2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

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

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

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

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

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

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

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Introduction

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

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

Fourth National Report on Human Exposure to Environmental Chemicals

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5.4.2'3.2-Dichloropropane 2.4.4'-Tribromodiphenyl ether (BDE 28) 2.4.1.2'.4.2'.4'.4'.4.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.3.2-Dichloroethene trans-1.4-Tribromodiphenyl ether (BDE 17) 2.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.2-Dichloroethene Dichloromethane (Methylene chloride) 1.5.1.4'.3. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.5’.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.6-Heptabromodiphenyl ether (BDE 183) 2. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4.2'.4. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.What’s New in this Report What’s New in this Report In this Fourth Report.5.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .2'.3'.4-Dichlorobenzene (p-Dichlorobenzene.3-Tetramethylbutyl] phenol) Triclosan (2.5'-Tetrachlorobiphenyl (PCB 44) 2.gov/exposurereport/chemical_selection.1-Dichloroethane 1.4'-Tetrabromodiphenyl ether (BDE 66) 2.2-Dichlorobenzene (o-Dichlorobenzene) 1.4’.5.4.3-Dichlorobenzene (m-Dichlorobenzene) 1.1-Dichloroethene (Vinylidene chloride) cis-1.2'4.3.5-Pentabromodiphenyl ether (BDE 99) 2.4'-Tetrabromodiphenyl ether (BDE 47) 2.2'.6'-Hexabromodiphenyl ether (BDE 154) 2.4.3’.5'-Tetrachlorobiphenyl (PCB 49) 2.5'.4.2-Trichloroethane Trichloroethene (Trichloroethylene) m.4'-Pentabromodiphenyl ether (BDE 85) 2.2'. Paradichlorobenzene) 1.4.1.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.4'.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.2’.1.html.3.2'. Table 1.5'-Hexabromodiphenyl ether (BDE 153) 2.4’. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.1-Trichloroethane (Methyl chloroform) 1.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.2.6-Pentabromodiphenyl ether (BDE 100) 2.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.2'.2-Dichloroethane (Ethylene dichloride) 1.4.6.4'.cdc.2'. The process for selection is described at http://www.

Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e.1). and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. Details of this procedure are provided in Appendix A. the presence of an interference) that produced results of inadequate quality. Data for other pesticides are included only for 1999-2000 and 2001-2002. urinary 2. and these data will be included in the next release of the Report. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available.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.5-dichlorophenol for the 1999-2002 survey periods. 2001-2002.4-dichlorophenol and 2. Fourth National Report on Human Exposure to Environmental Chemicals 3 . Only slight differences should be noted when one compares the recomputations to previous releases of the Report. Percentiles for all three NHANES survey periods (1999-2000. Explanations for each change are provided in Appendix B...g. five results that all have the value 90. 2003-2004) have been re-computed by use of this improved procedure.g. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period.

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

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

and a few other pesticides. Percentiles: Percentiles (50th. because this concentration determines the analytical sensitivity. For this reason. if the 50th percentile for males was < LOD in the table using weight per volume of urine. furans. Percentile estimates and 95% confidence interval estimates that are less than the limit of detection are indicated as <LOD in the data tables. Geometric mean and percentile calculations were performed separately for each of these concentrations. For chemicals measured in urine. Concentrations less than the LOD were assigned a value equal to the LOD divided by the square root of 2 for calculation of geometric means. concentrations less than the individual LOD were assigned a value equal to the individual LOD divided by the square root of 2.1). which uses Taylor series linearization for variance estimation. For the same chemical. 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. 6 a conservative rule was used for reporting percentiles: if any individual sample LOD in the demographic group was above the percentile estimate. Assigning a value of the LOD divided by 2 made little difference in geometric mean estimates. 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. 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). 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. and 95th) are given to provide additional information about the shape of the distribution. weighted percentile estimates for 1999-2000 and 20012002 data were calculated using SAS Proc Univariate and a proportions estimation procedure. the percentile estimate was not reported. Thus. geometric means were not calculated. A percentile estimate may fall on a value that is repeated multiple times in a particular demographic group defined by age. LOD values may change over time as a result of improvements to analytical methods.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. These analyses have an individual LOD for each sample. 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. PCBs. For these chemicals. care must be taken to use the LOD that applies to the survey period. For dioxins. organochlorine pesticides. The maximum LOD was the highest LOD among all the individual samples analyzed — typically. Geometric mean and percentile calculations were performed separately for each of these concentrations. Since the Third Fourth National Report on Human Exposure to Environmental Chemicals .e. In the lipid unadjusted tables. because this concentration determines the analytical sensitivity. The standard error was computed with SUDAAN’s Proc Descript (design=WR). If the proportion of results below the LOD was greater than 40%. For chemicals measured in serum lipid. In the Third National Report on Human Exposure to Environmental Chemicals. 90th. LOD calculations were performed using the chemical concentration expressed per amount of lipid. The LODs for each chemical and survey period are provided in each data table and collectively in Appendix D. mostly because the sample volume used for analysis differed for each sample. In the creatinine corrected tables.. the maximum LOD value is provided in each data table and in Appendix D. each individual sample has its own LOD. 75th. LOD results for chemicals measured in each data table and in Appendix D are in weight per amount of lipid. For this reason. LOD calculations were performed using the chemical concentration expressed per volume of urine. The same procedure for imputing values below the LOD in calculations of geometric means was used for chemicals with individual LODs for each sample. 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. in non-Hispanic white males 12-19 years old. LOD results for urine measurements in each data table and in Appendix D are in units of weight per volume of urine. for proper interpretation of LODs in the data tables. sex and race (e.g. That is. five results that all have a value of 90. the mean LOD was about 40-50% of the maximum LOD. it would also be < LOD in the creatinine corrected table. a better ability to detect low levels). Percentile estimates (see below) that are less than the LOD for the chemical analysis are reported as “< LOD..” For most chemicals. For chemicals that had individual sample LODs. 1987). a result for a geometric mean or percentile was reported as < LOD if the corresponding geometric mean or percentile was < LOD in the lipid adjusted table. A higher sample volume results in a lower LOD (i. 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). For example.

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

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

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

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

FAO/WHO.5 (52.S.1 (83.Acrylamide Acrylamide CAS No.1 (52.. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. FDA. are heated at temperatures used for frying and baking.5) 58.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. gels. the main source of exposure is from the diet. Survey Geometric mean (95% conf. Foods such as french fries and potato chips can contain acrylamide at levels up to 100 times greater than levels found in cooked fish or poultry (DiNovi and Howard.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. 2006). 2004.9 (60.4-89.0 μg/kg for adults (FAO/ WHO. EPA reference dose of 0. 2005).2 (58. pulp and paper production.8 (81.8 (91. ocular and dermal irritation from direct contact with acrylamide containing materials.S. Fennell et al.6 (56.9-105) 86.6) 71. Polyacrylamides are useful water-compatible polymers used in water treatment.7 (63. in some sealing grouts.6-66. 2005).5) 66. and binding agents. In humans.6-104) 82.9) 63.2 (62. soil conditioners. or to glutathione conjugates (Calleman et al.6 (51.9 (69. Animal studies indicate that acrylamide is well absorbed.4-83.2-93. but are generally above the U.8 (52. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.7) 54.3 (53.4) 100 (89.5-80. glycidamide. acrylamide is synthesized and used in the production of polyacrylamide polymer.6-65.7) 75th 79.6-108) 61. 1990..9) 57.7) 58.7-64.3 (55.2 μg/kg/day (U. Since acrylamide has limited volatility and high water solubility.S.8 (57.2-59.5 (79.6-75.0 (53. Elimination occurs mainly in the urine as mercapturic acid conjugates.9) 58.2-118) 98.4) 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. 2002).7) 73. Natural substances in the food are converted to acrylamide. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.4-60.4 (54. 1994).S. as an absorbent in disposable diapers.1 (73.1) 46.0 (69. In 1997. In the general population.6) 50.3) 70. 2006.4-60.4 (54. mineral processing.2-77.1 (47. 2005). 2004).5 (44.5-85. see Data Analysis section) for Survey year 03-04 is 3.3-71. Estimated intakes in children are about twice that of adults (DiNovi and Howard. and well below doses known to cause nerve damage or carcinogenicity in animals.1 (88. These estimated intakes are hundreds of times lower than occupational exposures..2-70. it was discovered that acrylamide is formed when starch-rich foods. and from dermal contact with products that contain residual acrylamide. Fourth National Report on Human Exposure to Environmental Chemicals 11 . Tareke et al.4 (53.S.1) 53.6 (81.4 (51.2 (75. Commercially.1-57. smoking. 2005. drinking water.7) 96. and an average daily intake is estimated as 0.0 (67.4-76. interval) 61.1) 55.8-57.0) 57.2-114) 163 (147-191) 96.7 (55.3) 86. 217 million pounds of acrylamide were produced commercially in the U. EPA.4) 57.9) 75. (NTP-CERHR.0. widely distributed in tissues.0) 85.0-49. Acrylamide is not thought to accumulate in the body at environmental doses.2-67.9-61. and in the synthesis or compounding of dye materials. acrylamide has produced upper airway irritation following inhalation of high levels.2-91.9-52.4) 57.0-108) 152 (139-175) 126 (111-142) 108 (86.2) 57.1-64. 2005). and is either metabolized to the reactive epoxide. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.4 (59.7 (65. in permanent press fabrics. EPA.7-60.1) 101 (95. Recently. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.6) 73.7-64.8-55.5 (74.1-64. and cosmetics (NTP-CERHR. People may be exposed to acrylamide from foods.2) 57.1-61.7 (58. 2005).0-66. but can covalently bind to form adducts with proteins.6-61.3) 63.0 (57.1) 62.9 (54.6) 90.3-2.0-58. population from the National Health and Nutrition Examination Survey.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. and in some cosmetics. such as potatoes and some grains.

2006).6-64. 2006) have been demonstrated after acrylamide dosing.5 (83. fetal death.9) 75. 2002. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al. Puppel et al.4) 46.. EPA.. 2005). respectively) are markers of integrated acrylamide exposure over the preceding few months..8-49.9 (57.1 (70.9) 65. Rice. reproductive effects (reduced litter size.0 (80.3 (56. 2006.1) 60.2 (72.S. although different analytic methods can affect results.8 (51.8) 45. 2008).1 (57.2-90.7 (87.. 2008).2-68.5 (59.0-93. and cancer (mammary.0. Axonal degeneration.9-64. 1997.9-138) 143 (130-159) 96. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.int/ ipcs/food/jecfa/summaries/summary_report_64_final. Mucci et al. 2005). 2005) have been demonstrated in animals.7) 60. 2001).5-94.1 (82. 2005..5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.9) 59. 2005.6-62. 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.1) 56. Maniere et al.. 2005) and sperm DNA adducts (Xie et al. and neuronal DNA reactivity (Doerge et al. AHA levels have been shown to increase with dietary intake (Hagmar et al.6 (90. Puppel et al. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. 12 Fourth National Report on Human Exposure to Environmental Chemicals .8) 60.4) 83..3) 59. 2005.7) 90.2) 65. Acrylamide is clastogenic and can produce dominant lethal mutations.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. scrotal. male germinal cell injury. U.1-56. and other sites) (FAO/WHO.3-101) 95..3) 59. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.4) 53.5-64.6-90. see Data Analysis section) for Survey year 03-04 is 4.5) 71. 1997.9-78.0-62.S.1 (66.5) 75th 85. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.8 (44. 2006). altered gene expression in testicular tissues (Yang et al.4 (81. 2005.. EPA. Glycidamide has been shown to react with DNA (Doerge et al.5-92.1-60.Acrylamide occupational exposures.0 (70. 2005).9) 87.4 (56. glycidamide (NTP-CERHR.4-103) 79. most non-smokers had levels less than about 100 pmol/gram hemoglobin..2 (63.5) 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. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. thyroid.. 2005. 2004). In addition.6 (66. uterine.4 (57. 2003.3) 85.S.. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. dominant lethality).1) 62. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.5 (56.5-66.1-70. Vesper 2005) and smoking (Bergmark..9-77. 2005.0 (75. Schettgen et al.3-78..4 (90.7 (84. 2005).1-62.4 (61. 2005.1 (56. presynaptic nerve terminal binding (LoPachin.pdf.4-98.. 2002. 2005..3) 59.7-62. 2005. Additional information is available from U..8-61. Klaunig et al.2) 55.4-59.0) 118 (103-126) 121 (112-134) 113 (94. adrenal. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).7 (57. probably through its epoxide metabolite.2-91. EPA at: http://www.5) 87. The degree of formation of the more toxic glycidamide and levels of GHA can be influenced by polymorphisms in several of the enzymes that metabolize acrylamide (Duale et al.S.0) 94. Schettgen et al. IARC classifies acrylamide as probably carcinogenic to humans. 2005.who... interval) 59. Vesper et al.8-48. After exposure ceases.7 (61.4 (51. population from the National Health and Nutrition Examination Survey.7) 61. Survey Geometric mean (95% conf. U.5 (42..9-62.7-86.epa. 2009).9 (58.0 (52.2) 87.9-76.2 (56.4-65.7) 74. NTP-CERHR. Hagmar et al.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. 2004. 2005.9 (81.7-64.

3:406-412. Wu Y. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 .niehs. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. smoking habits and gender.pdf. Calleman CJ.561:21-37. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Mucci LA.html#u1004. Aprea P. Twaddle NC. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. 64th Meeting: Summary and Conclusions (FAO/WHO). 2001). Adv Exp Med Biol 2005. Maniere I. 1993. 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. Mutat Res 2005. CFSAN/Office of Plant and Dairy Foods. Bergmark E. Kamendulis LM.56. Paulsen JE. Wilson KM. Cheong HK. smokers and nonsmokers. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al.cfsan. Nordander C. et al.. Snyder RW.85:447-459. J Agric Food Chem 2008. He F.120(1):45-54.Toxicol Appl Pharmacol 1994. Metabolism and hemoglobin adduct formation of acrylamide in humans. Becher G. NIH Publication No.580(1-2):119-129.pdf. Costa LG. Burgess J. Toxicol 2005. Hagmar L. Italy. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Costa LG. 6013-6019. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. 2005. Available at URL: http://cerhr. Acrylamide neurotoxicity: neurological. Zhang S.10(1):78-84. He F. Wirfalt E. Doerge DR. Calleman CJ. Food and Drug Administration (FDA). et al. Tornqvist M. Available at URL: http://www. Spicer R. Bergmark E. In another study. da Costa GG.fda. 1999).27(4):219-226. DiNovi M and Howard D. Chicago. Illinois. Toxicol Appl Pharmacol 1993.561:49-62.. McDaniel LP. Granath F. Calleman CJ. 2/3/09 Hagmar L. Perez et al.580(1-2):131-141. Joint FAO/WHO Expert Committee on Food Additives. Bruze M. morphological and molecular endpoints in animal models. Yang JS.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Toxicol Sci 2005. Bjellaas T.. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Magnusson AL. Chem Res Toxicol 1990. 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. gov/~dms/acrydata. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Mechanisms of acrylamide induced rodent carcinogenesis. Axmon A. 2004 Acrylamide in Food Workshop: Update Scientific Issues. et al. Alexander J. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake.. Kautiainen A. 2001. Bergmark E. Chem Res Toxicol 1997 Jan. Churchwell MI. 054472. Paulsson B. 2004. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. and Research Strategies. Scand J Work Environ Health 2001. 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. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. National Toxicology Program. Osterman-Golkar S. February. Malmberg B. [Epub ahead of print] Dybing E.who. Uncertainties. LoPachin RM. Toxicol Sci.nih.580(1-2):157-165. Haugen M. Laurentie M. Guffroy M. Adv Exp Med Biol 2005. 1994).43:365–410. Fennell TR. Survey data on acrylamide in food: individual food products. References Bergmark E. Beland FA. Hagmar et al. Churchwell MI. Mutat Res 2005. Rosen I. 2006. Godard T.126(2):361-371. Food Chem. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Human exposure and internal dose assessments of acrylamide in food. 2/3/09 Perez HL. 2009 Jan 8. The Updated Exposure Assessment for Acrylamide.gov/chemicals/ acrylamide/Acrylamide_Monograph. Andersen M.Acrylamide In occupational settings. July. Tornqvist M. Fennell TR. 2/3/09 Klaunig JE. Farmer PB. Mutat Res 2005. 8-17 February 2005. Duale N. Available at URL: http://www. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Rome. April 13-15. Bridson WE. et al. Summer SCJ. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Doerge DR.. Tian G. Acrylamide intake through diet and human cancer risk.

Schettgen T. Marko D. Han CH. et al. Environmental Protection Agency (U. Liu Y. Lee SH.206(1):9-14. EPA).Acrylamide glycidamide by gas chromatography-mass spectrometry. Toxicological effects of acrylamide on rat testicular gene expression profile.20(6):959-64. Vesper HW. Hemoglobin adducts of ethylene oxide.274(1):59-68.19(4):527-34. Karlsson P. Jin Y. 2/3/09. Office of Pollution Prevention and Toxics. Int J Hyg Environ Health 2004. Choi JH. Ingham L. 14 Fourth National Report on Human Exposure to Environmental Chemicals . 1994. Tornqvist M.gov/chemfact/s_acryla. Tjaden Z. Washington (DC). Drexler H. Int J Hyg Environ Health 2003. J Agric Food Chem 2002. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Meyers T. Chae C. Analysis of acrylamide. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Rapid Commun Mass Spectrom 2006.580(1-2):71-80. Angerer J. revised 1/3/06. Chemical Summary for Acrylamide.S.S. Eriksson S. Adv Exp Med Biol 2005. Environmental Protection Agency (U. Kutting B. Ding X. a carcinogen formed in heated foodstuffs. Tjønneland A. Letzel S. Myers GL.gov/iris/subst/0286. Integrated Risk Information System (IRIS).epa. Available at URL: http://www. Lee MH. Broding HC. Angerer J.561:89-96.50(17):4998-5006. Puppel N.56(15):6046-53.134(1-3):65-70. Schettgen T.163(2):101-8. Ospina M. Schettgen T. Fu D. Anal Biochem 1999.htm. Benetou V. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Reprod Toxicol 2005. Vesper HW. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Han DU. The carcinogenicity of acrylamide. Rice JM. Fueller F. et al. J Agric Food Chem 2008. Toxicol Lett 2002. Drexler H.epa. Sun H. Rossbach B.S. Weiss T. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Hallmans G. U. propylene oxide. Yang HJ. Meyers T. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Ospina M. EPA).txt. Toxicol Lett 2006. Angerer J. Slimani N. Rydberg P.S. Available at URL: http://www. 2/3/09 Vesper HW.207(6):531-9. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany.580(1-2):3-20. Licea-Perez H. Gray JG. Mutat Res 2005 Feb 7. September. Liu K. Xie Q. Drexler H. Agudo A. U. Mutat Res 2005. Smith A. Tareke E. Acrylamide.

