.03 (.49-2.178-.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .860 (.280 (.200-.13-1.80) 4.35-3.590-1.270) .17 (.500) .37) 1.400-.309 (.220 (.91) 9.43 (2.238-.275 (.10 (2.07-5.250 (.190-.330) .91-4.370-.450 (.83) 1.41) 1.730-1.32 (2.94 (1.700-1.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .96 (1.590) .280 (.380 (.490 (.37 (1.335-. population from the National Health and Nutrition Examination Survey.720) 90th 1.930) 1.316 (.730) .53 (1.362 (.280) .270) .73-4.44) 2.88-5.81 (1.437) .278) .640 (.550 (.365) 99-00 01-02 99-00 01-02 99-00 01-02 .00) 1.25) 2.440-.60) 1.210-.36 (1.64-5.19 (2.43 (1.290) .55 (1.86 (1.400) .261 (.49) 3.240-.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .580) .240 (.27) 1.67 (1.60-4.280 (.250 (.272 (.677) .43) 1.11 (.401) .210 (.510 (.40 (1.13 (.04 (.670) .52 (1.320) .357) .271-.19) 2.240 (.329) .17-1.220-.44 (1.329) .230-.73) 1.00) 1.05-3.240-.420-.229-.224-.216-.250) .321-.11 (.760) .

Fourth National Report on Human Exposure to Environmental Chemicals 175 . Sugiri D. Idel H. Angerer J. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Ranft U.46(3):281-288. Int Arch Occup Environ Health 2003. Levsen K. Third National Report on Human Exposure to Environmental Chemicals. Idel H. Lopez-Guzman OD. Arch Environ Contam Toxicol 2004. Grimaldo M. et al. Exposure to indoor pesticides during pregnancy in a multiethnic. Bartell S. Liu Z.76(7):492-498. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Olsson AO. Ball M. Bravo R. Environ Health Perspect 2003. Environ Health Perspect 2005. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Hadnagy W.209(3):221-233. Pearson M. Lapinski R. Ortiz-Perez MD. Environ Health Perspect 2006. Godbold J. et al.Pyrethroid Pesticides References Baker SE. Int J Hyg Environ Health 2006. Biological monitoring of workers after the application of insecticidal pyrethroids. Barr DB. Ranft U.111(1):79-84. Berger-Preiss E. Carranza C. Centers for Disease Control and Prevention (CDC).206(2):85-92. Berger-Preiss E. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.113(6):782-786. Kolossa-Gehring M. Atlanta (GA). Leng G. Sugiri D. Seiwert M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Berkowitz GS. 2005. Lu C. toxicokinetics. Barr DB.205(6):459-472. urban cohort. Hardt J. Deych E. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Int J Hyg Environ Health 2002. Hoppe HW. Leng G. Batres LE. et al. and genotoxicity in exposed children.114(9):14191423. Becker K. Torres-Dosal A. Obel J. Angerer J. Int J Hyg Environ Health 2003.

190) .300 (.280) .110) .080) .340 (.110 (.360-.390 (.130 (.500) .132 (.360) .470) .240-. ammunition.200 (.170 (.145) Selected percentiles ( 95% confidence interval) 50th .330) .115-.150-.220 (.240-.260 (.310-. Stibine is a metal hydride form of antimony used in the semiconductor industry.120 (.154) . see Data Analysis section) for Survey years 99-00. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.160 (.125 (.200-.310) .131-. It is also used in paints.280-.330) 1132 1335 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .210) .260 (.350) .140 (.320-.300) . storage batteries. Dermal contact with soil.144) .140) .350-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.190) .210 (.390-.220-.120) .350 (.120 (. enamels.430 (. to a lesser extent.04.300-.280-.123 (. solder.400-.105 (.400 (.157) .240 (.250 (.134 (.350 (. It is used in metal alloys.130 (.120-.143 (.270 (.140-.390) .190 (.120 (.300-.140 (.200-.160-.250-. People are exposed to antimony primarily through food and.440 (.200) .120-.110-.400) .220) 95th .370-.320) Total .320 (.220) .260) .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.141-.140 (. and 0.270-.360 (.145 (.114) .190 (.140) .160) .154) .197) .390-.280 (.220) . metal bearings.150) .230) .160) .220-.070 (<LOD-.210) .190-. The absorption.093 (. 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.230 (.210 (.360) .530) .210) .220) .137) .310 (.350) .130-.100 (.136-.160-.130-.230) .180-.330) .460 (.090 (.560) .098-.240 (. interval) .099 (.250-.260-.150) .250 (.200) .210) .120 (. < LOD means less than the limit of detection.150-.390-.095 (.340 (.160) .200 (.110-.250-. and +5.184) .220-.080) .410) .100-.160) . and glass.230 (.130-.320-.090-.470 (.200-.110-.175 (.130-.310 (.330) .350) .200 (.320-. and excretion of antimony vary depending on its oxidation state.130) . +3.108-.440) . from air and drinking water.120 (.220-.150-.310) .600) .120) .260) .142 (.230-. and refuse incinerators that process or release antimony.270) .350) .190-.250) .130) .330 (. distribution.126 (.220-.164-.190-.150 (. which may vary for some chemicals by year and by individual sample.169 (.108 (.120) .350 (.190-.180-.120-. 176 Fourth National Report on Human Exposure to Environmental Chemicals .240 (.07.130-.300) .570) .270 (.200 (.140) . castings.200) .290 (.200-.210-.070-.280 (.390) .090-.148-.S.136) * .200) .120-. coal-fired plants.270 (.350 (.150-.180-. sheet and pipe metal.070 (<LOD-. Workplace exposures can occur at smelters.320-.137) .350 (.210) .170-.490) .330-.300-. Antimony enters the environment from natural sources and from its use in industry.079-.200 (.180) .090) 75th .130-.370) .190 (.230 (.190 (.460 (.330 (.158 (.170-.109-.170-.410) .160 (.161) . fireworks.Metals Antimony CAS No.115) .320 (.180-.095-.130 (.270 (.130 (.260 (.220 (.140) .120-.170) .180 (.130 (. ceramics.300) .080-.154-.190) .280-.134-.130-.119) .280-.135) * .230-.103) .160-.310 (.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 . water.200 (.300 (.130) < LOD . or other substances containing antimony is another means of exposure.146 (.150) 90th .132 (.280-. 0.220-.176 (.130 (.150 (.150-.180 (. and pewter.100-.190) .350-.128 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3. and as a fire-retardant in textiles and plastics.340) .230-.120-.260-.230-.140) . 7440-36-0 General Information Antimony is found in ores or other minerals.260) .120-.180 (.190-.090 (<LOD-.180 (. and 03-04 are 0.087-.100) .133) * .128 (.122 (.400) .310-.120-. 0.290-.207) .330 (.160-.350-.130 (.04.510) .250 (.190 (.156-.460 (.160) .430 (.470) .210-.250-.180 (.140) .330) .110-.180 (.490 (.440) .500) .320) .230-.130) .390) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. respectively.119-.400 (.170 (.180) .142) * Sample size 2276 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .420) .290-.080 (<LOD-.178) .150 (.310 (.117-.400) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.400 (.270) .140 (.190) .120) .410-.180-.117-.240) .100 (.130 (.240 (.160 (. 01-02.170-.280) .150) .390) .230) .120-. population from the National Health and Nutrition Examination Survey.360 (.088-.240 (.112-.160) .330-.126-.170-.280) .430 (.280) .710) .460) .

148-.138) * .146-. and ulcers (Werrin.132 (.233) .124) .104-.343 (. 1953).181) .333 (.098-.195-.127 (.092) .149) .075 (.117-.120 (.321) .225) .178-.146) .111-.250-.176-.300) .429 (.207) . Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.133) .109-.188) .364 (.081 (<LOD-.261) .150-.117-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al. and kidney have been demonstrated in high dose animal studies depending on the dose.266 (.108-.140) .333-.129 (.250 (.068 (.085) .193 (.106-.159-. Ming-Hsin et al.209 (.30) .122 (.098) .364 (. 1962).115) .146-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman..308) .086 (.115-.126) .267-.145) .248-.271-.107-.129) ..068-.241-.485) .154-.164) .357) .217 (.152) .269 (.233-.159-.300 (. diarrhea.208 (.235-.333-1.163 (.228-.080 (.265 (.112 (.102-.117-.137 (.082 (<LOD-.178 (.107-.115 (.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 .113-.095-.077) .087) ..239-.253 (.183) .164 (.123 (.480) . Fourth National Report on Human Exposure to Environmental Chemicals 177 .113) .102-.206-. 1986).082) .140) < LOD .176 (.173-.076-.281-.115-.313-.250-. 1973).391) .182 (.259 (.268) .150-.245) .149-.209) .238 (.135) .078 (.173) .098-.194-.320) .338 (.179-.069-.295 (.385 (.135) .112 (.120 (.144-.135 (.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.135) . liver.267 (.172-.124-.196 (.263 (.294) Total .310) .124-.074 (.430) .130) .310 (.200-.127) . Acute antimony poisoning may cause a metallic taste.192) .727) .109 (.247) .224 (.195-.173 (.352) .171) .131 (.115 (.185-.119 (.250-.280-.357-.148) * .250 (.161) .097-.425) .200) .226 (. and gastrointestinal symptoms such as vomiting.120 (.071-.173 (.203) .121) .084) .080 (<LOD-.191 (.429) .225 (.204-. myocardium.256 (.126-.099-.135 (.116-.253-.162-.230) 95th .119-.333-.500) .320-.185 (.242-.255) .105-.250) .Metals than for trivalent compounds (Elinder and Friberg.741 (.167-.255-.109 (.373) .143) Selected percentiles ( 95% confidence interval) 50th .159-.380 (.130) .114 (.146-.438) .278) .. 1995).096-.156 (.069-. and route of exposure (Elinder and Friberg. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.114 (.089) .103-.741) .116 (.333 (.107-.119-.238) .277 (.131) .228 (.248) .400 (.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 .198) .318-.121 (.103-.170 (.229-. abdominal pain.338 (.417) .139 (.132) .286 (.143) .241-.121 (. population from the National Health and Nutrition Examination Survey.227-.161) .143) 90th .113-.352 (.300) .167 (.106-.138-.315) .123) .444) .S.075 (.148-.244-.128-.127) .147) .139 (.405) .250-.152) .118 (.130) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.131-.130 (.114 (.209-.164-.213 (.099-. The toxicity of stibine after acute inhalational exposure is similar to that of arsine. 1986).189 (. and eyes.125 (.122 (.127) .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 .317) .175 (.371 (.272) .143 (. 1954).086) 75th .447 (.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.276 (.. skin.238) .129 (.192-.267) .167 (.079 (<LOD-.320 (.124 (.199-.153-.095-.129) * .185 (.317) . Inorganic antimony salts irritate the mucous membranes.257) . Histopathologic inflammatory and degenerative changes in the lung.126 (.391) .278 (.092-.151) .263-.471) .125-.444) .338) .076-.143) .333 (.081) .471 (.298 (.236 (.318-.082) .127) .147-.160 (.228 (.120 (.104-.414) .288 (. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.310) .230-.111 (.333) .265-.192 (.118 (.209) .138-. 1958) and occupational exposures (Briegner et al.136) .333-.421) .163 (.188-.112-. 1988.200-.205-.181) . 1944).222 (.186) .320 (.214) .187) .308-.193) .061-.167 (.317) .200-.211) .417) .153 (.208-.203) .233 (.138 (.176 (.220) .280 (.134) .100 (.108-.108-.156-. species.181) .320-. interval) . resulting in hemolysis with abdominal and back pain (Dernehl et al.195 (.115 (.

and future strategies. and 2003-2004.. Ming-Hsin H.)1954. Sabbioni E. Dunkelberg. Urinary antimony in infancy. Int Arch Occup Environ Health 1987.48:93-97. Chen J-R. Shao-Chi C. Dernehl CU. 1991. Industrial Medicine and Surgery (Dec. External and internal antimony exposure in starter battery production. Antimony. Roland H. Element reference values in tissues from inhabitants of the European community. Delves HT.atsdr.67:119-123. Pulmonary edema of environmental origin.. Centers for Disease Control and Prevention (CDC).e. Kuo-Juie Y. environmental levels) and health effects is available from ATSDR at: http://www. Wade A.. 20012002. and antimony in optoelectronic industry workers. Schacke G..Metals to antimony have been established by OSHA and ACGIH. Kentner et al. Cullen A.. even when exposure levels were below workplace air standards (Bailly et al. Yu H-S. Chest 1973. Elinder CG. Mayer P.158:165-190. Review of elements in blood. Dezateux C. et al. J Trace Elem Med Biol 2002. Delves HT. Handbook on the toxicology of metals. Biomonitoring of a worker population exposed to low antimony trioxide levels. Industrial antimony poisoning. Nordberg GF.76:432436. Luedersdorf R.. Industrial Medicine 1944. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Bolten C. or exposure differences. Arsine. Ju-Sun P. Costeloe K. Schaller KH. Atlanta (GA).. References Berman JD. 1986. Kiberd B. et al. Petrucci F. Vouk VB. Mahieu P.46:931-936. Biological monitoring of exposures to aluminum. Friberg L.76(2):103-115. Trace element reference values in tissues from inhabitants of the European community I. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. J Clin Pathol 1998.51:238-240. 2005. 1994) have reported values slightly higher than those in this Report.S. population. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. EPA. Yang C-Y.cdc.. Liao Y-H. 1998) or compiled reference ranges (Hamilton et al. Stocks J. Pilgrim L. Cordasco EM.64(2):182-185. Stasney J. respectively. and hydrogen sulfide. Gallorini M. In: Friberg L. Matthews T. Suchenwirth R.html. gallium. Apostoli P. 1987). Carelli G. et al. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Sabbioni E. Antimony trioxide is rated by IARC as a possible human carcinogen. Third National Report on Human Exposure to Environmental Chemicals. Gebel TW. Van der Venne MT. Iavicoli et al. Sci Total Environ 1994. Semisch CW. stibine. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Environ Health Perspect 1998. which may be due to methodologic. pp. Leinemann M. Briegner H. 1995. Skulsukai G. eds... Alimonti A. Kentner M. 1997).106:33-39. 1998). Earlier measurements in general populations (Minoia et al. clinical efficacy. 1990. 2004. arsenic. 1998. Lauwerys R. Cheng-Wei L. Nau CA. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . 26-42. Mayne P. 2002. Liao Y-H et al. Int Arch Occup Environ Health 1995. 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. Ho C-K. Iavicoli I. J Occup Environ Med 2004. Caroli S. Biological assessment of exposure to antimony and lead in the glass-producing industry. VI. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony.. Piatnek DA. Fuchs A. O’Regan M. Br J Ind Med 1991. Paschal et al. Konings J. Antimony in blood and urine of infants. Arch Dis Child 1997. Chemotherapy for leishmaniasis: Biochemical mechanisms. Ludersdorf et al. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Lenert G.10(3):560-586. Bailly R. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. 2nd ed. Weltle D. Wu M-T.16: 33-39. Pietra R. Information about external exposure (i. Pozzoli L. Rev Infect Dis 1988. indium. New York: Elsevier. and a drinking water standard has been established by the U. Stead FM. Dezateux et al.521-523. Minoia C.. Buchet JP.59:469-474. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Hamilton EI. Stone FD. HH.13:361-362. Chin Med J 1958. gov/toxpro2. Chia-Yu H.

95:89-105. Paschal DC. Trace metals in urine of United States residents: reference range concentrations. Renes LE. 27:38-45. Ting BG. et al.76(1):53-59. blood. Morrow JC. and serum of Italian subjects. Environ Res 1998. Quarterly Bulletin of the Association of Food and Drug Officials 1962.Metals in urine. Pirkle JL. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Werrin M. Sampson EJ. Jackson RJ. Industrial Hygiene and Occupational Medicine 1953.99-108. Sci Total Environ 1990. Antimony poisoning in industry. Chemical food poisoning.

Although it is still widely used in the United States.90-11.8-61.70 (6. particularly arsenic trioxide.90-7.10 (6.7-95.08 (5.4 (24.10) 10.1 (38.10-10. arsenocholine. Gallium.9 (17.40) 7.6-35.4 (31. 180 Fourth National Report on Human Exposure to Environmental Chemicals .1) 290 725 1542 03-04 03-04 9. The United States no longer produces arsenic from mining but imports about 22.8) 33.8) 29.2 (41.90-8. arsenites. aluminum. though in some locations arsenite may be prevalent (WHO.80 (5. Arsenic trioxide is approved to treat acute promyelocytic leukemia.6) 618 722 1074 Limit of detection (LOD.57) Selected percentiles ( 95% confidence interval) 50th 7.5) 41.3) 10.27) 9.9) 21. and play sets. mostly for use in wood preservation (ATSDR.12-10. In the last century. and arsenates (oxidation states of -3.2-17.10-7. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. it is found in over 200 crystalline or mineral forms. arsenic as elemental metalloids may be used in some ammunition.7-83. psoriasis.90 (5.0 (11.50 (8. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. and as a cosmetic to lighten complexion.7 (11.1 (32.6-141) 53. interval) 8.8) 7. arsenic compounds. trimethylarsine oxide.2 (13.6-43.5-52. and other metals.7) 65. Arsenic trioxide (As2O3. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6 (15. Arsine (AsH3) is a reactive.70) 8. copper arsenates. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. population from the National Health and Nutrition Examination Survey.55 (7. grain.8) 30.000 metric tons annually.2) 15.30 (7.5) 66.8 (48. and.00-9. In nature. solders.Metals Arsenic CAS No.4 (48.0 (43.2-93.74.34-9.5 (14. gaseous hydride manufactured in small quantities for use in the semiconductor industry. cancers.2-20. lead.6 (32.8) 17.00 (6.0 (14. Also.12 (6.1) 15.1-18.7) 90th 37. black.5-178) 46. to a lesser extent.25-9. Various arsenic compounds were used in paint pigments and for tanning animal hides. were used as treatments for syphilis.80) 6.66-8.20 (8.3) 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 7.2-61. retaining walls. Water sources contain mostly inorganic arsenate. 2005).30) 17. pesticides.0 (15. Survey years 03-04 Geometric mean (95% conf.8) 34.2 (51. and indium arsenides are used in the semiconductor industry. sodium arsenite. semiconductors.4 (26.4) 40.90 (7. and in lead-acid storage battery grids. meats. and as homicidal poisons. and foods.90) 75th 16. ocean and fresh waters.90) 16.9) 68.9-62.0 (22.90 (7.1-40.84) 8. or rarely as elemental metalloids (yellow. the smelting of copper.2 (12.90-8.7) 24.77) 6. and produce.5-41. General population exposure to inorganic arsenic can occur through consumption of drinking water and. Arsenic is measurable in most soils. Before the 20th century. see Data Analysis section) for Survey year 03-04 is 0.S. from coal burning.84) 8.9-34. +3 and +5). referred to as inorganic arsenic compounds.3-15.9 (8. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.19-9.02-8.6) 11.5 (23.4) 60.5) 43.8) 7. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.0-60. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.9-46.1) 7.1) 1281 1276 03-04 03-04 03-04 9.6 (9. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.13-8.3-111) 78.34-10.3-19. Since the 1940s. to a lesser extent.6 (13. and gray forms).5-19.97) 8.29 (8.30 (6.90-14.2) 46. mental disorders.80-9. Arsenic and its compounds have had many uses in the past and present as medicines.5 (34. alloys.5) 95th 65.0-19.5 (36. as alloy in metal bearings. cacodylic acid.8-77.50-14. and arsenosugars. lead hydrogen arsenate.4 (7. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.4-65.70-9. 2001). such as arsenopyrite (FeAsS) and realgar (As4S4).4) 13.41 (7.5 (40.

44-11. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.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 8.6 (35. arsenocholine. gallium arsenide and indium arsenide.75 (5. and arsenosugars.04) 7.1) 6.01) 7.4) 54.g.33-10. Steinmaus et al.06 (4.7 (9.61 (7.1) 58.0) 1281 1276 03-04 03-04 03-04 8. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established. After absorption.5-120) 40.7-188) 27.4) 32.13) 8.1) 8.0) 14. Extremely high groundwater arsenic levels. 2001).2-15.40) 8.5-17.8 (21.8) 22.88) 7. dust.3-53. kelp.96) 12.1) 7.28-7. have caused clinical arsenic poisoning. and folate status (Chen et al.5 (9. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.3 (24. Direct exposure to DMA and MMA may result from use of the two pesticides.66-8.88 (5. 2007.45) 5.0) 12. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.24 (7.32 (5. 2001).3) 9. arsenic does not show biomagnification in the food chain (WHO. interval) 8.93-8.8 (11.7 (11.S. Chowdhury et al. 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.66 (7. age.0 (17.86-17.25 (6.1 (11.50 (6. 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. as observed in Bangladesh where millions of people have been exposed. In aquatic sediments.47 (6.2 (12.3) 6.. The semiconductor dopants.99-9.04 (5.8 (20.58-10.8-75.0) 26. Tseng. so exposure to the general population is extremely limited.0-69.75) 13. and some other seafood can contain organic forms of arsenic including arsenobetaine.76 (6..9-56.2) 15. WHO.93-9. Though modest bioconcentration occurs in some aquatic life.9) 53. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. 2007.23-7.. 2001).9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . shellfish. Survey years 03-04 Geometric mean (95% conf.4 (40..1 (14. dose level. Fish.5) 290 725 1542 03-04 03-04 8.. Gamble et al. and contact with CCA-preserved wood structures. though some reduction may occur in the gut prior to absorption.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.3-41.7 (25. 2006.07-9.1) 24. are used in enclosed ultraclean operations within the semiconductor industry.47-6.4 (42.47 (7. selenium.4 (26.8 (12.0 (31.2) 90th 30.59) Selected percentiles ( 95% confidence interval) 50th 7.6) 45. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. cacodylic acid and monosodium methyl arsenate.44) 6. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. NRC. mine tailings).S. organic arsenic can be converted back to methylated and inorganic arsenic.2) 40. 2001).64 (7. U.0-38.1-36.4 (24.10-16.10-8.33 (6.30-9.3-62.6 (17. Children may have additional exposures from ingestion of contaminated soils (e..9 (45.7-17. WHO. but is poorly absorbed dermally (WHO. 2001).8-32. 2007.3-64.12-10. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.66-8.41) 6. Inorganic forms of arsenic demonstrate high acute toxicity. inorganic arsenic is widely distributed within the body.0) 33.31 (6.2-46. 2001). 2006.6-17.3 (27.S.7) 95th 50.38-10.7) 28. EPA’s maximum contaminant level (Hughes.18 (5.4-64. 2001.81-9.4 (12.5) 17.9) 13. Arsenate is reduced in the body to arsenite (oxidation state +3).51) 75th 14.8 (27. EPA.8-62. 1988).35) 7.6 (10.25-9. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.11 (5.0-18. 2003.20-9. 2001).0-26.8) 27.00 (6.4 (11.7-34.7-35.0) 42. population from the National Health and Nutrition Examination Survey. Smoking tobacco is also a source of inorganic arsenic.7-18. 2001. In aquatic organisms. trimethylarsine oxide (TMAO).01) 11. 2001).

50) 621 725 1078 Limit of detection (LOD. and childhood neurodevelopmental effects in observational human studies. and diarrhea. respectively. leading to a decrease in adenosine triphosphate energy production. cell transformations. Cellular glucose uptake. drinking water have not been associated with increased cancer rates (Schoen et al. noncirrhotic portal hypertension. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. gluconeogenesis. renal failure. < LOD means less than the limit of detection. Studies of arsenic at levels typical of U. WHO. 1998. WHO. population from the National Health and Nutrition Examination Survey. The U. and production of glutathione may be affected as well.. substitution in phosphate metabolism. 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..S.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. Although arsenate is reduced in the body to arsenite. 2004). and it also will inhibit succinate dehydrogenase.. The organic forms of arsenic occurring in seafood have little known toxicity. Acutely.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.10 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 1. 2001. WHO. 2001.EPA.g.. and DNA repair inhibition (Cohen et al. and bladder cancer (IARC. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. hepatotoxicity.. 2001).S. including drinking water sources with elevated arsenic levels (e. 2006. hematocytopenias. 2001). arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. which can lead to dehydration and shock.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. cytotoxicity. peripheral vascular disease.. Raml et al. Taiwan. and by uncoupling oxidative phosphorylation (NRC. and endothelial injury (Kumagai and Sumi.g..50) 1. some of these effects may take years to develop. 2007). OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. Laboratory studies using inorganic arsenic have shown chromosomal aberrations.10 (<LOD-1. Cardiac arrhythmias. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. 2007.. 2006) or when exposure occurs in smokers (Chen et al. lung. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. Such actions may lead to decreased energy production. hyperkeratosis.EPA has established drinking water.10 (<LOD-1.S. increased oxidative stress. and hyperpigmentation of the skin (NRC. Arsenic has many actions demonstrated in cellular studies. U.20 (<LOD-1. can cause peripheral sensorimotor neuropathies. fatty acid oxidation.. 2001).. interference in signal transduction pathways.80) 1.0. 2006. 2006.30) 1. Chronic arsenic exposure in humans is considered to be a cause of skin. 2001).S.60) 1. 2001).60) 1. Bredfeldt et al. Chile). Chronic human intake of arsenic at less than acutely toxic doses. Bangladesh. including inhibition of numerous enzymes. 2004. and altered gene expression. but additional or confirmatory research is needed (Kapaj et al.20 (<LOD-1. hypertension. Survey years 03-04 Geometric mean (95% conf.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. NRC. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. 182 Fourth National Report on Human Exposure to Environmental Chemicals .20 (<LOD-1.. 2007.20 (<LOD-1.10 (<LOD-1. apoptosis. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2001). vomiting. 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. 2000. WHO. food residue. 2004). which may vary for some chemicals by year and by individual sample. NRC..10 (<LOD-1. Chronic elevated arsenic intakes have been associated with diabetes. arsenic trioxide) includes hemorrhagic gastritis with nausea. Cohen et al. With chronic exposure.

Additional information about external exposure (i.. 2006.. 2007. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.18) 3. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. population in the National Health and Nutrition Examination Survey (NHANES) 2003–2004 were similar to levels reported in the National Human Exposure Assessment Survey (NHEXAS) 1995–1996 for about 80 children residing in the Great Lakes region (Caldwell et al. Caldwell et al. Meza et al. population in NHANES 2003–2004 (Schulz et al.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 1999.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 2001). 2006).75 (<LOD-2. 2000). arsenic has been fetotoxic and teratogenic.. 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. 2006). 2004.61 (<LOD-3. environmental levels) and health effects is available from ATSDR at: http://www.04 (<LOD-3. hand washings from children playing on CCA-treated wood compared to children playing on non-CCA-treated wood playground equipment were slightly to fivefold higher (Kwon et al. 2006. Calderon et al... Pellizzari and Clayton. gov/toxpro2.. Vahter et al.. 2001)... 1999).80 (<LOD-4. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. median urinary total arsenic levels in 4052 adults varied with seafood intake. Compared with this Report. In a Nevada town where groundwater levels were naturally elevated. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. Fourth National Report on Human Exposure to Environmental Chemicals 183 ... 2006.19) 3. Consequently. Survey years 03-04 Geometric mean (95% conf.. Caldwell et al.S. 1992. 2006).S.. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Shalat et al. 2000..atsdr... urinary arsenic levels have been accepted as a good biomarker of dose (WHO. Offergelt et al. although urinary arsenic levels were not associated with CCA contact (Shalat et al.. population (Rubin et al.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. and the FDA has established a bottled drinking water standard.Metals compounds. Pellizzari and Clayton 2006). 1999..50) 1. 2006)..18 (<LOD-3. Shalat et al. Josyula et al.00) 1.33 (<LOD-3.cdc. WHO. 1986).33 (<LOD-3.75 (<LOD-2. Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al. and were about two-fold lower than those for the U. Pellizzari and Clayton. In the German Environmental Survey III of 1998. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2008.S. 2003.html. but generally only at maternally toxic doses (WHO. 2008). 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. In animal studies. 1998. 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. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al.41) 3.e. 2008).. Levels of total urinary arsenic in the U.. 2004. DMA produced bladder cancer in some chronic rat studies (Cohen et al. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. population from the National Health and Nutrition Examination Survey.. Valenzuela et al. had decreased since the prior 1990– 1992 survey.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.69 (<LOD-3. 2001).. 2007.

Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7 (13.0 (27.Metals other areas of the world (Ahsan et al.0) 29.8 (17.600 (.700-1.S. arsenite. 2005.5 (26.50) .70) 6.70 (5.3% of a representative sample of the U. Pellizzari and Clayton... DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. arsenite.70-21.700-1. see Data Analysis section) for Survey year 03-04 is 0.800-1. China. when seafood organic arsenic is subtracted).37 (1.83) Selected percentiles ( 95% confidence interval) 50th 1..800 (. 2000.20) 18.20 (2.. arsenocholine.30) 10.00 (. population showed a higher contribution of arsenobetaine (Caldwell et al. population in the NHANES 2003–2004 subsample.40-7. Total arsenic measured in the urine includes all species of inorganic and organic arsenic. 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. dermal keratosis.28) 1. and TMAO were detected in only 7. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.20-190) 31.70-21.900-1. After recent seafood ingestion.45 (1.3) 1284 1284 03-04 03-04 03-04 1. in NHEXAS 1995–1996. and other factors such as nutrition.S.90-7. 2008).3-39. 2005. Caldwell et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In the residents of a Chilean town who consumed water with high levels of arsenic. 2001.2-38..19 (. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.S. 2008).4-35. MMA. arsenocholine. 1996.20) 7. and two methylated metabolic products.5) 32.. These associations are stronger at higher urinary levels. 4. In the late 1980s.6 (25.5) 29.4) 31.3 (9.30) 2. 2008.11-1. population from the National Health and Nutrition Examination Survey. respectively. WHO.1-25.20-25.60-3.50) ..43-1.5 (14..9 (6. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. with DMA. Aposhian et al.90-29.48-2.6-44.74 (1.00-1.800-4..3 (21. Individually measurable species resulting from inorganic arsenic exposure are arsenate. For residents of Inner Mongolia.9 (7...20 (4.4 (16.6 (13.80) 1.60) 1.8) 35.871-1.0) 4.4. 1. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.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.S. Valenzuela et al.S..6 (11..800) 1.3) 95th 35.6.68) .30 (1. The higher percentiles of total urinary arsenic levels in the U. and 0..0-23.500-1. Sun et al.5) 621 725 1078 Limit of detection (LOD. Survey years 03-04 Geometric mean (95% conf.30 (2. Caldwell et al. vasospasm.93) 1.20 (1.00 (1. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.0 (26.8 (12. Arsenate. 2006).8-40.31-1. arsenobetaine.7) 13.. Blom et al. Caceres et al. 184 Fourth National Report on Human Exposure to Environmental Chemicals . 2000.80 (3. 1990.00-6.7 (21..g..900 (. 2005.9) 13. 2003).29 (1. 2000. 2008). Measurable organic arsenic species in this Report are three biologically generated environmental forms. In most human studies.40) 5.800 (. Also..17-1. 2007) with higher levels of arsenic in the drinking water. 2008.5) 292 728 1548 03-04 03-04 1. 1985. When seafood intake is avoided.1) 18.1-51. Some noncancer effects of arsenic (e. geometric mean levels were about 70-fold higher than for the U.. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.00-12.40-6.00) 3. and TMAO. 2008).20 (.05) < LOD .1-94. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.7) 15. Tseng et al.50) 90th 16.20-3. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.66 (1.6. which may vary for some chemicals by year and by individual sample.70 (3.3) 35. DMA and MMA.7-22. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.2-35.10) 8.4) 23. 2001).80 (4.2 (6.55 (1. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.8-50.20) 3.1) 45. population (Ahsan et al.80-5. < LOD means less than the limit of detection. Chowdhury et al. population (Sun et al. methylation capacity.80 (.8. 2007).400-.9-23.10 (4.62) 2.00-4. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.50-6.e. interval) 1.10) 4. Caldwell et al..40) 75th 5. and duration of exposure are also considered important.

13-39.80-153) 17.15-4.4 (11.9-18.9 μg/L. 2006.400-.50-7.4-28.8) 29.58 (3. 1986.78 (3. Sun et al. 2001). 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.2 (13. 2008)..00 (3.83) 8.2 (4.68 (1.3 (10.S.80) .05 (.3) 95th 29. Fourth National Report on Human Exposure to Environmental Chemicals 185 .43) 75th 5. In recent years.82) Selected percentiles ( 95% confidence interval) 50th 1.3) 1284 1284 03-04 03-04 03-04 1.25 (.9) 14.37-2.7) 9.29 (4. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3 (10.7) 30.S.4-82. Vahter et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.11 (.53 (.16 (.25-7.6-32. 2001). WHO.64-29.30-1.32-7.29-14.786-1.14 (1.88 (5.5) 26. 1998.39-3.62-6...51) 5.. Survey years 03-04 Geometric mean (95% conf.1-18.5-20.1-36.47 (1.91) 90th 16. which is below the ACGIH BEI (Caldwell et al.4 (24.51-2.40) 1. Caldwell et al.0 (9.7) 17.91 (4.Metals as with DMA.82) 4. The 95th percentile of the U.55) 1.15-1.2 (12. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.531 (.28) 1.959-1.938-1. Offergelt et al. 2007).78-5.72) 12.81 (4.18-1. Information about the biological exposure indices is provided here for comparison. population for the sum of inorganic related species was 18.43) 14.19-2. 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.67) 4.44 (1.6 (9. 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.5 (18.83) 2. not to imply a safety level for general population exposure.88) 2. 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.30) 1..6-46.21) 5.36) 2.4) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.5 (18.877 (.76-27.65 (1.5) 17. 1992.2 (12.9 (25.40 (1.47 (2.70) 5.901-2.93 (1.05) 1. interval) 1.1 (26..61-6. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.638) 1.9) 32.54 (1.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine..1) 26.79 (1.6 (6.612-1.6-29. 2008). 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.0-36.50-15.15-1.4) 32.45) 1.3-24.833-1. population from the National Health and Nutrition Examination Survey. 2003.12) < LOD .73-6.10 (.00 (1.9 (13.4-21.6) 19.4) 292 728 1548 03-04 03-04 1.909-1.67) 1.4) 13..