140-.086 (.188) .990) .104-.770) .030-.050 (<LOD-.77 (2.100-.50 (1.54) 1.S.960-1.150) .087-.50) 3.93) .197) . which may vary for some chemicals by year and by individual sample.164 (.770-1.39 (1. cardiovascular disease.187) .02) 1.49) 1.050) .120 (.040-.071 (.050 (<LOD-.110-.148-.120) .28-1.059-.30) 2.137 (.310-1.160 (.070-.111-.28) .230) . DHHS.63 (2.080 (.068) .533-.540 (.57) 2.14-1.400-.68 (1.20 (.480-1.130) .110) .310) .260) 1.163 (.S.930 (.070) .058 (.40) .12) 1.66) 1.060-.110-.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * . acute respiratory illness.180 (.220) .110 (.01) 3.70) 2.950-1.20-2.015.33-2.164 (.55 (1.410) .080) < LOD .53 (1.130 (.066) . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.88 (.220) .073) < LOD . The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.505 (.120 (.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th . Fourth National Report on Human Exposure to Environmental Chemicals 15 .770) .052 (<LOD-.120-.050) .790) .050 (.30) 2.302) .42 (1.710 (.154-.850 (.95) 1.740-1.81-2.05.216 (.70-2.430-1. Serum Cotinine Metabolite of nicotine (component of tobacco smoke) Geometric mean and selected percentiles of serum concentrations (in ng/mL) for the non-smoking U.480-.48-3.506 (. respectively. population from the National Health and Nutrition Examination Survey.14) .12 (1.080-.580-1.124 (.160 (.570-1.040 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.047-.350-.070 (<LOD-.600-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.53-4.300) ..89) 1.510 (.077) .99) 2.00) .470-.193) .83-2.690 (.175 (. acute respiratory infections.88 (1.115-.060-.145) .120 (.630 (.84-3.85 (1. and various other disorders (U.76 (1.78) 2.02) 1.54 (1.44) 2.350 (.080-.43 (1.860 (.180) .23 (1.63-2.19) 1.030-.071) .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 .057-.190-.910-1.310-1.054 (.14) .015 ng/mL.950 (.34 (1.65 (1.090-.180) .44) 2.21-1.020-.48-2.997-3.Cotinine Cotinine CAS No. < LOD means less than the limit of detection.142-.5% nicotine by weight (Kozlowski et al.22) 2.30) * .370-.201) .090-.670) .99) 2.140 (.66 (1.167 (.153-.44 (2. Children exposed to ETS are at increased risk for sudden infant death syndrome.44 (1.110) .126) . DHHS.17) .990 (.68) 2.35 (2.110 (.580 (.050 (<LOD-.120 (.066-.312) .110 (.570 (. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.45) 1.18-3.089) Age group 3-11 years 99-00 01-02** 03-04 . emphysema.140 (.280 (.50-4.20) .62) 2. maternal exposure during pregnancy can result in lower birth weight.12-4.075 (.030 (.32-2.15) 2. and 0.630 (.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. and 03-04 are 0.131 (.163) .92 (1.144 (.62 (2.030-.580) .625) .15 (2.080-.068) .920 (.23-2.09-2.740-1.084) .063) .19) .23 (2.621-1. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease. 2006).21-1.32-2.088-.726) .120-.500 (.450-.77 (1.190-.66-3.070) . ear problems.96) 2.110 (.053 (<LOD-.160 (.428-.077) .87-3.180) .39) 3.310) 90th 1.066 (.087 (.520 (.12 (2.060-.150) . and exacerbated asthma (U.050-.213) .49) 1.730 (.01 (1.77 (1.96-4.076-.50-1.160) .04 (1.047-.137-.11) .320) .42-4.061) < LOD . 2004).16) . ** In the 2001-2002 survey period. 83% of measurements had an LOD of 0. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.350-.110-.040 (.660) . see Data Analysis section) for Survey years 99-00.059-.02 (.840) 3.160-.094) .070) 75th .20 (1.200) 1.47-3.087) < LOD < LOD .68) . and 17% had an LOD of 0.160) .26-1.140-.198) * .60-2.050-.94) 1.240 (.139) * . 2004).620 (.080 (.043-.180) .21 (.060 (<LOD-.00) 1.360) .19-2.234) .106-.308 (.17 (.108) * .09-3. stroke. 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.220-.110 (.260-1.230 (.20) 1.800 (.38-2.040-.060 (.09-3.090-.060) .210 (.96 (1. 1998).620-1.900-1.120 (.32) 1.190-.S.79) 3.55-2.060 (.820) .080-.05) 1.060 (<LOD-.080) < LOD < LOD .17 (1.05 ng/mL. Survey Geometric mean (95% conf.75) 1.630 (. Cigarettes contain about 1.050 (<LOD-.54 (1.540-.180) .180 (.062 (.23 (.052 (<LOD-.040 (.

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

Ethnic differences in N-glucuronidation of nicotine and cotinine. Jacob P III. National Center for Chronic Disease Prevention and Health Promotion.S. Pechacek TF. DHHS).114(6):853-858. Herrera B. DHHS). Metabolism and disposition kinetics of nicotine. Benowitz NL. Brody DJ. Kira S. Available at URL: http://monographs. and the United States.56:483-493. Jacob P III. U.niosh.gov/tcrb/monographs/10/. Dollery CT. Available at URL: http:// cancercontrol.gov/ntp/roc/eleventh/profiles/ s176toba. Coordinating Center for Health Promotion. Schober SE. References Armitage AK. Available at URL: http://monographs. National Toxicology Program (NTP). Pickett MA. In Report on Carcinogens. Pharmacol Rev 2005.15:302-307. 4/13/09 National Cancer Institute (NCI). 1988-1991. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Bernert JT. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. June. 4/13/09 Perez-Stable EJ.280:135-140. Nicotine metabolism and intake in black and white smokers. Tobacco related exposures. Int Arch Occup Environ Health 1991. Fong I. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Jacob P. U. Am J Public Health 2004. U. 2004. Pollack HA.S. iarc.php. Perez-Stable EJ. Centers for Disease Control and Prevention. Coordinating Center for Health Promotion. Office on Smoking and Health [online] 2006. Trends in the exposure of nonsmokers in the U.18:188-204.gov/library/ secondhandsmoke/. International Agency for Research on Cancer.fr/ENG/Monographs/allmonos90.niehs.S. Etzel RA. Benowitz NL. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Department of Heath and Human Services.S. Mehta NY.gov/eid/rmca/critdocs/ criteriadoc/33.S. 11th ed.S Department of Health and Human Services (U. George CF. Richter PA. [online].surgeongeneral. Summary of Data Reported and Evaluation [online] 2004. population to secondhand smoke: 1988-2002. Bernert JT. 4/13/09 Iwase A. Modin G. Caudill SP. Third National Report on Human Exposure to Environmental Chemicals. Strauss WJ. Lewis PJ. 1991. Turner DM. Giovino G.57(1):79115.pdf.pdf.7:369-375. Pirkle JL. Vol 83. Giovino GA. Clin Pharmacol Ther 1994. Aiba M. 4/13/09 U. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Respiratory nicotine absorption in non-smoking females during passive smoking. IARC Monogr Eval Carcinog Risks Hum. et al.php.275:1233-1240. Epidemiol Rev 1996. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Cotinine as a biomarker of environmental tobacco smoke exposure. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. available at URL: http://mtn.4:313-316. Environ Health Perspect 2006. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. 4/13/09 International Agency for Research on Cancer. Summary of Data Reported and Evaluation [online] 1986. JAMA 1998. Maurer KR. BMJ 1975. Schwartz SS.S. Tob Control 1998.94(2):314-320. 1999.63:139-43. IARC Monogr Eval Carcinog Risks Hum. Smoking and Tobacco Control Monograph 10 [online]. Brody DJ. Benowitz NL. Herrera B. Tobacco Smoke.nih. Department of Heath and Human Services. Available at URL: http://www. JAMA 1998. JAMA 1996. Hukkanen J. Sweeney CT. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects.S. 4/13/09 Centers for Disease Control and Prevention (CDC). Pirkle JL. Tobacco Smoke and Involuntary Smoking. Benowitz NL. Centers for Disease Control. Curtin LR. Tob Control 2006. Jacob III P. cigarette smokers: the Third National Health and Nutrition Examination Survey.cancer. Sosnoff CS. Kozlowski LT. Available at URL: http://ntp. the United Kingdom.S Department of Health and Human Services (U.291(3):1196-1203.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Exposure of the U. Racial/ethnic differences in serum cotinine levels among adult U. Mowery PD. Warner K. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.cdc. National Institute for Occupational Safety and Hygiene (NIOSH). IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.280:152-156. Soliman S. J Pharmacol Exp Ther 1999. Pechacek TF.fr/ENG/Monographs/ allmonos90. Vogler GP. Atlanta (GA): 2005. Houseman TH. 1999-2002. Absorption and metabolism of nicotine from cigarettes. 1988-1991. Vol 38. et al. Benowitz NL. Flegal KM. Jarvis MJ.iarc. Centers for Disease Control and Prevention. Caraballo R. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary.

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

see Data Analysis section) for Survey years 99-00 and 01-02 are 0.130 (.180) < LOD .130-. 2005).100-.N-Diethyl-meta-toluamide (DEET) CAS No.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.110 (.EPA. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. Its use is recommended for prevention of several vector-borne diseases. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.S.100-. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.130-.110 (. 2002).140-.S. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. 2003). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .449 and 0. (U. including seizures and encephalopathy.130-. Additional information is available from U.150) < LOD .210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .120-. population from the National Health and Nutrition Examination Survey. DEET is not genotoxic. < LOD means less than the limit of detection. There are over 225 insect repellents brands containing DEET.gov/pesticides/. About 3-8% of dermally applied DEET is absorbed. 1998).210 (. Sudakin and Trevathan.100 (<LOD-.180 (. 1998). 2003).220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .120-.110 (.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample.240) < LOD .220 (. DEET can be applied to clothing and the skin to repel biting insects.EPA at: http://www.180 (.S. 134-62-3 General Information N. DEET is not registered for use on agricultural commodities.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1995. and it has not been rated by IARC or NTP with respect to human carcinogenicity.250) < LOD .140 (.N.100-.190) < LOD .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-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. After absorption. EPA. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. One survey detected DEET in 74% of sampled streams in the U.520) < LOD .1.epa.S.180 (.130 (.140) < LOD .N-Diethyl-meta-toluamide (DEET) N.110 (<LOD-. DEET is not a developmental or reproductive toxicant in animals (U.170 (. Urinary N..S.EPA.S.270) 688 678 518 700 598 956 Limit of detection (LOD.100-.. Fourth National Report on Human Exposure to Environmental Chemicals 19 . 2002).110-. DEET is also used in combination with dermal sun screens (U.560) < LOD . Survey Geometric mean (95% conf.130 (. and they range in concentration from 4% to 100%.100-.100-.140) < LOD .130) < LOD . have been reported as result of self-poisoning by ingestion or excessive dermal application. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.130) < LOD . (Kolpin et al.110 (.170 (.110 (<LOD-. Neurological effects in humans.160) < LOD .110-.130-. DEET has low acute toxicity.140) < LOD .

320) < LOD .250) < LOD .290-.270) < LOD .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 .270-.230) < LOD .150) < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.190 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .190 (<LOD-. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect. 1992).190-.640 (.200 (.150-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .. 2007).490) < LOD .410-.S.130 (<LOD-.93) < LOD .280 (.330 (.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.350-.270 (.S.230-.330 (.390-.230-.240) < LOD . population from the National Health and Nutrition Examination Survey.190 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.300 (.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.250 (. 2005).550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey Geometric mean (95% conf..370-.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 .630) < LOD .240-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350) < LOD . Urinary N.410 (.440) < LOD .170-.480 (. representative subsamples from NHANES 2001-2002. In this survey period.370) < LOD .410 (.320 (. Urinary DEET levels as high as 5.500 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.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 .N. 20 Fourth National Report on Human Exposure to Environmental Chemicals .280-1. 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. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.250-.140-.270 (<LOD-.

S. Tapia J. Third National Report on Human Exposure to Environmental Chemicals. Centers for Disease Control and Prevention (CDC).S.S. hormones. 1993-1997.gov/teach/chem_summ/ DEET_summary. Int J Toxicol 2002. Reregistration Eligibility Decision (RED): DEET. DeBord KE.N-Diethyl-meta-toluamide (DEET) References Arcury TA. Thurman EM. Environmental Protection Agency (U. Veltri JC. 1-118.gov/oppsrrd1/REDs/0002red.EPA.41(6):831-839.115(8):1254-1260. Washington (DC): U.S. EPA 738-R98-010. Available at URL: http://www. DEET: a review and update of safety and risk in the general population.2:341352.S.N.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography.EPA). Atlanta (GA). Furlong ET. Environ Health Perspect 2007. Schoenig GP.25:95-100. Human exposures to N.36(6):1202-1211.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. et al. EPA. streams. pdf. Hartnagel RE Jr. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . pp. U. Gabriel KL. Osimitz TG. Barr DB. Lowry LK. 1999-2000: a national reconnaissance. Bell JW.S. N.epa. Zaugg SD. 4/9/09 U. Page BC. Available at URL: http://www. Toxicity and Exposure Assessment in Children’s Health.EPA). and other organic wastewater contaminants in U.16(1):10-13. Trevathan WR. Pharmaceuticals. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. September 1998. Fundam Appl Toxicol 1995. Environ Sci Technol 2002. and excretion of N. U.pdf. Diethyltoluamide (DEET). Selim S. Sudakin DL. Absorption. J Anal Toxicol 1992. 2005 Kolpin DW. Meyer MT. Smallwood AW. Chemical Summary. Grzywacz JG. 2005. Barber LB. Quandt SA. J Toxicol Clin Toxicol 2003. metabolism.N-diethyl-mtoluamide following dermal application to human volunteers.epa. Environmental Protection Agency (U. Chen H.S.

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

2008.14(2):149-157. November 26. Joskow R. Sottas CM. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. J Am Dent Assoc 2006. Available at URL: http://cerhr. Barr DB. Twomey K. et al.europa. Joint Research Centre Institute of Health and Consumer Protection.102(19):7014-7019. 2007. 5: 505-523. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants.nih. August 2001. Marr MC.pdf .jrc. Hughes C. Chung MK. hormones. Endocrinology 2008. Koulova AI. Kawamura N. Pyo MY. Chem Res Toxicol 2001. Nippon Eiseigaku Zasshi 2004. NC. Furukawa M. Szigeti-Buck. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Han SY. Rhomberg et al. Proc Natl Acad Sci USA 2005. Toxicol Sci 2002. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). September.pdf . 32 Fourth National Report on Human Exposure to Environmental Chemicals . Ikka T. T. Hum Ecol Risk Assess 2004. Doull J. Howdeshell KL. Kiguchi M. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Barber LB. vom Saal FS.pdf. and other organic wastewater contaminants in U. DirectorateGeneral Health and Consumer Protection. Research Triangle Park. Serizawa S. Gray GM. Available at URL: http://ecb. Occup Environ Med 2002. Brine DR. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP).S. Environ Health Perspect 2008. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. streams.145:592-603.10:875-921. and Hajszan. Belgium. Ecotoxicity and the Environment (CSTEE). Kim YH. Klinefelter GR. Calafat AM. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Environ Health Perspect 2005. Cunha G. Yoshinaga J. Available at URL: http://ec. Pharmaceuticals.nih.35(2 Pt 1):238-254. Watanabe C. Life Sci 2001. 2002. An evaluation of the possible carcinogenicity of bisphenol A to humans. 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. Kuklenyik Z.S. National Institutes of Health. bisphenol A glucuronide. Barr JR. Hlywka JJ.69(22):2611-2625. Bradley S. Imai H. Tsugane S.. Calafat AM. Matthews JB. Brussels. Yang M. Exposure of the U.312(2):441-448.gov/chemicals/bisphenol/BPAFinalEPVF112607. Lynch BS.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Regul Toxicol Pharmacol 2002. Kolpin DW. Reidy JA. 2/4/09 Fujimaki K.niehs. Thurman EM. MacLusky. Environ Sci Technol 2002. Needham LL.149:988-994. Kroes R. 4.pdf.. Harazono A. Keimowitz AR. Reprod Toxicol 2001.137(3):353-362. Cha SW. May 22. K. In vitro and in vivo interactions of bisphenol A and its metabolite.J.pdf. Reidy JA. Available at URL: http://cerhr. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. European Commission. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Biochem Biophys Res Commun 2003. Zaugg SD.113(4):391-395. Richter CA. Endocrinology 2004. C.. N. Haighton LA.eu/ health/ph_risk/committees/sct/documents/out156_en. 1999-2000: a national reconnaissance. et al. Kim JC. Kim CS. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Tyl RW.59(4):403-408. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. U. Koh WS. Thomas BF. niehs. Ema M. Leranth. Department of Health and Human Services.gov/chemicals/bisphenol/bisphenol. Needham LL. 2/4/09 European Commission. Fujii S.59(9):625-628. Italy. Zacharewski TR. Meyer MT.68(1):121-146. 2/4/09 Ouchi K. Furlong ET. with estrogen receptors alpha and beta. McConnell EE. Hanaoka T.Environmental Phenols References Akingbemi BT. Needham LL. Available at URL: http://ntp.nih. Wong LY. Han SS. Ye X. Cohen JT. 2003. Caudill SP. Human Health.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Park S.36(6):1202-1211. Rubin C. Bisphenol A. Myers CB. niehs. Ekong J. National Toxicology Program. Barton L.Scientific Committee on Toxicity. J Chromatogr B Analyt Technol Biomed Life Sci 2002. and Hardy MP. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Hara K. Arakawa C.S. Rat two-generation reproductive toxicity study of bisphenol A.116(1):39-44.780(2):365-370. National Institute of Environmental Health Sciences. Shin HC. Timms BG. Munro IC. et al. Watanabe S. Ispra. Calafat AM. Gender differences in the levels of bisphenol A metabolites in urine. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats.

Environ Health Perspect 2005. Morgan MK. Chang SS. Wilson NK. Chem Res Toxicol 2002. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration.15:12811287.40(7):905-12. Nagel SC. Colnot T.147(6 Suppl):S56-69. Dekant W. An observational study of the potential exposures of preschool children to pentachlorophenol. Arch Environ Contam Toxicol 2003. Hughes C. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Kawamoto T.Environmental Phenols Volkel W. Witorsch RJ. III. Fourth National Report on Human Exposure to Environmental Chemicals 33 .113(8):926-33. Lordo RA. Vom Saal FS. Environ Res 2007. Food Chem Toxicol 2002. Kim SY. Biological monitoring of bisphenol a in a Korean population. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Yang M. Chuang JC. Large effects from small exposures. Endocrinology 2006. and nonylphenol at home and daycare.44(4):546-51. Filser JG. vom Saal FS. Welshons WV. bisphenol-A.103(1):9-20. Csanady GA. Sheldon LS. Lee SM. et al. Jang JY. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment.

389 (.497) * . Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. have demonstrated estrogenic effects particularly when injected at high doses in animals.10) 2.900 (. see Data Analysis section) for Survey year 03-04 is 0. industrial cleaners. 2000. Katsuda et al. During the 1980s and 1990s.3. and some personal care products.S.80 (1. Ying et al. an alkylphenol. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.40) 2.20-2.20) 1.00) 1229 1288 03-04 03-04 03-04 * . which are anionic surfactants used in detergents.500 (.369 (. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.1.200-.600) 1. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. the various alkylphenols have also been used as emulsifiers and modifiers in paints.10 (.200-.000 tons of alkylphenol ethoxylates were produced annually worldwide. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. Laws et al.60-3.300 (<LOD-.70 (1.10 (1. 4-octylphenol monoethoxylate was detected in 43.800-1..30 (1.900 (.500) . The alkylphenol ethoxylates enter the environment through human use of products containing them.50-2.70 (1. Less frequently. In rats.S. and the polyethoxy chain may consist of up to 50 ethoxy units.400 (. and from contact with some personal care products and detergents.70 (1.477) ..60) .50 (1.20) 314 715 1488 03-04 03-04 * * . including 4-tert-octylphenol.300 (<LOD-.30 (1..3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates. and through manufacturing waste streams (Warhurst. which may vary for some chemicals by year and by individual sample.20-2.500-1.60) 1.300-. and to alkylphenoxycarboxylates. streams in 30 states (Kolpin et al.20-2.300 (<LOD-. is used to manufacture alkylphenol ethoxylates. 2000...30-2. and some of their degradation products are toxic to aquatic life. fish) and drinking water.. Blake and Boockfor.90) 2. Several alkylphenols.274-.600-1. to shorter chain alkylphenol ethoxylates. 2002). < LOD means less than the limit of detection.10-2.400) 1. orally administered 4-tert-octylphenol was well absorbed.300-.80 (1.20-2. over 500.900 (.. impaired steroidogenesis.40 (1.400 (.60-3. Indoor and to a lesser extent. 1996).10 (. 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. 2002).10) 1.40) * 03-04 03-04 03-04 . Disposition in humans has not been studied sufficiently. population from the National Health and Nutrition Examination Survey.60-3.5% of 139 U. 140-66-9 General Information 4-tert-Octyphenol.600) . textiles.. 1997.299-.400 (.50) .20-2.30) 1.600-1.30 (1.30 (.300 (<LOD-.80 (1.600-1.50) 1.20 (1. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.Environmental Phenols 4-tert-Octylphenol CAS No.600-1.. In the 1990s. Bian et al.30) 2. pesticides.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 .600) .507) * < LOD .70 (1.60-3. and emulsifiers.300 (<LOD-.700-1. altered neonatal sexual development. In 1999-2000. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). * 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 2. 1995.80) 2.40) 2. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. testicular atrophy.30) 90th 1. The alkylphenols can bioaccumulate in some fish. through sewage.600) . did not bioaccumulate.60-3.268-.00 (1.. leading to inhalation as another potential exposure route (Rudel et al.900 (.g.20) 2. Urinary 4-tert-Octylphenol (4-[1.500) .30 (1.600-1.900 (.500) .500) 75th .2.40) 1.50) 1.20-2.40) 1. Saito et al. altered estrus cycles and reproductive outcomes.90) 2. 34 Fourth National Report on Human Exposure to Environmental Chemicals . 2006.600-1.00 (.g.60) 613 652 1092 Limit of detection (LOD. 2004).357 (. 2003. and was quickly eliminated from the blood (Certa et al.50-3.50) 1.60-3.500-1.50) .00 (. and impaired spermatogenesis (e.

00) 2. or their corresponding ethoxylates with respect to human carcinogenicity.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00 (.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 .860 (.00) 2. 2005.36-3.400) .73) 2.78) 3.560) .29) 2.50 (2..740 (.65-3. Sweeney et al.384) * .68) 2.276 (. 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.640-1.540-1.470-1.11-2.43) 1. In a small number of adult Japanese volunteers.43) 1.740 (.620) .470) 75th .05-2. 2000.96-4.570) . 2004).03 (1.62 (1.18-4. Fourth National Report on Human Exposure to Environmental Chemicals 35 . (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.10-2.00) 1.450) 1.270 (.43-3.300 (<LOD-. Urinary 4-tert-Octylphenol (4-[1.33) 3.11) 1. Calafat et al..06 (2. It is unclear if estrogenic or other effects occur in animals through oral dosing.890-2.59 (1..15) 1.270 (.500-1. at lower or environmentally relevant doses (Blake et al. population from the National Health and Nutrition Examination Survey.02-4.00 (.460 (.41) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.630-1.S.76 (2.370 (<LOD-.08) 1. representative subsample of NHANES 2003-2004. Survey Geometric mean (95% conf.31-2.3.81 (1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.730-1.270-. nonylphenol. 1999). 2001).470-1.550-1.40 (1. 2003.207-.54) * 03-04 03-04 03-04 .85 (1.24) 612 651 1091 < 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.850 (.40-4.64 (.03-6.530) .11) 2.410 (. IARC and NTP have not rated octylphenol.320 (<LOD-..280-. Yoshida et al.14) 314 713 1487 03-04 03-04 * * ..337-.22) .25) 90th 1..53-3.170-.17 (.S.269 (.349) * < LOD .1.199-.03 (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. 2004. Tyl et al.67-2.450) . 2001.910 (.380 (<LOD-.770 (.435 (.31 (1.33 (2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.25-2.59) 1.62) .160-.20 (1. Nagao et al.620-1.68-2.25) 2.78 (1.71) 2. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.78) 1228 1286 03-04 03-04 03-04 * .Environmental Phenols Myllymaki et al.260 (<LOD-.610) .60 (1. Kawaguchi et al. 4-tert-Octylphenol is not considered directly genotoxic.62 (1.420) .

121(1):21-33.36(6):1202-1211. and sertoli cell number. Song L. Maekawa A. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Furlong ET. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Certa H.18(1):43-51. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Environ Health Perspect 2008. Makino T. Wiegand HJ. Rudel RA. Ito R. Yoshimura Y. Izumi S. Spengler JD. Sakui N. Roche JF.folliclestimulating hormone.116(1):39-44.Environmental Phenols References Bian Q. Inoue K. Okada F. Qian J. Onuki A. pesticides. Fedtke N. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol.S. Environ Int 2002. nonylphenol. Kawaguchi M. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Tyl RW. et al.30(2 Pt 1):81-95. Toxicol Appl Pharmacol 2000. Calafat AM. Indoor air pollution by alkylphenols in Tokyo.uk/resource/reports/ethoxylates_alkylphenols. Takenaka A. Environ Sci Technol 2002. 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.pdf. Estrogenic activity of octylphenol. Yoshida M.co. Millette CF. Taya K. Boockfor FR. Brody JG. Muller AM. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Endocrinology 2000. Nicol L. et al. Phthalates. Kolpin DW. Brooks AN. Nagao T. Saito Y. Environ Sci Technol 2003.57(2):255-266. polybrominated diphenyl ethers. Brine DR. Arch Toxicol 1996. Myers CB. Boockfor FR. Katsuda S. and other organic wastewater contaminants in U. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Wong LY. Camann DE. Blake CA. Haavisto TE. Cooper RL. Barber LB.165(3):217-226. Nakagomi M. Meyer MT. Laws SC. Blake CA. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Reprod Toxicol 2001. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Wang X. McCoy GL. Exposure of the U. Bodman GJ. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. 2003. 36 Fourth National Report on Human Exposure to Environmental Chemicals . prolactin. and other endocrine-disrupting compounds in indoor air and dust.141(7):2667-2673.71(1-2):112-122. Williams B. Marr MC. Thurman EM. Biol Reprod 1997. streams. Zaugg SD. Myllymaki SA. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Ye X. Horie M. Ferrell JM. Katsuda S. Seely JC.foe.207(1):59-68. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Yoshida M.37(20):4543-53. Toxicol Lett 2001. 2/4/09 Ying GG.S.28(3):215-226. Saito I. et al.54(1):154-167. Watanabe G. Korn LR. Ono H. Fail PA.14(5):325-332. et al. Chen J. 1995. Warhurst AM. Two-generation reproduction study with para-tert-octylphenol in rats. alkylphenols.799(1):119-125. and testosterone. Regul Toxicol Pharmacol 1999. Xu L. Indoor Air 2004. Available at URL: http:// www. Usumi K. Nair-Menon JU.15(6):683-692. Carey SA. Taya K. Food Chem Toxicol 2006. Takai N. Reidy JA. Maekawa A. Yoshimura S. Anal Chim Acta 486:41-50. Toxicol Appl Pharmacol 2005.44(8):1355-1361. Pharmaceuticals. Watanabe G. Toppari J. Raychoudhury SS. Karjalainen M. Bolt HM. Paranko J. 1999-2000: a national reconnaissance. testis size. Toxicol Sci 2000. Inoue K. hormones. Needham LL. Reprod Toxicol 2004. Kawaguchi M. bisphenol A and methoxychlor in rats. Kookana R. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Sweeney T. Seto H.

S. mouthwashes.. the median urinary triclosan level of 7. streams sampled in 30 states (Kolpin et al. Veldhoen et al. Moss et al.Environmental Phenols Triclosan CAS No. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al.S. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. Matsumura et al.. 2008 has shown higher levels during the third decade of life and among people with the highest household income. In a U. 1988. Triclosan has been added to soaps... 1987). Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. 2006). 2007.. triclosan was found in 57.6% of 139 U. 1996.8-dichlorodibenzo-p-dioxin (Aranami et al. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent. and has also been impregnated into some kitchen utensils. In a study of 90 U.2 µg/L was comparable to the median level (8. General population exposure results from dermal and oral use of products containing triclosan.. young girls. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. Calafat et al. and wound disinfection solutions. It can be photochemically and biologically degraded.. toothpastes. 2000). Triclosan can be absorbed across skin into the blood stream.. 1976. Triclosan enters the aquatic environment mainly through residential wastewaters. but not by race/ethnicity and sex. Fourth National Report on Human Exposure to Environmental Chemicals 37 .S. It acts by inhibiting bacterial fatty acid synthesis.. Triclosan is not considered teratogenic at maternally toxic doses. acne medications. Biomonitoring Information Urinary triclosan levels reflect recent exposure. In animal studies. (Sandborgh-Englund 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. it has low acute toxicity. 2007). and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. In 1999-2000. representative subsample of NHANES 2003-2004. Triclosan has a low bioaccumulation potential in fish. 2002). Some reports show endocrine effects are observed in amphibians and fish (Foran et al. 2000. Lyman and Furia. 2007. Calafat et al. deodorants. In the body it is conjugated to glucuronides and sulfates (Bodey 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.. and medical devices..2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. In animal and human studies. toys. Triclosan formulations may rarely cause skin irritation. 2007). Mezcua et al. IARC and NTP do not have ratings with respect to human carcinogenicity. 1969). 2004).... a process that can result in the formation of small amounts of 2. 2005. 2008).

9 (8.0-73.4 (12.0) 9.Environmental Phenols Urinary Triclosan (2.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.6) 90th 212 (172-241) 03-04 03-04 03-04 9.9) 7.92-12.55 (4. population from the National Health and Nutrition Examination Survey.60 (6.1) 9.0-213) 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 (4.4-19.8-127) 37.2 (10.0) 65.S.20 (7.8-63. population from the National Health and Nutrition Examination Survey.7) 10.50) 10.9) 32. see Data Analysis section) for Survey year 03-04 is 2.7 (28.6) 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 9.16 (6.6 (9.6 (30.93 (7.5) 13.5) 20.74 (5.3.2) 9.45-13.38-18.8) 7.4) 90th 249 (188-304) 03-04 03-04 03-04 8.8-85. Urinary Triclosan (2.5 (11.3) 10.8-112) 30.9 (50.2 (11.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.2 (37.4) 25.20-11.4) 317 (231-433) 144 (96.6) 31. interval) 13.6-111) 33.4) 73.4 (11.6-14.9-61.2-46.2) 12.0-19.1-39.70-16.3 (26.1) 14.48 (8.9) 8.7 (9.4) 7.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2 (25.00-8.4) 51.3-35.1) 9.43-13.6 (10.89-11.30-14.29-12.0-15.0 (8.11-11.2 (13.10) 84.3) 47.10-9.1 (45.7) 292 (151-432) 132 (78.8) 9.0-15.5) 11.1) 11.3 (8.7) 123 (36.6) 39.6-14.5-14.1 (15.20 (7.6-15.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.8) 14.4-18.86-12.3-31.3-15.80 (5.94 (7.45-10.3-67.9 (33.6 (12.4) 357 (225-456) 203 (87.40-17.0 (26.50-10.6-65.90-10.9-236) 193 (90.21 (6.S.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.32-14.4 (32.40-11.8) 116 (39.7 (39.82 (8.54 (8.20-10.9 (11.8-60.6) 10.1) 50.0) 49.6) 12.1) 9.2 (27.0 (36.2-58.4.3 (11.0 (11.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.1) 7.4.1 (8.2-14.8 (21.7 (11.2) 13.1) 9.45 (5.2-58. Survey Geometric mean (95% conf.5) 66.4 (38.1) 13.6-37.20-13.3) 6.22-10.5-86.9) 75th 47.48-10.18 (5.60 (8. Survey Geometric mean (95% conf.72-13.4) 75th 43.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.7 (14.1) 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 9.0 (34. interval) 12.3 (9.6-20.

24(3):209-218. Toxicology of 2. Katsura E.115:116-121. Ekstrand J. Gunderson MP. Bhargava HN. 4’-trichloro-2’-hydroxydiphenyl ether. Wong LY. Meyer MT. Furlong ET. Aguera A. and other organic wastewater contaminants in U. Adolfsson-Erici M. population: 2003-2004. hormones.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Nagao Y. Environ Health Perspect 2008. Zaugg SD. Skirrow RC. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Hong HC.83(1):84. Arch Environ Contam Toxicol 1988. Matsumura N.28(9):1748-1751. Bodey GP. Wigmore H. Lyman FL.38(2):64-71. and phenols in girls. Foran CM. Pinney SM.7/2. Am J Infect Control 1996. Wolff MS.45 Suppl 2:S137-S147. Triclosan: applications and safety. Ebersole R. J Invest Dermatol 1976. Percutaneous penetration and dermal metabolism of triclosan (2. Calafat AM.36(6):1202-1211. Kanetoshi A. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Hernando MD. Mezcua M.116(3):303-307. Readman JW. Howes D. Moss T. Aranami K. Windham G. Erratum in: Aquat Toxicol 2007. Furia T. Gilbert RJ. J Toxicol Environ Health A 2006. Biol Pharm Bull 2005. Reidy JA. Pharmacokinetics of triclosan following oral ingestion in humans. phthalates. Osachoff H.. Environ Health Perspect 2007. Urinary concentrations of triclosan in the U. Barber LB. Needham LL. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Chelimo C.524:241-247. Williams PE. Teitelbaum SL. Watanabe N. Pharmaceuticals. Clapson DJ.67(4):532-537.Environmental Phenols References Aiello AE. Anal Chim Acta 1004.17(5):637-644. Br J Clin Pharmacol 1987. Sandborgh-Englund G. Pilot study of urinary biomarkers of phytoestrogens. 4.69(20):1861-1873. et al. The oral retention and antiplaque efficacy of triclosan in human volunteers.S. Environ Sci Technol 2002. Kolpin DW. Ye X.S. Mar Environ Res 2000. IMS Ind Med Surg 1969. et al. Thurman EM. Kaneshima H. Developmental evaluation of a potential non-steroidal estrogen: triclosan.4. Ogawa H. Ishibashi H.66:1052-1056.38(4):361370. Leonard PA. Ferrer I. Chemosphere 2007. Bennett ER.4’-trichloro-2’hydroxydiphenyl ether). Veldhoen N. 1999-2000: a national reconnaissance. Hirano M. Okui T. Evidence of 2. Food Chem Toxicol 2000. Larson EL. Levy SB. Benson WH. streams.80(3):217-227. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Britton JA. Fernandez-Alba AR.23(5):579-583.50(1-5):153-156. Williams FM. Photolytic degradation of triclosan in freshwater and seawater. Aquat Toxicol 2006. et al. Odham G. et al. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Shiratsuchi H. Gomez MJ.

30 (.70) .48-2.350 (.350-. algaecide and insecticide.990 (<LOD-2.40 (. which may vary for some chemicals by year and by individual sample.58-2.350) < LOD .350) < LOD .350 (.350-2.350-2. has been restricted.980 (.08-3.10 (.58-2. and dermal contact with PCP-treated products.350 (. 1979).5. are eliminated in the urine.350-. PCP cannot be used on wood in residential or agricultural buildings. Human exposure to PCP has become less common.00 (. Kohli et al..770 (. 40 Fourth National Report on Human Exposure to Environmental Chemicals .78) 1.76) . Survey Geometric mean (95% conf.350-.350) < LOD .860-2.390 (. To-Figueras et al.500-2. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.350-. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.350) < LOD . herbicide.350) < LOD .350 (. so it is relatively non-persistent. Effects including hyperthermia. mollusicide.42) 696 680 521 696 603 951 Limit of detection (LOD.75) 2. Since 1984. bactericide.10 (1.350 (.83 (2.650) 1.890 (..350-1.350 (.S.350-. After absorption.510-5. PCP use in the U.04) 1.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350-2.350) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. with repeated or chronic exposure.350-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.650 (.65 (.350) 90th .350 (.10 (<LOD-1. the elimination half-life may be a week or more (Uhl et al.590-1. The parent compound and conjugates.76) 1.90 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. along with small amounts of tetrachlorohydroquinone and conjugates. and animals. and it is used primarily as a preservative for wood to be used outdoors (e.350) < LOD . ingestion of contaminated food or water.S.67) 1.350 (.47-5.350-.g.660 (.65 (.30 (1. utility poles and fence posts). 1997).70) 2.350 (. hypertension.350) < LOD . < LOD means less than the limit of detection.350-..350-1.350) < LOD .98 (1.350-.350 (..350) < LOD .33-2.00) 2.350-.990-2. Acute. PCP is absorbed rapidly and well by all exposure routes.350-.23 (.90) 1.30 (.630 (.37 (.350) < LOD .53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .64) 1. After a single dose.890-1.510-3. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. other polychlorinated benzenes.350 (.350 (. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.32 (.80) .94 (1.350-2. General population exposure to PCP may occur by inhalation of contaminated air.530) 1.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350) < LOD .18 (<LOD-1.350-. 1986). PCP is distributed to most tissues and is not extensively metabolized. population from the National Health and Nutrition Examination Survey. PCP is degraded by sunlight and metabolized rapidly by microorganisms.47-3.350-.09) . PCP is eliminated over a few days (Braun et al.350-2.10) 1.30) 1..350-.350) < LOD < LOD 75th .60) 1.350-.350 (.30) .60) 1.350) < LOD . plants.25 and 0.850-2.350-. water and sediments because of the large amounts that were produced and used historically. PCP has been detected in soils.01 (<LOD-1.350-.62 (.350-.00) 1.10) 1.33) .350-.350-.350 (.90) 2.350 (.94 (1.390 (.350-.960) 1. and possibly of lindane (IPCS. 2002.37) .73 (1.350) < LOD . In the environment.350 (.350 (.350 (.480-2.350) < LOD . and metabolic acidosis were observed in CAS No.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 . air.48 (.680-1.91 (1.350-1.50) 1.45-2.350 (. 1976.350 (.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .54-2.350-.350 (.00) 1.350) .51) 1.350) < LOD .350-.30) 1.

95) 3.950-1.40) 1.330-.780-1.epa.00-1.10-2.. respectively) (Becker et al. In a small sample of U.380-.440 (.S. Pentachlorophenol is not mutagenic or teratogenic.25-2.560) < LOD .220-.40) 1. 1991). 2004.370 (.250 (. van Raaij et al.420) < LOD . In NHANES 2001-2002 subsamples.300 (.780) < LOD .35-2.510-.310-.html.52 (<LOD-1.340-.09 (<LOD-2.18) .500-1.320 (.cdc.gov/ toxpro2.13 (.590-1. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.25-1.570 (.16-1.atsdr.S.650 (.35-2.950-1.48-2.S.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .650 (.00-1.52 (<LOD-1.30-2.57 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67-3.83 (1. Fourth National Report on Human Exposure to Environmental Chemicals 41 .94 (1.67 (1.67 (1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. environmental levels) and health effects is available from the U.92) 1.. Survey Geometric mean (95% conf.25-2. OSHA has established an occupational standard.800-1.EPA.78) 1.560-.19 (1.290-.30) 1.26 (1.11) 2.270-. population from the National Health and Nutrition Examination Survey.78) 1.360-.67 (1. Biomonitoring Information In NHANES 1999-2000 the median urinary PCP levels among children aged 6-11 and 12-19 years were as much as thirteen times lower compared to a sample of German children aged 6-14 years in 1990-1992 (4.9 mg/L.19) 2.26 (1.990 (.40-2. and the FDA has established a standard for bottled water.320) < LOD < LOD 75th .220-.290-. 2000).84) 1.430-.25 (1.350) < LOD .06) 1.300 (. 1989).270-.30) 1.S. and adversely affected thyroid function (U.18 (1. 1989).21-2.490) < LOD .730) < LOD ..16 (.e.830) < LOD .36) .67 (1.260 (.19) 2.S.250 (.950-1.920 (.90) 1.300 (..35) 1. carcinogenic.35) 1.67-3. respectively) (Seifert et al.700-2.25) 1.400 (. The U.650) 90th 1.320) < LOD . children in the 1980’s.Fungicides adults and children severely exposed to PCP through ingestion.470 (.610 (. 1995).56) 1.94 (1.800) < LOD 1.320) < LOD .500 (.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * . chronically administered high doses of PCP were hepatotoxic.21 (.240-.84-4. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.590) < LOD .52 (1. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.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 .500-.94-3.08 and 5.760 (.82) 1.30 (. inhalation.55) 1.710-1.34 (.510-.75 (<LOD-2. Urinary Pentachlorophenol (creatinine corrected) Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.52) 1.19) 2. 2003).67-2.06 (.29-3..280) < LOD .84 (1.900-1.40) 1.09-1. Death can result from seizures and cardiovascular collapse.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .580-.10 (1.57 (..67 (1.0 mg/L. 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.360 (.430) < LOD .40) 1.560) < LOD ..850 (. In animals. EPA at: http://www.69 (1.290) < LOD .79) 1.gov/ pesticides/ and from ATSDR at: http://www. EPA has developed standards for PCP in drinking water and the environment.40) 1.75) 1.00) 1.73 (1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.51) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.. More information about external exposure (i. or skin absorption.25 (1.06-3.82 (1.910-1. Among adults in the NHANES 1999-2000 subsample. 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.310) < LOD .6 and 14. 2003).630 (.

Needham LL. Can J Biochem 1976.inchem. Arch Environ Contam Toxicol 1989.4:289296. The metabolism of higher chlorinated benzene isomers. Jones D. Phillips DL. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Needham LL. Environ Health Perspect 1997. EPA). Seiwert M.10:552-65.org/documents/jmpr/jmpmono/2002pr08. Safe A. Holler JS. Schmid P. Cline RE. J Expo Anal Environ Epidemiol 2000. Int J Hyg Environ Health 2003. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood.S. Shealy DB. Arch Toxicol 1986. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. available at URL: http://www. Schulz C. 4/21/09 Kohli J. Toxicology 1991: 67(1):107-16. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Uhl S.58:182-186. Helm D. Schulz C. Arch Environ Contam Toxicol 1989. Notten WR. Engel R. 206:15-24. Hill RH. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. van den Berg KJ.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. 42 Fourth National Report on Human Exposure to Environmental Chemicals . r e g u l a t i o n s . drinking water and indoor air. et al. International Programme on Chemical Safety (IPCS). Baker S. Fast DM. house dust. Pesticide residues in urine of adults living in the United States: reference range concentrations. Otero R. Barrot C. Chenoweth MB. Seifert B.18(4):469-474.S. To T. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Bragt PC. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. 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. 2002. et al. Becker K. urine. Head SL. Hill RH Jr. Pharmacokinetics of pentachlorophenol in man. References Becker K. 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. Bailey SL. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Santiago-Silva M. Rodamilans M. Sala M. htm. U. Kaus S. Krause C. Hill RH Jr. Environ Res 1995.54(3):203-208. Seiwert M.18:475-481. Seifert B. 4/21/09 van Raaij JA. et al. Schlatter C. Environmental Protection Agency (U. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Available at URL: h t t p : / / w w w. Gregg M. hair. Braun WH. Dev Toxicol Environ Sci 1979.105(1):78-83. Blau GE. Lindane. To-Figueras J. 11/30/2004. Smith SJ.71:99108. PCP: Human Risk Characterization [online].