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

00 (<LOD-3. * 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) 1.08 (<LOD-4. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. which may vary for some chemicals by year and by individual sample.S. see Data Analysis section) for Survey year 03-04 is 1.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. < LOD means less than the limit of detection.00 (<LOD-2. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey years 03-04 Geometric mean (95% conf.S. Fourth National Report on Human Exposure to Environmental Chemicals 187 .70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.80) < LOD 621 725 1078 Limit of detection (LOD.2.40 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. population from the National Health and Nutrition Examination Survey.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3.20 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.95 (<LOD-2. population from the National Health and Nutrition Examination Survey.44) 2.

00 (5.10) 6.00 (3.30 (7.46 (4.7 (10.12 (3.95-6.00-4.16 (2. Survey years 03-04 Geometric mean (95% conf.71 (3.71-4.31-4.00 (4.86 (2. population from the National Health and Nutrition Examination Survey.11) 4.00-15.20) 11.0 (9.0) 292 728 1548 03-04 03-04 4.88 (4.00) 5.32 (8.0) 13.6 (9.31) 4.30) 3.74) 90th 9.00) 3.0 (8.34) 3.6) 1284 1284 03-04 03-04 03-04 4.0-16.32 (4.00-7.71 (4.25 (4.65-8.0-18.0 (10.00 (6.00) 7.94) 3.0-17.80-6.00-7.27-5.00) 12.7.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.33-4.65-6.82-5.95-4.3 (8.5) 95th 13.1 (8.7) 12.14) 3.24) 3.00-22.18 (6.1-22.70-12.60-4.0-12.61-16.0) 95th 16.42) 3.86-21.0 (11.98) 4.48 (3.60-7.0 (12.05) 5.0) 11.1-15.00 (6.38 (3. interval) 3.78 (4.84-8.70-3.59 (6.72 (4.00) 9.0 (14.00-11.S.32-10.17-6.0-17.90) 5.74 (2.0 (13.8) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 3.00-3.1-18.20-4.60-3.79 (3.0) 17.9 (7.03-6.0 (10.05) 3.80) 2.0) 16.00 (3.0) 11. see Data Analysis section) for Survey year 03-04 is 1.57-5.2) 10.0 (10.73) 6.50-5.69-6.8) 7.13-4.09 (7.92-12.00-10.10) 3.77 (3.00-4.69-3.14) Selected percentiles ( 95% confidence interval) 50th 3.03 (3.00) 6.17-4.0) 9.50-15.00 (6.91) 75th 5. interval) 3.94-3.73 (3.69 (3.67) 9.81 (5.00) 4.00 (3.7-16.67) 8.00-13.00) 6.00 (5.5 (11.90) 2.00 (5.00-4.0) 9.0 (10.27 (2.00) 75th 6.9) 5.82) 3.00-3.6) 292 728 1548 03-04 03-04 3.50 (4.00-4.00) 6.24-4.00-8.45) 8.9) 11.7) 13.0) 9.33) 3.70) 5.92) 3.34-4.19) Selected percentiles ( 95% confidence interval) 50th 3.82-9.00 (5.62) 4.55 (2.0 (13.28) 2.17 (2.84-18.27 (3.3 (7.29-4.6-18.16-11.00 (7.00-11.0) 10.80-3.80-5.90 (3.34 (3.00 (3.9) 12.0) 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 4.0-16.00) 6.08 (2.00-4.86-7.0 (9.44) 5.16 (4.0) 14.89 (3.0-19.85 (3.00-7.0) 16.00 (3.00-11.00 (7.0 (8.00) 4.06) 5.22) 4.95-3.57 (3.5) 12.00-5.0-25.45 (8.34 (3.20-12. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.7) 1284 1284 03-04 03-04 03-04 4.00-4.0 (12.00-15.0) 17.4 (7.00-12.0 (9.80 (4.69 (3.71) 3.0) 13.70-4.00-7.49) 10.52) 3.00) 3.60-6.44 (2.49-4.15) 4.05) 10.00-12. population from the National Health and Nutrition Examination Survey.37 (3.12-4.48 (2.3 (8.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .95 (4.34-4.70 (3.S.0) 621 725 1078 Limit of detection (LOD.00-15.37 (2.78) 4.00-9.45) 3.61-11.9 (11.9) 13.27-2.00 (5.97-3.39-3.11 (3. Survey years 03-04 Geometric mean (95% conf.8) 7.0) 12.00 (3.80) 7.00) 90th 11.

61-3.40-2.96-2.70-2. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.70-2. population from the National Health and Nutrition Examination Survey.16 (2.20 (1.28 (1.20-3.900-1.00-2.00-1.54) 90th 2.60) 2.63 (<LOD-1.50) 1.40-2.50 (2.90) 1.80 (2.00 (<LOD-1.79) 2.31 (1.58) 2.07 (1.61) 2.22 (1.00-4.34) 2.80) 1.30) 2.17) 2.9.00) 1.07) 2.40) 1.00 (2.00) 2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.45) 3.80 (1.10) 95th 2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.53-2.10) 2.10-3.30 (1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.18-1.07-3.30 (1.11-1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.20-1.00) 2.50-2.985) 1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00 (1.30-2.71-2.86 (2.46 (1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.35-3.00) 1.816 (<LOD-.20 (1.80 (1.77) 1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.36 (1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.85) 2.43-3.90 (1.00 (2.30-1.40 (2.70-2.36) 1.20 (1.85) 1.20 (1.60 (1.10 (1.80-2.57) 95th 2.33 (1.853-1.28 (1.93) .73-2.20) 2.37 (1.18-1.90 (2.70-2.62) 2.82-2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.80 (1.88 (1.81) 1.30 (1. see Data Analysis section) for Survey year 03-04 is 0.50) 621 725 1077 Limit of detection (LOD.30) 1.70) 2.40 (1.80) 1.15-1.70-3.40-3.60 (2.05-1.31-3.10 (1. Survey years 03-04 Geometric mean (95% conf.52 (2.10 (.S.60) 2.30) 1.88-2.40-3.00-1.50 (1.90) 2.82-2.84-3.S.60-2.20 (1.86) 3.30-1.30) 90th 1.23) 1.80-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .90) 2.40) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) 2.10 (<LOD-1.00-2.33 (1.20 (1.60) 1. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.53 (1.10-1.00 (<LOD-1.50 (<LOD-1.88 (1.86) 2.86 (2.30 (2.14-1.50 (1.80 (1.10 (.46-2.22) 3.10-1.

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

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50 (1.20 (1.25 (1.46-1.1) 9.90) 2.50 (4.38 (1.50 (1.00) 4.90-13.11 (2. fireworks.38) 2. 2001).76 (3.74-3.07 (2. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).76) 1.65) 1. and 0.81-3.53) 1. glass.35-1.39 (1.14-1.73) 3.03 (1.38 (1.87-9.39) 1.10 (4.57) 3. 7440-39-3 Medically.52 (1.48) 1.93 (4.50 (4. such as brazil nuts. barium sulfate and barium carbonate).20-1. Some barium salts are freely soluble in water.36 (1.40 (1.30-2.12 (2.71) 95th 6.80 (1.60 (2.45 (1.95-6.76-3.50-1.32-1.15 (1.43 (5.69 (1.54) 1.48-4.12.50) 4.70 (5.70 (1.22-1.81-2.43) 2.09 (2.43 (1.74-2.11 (3.20) 2.20-1.00 (2.35-4.8) 5.64-3.50) 2.34) 2.4) 6.11-1.50) 2.05-2.90) 1.20-8.27 (1.35 (3.54) 2. water.57-7.47) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80 (5.46) 1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.72) 75th 3.54 (2.61 (1. and food. interval) 1.70-3.56 (1.71) 1.98) 1.17-1.10-5.80 (1.70) 1.80) 7.20-8.12.50-6.64 (1.31.06-1.18-1.50 (1.51) 2.37-1.12) 6.80-2.36-1.82) 2.37) 1.55-3.40-13.00-3.15-11.49-9.32-7. rubber.70) 4.38) 8.50-1.87-7.50 (1.90 (1.2) 6. Barium salts have also been available as rodenticides. such as barium chloride.39-1.10) 1083 1335 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.50 (3.90 (4.67) 6.11 (3.18) 3.S.00-8.77-3.30) 3.34 (2.00-76.8 (6.71-9.16 (1.00) 1.85) 1.90 (6.37) 5.30 (5. soluble forms of barium.80-3.61 (2.20-5.31-2. tiles.47-1.80 (2.65-8.60) 4.87-3.73 (5.30) 8.05% of the earth’s crust. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.88) 1.80 (2.34 (1.76-2.63 (2.56 (1.70-6.75) 2.56 (6.00) 1.96-2.54-1.91) 6.60-10.37 (4.63) 1.08-8.60-6.39) 4.59) 3.30 (5.68 (1.28) 90th 5.21 (1. The general population can be exposed to low amounts of barium in air.88) 4.70) 5.40 (1.30) 4.8) 9. In single dose animal studies.73 (6.63 (1.30-2.70) 1.65 (5.82-6.30-1.63) Total 1.50 (2.40 (5.30) 2.49) 11.43 (1.21-2.65-5.14 (6.43) 6.42 (1.71) 2.26-1.12-1.80-7.55-7. are high in barium (Genter.31 (2.85) 1.53-5.78) 1.60 (1.57 (5.01-7.60) 3. Workers employed by industries that make or use barium compounds can be exposed to barium dust.10 (3.78-2.93-2.91 (2.30 (3.35 (2.40 (4.61-8.18 (6.62 (1. respectively.40 (1.50 (4.15 (2.27 (1.24-1.20-6.66) Selected percentiles ( 95% confidence interval) 50th 1.30 (1.93-8.44-2. In nature.70-8.19-1.51) 7.40) 7.20-8.34 (1.36 (4.86 (4.40) 3.15-1.g.60-3.14-6.90-9.61 (1.95 (4.10 (2.81-2.87) 7.37-8.49 (1.41-3.Metals Barium CAS No.73-5.99 (4.48-4.29) 5.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70-2.52 (4.72) 1.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.80 (1. and 03-04 are 0.26) 5.48) 1.80) 6.28-1.10-4.62) 1.50) 1.87 (5.35-1.50 (5.54) 1.08 (6. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.04-6.25-1.9) 5.15) 5.50 (1.94-6.19) 2.65-1.35) 5.32) 8.60-2.49) 4. and ceramics.84) 5.73) 1.00 (1.30) 5.88) 7.87-14. see Data Analysis section) for Survey years 99-00.50 (6. Certain foods.01 (4. Fourth National Report on Human Exposure to Environmental Chemicals 193 .75-3.20-1.66 (4.80) 1.15-1.09 (1. bricks. 0.76-7.4) 9.22-1.54 (6.63 (8.21-8.30-1.90) 4.25-11.26) 2.54-1.10) 5.74) 3.49) 8.41-1.33 (1. Barium compounds are used by the oil and gas industries to make drilling muds.24 (4.77) 1.63 (5.92) 2. Barium compounds are also used commercially in paint.56) 4.86 (4..36) 5.56) 1.21 (1.60) 1.49-1.29-5.47-1.30) 5.26-7.44 (1.88 (5.45) 7.64) 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 2.30) 5.29-1.30-5.16) 5.49) 2.30 (2.91) 2.87 (6.06-2.70) 7.82) 1.77 (3.20 (4.36-1.15 (6.40 (5.02 (7.20-1.40 (5.90) 2.59-11.12 (2.39 (1.86-4.62) 1.35 (1.78-3.56 (2.70) 3.86-5.90-2.10) 3.40) 7.70-5.24-1.78) 1. whereas others are practically insoluble (e. population from the National Health and Nutrition Examination Survey.51 (1.46) 1.71 (2.63) 1.60-6.72) 4.61 (3.27) 2.41) 1. depilatories.99-5.53) 2.44-5. it combines with other chemicals such as sulfur or carbon and oxygen. Small amounts of barium can be released into the air during mining and other industrial processes.00) 6.12) 7.22) 6.62 (1.65) 1.54-8.85 (2. 01-02.4) 7.61 (5.60) 1.70-2.51) 1.65) 3.97 (1.04-2.20 (3.80-5.48 (6.30-3.86) 6.50-6.

55-5. weakness.57-10.39-1.60) 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 2.04 (2.59 (1. hypertension.16-1.26-1.38 (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.03) 3.96) 7.03-1.61 (4.0) 7. population from the National Health and Nutrition Examination Survey. interval) 1.29 (1.31) 5.52) 1.40 (1.91 (3.2 (3.22-4.60 (5..64 (1.61) 2.963 (.51 (3.27-1.64 (1.97) 1.38 (1.54) 1.74 (5.09) 6.10-2.20-1.00-1.59 (1.49 (1.20 (1..55 (1.53 (2.64 (1.77-5. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.44 (1.99 (4.64) 7.10-1.99 (2.74) 1.38-5.42) 1.55 (4.04) 1. and route of exposure.52) 2.33-4.777-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.58 (4.85-5.18 (1.22-1.27) 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 .36-2.45 (1.51) 4.03) 2.703-1.59) 1.56 (1.77) 1.51 (1.33) 1.20-8.710-1. Toxicity from soluble barium salts is rare.39) 4.72) 6.60 (2.891 (. vomiting.10) 3.51 (1.8) 4.47) 1.39-5.88 (6.36-1.86 (2.47 (5.26) 4.36 (5.04) 5.50) 2.42 (4.77) 1.08-2.40-1.00) 6.59-7.27 (2.00) 4.96 (4.29-4.13-3.68) 3.37 (1.31-1.50) 1.81-6.45) 95th 6.18 (1.33 (1.77) Total 1.96) 4.68-3.86-7.54 (2.30) 2.39 (2.29-4.24-1.38) 1.97 (4.62 (4.97-4.59) 2.2) 6.02) 4.36 (1.25 (1.56 (1.16 (1.32) 2.34) 1.19-1.27) 7.37 (1.14-2.78 (2.41) 5.55) .23-2.00) 1.68 (2.58) 1.06) .48 (1.34-1.76-3.29-3.34-3. Symptoms following acute high dose include perioral paresthesias. Barium is not rated for human carcinogenicity.33 (1.02 (3.40 (1.90-2.24-1.57-7.38-1.28-1.75) 2.36 (3.08-1.28) 5.69-9.57-5.37-1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.81-7.06) 2.62) 2.53) . diarrhea.92) 2.62 (2. are not absorbed when administered.15-4.39-1.80-6.76) 2.24) 3.68) 1.20-2.48 (1.92 (4.63) 1.70) 4.56) 4.32 (1.38) 1.56) Selected percentiles ( 95% confidence interval) 50th 1.89 (2.47-8.63-4.43-6.16) 11.79-5.02) .25) 4.38 (4. NTP.82) 1.45 (3.24-6.75) 1.82) 1.01) 1.35-1.754-1.70) 10.24-11.77) 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 1.97 (5.42) 1.55-6.84 (3.00) 4.84) 2.60 (1.80) 3.3) 6.915 (.60 (1.49-1.41 (1.48) 2. 1984.65 (2.4 (5.31 (1.50 (4.48-5. water solubility.19-1.00-7.52 (3.45) 1.39 (3. 1986).29) 1.58-6.880-1.97-3.22-1.84-2.32) 2.69 (5.29-1.83) 3.51) 4.96) 4.Metals was eliminated primarily in feces and to a lesser extent.23-5.32 (2.55 (1.3 (6.28-11.73-4.31 (4.48-3.34 (1.02-5. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.30 (1.29-7.36-1..91-2.24 (5.21 (1.45-1. 1985.76) 1.74) 1.23-1.46) 2.35-3. 2001).49-1.43) 1.25-11.58 (2. Insoluble barium salts.72 (2. Wones et al.39 (2.40 (1.01 (4.03-1.80) 4.28-6.49 (1.S.67-6.68 (3.37) 2.75) 2. Following intravenous injection in animals.56-3.33 (5.44-2.87) 1.73) 2. such as those used in medical radiographic procedures.0) 5.98 (2.83) 2. 1994.45-1.76 (3.28 (1.921 (.70) 1.41 (2.99) 1.44-2.39-10.55 (5.33-1.47) 4.31-1.57) 2.84-5.46-22.26-4.47) 10.03) 1.50) 1.00 (2.33) 6.51-3.905 (. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.96-6.4) 5. Chronic high doses in animals resulted in kidney damage (McCauley et al.51) 6.58) 4.73-2.31-1. 1990).0) 6.46 (2.00 (5.48 (1. chemical form.29 (3.37-2.75-3.64 (1.46) 1.79) 1.00 (3.54) 2.88 (2.91 (3.32 (1.47 (2.24-3.35-1.68-3. Perry et al.26-1. paralysis.38 (4. 1989).72) 4. and cardiac dysrhythmias.19-2. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.71 (5.26-1.26-1.38) 4.49-1.12) 2.39 (2.57 (6.2) 5.52) 7.96) 4.53-21.10) 6.11) .34-5. a benign condition that may occur among barite ore miners.36 (3.68 (3.77) 1.89) 90th 4.13-2.65 (5.91) 2.76 (2.881 (.36 (1.19-1.52-4.52-10.01 (5.24 (3.66 (1.45-8.00 (3.86) 5.48-1.62 (1.76 (4.46) 3. in urine.30 (1.54 (1.41) 4.47) 1. The health effects of exposure to barium compounds depend on the dose.22-2.64) 7.38-7.58) 75th 2.41 (1.60 (2.45-6.81-6.20) 4.11-2.24-6.59) 1.10 (6.832-1.75) 1.96 (4.75-22.27-3.76) 2.28-7.11) .05-1.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.

References Brenniman GR.. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). 1989. Ting BG. Available at URL: http://ntp. Trace element reference values in tissues from inhabitants of the European community I. Powell C. 1984. Genter MB. Exposure to soluble barium compounds: an interventional study in arc welders. A study of 46 elements in urine. Inc. Vouk VB. Pirkle JL. barium. PS.cdc. Apostoli P. In Friberg L. Epidemiological study of barium in Illinois drinking water supplies.. In: Calabrese EJ. and radium In: Bingham A. Princeton NJ: Princeton Scientific Publications. Pietra R. Kopp SJ. Nordberg GF.html. EPA. Wones RG. Comparison of representative ranges based on U. Weltle D. p. Reeves AL. Zschiesche W.. Schaller KH.S. calcium. 4/8/09 Paschal DC. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Minoia et al. Stadler BL. [online]. Environ Health Perspect 1990. Advances in modern toxicology. Trace metals in urine of United States residents: reference range concentrations. 2005... Int Arch Occup Environ Health 1992. Fourth National Report on Human Exposure to Environmental Chemicals 195 .. p. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. New York: John Wiley & Sons. 84-94. Laurie RD. Biomonitoring Information Levels of urinary barium reflect recent exposure. Princeton (NJ): Princeton Scientific Publications. the welders had no obvious adverse clinical effects (Zschiesche et al. environmental levels) and health effects is available from ATSDR at: http://www. Gallorini M.e. Environ Res 1998. et al. Vol 2: Specific Metals.gov:8080/cs. Howerton K.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en.76(1):53-59. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report.. 221-252 Komaromy-Hiller G. 2nd Ed.. 1986.95:89-105. Third National Report on Human Exposure to Environmental Chemicals. Magnesium. Minoia C.85:355-359. Lack of effect of drinking water barium on cardiovascular risk factor. LA. pp. 2001-2002. ed.atsdr. 1994. Barium. Morrow JC..28(3):373-388.niehs. J Toxicol Environ Health.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA.html?charset=iso-88591&url=http%3A//ntp. Douglas BH. ed. Calabrese EJ. 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. eds.S. Frohman. New York: Elsevier. et al. patient population and literature reference intervals for urinary trace elements. National Toxicology Program (NTP). blood. p. Sabbioni E. and a drinking water standard has been established by U.niehs. 1998). and 2003-2004 (CDC. Patty’s toxicology. Sci Total Environ 1990. Handbook on the Toxicology of Metals. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. Information about external exposure (i. 1992).197210. and serum of Italian subjects. Centers for Disease Control and Prevention (CDC).296(1-2):71-90. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Jackson RJ.nih.gov/ntp/htdocs/LT_rpts/tr432. Levy. Perry EF. Pozzoli L. Atlanta (GA). 231-249. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. Perry HM. 2000) to levels in NHANES 1999-2000 and 2001-2002.gov/toxpro2. Sampson EJ.64(1):13-23. Costa R. 1990. et al. et al. In: Inorganics in drinking water and cardiovascular disease. eds. McCauley PT. NTP.nih. 5th ed. Cohressen B. 1985. Clin Chim Acta 2000. Ash KO. 2005. Jr. 2001. Paschal et al. Investigations into the effect of drinking water barium on rats. strontium. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no.

respectively. 7440-41-7 General Information Pure beryllium is a hard gray metal. 0. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 01-02. and can be found in mineral rocks. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. electrical. and machine-parts industries. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. and 03-04 are 0. the lightest of all metals.13. < LOD means less than the limit of detection. In studies of laboratory animals.150) < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . beryllium is used in instruments. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . bertrandite and beryl. coal.Metals Beryllium CAS No. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. In medicine. Beryllium compounds are commercially mined. which may vary for some chemicals by year and by individual sample. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. or drinking water containing the metal. Two types of minerals. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. aircraft. and 0. near some hazardous waste sites. eating food. Low-level beryllium exposure in the general population can occur through breathing air.130 (<LOD-. and refined beryllium is used in mirrors and special metal alloys for the automobile. x-ray machines.140 (<LOD-.S. Exposure to beryllium occurs mostly in the workplace. see Data Analysis section) for Survey years 99-00. soil. are mined for commercial recovery of beryllium.13. and volcanic dust.130 (<LOD-. nuclear. and dental bridges. 196 Fourth National Report on Human Exposure to Environmental Chemicals . computer.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 .13. population from the National Health and Nutrition Examination Survey. and from breathing tobacco smoke.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure.S. Costa R. References Apostoli P. blood.. Hamilton EI. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i.23:827-839. Schaller KH. Available at URL: http://www. In other studies.157:388-398.. Levels of beryllium in urine for the U.74:162-166. Maier L. Minoia et al. Pirkle JL.S. Atlanta (GA) 2005. 1990.Metals (i. it is likely that urinary beryllium levels in the U. 1998). Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Ting BG.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller.gov/toxpro2. McCanlies EC. environmental levels) and health effects is available from ATSDR at: http://www.. Comparison of representative ranges based on U. Sampson EJ.html. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Van der Venne MT. 0. Clin Chest Med 2002. less than 0. et al.95:89-105. Pietra R.atsdr. et al. Given these results. Pozzoli L. A study of 46 elements in urine. and the fact that most NHANES participant levels were undetectable. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al.12 to 0. Trace metals in urine of United States residents: reference range concentrations. Int Arch Occup Environ Health 2001. Minoia C. Paschal et al. Centers for Disease Control and Prevention (CDC). 106. Gallorini M.htm. Element reference values in tissues from inhabitants of the European community. Andrew M.296(1-2):71-90. Trace element reference values in tissues from inhabitants of the European community I. Hamilton et al.1 μg/L).inchem.158:165-190.13 μg/L. patient population and literature reference intervals for urinary trace elements. Environmental Health Criteria. Ash KO. 2001). Weston A.. and the 95th percentile for males in NHANES 2001-2002.. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Sci Total Environ 1990. 198 Fourth National Report on Human Exposure to Environmental Chemicals . 3/27/08 Komaromy-Hiller G. 20012002. International Programme on Chemical Safety (IPCS). Kriess K. Howerton K. and 2003-2004. Apostoli P. Sci Total Environ 1994. Review of elements in blood.e.cdc. VI. Environ Res 1998. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Morrow JC. Genetic and exposure risks for chronic beryllium disease.e. population were generally undetectable in NHANES 1999-2000. Jackson RJ. Sabbioni E. Am J Epidemiol 2003. Third National Report on Human Exposure to Environmental Chemicals. Clin Chim Acta 2000. 1990. 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.76(1):53-59. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. 2000. population are lower than levels in workers. Beryllium [online]. Sabbioni E. which approximate this Report’s limit of detection. Paschal DC. They reported urinary beryllium levels ranging from 0.org/documents/ehc/ehc/ ehc106. HLA-DPB1 and chronic beryllium disease: a HuGE review.S. and serum of Italian subjects.

500-.30-1.300) 1.283 (.300) .400 (.300 (<LOD-.300) . Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil. population from the National Health and Nutrition Examination Survey.300 (.300 (.900 (.300 (<LOD-.255) .40 (1.20-1.70) 1.296-.500) .400) .10) 1.427) * .400 (.300-. interval) .00 (1.10) 1.400-.3.60 (1.400) .441) * .40) 1.40) 1.20) 1.00 (.300 (<LOD-.10 (1.60 (1.50 (1.333 (.800-1.300) .500) .900-1.200-.700-1.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .S.500 (.300) .800) .300) .500) .300 (.30) 1.500-.50-1.400) .60 (1.300 (.00 (.398) < LOD < LOD < LOD < LOD < LOD < LOD .400-.30) .600 (.500-.424) * .395 (.600 (.20) 1.20) 1.500) .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 * * * * * * .10 (1. Cadmium also may be emitted into the air from zinc.393 (.20 (1.500-.600 (.313 (.00 (.376-.700) .80) 1.500 (.60) 1.600-.700 (.378 (.10) 1.300) .00-1.700) .500 (.400) .600 (.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 .403 (.368-.700) .300 (.600-1.70) 1. lead.300-.300) . EPA.00 (.300-.400) .600) .300-.500-.400 (.500-.300-. and 0.600) .400) .425 (.500-.80) 1. or copper smelters (U.20-1.500-.200-.30-1.900 (.10) 1.00 (.500-.600) 1.500-.S.386-.00-1.300-.30-1.800 (.200 (.00 (.400 (.20) 95th 1. malleable.10 (.900-1. and 03-04 are 0.60 (1.20-1.10 (1.500) .460) .331) .300 (.00-1. U.400 (.700) .400) .60) 1.00-1.400 (.400-.200) .900-1.50) 1.468 (.500 (.300) .600) 90th 1.200-.700) .513) .500-.700) .900-1.50 (1.500-.30 (1.600 (.600) .900-1.400) .500 (. and incineration of municipal waste materials. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (. and nonferrous alloys.700) .40 (1.600 (.326 (.50) 1.20) 1.359-.300 (.400-.366) * * .400) < LOD . 01-02.400 (.40 (1.10) 1.10 (1.400 (.usgs.300-.400-.00 (.700) 1.400 (.600) .600 (.309-.50 (1.00 (.700-1.40 (1.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400) < LOD .300) .400 (.30) 1.300 (.800) .452) .300-.800-1. 7440-43-9 General Information Cadmium is a soft.300 (.600) .470) * .600 (.900-1.500-.10) 1.00 (1.300-.600) .10 (1.300-.304 (.200-.275-. see Data Analysis section) for Survey years 99-00.400) .500 (.300-.10) 1.412 (.600 (.500) .20) . cadmium use has declined in response to environmental concerns (http:// minerals.400-.400) < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.800 (.50-1.266-.600) .300-.300) .00) .400 (.300) .420 (.300 (.900-1.50 (1.20-1.20) 1. 0.300 (.900-1.400) .300-.400) .30) 1.00 (.300-.14.20) 1.S.60 (1.400-.900-1.200 (<LOD-.400-.00) .20) 1.10 (1.382 (.80 (1.400 (.20-1.400 (.400) .337) .600 (.600) .600-.60-1.700) .40-1.300-.70) 1.300-.300-.00-1.289-.10) 1.362-.00-1.300) 75th .60) 1.400-.00-1.20-1.300-. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.00-1.30-1.40-1.gov/minerals/pubs/commodity/cadmium).200 (.400) .3.200-.449) Selected percentiles ( 95% confidence interval) 50th .367-.344) . < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 199 .500-.300) . Other uses include pigment production. Since 2001.600 (.200 (<LOD-.235 (.800) 1.50-1.500 (. coatings and plating.40 (1.600 (.300 (.300-.400 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.500 (.300-.20) 1.400) < LOD .00 (.20-1.400 (. The predominant commercial use of cadmium is in battery manufacturing. as zinc sulfide) and to a lesser extent.400 (.500) .216-.300 (.40 (1.50) 1.300) . plastic stabilizers.403) .00-1.421 (.400-.500-.Metals Cadmium CAS No.50-1.30-1.600-.200 (.600 (.500-.70) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.400 (.500-.300 (<LOD-.361-.378-.300-.900-1.200) .300-.300 (. during refining of lead and copper from sulfide ore.90) 1. respectively.500 (.10 (1.400) .426-.700-1.304-.500-.400-.304 (.600 (.40 (1.60) Total * .20) .600) .

249) .295) . Renal tubular and glomerular damage.211 (.412) .02-1.43) 1. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.960 (.817 (.148-.165-..170 (.580) .15) 1.284) .20 (1.260 (.479) .481) . The kidney is a critical target and shows the earliest sign of cadmium toxicity.260-.198) .551 (.148) .210 (. 0.272-.229) .135 (.09-1.285-.239 (.22 (1.539) . Inhalation of cigarette smoke is a predominant source of exposure in smokers.281 (.189-. 1999.061 (<LOD-.892 (.892-1.940-1.077 (.15 (.151-.184-.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .078 (.843-1.990) .329 (.199 (.388-.452 (. population from the National Health and Nutrition Examination Survey.134) . a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.500) 90th .157-.167-.178-.34) 1.15) .800 (.189-.07-1.193 (.38) .476-.362) .219 (.890-1.700-.101) .886) . and various seeds.193-.04 (.219 (.20 (1.214-. 01-02.261-.717-.202-.390 (.160) . rice.366-.430) .170-.01 (.249-.255) .836-1. zinc.Metals 2000).17 (.38) .530 (.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 .339) .289-.30-1.810-1.232) . Cadmium in soil is absorbed by plants.308) .270 (..366-.848 (. 1994). an inducible metal binding protein.860) 1. Horiguchi et al.112-.713) .190-.10 (1.220) .980) .680 (.273 (.310 (.080 (. see Data Analysis section) for Survey years 99-00.060-. Diamond et al.394-.36) 1.20-1.299) .25 (1.290-.06.445 (.210 (.326) . 2003).490) 1.500) .196-.52 (1.257) . The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.265 (.510-.480) .03) .813 (.519) .201 (.226) .886-1.157) .730-.57) 1.714-1.243-.177-.366) ..06.507) .41 (.190-. With chronic exposure.980-1.13 (.203 (.135-.74) 1.700-.220-. and 03-04 are 0.20 (1.247) .114-.400-.980 (.175 (. and 0.204 (.492 (.173) .06) .32 (1.360) .160 (. To a lesser extent.790 (.S. Cadmium is absorbed via inhalation and ingestion.440 (.238) .989-1.241) .545 (.160) .160-.48 (1.067-.455 (.210 (. interval) .077 (.100-.450 (.171-.530) .733-. copper) and protein.280 (.265) .12-1.01-1.972 (.623) .061-.17 (.313) .19) 1.870) .220-. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.820-1.38) 1.200-.233) .192-.107-. calcium.210) .300 (.686-.633-1.283 (.540) .482) .183-.090) .120 (.229) .490) .610) .327 (.234 (.179-.202 (.875) .390-. potatoes.109 (.351-.400-.72) 1.17) .260-.207-.263) .700-.475 (.110-.01) .175 (.191-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.150) .277 (.372) .253-.550 (.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 .189) .220 (.918-1..733) .12 (. drinking water is a source for cadmium intake.817 (.551) .246) .445 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.216 (.748-1.219 (.310) .221 (.855-1.067-.279 (.251) .82) 1.28-1.316 (.22 (. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.121 (.890 (.520-.237-.230) .426 (.130 (.232 (.210 (.839 (.423-. including many food crops such as cereal grains.462 (.510) .262) .430-.208-.191 (.980-1.790 (.231) . respectively.440 (.466 (.233) .450 (..235) .607) .83) 1. Kikuchi et al.092 (.28 (1.381-.115-.493-.875 (.858 (.065-. however.081) .210) .330-.596) .06.227 (.387) .240) .763-.436-.13-1. 2004a.04 (.136) .13) .240-.820) 1.440-.753-.306 (.470-.20) 1.433-.210 (.187 (. For nonsmokers who are not exposed to cadmium in the workplace.200 (.766 (. ingestion through food is the largest source of exposure.128 (.589 (.559 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .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. **All results are corrected for molybdenum oxide interference in the ICP-MS method.200 (.336) .206 (.203) . 2003).919) .191-.300) .963-1. whose body burdens of cadmium can be approximately twice that of nonsmokers.229-.393-.150-.741-1.180 (.209 (.221) .087-.153-.458 (.200-.322 (.980) .350 (.705-.195-.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.818 (.960) 1.109-.447 (.320) ..51 (1.222) . wheat.519) .257-. 200 Fourth National Report on Human Exposure to Environmental Chemicals .270 (.640) . individual values vary and are affected by factors such as dietary intake of essential nutrients (iron. 2003).806) .255) .47) 1.800-.190-.633 (. Cadmium absorption may be increased with iron deficiency (Berglund et al.38) 1.140 (.170-.194-.238-.282 (.230 (.126) .261-.498-.354) .456-.169-.820 (.302 (.28) 1. 2003.255) .977) .090) .192-.181 (.211-.25) 1.06-1.24) 1.223 (.** Survey Geometric mean (95% conf.141 (.390-.206) .06-1.880) .17 (. 2001).092) .230) 75th .