22 (. Estimated human intakes have been below recommended intake limits (U. 2006).S. OPP is considered to be moderately toxic after acute oral doses in animal studies.600) < LOD . EPA.840-1. 90-43-7 General Information Ortho-phenylphenol (OPP.490 (<LOD-.. Workers who manufacture.640) < LOD . OPP is volatile. Timchalk et al.10-1.50-4.50) < LOD .27 (. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. such as fruits and vegetables.00 (1.580-1.90 (1.40-2.50-3. and sanitizers.60 (1.350-1. interval) . or apply these chemicals may be more highly exposed than the general population.740 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.90) .560-8.696) * .570-1..50 (1.790) 2.03) 1.890) 1. and it has limited water solubility.30) < LOD 1.420 (<LOD-.60-2.20) 2.30) < LOD . Most agricultural food applications have been revoked.450 (<LOD-.00) < LOD .370-.590-2.30) < LOD 90th 1. Both have been used in agriculture to control fungal and bacterial growth on stored crops.30) 1.710-2.498 (. 1998.60 (1.402-.10) .433-.33 (.890 (.500-2.90 (1. however.645) * .07 (.600) < LOD .860) * 99-00 01-02 99-00 01-02 99-00 01-02 .30 (1.00) .10) 1. fungicides.10) .10 (1. Cnubben et al.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.17 (.509 (.90) 1. are antimicrobial agents used as bacteriostats.50) 1.490 (<LOD-.61) 2.50 (1.950) < LOD .410-.496 (.88) 1.19 (.3.349-. formulate. 1998).10) .570 (.50) .370-.00 (1. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.621) * .860 (.40-5..S.550-1.10-2.00 (1.490 (<LOD-.34) 1. < LOD means less than the limit of detection. General population exposure can occur via dermal. In the past. SOPP is applied topically to the crop and then rinsed off.480-1.76) 1.50-2.S.520 (. 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.567 (.90) 2.90) . Survey Geometric mean (95% conf.20 (1.00) .23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .30-2.28 (.570-2.600-1.92 (.80) 1.20-2.40 (. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.20-3.610 (.20 (.820 (.638) * .600-1. Both chemicals degrade within hours to weeks in the environment (U. 1989). it was used in home sanitizers for surfaces.10) 2.389-.389-. 2002.EPA.750-2.800-3.630) < LOD .600-1. Fourth National Report on Human Exposure to Environmental Chemicals 43 .780) < LOD .20) < LOD 1.80-3. which may vary for some chemicals by year and by individual sample.50) < LOD .Fungicides ortho-Phenylphenol CAS No. and as a wood preservative.09) 2. 2006).S.14 (<LOD-3.386-.50) < LOD .466 (.EPA.930 (.742) * .880-2.600) < LOD 75th .490 (<LOD-.497 (. 2006). whereas SOPP is not volatile and is more water soluble.470 (<LOD-.570 (.30-7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.490 (<LOD-.836) * .450 (<LOD-.370-. population from the National Health and Nutrition Examination Survey. or 2-phenylphenol) and its water-soluble salt. Available evidence suggests that OPP does not accumulate in the body.80 (2.02) 1.00 (1.770 (.80) 1. leaving the chemical residue OPP.450 (<LOD-.23) 695 680 520 695 603 953 Limit of detection (LOD. sodium ortho-phenylphenate (SOPP). 2006).770 (. in paints.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .670) 2.3 and 0.85) 2.970 (.690) < LOD .890 (.636) * .50 (1. on ornamental plants and turfs.20 (1. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.570-.690-1. inhalational.60 (1.40-7.540-2.493 (.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 .710) 3.760-2.600) < LOD 1.40-5.20) < LOD 2. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.10) 1. OPP is still used as a disinfectant fungicide for industrial applications. but OPP and SOPP are still used on pears and citrus (U.00-2. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.850 (.10 (1.830 (.364-.624) * .610-1.508 (.390-.552 (.22) 2.60-3.28-3.

666) * .01) 1.453 (. 1999.S.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 .291-.61 (.96) 1.301-.33-2.96-4. 1993.670 (..17) 2..410 (<LOD-. Murata et al.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.32) 1.02 (.S.00 (.59) 1.52 (.S.61 (2.00 (1.06 (1.780-14.75 (1.EPA at: http:// www.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 . Pathak and Roy.656) * .44 (1. population from the National Health and Nutrition Examination Survey.74 (1.500) < LOD .329-.33) .353-.4) 3.311-.514 (.81) 1.690 (.570) < LOD 1.89 (1.05-2.43 (1.0) 1.550 (.28 (2..59) . 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..09 (1. reproductive.12) < LOD 1.810-1.40-13.670 (. CDC.S.96 (1.17 (.320 (<LOD-.07) 2.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .860 (. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Biomonitoring Information Urinary OPP levels reflect recent exposure.EPA 2006). Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. 2005). 1984.38-3.64 (2. OPP was not found to be mutagenic. leading to production of two metabolites.11-1.32) 3. or.580-1.473) * . Zhao et al.96 (1.51-3.09-6. interval) . 1984.29) 1. U.650-1.88-4.21 (.480-.31) < LOD .28 (<LOD-4.13) 1.361-.93 (1.58) 2. by possible genotoxic mechanisms (Hagiwara et al.06-4..980 (<LOD-1.27) < LOD .53) 1.62) .08) 1.11) 4.484) * .900) < LOD .420 (<LOD-. In high dose animal studies.780 (. IARC has classified SOPP as a possible human carcinogen.860 (.950) < LOD .06-5.26) 1.510 (<LOD-.43-2. 1992.86 (1. Bomhard et al.970) 1. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.93) .403-.810) < LOD .11) < LOD 90th 1.550-.EPA 2006).620-1. Ito et al.08-2.21-2. 2000.17 (.560) < LOD 75th .61 (1. 2002.600-1.38) 1.360 (<LOD-.610) < LOD 1.43-2.97 (2..91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.550) < LOD .24-2.580) < LOD . These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.910-1.S.25-6. 1998. Additional information is available from U.568) * . 44 Fourth National Report on Human Exposure to Environmental Chemicals .470) < LOD .880-1. Kwok et al.43) 3.04-4.78 (2.910 (.420 (<LOD-.750-2.750 (.800-1.382 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.750 (..343 (. Brusick. 2005.12-2.38) 2.75 (1. and it has classified OPP as not classifiable with respect to human carcinogenicity.620-1.455-.460-.508) * .47) .558) Selected percentiles ( 95% confidence interval) Sample 95th 2. less likely..560-2.640-1. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.470 (<LOD-. Survey Geometric mean (95% conf.670) < LOD .590) * . Volunteers exposed to 0. Detectable levels were seen in over half the U.385 (.496 (.08-1.270-.93) 1. 2002).29) 1.380 (. 1986). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. but no neurologic.900-1.980 (.940-2.248-. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.46) < LOD 1.440 (. Nakagawa et al.09-3. U. or developmental toxicity was observed (Bomhard et al.21) 1.24-2. 2005). 1997.840 (.910 (<LOD-1.990) < LOD .. 1999.18) 2.91 (1. Smith et al.93) .410 (<LOD-. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.epa.Fungicides anemia.84 (1. 2002.gov/pesticides/.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .444 (.770-2.20) < LOD 3.69 (1..791) * .11 (.510-.11 (.

Hagiwara A. IARC Sci Publ 1984. EPA-560/5-89-003. Xenobiotica 1998. The carcinogenicity of the biocide ortho-phenylphenol. Shirai T. et al. Stanley JS. Timchalk C. Office of Toxic Substances.17(8):411-417. National Toxicology Program (NTP). Carcinogenesis 1999.45(5):460-481.20(5):851-857. Christenson WR. Hakkert BC. Ito N. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). et al. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Tayama S. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Atlanta (GA). U. Environmental Protection Agency (U. Cnubben NH. Drugs. Environmental Protection Agency (U. Bartels MJ. Nakagawa Y. Selim S. Bromig KH. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol.nih. Bartels MJ. Imaida K. EPA). Fukushima S.28(6):579594. Environ Mol Mutagen 2005. Mendrala AL. Narang A. Murata M.S.150(2):402-413.EPA). Sangha G. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats.74(2):61-71.S.32(6):551-625. Gierthy J. Bormett GA. Eadon G. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Inoue S. Regul Toxicol Pharmacol 2002.pdf. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Shibata M. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Toxicol Appl Pharmacol 1999. Buchholz BA. 1989. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Moore GA. Christenson WR. Brzak KA. Ito N. Zhao S.S.50(11):3351-3358. Moriya K. van de Sandt JJ. Bartels MJ. 2005.54(16):5731-5735. Smith RA.niehs.159(1):18-24. Available at URL: http://www. Turteltaub KW. Kawanishi S. Toxicol Appl Pharmacol 1998. Herbold BA.epa. 2006. Third National Report on Human Exposure to Environmental Chemicals. Bartels MJ. rat and man. 4/9/09.gov/ntp/htdocs/LT_ rpts/tr301. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Crit Rev Toxicol 2002. St John MK. Roberts AL.Fungicides References Appel KE.22(10):809-814. Vogel JS. Cano M. Hirose M. Eastmond DA. J Chromatogr B Biomed Sci Appl 1997. Kwok ES. Comparative metabolism of orthophenylphenol in mouse. Freyberger A. Meuling WJ. Roy D.35(2 Pt 1):198-208. Pathak DN. EPA 739 R-06004. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. McNett DA. Coelhan M. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Mutat Res 1993.S.pdf. Hagiwara A.(56):399-407. Food Chem Toxicol 1984. J Agric Food Chem 2002. Fukushima S. 4/13/09 Onstot JD. U. Elliott GR.43(7):14311437. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Richter M.. Timchalk C. Brendler-Schwaab SY. 90-43-7) in Swiss CD-1 mice (dermal studies).286(2):309-319. Identification of SARA compounds in adipose tissue. Arch Toxicol 2000. Bomhard EM. Glas K. Centers for Disease Control and Prevention (CDC). Available at URL: http://ntp. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. March 1986. Leser KH. Biochem Pharmacol 1992. Sangha GK.703(12):97-104. J Agric Food Chem 2006. July 28. Moldeus P. Brusick D. Hum Exp Toxicol 1998. Arnold LL.gov/oppsrrd1/REDs/ phenylphenol_red.

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

S. 2005). However. 2000. environmental levels) is available from U.EPA. Feng and Wratten. and hydroxymethyl ethyl aniline (U.. In animals. 1996)... People exposed to acetochlor will excrete acetochlor mercapturate in their urine. 2006).S. and neurologic movement abnormalities (U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. but it has produced testicular atrophy...epa. Estimated human intakes of acetochlor have been below recommended limits (U. EPA at: http://www. and has been detected in watersheds of agricultural lands (Battaglin et al. remains in soils for up to 3 months. 2005.EPA 2000.0 μg/L (Curwin et al. 1989. Fourth National Report on Human Exposure to Environmental Chemicals 47 . General population exposure to acetochlor may occur through diet or drinking water. 2006). NTP and IARC do not have ratings regarding human carcinogenicity.EPA. Hladik et al. Plants can degrade acetochlor to 2-ethyl-6-methylaniline. 2006). Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. which are often more prevalent in the environment.S. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Acetochlor is microbiologically degraded. nasal epithelia.. but other pathways occur. Jefferies et al.EPA. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8.S. 2000.S. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies. Additional information about external exposure (i.. and it is unlikely to be genotoxic at relevant doses (Ashby et al. mainly corn. U. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid. 2007). 2000. Acetochlor is not mutagenic.gov/ pesticides/. Davison et al.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al. Acetochlor is moderately toxic to fish and honey bees. this metabolite is not a marker of exposure to most plant metabolites or environmental degradates.. Acetochlor has low acute toxicity.Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure. a major pathway for acetochlor metabolism involves mercapturate conjugation. 1998). the latter which may account for some observed effects (Coleman et al. renal injury. CAS No. in some species and at doses above maximum tolerated doses.EPA considers acetochlor likely to be carcinogenic in humans. Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect. however.e. Urinary acetochlor mercapturate levels of 0. Kolpin et al. 2006). It is absorbed by plants and inhibits plant protein synthesis.. 2000). 2005). 1994.S.. animals have demonstrated tumors of the lung. including one that produces 2-methyl-6ethylaniline and its reactive metabolite. 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. and thyroid (U. 2-hydroxyethyl-6-methylaniline. 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.

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

11(4):353359. Bravo R. Wratten SJ. Furlong ET. Hsiao JJ. EPA 738-R-00-009. Hum Exp Toxicol 1996. Andrews HF. Green T. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Kier L. Hladik ML.S. Fourth National Report on Human Exposure to Environmental Chemicals 49 . EPA). Heederik D.EPA): http://pmep. Number 15. epa. Tinwell H. 1998. Reynolds SJ. Third National Report on Human Exposure to Environmental Chemicals. Hodgson E.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Olsson AO. Xenobiotica 1994. et al. Centers for Disease Control and Prevention (CDC). 5/30/06 U. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry.248(2-3):115-122. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Larsen GL. U. Dialkylquinonimines validated as in vivo metabolites of alachlor. Striley CA.cce. Kolpin DW. Barr DB. Coleman S.pdf. Deddens JA. Jefferies PR. Federal Register: January 24. Barr JR. Comparative metabolism and elimination of acetanilide compounds by rat.S. pages 3682-3690. Chem Res Toxicol 1998. Hein MJ.108(12):1151-1157. sulfonamide. acetochlor. Peter CJ.html. Sci Total Environ 2000. and metolachlor herbicides in rats.17(6):559-566. Alavanja MC. March 2006.248(2-3):123-133. Available at URL: http://www. Sci Total Environ 2000. Rose RL. Casida JE.24(10):1003-1012. imidazolinone.37(4):10881093. J Expo Anal Environ Epidemiol 2005.15(9):702-735. Acetochlor (Harness) Pesticide Petition Filing 1/00. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Environ Sci Technol 2005. Ward EM. and other herbicides in rivers.111(5):749-756.Herbicides References Ashby J. Feng PCC. Available at URL(non U. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Camann DE.cornell. Whyatt RM. 2005. Wilson AG. Environmental Protection Agency (U. Environmental Protection Agency (U. Volume 65. Quistad GB. Feil VJ. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Linderman R. Environ Health Perspect 2003. 5/30/06. Battaglin WA. Kinney PL. et al. Linhart SM.S.15(6):500-508. Atlanta (GA). 2000. Curwin BD. Sanderson WT. EPA).S. Environ Health Perspect 2000.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Barr DB. et al. Roberts AL. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. reservoirs and ground water in the Midwestern United States. J Agri Food Chem 1989.39(17):6561-6574. Thurman EM. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Occurrence of sulfonylurea.S. Hines CJ. Barr DB. Burkhardt MR. J Expo Sci Environ Epidemiol 2007. Davison KL. Lefevre PA.

U. 2003). ranged from 0. 1996. U.. Hill et al. 1996). mercapturate conjugates were predominant metabolites. mean values of urinary concentrations of alachlor metabolites. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure.. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. Feng and Wratten. (2003) showed that 2. 1998. WHO. 1998). whereas 60% of applicators had detectable amounts. 1999 and 2007. Hines et al. 1998). but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. 2005).EPA. Estimated human intakes have been below recommended limits (U.S.S.epa. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2000.1 to 1. formulators. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. In animals.EPA. Kolpin et al. Because it can be absorbed through skin. soybeans. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. 1996.1 mg/L at various collection times (Sanderson et al. 2005. In a study of applicators and workers exposed to alachlor. U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. about 20-25% of the U. Biomonitoring studies on levels of alachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of alachlor than are found in the general population. hemosiderosis.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. 1988.. WHO. 1995).EPA considers alachlor to be a probable human carcinogen at high doses. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. Since the late 1980s alachlor use has been declining.S. 1998). 50 Fourth National Report on Human Exposure to Environmental Chemicals .. 1998. USGS. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. In chronic animal testing.Herbicides Alachlor CAS No. Alachlor has low potential for acute toxicity. 1998. corn cropland was treated with alachlor. and field workers. alachlor has demonstrated hepatotoxicity. 1994.. 2000. It is absorbed by plants and inhibits plant protein synthesis.. but shows little bioaccumulation. U. In 1993-1995. 1997. IPCS. and uveal degeneration. but not likely at low doses. 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.EPA. 1989. Alachlor has a soil half-life of a few weeks.. peanuts and other crops.S. the latter may account for some observed effects (Davison et al. EPA at: http://www. including corn. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. but another metabolic pathway can produce 2. as measured through conversion to deethylamine. stomach. 2003).gov/pesticides/. 1995. 2003). It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. NTP and IARC do not have ratings regarding human carcinogenicity.EPA. 1999..S. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. but has not shown developmental or reproductive toxicity in mammalian systems (U. Tessier and Clark. Additional information about is available from U.EPA.S. WHO. WHO. the dermal exposure route is potentially significant for applicators.S.6-diethylaniline and its reactive metabolite.. Alachlor itself is not considered mutagenic. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. and on non-crop land for general weed control. Hladik et al.S. Jefferies et al. 2003). 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.. In animal studies.

population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey. Urinary Alachlor mercapturate (creatinine corrected) Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 99-00 is 1.18. Fourth National Report on Human Exposure to Environmental Chemicals 51 . < 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 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Herbicides Urinary Alachlor mercapturate Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. 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.S.

Third National Report on Human Exposure to Environmental Chemicals. Environmental Protection Agency (U. Tolos W.39(17):6561-6574. 4/2/09 U. Clark JM.pdf. Life Sci 1988. Xenobiotica 1994.gov/oppsrrd1/ REDs/0063. EPA). 86. Environ Health Perspect 2003. No.inchem. Linhart SM.usgs. Furlong ET. March 2006. Larsen GL. California. Whyatt RM. Camann DE.56(6):853-859. Sacramento. Environ Sci Technol 2005. 2/27/09 Jefferies PR.htm. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Background document for development of WHO Guidelines for Drinking-water Quality. Driskell WJ.44(18):1325. Martens MA.int/water_sanitation_health/dwq/chemicals/en/alachlor. Davison KL. 1999. Geological Survey (USGS). Kier LD. Geneva. Thurman EM. Deddens JA. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Kolpin DW. 1996. Hum Exp Toxicol. Available at URL: http://water. Occurrence of sulfonylurea. Gilliom RJ).43(25):2087-94. Barr DB. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Henningsen G.org/documents/pds/pds/pest86_e.24(10):1003-1012. December 1998.37(4):10881093. et al. Erratum in: Life Sci 1989. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.43(9):2504-2512. Atlanta (GA). Casida JE. Casida JE. U. Kimmel EC. Wratten SJ. Centers for Disease Control and Prevention (CDC). Finding minimal herbicide concentrations in ground water? Try looking for their degradates.pdf. 2003. 1999.Herbicides References Battaglin WA. ALACHLOR. Available at URL: http://www. et al. Peter CJ.18(6):363-391. Casida JE.248(2-3):115-122. and other herbicides in rivers. Burkhardt MR. Am Ind Hyg Assoc J 1995. Hill RH Jr.47(6):503-517. Sanderson WT. Available at URL: http:// www. Heydens WF. 2005. Supplemental Technical Information (available on-line only).S. Jefferies PR. J Ag Food Chem 1995.248(2-3):123-133. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. EPA 738R-98-020. Geological Survey (USGS). Striley CA. imidazolinone. Quistad GB.11(4):353359. Kolpin DW. Biagini R. Hsiao JJ. Thelin GP. Alachlor in Drinking-water. reservoirs and ground water in the Midwestern United States. Comparative metabolism and elimination of acetanilide compounds by rat. Andrews HF. Reregistration Eligibility Decision (RED) Alachlor. Hladik ML. Brown MA. 1998. World Health Organization. Hill AB. acetochlor. Biagini RE. WHO/ FAO Data Sheets on Pesticides. Roberts AL. 1992-2001. J Agri Food Chem 1989.S.epa. Tessier DM. Bull Environ Contam Toxicol 1996. Barr JR. and metolachlor herbicides in rats. Chem Res Toxicol 1998.111(5):749-756. Sci Total Environ 2000. Shoemaker DA. Hines CJ. World Health Organization (WHO). Identification of a major human urinary metabolite of alachlor by LC-MS/MS.S.395(2-3):159-171.php. 2/27/09 U. Shealy DB.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Wilson AG. Brown KK. International Programme on Chemical Safety (IPCS). Dialkylquinonimines validated as in vivo metabolites of alachlor. Circular 1291. Feng PCC. revised February 15. DNA adduct formation by alachlor metabolites. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. MacKenzie B. Quistad GB. Hull RD. Thake DC. 98-4245 (by Barbash JE.S. Mutat Res. Hines CJ.56(9):883-889. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Kinney PL. 1997. An evaluation of the carcinogenic potential of the herbicide alachlor to man. sulfonamide. Sci Total Environ 2000. 2007. Available at URL: http://www. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. who. Ann Occup Hyg 2003. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Lau H. Feil VJ.