.181 (.161-.441-.255-.444-.266) . 1999).16) 1.245 (.086 (.00 (. 2003.236-. However.130-.235) .183) .104) .126 (.184-.084 (.391-.767 (.204-.962) .381-.209) Selected percentiles ( 95% confidence interval) Sample 95th .666-.156-.784) .234-.813-.224 (.873 (.187-.100 (.537-.941 (.078 (.247-.253 (.722-.077-.207-.708-1.181 (.247-. 2002.308) .426-.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 .150-.270 (.136-.293-.541) .693 (.106) .382) .331 (.170 (.101) ..197-.325 (.206-.175 (.507-.690-.653) .712 (.321) .792 (.182) .282 (.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 .281) .340) .232) .219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .175 (.182) .551) .268 (. 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.433-.163) .414 (.144-.12) 1.421 (.998) .183 (.470) .449) .650-.146-.729 (. can result from high dose chronic exposure.560-.927-1.177) .335 (.850) .631) .168-.446) .210) .176 (.09 (.159 (.767) . 1999).261-.223) .176 (.182) .909-1.181-.226) 75th .687-.202 (.184-.668-.826-1. At lower environmental exposures.143-.219 (.388-.104) .950) .111-.300-.440) .222-.700 (.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .084-.364) .716) .686 (..113-.252 (.16) .387-.440) .173 (.377-.329 (.518) .296 (.906) .181) .263 (.289) .199-.159 (.274) 1.865 (.178) .201-.162 (.157-..481 (.979 (.233 (.316 (.091) .674-1.500-.280 (. 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.085-.097) .267 (.240) .281) .412 (.484 (.473 (..725-1.10) 1.225) .093 (.304-.234 (.830) .098) . 1999).740 (.283 (.178-.218) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.827) .288 (. Fourth National Report on Human Exposure to Environmental Chemicals 201 .191-.112) .232) .209) .192) .850) .818) .123-.140-.423 (.856) .123-.278) .434 (.06 (.189-.122 (. 1996.690 (.622 (.148 (.256-.783 (.667) .318 (.795) 1.769 (.147-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.487 (.931 (.727-.38) . Jarup et al.229) .171-.156 (.839) .297) .140-.063-.783) .205 (.096) .219 (.536 (.387 (.207) .719 (.147 (.137 (.227-.090 (.166 (.** Survey Geometric mean (95% conf.221-.17) .830-1.261) .917 (.191 (.02 (. interval) .00 (.538) .085 (..157-.687 (.242) .250) .174-.884) .253) .917) .718 (.198) .208-.813-1.591 (.238) .191) . 2002.336-. 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.919 (.13) .802 (.083-.239-.238-.051-.415) .143-.438-.216-.273 (.168 (.156) .490 (.067-.247-.137-.343-.304) .700) .316) .404) .07) .940-1.398-.208 (.185 (. 2004b).107) .479 (.228-.818) .07 (.607) .136-.200 (.828) .645-.199 (.194-.472) .175-.691-.690-.688-..212 (.078-.431) .516-.418) .187) .617 (.614) .438) 90th .350) .757) .414-.338 (.470) .404 (.308 (.190 (.833-1.423-.185) .779 (.678-.696-. most often a result of occupational exposure (Roels et al. population from the National Health and Nutrition Examination Survey.501 (. 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.545) .789 (.562-.263-. Horiguchi et al.158-.418-.647-.716-.876-1.929) .874-1.663 (.240) . a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.940 (.241) .267 (.432 (.234) .091 (. Noonan et al.382-.985 (.856 (..288) .476) .210 (.184) .261 (.163 (. 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.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.074-.091 (.531 (.559-.154-.220 (.826-1.168-.289) .173-.311) .05) 1.352) . Olsson et al.754) .190 (. Staessen et al.533) .806-1.292) .630-.147-.757 (.215 (.075-.211 (.170-. 2002.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate. 2000.075 (<LOD-. During the 1950’s and 1960’s.678 (.210 (...143) .288-.196 (.131-. 2004).266-.071 (.094) .491-.154 (.303) .S.08) .221 (.135) .225) .

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

Hotz P.296(1-2):71-90. Olfactory function in workers exposed to moderate airborne cadmium levels. et al. Komaromy-Hiller G. Thorax 2004. Miyamoto K. Atlanta (GA).S. Bernard A. Taylor AJ. Fayers PM.110:699-702. Environ Res 2006. Int J Hyg Environ Health 2003.24:717-724. et al. Sasaki S. Bregante G. Bo M. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Jarup L. Thayer WC. Seifert B. Miyamoto K. Furuki K. Savage-Brown A. Cadmium fume inhalation and emphysema. Occup Med 1996. Vahter M. 196:114-123. Kaus S. Kumagai N. Seiwert M. diabetes mellitus. Ash KO. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Becker K. Tsukahara T.atsdr. Serra J. 1999 [online]. Machida M. Comparison of representative ranges based on U. Greves HM. Krause C. Chiappino G.000 women in the Japanese general population: a nationwide large-scale survey. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. et al.76:186-196.102:83-89. Toffoletto F. Horiguchi H. Lancet 1999. References Akesson A. et al. Diamond GL.57:668-672. Alfven T. Vahter M. Oguma E. Ye T. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Mannino DM. 206:15-24. Lauwerys R. Hellstrom L. Toxicol Lett 2004. 102:10581066. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. et al.gov/toxprofiles/tp5. Fukui Y. Ukai H.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. Centers for Disease Control and Prevention (CDC). Sanz P.html. Environ Health Perspect 2005. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Nermell B. Lukyanova EM. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Berglund M. Nomiyama T. et al. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Ezaki T. Venables KM.13(11):1627-1631. Dekio F. Choudhury H. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Third National Report on Human Exposure to Environmental Chemicals. et al. Moriguchi J. Ikeda Y. Neurotoxicology 2003. Available at URL: http://www. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002.cdc.148(1-2):11-20. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Carlsson MD. Okamoto S. Occup Environ Med 2000. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Tsukahara T. J Toxicol Environ Health 2003.59:194-8. Mucha A. Darbyshire J. environmental. Ikeda Y. Seiwert M. Consonni D. Costa R. Zhu G. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. possibly better than b2microglobulin. Int Arch Occup Environ Health 2003. Stock AL. Uemura T.S. Gadea E. Schulz C. Furuki K. Nordberg G. Becker K. Anthropometric. Machida M. Chislovska NV. et al. Toxicol Appl Pharmacol 2004a. Davison AG. et al. Pickering CA.46:372-374. Horiguchi H. Buchet JP. Lancet 1988. Jones RL.354:1508– 1513. Fernandez MA. Nerbrand C. Elinder CG. ShkiryakNizhnyk AZ.45:43-52.205:297-308. Environ Health Perspect 2002. Lepom P. Takebayashi T.1(8587):663-667. Jin T. Persson B. Clin Chim Acta 2000. Bellerup P. Kikuchi Y. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Lidfeldt J. Fukui Y. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Friedman LS. Environ Res 2004. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. patient population and literature reference intervals for urinary trace elements. 4/8/09 Alfven T. population. J Occup Health 2003. Howerton K. Fatal chemical pneumonitis due to cadmium fumes. Moriguchi J. Wang H. Palomar M. Environ Res 2004b. iron deficiency. 2005. Int J Hyg Environ Health 2002. Comprehensive study of the effects of age.95:20–31. Jarup L. Environ Health Perspect 1994.59:497]. Mascagni P.66(Pt A):2141-2164. et al. Holguin F. Grubb A.96:353-359. Sasaki S. Akesson A. Kundiev YT. Ezaki T. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Schulz C. Kaus S. et al. Oguma E. Agency for Toxic Substances and Disease Registry (ATSDR). Lundh T. Lison D. Toxicological profile for cadmium update.

Schultz C. Ottosson H. Nakagawa H.html. J Environ Sci Health B 2004. age. et al. Nordberg M.533(12):107-120. Biological monitoring of toxic metals.gov/ttn/atw/ hlthef/cadmium. Staessen J. Okubo Y. Revised 2000 [online]. et al. Gangemi S. Zhu HD. Wang JX. et al.39:2507-2515.110:151-155. Hoet P. Arch Environ Health. Salpietro CD. Lauwerys R. Environ Res 2000. Schwenk M. Noonan CW. Wennberg M. lead. Available at URL: www. J Cardiovasc Risk 1996. New York: Plenum Press. Kuznetsova T. Nordberg GF. Mutat Res 2003. 4/8/09 Waalkes MP. 204 Fourth National Report on Human Exposure to Environmental Chemicals . lead. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Buchet JP. Kobayashi E. J Perinat Med 2002. Lijnen P. Zhao YC. Toyama. Tawara K. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China.100:330-338. Thijs L. United States Environmental Protection Agency (U. Tanebe K. Emelianov D.59:394-397. Friberg L. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Lison D. Nogawa K. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. Sager PR. Kathman SJ. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Vangronsveld J.353:1140-1144. forearm bone density. 2000. Roels HA.21(3-4):251-262. In: Clarkson TW. Usefulness of biomarkers of exposure to inorganic mercury. Suwazono Y. Zhang YL. Olsson IM.30(5):395-399. lead. Kido T.epa. 2004. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. pp. dietary intake. Stegmayr B. Occup Environ Med 2002. Honda R. et al. Japan.3:26-41. Lundh T. Cadmium carcinogenesis. Skerfving S. Sarasua SM. Saito S. Environ Res 2006. Campagna D. Staessen JA.Metals Nishijo M. Ren Fail 1999. eds.84 (Section A):4455. and former smoking – association of renal effects. 151-168. Liu QF. Nishijo M. Merlino MV. Int J Hyg Environ Health 2006. cadmium. Environ Health Perspect 2002. EPA). or cadmium in controlling occupational and environmental risks of nephrotoxicity. et al. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. Roels HA. Revised and new reference values for arsenic. Bruiglia S. Environmental exposure to cadmium. Mueller PW. Nordberg GF. Lancet 1999. Jansson J-H. Honda R. Time trends in burdens of cadmium. Tanebe K. 2001. and risk of fractures: prospective population study. created 1992. iron status.209:301305. et al. Lybarger JA. Bergdahl IA. Relationship between newborn size and mother’s blood cadmium levels. Minciullo PL. Bensryd I.59(1):22-25. Hazard Summary. Biological monitoring of cadmium. Roels H. Nakagawa H. Wilhelm M. Cadmium compounds. and mercury in the population of northern Sweden. Ginucchio G. Environ Health Perspect 2002. Cadmium in blood and urine – impact of sex. Lundh T. Stelitano A.110:1185-1190.S. Nakagawa H. Oskarsson A. Gallmans G. Fan YG.

4) 9. cesium hydroxide is corrosive and irritating at high concentrations.30) 7.99-6. and 03-04 are 0. and 0.04 (4.81-14.97) 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 4.81) 9.94-4. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.87 (4.05) 5.84 (4.4 (10.09) 5.8) 9.91-8.26) 7.82) 5.87 (4. semiconductors.70) 7.71 (4.86-12.42) 6.81) 4.47-4.6 (9.95-4.3-13.59-5.45-8.07-11.90-12.10-8. Little is known about the health effects of this metal.7 (9.1) 9.40-5.74-5.50 (4.68) 9.2 (9.33 (6.17 (6.90) 9.80-10.24) 4. scintillation counters.37) 5.6 (11.49 (4.57-5.9 (10.64) 5.13 (7.80 (8.1 (11.14.8) 11.0) 12.25-5.00-9.6 (9. photographic emulsions. diarrhea.34 (4.0) 12.3 (8.73-11.0) 10.61-6.99) 9.60-6. 2004). and clay. nausea.21 (4.70 (5.03 (4.6 (9.90) 4.3) 9.36 (6. Whether cesium compounds are carcinogenic is unknown.2) 12.35 (4.93 (4.70-8.04) 7.80-10. soil.98 (7.83-4.87 (4. Radioactive 137Cs has been used medically to treat cancer.26) 4.36 (3.23-4.80 (4.63) 6.20) 7.6) 10.07) 4.2 (9.5-16.4) 10.40) 5.10 (8.83) 6.08 (6.40) 7.7 (9.40-5.9 (11.39) 7.80 (4.64 (4.20-8.29 (4.39-4.00-4.13 (8.00-10. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.66 (7.70 (6.70 (8.12 (4.2-13.4 (9.84) 8. infrared lamps.50 (7.5) 9.50 (4.32-5.7) 10.8-13.0-15.71-8. and high-power gas-ion devices.60) 5.9 (11. For absorbed cesium salts.00 (7.00) 4.4) 10.54-11.64) 5.88 (8.97 (7.70) 5.72-7.1 (10.40) 5.1-12.60-7.7 (10.70-5.70) 5.53 (6. see Data Analysis section) for Survey years 99-00.5) 12. Most human exposure to cesium occurs through the diet.97) 4.35-5.1) 10.60 (7.8) 11.9 (11.81) 4. population from the National Health and Nutrition Examination Survey.20-7.89) 4.71) 4.0) 11. 0.0 (9.4 (9.2-14.70 (6.01-8.47-8.8 (11.2-13.50) 9.03 (4.77-8.08-5.61) 7.42) 7.2-13.63 (4.23) 9.54) 4.64-10.4-13.50 (4.53-11.34) 9.32 (3.17) 4.5-14.4) 12.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4.94) 4.1) 9. and cardiac arrhythmia (ATSDR.17-6. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.40 (4.5 (10.84-9. the body half-life is estimated to be 70-109 days based on 137Cs exposures.26 (3.52-9.62 (5.05-5.14.43 (5.90-10.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.22 (4. Fourth National Report on Human Exposure to Environmental Chemicals 205 .90-10.59) 7. However.4) 12.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3) 10.10-7.99-11.89-5.67 (4.98 (7.44 (8.2.8 (10.80-6.80 (4.16-6.56 (4.12-5.33 (5.26-11.7-14.01) 7.82-4.92-13.29) 4.56-11.40-5.2) 11.14 (4.90 (6.90) 5.20) 8.43-8.72) 4.84) 5.59-5.15-8.60-7.3-13.03-4.S.0-13.40-11.9) 8.3) 12.50 (6.45-5.55 (7.27 (7.9) 12.00-8.16-6.20 (6. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.64-5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.99) 7.30-10.0) 9.40-11.76-6.30-5.77 (9.3 (8.32) 4.Metals Cesium CAS No.9 (11.10 (6.7 (10.13-8.1) 11.02 (4.12) 5.5-13.74 (4.87-7.5) 10.60) 7.80-10.7) 11.30 (6.36) 3.25) 4.50-7.80 (8.3) 10.90-10.05-5.08) 7.97-7.27-5. although cesium was generally of low toxicity when given to animals.94 (4.63-4.8) 12.94 (4.40-7.84-5.1-13.89) 5.7) 10.95 (3.35 (4.20-5.42-7.56 (4.8) 12.33-5.20) 5.80) 7.21) 90th 9.7) 11.38) 5.64) 4.73-5.60-6. 01-02.09-5.80-11.77 (4.90-8.10-5.68 (7.71-9.49) 4.90 (4.8) 12.22-4.2-12.00) 6.86 (7.7 (8.10-9.9 (10.0) 11.9) Total 4.00) 7.90) 5.71 (8.70 (4.7 (9.00-8.7 (11.10 (6.5-14.79 (4.8) 9.87) 5.59 (5.96 (6.20 (4.50) 5.08-5.80-13. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.1-12.70 (8.27) 4.7 (10.4) 11.3) 10.40-5.31-8.8 (10.3) 10.49 (5.13 (5.01-6. interval) 4.59-5.12-11.25 (3.77 (9.6 (9.86-11.1) 11.30 (6.99-11.5 (8. and as polymerization catalysts.46) 7.60 (8.62) 4.80 (8.30) 5.1 (9.60) 7.74) Selected percentiles ( 95% confidence interval) 50th 4.6 (11.9) 11.4) 95th 11.91 (7.81 (4.10 (8.90) 7.70 (9.95) 5.69-6.52) 7.37) 7.55-11.08 (7.6) 11.71-5.90-12.56) 5.49) 75th 7.05) 5. respectively.0 (10.20) 4.62 (5.60-5.3-15.0) 12.55 (4.60-12.20-4.

05-4.35-7.95 (5.08) 4.08 (5.70) 7.20-4.85) 4.10-4.29) 4.66-6.79) 9. (2000) found urinary cesium levels that were slightly lower than those reported for the U..94 (5.60 (5.3 (9.71 (7.08-7.78 (3.99 (3.66 (6.09 (4. population from the National Health and Nutrition Examination Survey.79) 4.20-8.67) 5.77 (6.17 (6. interval) 4.43-11.30 (7.41-7.68-11.85-4.64-6.82) 7.31-6.78 (3. 1990).63-6.48-6.43 (4.84-7.9 (10.63-6.9) 10.94) 7.21-4.46-4.03-5.76-6.68) 4.17-4.99) 4.S.00 (8.27-4.70) 6.64) 5.70 (7.33 (5.5) 9.09) 8.54 (3.90-8.03-6.50 (7.41 (8. 2004).96-4.99-9.38 (3.18) 8.06 (3.43) 8.41 (5.56 (4.05-3.07-4.35 (4.60-20.93-9.14) 4.15) 95th 8.38-7.21-3.39 (5.00-8. Minoia et al.83-7.95) 4.50 (6.56) 3.87 (5.0) Total 4.79-5.7) 10.20-4.57) 3.84-9.99-4.16-8.19-3.56) 4.99-9.44) 3.20-4.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .47) 6.8) 10.35) 3.55-5.31-4.00-4.88-10.98) 5.96) 4. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.10) 7.00) 6.58 (6.55) 4.33-8.42 (4.48) 90th 7.63) 6.8 (9.84-11.02 (5.63 (7.68) 6.14) 4.18-6.53) 6.27 (8.98) 5.43 (8.43-6.03) 5.38-12.05) 3.S.91) 5.91 (5.66 (5.30) 10.16) 5.34 (5.75-11.65 (6.21-5.10 (3.2 (8.33-3.71) 6.74) 75th 5. Komaromy-Hiller et al.29-3.72-5.5 (9.67 (6.60-10.08-3.42 (5.83-6.07 (5.41 (4.74 (5.54 (5.96 (4.64) 9.25) 4.46) 6.81 (4.42-4.73 (3.65-3.49) 3.81 (4.40) 6.04) 5.1) 11.64) 4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.41) 4.14 (6.77 (4.25) Selected percentiles ( 95% confidence interval) 50th 4.61-3.0 (7. Using clinically submitted specimens.63 (4.58 (4.05) 6.84-9..47) 7.10 (5.45-6.42-6.87) 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 5.29) 4.20) 5.98 (6.54 (4.44 (8.98 (7.93-7.24-4.51 (3.74 (4.21 (2.14-4.56) 4.82-4.90-3.95-6.95) 10.56-10.39) 8.15-4.23 (7.37-3.3) 11.04-11.8) 6.8) 5.48) 7.38) 10.31 (4.05 (4.96) 4.68) 3.26 (4.78) 4.26 (3.19-6.79 (5.13) 7.29-3.31 (4.77-5.59-8.85) 5.73-4.95) 8.67 (5.6) 6.36-6.06 (5.9 (9.50 (5.91-6.09) 4.92 (5.06) 5.97-5.40-5.51) 4.5) 9.75 (7.46-8.17) 9.59) 4. population results shown in this Report (Alimonti et al.30-4.64 (4.46 (8.11 (5.15 (7.12 (3.12-6.88-4.0) 7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.58) 8.13-9.95-12.24-10.75 (6.08 (6.30 (3.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.47 (4.77 (7.27 (6.27) 4.00-9.51 (4.14-6.78) 4.13-9.7) 10.08 (3.38 (3.6 (9. Biomonitoring studies on levels of cesium can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cesium than are found in the general population.50-5.62-8.42-4.00-10.50) 4.46 (7.22) 6..28) 7.39) 5.74) 3.04-5.16-5.58) 3.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.30) 10.12) 3.40) 7.07) 8.55 (3.50) 4.53 (4.87) 5.43 (4.92) 3.11 (5.90 (7.51 (7.S.4) 10.27 (6.87-4.35-11.7-12.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.96-4.72) 4.28 (5.3-15.3) 9.65-4.14-7.41) 9.64 (8.08) 3. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.53 (6.30-4.29) 5. Two small studies of European populations reported urinary cesium levels similar to U.2) 11.68 (4.03) 6.44-5.51 (3.58-5.10 (3.16-8.33 (5.36-3.74-11.86 (4.84-7.60) 3.66 (5.28) 8.97) 8.05-3.47) 6.91-7.22 (3.07) 8. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.91) 4.27-6.60 (3.47 (7.89-4.95 (3.02-4.91) 5.90-8.01-8.91 (5.52-5.35 (3. and were also roughly similar to those in this Report.83) 8.08) 4.30 (4.26-6.43 (3.6 (9.61 (7.77) 4.47) 4.76-9.06) 4.5) 7.15-11.63 (6.80) 6.04) 6.3 (10.00-5.53) 3.91-9. 2005.24 (3.79) 6.28 (4.00-5.36-10.13 (3.50) 4.44 (4.72 (4.50) 8.97-4.22-11.45 (4. population.44-9.37) 4.51 (4.62) 5.41-4.18-7.18 (7.54 (4.17) 4.3 (8.2 (8.

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

03 (.740-.450) .370-.375 (. seawater.377-.470) .450) .06 (.28-2.680) .47 (1.414) .431) .600-.700) .410-.12) 1.04-1. steel-belted radial tires.460 (.850) 1.398) .427-.08.620-.410 (.520) .03) 1.373-.07.350-.460-.316 (.26-2.04 (.04-1.461 (.59 (1.08-1.590) .700) . and kitchenware.630 (.379 (.450-.940 (.46 (1.360-.07-1.47) 1.75 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.630 (.24 (.56) 1.430 (.543) .386) . 208 Fourth National Report on Human Exposure to Environmental Chemicals .465) .26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.374 (.05) 1.400-.890-1.355-.99) 1.380-.22-1.410 (.430) .12) 1.380 (.305-.530 (.17 (.520 (.830-1.14) . and magnetic recording media.350-.760 (.280-.740-.348-.33-1.520 (.820 (.419) Selected percentiles ( 95% confidence interval) 50th .32) 1. interval) . It is emitted into the environment from burning coal and oil and car and truck exhaust.16) 1. and soil.750 (.26) Total .42) 1.930 (.340-.515 (.45 (1.480 (.330-.540-.05 (.750-.410 (.800) .01 (.07.940-1.410) .500 (.980-1.590 (.22 (1.580 (.680 (.270-.316-.880-1.339 (.790 (.07-1.17 (1.880 (.570-.750 (. 0.359 (.581) . and inks.950) . hard metal (alloys of cobalt and tungsten carbide).540-.730) 1.570-.370 (.850) .540-. Usual human exposure is from food sources.00) .870-1.04) 1.460) .410 (.04-1.650-. industry is imported or obtained by recycling scrap metal that contains cobalt.460) .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 .870 (.800-.550) 90th .790) .03-1.48) 1.600) .440-.417) .520-.650 (.17-1.14) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .710 (.420) .23-2.680 (.380 (.660) .620-.22) 1.21) 1.890-1.331-.32-2.610) .670-.319) .900) .47) 1. see Data Analysis section) for Survey years 99-00.310 (.640) .487) .520) .570) .32 (1.950 (.520-.16) 1.334) .16 (1.480-.502) .333-.740 (.390 (.590-.610) .452 (.850-1.550 (.920-1.430-.300 (.650 (.32) 1. Cobalt is used as a drying agent in paints.24 (1.410 (.352 (. Cobalt compounds are also used in manufacturing battery electrodes.15-1.371 (. large appliances.28 (1.418 (.S.14-1.364-.336-.270-.394) .380 (.519 (.17 (1.463-.450-.540) 1.405-.390 (.810) . and fertilizers.670 (.50) 1.09 (.373) .790-.564) .03 (.620) .25-1.05 (.28 (1. It is also a component of porcelain enamel applied to steel bathroom fixtures.640) .570) .16 (.930-1.690-. shiny.343 (.590-.01 (.670 (.610 (.940-1.600 (.950-1. varnishes.290-.08) .810-.52 (1.16-1.770) .68 (1.820 (. blue-colored pigments.680) .760) .92) 1.450) .16 (1.16-1.320 (.340) .570 (.670-.327-.360-. automobile airbags.301 (.690-. Cobalt occurs naturally in airborne dust.430 (.860 (.09 (.410-.03) 1.499 (.372) .50 (1.430) . Cobalt compounds are used as catalysts in producing oil and gas.480 (.950 (.950-1.64) 1.670 (.47 (1.Metals Cobalt CAS No.840) .350-.930) . 01-02.520 (.870 (. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.810) .523) .404) .430 (.399) .308-.710) 1.390 (.388-.370) .330) .420) .48) 1.469-. The cobalt used in U.65) 1.900) .390-.19) .460 (.710) .690 (.550-.431) .800-. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.390) .890-1.333-.960-1.379 (.410) .490-.520 (.620-.03) .367 (.450) .520-.26-1.330 (.910-1. and in synthesizing polyester and other materials.470 (.259-.510) 1.09) . population from the National Health and Nutrition Examination Survey.530-.370-.369 (.53) 1.81) 1.900) .380-.428-.340-.420 (.350) 75th .60 (1.36) 1. hard metal or in combination with other elements.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 .S.67) 1.81) 1.560 (.410-.73) 1.900-1.291-.270-.26) 1.640) .294 (.285 (.580 (.28 (1. diamond-polishing wheels.435 (.490-.348-.310-.01-1.370-.750 (.37-1.500) .350 (.580 (.44) 1.530) .416) .520-.02-1.393-.980) .338-.360-.07 (.454 (.424) .13) 1.313) .398 (.820 (.660-.06 (.39) 1.20 (1.890) 95th 1.460) .890) .900-1.15 (1.583) . 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.23) .630-.06-1.32 (1.610-.540-.920) 1.01-2. and 0.496) .340) .340 (.29 (1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.33 (1. and 03-04 are 0.850-1.434 (.660) . respectively.300-.

352 (.689 (.898 (. in the feces.251-.388 (.313-.296-.821-3.36) 1.12 (.29) .50 (1. Once absorbed and distributed in the body.09) 1.435-.04-1.850-1.503-.44 (.363) .391 (.24) .911-1.786-.329 (.300) .393-.990) .328 (.434-.55) .313-.728 (.234 (.407 (.248-. A portion of cobalt retained for long periods is concentrated in the liver.554 (.400 (.421) .562) .500-.630-.23 (1.378-.662) .293 (.582-.585) ..15) 1. Cobalt is absorbed by oral and pulmonary routes.00 (.14 (.983-1.433) .554 (.560-.515 (.362-.30 (1.691 (.733-1.215-. Smith et al.609) .938-1.857-1..349) .36) 1.476-.949) .304) .248-. 2003).50) 1.468) .548 (.355) .271 (.280-.694) .310) .73) 1. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.313-.278-.952 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.463-. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.838 (.457 (.328) .563-.833-1.328 (.469-.29 (1.847) .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 .523 (.342-.361-.481) 90th .707) .57) 1.744) 1.296) .29) 1.16 (1.824 (. respectively.963-1.917) .462) .606 (.380-.339-.533 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin). Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.895-1.444 (.495 (..438) .737 (.361 (.378-.407) .861-1.626-.301) . Exposure in the workplace may come from electroplating.442-. and to a lesser extent.259-.700 (.331-.00) .294-.667-1. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.291 (.425) .632-.28) 1.756 (.634-.963) .640) .479-.760-1.12-1.673-.378 (.821 (.353 (.382-.301-.279 (..290 (.257-.381) . population from the National Health and Nutrition Examination Survey.409) .10) .297-.471-.327 (.708) .848 (.396) .964 (.679-.54) 1.461) .19) .275-.290 (.872 (.591 (.615) .408 (.543) .352) .S.243-.16 (.237-.03 (.932-1.302-.955) .257 (.278 (.647) .326-.378-.49) 1.396) . 1972).753) 1.11-1.781-1.309) .289) .281) .608 (.750) .937 (.306) 75th .449-.471 (.574-.29 (1.593) .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 .850 (.275-.298 (.83) 1.428-.10-1.479) .727 (..938) .552 (. or using diamond-polishing wheels that contain cobalt metal. cobalt is excreted predominantly in the urine.376 (.929) .534-.426 (.844 (.449) .60) 1.457-.960 (.333-.329-.25 (.387) .598 (.304-.826-1.391) Selected percentiles ( 95% confidence interval) 50th .738 (. using hard metal cutting tools.00 (.27) 1.360) .404-.353-.419) .905) .344-.990-1.343-.334) . Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.513 (.16) .392 (.368 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.346 (.358 (.394) .704-.534 (.316 (.561) .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 .306 (.274-.259 (.736-.00) .402 (.829) .17) .740-1.975 (.388 (.660-.505) .879-1.976 (.738 (.10) Total .508-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.425-.750-.417) .352 (.785) .550-.250) .439) .599) .417 (.595) .384) .27) 1.303-.Metals fabricated from cobalt alloys (Lhotka et al.297) .851 (.487-.542 (.282 (.792 (.955) .513-.513) .314 (.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 .286) .669) .279) .523 (.455 (.290 (.386 (.337) .452-.33) .361 (.333-.00 (.829-1. 1972).324) .35) .537 (.500 (.467-.317 (.335 (.268 (.10 (.547 (.319-.313 (.500-.703-.361-. 1994.33) 1.457) .348) .638-1.362 (.337 (.313-.757-1.774 (.368) .372) .471-.343 (.256-.259) .362) .529 (.239-.365-.06 (.804) 1. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH. 1979).35) 1.25 (.369 (.16 (.324-.487-.616-.60) 1.365) .562) .842) .522) .644 (.723 (.611) .00 (.581) .368) . refining or processing alloys.435 (.393 (..11-1.635 (. interval) .963) .611) .272-.830 (. 1994).700 (.777-.50) 1.630-.333 (.15 (.488) .861 (.683-.895-1.667-1.277-.792-1.282-.728) .594) .781) 95th 1.333-.983) .900-1.247 (.04 (.313-.429) 1.475 (.327-.273 (.753-.03-1. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.00-1.29 (1. an essential human nutrient.02 (.323) .963-1.600-.