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

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

demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Striley CA. Quandt SA. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Gammon DW. et al. Ferrell JM. et al. 2003. et al. J Toxicol Environ Health 1994. Lioy PJ. Sanderson WT. Fleenor-Heyser DG. Breckenridge CB. Chen H. Goldman JM. Ferrell JM. 1993). The geometric mean of urinary atrazine mercapturate was 1. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Gillis JH.109(6):583-590. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Barbieri F.htm. Barr DB. 82. Jones AD. Blewett C. 3/11/09 Arcury TA. et al.atsdr. Toxicol Sci 2003. In a study of 60 farm worker children. Heederik D. Lee M.gov/toxprofiles/tp153. Simpkins JW. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. et al. Clayton CA. 2005). International Programme on Chemical Safety (IPCS). Tapia J. Bersani M. Third National Report on Human Exposure to Environmental Chemicals.61(4):331-355. Bradway DE. levels of atrazine mercapturate were generally not detectable (CDC. Stoker TE. Available at URL: http:// www. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Toxicol Sci 2000. Saiz SG. Atlanta (GA). Reynolds SJ.. Carr WC Jr. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Catenacci G. Biological monitoring of human exposure to atrazine. Barr DB. Curwin BD. Available at URL: http://www. 3/11/09 Laws SC.76(1):190-200. In small studies of Maryland residents in 19951996 (MacIntosh et al. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure.inchem. Schmid J.15(6):500-508. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Environ Health Perspect 2007. Hein MJ. Hines CJ. Eldridge JC. McElroy WK. 1996. Stevens JT. Hermaphroditic. Eberly LE.43(2):155-167.64(9):672-678. Proc Natl Acad Sci USA 2002. Mendoza M. Perry et al. Laws SC. Vonk A. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Barr DB. 2000). Toxicol Sci 2000.69(2):217-222. Freeman NC.47(6):503-517. Biagini RE. Brown KK. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.org/documents/pds/pds/pest82_e.cdc. Steroids 1999. Extrom PC. Tyrey L.. Maroni M.99(8):5476-5480. Environ Health Perspect 2001. diamino-S-chlorotriazine and hydroxyatrazine.. Grzywacz JG. 2007). Geneva. Ann Occup Hyg 2003. Goodrow MH.53(2):297-307. References Adgate JL. J Expo Anal Environ Epidemiol 2005. Toxicological profile for atrazine. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In the NHANES 2001-2002 subsample.. Hayes TB. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Stoker TE. World Health Organization. Centers for Disease Control and Prevention (CDC). Cooper RL.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Toxicol Lett 1993. Stuart AA. Wetzel LT. Seiber JN. Pfeifer KF. J Toxicol Environ Health 1994. Noriega N. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Collins A. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.html. Aldous CN. Deddens JA. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. atrazine was detected in only four children (Arcury et al.. Ferioli A. et al. ATRAZINE. 2005. Moseman RF.115(8):1254-1260. Pest Manag Sci 2005. Cooper RL. WHO/ FAO Data Sheets on Pesticides.. Sanborn JR.43(2):155-167.58(2):366-376. Eldridge JC. Cooper RL. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Lucas AD. 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. Agency for Toxic Substances and Disease Registry (ATSDR). Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . A risk assessment of atrazine use in California: human health and ecological aspects. 2001 [online]. Shoemaker DA. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). 2005). Wetzel LT. Gillis JH.. Stoker TE. No. Cottica D. 2001). J Agric Food Chem 1982.30(2):244-247. In a small number of field workers.

U. Langvardt PW. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Dryzga MD. J Expo Anal Environ Epidemiol 1999.182(1):44-54. Ann Epidemiol 2000. Toxicol Appl Pharmacol 2004. Christiani D. Lansbergen GW. Ryan PB. Cooper RL.S. Osborne DW. EPA). 0062.S.pdf.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Geological Survey (USGS). Environmental Fate and Effects Division. Boerma J. Cooper RL. Delzell E. Case No.gov/oppsrrd1/REDs/ atrazine_ired. MacIntosh DL. May 2003a.56(2):69-109. J Toxicol Environ Health A 1999. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Environmental Protection Agency (U.epa. Circular 1291. March 2006. Toxicology 1990. Sathiakumar N. 2007. Chem Res Toxicol 1993.pdf. Crit Rev Toxicol 1997. Office of Prevention. Stoker TE.usgs. Sanderson JT.S. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Wood C. Available at URL: http://www. Hammerstrom KA. EPA). Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. The Quality of Our Nation’s Waters.9(5):494-501.S. EPA Office of Pesticide Programs.epa.6(1):107-116. A longitudinal investigation of selected pesticide metabolites in urine. Tortorelli J. Toxicol Sci 2002. 3/11/09 U. Dagenhart D. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine.61(1):27-40. Singzoni B. Environmental Protection Agency (U. Interim Reregistration Eligibility Decision For Atrazine. Supplemental Technical Information (available on-line only). Washington (DC). Fenton SE. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Laws SC. Laws SC.10(7):479. 2003b. Toxicol Appl Pharmacol 2002. Wetzel L. Perry M. Pesticides and Toxic Substances. Kastl PE. Available at URL: http://water. Rayner JL. Breckenridge CB.58(1):50-59. White paper on potential developmental effects of atrazine on amphibians. van den Berg M. A review of epidemiologic studies of triazine herbicides and cancer.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.S.27(6):599612.php. Guidici DL.67(2):198-206. 6/1/09 U.195(1):23-34. Needham LL. Guidici DL. Toxicol Sci 2000. Pesticides in the Nation’s Streams and Ground Water. Timchalk C. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Available at URL: http://www. revised February 15. 1992-2001.Herbicides development of a biomarker of exposure. Stevens JT. Stoker TE. A risk characterization for atrazine: oncogenicity profile.

02-1. Kohli et al.S.210-.4-D were used in the U. Survey Geometric mean (95% conf.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.690 (. It was first registered with U. 2. 2004). population from the National Health and Nutrition Examination Survey.310) < LOD .05-2. abdominal pain. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.80) 1.330 (. and aquatic environments.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .890) < LOD .07 (.S.32 (1. 1974.690 (. < LOD means less than the limit of detection.810-1.27-2.560-. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.40) 1.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.03) 695 659 520 668 589 892 Limit of detection (LOD.4-D) controls broadleaf weeds in residential. 2005). by direct contact with agricultural and residential areas after applications.680-1.4-D has low acute toxicity.930-1. and by consuming food or drinking water contaminated with 2.EPA in 1948.690-1.20 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. hypotension. 2. Human health effects from 2.27 (1. but at higher levels they are herbicidal. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.43) 1.230 (<LOD-. these herbicides can enhance plant growth.. General population exposure to 2.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .740 (. Sauerhoff et al.70) 1.4-Dichlorophenoxyacetic Acid CAS No.230-. 4-D.410) < LOD .10 (<LOD-1.66) < LOD 1. 2.20 (<LOD-1.16) < LOD .48) < LOD 1.610 (.10) < LOD 1.60) 1. myotonia.2.730 (. It is rarely detected in ground waters (USGS. renal and hepatic injury. it acts as a plant growth hormone.Herbicides 2.910) 1. Similar to other chlorophenoxy herbicides.13) < LOD . and delayed Urinary 2.250 (<LOD-.08) < LOD .490 (.260 (<LOD-.960-1.690 (..560-1.EPA. 1989.4-D can be applied either as an aqueous salt or as oil-soluble esters.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 . the chlorophenoxy herbicide 2. in 2001 (U.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.952 and 0. It is not well absorbed through the skin. As much as 62 million pounds of 2.4-D may occur during residential applications.51 (1.420-. 2.660) 1.540-.00-2.27 (.610-.EPA.4-D have been below recommended intake limits (U. It is poorly bound in soils.4-D or exposed for prolonged periods.55 (1. 94-75-7 General Information Widely used throughout the United States. Once absorbed.420) < LOD . MCPA. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.930 (.30 (<LOD-2. 1977).21) 1. Fourth National Report on Human Exposure to Environmental Chemicals 57 .22) < LOD .670-1.10 (<LOD-1. At low levels.250 (<LOD-.440-1. with a half-life of several days to several weeks.890 (. and mecoprop). Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.760 (.320) 90th .400) < LOD .350) < LOD < LOD < LOD . headache.4-dichlorophenoxyacetic acid (2.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.910) < LOD .4-D is rapidly absorbed via oral and inhalation routes.24 (.490) < LOD < LOD < LOD .210 (<LOD-. agricultural.310 (. which may vary for some chemicals by year and by individual sample.370-. dizziness.550-1.S. Recent estimates of chronic intakes of 2. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. 2007).. nausea.

or to contaminants in the herbicide formulations (specifically 2. U. IPCS.08 (.640 (. 2004).380-.570) < LOD .780) .S. 1995. The acid and salt forms of 2.S.440 (. myotonia. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans..270 (<LOD-.270-. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.410) < LOD 1.390) < LOD < LOD < LOD . Pearce and McLean.670 (. 2005. 2002. IPCS.470) < LOD .780 (.13 (.920) < LOD 1. 2005. 1994). in small samples of children (Hill et al.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .EPA.27-1. 1996. eyes.S.790) < LOD . 2005).S. U.350 (<LOD-.410) < LOD < LOD < LOD .930-1.gov/pesticides/.56) .29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . Acute high doses administered to laboratory animals produced ataxia.520-. 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. Hill et al.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.590 (<LOD-1.14 (. population (Hill et al.39) < LOD 1. Survey Geometric mean (95% conf. 2002. IOM.13 (. It is unclear whether these associations are related to the chlorophenoxy herbicides.670 (.790) 1..610-.820-1. 2005.380 (<LOD-.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.08 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (. U.380 (<LOD-.810-1.680) < LOD .. Kutz et al. other exposures.7.S.16) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.810-1.380) < LOD .. 2005).08 (.epa.330-. U.4-D reflect recent exposure.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. Frank et al. 1996.EPA. Additional information is available from U.Herbicides neuropathy (Bradberry et al.EPA.4-D production plant workers and a few forestry workers spraying 2.560-.S.590 (<LOD-1. 2005).610-. In previous samples of the U. 2001.S.41 (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 .. and evidence of histological injury to the kidneys. 2000).4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. 2003.410 (<LOD-. 58 Fourth National Report on Human Exposure to Environmental Chemicals .35) < LOD ..740 (. developmental.490 (. urinary 2.17 (.480 (.73) .780-1.340-.980) < LOD 1.990-1..660) < LOD . 1989).. 2.580-.4-D are eye irritants. 1980.24) 1.550-. Kolmodin-Hedman and Erne.660 (. CDC.05) . adrenals and gonads (NTP.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .560-.340 (. or teratogenic effects in chronic rodent studies (Charles et al. 1995).32 (<LOD-2.EPA at: http://www.620-. 2005).EPA 2005).4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 1985. population from the National Health and Nutrition Examination Survey.19) . Post-application levels in farmers and home gardeners were dependent on Urinary 2. IPCS.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. 1992). 2. thyroid. 2005.670 (<LOD-1. 2.890) < LOD 1. Biomonitoring Information Urinary levels of 2.850) < LOD . Average post-application urinary levels of 2. 2006.720 (. Knopp et al.410) 90th . Epidemiological studies have reported associations of several types of cancer.4-D levels were detectable in less than a quarter of the individuals studied.4-D does not have significant reproductive. liver. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. 1996. and of adults and children (Baker et al.890-1..3..

other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.4-D and 2. Sirons G J. 2003.. 1992). Toxicol Sci 2001. Smith SJ.4-D will result in an adverse health effect. the number of acres to which it was applied (Curwin et al. Beasley VR.4-Dichlorophenoxyacetic Acid). Chapman P. Shealy DB. Pesticide residues in urine of adults living in the United States: reference range concentrations.27(1):23-38..4-dichlorophenoxyacetic acid in man. Harris et al. Reynolds SJ. Available at URL: http:// www. Arch Environ Contam Toxicol 1989. Cole DC.51(3):152-159. Crit Rev Toxicol 2002.60(1):121-131. Dichlorophenoxyacetic acid. Review of 2. Stephenson GR. Needham LL. Sanderson WT.Herbicides the time since application. Assessment of exposure to 2. Carter-Pokras OD.31(2):121-125. Pesticides residues in food: 1996 evaluations Part II Toxicology. Exposure of homeowners and bystanders to 2.4:97-100. Scand J Work Environ Health 2005. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.. Survival and Growth Curves from NTP Toxicity Studies. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. 2005). Khanna RN. Tandon JS. Murphy RS. 2006.71(2):99-108. Needham LL.4-dichlorophenoxyacetic acid (2. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Xenobiotica 1974. To T.4-D). Hill RH Jr.edu/catalog. Board on Health Promotion and Disease Prevention.4 dichlorophenoxyacetic acid (2. Frank R. Head SL.4-D than levels found in the general population. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. In farm families. Harris SA.4-D) epidemiology and toxicology.4-D. 2005). International Programme on Chemical Safety-INCHEM (IPCS).org/documents/jmpr/jmpmono/v96pr04. Holler JS. van Ravenzwaay B. TOX-63 Peroxisone Project (2. Kolmodin-Hedman B. Campbell RA. Brody D. Developmental toxicity studies in rats and rabbits on 2. J Toxicol Environ Health 1992. Beeson MD.4-dichlorophenoxyacetic acid (2. J Environ Sci Health B 1992. Acquavella JF. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Biomonitoring for farm families in the farm family exposure study. Selected pesticide residues and metabolites in urine from a survey of the U. National Toxicology Program (NTP). Honeycutt R. Gregg M. 2005 Charles JM. Ritter L.4-. Ripley BD. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . and the use of protective clothing or equipment (Arbuckle et al. 2005. Cook BT.nih. Gupta BN. Finding a measurable amount of 2.gov/index.nap.. Atlanta (GA).inchem. Wilson RD. et al. References Arbuckle TE. Occup Environ Med 1994. Estimation of occupational exposure to phenoxy acids (2. the amount of pesticide applied. Arch Toxicol Suppl 1980. Washington (DC): National Academies Press. Tables.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Centers for Disease Control and Prevention (CDC). TOX-63: TOXICITY REPORT CURVES.4:318-321. Veterans and Agent Orange: update 2002. Erne K. Bailey SL.4.10(6 Pt 2):789-798. general population. Barr DB. Mandel et al.4-dichlorophenoxyacetic acid and its forms. Biomonitoring of herbicides in Ontario farm applicators. Heederik D. Baker BA. J Expo Anal Environ Epidemiol 2000.15(6):500-508. Updated March 7. 3/17/09 Institute of Medicine (IOM).php?record_id=10603. Baker S. Hill RH Jr. Forestry workers involved in aerial application of 2.5-T). Fast DM.S.32(4):233-257. Kohli JD.18(4):469-474.31 Suppl 1:90-97. 3/17/09 Knopp D. Solomon KR. 2. Dhar MM. J Expo Anal Environ Epidemiol 2005 Nov. 914.4-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 2.31 Suppl 1:98-104. Curwin BD. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.4:427-435. Hein MJ. Barr DB. Sircar KP.4-D): exposure and urinary excretion.37(2):277-291. Alexander BH. Philbert MA. Available at URL: http:// www. Biomonitoring studies of 2.4-D were highest in the farmers who applied the 2.htm. Mandel JS. Third National Report on Human Exposure to Environmental Chemicals. Garabrant DH. Arch Environ Contam Toxicol 1985. Arnold EK.niehs. Environ Res 1995. Bus JS. Driskell WJ. Kutz FW. Hanley TR Jr. Baker SE. Scand J Work Environ Health 2005.4-D in urine does not mean that the level of the 2. Vet Hum Toxicol 1989. Available at URL: http://ntp. Absorption and excretion of 2. geometric mean urinary levels of 2. et al.

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

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

< LOD means less than the limit of detection.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.240) 679 701 957 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. see Data Analysis section) for Survey year 01-02 is 0.440 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.S. 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 . 62 Fourth National Report on Human Exposure to Environmental Chemicals .670 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2.200 (<LOD-.200 (<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. * 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.S. Survey Geometric mean (95% conf.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.

Feng PCC. streams and groundwater. Andrews HF. Jefferies PR.111(5):749-756.S.248(2-3):123-133. Quistad GB.html. Camann DE.47(6):503-517. Kinney PL. Supplemental Technical Information (available on-line only). California.gov/nawqa/pnsp/pubs/files/051507. Feil VJ. J Expo Anal Environ Epidemiol 2005. Environ Health Perspect 2003.pdf. Burkhardt MR. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Available at URL: http://water. et al. Gillion. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Atlanta (GA).41:3409-3414. Xenobiotica 1994. Thelin GP. Centers for Disease Control and Prevention (CDC).ESTfeature_gilliom. Wratten SJ. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.248(2-3):115-122.108(12):1151-1157.15(6):500-508. Comparative metabolism and elimination of acetanilide compounds by rat.epa.11(4):353359. and metolachlor herbicides in rats.39(17):6561-6574. imidazolinone. Ann Occup Hyg 2003. sulfonamide. Available at URL: http://water. Thurman EM. Peter CJ.pdf 3/30/09 Hines CJ. Hladik ML. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Ward EM. Roberts AL. 1998.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Davison KL. Linhart SM. Dialkylquinonimines validated as in vivo metabolites of alachlor.37(4):10881093.S. et al.usgs. R. Metolachlor in Drinkingwater. Available at URL: http://www. Gilliom RJ).usgs. Occurrence of sulfonylurea. Available at URL: http://water.int/water_sanitation_health/dwq/chemicals/ metolachlor. 2003.S. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . 1992-2001. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.Herbicides References Battaglin WA. Biagini RE. World Health Organization (WHO). J Agri Food Chem 1989. Barr DB. U.php. Hein MJ. and other herbicides in rivers. Casida JE. Striley CA. revised February 15. Environ Sci Technol 2007. Curwin BD.S. Linderman R. usgs. Sci Total Environ 2000. Reynolds SJ. 2005. Environ Sci Technol 2005. Barr DB. Environ Health Perspect 2000. reservoirs and ground water in the Midwestern United States. Chem Res Toxicol 1998. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. 98-4245 (by Barbash JE. Reregistration Eligibility Decision (RED) Metolachlor. Kolpin DW. Coleman S. Environmental Protection Agency (U. Circular 1291. Geological Survey (USGS). acetochlor.gov/oppsrrd1/ REDs/0001.gov/nawqa/ pnsp/pubs/wrir984245/text. Geological Survey (USGS). Larsen GL. 6/1/09 Whyatt RM. Hodgson E. Background document for development of WHO Guidelines for Drinking-water Quality. Sanderson WT. Kolpin DW. 2007. EPA). Rose RL. Barr JR. Brown KK. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Available at URL: http://www. Sacramento. Hsiao JJ. 3/26/09 U. Sci Total Environ 2000. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Pesticides in U. Shoemaker DA.pdf. Alavanja MC. Heederik D. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.24(10):1003-1012.S. Deddens JA. EPA 738R-95-006. Furlong ET.who. 4/2/09 U. April 1995. 1999. Third National Report on Human Exposure to Environmental Chemicals. March 2006.

see Data Analysis section) for Survey years 99-00 and 01-02 are 1. but higher levels are herbicidal. The half-life of 2. dizziness. Omer.5-T (Holson et al..5T is rapidly absorbed via oral and inhalation routes. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.5-T. with an elimination half-life of approximately 19 hours (Arnold et al. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.g. 2.4.5-Trichlorophenoxyacetic Acid CAS No.5-trichlorophenol and other degradates.3.5-T degrades to 2. abdominal pain. renal and hepatic injury.5-T and 2. hypotension. and delayed neuropathy (Bradberry et al. 1992.4.4. 2. ranging from several weeks to many months.2 and 0.4.4-D were used as defoliants in the Vietnam War (e.4. Survey Geometric mean (95% conf.. 1974). and concern about contamination with 2. Although 2.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.4. Kohli et al. these herbicides can enhance plant growth. 2007).4. 2.4. nausea. which may vary for some chemicals by year and by individual sample. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Mohammad and St. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2..7.S.5-T has been rarely detected in ground waters (USGS. 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.4. the general population is unlikely to be exposed to it.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Ester forms of 2.4.4. myotonia.1.. headache. Epidemiological studies have reported associations of several types of cancer.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. it is not well absorbed through the skin. 93-76-5 General Information 2. 64 Fourth National Report on Human Exposure to Environmental Chemicals . Human health effects from 2. 1989.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. Nelson et al. 1986. population from the National Health and Nutrition Examination Survey.5-T use as a herbicide in 1985.4. < LOD means less than the limit of detection. At low levels. 2004).Herbicides 2. 2.5-T is eliminated mostly unchanged in the urine.4. 1992).5-T in soil varies with conditions. Agent Orange).4. Given the commercial unavailability of 2.. Chlorophenoxy herbicides act as plant growth hormones. Once absorbed into the body.5-Trichlorophenoxyacetic acid (2..4.5-T was once applied as either an aqueous salt or as an oil-soluble ester.

2005).S.4. 2002.epa. urinary levels of 2.5-T were generally below the limit of detection. Pearce and McLean. similar to results of NHANES II (19761980). population from the National Health and Nutrition Examination Survey.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5-T does not mean that the level will result in an adverse health effect. 2003.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2.4. It is unclear whether these associations are related to the chlorophenoxy herbicides. in which urinary levels of 2.4. 2005. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.gov/pesticides/. IPCS. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. Biomonitoring Information Urinary levels of 2.5-T than levels found in the general population. 1996. Mean urinary levels of 2. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Additional information is available from U. 1980). Finding a measurable amount of 2. IOM.3. Urinary 2.EPA.5-T also were below the limit of detection (Kutz et al.5-T itself is not mutagenic.4. U.5-T reflect recent exposure.4.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. other exposures.Herbicides or contaminated herbicides. Biomonitoring studies on 2. Fourth National Report on Human Exposure to Environmental Chemicals 65 ..4. 2004).7. or to contaminants in the herbicide formulations (specifically 2. Survey Geometric mean (95% conf.4. 1992).S.S.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.EPA at: http://www.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. 2.4. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

Wolff GL. Fundam Appl Toxicol 1992. Pearce N.32(4):233-257.edu/catalog. Bradberry SM.S. Mohammad FK. 2. Nelson CJ.pdf.31 Suppl 1:1825.htm. Arch Int Pharmacodyn Ther 1974. Review of 2.S. Developmental toxicity of 2. May. 3/17/09 Kohli JD.5-T).nap.org/documents/jmpr/jmpmono/v96pr04.4-dichlorophenoxyacetic acid (2. Washington (DC): National Academies Press.EPA. Estimation of occupational exposure to phenoxy acids (2. Gaines TB. St Omer VE. Khanna RN. Vet Hum Toxicol 1989.4. Centers for Disease Control and Prevention (CDC). The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Garabrant DH. Pesticides residues in food: 1996 evaluations Part II Toxicology.epa.5-T).S. Board on Health Promotion and Disease Prevention. Neurobehav Toxicol Teratol 1986. II. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Gaines TB. Selected pesticide residues and metabolites in urine from a survey of the U. Philbert MA. Available at URL: http://www.19(2):286-297.4.inchem. Available at URL: http:// www. Holson JF. Proudfoot AT.5-T). Poisoning due to chlorophenoxy herbicides. Gaylor DW.4-. LaBorde JB. Available at URL: http:// www.4. Environmental Protection Agency (U. et al. 2004. 2005. Dhar MM.4. I. Scand J Work Environ Health 2005. Sheehan DM. S.4. et al. Developmental toxicity of 2. Absorption and excretion of 2. 210:250-255. general population.4.4-D) epidemiology and toxicology.EPA). Behavioral and developmental effects in rats following in utero exposure to 2.37(2):277-91. Veterans and Agent Orange: update 2002.5-T in four-way outcross mice. Carter-Pokras OD.2000 and 2001 market estimates. Brody D.5-trichlorophenoxy acetic acid in man. Washington (DC): U. Cook BT.5-trichlorophenoxyacetic acid (2.4-D and 2. Crit Rev Toxicol 2002. 2003. Kolmodin-Hedman B. Pesticide industry sales and usage . Fundam Appl Toxicol 1992. Holson JF. Sircar KP. Nelson CJ. Kutz FW. Tandon JS. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Agricultural exposures and non-Hodgkin’s lymphoma. Vale JA. Murphy RS. International Programme on Chemical Safety-INCHEM (IPCS). McCallum WF. McLean D. U. gov/oppbead1/pestsales/01pestsales/market_estimates2001. discussion 5-7. Office of Prevention Pesticides and Toxic Substances. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4. Atlanta (GA). 3/17/09 Institute of Medicine (IOM).4:318-21.Herbicides References Arnold EK.5-trichlorophenoxyacetic acid (2.31(2):121-125. Third National Report on Human Exposure to Environmental Chemicals. Dichlorophenoxyacetic acid.4-D/2.5-t mixture.8(5):551-60. Gupta BN. Beasley VR.php?record_id=10603. 914. LaBorde JB. Erne K. Toxicol Rev 2004. Multireplicated dose-response studies with technical and analytical grades of 2.4. Arch Toxicol Suppl 1980. J Toxicol Environ Health 1992.23(2):65-73.19(2):298-306.

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

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

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

which may vary for some chemicals by year and by individual sample.100 (.101) .7) 15.120 (. population from the National Health and Nutrition Examination Survey.5-17.1-19.9-38.147) 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 .4 (12. 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 9.4) 20.103 (.5) 21.4) 21.112-.110-.6 (15.1-24.9 (12.130) .2) 15.9 (13.0) 19.062 (.109 (.9-23.158) .182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .1 (13.5-17.1-16.084-.058) < LOD .170) .90) 90th 15.064 (.5) 19.124) .10 (<LOD-16.102 (.0 (15.110) .160 (.089 (.070-.190) .4) 14.110 (.6-24.139 (.109-.086-.3 (18.30 (8.60-10.100) .150 (.5 and 7.242) .7-19.077-.5-15.80 (<LOD-10.4) 539 456 484 487 980 885 Limits of detection (LOD.054-.113 (.064) 90th .069) < LOD < LOD .053 (<LOD-.0 (11.120 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 15.130) .130-.8) 14.7 (15.1) 14.8 (9.056-.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD . Survey years 01-02 03-04 Geometric mean (95% conf. Survey years 01-02 03-04 Geometric mean (95% conf.3-21.090-.7 (<LOD-15.6-33.0) 21.1) 13.5) 15.8 (18.50 (8.075) < LOD .6 (15.70 (7.3 (14.8.130) .080) .8-25.130-.062 (.120-. Fourth National Report on Human Exposure to Environmental Chemicals 79 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3 (18.110 (. 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 .5 (16.9 (13.100-.080 (.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.50) 15.090-.0 (10.088-.096-.40-9.1 (18.070) .059 (. see Data Analysis section) for survey years 01-02 and 03-04 are 10.140) .8-17.7-22.120 (.8 (11.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.100-.130 (.7 (14.4 (12.4) 19.117) < LOD .116) .2) 14.1-18. < LOD means less than the limit of detection.054-.138 (.4-18.120) .0-21.40-10.055 (.138) .1) < LOD 9.8-24.080-.9 (14.00-14.9-22.130-.090 (. 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.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.100) .6) 19.090 (<LOD-.8) 15.1) 20.090-.6 (14.112) 95th .8-19.2) 12.149) .093) .180) .077 (.4) < LOD < LOD 16.180) .80-10.140-.0) < LOD 9.3 (19.0 (10.S.S.109-.110) .048 (<LOD-.108-.070 (<LOD-.049-.8-17.2) 11.2-15.083-.00 (8.9 (12.098 (.150 (.1) 10.054-.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 8.160) .2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.062-.6) 16.160 (.139 (.190) .3 (13.0-25. which may vary for some chemicals by year and by individual sample.30 (8.4-17.110 (.060) .100-.140 (.6) 9.103 (.147 (.063-. population from the National Health and Nutrition Examination Survey.4) 95th 20.8) < LOD 8.80-9.6-24.1) 15.5 (<LOD-11.073-.

Jr and Laws ER. 1992-2001. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Vol.gov/ circ/2005/1291/. either singly or in combination. Ellis H. 15. Food and Drug Administration (FDA).54:1431-1443. Int Arch Occup Environ Health 1994. Serrano FO. McIntosh LJ. References Agency for Toxic Substances and Disease Registry (ATSDR).cfsan. Six high-priority organochlorine pesticides. Buckland SJ. J Toxicol Environ Health. Chemosphere 2004. toxicology.66(4):229-234. Soto AM. et al. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Toxicological profile for aldrin/dieldrin [online]. Patterson DG Jr. Facca A. Daniel SE. 6/1/09 Ward EM. Tully DB. International Programme on Chemical Safety (IPCS). Corrigan FM. Fernandez MG. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Handbook of Pesticide Toxicology. bioaccumulation.109(Supp1):113-139. Available at URL: http://www. 2007 [online]. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Wienburg CL. 4/21/09 Hoyer AP. PA. and lymphocyte sister chromatid exchange. 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. Sanchez-Ramos J. New York. Finley B. Edwards JW.91(1):122-126. Sonnenschein C. 4/21/09 Jorgenson JL.352:1816-1820. Stehr-Green. Patterson DG Jr.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994).27:405-421.cdc.14:95-102.usgs. Kanthasamy AG. Revised Feb. Chung KL. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Mumtaz MM. Grandjean P. 731-915. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Grajewski B. Psychopharmacology (Berl) 1987. Needham LL. 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. David VL.103(Suppl 7):113-122. Part A 2000. Chlorinated Hydrocarbon Insecticides. Environmental Health Criteria 91.47:1059-1087.64-65 Spec. Basit A. Smith AG. Jr. Cox. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Kanthasamy A. Schulte P. Teta MJ. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Li AA. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Roy ML. Cancer Epidemiol Biomarkers Prev 2000. 1989. Shore RF. plasma dieldrin. Hartvig HB. Available at URL: http://www. Available at URL: http://pubs.9:1357-1367. Mink PJ. United States Geological Survey (USGS). Mann D. In Hayes WJ. Toxicol Lett 1992.59:229-234. Jorgensen T. Song S.html. Pesticides in the Nation’s Stream and Ground Water. Carlson JN. Garrett N. Eds. Neurotoxicol 2005.html. Academic Press. Anantharam V. J Toxicol Environ Health 1989. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Exp Neurol 1998.26:701-719.150:263-271. Environ Health Perspect 2001. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Lancet 1998.org/documents/ehc/ ehc/ehc91. are nonestrogenic in transfected HeLa cells. Environ Health Perspect 1995.htm. Priestly BG. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. September 2002. Turner W. 4/21/09 Bates MN. Chapin RE. et al. Narahashi T. Rosellini RA. Inc. and epidemiology in the United States. Demographic and seasonal influences on human serum pesticide residue levels. Kitzazwa M. Olea N.inchem. Reprod Toxicol 2000. Brock JW. J Occup Environ Med 2005. 1991. August 2008.atsdr. VT. Andersen A. Aldrin and Dieldrin [online]. Ginsburg KS.gov/~dms/ pesrpts. No:429-436. 2 Classes of Pesticides. Available at URL: http://www. Frey JM.gov/toxprofiles/ tp1. pp.fda. Organochlorine exposure and risk of breast cancer.

9 (36.7) 19. see Data Analysis section) for Survey years 99-00. 01-02.10 (8.2) 37.6-24.3 (11.1-50.8-73.7 (10. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.2 (36.20 (<LOD-11.0) 27. and 03-04 are 14.8-20.5) 9.4) 18.4 (30.5) 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 * * * * 11.9 (18.2) < LOD 11. respectively.5-13.8-61.8-42.7) 35.0) 37. < LOD means less than the limit of detection.5-43.37 (8.3-24.2-28.2-56.2) 34.7 (17.3 (28.7-14.3 (<LOD-19.2 (28.5-32.4-40.8-32.3) 37.8 (18.6 (25.2) 22.1) 30.7-56.5-41.3) 18.9 (26.10-11.7-25.82-11.1 (16.9) 37.4) 29.2 (41.6 (16.2 (21.8 (17.70 (<LOD-10.0 (26.0) 20.9) 36.3) 10. 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.3-45.6) 48.6) 49.9 (21. population from the National Health and Nutrition Examination Survey.4-45.1 (44. 57-74-9 Heptachlor CAS No.9) 13.1-25.9 (29.4-14.7) 31.1) * 11.3 (9. Chlordane is not currently produced or used in the U.2 (37.2) < LOD 11.4 (<LOD-12. As a result of the manufacturing process.Organochlorine Pesticides Chlordane CAS No. and in soil.1-15.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.5-40.6-24. Until 1988.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.5) 56.6) 20.63 (8. the technical grade product of each chemical contains 10%-20% of the other chemical.8 (10.7 (34.9 (11.8) 52.2-21.2-49.10-18.9-21. Consequently.1 (20.3 (27.2-49.7 (<LOD-13.9 (15.8) 27.2-26.36-11.0-18.7) 9.4) 22.7 (42.2) * 12. and dairy products are the usual sources of exposure to these chemicals in the general population.0 (<LOD-12. lawns.7 (43.5 (34.S.6-12.3) 10.3) 41.1 (15.4 (30.6) 23.4 (22.8 (42.7 (<LOD-32.7) 28.8-23. 1994).1 (<LOD-12.4 (10.2) 36.8 (40.0-61.3 (25.1 (<LOD-12.5) 37.5 (31.4 (31. 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. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk. Since 1992.4-51.89-10.8.0) 75th 20.7) 19.6) 9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (9.5-42.4) < LOD < LOD < LOD 23.20-10.5) 38.2) 33.0 (16.9 (17.9 (15.1-19.20-11. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.30-11.8 (17.9 (31. 10.5-47.2 (39.9) 47.7 (34. from the early 1950’s until the mid-1980’s.74 (<LOD-10. Survey Geometric mean (95% conf.4) < LOD 11.1) 16.4-21.0-67. 2007).0 (32.9) 23.3 (20.9) 11.9) 39.1-51.1 (40.3) 18.9) 17.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.9) 10. Fourth National Report on Human Exposure to Environmental Chemicals 81 .0-12. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.7) 42.2 (10.3-49.1-65.9-40..S.69-10.1-25.1) < LOD < LOD < LOD < LOD < LOD 8.6) 9.90 (8.5 (41.6-18.5-65.1) 22.7-70.6 (43. which may vary for some chemicals by year and by individual sample.8) 52.7-12.5.6) 11.8-33.5 (8.0 (37.5 (<LOD-12.9) 11. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.9) 31.2 (9.6-53.9 (11.6 (9.7-39.1 (11.8) 18.0-13.3-45.6) 48.5. buildings.9-42.5) 21.3-43.0 (20.0) 41.5) 44.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 1994.6-45.9-21.5) < LOD < LOD 9.6) 39.1) 30. chlordane was used to kill termites and other insects on agricultural crops.4) 37.2) 46. in addition to trace amounts of numerous other related compounds (ATSDR. 2007).0) 31.1 (27.1 (<LOD-12.9) 23.7 (19. heptachlor use has been limited to treatment of fire ants near power transformers.8) 44.8-33. and 7.0-25.7 (32.S.0) 21. foods high in fat such as meat.3 (26.0-33.4) 39.6) 36.5-44.3 (21.6) 8.8-43.9-38.5-38.9 (26.8 (10. 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. Technical grade chlordane had contained 7% trans-nonachlor.6) < LOD 11.1) * 11.4 (35.5) < LOD < LOD < LOD < LOD 13.1) 90th 34.8) 53.1 (25.5 (33. fish.3-32.1 (17.8-31.4) 12.

119 (.340) .170) .290 (.240) .047 (<LOD-.250 (. and inhalation exposure.227) < LOD .090) .430) .130-.290) .510) .207 (.090-.280-. 1981). 1996.320) .050 (<LOD-.300) .148) .080) .130 (.160 (.140 (.204 (.070 (<LOD-.108-.330 (.213) * .189 (.240 (.170) .320 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.130) ..230 (. Takahashi et al.260-.370 (.090) .120-.225 (.242-.073) < LOD < LOD < LOD < LOD . 2007).126 (.146) < LOD < LOD .400) .245-. 1991).250 (.100 (.203-. In laboratory animal studies.300 (.130-.230 (.150 (.310) .260 (.231) .083 (.190-.100-.310) .077) .210 (. Survey Geometric mean (95% conf.230-.075 (. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.350) .070) .056 (.410) .066 (.110 (<LOD-. and alterations in immune function of offspring.310) .269 (.380) . Le Marchand et al.199-.130-..208 (.286 (.070-.450) .450) .130 (. The U.092) .320 (.140 (.048-.280-.126) .190-.104-.080) .070 (.370 (.190-.130 (.280 (.260 (. which is also persistent in the body (ATSDR.240-.049 (<LOD-.280) .302) .320) .071 (.057-.063-. 82 Fourth National Report on Human Exposure to Environmental Chemicals . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP. 2007.290-.189-.074-.063 (. Rogan.062) < LOD .370 (.440) .057 (. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.104) .230-.061-.348) .320 (.140 (.080 (.210 (.290) .077) ..300-.128 (.287) .058-.148-.223) .200 (.130-.130-.080 (.250-.068) 75th .271 (.258 (.310-.067 (. and heptachlor epoxide in foods and bottled water.140) . Acute.170-.350 (.063) * .053-.180-. chronic doses of heptachlor have produced liver enlargement and injury. dermal. and the U.150) .066 (<LOD-. 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.300) .350 (. heptachlor.230-.160) .150 (. population from the National Health and Nutrition Examination Survey. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.112 (.055-.106-.260 (.373) . EPA has established environmental criteria for chlordane and heptachlor. characterized by seizures and paralysis.083) .063) .331) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .070 (<LOD-.068-.053-.057) * .063 (.S.091) .133) 90th .120 (. 1977b.058 (.210-.253-.216-.149 (.115 (.180) .150-.130) .082 (. and breast milk is a major excretion route in lactating women.Organochlorine Pesticides (Dallaire et al.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .070 (<LOD-.300) . IARC. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al. The major metabolite of heptachlor is heptachlor epoxide..064) < LOD .170) . Chlordane is metabolized primarily to oxychlordane and to a lesser extent. Shindell and Ulrich.200-.270 (. Chlordane and heptachlor are absorbed after oral. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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.300) . 2006).220 (. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.280-.430) .286 (. to heptachlor.200-.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .058-.070-.310 (.068) .115-.170) .160) .066-.146) .200-. Smith.140-.220-. Elimination of all these chemicals from the body occurs over months to years. FDA established allowable residues of chlordane.120-.079) < LOD < LOD < LOD .077) . 1986).077) .060 (<LOD-.136) .315 (.050-.170) .560) .063 (.150 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.165-. neonatal mortality.S. 1977a.270 (.069 (<LOD-.246-. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.168-.100 (<LOD-.280 (. 2001.063 (.160) .120-. 1986).066-.320 (.140-.400) .240-.258-.360) .087-.079) .270 (.140 (.080) .180-.220-.110-.076) < LOD .070) < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.290-.290-.070 (<LOD-.S. OSHA has established occupational exposure criteria.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .180) . 1991.207) .340) .100-.065-. 2002.073 (.070-.230) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .