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

Health Phys 1979. Am J Epidemiol 1998. Robinson C. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Kusaka Y. Edmonds CJ. Buchet JP.148:241-248. DeSantis V. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Kiilunen M.34:620-626. Fourth National Report on Human Exposure to Environmental Chemicals 211 .95:29-37. Wild P.55(4):269-276. Weyher I. Co-sensitivity between cobalt and other transition metals. Linnainmaa M.216:253-270. Lhotka C. Swennen B. Mosconi G. The release of metals from metal-onmetal surface arthroplasty of the hip. Bourne RB. Lauwerys RB. Kirsch-Volders M. Epidemiological survey of workers exposed to cobalt oxides. Int Arch Occup Environ Health 1997. et al. Lison D. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Moulin JJ. Uitti J. Sci Total Environ 1994. Goto S. Lauwerys R. Zobelein P. Steffan I. Thomassen H. Thabe H. 1985. Vitali MT.150. Unwin P. Occup Environ Med 2001. J Bone Joint Surg Br 2005. J Bone Joint Surg Br 2006. Shirakawa T.45:246-247.36:732-734. Lison D. Lisi P. Salama A. De Boeck M.157:117121. Roto P.50(9):835-842. Sanghrajka AP. Heki S. et al. Swennen B.28(5):1121-1128. Diepgen TL. Laippala P. A report of two cases from mineral assay laboratories and a review of the literature. Zhuber K. Szekeres T. Meyer zum Buschenfelde K-H. Dunning SP. Iavicoli I. Lasfargues G. Health Phys 1972.150:177-183. Schramel P. Cannon SR. Sabbioni E. Clin Orthop Relat Res 2003. Tilley S. Pisati G. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. McCalden RW. Radulescu M. Bunn HF. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Stanescu D. X. Lung cancer risk in hard-metal workers. Barnaby CF. Sci Total Environ 1998. Peltier A. Lison D. Ghat IS. and hard metal dust. et al.87(5):628-631.44:124-132. Cobalt cardiomyopathy. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up.150(1-3):167-171. Ichikawa Y. Sabbioni E. J Orthop Res 2003. Kristiansen J.204:147-160. Contact Dermatitis 2003. 3rd ed. Sabbioni E. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Int Arch Occup Environ Health. MacDonald SJ. Sci Total Environ 1997. Biological monitoring of workers exposed to cobalt metal. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Bozec C. Kato M. Am J Ind Med 2003. Meier R. Rorabeck CH. Pradhan C. Cresti R. Chest 1989. Jarvis JQ. Occup Environ Med 1994. Thakker DM. et al. Bacis M. Absorption and retention of cobalt in man by whole-body counting.88(4):443448. Angerer J.58(10):631-634. Kraus T. Respiratory health of cobalt production workers. Christensen JM. Blunn G. Dickel H.21(2):189-195. and cobalt metals. Falcone G. Romazini S.406:282-296. Ziaee H. Trace element reference values in tissues from inhabitants of the European Union. Buchet JP. Molders J. Weber A. Fujimura N. Smith T. Occupationallyinduced “isolated cobalt sensitization. White MA. Outcome of occupational asthma due to cobalt hypersensitivity. et al. 2001. oxides. Science 1988. Chess DG. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Zedda S. Mutat Res 2003. J Rheumatol 2001. a study of 13 elements in blood and urine of a United Kingdom population. J Trace Elem Med Biol 2006. Cleland D. Schaller KH. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust.48:172-173. Zweymuller K.22:359367. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group.(1-3):133-139. Kuska Y. Gross RT. Goto S. McMinn DJ. Kriss JP.69(3):193-200. Salvatori S. HoffmannB. Long-term clearance of inhaled 60Co. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Daniel J. Dunstan E. Sci Total Environ 1994. Hedge AG. Carnes WH. J Occup Med 1992.Metals effects of cobalt. Hammon E. Alessandrelli M. Oksa P.533:135-152. Boca Raton (FL): Lewis Publishers. et al. Leghissa P. Hoher T. Lauwerys R. Goldberg MA. Arch Intern Med 1990. Cobalt and antimony: genotoxicity and carcinogenicity. Schank M. Linna A. Br J Ind Med 1993. Iversen BS.51(7):447450.” Contact Dermatitis 2001. Industrial Chemical Exposure: Guidelines for Biological Monitoring.242:1412-1415. Palmroos P. Hoet P.20(1):25-31. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. salt. cobalt salts.

30-1.70 (5.95) 1.40-2.28.40 (4.10-2.70 (2.20-6.50 (1.43) 1.90-4.70-6. brass.40-6.10-2.20 (3.90-4.40) 2.60) 3.00) 1.50) 1.70) 2.50-5.30 (2.20 (1.30 (2.50 (4.62) 1. antique-molded or cast ornaments.00 (2.40-3.20) 4.30 (2.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.60 (1.80) 3.00) 5.20 (3.60) 4.40-1.80) 1.20) 3.72) Selected percentiles ( 95% confidence interval) 50th 1.30 (2.70) 4.60-1. see Data Analysis section) for Survey years 99-00.70-2.10-1.50-2.19 (1.80 (1.90) 5.20) . lead was added to gasoline and residential paints and used in soldering the seams of food cans.90) 3.90-3.20 (3.55-1.10-3.30 (2.00) 2.69 (1.10 (1. Lead has a variety of uses in manufacturing: storage batteries.50 (1.60) 2.70-1. respectively.10-2.60 (3.10-2.70) 1.80 (5.00) 2.75-1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.40) 2.30-5.40-5.10) 4.10-4. 0.90) 2.60-1.40-1.80-3.60) 1.80) 2.70-2.80 (1.80-4.30 (1. and for radiation shielding.52 (1.10) 1.60 (1. ammunition.83 (1.40 (3. metal alloys (e.25) 1.80-4.50 (1.50 (2.900 (.69) 1.90-4.80) 2.40-1.78 (1.00) 6.60-4.20) 3.800-1.36) 1.50) 5.20 (3.80 (1.00-4.00) 4.60-2.56 (1.90 (1.80-4.31) 1.40 (1.30) 5.20-1.50) 5.90 (3.70) 4.60-2.10-2.45-1.70-1.50-1.60-4.50 (2.30 (4.20-3.942 (.3.10 (1.50-5.00) 1.52-1.60) 2.51) 1.80 (2.30 (1.30) 1.90) 1.66) 1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .90-2.70-1.70 (1.60) 4.40-3.52-1.40-6.80) 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 1.10 (2. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.30) 95th 5.50) 4.60 (1.14-1.30) 2.30 (3.90-2.30-4.50-2.80 (2.00-4.62 (1.60 (1. ceramic glazes.60) 3.00) 2.50 (2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20-1. 7439-92-1 General Information Elemental lead is a soft.43 (1.00) . solders. population was aerosolized lead emitted from combustion engines that used leaded gasoline.20 (3.14-1.10 (2.55 (1.00-4.23 (1.70) 4.36-1.86) 1.60-3.900-1. population from the National Health and Nutrition Examination Survey.00 (1.20 (1.00 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.91) 1.51 (1.70-2.20) 2.37 (1.50) 1.90 (3.01 (1. blue-gray metal that occurs naturally in soils and rocks.40 (1.40-2.48) 1.60) 1.65 (1.30-2.40) 1.30 (1.00) 4.50-3.80 (5. interval) 1.40) 1.40 (2.46 (1.20) 3.87 (1.60 (3.50) 1.40) 2.80 (1.90 (3.50-1.30 (4.50 (2.10-2.40) 1.75-2. malleable.25 (1.12-1.10) 2.90 (4.40-1.20-2.00) 1.40-2.10) 2.g.30) 2.70 (2.90-6. dense.90 (2.00 (3.09) 1.00 (4.00) 2.80 (3.50) 4.50-1.37 (1.20-4.00-2.36-1.43 (1.40 (1.50-3.60) 2.3.20 (2.75 (1.10 (1.80-3.30-1.90 (2.70) 3.04-1.80) 2.40-1.50) 3.50-4.80-2.55-1.00) 1.70) 4.14-1.10-6.60) 3.80) 1.17) .10-8.60 (2.00 (1.00-6.70) 3.40-1.10 (4.90) 2.77 (1.00) 1.20 (4.70 (1.50-6.90) 3.40 (5.32-1.90) 1.50 (4.60-6.60) 3.S.70 (2.43-1.50-2.30) 2.90) 1.90-2.45 (1.75) 1.20 (1.00) 3. bronze). and 03-04 are 0.60-1.60 (3.30-1.10-1.89) 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 2.20 (3.40) 2.80-5.20) 90th 3.10-3. plastics.00-1.87) 1.50 (3.20-3. and 0.30 (4.20-3.50 (3.60) 4.60 (2.10-3.70 (3.30 (2.81) 1.60 (3.50-1.60 (1.30-6.30-1.70-3.00) 3.30 (2.20) 5.90 (3.00-1.80-3.10-6.25 (1.90-4.80 (2.40-3.20 (2.90) 2.60 (1.90) 2.30-1.S.66 (1. Lead was used in plumbing for centuries and may still be present.49-1.60) 1.20) 1.80) 1.90 (1.40-4.69) 1.70 (1.30-1.39-1.10) 3.80-3.40) 3.30-2.40) Total 1.50) 2.50 (1.30 (1.60) 2.90) 2.10) 5.00 (5.71-1.60 (4.10-4.50-4.80 (1.60) 1.10 (3. the main source of lead exposure for the general U.10) 3.60) 1.60 (2.62-1.90 (3.10) 1.00-5. such as lead phosphate and tetraethyl lead.80 (1.60 (2.80) 2.80) 1.878-1.70 (3.70 (1.90-2. In the past.50 (2.20 (1.40 (1.70) 1.60-1.946 (.40) 5.40 (2.70) 1.00 (4. Since lead has been eliminated from gasoline.34-1.60 (1.20-2.96-2.70-4.10-3.39) 1.10) 3.10 (2.69 (1.60 (2.40) 4.60) 5.20 (3.986) .Metals Lead CAS No.50) 1. leaded glass.53) 1. Elemental lead can be combined with other elements to form inorganic and organic compounds.50) 2.22 (1.60 (2.50-1.68-1.50) 7.10) 1.20 (1. 01-02.60) 4.37-1.30-2.70) 1.899-.80 (4.80 (4.60) 5.32-1. Lead is most often mined from ores or recycled from scrap metal or batteries.70) 3.93-2.70) 1.70-5.20) 3. Before the 1980’s.50) 75th 2.02) 1.900 (.43) 1.20) 4.50-2.30-2.60) 2.10-1.20-3.80) 1.

Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.80 (1.50 (1.82 (2.20) .80) 1.30 (2.820-1.07-1.40) 2.00-1.560-.752 (.S.688 (.10 (1.970-1.90-2.674) 1.00-1.660) .700 (.80) 3.80) 2.80) 2.Metals occupational (e.650) 1.790 (.90) 2.90 (2.00) .06) .50 (2.86 (1.613) .600 (.20 (3.564 (.50 (2. In the blood.700 (.90-3.19 (1.10) 2.640 (.75) 3. bullet fragments retained in human tissue. 2000).570-.50-2.800-1.30) 1.70 (1.90-2.800 (.661-.70) 1. dust.70 (2.815 (.60-1.80-3.923 (. 2007.600-.29 (2.900) .960-1.600-.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 .595-.40 (1.66 (2.80) 3.900 (.20 (1.700) .800 (.20) 1.20-1.90 (1.00 (1.20 (1.900) .03 (1.10) 2.480-.810-1.60-2.82 (1. and 0.671-.604 (.960-1.40-5.75) 4.70 (2.30-1.10-1.800) .10) 1.60 (1.580-. However.62) Total .90-2. Approximately half of the absorbed lead may be incorporated into bone.86) 1.40) 1.52-1. older plumbing systems with leaded pipes or lead soldered connections.50 (1.753 (.50-2.33-2. interval) .800) .00) .700-.848 (.70) 1.30) 1..90) 1.986) .70-2.50-3.30) 1.10-3.50) 1.30) .50-1.11 (1.90 (2.80) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 0.04-2.910-.10 (1.30) 2.00 (.86-2.700) 1.78-2.990) 2.940 (.800 (. battery and radiator manufacturing) and recreational sources.29) 2. CDC.960 (.09) 1.955-1.920 (.572-.40-1. respectively.785) .30) 1.90 (1.80 (1.00) 2.80 (2.40) 1.91) 2.900-1.78-2.07 (.40) 1.600-.03-2.30-1.50) 2.30-2.50) 2. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.00 (2.31-3.30) 2.70 (2.g.556-.637-.800 (.89) 2.70-3.17 (1.90) 2.50) 1.90-2.600) . imported children’s trinkets and toys.50 (2.900-1.70) 1.640-.691-.20 (1.11) 2.850 (.60 (1.40 (1. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.90-4.20-2.610 (..800) .22) 1.690) 75th 1.630 (. and 03-04 are 0.31 (1.70) 2.700 (.990) 1.700-1.800-1.641-.30-3.20 (2.857) .636 (.540 (.700-.40-2.10) .540-.10-1.50-2.80-2.10 (.695 (.708-.20) 1.40 (2. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.900) .628) 1.72) 1.40) 3.33 (2. population from the National Health and Nutrition Examination Survey.12) 90th 2.900-1.773) .20) 1.18-1.600-.27) 1.10-1.00 (1.900) .13) .900-1.86) 95th 2.27 (1.40-1.620) 1.20 (2.02) 1.10-5.500-.730 (. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.941) .13-3.920 (. 01-02.80) 1.14 (1.40 (1.700 (.20 (1.04 (.00) . lead-based painted surfaces undergoing renovation or demolition.00-2.90-3.20 (2.00-1.10-3.00 (1.40 (1.795 (.00 (1.700 (.78-2.862) .66 (2.64) 2. 1991).00) 2.10-1.757-.60 (2.573 (.822-1.818) . Fourth National Report on Human Exposure to Environmental Chemicals 213 .10 (. or water contaminated by mining or smelting operations.659 (.616) . see Data Analysis section) for Survey years 99-00.50) 1.10 (1. stained glass framing.20) .60-3.90 (1.70) 3.70 (2.766 (.700 (.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. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.651) .30) 2.800-.590 (.579-.840 (.10) .800-.579-.40 (2.21 (2.20) .35 (.30 (1.59-2. and contact with soil.677 (.729-.40) 1.60-2.52-1.40) 2.745-.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.1.14-1.738) .833-1. pewter utensils and drinking vessels. 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.70) 3.30-5.90) 2.80) 2.526-.710-1.52 (1.718) .20-1.931) .00) 1.40) 1.558 (.642 (.605) .40) 2.900) .589-.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 1.680-.1.49 (1.40-1.59) 1.30-1.80) 2. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.900) . lead-contaminated dust in indoor firing ranges.60 (1.40 (2.30) 1.20 (1.600-.04 (.680) .50) 3.620 (.625 (.828) Selected percentiles ( 95% confidence interval) 50th .23) .14 (1.20 (1.553-.04) 2.41) 2.935) 1.00-2.701) .600 (.833 (.591 (.23-4.32 (1.749) .60 (1.73 (1.90 (2.900 (.700-.80) 2.40 (2.915-1.800) .800) .10-3.20-2.40-3.02 (.20) .10 (1.00) .30 (3.33.808 (.04) .00-2.10-1.700-.700-.506-.900 (.20-1.80-2.680-.710-.24-1.40-1.97) 4.30-1.40) 2.40 (1. or after soluble lead compounds are ingested.62-4.535-.60) 2.44-2.60-3.600) .625-.731 (.10 (. lead-containing folk remedies and cosmetics.

2004.09) 1.375 (.510-.658 (.38 (2.64-2.31 (1.62) 2.08) .40-1.44 (1. with a half-life of years to decades.612-.85-2.36-2.64) 95th 2.535) . Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.682) .09-1.02-1.22) 1.68 (1.603 (.33) 2.793-1. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.648 (.408-. BLLs and associated toxic effects differ in children and adults.73-2.432 (.702) .65 (1.06) 1.17-1.718) .404 (.681-..98-2. CDC.639 (.710) . Lead can cross the placenta and enter the developing fetal brain.83 (2. Schwartz.52 (1.667-.00 (. seizures.603-.44 (1.681-.66) 2.722 (.963-1.853-1.698) .11) .07-1.89-5.10) 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 .85) 1.00 (1. scant amounts are lost through sweat.587-.07) .50-2.667) . 2007). 1991.35) 2.47 (2.918-1.03) 90th 1.18 (1.66 (1.00) .01) .43) 1.62-1.812-1.712 (. and nails (Leggett.83) 1.64 (1.06) .78-4.92) 2.26) 2.679) 1.72-2.43 (2.49 (1.763) . and paralysis.460-.63) 1.725) .11-1.677 (.887 (.918 (.559-. encephalopathy.667-.569 (.87) 1.97 (1.742) .12-1.47 (1.89-2.492-.43-1.79 (1.28) 2.606-.693 (.615 (.19) 1.810 (.977) 1.622 (.838) .05 (1.S. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.97) 1.649 (.85 (1.75-2.701 (.702-.615 (.09-1.862-.22) 1.645-. Staessen et al.00 (1.11 (1.677) .15) 1.841-1.31 (1.914 (.97) 1. 1993).61) 1.37-1.655) .10 (.41 (1.06 (1.721 (.765) .796-1.644 (.45 (1.50-1.571-.774 (.933) . Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.607-.94 (1.579-.77) 2.0) 3.20) .55 (1.608-.18) 1.676) . 1993. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.05 (.698) . based on prospective population studies.609 (.755 (.62-3. 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.50 (1.88) 1.59-3.11 (1.23 (1.43 (1.00 (1.88 (1.50) 1.635 (.64) 2. Large amounts of lead in the body can cause anemia.34-1.917-1.671 (.971 (.588-.876-1.529-. 1996).718) 1.593 (.938 (.709 (.56 (1.594-.18) .652 (.603-.592-.618 (. and through binding to ion channels and regulatory proteins.11 (.633 (.893) .638 (.79) 1.04) 2.69 (1.496 (.47) 1.41-1. For instance.608 (.604-.51 (1.14 (1.670) 1.870 (.11) 1.43) 2. The skeleton acts as a storage depot.790) .73) 2.541-.617-.56-3.38 (2.44) 1.639 (.72-2.85-2.24 (1.55 (1.992-1.63) 4.03 (.469 (.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 .06 (.701) .03) 2.688) .61) 3.53) 1.75 (2.900 (.72) .31) 1.39-1.725) .673) .639) .04-3.15) 1.428) .33-1.720 (.730) 1.938-1.962 (.58) 1.655) 75th 1.88) 2.702) .828-1.882-1.26) Total .98) 2.686) .41) .52) 1.571-.29 (1.914 (.38 (2.01 (.508) .03 (1.933-1.56) 3.61) 1.03) 1.828) .03) 2.Metals 90% of the body lead burden in most adults.67-4.11 (.404-.957-1.79) 2. 2003.696 (.03) 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. O’Flaherty.27 (1. kidney injury.78 (2.88) 2.781-1.25-1.561-.51) 1.975-1.708 (.86 (1.926 (.28-1. abdominal pain.71-2.623 (.03) .677-.659-.641 (.37-1.74 (1.722 (.50-2.14) 1. Approximately 70% of lead excretion occurs via the urine.48 (1.05-1.33) 1.88-2.62-2.981-1.98 (1. In 1991.18) 1. hair.31) 1.22-1. zinc.82) 1.15-2. and iron. 1995).997-1.594-.66 (1.654) .07 (.03 (.679-. through the inhibition of certain enzymes.988 (.639 (.61) 1.920-1.645-. interval) ..657) 1.97-18.851) .655-.28) .668-. The toxic effects of lead result from its interference with the physiologic actions of calcium.53-1.17 (.03) .436) .08) .10 (1. population from the National Health and Nutrition Examination Survey.71 (1.50-2.46 (2.03-2.08-2..400) .15-2.898) .992-1.625 (.404 (.601-.10) 1.20) .707 (.56-2.551-.746) .09-1.734) .02) 1.96 (1.46 (1.94-2.31 (2.19-5.753) .25-1.22-2.12) 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 .20-3.623 (. with lesser amounts eliminated via the feces.70 (1. 1995.461) .03 (.61) 1.586-.731-.758) .33 (1.18) 2.739) . and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.988-1.588-.946-1.800-.914-1.383-.65-2.632 (.583-.683-.742) Selected percentiles ( 95% confidence interval) 50th .15-3.05-1.979 (.700-.605-.22) .342-.720 (.990 (.621 (.644) .940 (. Nash et al.703) .380-.

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

Aug 2007 [online]. Lepom P. Pediatrics 2004. Manton WI. Lead.cdc. Coresh J.htm. Semen quality of men employed at a lead smelter. Third National Report on Human Exposure to Environmental Chemicals. Environ Res 2000. Chiodo LM. Vupputyuri S. Apostoli P. Jacobson SW. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 4/14/09 Centers for Disease Control and Prevention (CDC).htm. Am J Epidemiol 1999. Bavazzano P. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . MMWR Morb Mortal Wkly Rep 2006. MMWR Morb Mortal Wkly Rep 2005a. Available from URL: http://www.348:15171526. Available at URL: http://www. van Netten C. CDC. Occup Environ Med 1996. Korrick S. JAMA 1996. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Farias P. Rios C. gov/mmwr/preview/mmwrhtml/mm5420a5. Pediatrics 2009. Jusko TA. Atlanta (GA). Sci Total Environ 2002.10:43-50.gov/mmwr/preview/mmwrhtml/ mm5532a2.115:521-529.87:1-471. 4/14/09 Centers for Disease Control and Prevention (CDC).atsdr. Birth Defects Research (Part A). Speizer FE. Sparrow D. Hu H. Mantere P. Cory-Slechta DA.89:330-335. 4/14/09 Centers for Disease Control and Prevention (CDC). Meyer PA. Available at URL: http://www. IARC Monogr Eval Carcinog Risks Hum 2006.275(15):1171-1176. Blanco J. Acquisition and retention of lead by young children. Ganzi A. 2005. Weiss ST. Seiwert M.cdc.cdc.gov/nceh/lead/publications/ books/plpyc/contents. Stanek KL. Henderson CR. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. doi:10. Hunter DJ. et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Pirkle JL. Hu H. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Am J Public Health 1999. Lead and hypertension in a sample of middle-aged women. Baghurst PA. Kaufman JD.82:60-80. Wager C. Dietrich K. Toxicological profile for lead. Jacobson JL.cdc.8(3):395-401.gov/nceh/lead/ CaseManagement/caseManage_main.113(4):1016-1022. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 2003-2004. Auinger P.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. Reese YR. Roberts RR. Kuehnemann TJ. McMichael AJ. Schulz C. Aro A. Age-specific kinetic model of lead metal in humans. Vimpani FB. Robertson EF. Muller CH. Canfield RL. Atlanta. et al.205:297-308.73:409-420. Becker K. Rotnitzky A. Caldwell KL.gov/toxprofiles/tp13. Bellinger D.150(6):590-597. Rojas LM. et al. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Inorganic and Organic Lead Compounds. Centers for Disease Control and Prevention (CDC). Weiss ST. 1991 [online]. Leggett RW. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. N Engl J Med 2003. Ewers TG. Luukkonen R. Jones RL.cdc. Sparrow D. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Muntner P. Available at URL: http://www. Scand J Work Environ Health 1984. Wigg NR. Ronchi L.1542/peds:2007-3608. Korrick SA. Lanphear BP. Hänninen H. Hertz-Picciotto I. Kim R. Checkoway H. Neurotoxicol 1987. Adult blood lead epidemiology and surveillance—United States. Int J Hyg Environ Health 2002. Blood lead levels—United States. Available at URL: http://www.53:411-416. Hernberg S. 2002 [online].55(32):876-879. Rotnitzky A. et al. The relationship of bone and blood lead to hypertension.26:359-371. Batuman V. Homa DM. Neurotoxicol Teratol 2004. Neurodevelopmental effects of postnatal lead exposure at very low levels. 2005b.287:1-11. Cox C. 4/14/09 Alexander BH. Cox C. 4/14/09 Centers for Disease Control and Prevention (CDC).54(20):513-516.htm. Bellinger D. Neri A. Baj A. Managing Elevated Blood Lead Levels Among Young Children. 1999-2002. Krause C.123:e376-e385.101(7):598-616. Blood lead reference values: the results of an Italian polycentric study.html. 1988-2004. Payton M. JAMA 1996. Preventing Lead Poisoning in Young Children. Public Health Rep 2000. Brody DJ. Angle CR. et al. Teratogen update: lead and pregnancy. Kaus S. Blood lead levels measured prospectively and risk of spontaneous abortion.htm. Ga. Hu H. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study.275:1177-1181. Lanphear BP. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Environ Health Perspect 1993. Atlanta (GA). Borja-Aburto VH.

IV. Nash D. Kaufmann RB. JAMA 2003.9:303-327. Kinetics of lead disposition in humans. Pirkle JL. Pizent A.209:301305. Soldin OP. Stewar WF. population to lead: 1991-1994. Exposure of the U. Schwartz J. 50:31-37.106:745-750. Revised and new reference values for arsenic. Lee BK. Kaufmann R. Lee SS.140:821-829. Flegal AR. et al. Wilhelm M. Hanak B. Int J Hyg Environ Health 2006. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Am J Epidemiol 2001.289(12):1523-1531. Environ Health Perspect 1998. et al. Am J Epidemiol 1994. Soldin SJ. and hypertension in perimenopausal and postmenopausal women. Sparrow D. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Brody DJ. Lauwerys RR.104(1):60-66. lead. Hickman T.327:109-113. Schwenk M. Payton M.S. Schwartz BS. Physiologically based models for bone-seeking elements. Cvitkovic P. Hwang KY. dimercaptosuccinic acidchelatable lead. blood pressure. Paschal DC.118:16-29. Lustberg M. Low-level lead exposure and renal function in the Normative Aging Study. Staessen JA. Use of endogenous. J Hum Hypertens 1995. Rubin R. Osterloh JD. Amery A. Association of blood lead. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Hu H. Gavella M. Weiss ST. cadmium. Blood lead concentrations in children: new ranges. Schulz D. blood pressure and cardiovascular disease in men. Arch Environ Health 1995. Telisman S.108(1):45-53.63:1044-1050. Smith DR. Blood lead. stable lead isotopes to determine release of lead from the skeleton. Low-level lead exposure and blood pressure. cadmium. zinc. Clin Chim Acta 2003. Roels H. Lead. Magder L. Lee GS. Environ Health Perspect 1996. and tibia lead with neurobehavioral test scores in South Korean lead workers. Rocic B. Sherwin R. Gunter EW. Jurasovic J. Kidney Int 2003. Toxicol Appl Pharmacol 1993. and copper in men. O’Flaherty EJ.Metals results from NHANES III.153(5):453464. Environ Health Perspect 2000.

Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.40-2. In addition.900) 1.700) . sulfur.70 (4. 1980.90 (1. thimerosal.700) .30-2.00-1. Apart from methyl mercury.80) 3.00 (2.g.300-.g.30) 1. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements. thermometers.900) 75th 1.50) 2. an organic form of mercury.800-1.30) 4132 4241 03-04 03-04 03-04 . and is distributed to most tissues.S.500 (. such as chlorine (e.860-1. Elemental mercury is a shiny. population from the National Health and Nutrition Examination Survey.50-3.60-6.10-3.781 (. thermostats and switches).60-6.40-2.300 (.70 (3.40) 3.02) .g.40-1. inorganic. The kinetics of the different forms of mercury vary considerably.877 (.80 (1.753-1.60-5.20-4.00) 4. Woods et al..672) .50-1.90-3. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.30-6.363-..80 (1.814 (.. interval) . and mercury compounds are still used as preservatives (e.00 (2.10) . After elemental mercury is absorbed.500) .00 (2.S. Also.419 (.50-2.484) .00 (.90) 90th 3.00) 1.326 (.2.50) 4. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.797 (.400 (. phenylmercuric acetate) or topical antiseptics (e.30) 5..300) . synthetic organomercury compounds were once used in pharmaceutical applications.40 (3.30 (1.800 (.. merbromin).00) 3. Some cosmetic skin creams from countries other than the U.30) 3.418-.500-. The ingestion of methyl mercury.90 (1.600 (.700-.500-.50) 5.700-. which can bioaccumulate in aquatic and terrestrial food chains.00) .30-4.372) . 1993).714-. Other major uses include electrical equipment (e.900) 1.30) 1.800 (.979 (. 1994. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.800-1.40) 1. elemental mercury is absorbed mainly by inhaling volatilized vapor.700-.689-. Survey years 03-04 Geometric mean (95% conf.563 (.12) . predominantly from fish and other seafood. and dental amalgam.20-3.40 (4. Accidental spills of elemental mercury.800 (.700 (. solid-waste incineration.490 (.80 (1. to form inorganic mercury compounds or salts.00 (1.400-.90 (4.776 (. or oxygen.70 (1.80 (3. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).900) 1.60-3.60) 1.900) .g.800-1.60-2. have often required public health intervention (Zeitz et al..472-.285-.574) .70) 911 856 2081 4525 03-04 03-04 . electrical lamps. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore. sphygmomanometers and barometers.40-3.700-.30 (2. Hursh et al. with the highest concentrations occurring in the kidneys (Barregard et al.40 (3. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.800-1. and mining and smelting. and organic forms.800 (.900 (.903) Selected percentiles ( 95% confidence interval) 50th .703-.80) 1. mercuric chloride). Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.00 (.30-5.30) 3.70 (1.00-5. Poorly absorbed from the gastrointestinal tract. 1998. may contain inorganic mercury. 1999 .20 (2.60 (1.90) 3.886) . Atmospheric elemental mercury can be deposited on land and water. IARC.20) 2.40 (4.400-.919) .655-.700-.00 (.20-4.50) 1. 2002).. which create an episodic potential for volatization and inhalation of mercury vapor. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).70-2.90) 95th 4.500 (.800-1.Metals Mercury CAS No. 2007). Kingman et al. 218 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey year 03-04 is 0.00 (.40-1..60) 2085 2293 3478 Limit of detection (LOD. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.80) 4.60) 1..927) . constitutes the main source of dietary mercury exposure in the general population.60 (2.50) 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 .600) 1.00) 1.60 (1.

70-5.500 (.00 (1.800) 1. Excretion occurs by renal and fecal routes.738-.. 1992)...343 (.871-1. Geometric mean Survey years (95% conf.200-.60 (3.90 (3.0) 4.00-2.500-. 1992 and 1999. 1999-2002. and a useful marker of exposure in epidemiologic studies (Grandjean et al. 1994.500-. 1999). 1998).30-2.500-.30-4.700) 2.14 and 0.30) 3.90) 3.70) 4. 1991.50-3.700 (. and the newborn’s levels decline gradually over several weeks (Bjornberg et al. 1994) and then undergoes slow dealkylation to inorganic mercury. Vimy et al.50) 1.300) .80 (3. 1971).00-2.00) 6.70-6.70 (1.. 2004.30-11.7) 4.30) 1. 1994).297-. for both acute and chronic exposures.30 (1.300 (.200-.30) 1.80) 579 527 370 436 588 806 Limit of detection (LOD. 2003).06-1..60 (1. Smith et al. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.00-6.900-1. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.600) .200-.73) 1.50) 95th 2.3) 4. 1996.317 (.307 (.369) 1.60) 1.475) .800-1.80-3.300) .395) .200-.50 (2.900 (.800) 1. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.50) 1.90 (1. 1996).200 (.60 (1. interval) Selected percentiles (95% confidence interval) 50th ...600 (.726-1. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.10-1.00 (2.944 (.70-3.00-2. Vahter et al.10-3.23) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.35 (1.60 (3.90 (4. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.30-6.90) 5.30-6.29) .40-2. Suzuki et al.541-.00) 1.500-. After exposure to elemental mercury.00) 7.299-. with most elimination occurring through in the feces (Sherlock et al. Sandborgh-Englund et al. 1995.500 (. 1998).20) 1.10) 1.S.900 (.800) .500-.60 (2.00) 2.70) 4.10 (.30 (.70-5.833 (.256-.919) . 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.70-3. Jonsson et al. 1993).60) 3. Methyl mercury enters the brain and other tissues (Vahter et al. 1975. 1992.02 (.60 (1.269-..40) 1.300) .900-1.824) 1.00-1.90 (1.70) 1.40-1.40) 5.820 (...800-1.200-.800-1.90) Sample size 705 872 318 432 387 440 1709 1928 Age Group 1-5 years (females and males) Females Males 16-49 years (females only) 99-00 01-02 99-00 01-02 99-00 01-02 99-00 01-02 .20-3. Smith and Farris.700-1.30-4. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al..400-.90) 90th 1.06 (.300 (.30-5. 1993).00 (2.50-2.40-2.50 (1.90) 2..407) .50-12.667 (.700 (. 2003). McDowell et al.377 (.90 (4.800 (.20) .700-.377) . Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.10 (1.14.10 (1.700 (. National Health and Nutrition Examination Survey.90) 2.318 (.50) 3.20-3..300 (.40 (1.27) .40) 2.00) 4. 1990).10) ..10 (3. 2005).80) 1.20 (.20 (2.664-1.10) ...30 (1. a measure of accumulated dose (Cernichiari et al. 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. Myers et al..30 (1. Miettinen et al.01) . Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.00 (2.20-3... The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.800) . Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.697-.00-3. Methyl mercury is incorporated into growing hair.500-1. Fourth National Report on Human Exposure to Environmental Chemicals 219 .10 (.20-11.800 (.800 (.265-. thereafter.60) 1. 1984.00 (3.Metals the tissues to mercurous and mercuric inorganic forms.30-3.00) .300) .268-.900 (.200 (.10 (5.700 (. 1973). 1969.800) 75th .700-1.60) 2.70 (1.20) .374) ..700-.50) 2.940) Race/ethnicity (females.00) 1. population.300) .10 (1..40 (1.30-6.300 (.600) .825-1. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .20-2.70 (1.80 (1..329 (.200-.300) . Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.