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

population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.8) 15.10-13.6) 14.8) 20.3-18.2 (<LOD-62.0-17.8 (<LOD-23.2) 26.2 (18.0 (15.6 (12.8) 13.4) 21.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) 15. 10.2-27.7-19.2) 13.8 (18.0-17.9 (12.4 (11. Survey Geometric mean (95% conf.5 (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 8.2-17.7 (10.6 (13. 84 Fourth National Report on Human Exposure to Environmental Chemicals .7-18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 10.6) 13.6 (<LOD-27.0-19.9-23.50) < LOD < LOD < LOD 17.2-16.7 (16.6 (11.3) 16.8) 19.90 (<LOD-9. respectively.9-16.8 (18.0) 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.S.2 (<LOD-25.1-15.6 (16.4 (<LOD-54.1-29.9) 15.6 (8.8) 13.5 (<LOD-32.3) 18.6-17.0 (11.1) 13.3) 22.8) 14.3) 27.0) 13.5.9-25.3) 18.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.5) < LOD 14.4 (<LOD-19.8-24.1) 20.6) < LOD < LOD < LOD 27. < LOD means less than the limit of detection.8) 21.8) 14.0-54.0-16.8 (13.5 (11.3 (<LOD-25.5) 19.6 (16.7 (13.9-29.6.5 (18.5 (<LOD-21. which may vary for some chemicals by year and by individual sample. and 7.3) 23.8) 19.20 (<LOD-9.3) 18.7-25.8-46.8 (15.1 (16.8-24.9 (15.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.1) 23. and 03-04 are 14.6) 22.8-23.2) 20.1 (19.8-24.1-38.6-21.4 (11.8. 01-02.1-16.4) 18.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.4 (15. see Data Analysis section) for Survey years 99-00.8) 16.40) 15.8 (13.2 (<LOD-16.5 (10.9-29.2-27.6 (14.3 (13.

220) .069 (.135 (.108) .090-.130-.077-.090-. Fourth National Report on Human Exposure to Environmental Chemicals 85 .107-.055 (<LOD-.110 (.130) .200) .116) < LOD < LOD < LOD .113-.090-.180 (.133 (.070-.063) .200) .100 (.130-.190) .100 (.120) .110 (.077-.104) .S.120 (<LOD-.135 (.130-.170) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110-.100 (<LOD-.101 (.161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .140) .120 (.094 (. Survey Geometric mean (95% conf.200 (.170 (.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 .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 .180) . population from the National Health and Nutrition Examination Survey.053-.180) .240) .120) .100-.090 (<LOD-.098 (.096 (.140) .120-.150 (.130 (<LOD-.190) .157) .074-.110-.190) .090-.097) < LOD .180 (<LOD-.310) .106-.270) .190 (.120 (<LOD-.173) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .071-.150 (<LOD-.063) < LOD < LOD < LOD .380) .110 (<LOD-.149) .090-.110) .170) .128 (.130 (.150 (.126 (.310) .100 (.090 (.108-.100-.130-.180) .067-.090-.087 (.170 (<LOD-.113) .100 (.117) .170) .170 (.076-.170 (.111-.094 (. which may vary for some chemicals by year and by individual sample.101 (.180) .110 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .057 (<LOD-.110) .140-.082-.111) .180) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.130) .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.

1 (47.5) 77.6 (12.7) 52.8) 47.0-37.9-69.3) 32.8 (26.2) 20.9-65.0-123) 74.1-22.7) 14.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.0) 49.5) 35.8-77. interval) 18.7-20.5-20.3 (49.4) 20.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.2) 39.5-19.0 (14.2-88.0 (48.2 (26.1) 17.7 (18.5 (15.5) 20.3 (56.6 (<LOD-14.1) 62.1 (41.4-23.0-23. see Data Analysis section) for Survey years 99-00.1) 16.5) 90th 55.8 (28.8 (28.6-54.3) 32.1-55.1) 17.2-17.4) 19.1 (65.3-57.4-36.2 (7.5) 78.2 (59.5) 19.8-16.1 (48.1-126) 67.9-20.8 (49.9 (47.9 (51.8-21.1 (17.1) 17.0-38.2 (60.7) 78.5-95.1) 17.0) < LOD < LOD 8.6-20.2 (27.7-77.2) 19.9-22.1-34.4-22.4 (30.86-13.3) 25.8.2 (64.7-113) 68.7 (16.0-24.8) 19. and 03-04 are 14.4-67.0) 75th 31.6 (57.3-50.9 (36.3-32.0-22.5 (25.5-17.5) 9.7) 73.9 (16.8 (30.3) 18.5) 30.0 (60.1) 17.4-62.5 (45.4 (12.8 (45.5) 36.7 (13.2 (14.1-20.7-32.8-90.6-22.2) 17.3-86.8 (71.3-30.1) 31. 01-02.0-23.8-90.6) 10.7) 15.7-29.6 (15.9) 14.9-40.6 (50.0) 40.7 (35.8-129) 74.2-21.9 (<LOD-14.8 (13.0-93.0-143) 112 (68.0 (13.8 (16.1-16.3-21.3 (58.3) 36.8 (11.3) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.7 (59.0 (42.0) 13.3) 19.9 (28.6) 54.7 (11.0-93.2) < LOD 10.9-45.6-88.6) 34.7) 78. < LOD means less than the limit of detection.7-35.9) 51.8 (26.1 (22.0) 19.9-64.4) 107 (84. population from the National Health and Nutrition Examination Survey.7 (74.1) 17.5 (13.0-20.8 (15.1) 78.5.0 (62.2 (36.9-35.0-59.3 (14.1) 78.1-28.9 (29.7-21.1) 18.4-35.8 (42.7 (28.0 (42. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3-39.6) 82.5) 26.6 (16.2-18.8-110) 59.7-17.6) 56.4) 55.70 (<LOD-12.10 (<LOD-11.4 (28.8-67.2-37.9) < LOD < LOD < LOD 20.0 (16.5 (44. and 7.8 (19.3) 30.3) 16.4 (45. 10.4) 16.3) 18.0 (13.7 (59.1) 32.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.1 (10.7-23.4 (67.3-74.4) 59.9-36.6) 25.9-65.9-58.2 (19.0 (15.6-66.6 (56.6 (32.6 (52.5) 22.S.1) 14.4 (16.9 (15.6-82.7 (30.1-18.0) 33.1-51.8-79.4-18.6) 60.9 (15.8 (26.5-87.9 (51.5-111) 68. Survey Geometric mean (95% conf.6) 56.7) 56. respectively.5-36.8 (<LOD-20.0 (16.3 (17.7-160) 86.8 (28.3 (16.8-16.2) 30.0 (19.9) 51.0 (29. 86 Fourth National Report on Human Exposure to Environmental Chemicals .9-89.7) 28.2 (14.5 (15.7) 35.8) 51.7-18.2-16.6) 13.9 (19.1) 18.5) 48.6-19.8) 80.6 (56.2) 34.3 (45.4-52.5) 14.4) 48.3 (14.5.5) 14.8 (17.8-41.2) 59.7-22.1-16.0-113) 68.0-68.1) 30.8-19.8 (12.8-19.7) 17.1-34.3-58.4 (11. which may vary for some chemicals by year and by individual sample.3) 30.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.0) 18.3) 15.2-18.9 (66.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.2-23.2 (15.5-69.2 (25.8 (13.7-34.6) 84.0 (15.7-38.9) 14.7) 59.1) 17.

093-.120) .122) .220 (.120-.590 (.090) .079-.651) .047-.397-.128 (.089 (.310) .069-.630) .250) .124) .130) .490 (.062 (.120-.116 (.130) .367) .20) .690) .110) .110 (.640 (.600 (.100 (.240) .093-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .360-.400-.190-.120-.210 (.317 (.098 (.470 (.190-.684) .095-.078-.400 (.242) .630) .160 (.210 (.370 (.110 (.113) .409-.180-.286-.202 (.160-.310-.134) .186 (.420 (.141) .210) .370 (.122) .330-.078 (.458 (.220 (.090-. interval) .099-.090-.573 (.330 (.126) .130) .210-.210) .420) .120 (.106 (.080-.150) .410-.220 (.090 (.272-.060) .390-.130) .173-.183 (.830) .260) .092 (.120 (.112 (.080) .130 (.116) .130) .300-.100-.220 (.540) .190-.110 (.310 (.240 (.070 (.280) .320-.096-.260) .158-. which may vary for some chemicals by year and by individual sample.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.170 (.080 (.120 (.565) .125) .580 (.191 (.145-.171-.340-.288 (.108) .210 (.390 (.390) .141) .300) .082) .279-.130) .461 (.120) .110 (.310-.430-.320-.090-.380 (.112 (.091-.087 (.111 (.186-.690) .470-.460-.106 (.390 (. Fourth National Report on Human Exposure to Environmental Chemicals 87 .580 (.211) 90th .270-.110-.099-.060-.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.480) .093-.470-.520 (.080-.220 (.103 (.510-.069) .460) .500) .180-.430-.285-.390 (.590 (.150) .119) < LOD < LOD < LOD .111-.180-.250) .140) .395) .071 (<LOD-.580 (.210) .190-.085-.096-.120) .350-.340-.130 (.130) .108) 75th .400 (.105 (.103 (.559) .091) .220) .054-.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 .119) Selected percentiles ( 95% confidence interval) Sample 95th .324 (.310-.490) .410-1.098 (.090-.090 (<LOD-.106 (.100 (.100-.092 (.680 (.343 (.109 (.960) .460) .090-.117) .232) .520) .327 (.125 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .680) .440-.205 (.113) < LOD .129) .400-.098-.630) .490-.131) .240) .350 (.109 (.590) .S.220 (.360-.520 (.490 (.371) .081-.470 (.210-.098) .330-.930) . population from the National Health and Nutrition Examination Survey.100-.220 (.104-.080-.161-.230 (.135 (.190-.340) .417 (.470 (.120) .093) .041 (<LOD-.301-.068-.084-.600) .234) .055 (<LOD-.760 (.060 (<LOD-.161) .390 (.510 (.085-.405) .390) .290-.250) .090-.355 (.080-.085-.190-.104 (.440) .450) .288-.237) .094 (.127) < LOD < LOD .414 (.116-.079-.177-.097) .497-.395-.240-.114) .110 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.550 (.430-.830) .565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .237) .100-.594) .081 (.220 (.800) .840) .108 (. Survey Geometric mean (95% conf.096) .110 (.240) .400) .061-.310-.

An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. 2001.8:1-123. 4/21/09 James RA.cdc. Jr and Laws ER. Barker J. Natl Cancer Inst Carcinog Tech Rep Ser 1977a.niehs.html. Siegel BZ. Bleiweiss IJ. May 1994. Handbook of Pesticide Toxicology.inchem. KalubaSkotarczak A. Wong L. LeMarchand L. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. International Agency for Research on Cancer (IARC). Keller JA. 731-915. Dendle WH. Toxicological profile for heptachlor and heptachlor epoxide [online]. Berkowitz GS. Hawaii Med J 1991. Mortality of workers employed in the manufacture of chlordane: an update. In Hayes WJ. Baker DB. 9/25/07 International Programme in Chemical Safety (IPCS).org/documents/iarc/ vol79/79-12. Chashchin V. Arch Environ Health. 1994-1997 organochlorine compounds. Bioassay of chlordane for possible carcinogenicity. Available at URL: http://www. Available at URL: http://www. Glynn AW.inchem. Available at URL: http://www.50(3):108-118.372:20-31. National Toxicology Program (NTP). 1986. JAMA 1988.atsdr.Summaries & Evaluations. Granath F.9:1-109.atsdr. Eds.nih. Circumpolar maternal blood contaminant survey. Bioassay of heptachlor for possible carcinogenicity.heptachlor. Dewailly E.84:151-161.cdc. Takei G. 4/21/09 Baker DB. et al.gov/ntp/ htdocs/LT_rpts/tr009. Distribution of polychlorinated biphenyls. Charles MJ. Wolff MS. Senie R.gov/toxprofiles/tp31. Available at URL: http://ntp. 4/21/09 Dallaire F. Canada). Willman E. Pollutants in breast milk. 1991 pp. Vol.gov/ntp/ htdocs/LT_rpts/tr008. Environ Health Perspect 2002. et al. Environ Health Perspect 2003. Available at URL: http://ntp. Toxicological profile for chlordane [online]. Arch Pediatr Adolesc Med 1996. Takahashi W. J Occup Med 1986. Poland. Available at URL: http://www. Shindell S and Ulrich S. Atuma S. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Voorspoels S. 1963-1967. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Chlorinated Hydrocarbon Insecticides. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum.niehs.110(8):835-838. Dewailly E. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Organochlorines in Swedish women: determinants of serum concentrations.html. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Sci Total Environ 2004. Inc. Head SL.pdf. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Environ Res 2000.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Smith AG. Organochlorine exposures and breast cancer risk in New York City women. Stehr-Green P. Kolonel LN. Tartter P. 1993. Gilman A. Laliberte C. Ayotte P. 2 Classes of Pesticides.150:981-990. Chlordane and heptachlor [online]. Bull Environ Contam Toxicol 1981:27:506-511.nih. et al. 1979-1980. Organochloride pesticide residues in human milk in Hawaii. Saidein D. Concise International Chemical Assessment Document 70 Heptachlor [online]. Bjerselius R. A Report to the Hawaii Heptachlor Research and Education Foundation. Odland JO.org/ documents/cicads/cicads/cicad70.259(3):374-377. Wohlleb JC.html.28:497501. Hertz-Picciotto I. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. International Agency for Research on Cancer (IARC) . Muckle G. New York.org/site/foundation/ research/projects2.110:617-624. Royce W.330:55-70. 6/1/09 Rogan WJ. Brower S. Available at URL: http://www. 6/1/09 National Toxicology Program (NTP). Van Oostdam JC. Hansen JC.htm. Sci Tot Environ 2006. Lawrence River (Quebec. August 2007. gov/toxprofiles/tp12. Lulek J. 2006. Darnerud PO. Environ Health Perspect 2002. Loo S. Academic Press. maternal serum and milk from Wielkopolska region. Jr. et al.111:349355.41:145–148. Vol. Jaraczewska K. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Drews K.pdf.htm. Aune M. 79. Covaci A.

10-13.0) 19.5-36.9) < LOD < LOD 9.4) < LOD 17.0-53.3 (27. 2008. or dermal exposure. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.3-16. sediments. 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. particularly for endemic vector and malaria control. o.0-35. It was produced and used in the U.3-590) 293 (104-541) 48.1 (23. population from the National Health and Nutrition Examination Survey. and dairy products.9) 17.6 (9. resulting in fetal exposure.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. DDT is converted to DDE and several other metabolites.1-71.9) 14.7.9-28. particularly meat. DDT can be absorbed after ingestion.0-27. including 1. < LOD means less than the limit of detection. 1991). which may vary for some chemicals by year and by individual sample.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. Fourth National Report on Human Exposure to Environmental Chemicals 89 . In the body.0 (10. In the general U.1’-dichloro-(2.4) < LOD < LOD < LOD 61.00 (<LOD-10. Survey Geometric mean (95% conf.3) 22.5-54.0-155) 83. DDT is converted in the environment to other more stable chemical forms.0) 20.5) 25.0 (18.5 (23. see Data Analysis section) for Survey years 99-00.1’-(2.7-16.7) 12.5) 23.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.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.2 (11. Both Serum p.2 (<LOD-40.1 (<LOD-39.6 (22.70 (8. Gunderson.7 (19. 1988). 01-02.0 (21.9 (21. food.1 (33.0) 26.S.0) 40.2-95. DDT was used at one time as a treatment for head and body lice. inhalation. 1991).3) 21.7) 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 10.5 (23.2) < LOD < LOD 9.8. 17.50-11.8-39. after World War II until 1972.p’-DDT (65%-80%). and 03-04 are 20.8-23. air.0-37.8-17.9-34.S. population.2) 30. continues to be the primary source of DDT exposure.2-65.0-15.6 (25. as well as in plant and animal tissues. and water.10 (<LOD-12. which is a mixture containing p.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.4. These chemicals are highly persistent in soil. and trace amounts of several related compounds.6 (<LOD-25.0 (18.8) 30.3-236) 24. depending on conditions. fish. Food imported from countries that still use DDT may contain the chemical or its residues.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5 (14. The biodegradation half-life of DDT in soil varies from 2 to 15 years. DDT and DDE can cross the placenta.7) < LOD 18.8-26. p.4 (23.5 (15.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.9 (10.2) 155 (59.90 (<LOD-12.5) < LOD < LOD 9. Only a small proportion of DDT is metabolized and excreted (Smith.1) 31.8) 799 1073 959 880 1232 1006 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.3 (<LOD-31.3) 21.1-27. Smith.9) 29. It is still used in some countries.6 (31. when virtually all use of it was banned. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-33. respectively.7 (15.2-bis(p-chlorophenyl) ethane (DDD).8) 15.9 (<LOD-20. DDT usually refers to the technical product. and 7.3) 28. 2002.p’-DDT (15%-21%).8) 36.9 (10.9 (10. although DDT and DDE intakes have decreased over time (FDA.p’-DDD (4% or less).3 (<LOD-21.

064 (. 2002. other organochlorines.128 (.180-. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.106-. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.140) ..120 (<LOD-.160-..146 (.. In high dose.240 (. polychlorinated biphenyls.150) . 1956). 2000. Jusko et al.. 1996). 2006)..048 (<LOD-.078 (.343) < LOD . Survey Geometric mean (95% conf. 2006. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.00 (. 2001).112 (. 1995. Jusko et al.290) .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 .079) < LOD < LOD . have not been consistently demonstrated (Beard.170 (. 2006).071-.230) .054-. 2002.086 (.065-. resulting in exposure to nursing infants (Rogan.132-.200 (.530 (.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .400 (. Gladen and Rogan.250-1.140-.180) .400) .330-4. lung cancer. dioxins and furans). although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.130 (<LOD-.080-.189-.068-. premature delivery. 2001). population from the National Health and Nutrition Examination Survey.. Mariussen and Fonnum. reproductive organ abnormalities.061) < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and seizures. overt signs of acute human toxicity include vomiting.g.146 (.260) .074-. Studies of DDT exposure and pancreatic cancer.150 (<LOD-.313 (. A workplace standard for DDT has been established by Serum p. 2004.105-. Reproductive effects in humans affecting birth weight. Animal studies reported reduced fertility. Beard. 2002. 2006.063 (<LOD-.p’-DDE can produce anti-androgenic effects (Gray et al.420) . Gray et al.220) . 2001).S.106) .051 (<LOD-. DDT may bind to estrogen receptors (Chen et al.130-.190 (. tremor.230) . Longnecker et al.075) 1.108 (.220) .071 (..114-.62 (.106) < LOD < LOD .570-4.. fertility.069) . and o. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Snedeker.34) . 1998). Hayes et al.170) .00) .059-.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 .150-.190-1.120-. 2002. accidental exposures.250 (.180) .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.170-.143) < LOD < LOD . Calle et al.26) 1. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.Organochlorine Pesticides chemicals are excreted in breast milk.130 (<LOD-.078-.142 (..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. 2006.190 (.150-..p’-DDD and p.180 (.201 (. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.084 (. 90 Fourth National Report on Human Exposure to Environmental Chemicals . In laboratory animals. and duration of lactation.627) . 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.240) .150 (<LOD-. which may vary for some chemicals by year and by individual sample. 1997).087 (.. and altered behavior after neonatal exposure (Eriksson and Talts. and leukemia have also been inconclusive (ADSDR. 2001).095) < LOD . 2006).530) .203) .180 (.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 .130 (<LOD-.01) .098-..

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 declined by about fivefold to tenfold. More information about external exposure (i.p’-DDT) as a possible human carcinogen. Link et al.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.e. In a population-based sample of men and women from eastern Slovakia.8.3. 2003. Stehr-Green. environmental levels) and health effects is available from the U.gov/ toxpro2. 2004). respectively..7-119) 113 (100-140) 93. Compared to females in the NHANES 1999-2000 subsample.6. 01-02. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. IARC classifies DDT (p. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. respectively..6 (81. 2005).. Declining DDE levels over time have also been observed in the German population. Fourth National Report on Human Exposure to Environmental Chemicals 91 .. 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.gov/ pestcides/ and from ATSDR at: http://www.. 2002. Smith. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. In general.atsdr. 2004). for males and females in the NHANES 19992000 subsample (Pavuk et al. and 7.p'-Dichlorodiphenyldichloroethene (DDE) (lipid adjusted) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. 2003).epa. 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.cdc.html.S. compared to levels observed in this Report (Anderson et al. 1991). 2002. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.S. 1989).. Heudorf et al. and 03-04 are 18..S. NTP considers DDT as being reasonably anticipated to be a human carcinogen.Organochlorine Pesticides OSHA and a guidance established by ACGIH. Survey Geometric mean (95% conf. mean serum levels of DDT and DDE in the U. 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.. population from the National Health and Nutrition Examination Survey. EPA at: http://www. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. 1998. 8. Since the 1970’s. see Data Analysis section) for Survey years 99-00. Biomonitoring Information DDE persists in the body longer than DDT.