. 1993).500-.600 (.500-.600) .600 (. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. DeRouen et al. the existence of a causal relation is unresolved (Chan and Egeland.. altered physical growth. 1996). sensory impairments.42.. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. anorexia. fatigue. 2006. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.600 (. 1995..600) . irritability. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.800) . high-dose exposure to elemental mercury vapor may cause severe pneumonitis.600) .600) . Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.500-.600-. 2000).. Salonen et al. Once absorbed. Rissanen et al.600) . maculopapular rash. dysarthria. Oskarsson et al. causing parasthesias. Rice.500-. 2006.500 (.. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.500-. Sakamoto et al.500-... Sakamoto et al.700 (. particularly irritability. 1987). which may vary for some chemicals by year and by individual sample. 1970.600 (.700 (. Drexler and Schaller. 1963). and neurocognitive and behavioral disturbances. 2004. 2002.600) .. 1995. 2005). 2000.500-.600 (.. Acute. 1951. Bellinger et al.500 (<LOD-. 2004.500 (<LOD-.600 (.500 (.500-.700 (. 2005. Factor-Litvak et al. In recent epidemiologic studies.500) . short-term memory loss.700-.. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.600-.S. 2000. depression.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . Inorganic mercury exposure usually occurs by ingestion. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. At levels below those that cause acute lung injury. Smith et al.500-. hypertension.600 (.700 (. Overt poisoning from methyl mercury primarily affects the central nervous system.. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. 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.700-.600) . 2004).700 (. 2003).600) .. 220 Fourth National Report on Human Exposure to Environmental Chemicals . and pinkish discoloration of the hands and feet (Tunnessen et al.. 1998.600-.Metals may be more efficient for inorganic mercury (Grandjean et al.700 (. Smith 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.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 . 2004). ataxia. typically after a latent period of weeks to months.800) . cerebellar ataxia.600-.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . gingivitis.600 (. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. The constellation of findings may include anorexia.700-. hearing impairment. and progressive constriction of the visual fields. 1983).700) . 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. overt signs and symptoms of chronic inhalation may include tremor.. insomnia. limb deformities.. and sleep disturbance (Bidstrup et al.700) 2007 2240 3406 Limit of detection (LOD. Vupputuri et al.. Stern 2005.600) . < LOD means less than the limit of detection. pain in the extremities. dysarthria.. and cerebral palsy (NRC.

03-4.441 (.420 (. Survey years 03-04 Geometric mean (95% conf.77-2.840-1.416 (. Kingman et al.05) 3. Grandjean et al.14) 90th 2.atsdr.76-4.430 (.408) .442-.476 (.350-.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 .610-1.. average age 33 years.890 (.14.396-. Over the NHANES 1999-2006 survey periods.28) 1.66) 3.463) ..16 (1.08 (1.90) 2.96 (1. aged 18 to 69 years.epa.gov/toxprofiles.63-2.88) 287 722 1529 03-04 03-04 . 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. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.99-6.76-3.55 µg/L.13-2.89) 3.360-.54 (2. 2006). particularly methyl mercury.555) .65) 1.870-1.97) 2. Sanzo et al. 2009). slightly higher total blood mercury levels were found in U.313-.09 (2. EPA at: http://www.330-.433 (..S.12 (. average age 9.330-.400 (..60-2.570) .78-2..S. 758 children.8 years. interval) .530-. Total blood mercury levels increase with greater fish consumption (Dewailly et al. 1998).410-. 2004.480 (.19 (2.61) 1.340-. 2002).460) . who participated in a 1998 representative population survey (Becker et al.S. Information about external exposure (i.360-. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. 1997.85-2. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC..96 (1.e. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.840) 1.08 (1. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.460 (.16 (.534) . 2009).440 (.19 (1.46) 3. range 40 years to 78 years) had an average total blood mercury concentration of 2.67-2.33 (2. Mahaffey et al.930-1. Fourth National Report on Human Exposure to Environmental Chemicals 221 .580) .430) .9 years)...430 (.78 µg/L for adults and 0. 2000).76-3. see Data Analysis section) for Survey year 03-04 is 0.. In NHANES 19992002. and increased slightly in non-Hispanic white children (Caldwell.495 (.cdc.700-1.250) .509) .S.520) .60) 619 713 1066 Limit of detection (LOD. 2003). 2003). (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.88-3. 1998). Among the three racial/ethnic groups. total blood mercury geometric mean levels in females aged 16-49 years did not change.14-2. Benes et al.58 µg/L for 4645 adults.200 (..68 (2. However.88 (1. 2001.549) ..24) 1.52) 2.01 (. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.29) 1. the total blood mercury concentration is due mostly to the dietary intake of organic forms.213-.05) 1.492) Selected percentiles ( 95% confidence interval) 50th .20 (1. In Germany the geometric mean for blood mercury was 0.gov/mercury and from ATSDR at: http:// www.360 (. These distinctions can help interpret mercury blood levels in people.00 (.23) . Biomonitoring Information In the general population.406-.254 (. 1995. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.370) .304) .39-3.46 µg/L for children. adult women in several ethnic subgroups (Hightower et al.358 (.26 (1. and the age-related changes differed across the groups (Caldwell et al. Schober et al.60 (1. et al.34-3.870-1. EPA.S. environmental levels) and health effects is available from the U. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning..31) 1266 1272 03-04 03-04 03-04 . 2001.480) 75th 1.509) .. total blood mercury increased with age.405-.840-1.447 (. A cohort of 1127 U. the median concentration of blood mercury was 0.07 (. population from the National Health and Nutrition Examination Survey.330 (.290-.24 (2.18) 2.330-.93 (1.700 (.Metals standard for inorganic mercury has been established by U.413-.31) 2. During the same survey periods..530) .530) .42) 95th 3.280-. military veterans (mean age 52. From 1996 through 1998.940 (.960 (.770-1.00) 1.23) 2.420 (.382-.67-3.160-.30) 3.

88-2.13-2.696 (.12-3. 2002) adult population surveys were similar to those in a U.67 (1.455-. mean urinary mercury was 3.S.368) . et al.535) 1.00) 90th 1.588) .301-.217 (.S.785-1. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.391-. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al. 2005). Czech (Benes et al. DeRouen et al.41-2.309-.455) .61) 1.964-1. a biomarker of perturbation in renal tubular function.476 (.88 (1.18-1. Department of Health and Human Services noted that several studies have observed a modest..652) .376-.537) .297 (.1 µg/L. Urine mercury and the number of dental amalgams were correlated.486) Selected percentiles ( 95% confidence interval) 50th .04-3.464 (.545 (.532 (.472-. Levels in U.S.630) . Urinary mercury levels in recent German (Becker et al..358) ..768 (. military veterans with dental amalgams. 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.67 (1.88-2.400) . 1998).65 (1. 2009).. reversible increase in urinary N-acetyl-glucosaminidase. 2009).667-1.44) 1.687) .11) 1.970 (.347) .391) . 2002).78-4. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.01) 2.400-.79) 1.40 (1. population from the National Health and Nutrition Examination Survey. 2006).365 (. 1992).384 (. not to imply a safety level for general population exposure. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.51-2.54 (2.40-1.385-. Information about the biological exposure indices is provided here for comparison.508 (.S.417) .00) 286 722 1529 03-04 03-04 ..39) 1. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.280-.00 (.Metals 2000).404-.76 (1.265-.306 (.616) . An expert-panel report recently prepared for the U.03) 2.31 (1.392-.11-2.447-.800-1.30) 2.784) 1. In the study of U.23-2.09) 1. the urine mercury increased by approximately 0.480) .46-2.485 (.969-1.13 (1.307-.522-.56) 1266 1271 03-04 03-04 03-04 ..63) 1..276 (.07) 1.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .28 (.343 (.16) 1.275) . ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L. Survey years 03-04 Geometric mean (95% conf.619-.255 (.714-1.599) ..909 (.525 (.64-2.875-1.1 µg/L for each surface with a dental amalgam (Kingman et al.498) 75th ..225-.87) 2.990) .11) 2.87 (1.35 (1.362 (.587 (.333-. 2006.620-.77 (2.. and Italian (Apostoli et al.365 (.S.32-2. Langworth et al.62 (1.289) . interval) . women of childbearing age have generally been much lower than these levels (CDC.06 (.208-. 2003).32 (1. 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.455-.21) 1.566) . Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.06 (.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 .246-.25 (. 1988.447 (.443 (.79 (1. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.196-. et al. and on average.86) 95th 2.463 (.30) 1.

population.68-3.560-.721 (.41 (2.13-4. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.560 (.709) .833) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.61-6.51) .41 (1.30 (1.650) 1.30-2.35) .526-.632 (.50 (1.56) 4.966) .32-3.620 (.62 (4.10-4.55) 90th 3.50-4.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.850-1.520-.21 (2.665) .04-10. 1999-2002.610-.710) 1.45-2. 16-49 years) 99-00 01-02 .606 (.657 (.622-.27-1.832-1.76) 2.92) 4.670) 75th 1. population.709) 75th 1.30 (2.28 (1.84 (2.47) 1.03) 1.45-3.799) .42-3.51 (3. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.38) 4.580 (.580-.45 (1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for females aged 16 to 49 years in the U.45) 2.76-5.41 (1.650 (.508-.16-5.579-.48 (2.540-.68 (3.59-5.691) .553-.22-3.76 (1.56 (1.742-1.639 (.09-1.07-2.95 (2.87-4.79) 3.53-3.65-4.85) 4.57-4.69 (1.14) 3.27 (2.740 (.56) 3.81 (3.91-7.810) . interval) Selected percentiles (95% confidence interval) Survey years 50th .892) .17) 95th 5.98 (5.52) 3.569-.30 (2.92) 3.870) .97 (1.846) .596 (. 1999-2002.650 (.03 (.05 (3. 16-49 years) 99-00 01-02 .21-3.636-.516 (.23-1.23-1.81-6.10-2.39-3.624-.46-4.43-1.710 (.14.760 (.03 (.631-.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .07-5.15 (2.65) 1.45) 2.83-3.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .31 (1.578-.450-.719 (.77) 1.724 (.14 and 0.14-2.32 (1.00 (2.97) 2.655 (.706 (.772 (.97) 2. Geometric mean Survey years (95% conf.387-.22 (.68) 3.15-1.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .475-.00 (3.774) .685 (.62 (1.62 (3.699) 1.46) 3.520-.501-.25) 2.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.420-.410-.99-2.92) 2.600 (.00) 2.14-1.500-.664) .522 (.06 (.909-1.18 (3.89 (2.32) 2.658 (.37) 1.605-.91 (2.05 (2.24-1.77) 2.686) .35 (1.21 (1.54) 595 531 381 442 594 826 Limit of detection (LOD.615 (.72) 1. Geometric mean (95% conf.79) 1.S.84 (2.24) 6.97) 2.S.426-.42) 2.99 (2.831) .45) 95th 3.61) 1.809) .03-2. interval) Selected percentiles (95% confidence interval) 50th .37 (1.592 (.744) 1.99) 1.656-.910) . National Health and Nutrition Examination Survey.41-6.55-3.31-1.85-3. National Health and Nutrition Examination Survey.806) .582-.565 (.16) 5.94) 1.540 (.99 (3.723 (.70 (2.18) 3.42) 90th 2.Metals Urinary Mercury−Females Aged 16-49 Years Old.824) .557-.710 (.790) .04-1.09-1.47) 1.3) 5.07) 1.69-3.616-.502-.637) .831) .44) 3.27 (1.50 (2.46 (1.13 (2.930) .

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Osterloh J. Mottet NK. Suzuki T. Tunnessen WW. Environ Health Perspect 2003. Fisher HL. Smith RG.97(2):195-200. Stern AH. Smith JC. Longnecker MP. et al. Hongo T. Acrodynia: exposure to mercury from fluorescent light bulbs.115(10):1527-1531. Patil LS. Turner MD. Takahashi Y. Woods JS. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Farris FF. Nakazawa M. Dorronsoro M.Metals Sanzo JM. Shen DD. 1999-2000. 226 Fourth National Report on Human Exposure to Environmental Chemicals . McDowell M.31:687-700. Mooney TF. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Vimy MJ. 1993-1998. et al. Friberg L. Sherlock J. Vahter M. Am J Physiol 1990. Blood mercury levels in US children and women of childbearing age. Baser M. Most B.110:129-132. Smith AE. Orr MF.258(4 Pt 2):R939-945. Amurrio A. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Vupputuri S. Methyl mercury pharmacokinetics in man: a reevaluation.4(5):981-988. Amiano P. Kaye WE. Guo S.79:786789. Allen PV. Hislop D.289(13):1667-1674. Am Ind Hyg Assoc J 1970. McMahon KJ. Newton G. Hum Toxicol 1984. Toxicol Appl Pharmacol 1994.111(12):1465-1470.98(1):133-142. Jones RL. Leitao JG. Effects of occupational exposure to elemental mercury on short term memory. Imai H. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Bernardo MF. Lorscheider FL. Environ Res 2005. et al. Leroux BG. Pediatrics 1987.124:221-229. Toxicol Appl Pharmacol 1996. Public Health Nutr 2001. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Azpiri MA. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment.2:117-131. Br J Ind Med 1983. Sinks TH. Smith JC. Goldberg J. JAMA 2003.40:413-419. The contribution of dental amalgam to urinary mercury excretion in children. Environ Health Perspect 2002. Aguinagalde FX. Hall LL. Matsuo N. Lind B. Daniels JL. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Langolf GD.37:245-252. Bolger PM.128(2):25125-25126. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. DeRouen TA. Martin MD. Sandler DP. The hair-organ relationship in mercury concentration in contemporary Japanese. Schober SE. Burbacher T. Effects of exposure to mercury in the manufacture of chlorine. Environ Health Perspect 2007. Vorwald AJ. The kinetics of intravenously administered methyl mercury in man. Toxicol Appl Pharmacol 1994. Whittle K. Arch Environ Health 1993. Zeitz P. Topping G. Smith PJ. Environ Res 2005. Yoshinaga J. Stern AH.48(4):221229.

semiconductor and battery industries have begun to use molybdenum.6-96.2) 48.8) 46.6) 71. 1997).4 (72.5 (49.4) 52.7) 51.7 (50.7-84. which exert homeostatic regulation over molybdenum balance.7 (44.2-91. see Data Analysis section) for survey years 99-00. interval) 45.4 (48.0) 39.1) 82.6 (43.0) 84.9) 62.0) 97. respectively.9 (73.0-77. 2001).7) 78.2) 53.9-82.5 (67. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.3-44.7) 46.Metals Molybdenum or ore deposits.7 (45.4 (48.0 (76.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.2 (49.0 (42.5) 80.3 (53.4-52.3 (38.3) 47.5) 60.5-66.9-85.9-109) 97.1) 35.8-94.6-62.2 (49. and xanthine oxidase (Kisker et al.0-85.7-39. and 1.7-41. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.8-46.9 (33.4-75.3 (37. Compounds of molybdenum are also used as corrosion inhibitors.5 (37.7) 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 78.3 (73. and in pigments for ceramics.6 (52.7-47.6-46.8.8 (67.5-91.9 (78.4) 56.8.9 (44.3-75.6-55.0-53. In humans.1 (91.5 (41.0) 62.2) 37.3) 37. and 03-04 are 0.9-55.2 (83.7) 78.0-100) 63.5 (43.0 (48.2) 79.0 (42. 2001.3 (84.9 (34.7 (36.1-51.7-92.2) 41.8 (42.6-82.2) 52.5-68. 01-02.7) 57.4 (80.8 (82.8-49.2-53. hydrogenation catalysts.2-79.0-101) 82. chemical reagents in hospital laboratories.6-72.3) 83.7-50.5-52.0-62.8) 44.2-59.1-59.2-59.7 (58.5) 44.0) 54.7-96.4) 45.3-115) 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.3 (79.2 (63.4) 41.8) 40.8) 39. 1996).5 (74. 7439-98-7 General Information Elemental molybdenum is a silver-white. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.7) 75th 84.6-111) 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. lubricants.8-90.2 (38.3 (47.5) 85.1) 59.0-71.6-58.9 (40.2-37.9 (52.2 (69.1) 46.0) 55.6 (40.5-41.2-70.5 (41.8-106) 88.8) 75.3) 65. At a daily oral molybdenum dose of 24 µg.4-61.7) 77.5-52.0 (43.2 (56.2) 40.9) 67.5) 80.5) 47.1-55.1-63.4) 49. 0.4) 76. inks.6) 53.5.2 (40. and paints.3 (55.9-55.8) 48.8 (85.7-51.4) 42. aldehyde dehydrogenase. Fourth National Report on Human Exposure to Environmental Chemicals 227 .3-91.4 (34.3 (55.8-108) 87.6 (55.5 (81.7 (51.2 (61. More recently.9) 34.6 (40.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.0) 45.7-122) 93.1) 126 (106-147) 109 (94.3) 85.9 (37.7 (73.6-42.5-46.4 (79.5-124) 108 (92.1-88. population from the National Health and Nutrition Examination survey.6 (73.6) 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 (99.4-82.7 (71. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1-52.3-47.0-110) 90.3) 54.6) Selected percentiles ( 95% confidence interval) 50th 50.2-42.6) 93.7-91. 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.6) 51.7-68.7-105) 69.1-44.1 (34.2 (55.0-56.1-48.5 (48.0-38.7 (37.7-73.3) 41..7-60.3 (46.0 (46.6 (55. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.2) 178 (147-259) 169 (138-197) 138 (127-152) 146 (112-171) 145 (129-159) 118 (105-125) 126 (114-134) 114 (103-124) 105 (98.3 (64.7) 45.1) 60.6) 71.0) 60.0 (81.1) 57.5-65. Excretion occurs predominantly via the kidneys. urinary excretion over six days CAS No.0-65.1 (38.9-56.3-108) 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 47.9 (32. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.S.3 (71.9-83. WHO.0 (41.1 (71.7) 86.1-52.

7) 62.2 (37.5-48.7) 41.1-100) 86.3 (36.5 (59.8) 45.0) 38.2) 42.5-45.2-65.3) 56.9 mg/kg/day and established a tolerable upper intake level of 0.9 (35..4) 61.5) 90th 108 (97.7) 45.4-106) 85.1 (82.7-38.2-121) 107 (92.1 (37. 1997).0-103) 103 (90.8-67.5 (35.3) 37.3-68.8) 71. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.0) 44.3 (37.2-103) 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 42.4-66.4 (55.4-107) 85.9-87..4) 40.2-96.8) 38.5 (78.4 (67.5) 72.5 (50.9-117) 57.1) 40. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.4-76.1 (30.8-47.3 (36.4) 47.0 (35.1 (54.8-84.1) 37.5 (40. urinary excretion over six days rose to 50% and 67%.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.4-42.1) 56.5 (83.4-41.9-68.2 (33.1-79.7-52.0) 39.2 (40.2-49.3-115) 98.4 (37.7-100) 77.7) 53.0) 72..4-120) 101 (84.5 (35.3) 61.5-92.9-45.4) 44. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.5) 60.1-45.5 (37.5 (79.2-80.3) 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 85.6) 48.6-61.9-42. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.9) 40.1-41.8) 37.5 (65.0) 36.6 (71.4-39.9 (64.2) 39.9-45.1-39.6) 36.5-99.0 (80.3) 40.7-137) 129 (109-155) 112 (97.4 (78.8-46.3-56. U.5 (39.7-93.7-62.1 (40.3) 57.8 (56.8-42.5 (39.4) 58.9-41.2 (43.4 (40.8-52.7) 42.7) 112 (95.5) 73.7) 115 (93.0) 88.5-46.5-60.3) 64.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.2) 58. In industry.9-40.5-97.7 (75.9 (36.0) 33.0-46.3-141) 109 (81.4 (59.0-133) 119 (88.6-41. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.9-118) 91.03 mg/kg/day in humans (IOM.8 (37.3 (37.8) 62.5-44.5) 63.3 (53.3) 41.1-38.8 (57. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2) 42.2) 55.2-40.0-41.6 (36. 1999).6 (57.1-112) 78.8) 79.2 (73.9) 44.6) 43.3-43. Molybdenum is generally considered to be of low human toxicity.4 (53.9-71.6-88.9 (39.7) 75th 63.8-118) 81.2) 39.6-61.5-119) 90. 1961.5 (65.0-46.0) 39.9 (73. population from the National Health and Nutrition Examination survey.5 (37.3) 44.2-96.7 (30.6) Selected percentiles ( 95% confidence interval) 50th 41.0) 53.8-65.1-67.8 (75.4) 122 (107-133) 109 (99.7-120) 87. but available epidemiologic data are scant.S.5-50.4-185) 106 (94.8) 39.1 (38.7-40.2) 37.1-109) 89.5 (54. EPA.0-56.3 (55.5 (36.3-46. at daily oral doses of 95 µg and 428 µg.1) 43.2 (40.6-78.8-47.2 (69.4) 60.3-45.1-81.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.5 (40.9 (64. 2001).6) 39.1 (42.2-41. interval) 43.7-43.9) 41.6-76.2 (36.7) 57.S.6 (38.1-43.3-44.5-62.2-46.2 (52.4) 77.5 (41.9 (49.2 (50.4 (56.0 (74.6-45.1) 37. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.8 (36.8 (90.6-63.9) 92.5-35.4-118) 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) 71.1-40. respectively.4 (44. and urinary levels reflect intake from all sources.1-39.9 (39.5 (34.1 (38.2 (57. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.9-96. 1993).3 (51.5 (80.3-102) 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 40.1-43.0) 62.3 (58.6 (42.5 (38.4) 48.1) 101 (83.9) 31.9) 79.7 (66. Biomonitoring Information Molybdenum is an essential element for health.0-38.4) 89.9-61.Metals was 18% of the ingested dose. Based on studies finding adverse reproductive effects in rats and mice.3) 43.2) 38.5-70.1-127) 90.9 (40.5-69.7-44.6 (36. of the ingested dose (Turnlund et al.8-66.8) 61.1) 65.2 (40.6 (59.1 (39.1 (49.0 (58.1-34.2-47.8) 38.3-52. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2) 43.1 (33.4) 116 (101-126) 104 (88.5 (41.3 (71. and clinical or epidemiologic evidence of adverse effects is limited.2) 37.9 (79.1 (44.3-59.3 (83.0-120) 85.6) 39.3 (71.7 (77.6-63. 1995).

et al. Menne C. 56:322-327.22(3):179-191. White MA. 2005). Vermeire PA. Available at URL: http://www. TR-462. Turnlund JR. Occupational risk factors of lung cancer: a hospital based case-control study. 2001). Sciarra G.gov/index. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. 1998. molybdenum. boron. Environmental Protection Agency (U..nap. and zinc: a report of the Panel on Micronutrients. 420-441. 4/14/09 White MA. References Centers for Disease Control and Prevention (CDC). X. pp. Ann Rev Biochem 1997. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Am J Clin Nutr 1995. Minoia et al. vanadium.S. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. White and Sabbioni. Minoia C. excretion. Gatti A. Molybdenum 1993 [online].htm. Sabbioni E.niehs. Molybdenum. Molybdenum in infancy: methodical investigation of urinary excretion. Christensen JM.66:233-267. nickel. 2001. Weyler JJ.Metals in urine for the U. (DC): National Academy Press.. 1996. EPA). A study of 13 elements in blood and urine of a United Kingdom population. Washington. Rees DC. vitamin K. iron. Occup Environ Med 1999. Peiffer GL.62(4):790-796. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Available at URL: http://ntp. Trace element reference values in tissues from inhabitants of the European Union.S. In: Trace elements in human nutrition and health. van Sprundel MP.gov/iris/ subst/0425. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Dietary reference intakes for vitamin A. pp. Geneva: WHO. 4/14/09 Sievers E.nih. Koval’skiy GA. 1998). Rapid Comm Mass Spectrom 2002. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. J Trace Elem Med Biol 2001. Analyst 1998. Food and Nutrition Board. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC.15(2-3):149-154. iodine. Keyes WR. 144-154. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. 2005. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Available at URL: http://books. copper. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. 16:1313-1319. Atlanta (GA). Schindelin H. Turci R. arsenic. chromium. Shmavonyan DM. National Toxicology Program (NTP). silicon. Yarovaya GA. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Zhurnal Obshchey Biologii 1961. Institute of Medicine (IOM). Sci Total Environ 1998. Schleyerbach U. Third National Report on Human Exposure to Environmental Chemicals. U. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. 2002.S.epa.216:253-270. Molybdenum absorption. Droste JHJ. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. World Health Organization (WHO). Ronchi A. Sabbioni E. Kristiansen J. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Aprea C. edu/openbook. manganese. Van Meerbeeck JP.php?record_id=10026&page=420. Schaub J.. 4/14/09 Iversen BS.123(1):81-85. Kisker C.

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

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

Saindelle A. Influences on human internal exposure to environmental platinum. Schierl R.35:313-321. Available at URL: http://www. Campbell K. palladium. Biomonitoring Information Urinary platinum levels reflect recent exposure. 1998). and in blood and urine in the United Kingdom. 2004. 1998).. Angerer J. Huber R. Herr et al. Schierl R. et al. Kuster W. Schulz C. pp. 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. et al. 206:15-24. Environmental Health Criteria 125.04 µg/L) in this Report.. eds. 2000... Schulz C. Begerow J. Occup Environ Med 1998. Parrot JL. Environ Res 1975a. Seifert B. Stilianakis NI.S. Rommelt H.4(1):27-36. Petrucci F.. rhodium.inchem. Carelli G. Kazantzis G. Int Arch Occup Environ Health 1997.htm.207(1):69-73. Duneman L:Long-term urinary platinum. Fruhmann G. Analyst 1998.inchem. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. 1991 [online]. Ruff F: Histamine release by sodium cholorplatinate. Raab W. Neuendorf J. Cohrssen B. 2001). 3/31/08 Moore W Jr. Arch Environ Health 2001. Blanks R.htm. Int J Hyg Environ Health 2004. Arch Environ Health:1969. Hauff K. Uptake of antineoplastic agents in pharmacy and hospital personnel. Seiwert M. 2003. Biomonitoring of traffic police officers exposed to airborne platinum. Ruff F: Platinum and platinosis. Hebert R.10:63-71. Iavicoli I.123(3):451-454. Farago ME. 2003. Kaus S.55(2):138-140. Powell CH. Bocca B.. Schierl. J Expo Anal Environ Epidemiol 2003. et al. ruthenium. Czerczak S. Turfeld M. Schierl R. 1997. population were below the limit of detection (0. van de Weyer C. Hall L. Pethran A. International Programme on Chemical Safety (IPCS).70(3):205-208. Jankofsky M. Kavanagh P.. Schierl et al. Biomarkers 1999.. In: Bingham E. et al. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Fries HG. 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. References Becker K. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. 289-380. Senofonte O. Platinum concentrations in urban road dust and soil. 2004) or less than 0. Urinary excretion of platinum from platinum-industry workers. Ensslin AS. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum.76(1):5-10.9:152-158. 232 Fourth National Report on Human Exposure to Environmental Chemicals . and platinum. 1999.01 µg/L (Becker et al. Kelly J. 2003. Crocker W.19:685-691. Herr CE. Urinary platinum levels associated with dental gold alloys. Grimm CH. Gromiec JP. Herr et al. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect.org/documents/ehc/ehc/ehc125. and gold excretion of patients after insertion of noble-metal dental alloys. Alimonti A.. Int Arch Occup Environ Health 2003.56(3):283-286. Occup Environ Med 2004. Thornton I. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. which elevate urinary platinum by five to twelve-fold (Begerow et al. Environ Health Perspect 1975b. palladium. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. International Journal of Hygiene and Environmental Health 2003. Ewers U. Allergy and histamine release due to some platinum salts. Platinum..org/documents/ehc/ehc/ ehc125. Levels of platinum in urine for the U. Br J Pharmacol 1969. Saindelle A. Nickel. Moore W Jr. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Hysell D.61(7):636-9. 2003). 5th ed. Gieler U. Pethran A. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Part 1: monitoring of urinary concentrations. Patty’s Toxicology. Several studies have shown that background concentrations in general populations were usually less than 0. Boos KS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Wilhelm M. osmium.005 µg/L (Iavicoli et al. Hysell D. Pethran et al.13(1):24-30. Wilhelm et al.Metals the International Programme on Chemical Safety at http:// www.. 2004). Schierl R. New York: John Wiley & Sons. Nowak D. Kulka U.

450 (.420) .470 (.200 (.380-.370 (.360 (.290 (.218) .370) .150-.184 (.390-.170-.300 (.149 (.220 (.480) .135-.159 (.160 (.270 (.460 (.390-.188) .217 (.430-.150-.250-.300) .480) .200) .180-.230) .450 (. respectively.360-.260 (.145-.360-.210 (.440) .180 (.290 (.440) .410-.370-.165 (.290 (.157-.640) .180 (.510 (.S.260-.430) .320-.390) .300) .420-.160 (.420) .240) .350-.380-.300) .133-.200-.175) .630) .300 (.158) .159 (.390 (.500) .217) .590) .420-.380) .200-.370-. In the United States. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.240) .360 (.202 (.360) .180) .170 (.159 (.220 (.270-. 2005).197-.300) .230-.170-.460-.280 (.280 (.380 (.340 (.156-. 01-02.201 (.520) .220) .450 (.520) .206) . It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.350-.190 (.200-.240-.450 (.170 (.260) .200) .179-.230) .450 (.160-.145-.320) .290-.170-.520) .250) .250 (.310) .155 (.490) .450) .280-.250-.170-.230) .400) .360 (.225) .560) . thallium readily crosses the placenta and also distributes into breast milk.02.440 (.202) .450 (.180-. Fourth National Report on Human Exposure to Environmental Chemicals 233 .690) .430-.240) .177) .550 (.410 (.320) .153-.185 (.400) .191 (.400-.350-.420) . interval) .340) .370 (.330-.330-.410-.420-.230 (.190 (.240-. thallium was obtained as a by-product of smelting other metals.144 (.243) . From these and other sources.167-.170) ..500) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.370 (.490) .400-.181-.350-.146 (.290) .380 (.390) .330-.410-.210-.215) .480) .171 (.400 (.220) .145 (.290) .150-.420) .260-.440 (.330) .239) .350) .510) . it has not been specifically mined or refined in the United States since 1984.290 (.260 (.370 (.172 (. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.370-.490 (. In the past.270-.330-.370) .310 (.390-.230-.470) .270 (. In addition.350-.192) Selected percentiles ( 95% confidence interval) 50th .160-.160-.490) Total .490) .196) .200) .260-.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 .170 (.290) .230-.170-.183) .140-.240-.147-.390-. representing distribution into other tissues.250-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.340-.170-.340-.400) .430 (.150-.410) .390 (.420 (. however.460) .270 (.Metals Thallium depilatory cosmetics. and 03-04 are 0.400-.410-.163) .02.350-.280) .02.430 (.350 (.270) .196) .400-.220 (.183) . Human health effects from thallium at low environmental CAS No.410 (.270 (.200) .190 (.410 (.430) .170-.420) .162-.187-.176 (. 0.280) .410 (.167-.250 (.400 (.480) .200 (.230) .440) .190 (.190 (.330-.320 (.300 (.160 (.410-.148-.370 (.360 (.500) .180-.170) .250-.470) .160-.390) .190-.147-.310 (.290-. see Data Analysis section) for Survey years 99-00.147-.280) .200 (.420-.202 (.330) .280 (.370 (.330) .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 .172) .410-. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.400 (.450 (.200) .400) 95th .340) .290 (.400-.430 (.220) .250-.400 (.173) .360-.250-.370 (. and 0.180-.160 (.178) .370-.197 (.340-.154-. Thallium disappears from the blood with a half-life of several days.220) . the latter being the current major industrial consumer of thallium in this country.150-.290 (.200-.200 (.310-. population from the National Health and Nutrition Examination Survey.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 .173-.350) .220) .220 (.300-.320) .250-.210 (.180 (.201 (.270-.218) .470 (.500 (.260-.410 (.350 (.440 (.390) .400) .200 (.260 (.210) .150-.430 (.440-.360-.520 (.220) .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.450 (.270 (.340-.470) .172 (.400 (. 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.167 (.173) .160 (.134-.290) .270) .440 (.450 (.220 (.250-.420) .330-.280-.290) 90th .420) .330) .330-.480) .190 (.137-.310 (.156) .410 (.180) 75th .590) .200) .220-.170) .185-.430-.200 (.156) .160-.360-.260-.182-.

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

Manke G. Wiegand H. Schaller et al. 1998).S. Jackson RJ. Brockhaus A. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. A study of 46 elements in urine. Paschal et al. 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. Sci Total Environ 1990. Schmidt M.5 μg/L. Cassot G. blood. White and Sabbioni.265 people living near a thallium-emitting cement plant in Germany. Sampson EJ. population) are thought to correspond to workplace exposures at the threshold limit value of 0. et al.35(1):4-9.76(1):53-59. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Sabbioni E. et al. Investigations of thallium-exposed workers in cement factories. Fourth National Report on Human Exposure to Environmental Chemicals 235 . et al. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium.cdc.Metals (CDC. Apostoli P.. Atlanta (GA). with concentrations ranging up to 76. Ting BG.95:89-105. Pirkle JL.html. References Agency for Toxic Substances and Disease Registry (ATSDR). Marcus RL. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust.. (1981) studied 1. Soddemann H. 1992 [online]. Gallorini M. Sabbioni E. Raithel HJ. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. X. Brockhaus et al. Trace element reference values in tissues from inhabitants of the European community I. 1981. 2005. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Buhlmeyer G. Centers for Disease Control and Prevention. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Investigation of a working population exposed to thallium. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Radiat Prot Dosim. 1980.47(3):223-231. Minoia C. Int Arch Occup Environ Health 1980. Environ Res 1998.. 1990. Toxicological profile for thallium. Minoia et al. Third National Report on Human Exposure to Environmental Chemicals. Kramer U. and serum of Italian subjects. Available at URL: http://www. Schaller KH. White MA. J Soc Occup Med 1985. 2005) and are shown with results from NHANES 2003-2004 in this Report. Challeton-de Vathaire C. Boisson P. Biomonitoring studies on levels of thallium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of thallium than are found in the general population.216:253-270. Trace element reference values in tissues from inhabitants of the European Union.48(4):375-389. Celier D. Paschal DC. Dolger R. Pietra R. Martin J-C. Sci Total Environ 1998. A study of 13 elements in blood and urine of a United Kingdom population. Pozzoli L. 7/15/09 Blanchardon E. 2005.atsdr. Ewers U.gov/toxprofiles/tp54.1 mg/m3 (Marcus. Morrow JC. 1998. 1985). Trace metals in urine of United States residents: reference range concentrations. Valentin H..113(1):47-53. Int Arch Occup Environ Health 1981.

090) .330-.550) .290 (.060 (.450 (.370 (.270-.320) .110) .430 (.160-.410-.130-.137 (.520) .260-.290-.160 (.250) .190) .430 (.320-.160 (.070-.080) .420-.440) .360) . which is used in the steel industry.100-. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.060-.073 (.330 (.093) .093-.210 (.120-.135) .180-.250-.100) .230-.120) .620) .073) .350-1.290) .120) .101 (.450-.087-.190-.510 (.140-. mainly as scheelite (CaWO4).410 (.092) .180) .380) .060-.170 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.310-.650) .520) .110 (.180 (.360-.210 (.070-.113 (.090 (. which are used in rock drills and metal-cutting tools.340-.460 (.076 (.092 (.060-.790) .204) .200 (.060-.310-.270 (.400) .087) .120) .310) .830) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).00) .160) .090-.220) .590) .530 (.460 (.060 (.090-.550) .160 (.520) .200-.070 (.050-.170) .470-.130) .140) 90th .090-.120 (.390) .084 (.056-.086 (.430-.090) .380 (.080) .210 (.096 (.082-.470) .340) .180-.460) .190-.066-.100 (.080-.380-.380-.120-.500) .111-. bronzes in pigments.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 .060 (.071-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.160-.570 (.100-.300 (.240 (.260-.270-.250) .280-.070 (. respectively.140 (.04.380 (.151) .400-.530 (.230-.116) .210) .091) .093 (.113 (.060 (.073-.240-.350) .270 (.050-.110 (.100 (.690) .120-.380-.170) .210-.200) . Evidence is lacking for the carcinogenicity of tungsten.080-.110 (.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 .084-. Occupational exposure is from dusts released during grinding or drilling of hard metals.300) 95th .490 (.070-.250) .080 (.490) . Little information is available on the toxicity of tungsten.180) .53) .060 (.170-.370 (.080) .070-. Tungsten compounds are used as lubricating agents.060-.100) Selected percentiles ( 95% confidence interval) 50th .560) .320-.950) .470 (.400 (.580) .082 (.120) .620) .360 (.120) .290) .480) Total .640 (.090) .510-1.430-.090-.090 (.180) .090-.350) .068) .132) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.150 (.170 (.100) .097-. and 03-04 are 0.130-.Metals Tungsten CAS No. interval) .065-.130 (.430 (.090-.100) .069-.088 (.250) .140 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.230-.130) .170) .120-.630) .088) .190 (.140 (.360 (.330) .064-.560) .400 (.360 (.810) .069) .070 (.500 (.190 (.800) . population from the National Health and Nutrition Examination Survey.340-.160 (.670) .100) .460 (.300) .550) .113 (.510-. see Data Analysis section) for Survey years 99-00.360-.190-.260-.400 (.560) .080 (.770 (.109) .076 (.120-.530 (.190-.260) .800) .310-.070) .140-.084) .113 (.260 (.060 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.095-.310-.460) .140 (.350 (.080) 75th .470) .150 (.096-.270-.105) .110) .130 (.230) .300 (.100-.120-.620 (.400 (.310-.550 (.074-.04.180-.370-.180-.160 (.058-.430) .100 (.070) .220) .340-.290-.420-.220 (.390 (.310 (.150 (.078-.270-.130) .320 (.130) .080 (.280 (.095-.092 (.160) . Tungsten is used mainly for producing hard metals.270 (.056-.150) .250) .110-.110-.160-.130-.080-.290-.330) . filaments for incandescent lamps.104) .370-.380-.090 (.100 (.080 (.230 (.110 (.300-.101-.470 (.081 (.070) .110 (.210 (.060-.250-.S.105 (.123-.220-.073-.122) .070-. and as catalysts in the petroleum industry. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.350) .300 (.090-.500 (.110-. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.570 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .160-.130) .107 (.126) .560 (.330-.130-. and 0.070) .071 (.220) . 0.180 (.230-. and for producing ferrotungsten.050-.090) .210 (.090-.260 (.082) .065 (.062 (.170) .370 (.04.230) .250) . 01-02.062 (.080 (.082 (.100) .180) .050-.560) .120) .320 (.077-.133) .150-.370) .158 (.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 .280 (.

484) .216 (.287) .293 (. 1997).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 . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.353 (.308) .431) .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 .201) .283) .151 (.180-.109-.085 (.431) .148) .063-.109 (.091) .S.375) .302-.080 (.108-.073 (. interval) . (1987) found possibly due to methodologic. population. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.124 (.077-. 2003.074-.061-.136-.354) .823) .065) .237-.079) .347 (.279 (.267-.133) 90th .333 (.145 (.331-.094-.339 (.098-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.187) .253) 95th .270 (.081) .059-.091 (.150-.064-.333) .157) .381) . similar to those in this Report (Schramel et al. measure urinary tungsten.133) .161) .055-.(Kraus et al.136-.084 (.265 (.426) .064-.060-.083) .079) .090-.084 (.085-. Using neutron activation analysis to 2000.339 (.063-.054-.053-.465) .091 (.181 (.165) .267) .197) .079) .084) .353 (.358) . Nicolaou et al.082) .197 (.272-.060 (.299 (.070 (.120) .217-.079 (.222) .200-.098-.091) .727) ..279 (. 2001-2002.436-1.153-.122-.797) .125) .158) .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 .096) .143-.253-.333) .333 (.090-..056-. and 2003-2004 (Paschal et al.203-. 2005).081-.075-.237) .158) .198) .080-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.075) .554) .100) .188-.214) .224) .186 (.174) .167-.083-.059-.28) .083) .198-.286-.237) .079 (.119 (.197) .174 (.139) .071) .136 (.383 (.063 (.069-.078 (.167-.317 (.300 (.294 (.284) .439 (.462) .131-.065 (.216 (.436) .379 (.255 (.133) .075) .359 (..301) .184 (.130-.231-.080 (.138) .333 (.077) .150-.065-.146 (.S.333-.071 (.414) .329 (.074) .216-.088) .208-.069 (.059-.061-.117) .176-.144 (. 1998).087 (.067-.138 (. 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.364 (.095-.098) .605) .089 (.341 (.S.255-.329-.068 (.065-.074) 75th .340 (.158 (.078 (.094) .306) .088) .250 (.315-.154) .285) .070 (.073 (.092) .199 (.410-.538) .063 (.218 (. population (CDC.081 (. 2001).278-.139 (.083 (.255 (.072-.098 (.119-.148 (.317) .301) .107-.386) .215) .108) .121-.056-.169 (.066 (.061-.155-.084) .459) .216-.100 (.075 (.116 (.333-.179-.170-.153) .344-.333 (.250 (.091) .072 (.392) .078-.080-.261-.152-.067 (.071 (. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.077-.452-.179-.106 (.205-.139-.063-.058-.439) Total .082 (.116) .093) .279 (.071) .075-.130 (.125 (.057-.071) .126-.082) .066 (.300) .164 (.111 (.880) .168 (.105 (.326) .146 (.057-.465) .201 (.122-.739) .222-.105 (.124-.385 (.068-. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.555 (.121 (.231 (.074 (.317-.065 (.144-.093-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher. Patients with medically-inserted tungsten found at increased levels in drinking water. or exposure that a control group of non-metal workers had mean levels differences.071-.634 (.300-.214-.067 (.094) .302-.120) .063-.078) .497 (.484 (.216-.116-.086) .258 (.077) .197-.071 (.074-.083 (.136-.086) .079) .453) .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 .209-.169) .100) .300-.136-.308) .250-.098-.086-.167) .103-.150 (.073 (.078) .354-.104-.233-.426) .582) .086) .431) .054-.081 (.059 (.245-.075 (.301) .275 (.143 (.667) .500) .154) .412 (.138 (.253 (.089) .122 (.360 (. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.167) .667 (.072-.117 (.091) .049-.439 (.217-.258-.069 (.176-.482 (.240-.065-.099-.211 (.200-.206-.085) .060-. population from the National Health and Nutrition Examination Survey.062 (.215 (.158) .095) Selected percentiles ( 95% confidence interval) 50th .199 (.146) .073 (.359 (.190) .087) .

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

006-.008-.040) .012-.009) .010 (.073) .009) .009-.010 (.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 .040-.016-.007-. 01-02.019-. Since the 1990’s.052 (.008 (.011) .008-.017) .011-.017-.026 (.032 (.009 (.023-.019-.158) .007-.005-.020-.011-.018) .017-.005-.006-.008 (.014 (.008 (.017 (.034-.039) .048 (.053 (.030 (.004.015) .010) .013 (.012) .051) .011) .009 (.010-.008) . in some ceramics.010) .017) . It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.047 (.015) .007 (.030) .056) .009 (.007 (.010) .012 (.013) 90th .009-.016 (.021 (.010) .010-.013 (.041 (.016-.007-.007 (.013 (.005-.066) .026 (.030-.063) . respectively.Metals Uranium CAS No.022 (.046-.026-.013 (.046 (.011-. see Data Analysis section) for Survey years 99-00.040-.018 (. and 03-04 are 0.013 (.008 (.008 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.031 (.027 (.010) * .008 (.007 (.009-.008) .022-.010 (.009 (.018 (.069) .044 (.011-.039-.035-.010) .027-.009 (.008-.007-.011-.010) .023) .037) .008 (.011 (.007-.020-.009) .017 (.013-.035) .012 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.006-.016) .037 (.017) .015 (.038) .019-.024 (.031-.015 (.037) Total .025-.009) Selected percentiles ( 95% confidence interval) 50th .018-.039) .007 (.008) . population from the National Health and Nutrition Examination Survey.027-.046 (.021 (.054) .021) .009-.011) .046 (.008 (.014 (.009 (.026 (.015 (.012) .027) .036 (.023) .010 (.013) .007) .024-.007-.006-.020-.022) .011-.037-.008 (.009-.008 (.009) .007 (.023 (.006-.008 (.042 (.007 (.008 (. nuclear fuel.127) .009) .008 (.026) .009-.006-.018) . and 234U.027 (.008 (.009 (.024-.019 (.013 (.023-.036 (.006-.013 (.016) .008 (.009) .027-.049) .022-.067) .S.012-.017-.034-.012-.014 (.031 (.009) .026) .005.009) .033) .046 (.009) .050) . 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. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.018) .023-. 0.045) .065) . and 0.036) .010) .028-.008-. In workplaces that involve uranium mining.031 (.009) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.017) .009) .028 (.012-.017-.013-.065) .006-.037) .007-. Uranium has many commercial uses.017-.006 (.017) .010-.007-.015-.005-. Exposure to DU may occur in military personnel from retention internal shrapnel that contains DU or exposure to dust generated from ammunition Urinary Uranium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.010-.028-.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 .007) . human exposure occurs primarily by inhaling dust and other small particles.088) .008-.008) .011-.007-.015 (.016) .011 (.114 (.020-.040 (.007) 75th .041 (.007-.049) .007 (.023 (.72%).007-.072) .027 (. Variable concentrations of uranium occur naturally in drinking water sources.016) .031 (.054) .014 (.031 (.035) .007) .020) .043) .021-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.054-.007-.029-.006-.010) * .008-.067) .043 (. 235U (about 0.004.021) .027) .056) .012 (.026) 95th .012) .062) .030 (. or processing.005-.009 (.021) .029-.007) .019-.016) .034) .007-.006-.012 (.033 (.009 (.050) .007-.030 (. milling.009-.006-.028 (.023) .042) .017-.040) .009-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).014 (.007 (.020-.007) .008 (.012 (.018) .029 (.023-.007 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 . Thus.021 (.007-.008-.009-.012 (.020 (.009) * .010) .016) .012-. and as an aid in electron microscopy and photography.009) .014 (.033 (.009) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.007 (.046) .013-.011) .048) .021-.279) .028 (.037) .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-.036-.036-.016-.008 (.011) .026-.010 (.007-.060 (.027 (.036) . interval) .009 (.022-.012) .020) .006 (.011) .011) .006-.007-. including nuclear weapons.009-.053) .008-.010-.024-.012-.027) .033-.027) .055 (.023 (.006 (.038 (.064 (.006-.040 (.008) .045) .007-.006 (.

015-.058) .006-.027-. 1992).020) .020-.016) .011) .013 (.015-.010-.008) .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.008-.037 (.006-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.010) .008 (.010) .029) .005-.007) .007-.005 (.043 (.016) .007 (.270) .015) .013) .004-.007 (..007-. Inhaled uranium-containing particles are retained in the lungs. 2003).042-. Radiation risks from exposure to natural uranium are very low.009 (.026 (.034 (.014) 90th .016) .034 (.021-.007 (.080) .020-.029) .027-.015-.007 (.016) .058) .022-.014-. After inhalation.008-.023-.005-.006-. where limited absorption occurs (less than 5%).016) .010-..008 (.020-.014 (.008) .016-.006 (.016 (.015) .013 (.006-.007 (.026-.027) .034 (.048) .014-.014-.005-.008-.026 (.027-.034-.013 (.050 (.017-.008 (.054) .006-.019) .030-.008) .033 (.005 (.012) . 240 Fourth National Report on Human Exposure to Environmental Chemicals .024-.007 (.009) .013 (.034-.018 (.1%-6% of an ingested dose may be absorbed.015-.009) Selected percentiles ( 95% confidence interval) 50th .018-.012 (.011) .033 (.031 (.011-.006 (.030) .006-.006-.042) .012-. the shrapnel acts as a source of chronic.047) .010 (.021) .006-.051 (.053) .033 (.018-.009) .027 (.017) .005 (.006-.013 (.021 (.009 (.028) .038) 340 368 289 719 762 725 1405 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .033) .010-.015 (.017-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.014 (.039) .006-.019) .008) .010-.022) .022 (.008 (.022-.008 (.025-.016-.008) .024) .Metals impact.019 (.004-.007 (.010 (.013 (.011-.008) .020-.009) .010-.032) .015 (.006-.012-.012) .009) * .019-.018) .007) .008) .025-.008 (.009 (.048) .019-.051) .007 (.034) .061) .012 (.010) * .012) .009 (.010 (.146) .010 (.018-.041) . In cases of retained DU shrapnel.012 (.050) .007-.006) .006) .028) .007-. kidneys. 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.006-.029 (.012 (.009) . liver.021 (. Health effects from uranium exposure result from chemical toxicity to the kidney.025) 95th .029) .030 (.011-.007 (.011-. Depending upon the specific compound and solubility.024-.009-.051) .039) .006-.013 (.007 (.050) .010) .009-.006) .021 (.007-.014) .027) .017-.014) .030 (.011) .007 (.006 (.025 (.029 (.010) .006-.006-.016) . Uranium is eliminated in feces and urine.030 (.015) .006-.013) .040 (. 2005).024 (.014) .027 (.007 (.033 (.007-.008-.074) .007-.027 (.013 (.013 (.030) .006-.010-.009) .028-.022 (.025-.010-.010-.039) .010-.011-.009) .010-.030-.013) .009) .012 (.006-.024 (.024 (.008-.011 (.041) 1227 1334 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .007 (.008 (.008 (.009-. which represents distribution and excretion.006-.024) .007) .008) .011-.006-.011) * . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.028 (.045 (.024) .019-.027-.022-.005-.008) .019-.044) .017) . Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.015 (.018-.026) . 0.020 (. low level exposure.031-.020 (.006-.029 (. which can occur occasionally from high occupational exposure.024-.010 (.009-.008) .005-. After exposure to soluble uranium salts. After long term or repeated exposure. the initial half-life of uranium is about 15 days (Bhattacharyya et al.035 (.006 (.006 (.010-.009) . population from the National Health and Nutrition Examination Survey.008) 75th .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 .007-.009-.016) .S.032) .015 (.028) .011-. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.007 (.017) .017-.011-.028 (.053) .034 (.005-.011 (.009-.006) .007 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.059 (.006-.077) .007 (.. with much slower elimination from bone.011-.016) .016-.007-.007 (.007-.022 (.008-.019 (. interval) .067) .042) .026 (.024) .017 (.029) .006) .007 (.009) .006-.028) .017 (.007 (.063) .010) .006-.015) .012 (.007 (.025 (.025-.034 (.018-.010) .020 (.039) Total .007 (.051) .009) .056) .012 (.006 (.013 (.019-.021 (.008 (.015-.005-.013-.035 (.024) .019 (.016-.100 (.005 (.008 (.008) .009) .009 (.

2006). 2004). Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. Zimmerman I.107:143-157. Information about external exposure (i.1992. the median urinary uranium concentration was 2.. 2001-2002.65 μg/L). soldiers evaluated before. McDiarmid et al. Hamilton MM. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000.1996. In a study of 105 persons exposed to natural uranium in well water. 2005. Fourth National Report on Human Exposure to Environmental Chemicals 241 .. Thomas RG. 1978). Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al.011 μg/L (McDiarmid et al..atsdr. 1991. Third National Report on Human Exposure to Environmental Chemicals. Hamilton et al. 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. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Carmichael AJ. 2004)..78:143-146. Galletti. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. population. The U. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. Uranium content of blood. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. 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. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.55 μg/L (median 0. Atlanta (GA). 1994. and 2003-2004 (Dang et al... IARC and NTP have no ratings for uranium human carcinogenicity. 2000). Six workers in a depleted uranium program showed concentrations of 0. 2004). Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Durakovic A. Health Phys 2000. 2003. but in whom no shrapnel was embedded.S. during. Karpas et al. environmental levels) and health effects is available from ATSDR at: http://www. had a mean urinary uranium concentration of 0. 2000).gov/ toxpro2. with emphasis on quality control. Metivier H.. 1992. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. in that the levels were below their respective detection limits (Byrne et al. respectively. et al... although slightly increased during and after deployment. 2006). (May et al. (Kurttio et al. 2004).. 28 soldiers who may have been exposed to DU by inhalation.cdc. eds.. 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.S. 2006. References Bhattacharyya MH. Horan P. Dietz LA. Radiation protection dosimetry. 2006). 2002). urinary levels of uranium were as high as 9. Squibb K. Byrne AR. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.... Volf V.078 μg/L (ranging up to 5. Tolmachev et al. Sci Total Environ 1991. or wound contamination.S. Pullat VR. Komaromy-Hiller et al.. the geometric mean urinary uranium concentration was 0. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. EPA. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. In 17 U.61 μg/g creatinine..066 μg/g creatinine (Gwiazda et al.110 to 45 μg/L (Ejnik et al.62:562-566. In the same study. 1-49. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Benedik L. the median urinary concentration was 0.html. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU.e. Dang HS. Boyd P. Ejnik JW. 2002. A cohort of 46 U. 2006). Breitenstein BD. Stradling GN. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.S. Vol.Metals injury associated with elevated urinary uranium levels (Kurttio et al.. NRC.S. Mil Med 2003. Drinking water and other environmental standards have been established by U. Health Phys 1992. Muggenburg BA. Kent (England): Nuclear Technology Publishing.. 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. 41 (1). ingestion. Pillai KC. In: Gerber GB. pp.162 μg/L) (Orloff et al. and no consistent effects on multiple endpoints of kidney function were found.168(8):600-605.S. Centers for Disease Control and Prevention (CDC). McDiarmid M.

47(6):972-982. Health Phys 2004. Review of elements in blood. Renal effects of uranium in drinking water. Van der Venne MT. Li WB. Roth P.S. Costa R. Sabbioni E. Nuclear Regulatory Commission (U. Bennett LG.94:319-326. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Environ Res 2004. Noguchi H. Auvinen A. rapid. Washington (DC): NRC.86:12-18. Int Arch Occup Environ Health 2006. Jackson RJ. Am J Kidney Dis 2006. Kane R.22–Bioassay at uranium mills. 242 Fourth National Report on Human Exposure to Environmental Chemicals .Metals Galletti M. Hollriegl V. Nuclear Regulatory Commission (NRC) Guide 8. patient population and literature reference intervals for urinary trace elements. et al. McDiarmid MA.296(1-2):71-90. Cordero S. Environ Health Perspect 2002. Salonen L. Radiat Environ Biophys 2005. Sci Total Environ 1994.S. Gwiazda RH. J Toxicol Environ Health A 2004. Kurttio P. et al. Metcalf S. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. concentration and daily excretion of uranium in urine of Japanese. Shelly T. Sampson EJ.67(8-10):697-714.S. Squibb K. U. Pinto V. Hancock RG. Comparison of representative ranges based on U. Saha H. McDiarmid M. Wahl W. Tolmachev S. Ash KO. Lewis BM.85:228-235. Scott K.87:51-56. Engelhardt SM. et al. Cremisini C. Saha H.82(4): 527-532. Biologic monitoring for urinary uranium in Gulf War I veterans. Biokinetic modeling of uranium in man after injection and ingestion. Wilson PD.79(1):11-21. U. Element reference values in tissues from inhabitants of the European community. Smith D. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Health Phys 2003. Oeh U. Health Phys 2004. Hamilton EI. et al. Halicz L. Paschal DC. NRC).71(6):879-85.110(4):337-342. Inductively coupled plasma mass spectrometry as a simple. Health Phys 2002. Marko R. Karpas Z. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Jarrett JM. Mistry K. Paretzke HG. Karpas Z. Ejnik J. Englehardt SA. Marino R. Uranium daily intake and urinary excretion: a preliminary study in Italy. Harmionen A. et al. McDiarmid MA. Komaromy-Hiller G. Uranium and thorium in urine of United States residents: reference range concentrations. Kuwabara J. Health Phys 1996. Katorza E. Makelainen I. Human exposure to uranium in groundwater. Gucer P.S. Ting BG. et al.44:29-40. Andrews WS. Pekkanen J. Clin Chim Acta 2000. Pirkle JL. Orloff KG. Roiz J. Ough EA.158:165-190. D’Annibale L. Salonen L.91(2):144-153. Kidney toxicity of ingested uranium from drinking water. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. July 1978. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. May LM. Komulainen H. VI. Lorber A. Oberbroekling KJ. Squibb K.81:45-51. Health Phys 2006. Howerton K. Heller J. Kalinsky V. Kurttio P. Auvinen A. Oliver M. Charp P. Environ Res 1999.

80-8.0) 15.11) 4.40 (4.10) 5. 2007).90-3.0 (11.0-18.90-12.80-15.90 (3. certain catalytic metals. laboratory analysis.00) 3.10-11.0) 15.20 (6.03) 3.90 (2.00) 3.0) 10.20 (4. and reducing agents.00) 4.0 (11. milk..16) 3.10 (6.10) 3.0) 14.0-15. interval) 3.08-3.30-19.0 (9.0) 14.90-10.0) 10. population from the National Health and Nutrition Examination Survey.30) 6.70-3.22-5.49-3.0-23.32 (3.0 (8.18-3.20 (5.90-6.50 (3.01 (2.70-3.0) 13.46) 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 3.66) 3.0 (13.50) 6.90 (5.30) 6.0) 9.40 (8.40 (3.39-4.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.19-4.00-5. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.80-6.0 (11.50-7.70-6.0) 11.50) 5.50) 3.0) 9.10-4. and certain plants with high water content (e. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism. 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.30 (5. Survey years 01-02 03-04 Geometric mean (95% conf. 2002).50-4.0) 9.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.76 (3.0) 9.30-17. leather tanning.80) 75th 6.20 (4.0) 13.10-7.30-7. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 . Perchlorate is stable under most environmental and physiological conditions.0-29.40-4.51 (3.0) 10.0 (12.10 (2.10) 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.74-3.93-3. Drinking water.90-11.40) 3.0-17. and electroplating.0 (11.10-11.0) 95th 14.0-18. matches.96 (3.50-4.0 (12.87-3.0) 11. fabric dyeing.0) 8.90) 5.40 (5.44-4.60 (4.60) 8.0) 13.40-6.75 (3.0) 8.0 (11. 2005). lettuce) can be the main sources of intake for humans (FDA.05 and 0.90 (5.0) 13.40) 2.65) 3.0) 13.50 (8.62 (3.00) 5. but has strong oxidant properties in the presence of concentrated acids.19 (3.11) 3.12) 3.90-9.10 (5.70 (3.80-12.0) 16.05 (2.0 (9.80 (7.0) 9.30 (2.0-17. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.0) 11.40-13.0 (9.0) 19.70-7.50) 11.S.93 (4.20 (2. 1998).90 (5.0) 708 617 681 652 1228 1092 Limit of detection (LOD.80) 7.0-19.00) 7.60-7.70 (3.56) 3.0) 9.88) 3.0-18.40-11.0 (12.40 (5.50-11.89-3.40) 6.30 (5.40) 3.90-3.0) 14.70-12.38) 5.80) 12.70-5.EPA.0-17.0 (11.20-3.0 (9.Perchlorate Perchlorate (Urbansky.26 (2.0 (8.67-5.0 (11.0 (9.60) 3.47-4.60) 5.30-7.40) 90th 10.0 (11.70-11.80-4.0-15. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.40 (5.0) 13.40-7.. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.0-17.S.0) 13.51 (3.5 hours and has a small estimated volume of distribution (Crump and Gibbs.70) 3.0 (11.30-6.0 (8.50) 5.20) 4.0 (12.0) 13.40) 3.80 (3.54 (3.20-11. Perchlorate was added to the U.70-9.60-6.80 (6.29-3.90-11.90 (4.20-12.S.20-4.70 (3.0 (8.90) 6. Other manufactured uses include fireworks.10) 5.81-16. or ammonium salt.21 (2.81) Selected percentiles ( 95% confidence interval) 50th 3.84) 14.10-12.0 (9. In addition.60 (7.0-17.0 (10.09) 3.10) 12.40 (3.50-3.80 (3.60 (4.20 (7.g.02 (3.68) 4.0 (9. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.0 (11.00-6.31) 2.80) 3.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.80-4.20) 7. It is normally found and produced as the anion of a sodium.79 (2. 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.20-4.07-4.0) 12.40) 4.22 (2.0-14.05.75-3.20 (2.10 (7. 2005). potassium. and limited applications in pharmaceutics.0 (8.0-17.35 (3.76) 4.90-9.93-4.40 (4.00-6.20) 3.30 (2.10 (6.40-4.45-4.0-20.50 (5.40-5.20 (8.

60-5. thiocyanate.0) 12. 2005).60 (3.3) 8.67) 5.60-3.04-3.89-3.40 (7.30-10.53 (2.60) 10..70-5.50) 95th 12.30) 5.42 (3.0) 14.36 (8. 2005. Many factors may be important in consideration of perchlorate action on the thyroid: dose..19-10.76 (3.90-3.S. U.4 (10. 2007).20-3.22 (2.46 (3. dietary iodine intake.20-3.70 (2. 2002. However.46-13.09) 3.43) 6.g. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.2) 8.60-15.66) 3.50) 2.40 (4.4 (11. 2003. NAS.60-8.10) 3.09 (7.95 (2.98) 3.00-11.89 (2.99-3.56-3.12-2.33 (7.0) 4. 2002).93) 3..21 (2.44) 3.0-44.0) 11.96) 2. gender.20) 8.87) 2.35 (2.0 (9..4-16. Survey years 01-02 03-04 Geometric mean (95% conf.61-10.6-17.20-9. 2005).10-7.10) 13.93-7.80 (7. nitrate.0 (9.70-3. In the U.50 (3.40-10.20 (7.77 (3.4 (8.1) 8.83 (5.87) 7.70) 2.75) 3.26) 4.EPA. Lamm and Doemland.97-5.25 (3.84) 2.90 (2.22-6.1-14.40 (3.10) 6.6) 12.90 (7.50-9. 1999.50-5. chronicity of exposure.52 (8.58) 2.. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.50-3.87 (7. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.02) 3.50) 6.3) 12. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.40) 3. up to 68% RUI has been demonstrated. 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. 2000). Also.30) 3. Ecologic studies from screening programs with elevated perchlorate in the regional drinking water have indicated no increased prevalence of abnormal neonatal screening tests for this disorder in these regions (Kelsh et al.0 (8.80) Selected percentiles ( 95% confidence interval) 50th 3.80 (4.90-2.0) 12.99 (5.4) 8.39-4.73) 3.20 (3.10 (1.74) 7.0 (11.50) 9.0 (9.0) 6. medications).20 (2. levels.16-3. Steinmaus et al.81-3.20-10. and the presence of other substances known to affect thyroid function (e.0-17.59) 3.03 (2.0) 13.20) 3. women with urinary levels of iodine less than 100 micrograms per day.S.35) 3.10 (4.41-9.30 (6.0 (10.22-4.72 (3. interval) 3.0) 12.47) 2.40 (3.04-3.90-20. 2005.15-12..10 (6.00 (4.3) 11. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.10-3.51-4.70-15..1-22.10 (2.54 (2.1 (11.93-5.18-3.82 (5.1-13.39 (3. Lawrence et al.50 (6.64) 5.25) 5.50) 5.1-16.22-4.5) 8.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.7 (11.87-3.S. 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.30 (5.30 (3.0 (11.40) 17.S.29) 2.20 (6. population from the National Health and Nutrition Examination Survey.0) 7.40) 5.0) 9.70) 10.71 (5.34-3.EPA.30) 75th 5.S.60-8.00) 4.24 (4.61 (5.20-4.44-6.30) 90th 9.80-3..60) 3.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.32) 5.0) 9.05 (4.90-15.56 (3.08) 3. Li et al.5 (13.91) 4.4) 13.2) 8. 2001.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.3 (10.25) 5.80 (7.30-5.00) 3. perchlorate is negative in most genotoxic assays (U.14 (2. 2002.4 (11.80-3.90) 5. During gestation and infancy.87 (5.0-14.51 (3. levels and sufficient in most participants (Tellez et al. 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. Greer et al.00-2.00 (2.54 (3.70 (2.37 (4.70 (4.45-2.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.00 (6.50) 2.19-6.64-3.90 (2.20 (4.61-5.76-3.24-2.0) 13.00) 9. in a representative sample of U.07 (2.10 (4.6) 20.30-5.70-4.S. menopausal status.8 (11.0 (8.93-8.0-14.37-13.1 (8.10) 4.33-12.0) 12.60-11.60-5.90-11.Perchlorate inhibition (RUI).00-3.46-4.39) 2.35 (4.0-19.60-11.45) 3..60) 8.90-9.0) 10.3-14.60-6.52-9.90 (4..0 (11.93-5. although iodine intake was higher than U.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 .26 (3.33-6. age. 2006.86) 4.S.12 (6.02-4.25) 5. 2005).08 (3. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.29-6. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.

Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. and environmental perchlorate exposure among residents of a Southern California community. Daaboul JJ. J Occup Environ Med 2003. Dasgupta PK. Li FX. The effect of perchlorate. Additional information about exposure and health effects is available from the U. Environ Health Perspect 2002. Environ Health Perspect 2005. Primary congenital hypothyroidism. Lamm SH. Miller MD. Health Implications of Perchlorate Ingestion. Benchmark calculations for perchlorate from three human cohorts..10(8):659-663. Blount BC. Landingham CB. Gibbs JP. References Blount BC. Pirkle JL. Crump KS. Lawrence JE.html. 2005). J Expo Sci Environ Epidemiol 2007. Pirkle JL. et al. Neonatal thyroxine level and perchlorate in drinking water. Caldwell KL. Thyroid 2000. Erratum in: Environ Health Perspect 2005. Environ Health Perspect 2007. Valentin-Blasini L. Crump KS.90(2):700-706. Braverman LE. Blount BC. 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. Buffler PA.11(3):295. Braverman LE. J Occup Environ Med 2000. Barnard JC. population. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Perchlorate Exposure of the US Population. Richman K. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.17(4):400-407. Erratum in: J Occup Environ Med 2004.S.46(5):509. Byrd D. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. (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. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 .gov/toxpro2.113(11):A732. Dyke JV. Howd R. Washington (DC): National Academy Press. Magnani B. Lamm S. Greer SE. Skeels MR. Abarca CR. Environ Health Perspect 2006. Osterloh JD. Blount et al.gov/safewater/ccl/perchlorate/perchlorate. thiocyanate.html and from ATSDR at: http://www.S. et al. Steinmaus C. 2005). newborn thyroid function. Kelsh MA. Kirk AB. Valentin-Blasini L.. Deyhle GM. National Academy of Sciences (NAS).40(21):6608-6614.htm. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.atsdr. Braverman LE. He X. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data.. Tellez RT.cdc. National Research Council of the National Academies. Lamm SH.114(12):1865-1871. Lamm SH. most of the population is considered to be below the U. Environ Sci Technol 2006. Low dose perchlorate (3 mg daily) and thyroid function.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Biomonitoring Information Urinary perchlorate levels reflect recent exposure.113(8):10011008. Sesser DE. Thyroid 2001. CFSAN/Office of Plant & Dairy Foods. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. epa. Li Z. Goodman G. Rutherford GW. Also. Pleus RC. EPA reference dose (Blount et al. The effect of short-term low-dose perchlorate on various aspects of thyroid function. 2001-2002.fda. 2005. J Clin Endocrinol Metab 2005. Food and Drug Administration (FDA). Pino S. Perchlorate in the United States.S. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. 2007).Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Osterloh JD.EPA at: http://www. Cross M. Available at URL: http://www.41(5):409-411. Analysis of relative source contributions to the food chain. 6/2/09 Greer MA. Lau EC. Pino S. Mauldin JP.115(9):1333-1338. 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. 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. Page Last Updated: 05/28/2009. May 2007. Chacon PM.110(9):927-937. et al. Jackson WA. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. and nitrate on thyroid function in workers exposed to perchlorate long-term. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002.42(2):200-205. Doemland M.45(10):1116-1127. Lawrence J.

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

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

The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. 2005). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. population from the National Health and Nutrition Examination Survey. there is limited information on the sources. human toxicokinetics. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. C5.... < LOD means less than the limit of detection. Bookstaff et al. may metabolize or degrade to PFOA (Dinglasan et al. All sources of human exposure are uncertain. 2000.. in a wide variety of marine and land animals (Kannan et al. 2006... and in offspring. thymus and spleen... The elimination half-life of PFOA in humans is roughly estimated to be 3. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. the 8-2 telomer. 2007). 2003). and β-oxidation of lipids (Kudo et al. 1993).4..5 years and for PFOS... 2004. but still can have long residence times in the body.. 2004..e. Taniyasu et al... 2004). 2005). Prevedouros et al. Tittlemier et al. Keller et al. 2005). but probably include dietary sources (Kannan et al. 2003a and 2004a). For instance. 2005. PFCs have been identified in surface coastal and ocean waters (Yamashita et al.. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins. 2005. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD. 2005. Lau et al. The PFCs often measured in human serum are listed in the table. 1995. kidney.8 years (Olsen et al. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels).. In some cases. C7). including immunologic effects and tumor induction. which may vary for some chemicals by year and by individual sample. Guruge et al. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.. Lau et al. U.. by high protein binding in plasma and other proteins. PFOA has been reported to cause liver. Vanden Heuvel et al. Unlike many organohalogen contaminant chemicals. 2004. 2006a. 2004). The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. 1990). endocrine and immune effects. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. Survey Geometric mean (95% conf.S. 2003).. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. and in human blood and semen (Calafat et al. 2002.. peroxisomal proliferation. heptadecafluoro-1-decanol. in part. or effects of other PFCs. Excepting PFOS and PFOA. hepatotoxicity. Kannan et al. approximately 4. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. pancreas. 248 Fourth National Report on Human Exposure to Environmental Chemicals . growth retardation and delayed sexual maturation (Kennedy et al. 2003. Olsen et al. environmental fate. PFOA is mostly excreted in the urine in animal studies. 2004. 2007a). It is unclear if environmentally degraded telomer products are a major source of other PFCs.. Some of the effects in animals may be mediated through peroxisomal proliferation. 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.. see Data Analysis section) for Survey year 03-04 is 0.S. EPA. C6.. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al.

monkeys.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al.40) . Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. 2003.. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. reproductive.500) .00) .. U.S.300 (<LOD-. 2004.00 (.600-2.800 (.900 (.900 (. Fourth National Report on Human Exposure to Environmental Chemicals 249 . 2007b). Olsen et al. 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... animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. thyroidal). Harada et al. PFOS. Thibodeaux et al. PFOA..80) 485 538 962 Limit of detection (LOD. However.3. 2003. 2004). In such studies. 2003a). 2003a.108 times higher than background serum levels in humans (Butenoff et al.500-1.. 2005).400-.400 (<LOD-. 2004b). which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th .600 (. 2007... and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400-1. Olsen et al.20) . and changes in thyroid hormone concentrations (Grasty et al. 2003a).. 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.00) .300 (<LOD-. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 0. 1999. 2007a.80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .800) 1. 2004. hepatotoxicity.500-3.. or increased cancer rates (Alexander et al. 1992.10) * 03-04 03-04 * * < LOD < LOD < LOD .. Fei et al.400-1.500) 90th .400-.500-1. PFOA.900 (. 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. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. population. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.80) 640 1454 03-04 03-04 * * < LOD < LOD . In comparing three separate reports on adults. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. EPA..400 (<LOD-. possibly related to lung immaturity (Lau et al. 2004a. population from the National Health and Nutrition Examination Survey.00) .. 2003).800 (. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. elderly and children. 2003)..700 (.400-1. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.10) .500) .700) . development in offspring was stunted and hypothyroxinemia was observed.400 (<LOD-. and humans.500 (.600 (. 2003).10) .. 2007). Cook et al. PFOS. perfluorohexanesulfonate (PFHxS).. 2003.50) .800 (.800) 1. 2004)..300 (<LOD-..500-1.400-1. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. 2005).S. 2007a. Kennedy et al.500) . Olsen et al.600 (.500 (.500 (<LOD-1.400-1.300-1. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. 2007b.S. Lau et al.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.500-.S.. At doses causing maternal toxicity. 2001. the potential to estimate risks to humans from animal doses is uncertain. 2003a.10 (.500-1. developmental and teratogenic effects were demonstrated in offspring. EPA. Animal studies of PFOS have demonstrated weight loss.. Survey Geometric mean (95% conf. At high but non-toxic maternal doses of PFOS. < LOD means less than the limit of detection. and there was no clear evidence of excess all-cause or diseasespecific mortality.. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.500) . U.800 (.400) . 2003a.

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

400) . see Data Analysis section) for Survey year 03-04 is 0. see Data Analysis section) for Survey year 03-04 is 1.500) 485 538 962 Limit of detection (LOD. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300-. 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.600 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .400 (<LOD-. < LOD means less than the limit of detection.S. which may vary for some chemicals by year and by individual sample.300 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 251 .3.0.400 (. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (<LOD-. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500 (<LOD-.S.400 (<LOD-.500-.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 . < LOD means less than the limit of detection.600) < LOD .900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .900) < LOD . Survey Geometric mean (95% conf.

50-6.600-.60 (1.80-12.80-7.42 (1.44 (2.12) .40) . Survey Geometric mean (95% conf.20 (1.51) 1.50) 6.700 (.5) 5.00-6.09 (.50-10.00-8.10) 5.5) 8.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.50 (1.30 (3.20 (1.70) 2.90) 90th 5.62-2.50 (1.20) .900-1.10 (4.80 (1.70) 1.40-1.900-1.50 (6.900-1.90) 3.10) 1053 1041 03-04 03-04 03-04 .40 (1. 252 Fourth National Report on Human Exposure to Environmental Chemicals .60) 1.80 (1.00-7.10) 1.900 (.60-2.80-4.54) .30-12.77-2.91) 2.40) 4.30-6.809) 1.689 (.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.697-1.20-2.10 (.0) 1053 1041 03-04 03-04 03-04 1.10) 1.70-6.00 (5.40 (1.30) 3.00 (1.80-8.10-9.3 (9.00 (1.60) 3.00-1.40 (1.56-1.966 (.40) 640 1454 03-04 03-04 2. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50) 2.834-1.60 (1.40-1.30) 03-04 03-04 .16) .17 (1.90 (1.70-2.6) 7.14 (.90-2.900-1.80) 5.900-1.50 (4.80 (4.70-7.17-1.20) 1.80-3.852 (.20-1.10) 6.30-9.20-1. interval) .30 (1.816-1.90-19.92 (1.1) 485 538 962 Limit of detection (LOD.60-4.90 (4.10) 4.50 (2.20-3.80) 1.00 (2.80) 4. Survey Geometric mean (95% conf.60 (1.40) 1. population from the National Health and Nutrition Examination Survey.80) 3.30 (2.70) 2.861 (.60-8.72 (1.00) 1.30 (6.900 (.73-2.60-4.26) 2.90 (4.90 (1.70-2.90) 1. interval) 1.30-2.800 (.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.50 (1.30) 3.80-8.86 (1.20) 1.70 (1.90 (1.90 (1.50) 2.50-6.20) 2.90) 8.00) 1.40-3.60-3.963 (.70) 13.800-1.912-1.900) 1.30) .40 (2. population from the National Health and Nutrition Examination Survey.60 (6.826-1.30) 3.05-2.20) 485 538 962 Limit of detection (LOD.1.60) 2.80) 90th 2.27) 1.72) 1.60-7.10) 6.20-1. see Data Analysis section) for Survey year 03-04 is 0.60-2.67-2.3.90) 1.80-2.90 (2.00) 2.93 (1.20 (6.10 (4.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.900-1.984 (.10) 8.30 (2.721-1.90) 1.80-7.00 (.70 (2.10-5.00 (1.30 (1.30 (7.90-10.80-6.00-1.20) 03-04 03-04 2.50 (6.586-.10) 4.10 (.20-1.80-4.01 (1.87-2.30 (1.60-2.80-4.20 (1.50-3.70-5.S.40 (1.30 (1.40) 1.40) 2. see Data Analysis section) for Survey year 03-04 is 0.60-3.50 (1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.08) 2.04) .03) 1.0) 8.60) 9.00 (1.10 (.20 (1.700-1.S.20 (6.835-1.70-10.50 (4.00) 3.80-3.10) 75th 1.70) 3.70) 1.10 (1.00 (.10-9.40) 640 1454 03-04 03-04 1.10) 75th 3.

1-36.3 (35.6 (19.S.40) 75th 5.0) 21.80 (6.0) 21.00 (5.4) 640 1454 03-04 03-04 23.20) 7.2 (16.80) 8.30-3.3 (35.7 (7.4) 75th 30.82) 4.9 (19.70 (5.5) 18.0) 03-04 03-04 19.8-30.1-33.8) 32.8-22.3) 42.1 (23.S.80-4.5) 19.3) 41.7-69.2-57. population from the National Health and Nutrition Examination Survey.07-4.7 (35.30-8.5-62.8-22.37 (2.4) 21.20) 7.40-6.70-9.60-9.5) 9.2-22. interval) 20.4 (23.0) 23.40 (6.1-24.8 (34.40-14.70) 6.20-5.20) 5.00 (5.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.8) 27.7-49.8-81.8-22. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.5 (28.60) 03-04 03-04 3.0) 90th 41.3) 28.7 (43.53) 3.70-10.3) 485 538 962 Limit of detection (LOD.7-33.7-23.90 (7.79) 4.60 (7.60 (3.70-5.6-24.5-21. Survey Geometric mean (95% conf.1.5) 7.91) 3.3-61.6) 7.3-22.1-25.6 (35.8 (37.2) 640 1454 03-04 03-04 4.2 (19.6-50.60-6.27) 4.40-10.60) 8.4-42.6 (44.6) 1053 1041 03-04 03-04 03-04 3.8) 46.10 (3.8-35.80 (5.30 (3.1 (24.9) 27.10) 5.4-25.5) 8.3 (44.70-7.2) 30.21-3.0 (20.90 (7.7 (13.0-70.4 (28.9 (22.18 (3.30-5.00) 3.60-13.00 (3.10 (6.1) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 4.40-6.7-30.40 (4.0-66.30) 7.7 (35.80-9.3 (28.70) 3.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.5-23.8 (45.6-45.50 (4.50) 7.4.40-17.9 (17.35) 3.70 (3.0) 36.40) 5.9 (13.90) 6.60 (4.2 (27.1-35.3 (17.20 (4.0) 43.9-19.80 (7. see Data Analysis section) for Survey year 03-04 is 0.6 (42.6) 62.9) 22.84-3.4) 20.85-4.7) 39.1) 15.2 (28.60-14.90 (5.30 (5.10-3.89 (3.0) 485 538 962 Limit of detection (LOD.6) 42.5 (28.5) 32.2 (21.60 (6.1 (19.9-38.47 (4.60 (6.4 (17.99-3.50-13. Survey Geometric mean (95% conf.2 (18.90-4.2) 45. population from the National Health and Nutrition Examination Survey.20) 10.2) 30.0-16.7 (19.60 (5.30-11.7 (43.80-12.4) 56.40) 90th 7.65-4.96 (3.50) 4.95 (3.70 (5. Fourth National Report on Human Exposure to Environmental Chemicals 253 .5) 57.8-78.20 (4.5-33.9-23.50-4.67-4.9) 22.90-4.50-6. interval) 3.70) 4.80 (6.4 (19.20) 5.20) 4.20-9.1) 57.6) 35.50 (3.6) 9.7-53.90 (7.70-7.20-4.40) 3.4 (19.1-52.30 (3.5) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 21.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.47-4.30) 6.6) 21. see Data Analysis section) for Survey year 03-04 is 0.9) 9.0 (27.6) 18.4-17.10 (3.11 (2.0-20.30-6.90-12.5) 1053 1041 03-04 03-04 03-04 14.

which may vary for some chemicals by year and by individual sample. 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 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (.200-.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300) .S.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (. which may vary for some chemicals by year and by individual sample.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .200-.300) .300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (<LOD-.300 (.300-.200-.300 (.300) .4.300) .300 (. < LOD means less than the limit of detection.300) .200-.300 (.300-.S.200-.300-.300) .500) < LOD 485 538 962 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th .500) 485 538 962 Limit of detection (LOD.300 (.300) .200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.200-.200-.300 (. population from the National Health and Nutrition Examination Survey.500) . Survey Geometric mean (95% conf. < LOD means less than the limit of detection.300-.300 (.500) . see Data Analysis section) for Survey year 03-04 is 0.300 (.400 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.200-.500) .200-.300 (.2. population from the National Health and Nutrition Examination Survey.300 (. 254 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf.

10) .40) 1.20-1.30) .10) * 03-04 03-04 * * < LOD < LOD .00 (.S.80) 1. Survey Geometric mean (95% conf.10-1.00 (.700) 90th 1.500 (<LOD-.30) 1.700 (<LOD-.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .900-1.600 (<LOD-1.10 (.10 (1.30 (1.300-2.700) 1. see Data Analysis section) for Survey year 03-04 is 0.900-1.900-1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .900 (.900-1.700 (<LOD-.700 (<LOD-.10 (.300 (<LOD-1.40) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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.60) 640 1454 03-04 03-04 * * < LOD < LOD .30) 1.700 (<LOD-.800 (<LOD-.700 (<LOD-.00 (.6.600 (<LOD-1.300 (<LOD-.700 (<LOD-.10-1.900) .70) 1.10-1.20 (1. Survey Geometric mean (95% conf.80) 1.800) .30 (1. population from the National Health and Nutrition Examination Survey.600 (<LOD-1. which may vary for some chemicals by year and by individual sample.10) 1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.700 (<LOD-2.600) .900-1.10 (.400 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 255 .00 (.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.90) .3.600 (<LOD-.30 (1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50 (1.900) 485 538 962 Limit of detection (LOD.00) < LOD .400 (<LOD-1.800) .10-1.10-1.S.10) 1.700) 1.60) 485 538 962 Limit of detection (LOD.10) .30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0.900-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .20) 1.00-1. which may vary for some chemicals by year and by individual sample.900 (<LOD-1.700) .50 (1.900-1. < LOD means less than the limit of detection.

Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Bandai N.1968--2003. Crit Rev Toxicol 2004.39(1):80-84. Calafat AM.S.104(2):322-333.41:2237-2242. Fei C. Herbstman JB. Reidy JA. Olsen GW. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. 2007b. Characterization of risk for general population exposure to perfluorooctanoate. Saito N. Yun SH. Tarone RE.124(2):119-132. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Seneviratne HR. Environ Sci Technol 2007a. Wong LY. Reidy JA. Kuklenyik Z. Kudo N.40:21282134. Olsen GW. Wijeratna S. J Environ Monit 2005. Environ Health Perspect. 256 Fourth National Report on Human Exposure to Environmental Chemicals .Koizumi A. Environ Sci Technol 2006a. Kannan K. The influence of time. Witter FR.7(4):371-377. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Guruge KS. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Mandel JH. Polyfluoroalkyl chemicals in the U. Grasty RC. Biegel LB. Rev Environ Contam Toxicol 2003. Arendt MD. and perfluorinated contaminants in livers of polar bears from Alaska. et al. Reidy JA. Olsen GW.Perfluorochemicals References Alexander BH. Saito N. et al. Birth Defects Res B Dev Reprod Toxicol 2003. Taniyasu S. Kamiyama S. Hurtt ME. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States.115(11):1596-1602. Katakura M.68(6):465-471. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Yoshinaga T. et al. Fillmann G. Day RD. Falandysz J. Frame SR. Regul Toxicol Pharmacol 2004. Yamashita N. Halden RU.34(4):351-384. Kuklenyik Z. Ye Y.and perfluorinated acids. Environmental and toxicity effects of perfluoroalkylated substances.134(1):18-25.60(10):722729. Harada K. Burris JM. Mandel JH. Chemosphere 2006b.S. Tully JS. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Koizumi A. Keller JM. Environ Res 2005. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Rogers JM. in vivo.60(1):44-55. Mohotti KM. Bookstaff RC. Chem Biol Interact 2000. Olsen J. Ingall GB. Mandel JS.39(23):9101-9108. Needham LL. Perfluorinated chemicals in selected residents of the American continent. Rodricks J.38(17):4489-4495. Lau CS. Toxicol Appl Pharmacol 1995.38(10):2857-2864.99(2):253-261. Calafat AM. Seacat AM. J Occup Health 2004. O’Connor JC. Toxicol Sci 2001.63:490496. Cook JC. Toxicol Appl Pharmacol 1990. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Morikawa A. Calafat AM. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Moore JA. Aguilar-Villalobos M. Environ Health Perspect 2007. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Suzuki E. Environ Sci Technol 2004. Needham LL. Jarnberg U. Bignert A. Moore RW. Kennedy GL Jr. Kuklenyik Z. Laane RW. Caudill SP. Hurtt ME. Murray SM. McLaughlin JK. Dinglasan MJ. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Edwards EA. brominated. Grey BE. and ex vivo studies. Tully JS. Environ Sci Technol 2005. Sasaki S. et al. Toxicol Appl Pharmacol 1992. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Kumar KS. Needham LL. Chlorinated. Needham LL. Harada K. Caudill SP.115(11):1670-1676. Evans TJ. Liu RC.39(23):9057-9063. et al. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea.179:99-121. Corsolini S. Calafat AM. Taniyasu S.46(2):141-147. Yamashita N. Serum concentrations of 11 polyfluoroalkyl compounds in the U. et al. Perkins RG. Occup Environ Med 2003. Hurtt ME. Cook JC. Calafat AM. Butenhoff JL. Frame SR. Environ Health Perspect 2007. Kuklenyik Z. Holmstrom KE. Loganathan BG. Kannan K. Watanabe T. O’Connor JC. Inoue K. The toxicology of perfluorooctanoate. Biegel LB. et al. Apelberg BJ. Kawashima Y. Environ Sci Technol 2005. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Peterson RE. Hekster FM. Inoue K. Yoshinaga T. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Reidy JA.39(3):363-380. Gaylor DW. Fluorotelomer alcohol biodegradation yields poly. Mabury SA. Environ Sci Technol 2004.115(11):1677-1682. Kannan K. Butenhoff JL. Environ Sci Technol 2005. de Voogt P. Cook JC.113(2):209-217.

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

Massey RC... Rhodes et al. van der Broek PH. pp. 2002). Albro PW and Lavenhar SR.. Silva MJ. Anderson WA. Environ Health Perspect 1982..gov/ reports/index. Food Addit Contam 2001. 2007. Available at URL: http://www. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. dibutyl phthalate (DBP).html). 2005. 2004. Lovekamp-Swan and Davis. Hauser et al. 1986). Springall C. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. and Sertoli cell abnormalities in the male animals and. Connor C. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 .html. Dirven HA. Vol. but there are known species-related differences in the hydrolysis of diester phthalates. atsdr. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. phthalates have been shown to induce peroxisomal proliferation in rodents. NTP-CERHR. Environ Health Perspect 1997. Pharmacokinetics. Mackay D. The monoester metabolites are thought to mediate toxic effects for some of the phthalates.805:49-56.atsdr.cdc. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for di-n-butyl phthalate update [online]. Also. Hoppin et al. Dave M. 2007). Slakman AR.... 2004. High doses of di2-ethylhexyl phthalate (DEHP). In Staples CA (ed). 2000b. Scotter MJ.cdc. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. Castle L. variation also occurs in the same person during repetitive monitoring (Fromme et al. McKee et al.. Drug Metab Rev 1989.gov/ toxprofiles/tp9. 2001. Coldham NG. and race/ethnicity (Silva et al..gov/toxpro2. Springer. gender. 2002). A biomarker approach to measuring human dietary exposure to certain phthalate diesters. 2000c. Jongeneelen FJ. Silvapathasundaram S. 2004.html.e.. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. McDonnell DP. Matthews HB. These differences may contribute to species-specific differences in toxicity (ATSDR.45:19-25. efficiency of intestinal absorption. Information about external exposure (i. Peck and Albro. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels.. Herbert AR.cdc.. 2001. 2000a. ovarian abnormalities in the female animals (Jarfelt et al.21:13-34.18(12):10681074. 2005). 2006). which may be a pathway to the development of liver toxicity and cancers in these animals.3. Kessler et al. Calafat AM. 4/20/09 Albro PW. Hauser et al.gov/toxprofiles/ tp135.html. reducing estrogen production.. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. phthalates produced anti-androgenic effects by reducing testosterone production and. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. 1982. In animals. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. 2003..Phthalates and metabolites have been tested. 2001). Available at URL: http://www. 1985. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. Cousins IT. Assessment of critical exposure pathways. Corbett JT. The Handbook of Environmental Chemistry. 2004. However. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. Population estimates of concentrations of specific phthalate metabolites may differ by age. and extent of metabolite conjugation to glucuronide (Albro et al. 2004). at very high levels. Clark K. 105:734-742. interactions with macromolecules and species differences in metabolism of DEHP. Metabolism of di(2-ethylhexyl) phthalate. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. 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. at higher doses. 227-262. Jordan S. The National Toxicology Program’s Center for the Evaluation of Risks to Human Reproduction (NTPCERHR) has reviewed the developmental and reproductive effects of specific phthalates (http://cerhr. Needham LL. 1982). 2002. Sauer MJ. 2003.. Evaluation of a recombinant yeast cell estrogen screening assay.New York. 2006). testicular atrophy. Schroeder JL.nih. Part Q: Phthalate Esters.niehs. References Agency for Toxic Substances and Disease Registry (ATSDR).atsdr. J Chromatogr B 2004..

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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 . Epidemiol 2005. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Toxicol Appl Pharmacol 2004. Biol Pharm Bull 2003. Meeker JD. Koch HM. Parker MG. Environ Health Perspect 2003. NTP-CERHR. Reprod Toxicol 2004. Environ Health Perspect 1998.19(4):505-515. Kano K. Hanaoka T.110(5):515-518. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Stringer WT. Calafat AM. Jobling S. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.22(3):688-695. J Androl 2004. Giwercman A. et al. Sumpter JP.382:10841092. Fromme H. Akesson B. Davis BJ.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. The estrogenic activity of phthalate esters in vitro. 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Meek MD. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. et al.58:339349. Clemons JH. et al. Parks LG.Phthalates phthalate (DEHP): a cross-sectional study in China. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Ostby JS. Environ Health Perspect 2006. Abbott BD. Jackson SJ. Orton TC. Environ Health Perspect 1986. Bratt H. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Peters JM. Urinary levels of seven phthalate metabolites in the U. Peck CC. Barlow NJ.36:459-479. Cunningham ML.45:11-17. Environ Health Perspect 2004. Toxicol Sci 1998. Wu ZF. Barr DB. Caudill SP. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Crit Rev Toxicol 2006. Matthews JB. Malek NA. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Environ Health Perspect 1982. Pratt IA. et al. Lambright CR. Silva MJ. Hodge CC. Rhodes C. 112(5):A270]. Zacharewski TR. Klinefelter GR. Rusyn I. Fielden MR.112(3):331-338.S. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man.114(11):1643-1648. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Batten PL. Reidy JA. Albro PW.65:299-308. Toxicol Sci 2000.46:282-293.

8-14.9) 14.7-15.4) 65.1) 13.3 (29.8.3) 15.9-16.0) 34.6) 13.9) 12.8-98.4) 81.9 (12.7-14.6) 15.6 (13.5-36.6) 14.4 (59.8) 14.1 (14.3 (29.1-15.7-16.8-16.6-150) 94. 2004.0 (12.2 (11.0 (23.6 (41.4 (27.5-97.7-35.7-16.8-14.5-33.6-132) 103 (84.7-25.9) 18.1) 32.2) 15.2-39.9) 15.1-16.9-27.5 (26.5) 65.3 (33.2-183) 101 (78.0 (27.8-121) 79. vinyl tile.1) 68.4-25.0) 24.3 (13..2 (25.0) 70.6-39.2-19.2-17.1) Selected percentiles ( 95% confidence interval) 50th 17.S.8 (30.6) 25. because it is not bound to products in which it is incorporated.5-41.1-116) 122 (93.1-61. BzBP can be released into the environment during its production and.5) 23.2 (10. including MBzP.1-35.4) 35. 2000). some personal care products. sealants.0 (30.3-130) 122 (88.5 (27. 2000).6-17.4) 129 (98.8 (12. 01-02.7 (70.6-29.1 (32.8 (10.2) 33.3-161) 99.0 (30.7 (80.0-85.8 (71.1 (55.8-48.4 (10.2-155) 91.3 (12.4-127) 80.2 (19. interval) 15.1-214) 166 (116-191) 145 (110-213) 88.0 (33.3-12.0-26.7 (53.5-18.0 (15.1 (20.3-125) Total 15. 262 Fourth National Report on Human Exposure to Environmental Chemicals .1-16.9 (28.3 (44.2 (14.9-14.1-15. and 03-04 are 0.2-38.0) 16.5 (55.8-41.2) 22.4 (10.5-36.6) 95th 103 (94.0 (14.3-74.2-31. can produce developmental and reproductive toxicity in rodents.7 (11.7) 38.4-24.7 (82.0 (34.4) 75th 35.2) 78.8-16.0 (11. High dose BzBP and its monoester metabolites.1) 12.7) 40.8-64. particularly male animals (McKee et al.7 (12.4 (48.5 (47.7-13.2) 17.1 (13.4-120) 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) 16.5-84.1) 76.8 (14.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.3-34.1-18.8 (86.8-35.6) 14. 0. and 2003-2004 were generally similar those reported in U.3 (22.7-82.7 (13.3-75.5-14.1 (58.4 (32.5-145) 138 (106-241) 143 (127-179) 120 (99. car care products.4) 71.3) 63.5 (61.1 (19. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4-92.3-91.7-16.0) 90th 67. 2001-2002.9-28.7-172) 103 (74. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.7) 23.3 (12.1.2) 13.6 (13.2) 14.6) 24.6 (12.5 (76.7-170) 169 (134-198) 152 (99.0 (55.6-116) 122 (102-142) 101 (85.3 (12. see Data Analysis section) for Survey years 99-00.5) 30.2-16.6) 50.9-30.4 (63.Phthalates Benzylbutyl Phthalate CAS No. and 0.3 (54.6-79.0 (20.1-43.8) 63.6) 37.8 (21.5) 15. 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.4 (53.9) 14.8-17.6) 63.. and diet is the major source for general population exposure.2) 69.1) 29. IARC considers BzBP not classifiable with respect to human carcinogenicity.7-17.0-130) 101 (86.2-16.3-18.8) 33.2 (47.1-39.5) 82.6 (53.0 (43.3 (30.3-82.8-133) 89.0 (26.3-27.8 (50.9-62.6) 35.9) 43.8 (28. and to a lesser extent. respectively.9-87.5-40.9) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 39.8) 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 16.2-116) 122 (102-143) 101 (84.1 (14.4) 38.4 (29.9-47. Food crops take up BzBP.5-62.4) 80.3-18.6 (13.4 (68.6-18.2) 12.9 (12.3-88. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.5) 16.3) 13.1-38.5 (66.3) 13.0-106) 58. residents (Blount et al.4) 14.8-13.8-72.6) 29.0 (15.9) 11.1) 67.2-20.1 (10.6-38.8-17.3) 23.6) 67.3.7 (15.4-15.8-76.4 (13.3-43.4) 33.2) 32.5) 15.0) 23.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6) 35.9 (70.9 (39.0-55.4) 49.2-40.7 (51.1 (13.8) 28.5-25.1-120) 52.8 (71.5-94.6 (13.3) 37.8 (38.6 (32.9 (22.5-35.9 (21.1) 31.6-92.7-119) 99.9) 13.0) 20.4-62.4) 12.4-16.6 (21.9-49.4) 51. NTPCERHR.8-18.2) 66.5 (13.6 (66.8 (80. it can be released into the ambient air during use or disposal of the products.6) 13.8 (53.6-72.9 (16.2 (43.8) 24.0) 32.4 (32.4 (53.4 (31.3) 94.6-92.4) 35.5 (57.S.9 (13.6-43.3-21.0) 33.4) 108 (96.9-190) 86. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.5) 27.5) 55.2-33.9 (11.7-58.5 (67.2) 14.2-115) 113 (91.1-90.4) 98. population from the National Health and Nutrition Examination Survey.1) 14.3) 54.2 (19.9) 49.

4 (69.8-16.8) 54.2-26.3-38. 2007).1-120) 77.3) 14.3) 18.2) 67. and in a small sample of German residents (Koch et al.0 (41.4-42.6) 25.6) 12..8) 26.3) 73.9-115) 57.1 (15.4) 44.2-78.0 (12.9) 11.4 (10.6) 13.1) 27.7 (13.8-60.6 (34.1) 24.5 (12.3) 55.8-64.4-142) 134 (116-176) 136 (85.9) 12.7-31.1 (9.8) 13.0 (12.9) 64.6 (11.7 (11.4 (33.3) 12..9 (54.8-13.8-27.9-83.8-69.4) 50.9) 42.8) 53.4 (13.2-57.1 (21.9 (15.1 (14.5-58.4-18.6 (30.1) 24.8) 34.7) 46.9) 12.0-53.0) 49.2 (56.3 (38.3) 90.1) 142 (99.8 (10.4) 90th 50.8-13.6 (24.0 (11.9) 100 (80.8-42.5) 17.7-14.2-21.9-16.1) 12.1 (21.1 (53.4 (11.3 (12.8 (46.8-48.9-40.0) 11.1 (34.4) 17.9) 11.9 (24.6) 30.1-58.7) 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 40.2) 15.7-69.8) 108 (75.3 (35.1) 39. 2005).7 (55.5) 13. Hoppin et al.8) 71.2-15. 2002.9 (29.2 (40.1 (25.5) 14.7 (23.5-31.4 (26. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.8 (13.4 (21.5 (56.1 (43.8-34. 2004..5-58.Phthalates York City (Adibi et al.1 (13.8 (50.7-12. population from the National Health and Nutrition Examination Survey.6 (11.73-12.5-42.7-15. in young Swedish men (Jonsson et al.4 (25.8 (11.2) 11.8) 33.4) 51.8) 15.5) 46.9 (55.8 (12.3) 16.7 (59.4-14.3 (39.2-17. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.2 (41.5) 16.8) 16.5-23.0 (13. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6-12. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4-15.3-73.8) 68.2 (27.4) 14.5 (9. 2003).6-20.2) 11.6 (57.5-29.5-16.1 (11.9 (15.8-14.1) 17.6 (15.7 (11.1) 80.1-12.7 (19.6-26.7 (14.3) 14.0 (49.7) 38.2) 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 12.7-56.6-47.3 (60.3-34.5 (48.4) 25..9) Total 14.0-90.4-19.6) 38.7-14.3-11.9-23.0) Selected percentiles ( 95% confidence interval) 50th 13.2-51.8-15.1-14.5) 20.6-116) 74.8) 56.6 (19.1-79.8) 24. 2004).9-104) 62.0) 24.4-23.7 (38.0-27.8-173) 195 (121-305) 229 (99.6-81.9-62.5-61.7-61.4) 12.9 (43.1-27.6) 73.2-117) 95.0) 13.1 (41.4 (46.9-69.5-76.6 (22.7-29.5-13.8 (49.8-85.7-90.9 (10.4 (34.5 (10. 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) 24.4-90.4) 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..0) 15.7 (11.8-80.9 (39.0) 12.0 (62.2) 12.9 (10.0-26.S.8-39.4) 104 (89.6) 75th 25.9) 52. 2002). DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.8) 46.2-13.1-12.1) 35.1-125) 86.8 (69.5 (10. and females compared to males (Silva et al.7-19. 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.7-20.4-27. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.4) 13.7 (54.5 (11.2) 26.1 (19. 2003).6-40.9 (22.4) 15.7 (18.1 (23.9 (24.2) 32.2) 11.8 (57.0) 60.4-99.3) 29.0-109) 65.6 (36.3 (23.5 (49.3) 37..8-14.5-79.6) 12.6 (14.5) 23.7-397) 70.7) 19.1 (13.0-48.3) 13.4 (74. 2007).8) 11.4 (63.7-15.9 (12.7 (12.4 (11.3 (15.8 (30.3-64.4 (12.3-16. In an annual sample of German university students.0-51.9) 12.9 (12.1 (21.1-35.4 (60.1-29.5-26.6) 58..5-26.6-15.7-20.5) 41.0 (41.5) 95th 77.4-14.4-17.4-60.3) 13.7-123) 77.7 (13.0 (38.3) 36.0 (10.9 (51.6-99.3 (24.6) 53.7) 25.9-28.2 (69.69-11. interval) 14.8-13.5 (42.5) 78.9-13.4) 28.6-86. Hauser et al.8-15.9-13.3) 67.3 (13..8) 80.7-19.3) 21. adolescents compared with adults..7) 56.1 (18.4) 60.4-102) 70.1) 23.9) 24.8) 53.6 (30. A small study of African-American women in Washington.9 (9..6-13.5-38.5-57.4-116) 73.7) 11.6 (51.5) 10.3) 13.2-49.5-213) 49.3) 89.4 (11.95-14. Weuve et al.6 (11.2-12.0 (67.0-15.8 (64.1 (46. in men attending a Boston infertility clinic (Duty et al.5-99.7 (21.4-93.4) 13.4) 21. In NHANES 1999-2000. 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.0 (33.2-13.8) 33.4-79.1 (21.9-14. 2005.2-15.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 . 2006).5 (35.

Silva MJ. Rylander L. Hu H. Available at URL: http://cerhr. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Brock JW. Reidy JA. Environ Health Perspect 2000. Environ Res 2003. Perera FP. Jedrychowski W. Davis BJ. Int J Hyg Environ Health 2007. Wittassek M. Brock JW. Chen Z. Butala JH. Brock JW. Meeker JD. Ryan L.111(14):1719-1722. Caudill SP.108(10):979-982. Giwercman A. Bull Environ Contam Toxicol 2002.68:309-314. J Androl 2004. Epidemiol 2005. Hauser R. Calafat AM. Weuve J. NTP-CERHR. Calafat AM. Centers for Disease Control and Prevention (CDC). Duty S.22(3):688-695. Koch HM.18(1):122. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Needham LL. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Atlanta (GA).html.S. David RM. Ryan L. Singh NP.Phthalates References Adibi JJ. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. et al. Angerer J. Jonsson BAG. McKee RH. Environ Health Perspect 2004. Pirkle JL. et al.210(3-4):319-333. Jacek R. Urinary levels of seven phthalate metabolites in the U. Hodge CC. Silva MJ.114(9):1424-1431. Blount BC. Levels of seven urinary phthalate metabolites in a human reference population. Gans G. Hum Reprod 2007. Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 2002. Helm D. Sampson EJ. Environ Health Perspect 2006. et al.93:177-185. Silva MJ. Poland. 4/20/09 Silva MJ. Camann DE. Research Triangle Park (NC). Caudill SP. Koch HM. Prenatal exposures to phthalates among women in New York City and Krakow. Schettler T. 2000 [online]. Dobler L. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Hilborn ED. Silva MJ. Baird DD.112(3):331-338. Green RA. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Sanchez GN. et al.niehs.25(2):293-302. et al. Reprod Toxicol 2004. Hagmar L.110(5):515-518. Caudill SP. Barr DB. Richthoff J. 264 Fourth National Report on Human Exposure to Environmental Chemicals .nih. Drexler H. Wiesmuller GA. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Phthalate monoesters levels in the urine of young children. 112(5):A270]. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). et al. Barr D. Hoppin JA.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Urinary phthalate metabolites and biomarkers of reproductive function in young men.16(4):487-493. Rossbach B. Malek NA. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Duty SM. 2005. Environ Health Perspect 2003. et al. Eckard R. Needham LL. Reproducibility of urinary phthalate metabolites in first morning urine samples.

4 (20.3-19.0) 24.33 (2. pharmaceutical coatings.90 (4.2-22.20) 7.50) 2.72-3.7) 14.3 (11.6) 17.00-6.5) 25.10 (3.71 (2.7-20.46) 2.1-17.9) 15.90-4.70 (5.20-12.20) 4.60 (2.10-9.5-16.3 (16.80) 75th 5.40 (7.0) 20. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.80 (2.10-2.20-2.8 (9.5) 22.10) 8.5 (17.43) 6.30) 6.5) 18.1-20.1) 16.68 (2.1) 25.26 (2.85-6.50-10.30-7.2 (8. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates. 2005). Koch et al.96) 3.6) 12.4) 5..07 (3.10) 2.40-4.97) 2.20 (3.S. 2001).30 (4.0 (13.82-3.S.6-14.00) 4.50) 8. in men attending a Boston infertility clinic (Duty et al.55 (3.46 (3.4-12. 2004.4-27.0) 12.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.10) 11.7-18.90 (6.3-48. 2003).6) 17.7) 7.30-13.60 (5.40-5.40 (2. Biomonitoring Information Median concentrations reported in the NHANES 19992000.6-34.1 (13.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.9-14.7-31. about 65% to 80% of a dose is eliminated in urine within 24 hours.0-14.17 (2. Hauser et al.2-33.22) 3.6 (13. residents (Blount et al.3. CDC.50) 7.2 (12.00 (7. 2000.7) 18..30-11.59) 3.5) 14..56-4.3-43.66) 2.1) 22. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate. 84-74-2 Di-isobutyl Phthalate CAS No. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al. 2000). Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.6 (13.0 (19.67 (5.00-11.40) 5.40-4.60 (8.4) 22.6 (10. they have been referred to as monobutyl phthalate (MBP).30-2. and insecticides.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.4) 12. 2004.5 (10.40-3. mostly as MnBP (Anderson et al.37) 6.. NTP-CERHR.50) 5.48 (2.50 (3.0 (11.60 (4.00-9.2-14.24-8.7 (9.30-3.20-12.6) 10. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.3) 18.50-4.84) 4.. OSHA has established a workplace air standard for external exposure to DBP.90-4.20-9. the median Urinary Mono-isobutyl phthalate (MiBP) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10 (4.46-5.80-5.6 (29.5) 23.90-2.28-5.3-30.. 2005.5) 12. population from the National Health and Nutrition Examination Survey.0) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2.5-29.5 (27.30) 10.80-5.5) 18.6-20.3 (16.30) 2.7 (18.40-17.00-4.0 (13.40 (6.0-38.90) 12.00) 4.6) 16.30-6.73-5.40-3.44-2.60-6.7 (17..00) 10.9) 10.10-9. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.0-25.81 (3.80 (5. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.0) 13. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.10 (4. Following oral administration of DBP to humans.50-2.9 (16. When total DBP metabolites have been measured.2 (11.70 (2.8) 40.6 (10.2) 5.6 (9.0-18.7 (16.22 (3.3 (19.7-31.6 (14. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.10) 3.1 (8.0 and 0.11-3.50) 90th 12.3 (13.70-8.30) 5.49-2.20 (7.80 (5. in a small sample of pregnant women in New York City (Adibi et al.73 (2.9-23.3-18.Phthalates Di-n-butyl Phthalate CAS No.80 (2.02) 4. Fourth National Report on Human Exposure to Environmental Chemicals 265 .5-24.90 (4.17) 4.3) 33.4 (14. In addition.6) 16.00 (5.20-6.3 (18.30 (1.00-6.30) 10.90-7. DBP can produce reproductive toxicity in male rodents (McKee et al.46 (2.5-16. 2005).7 (17.40-12.10) 9.8) 21.6-18.50-6.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.50) 18.19-3.55) 2.56 (5.90 (3.91) 4.1-25.70-4.3) 3.40-9.7) 15.70-4. interval) 2.0) 9.00) 6.6) 26.40 (3.5 (11. Survey Geometric mean (95% conf.97) 4.70) 5.3 (13.3-24.50 (6.56 (3.40 (2.6-26.7) 4.20 (6.30 (3.80 (3. and in a small sample of Japanese adults (Itoh et al.6 (11.56) 3. 2003).6 (14.5) 19.63) 3.00) 7. 2005).3-20.97-7.60) 3. 2007).5 (20.7 (7..70) 3.8) 677 652 703 699 1216 1088 Limit of detection (LOD.9 (16.30-6.. and also in some printing inks.1-12. Studies of children found age-related differences in urine MBP levels.

. interval) 2.02 (7.10-5.32 (3.33-9.43) 3.2 (11.21 (5.1-25.82) 4. 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.25) 5.52 (2.33) 3.2-13.26-2.14 (4.51) 2.72-7.9-26.0 (12.09-2.3) 16.7) 10.18 (1.6 (8.13 (2.66 (8.72) 5.02-10.28 (4.86-4.1) 4.20-2. 2005).57 (3.19 (2.80) 7.0-18.0) 3.07-5.69) 6. 2004).03-7.00-3.89-5.28-13.37) 3.2) 8.38 (6.0) 15.86) 6.98 (2. An analysis of NHANES 2001-2002 showed similar age.68) 5.81) 9.52-3.97-2.01-2.38-10.07 (2.32 (7.99-4.46 (2.1 (11.53-3. 2006).64-7. Weuve et al.11 (5.15) 3.6 (15.43) 3.95) 10. 2007).related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC. In an analysis of NHANES 1999-2000.5) 15. 2005).3 (17.47-5.18-10.22 (2.68 (2.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.43) 3.81 (3.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.88 (2.82 (4. Over this time.89 (3.1) 13. respectively.46-11.0 (8.52-20.41 (2.67-5.96 (3.20 (2.32) 7.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al..4-16.20-3.11-2.3 (13.9 (9.56-15.33 (2.4) 7..65-11.62 (6.18) 4.78) 8. ranging from more than one-tenth the NHANES median (Itoh et al. 2007).29-3.0) 7.6 (12.51) 15.79 (4.1 (10.5-19.6 (9.and gender.8 (8.93-6. while MnBP declined (Wittassek et al. samples from German university students had consistently higher median urine levels of MnBP and MiBP.83 (2.94-12.7 (13.00-3.7 (21.51) 5.30 (6.66) 4.91-6.2) 9. Between 1998 and 2003.6-19.7) 11.1-12.18 (4.9) 12.20 (2.42) 2.S. to about two to fourfold higher (Fromme et al.7 (9.2 (10.58-4.44 (3.61-3.17 (2. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al. 2002.95) 2.35) 3.39) 5.64-10.29-8.8-13.69) 4.31) 2.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.58-3. up to four and 13 fold.27-12.3) 28.6) 13.69-7.34 (3.65 (4.13-6.68) 3.76-3.54) 2.17) 90th 8.84 (4. 2004).5 (11.55-6.47 (3.56) 2.4) 23.78) 9.8 (10. population from the National Health and Nutrition Examination Survey.76 (3.54 (2.04) 7.5 (9.81 (6.03 (5.3) 18.79-8.00 (3.20 (7.92 (7.7) 19. the students’ median values for MiBP levels remained relatively unchanged.4) 15. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.08) 75th 4.20-4. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.26 (2.1-15.80 (3. Survey Geometric mean (95% conf. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.1) 15.36-7.85 (2.33 (3.15-4.5) 13.24) 3.66) 10.99) 7.05) 2.6) 11.36-2.9-16.21) 10.53-4.65-4.04) 3..95-3.31) 2. 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.4 (12.81) 4..89) 6.18-4.1) 7.6) 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 2.08-2.76-15.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .17-12.8-18.75 (4.59 (4..9 (15.80-3.04-5.94 (5.6 (10. than adults in NHANES subsamples during the same time period.18) 3.2-15.03-11..52) 3.11) 5.3) 13.6-19.31 (7.1) 11.54 (4.75 (6.31 (2.0 (10.39-3.56-4.84 (8.64-7.6 (8.8-18.73 (5. 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.9 (11.8-36.7 (11.76-3.1) 10.00-7.57-4.8 (9.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.2) 24.8) 10.7-28.66) 2.47-12.7) 3.94) 6.74-3.45) 3.74 (4.30) 2.69 (2.9-40.1-24.53-5.3) 13.79-6.78-8.56) 5.46) 3.57 (3.0) 11.62-12.

8 (19.2-24.8) 58. referred to as monobutyl phthalate (MBP).2-23.6-29.0 (78.5-60.3 (51.6-33.2-63.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.4) 52. and 0.7 (22.0-26.6 (55.1 (34.3-24.7 (24.7 (38.1) 17.2-56.2 (18.1 (41.2) 26.9 (79.2 (19.9.3-79.4-60.6 (16.5) 31.2 (78.7-42.0) 117 (104-131) 112 (84.3-76.6-20.4 (84.1 (19.5) 37.3 (23.0) 21.7) 124 (98.0-58.1) 31.5) 40.1 (19.0-24.1 (16.0-21.7-117) 118 (108-143) 93.0-19.4 (19.1-51.5-117) 95.0-51.8-22.6 (61.9-79.3) 18.5) 47.5 (74.3 (42.6) 35.1 (19.6-48.6) 46.1-27. respectively.3) 19.0 (15.9 (79.4-25.1-29.3) 21.1-75.7-106) 69.3 (23.1 (51.0 (30.4 (25.0-32.3-40.1-92.6-44.7) 28.7-92.6-29.4 (35.8) 43.5) 17.9) 71.4 (38.4 (35.7-26.8) 75th 51.2 (59.8) 23. 01-02.0) 120 (98.0-19.3 (30.0 (23.6-143) 127 (99.5-42.2-22.0) 30.0-73.9) 26.1) 25.2 (21.4-42.8-132) 95.9 (17.7 (51.7 (64.4 (36.1-24.1 (54.7-111) 64.1) 36.0-24.8-111) 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 23.7-116) 95.1 (28.7-20.4 (72.3 (30.1 (58.6 (32.0) 27.5-44.9 (20. Fourth National Report on Human Exposure to Environmental Chemicals 267 .0) 31.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.7) 92.6-31.4 (35.9-114) 116 (97.5-43. and 03-04 are 0.4-31.4) 22.7-91.6) 38.8) 62.7 (18.6 (26.2 (58.3) 23.9) 46.5) 20.9) 29.3-136) 137 (107-162) 119 (90.4 (21.5 (59.7-34.9) 21.9) 18.6) 20.7 (70.0 (25.5) 34.5) 78.0 (36.1) 23.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.6-49.1) 19. population from the National Health and Nutrition Examination Survey.0 (45.7 (18.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.2) 62.8-123) 101 (90.9-87.0) 38.2 (20.7) 74.1-80.2) 32.8 (57.4 (71.3-60.5-27.5 (29.8-42.2) 38.1 (31.5) 95.4) 20.2 (21.7-42.1-22.6-113) 108 (90.5-121) 106 (94. *In the 1999-2000 survey period.0 (31.4-20.2) 20.7 (16.0) 20.7-24.4-26.6-24.2 (79.3) 40.7-34.2) 90th 98.9-42.1 (21.2-159) 92.4-44.0 (18.3) 36.9-53.1 (17.9-92.9-33.5) 24.2-87.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.3) 24.2) 42.2 (74.7 (33. 1.1 (36.5-53.4.1.9-101) 77.8-119) 90.3 (17.4-18.6 (22.6) 80.6-36.7-127) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 22.8) 19.3 (36.2 (17.1) 23.5) 19.8-25.1 (18.9) 75.2 (75.5 (30.6) 39.0 (72.7 (28.3-96.5) 85.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.3 (37.6-37.1 (62.2-32.S.8-29.7 (19.4-159) 107 (84.3-67. Survey Geometric mean (95% conf.9-22.2-33.7 (43.6) 17.5) 21.0 (17.6-40.1) 23.5 (28.3-85.4) 59.8) 48.6) 21.5) 65.5-47.9) 36.5) 36.6) 71.4 (23.1-20.6 (65.1) 46.4 (35.3-21.5) 36.7) 52.2-114) 73.1-82.7) 42.6 (48.5) 26.9-22.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.3 (60.4) 64.2 (25.5-47.1 (19.0) 84. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.1) 30.9-28.1 (26.7-53.2-93.3-145) 85.5 (59.1) 47.2-21.3 (56.0 (20.3) 26.2-49.6 (90.6 (44.9 (17.7-121) 97.6 (19. interval) 24. see Data Analysis section) for survey years 99-00.2) 68.1) 20.6-69.

1 (15.3 (21.7) 36.7 (14.3-71.9-68.9) 28. population from the National Health and Nutrition Examination Survey.4 (53.4) 21.0 (52.8) 40.8-235) 137 (108-198) 88.1-21.4 (16.9 (39.3 (69.7 (57.3) 21.7 (27.6-155) 91.2) 31.7 (20.4) 62.8-43.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) 17.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.1-99.3 (17.3) 20.5 (15.4 (56.3 (55.4) 20.3-81.3 (16.1) 53.0 (16.1 (29.6) 23.6) 65.3 (24.8-23.8) 23.4 (31.6) 39.6) 64.6 (61.9 (37.6-22.6 (74.5-64.7 (28.9-68.0-19.2-61.5) 84.9 (30.5-70.8 (18.3-39.2-85.5) 17.9) 49.3 (46.2-22.7-23.1 (34.3 (28.2 (83.2-18.6-24.9 (35.0 (71.8-24.1-23.8-24.4 (50.6) 34.5-18.3-21.0) 19.7-21.4 (47.3-21.2-86.3 (48.9 (16.3-18.5-30.0 (19.8) 30.2-73.4-76.4 (31.3) 52.0-90.4 (18.9 (21.6 (19.5 (18.8 (22.4 (13.0-47.4-72.6) 31.7-19.7) 19.9 (64.4 (33.6-92.3-49.6 (29.9-105) 85.0 (27.4 (16.0) 35.3 (71.0) 25.3 (17.8) 34.S.0) 75.4) 15.5 (30.0-60.1) 20.0) 94.9 (30.4) 53.2-16.6-27.1-62.1-83.6-128) 96.2) 74.3 (76.4 (17.6) 38.2 (19. Survey Geometric mean (95% conf.2 (38.2-106) 64.8 (25.1) 21.0-92.2 (35.2) 59.6) 37.3) 67.4 (50.8) 13.9) 19.7) 20.5 (81.6 (27.3) 18.5) 60.7-20.4) 19.2-48.2-22.8) 20.8 (33.4-135) 71.0) 70.7 (12.3-26.3 (60.1) 44.6 (25.7 (60.9 (56.8) 17.4) 51.6-32.6) 24.7-51.9-56.6) 14.0 (18.0) 41.5-76.8 (13. 268 Fourth National Report on Human Exposure to Environmental Chemicals .5) 21.0 (69.2-179) 84.2 (19.7 (16.3 (19.9) 24.0-38.6 (41.7-39.0 (61.0) 108 (71.3 (52.3 (17.6) 24.0 (50.5) 134 (93.7-37.8 (50.6-53.3-20.9-100) 86.8) 34.4 (17.2) 159 (102-263) 147 (93.9) 39.4 (19.5) 91.2 (16.5-37.6-42.9-26.8) 35.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.0) 81.8) 63.4-61.9 (58.4) 16.9 (35.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.7-28.4 (37.0 (15.6-23.5-41.5-23.9) 14.6-50.0) 55.4-164) 96.9 (30.7-26.5-22.4 (45.0-17.4) 15.3-23.6 (25.8 (65.2-21.8) 19.7-42.1-18.9-84.1) 61.4-24.9) 62.0 (70.6-43.8 (17.9 (73.9-49.1 (46.3 (42.9) 20.9) 91.5-142) 81.6-23.3) 33.9-36.0 (18.0) 29.0 (34.2-27.1) 17.0-75.0) 53.5 (18.1) 20.4-47.3) 35.4-65.7 (81.1) 22.9 (20.8) 28.6 (31.3-114) 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 17.1) 42.7 (54.0) 28.5-21.4-103) 117 (83.8) 17.8-32.6-16.3) 59.7 (43.9) 30.0 (43.1) 50.6) 25.8) 20.6) 18.9) 52.6-26.6 (17.1-32.4 (20.7 (73.3 (52.5) 39.3) 17.6-44.8 (18.3-32.6) 83.3-38.1) 35.5) 82.5-15.1) 37.4-131) 81.9 (19.5) 90th 68.1 (61.3-40.3-78.6-24.2-28.5-16.7) 42.0-41.8 (18.0 (26.3) 19.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.6-44.8) 22.1 (56.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.0) 59.9-14.7 (19.6-19.7 (60.4 (68.2) 16.3) 19.8) 75th 38.3-17.9-70.3) 33.0 (20.1-99. interval) 22.2-22.9-34.3-106) 74.1 (32.6-74.8 (16.2) 65.4 (23.9-38.0-113) 104 (83.6-28.7-80.5 (14.6-119) 63.2) 21.6 (57.1-128) 97.7-19.5-142) 89.4 (31.1 (21.6 (72.7-78.4-34.0) 26. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.5 (64.

Levels of seven urinary phthalate metabolites in a human reference population. Reprod Toxicol 2004. Anderson WA.210(3-4):319-33. Brock JW. Sanchez GN. Hagmar L. Boehmer S. Caudill SP. Rylander L. Hilborn ED. Blount BC. et al. Sampson EJ. Springall C. Duty SM. Angerer J. Koch HM. Helm D. Centers for Disease Control and Prevention (CDC). Wittassek M.Phthalates References Adibi JJ.25(2):293-302. et al.111(14):1719-1722. Reidy JA. Caudill SP. Masunaga S.nih. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Environ Health Perspect 2003. Silva MJ. Barr D. Research Triangle Park (NC). Silva MJ. Koch HM. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Environ Res 2003.114(9):1424-1431. Calafat AM. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Environ Health Perspect 2004. 4/20/09 Silva MJ. Jonsson BAG. Malek NA. 2005. Camann DE. Green RA. Silva MJ. Duty S. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Eckard R. Int J Hyg Environ Health 2005. Needham LL. Angerer J.S. Needham LL. et al. Hum Reprod 2007. Food Addit Contam 2001. NTP-CERHR. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Pirkle JL. Scotter MJ. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. et al. Hodge CC.html. Singh NP. Giwercman A. Ryan L. Calafat AM. Urinary levels of seven phthalate metabolites in the U. Poland.22(3):688-695.112(3):331-338. Ryan L. Bolte G. J Androl 2004. Atlanta (GA). Fourth National Report on Human Exposure to Environmental Chemicals 269 .68:309-314. Silva MJ. 2000 [online]. Meeker JD. Koch HM. et al. Third National Report on Human Exposure to Environmental Chemicals.gov/chemicals/ phthalates/dbp/dbp-eval. Phthalate monoesters levels in the urine of young children. et al.niehs. Environ Health Perspect 2006. Available at URL: http://cerhr. Caudill SP. McKee RH.108(10)979-982. Bull Environ Contam Toxicol 2002. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Barr DB. David RM. Jedrychowski W. Castle L. Fromme H. Int J Hyg Environ Health 2007. Richthoff J. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Environ Health Perspect 2000.18(1):122. Wiesmuller GA. Hauser R.208:237-245. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Itoh H. Weuve J. Gans G. Drexler H. et al. Yoshida K.93:177-185. Brock JW. Drexler H. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Dobler L. et al. Epidemiol 2005. 112(5):A270]. Hu H. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Chen Z. Massey RC. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Perera FP.210:21-33. Rossbach B. Butala JH. Schettler T.18(12):10681074. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Int J Hyg Environ Health 2007. Prenatal exposures to phthalates among women in New York City and Krakow.16(4):487-493. Jacek R.

00) .700) . and polymers.500) < LOD < LOD . < LOD means less than the limit of detection.300-.500 (.300-.300 (.300 (.70) .9.900-1. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.300-.S.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.300-. 0.70 (1.90) .10 (. Survey Geometric mean (95% conf. and 03-04 are 0. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.500) .70) .700) .300-.500 (.400-.400 (.600) . Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.600) .10 (<LOD-1.400 (<LOD-. only levels at or above the 90th percentile could be characterized.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 .400) < LOD < LOD . which may vary for some chemicals by year and by individual sample.500) 1.400-.200-.00 (<LOD-1.500) < LOD < LOD .500 (.600) < LOD .Phthalates Dicyclohexyl Phthalate CAS No.10 (<LOD-1.400) < LOD 1. 01-02.500) . population from the National Health and Nutrition Examination Survey. and 0. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In this Report.400-.00-2.300) < LOD .400 (.600) .500) 1.20) .400-.600) .300-.50) .500 (.80) .500-. resins. 270 Fourth National Report on Human Exposure to Environmental Chemicals .400 (.500 (.400-.10 (<LOD-2.400-.00 (<LOD-1.400 (. respectively.500) .200-. including nitrocellulose.2.500 (.500) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.700) .200-.200-.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.300-.400 (.00-3.300 (.500 (.3.300 (. see Data Analysis section) for Survey years 99-00.10) .400 (<LOD-.200-.400 (<LOD-.00 (<LOD-1.400) 1.500) 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 .50) .500) 1.400 (. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-.300) < LOD .500 (.300 (.500) < LOD 1.300 (.400-.300-.400 (.500 (.600 (. polyvinyl acetate. 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.300 (.200-.70 (1.400) 1.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .400 (<LOD-.600) . and polyvinyl chloride.300 (<LOD-.200 (<LOD-.300-. 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.

630 (<LOD-.530 (.400-.10) .410 (.350-.910 (.16) .330 (.74) .910 (.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.22 (<LOD-1.530-.510 (.660) .370 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.00) .770-1.06) .500 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.360-.310-.12-1. Fourth National Report on Human Exposure to Environmental Chemicals 271 .670-1.590 (.880 (.480 (.790-1.710) .450 (.830) 1.610 (.250 (.18) .240-.910 (.82 (1.380-.11) .43 (1. Survey Geometric mean (95% conf.06) .560) 1.270) < LOD .950 (.690) < LOD 2.670 (<LOD-.53) .770 (.770) < LOD 2.00 (<LOD-3.800-1.36-1.690) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.530-1.220 (<LOD-.500-.34) .260-.500) 3.170-.420-.420-.620) < LOD .630 (<LOD-.400-.690 (.330 (.530) 1.740) < LOD < LOD .470 (.290-.490) .44) .740) .S.420-.53) .67 (1.Phthalates Urinary Mono-cyclohexyl phthalate (MCHP) (creatinine corrected) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .910 (.17) .470) 3.390 (.310) < LOD .660) < LOD < LOD .54) .54-6.380 (.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 .14 (<LOD-3.510-.690) < LOD < LOD .33 (<LOD-3.940 (.770-1.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .82) .450 (.590 (<LOD-.770-1.16 (<LOD-3.05) . population from the National Health and Nutrition Examination Survey.54 (<LOD-2.33) .690-1.

and also in men attending a Boston infertility clinic (Hauser et al. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. Products that may contain DEP include perfumes. 0.3 (74. A small study of children less than 2 years old reported mean urine MEP levels that were about twice as high as levels in children (aged 6-11 years) in NHANES 2001- Urinary Mono-ethyl phthalate (MEP) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2.7 (70.S. 2007). shampoos. and 0. 2002).4. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. 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.9 (61.8-111) 85. particularly those containing fragrances. 2001-2002. colognes. population from the National Health and Nutrition Examination Survey. respectively. see Data Analysis section) for Survey years 99-00. 272 Fourth National Report on Human Exposure to Environmental Chemicals . 2003) and African-American women in Washington. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and 03-04 are 1.1 (71..9-92.9.1-93.. Biomonitoring Information MEP levels in the NHANES 1999-2000. soaps. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 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. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine.7) 71.3-103) 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.5) 81. DC (Hoppin et al.3 (82.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75..Phthalates Diethyl Phthalate CAS No. 01-02. In contrast.2-102) 95.4 (62. and hand lotions. deodorants.

2 (66.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005). Survey years 99-00 01-02 03-04 Geometric mean (95% conf.S. 2003) were slightly lower than levels found in NHANES 2001-2002. interval) 163 (149-178) Selected percentiles ( 95% confidence interval) 50th 141 (129-157) 148 (133-162) 153 (137-177) 75th 360 (307-422) 388 (330-435) 452 (386-504) 90th 905 (753-1180) 969 (805-1180) 1110 (889-1290) Total 167 (150-185) 181 (163-202) Sample size 1950 (1670-2310) 2536 1840 (1450-2200) 2782 2040 (1640-2540) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 92. population from the National Health and Nutrition Examination Survey.Phthalates 2002 (Brock et al.6 (65. Other population estimates also differed by sex and race ethnicity (Silva et al. the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups. Median MEP levels found in a small sample of German residents (Koch et al. 2002). Analysis of NHANES 2001-2002 showed similar findings.5-114) 101 (87.6 (77.9 (82.. In an analysis of NHANES 1999-2000. Biomonitoring studies on levels of MEP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEP than are found in the general population. 2004).5-113) 122 (93.0 (66. This age-related trend is opposite the direction seen for other phthalates.7-110) 81.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.9-110) 96. 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.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. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.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 ..

274 Fourth National Report on Human Exposure to Environmental Chemicals . Drexler H. Silva MJ. Reidy JA. et al.110(5):515-518. 112(5):A270]. Barr D. Angerer J. Hoppin JA. Prenatal exposures to phthalates among women in New York City and Krakow. Meeker JD. Baird DD. Environ Health Perspect 2004. Hum Reprod 2007. Caudill SP. Koch HM. Davis BJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Hauser R. Reproducibility of urinary phthalate metabolites in first morning urine samples. Needham LL. Caudill SP. 2005.112(3):331-338. Jacek R. Silva MJ. Singh NP. Camann DE. et al. Brock JW. Poland. Centers for Disease Control and Prevention (CDC).111(14):1719-1722. Bull Environ Contam Toxicol 2002. Third National Report on Human Exposure to Environmental Chemicals. Phthalate monoesters levels in the urine of young children.Phthalates References Adibi JJ. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Silva MJ. Hilborn ED. et al. Ryan L. Jedrychowski W.S. Environ Health Perspect 2003. Environ Health Perspect 2002. Urinary levels of seven phthalate metabolites in the U. Hodge CC. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Perera FP. Rossbach B. Atlanta (GA). Duty S. Barr DB. Malek NA.22(3):688-695. Environ Res 2003.93:177-185. Brock JW.68:309-314.

00) 19.70 (3.07-4.7) 19.16 (2.6) 9.6 (10.7 (17.31-4.60) 9.10 (6.4) 33.20 (3.23 (2.70 (5.6) 14.80) 13.6) 95th 23.7) 22.10-11.90) 1.0) 31.00 (2.8) 15.70) 7.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.84-4.40) 4.70-5.9-49.94-3.40-9.0-18.40) 4.61 (3.96-5. Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8 (19. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.10 (2.80-9.00 (5.4) 22. and 0.1982). Survey years 99-00 01-02 03-04 Geometric mean (95% conf.86) 2.2-17.98) 2. see Data Analysis section) for Survey years 99-00.50-8.8-50.1-17.4-27.80-3.34 (2.4) 15.70-2.9) 27.00) 2.3) 28.60-11.00) 9.10 (3.84) 3.8 (19.40-1.7-32.0) Total 4.46) 3.3 (10.90) 7.1) 29.9-28.2) 29.2 (11.00-3.39) 3.6 (16.56 (2.50-20.83) 2.6 (20.5 (25.80-4.10) 8.4-20.9 (15.25-3.8-47.5-41.1 (11. and 03-04 are 1.1) 25.92-2.40-8.0 (13.10-5.60) 4.3-25.14 (1.49 (3.90) 3.9-29.8-36.1 (8.5 (12.7) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.8 (17.9 (16.10-3. After parenteral administration.1-29.4) 13.00) 5.10) 4.44) 4.15 (1.40-8.50-3. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).67-4.70 (8.9 (29. Concentrations in plastic materials may reach 40% by weight.2 (10.0 (19.5) 40.80-27.00-4.70 (1.9 (7.70 (1.70-4.60) 7.75-4.70-6.0 (21.4 (13.40 (4.00) 3.23) 3.69) Selected percentiles ( 95% confidence interval) 50th 3.90-3.90) 4.Phthalates Di-2-ethylhexyl Phthalate CAS No. packaging film.51) 4.1) 22.60) 10.40-11.10-2.37-4.2) 42.90 (1.0 (17.30-6.5) 21.9.9 (13.16-3.0) 23.6 (41.9) 15.50-3.23 (3.60 (6.80 (4.10 (4.30-13.5 (18.21 (2.4-40.6-23.6-25.0-18.70-3.70 (3. DEHP has been removed from or replaced in most toys and food packaging in the United States.43 (3.80 (8.80-4.90-5.2) 6.82 (3.40-12.6-130) 31.6 (12. 1989.10-5.0) 39.30 (4.87-2.10-11.10) 3.10 (4.30 (3.3-57.2) 4.40) 2.5 (24.57 (3.80) 9.00) 1.2 (31.3 (11.1 (8.90-8.50-5.20 (3.0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.9) 5.00) 1.70-8.40) 9.4 (21. as glucuronide conjugates (Albro et al. Albro and Lavenhar.50 (3. 01-02.0) 23.62) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.5 (31.4-20.03-2. ATSDR.50) 4.5-36.89-3.S.42-5.30 (6.60) 4.50 (8.9) 18.19-3.4) 23.4) 5.70) 16.7) 27.70-2.80 (8.3) 13.0) 11.4 (16.90-11.41) 3. 1982.5-28.91-3.3 (24.35 (1.90 (3.77 (2.5) 31.9 (26.82) 3.2.7) 35.9-55.90 (4.1 (10.50 (3.40) 11.0-29.50 (7.00) 11.9 (17.9 (29.3 (15.60-7.96) 4.4) 20. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.9-19.7