00-1.963-1. 2001-2002 and 2003-2004 subsamples. o.18) 1.3) 16.35) 1.55-9.4-19.9 (26.66) 3.18 (6.4) 13.20 (.7 (8.34-11.24-17.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.0 (12.6 (7.39) 1.85 (1. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.25) 8.18-4.49 (6.52 (3.34 (7.91-2.6) 11.13) 4.5) 22. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.57 (3.57) 2.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.02) 1.0 (9.97 (3.66-2.623 (.00 (.75) 2.32 (1..69 (1.18-3.66-17.10) .63 (1.81 (1.6) 8.63 (1.26-2.59 (1.97-4.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.62-6.82) 1.36 (3. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.6) 9.69 (2.456 (.45 (1.796 (.88 (2.75 (8.03-1.04-1.31-12.2 (9.27-1..00) 7.31 (1.57-2.1) 7.21) 90th 7.09-1.18-1.57-3.25-16.6) 13.5) 16.53) 7..43-4.680-1.39-1.10-5.68 (2.59) 6.516 (.51 (1.71) 32.69 (.1 (9.646) .820-1.88-35.14-9.40-4.1 (8.40-4.51-15.76) 1. 2004).1) 12.p’-DDT.3-43.03-4.36-11.8 (13.19) 4.23 (7.49 (1.14-1.45 (1.3) 10.66) 1.63 (6.22-1.32-1.7) 16.34-3.52-6. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.30-1. serum levels of o.37-16.557) 1.51-8.39-2.64-2.6) 12.59 (1.22) .31-2.53 (2.90) 22.01-11.32) 1.726) .84 (3. 1989).04 (6.46-2.S.07 (5.2) 19.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.9-17.68) 2.59) 3. considerably higher than levels in this Report (Smith.85-10.80) 1.10) 2. 1991).60-13.26) 3.07) 1.51-49.635) 1.43-8.49) 8.7-20.54-7.81-18.07) 1.90-8.8) 15.15-4.48 (6.36) 3.54 (1.7) 9.p’-DDT (Stehr-Green.870 (.80) 1.37-10.06) 1.01) 1.01-5.77 (1.01-1.77 (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.96) 1.17-3.2) 26.32-9.Organochlorine Pesticides nearby agriculture (Botella et al.28) 1.p’-DDT were below the limits of detection.46 (1.14) 2.68-4.18-1.81) 11.51) 3.71 (6.27) 3.3) 13.14) 2.26-10.38 (1.6 (8.50-17.37-4.7) 13.4 (8.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.75) 1.72) 1.13 (1.30 (1.56-6.16-1.2-32.7-48.600) .65 (1.12 (.19-14.53-15.80 (2.11-1.41-12.8 (14.61 (1.385-.91-3.4) 14. 309 versus 268 ng/g lipid. 2004). 2005).54) 8.69) 8.29 (1.3 (8.3 (9.9 (15.4 (12.61-2.25 (1.890-1.8-90.2 (19.81 (7.36-1.47) 3.14 (1.71) 12.10-1.860 ng/L) and DDE (about 14.590 (.05) 1.5) 7.58) 1.56) 2.70-3. Serum p.32-1.25 (.71 (5.534-.40-8.994-2.63-15.34) 6.52 (1.611-1.1) 40.00 (6. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.25) 1.51) 1.7-19.81-5.46 (1.37 (1.2 (6. In a subsample of NHANES II (19761980) participants.76-3.05 (3. In the NHANES 1999-2000.488-.47 (1.02 (2.965-1.66) 4.730) .33-1.6) 9.40 (3.36-2.2 (9.80) 3.34) 2.5) 5.01-1. Survey Geometric mean (95% conf.6) 9.17 (3.12-1.6 (9.69) 4.43 (5.p’-DDT. 1971).57 (1.76) 1. population from the National Health and Nutrition Examination Survey.06) 3.65) 1.22 (7. Finding a measurable amount of p.30 (1.57-13.75 (4.83 (1. interval) 1.55 (2.561 (.66-4.57 (1.32 (1.56-3.5) 10.11 (2.0) 2. less than one percent had detectable serum levels of o.76 (2.91 (6.59 (4.9) 5.43-4.38 (1.99) 1.66) 1.25-14.39 (3.64) 3.24 (1.6) 9.96) .16 (2.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.01-15.4) 9.79) 4..01-11.92 (3.93 (7.30-1.85-4.500-.50 (2.70) 1.58) 75th 3.72) 1.6 (17.75) 6.26 (1.78 (4.87 (5. or p.37-1.9) 7.24) 1.9-38.430-.8 (13.0) 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 .58) 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 3.84-3.01) 1.21) 3.12 (6.92) 1.49 (1.48-4.44) 1.56-2.87-16.520 (.53) 1.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 . High mean levels of whole blood DDT (about 3.13-2.02-8.419-.41 (1.82 (1.92 (3.91) 3.8 (9.

and 03-04 are 20.4. 17.Organochlorine Pesticides Serum o. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and 7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8. see Data Analysis section) for Survey years 99-00. 01-02. respectively. which may vary for some chemicals by year and by individual sample.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.S. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.7. Fourth National Report on Human Exposure to Environmental Chemicals 93 .

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

Klebanoff MA.52:301-309. and other chemicals.1-dichloro2. Notides AC.58:1185-1201. et al. selected elements.fda. Hurd C. Food and Drug Administration (FDA). Granath F. Brock JW. and dichloro(diphenyl)ethylene (DDE).gov/ toxprofiles/tp35. Ellis H. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Chen CW. Lambright C.53(8):1161-1172. Klebanoff MA. Kulkarni PK. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). HCH. Saiyed HN. Int J Hyg Environ Health 2002. The effect of known repeated oral doses of chlorophenothane (DDT) in man. et al. Henley SJ.206:485-491. Longnecker MP. Exposure of women to organochlorine pesticides in Southern Spain. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Toxicological profile for DDT. Hayes WJ. Zhou H. Durham WF. Bloom MS. Fourth National Report on Human Exposure to Environmental Chemicals 95 . and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Atuma S. Moysich KB. 4/21/09 Gladen BC. et al. Gladen BC. August 2008. Patterson DG Jr.71(6):1200-1209. Available at URL: http://www. Burse VW. Swanson MK. Crespo J.358:110-114. Schulz C. hexachlorobenzene. Link B. April 1982 to 1984. Krause C.355:7889. Baker RJ. Epidemiology 2006. Ostby J. Organochlorines in Swedish women: determinants of serum concentrations. Rivas A. Rogan WJ. Olea N. CA Cancer J Clin 2002. Bull Environ Contam Toxicol 2004. Maternal DDT exposures in relation to fetal and 5-year growth.17(6):692-700. Botella B. Needham LL. Available at URL: http://www. Kashyap R. Calle EE. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. and HCB residues in human blood in Ahmedabad. et al. hypospadias. Effects of environmental antiandrogens on reproductive development in experimental animals. Furr J. Am J Public Health 1995.cfsan. Gray KA. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.106(5):279-289. Jr. Olea-Serrano MF. Sci Tot Environ 2006. Drexler H. Aune M. Environ Health Perspect 2004. Maternal serum level of 1. Cueto C. Vorojeikina DP. Bjerselius R. Falk C. et al. Beard J. and polythelia among male offspring. Eriksson P. Frumkin H. Katz SH. Piechotowski I. Longnecker MP. Chemosphere 2004. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. dietary intakes of pesticides.html.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Hanrahan L. Willman EJ. Lepom P.. Wolf CJ. Environ Res 2005. Chemosphere 2005. Angerer J. et al. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Environ Health Perspect 1998. Int J Hyg Environ Health 2003. India. dichlorodiphenyldichloroethylene. lindane (g-HCH). et al. Biomonitoring of persistent organochlorine pesticides. Needham LL. Parks L. Biochem Pharmacol 1997. Bates MN. Vena JE. DDT and human health.21(1-2)37-48. Gray LE Jr. 4/21/09 Anderson HA. Seiwert M. Olson JR.155(4):313-322. Charles MJ.111:349355. Gunderson EL. Zhou H. Hum Reprod Updat 2001. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Zoellner I. Arnold SF. et al. Cerrillo I. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Greenfield TA. Darnerud PO. Garrett N. Koepsell TD. Barr DB. Buckland SJ. Talts U. Heudorf U.162:890-897. Paepke O.96:34-40. Herrman T. JAMA 1956. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Davis MD.72:261265.cdc. Environ Health Perspect 2003. DDE and shortened duration of lactation in a northern Mexican town.205:297-308. Kaus S.54:1431-1443. Jr. Am J Epidemiol 2002. DDE. and DDD [online]. Hediger ML. The Great Lakes Consortium. Thun MJ.97(2):178192.7(3):248-264. September 2002. Savitz DA. J Assoc Off Anal Chem 1988. Lancet 2001.gov/~dms/ pesrpts. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Jusko TA. Needham LL. Organochlorines and breast cancer risk. FDA total diet study. et al. Levels of DDT. Olson J. Environ Res 2004. Becker K. Zaidi SS. Glynn AW.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism.html. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Neurotoxicol 2000. Brock JW.atsdr.112(17):1761-1767. Klebanoff MA. Gabrio T. Profiles of ortho-polychlorinated biphenyl congeners.85:504508. Bhatnagar VK.

and DDD in male rat liver and cultured rat hepatocytes. Environ Health Perspect 2001. Smith AG. PA.53:455-477. Chemosphere 2004. Stehr-Green. Radomski JL. Rey AA. 2 Classes of Pesticides. Vol. Toxicol Appl Pharmacol 1971. Pollutants in breast milk. Astolfi E. Rogan WJ. Thomas PE. et al.Organochlorine Pesticides Mariussen E. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Chlorinated Hydrocarbon Insecticides. DDE. Lubet R. Cerhan JR. Handbook of Pesticide Toxicology. 731-915. Deichmann WB. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Petrik J. In Hayes WJ. Academic Press. Crit Rev Toxicol 2006. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. DDE. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Jr. Inc. Fonnum F.109:35-47. Reddy AB. Pesticides and breast cancer risk: a review of DDT. Snedeker SM. Demographic and seasonal influences on human serum pesticide residue levels. J Toxicol Environ Health 1989. et al.54:1509-520. Nims R. Comparative pharmacodynamics of CYP2B induction by DDT.150:981-990.27:405-421.36:253-589. Fox S. J Toxicol Environ Health Part A 1998. Arch Pediatr Adolesc Med 1996. and dieldrin. Jones CR. children and newborn infants. 1991 pp. Pavuk M. Schecter A. Chovancova J. Jr and Laws ER. New York. Lynch CF. Eds.20(2):186-193.

inhalation or dermal exposure routes. Smith. 1992. 72-20-8 General Information Endrin.. 1991). have been cancelled by the U. is no longer manufactured in the U. Endrin does not accumulate in body tissues (IPCS. 1981).50) < LOD 5.S. At high doses. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. unless the dose is high and the exposure is very recent.10 (<LOD-5. a stereoisomer of dieldrin. Endrin was not widely used as a termiticide. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. 1992). Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.09 and 7. endrin has been detected with declining frequency in U.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.S. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. EPA. Hepatic effects of endrin exposure have included necrosis. An epidemic of acute endrin poisoning. Endrin has been detected in soils. total diet surveys (FDA.Organochlorine Pesticides Endrin CAS No. rodenticide and avicide. Because it is metabolized so rapidly. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.40 (<LOD-6. endrin usually is not detected in serum of exposed individuals.S. 2008). Depending on soil conditions.30 (<LOD-6. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al.. and occasionally at low levels in sediment and surface waters. Endrin is absorbed rapidly after ingestion.20 (<LOD-5.70) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5.8.S.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. 1979. or from contact with contaminated soils and sediments in areas where endrin was applied. 1996. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. 1992). population from the National Health and Nutrition Examination Survey. anti-12hydroxyendrin.30) < LOD 5. Kavlock et al. 1992).50) < LOD < LOD < LOD 5. Ketoendrin is a major photodegradation product (IPCS.60 (5. unlike aldrin and dieldrin. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. manufactured.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. and inflammation (Smith. 1991). endrin can persist for years.S. < LOD means less than the limit of detection. Over time. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. Fourth National Report on Human Exposure to Environmental Chemicals 97 .10 (<LOD-5. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. endrin is converted rapidly to its major metabolite. Endrin was used as an insecticide. In the body. 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. 1987).40-5. or discarded.20 (<LOD-5... All uses of the pesticide in the U. fatty infiltration. IPCS.

24 ng/mL (about 6. 98 Fourth National Report on Human Exposure to Environmental Chemicals .S.gov/toxpro2.24 ng/g of serum) (Botella et al. population from the National Health and Nutrition Examination Survey. 2004).020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level.. with the highest value 6.. interval) Selected percentiles ( 95% confidence interval) Sample 95th .e. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.020-.Organochlorine Pesticides The U.020 (<LOD-. In a small study of Spanish women hospitalized for elective surgery.cdc.. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect.020) < LOD .020 (<LOD-.S..020 (<LOD-. Ward et al. 2000).020) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020 (<LOD-. This finding is consistent with other general population studies (Bates et al. Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Information about external exposure (i. Workplace exposure standards for endrin have been established by OSHA.020 (<LOD-.atsdr. endrin was detected in 9% of serum samples.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 . 2004.html. Biomonitoring studies on levels of endrin provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of endrin than are found in the general population. serum levels of endrin were below the limit of detection.020 (. which may vary for some chemicals by year and by individual sample.020) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020) < LOD < LOD < LOD .020 (<LOD-. EPA has established environmental standards for endrin.020) < LOD . IARC has determined that endrin is not classifiable with regard to human carcinogenicity. environmental levels) and health effects of endrin is available from ATSDR at: http://www. and the FDA monitors foods for pesticide residues. Survey Geometric mean (95% conf.

Olea-Serrano MF. Garrett N. 4/21/09 Kavlock RJ. Perinatal toxicity of endrin in rodents. Available at URL: http://www.org/documents/ehc/ehc/ ehc130. Rab MA. Eds. pp. Cerrillo I. Gray J. Gray JA. Grajewski B.9:1357-136.html. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.inchem. Ginsburg KS. 4/21/09 International Programme on Chemical Safety (IPCS). Patterson DG Jr. Handbook of Pesticide Toxicology.79(6):928-934. Fetotoxic effects of prenatal exposure in rats and mice.html. Smith AG. 1992. Available at URL: http://www. Rivas A. Hardjotanojo W. 1991. Burse VW.htm. Perinatal toxicity of endrin in rodents. Needham LL. Toxicological profile for endrin [online]. August 1996. Rowley DL. New York. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Chlorinated Hydrocarbon Insecticides. Ellis H. August 2008. Kavlock RJ.gov/toxprofiles/tp89. Available at URL: http://www.gov/~dms/ pesrpts. Olea N. Jr and Laws ER. Rogers E.13:155-165. Turner W.cfsan. Food and Drug Administration (FDA). Frey JM. Toxicology 1981. Whitehouse DA. Toxicol Lett 1992.21:141-150. Chernoff N. Vol. I. 4/21/09 Bates MN. Buckland SJ. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Chernoff H. Hanisch RC. Botella B. Environ Res 2004.cdc. et al. et al. Crespo J. Fetotoxic effects of prenatal exposure in hamsters. 2 Classes of Pesticides. Patterson DG Jr. Academic Press. 731-915. et al.fda. Jr. Roy ML. Exposure of women to organochlorine pesticides in Southern Spain.54:1431-1443. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Chemosphere 2004. Sokal D. Ward EM. Andersen A. No:429-436. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Inc. Cancer Epidemiol Biomarkers Prev 2000. Narahashi T.96:34-40. In Hayes WJ. Liddle J. Gray LE. II. Environmental Health Criteria 130. Toxicology 1979. Fourth National Report on Human Exposure to Environmental Chemicals 99 . et al. Schulte P. Endrin [online]. Pediatrics 1987. Gray LE.atsdr. Saleem M. Hanisch RC. Convulsions caused by endrin poisoning in Pakistan.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).64-65 Spec.

S.3) < LOD < LOD 29. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.6-33. air. and has been detected in soil.7-22.6) < LOD < LOD 26.6-26.6) < LOD < LOD 24.3 (22.8 (15.1) * * 15.2 (14.7) * * 14.0) < LOD < LOD 24.7-26. Urinary metabolites include pentachlorophenol (PCP).7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.1-20. HCB is slowly metabolized.7 (15.7-16.S.9 (25.4 (11.3) 24.5 (13.5-18. and 03-04 are 118.9-32. and 7. 100 Fourth National Report on Human Exposure to Environmental Chemicals .8) < LOD < LOD 27.4.9) < LOD < LOD 19. wildfowl. Therefore.7-16.0 (25.5 (14. Survey Geometric mean (95% conf.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.4.7-15.6) < LOD < LOD 26.5-TCP) and 2.7-30.1 (14. HCB has been detected in fewer foods since the 1980s (FDA.0) * * 15. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U. 01-02.6) < LOD < LOD 14.4 (18.0-25.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.7) < LOD < LOD 24. 31. Although it is not manufactured as an end-product in the U. 2002). The general population may be exposed to HCB through diet. Gunderson. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.8 (26.3-22. 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. HCB is well absorbed after oral administration. < LOD means less than the limit of detection.4) < LOD < LOD 33.1-16.4.2-15. or game taken from areas with HCB contamination.4-15.5-33. 2005).4-16.3) * * 15.3-20.1 (14.9) < LOD < LOD 28. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.4 (22.9-30.2) < LOD < LOD 29. 2.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.4) < LOD < LOD 14.3 (16.7 (15..3 (12.9-17.4 (18.9 (14.4) < LOD < LOD 22.5) < LOD < LOD 18.9 (25.2-15. The FDA dietary surveys have shown that over time.0 (18.9 (23.3) < LOD < LOD 20.1 (13. 1997). 1988).6 (21.5-15. which may vary for some chemicals by year and by individual sample.6-trichlorophenol (2.S.9) < LOD < LOD 20. particularly by consuming fish.3 (22. see Data Analysis section) for Survey years 99-00.5-14.2 (14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 (17.9-15.0-16. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.6-19.0) < LOD < LOD 15.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (18.9) < LOD < LOD 20. respectively.2) < LOD < LOD 13.0.0 (14.9) 19.. and foods with a high fat content.4) < LOD < LOD 18.5-trichlorophenol (2. and sediment (Barber et al.4) < LOD < LOD 23. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.6) < LOD < LOD 25.8-15.0) < LOD < LOD 15.8 (22.2-31.0-19. water. primarily as a fungicide and seed treatment until the U.6 (23.5-14..6-32.4) < LOD < LOD 19.9) < LOD < LOD 16.3 (20.9) < LOD < LOD 15..9-24. and elimination occurs by renal and fecal routes.7-21.6-44.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14. distributes widely throughout the body.5-15.3 (14.Organochlorine Pesticides Hexachlorobenzene CAS No.S.6 (24. 2008. breast milk is an additional route of elimination in nursing women.4.1) < LOD < LOD 15.2 (24.8. EPA cancelled its use in 1984.7 (27.9-20. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al. population from the National Health and Nutrition Examination Survey.7 (19.6-TCP) (To-Figueras et al.7-29.2 (13.0-28. and accumulates in fatty tissues where it persists for years.5 (13.3-26. 1976).2 (17.4.

098 (.107) < LOD < LOD .atsdr.191 (.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 * * . and liver and thyroid cancers (ATSDR. In humans. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .167 (.S.Organochlorine Pesticides chemical.090 (. 1960).065 (. arthritis. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.083) < LOD < LOD .086-.203) < LOD < LOD .120 (.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. 1982.095) * * .196) < LOD < LOD .097) .095-.169-.081 (.100) < LOD < LOD .072-.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .088-.062-. environmental levels) and health effects is available from the U.107-.123 (. Chronic feeding studies in animals have demonstrated kidney injury.069) * * .141) < LOD < LOD .130) < LOD < LOD . which may vary for some chemicals by year and by individual sample.159-.085) * * .176) < LOD < LOD .147 (.176-.e. Fourth National Report on Human Exposure to Environmental Chemicals 101 . acute doses produce central nervous system depression and seizures. The U.132) < LOD < LOD .152) < LOD < LOD . Infants were exposed transplacentally and through breast milk.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 * * . as well as hypertrichosis.html. EPA has established a drinking water standard.163) < LOD < LOD . and weakness.073-.078 (.118-.157-..104 (.089-. and many died before 2 years of age (Peters et al. With chronic exposure.090 (.175) < LOD < LOD . anorexia.178-.097) < LOD < LOD .114-.064 (. 2002).095) < LOD < LOD 75th < LOD < LOD 90th * * .129) < LOD < LOD .145-.135-. and the FDA has established a bottled water standard for HCB.113-.gov/pesticides/ and from ATSDR at: http://www.121 (.179 (. 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. Schmid.077-.147-.125 (.203) < LOD < LOD .094) < LOD < LOD . were seen in an epidemic of poisoning in Turkey that occurred from 1955 to 1959 when HCB-treated seed grain was diverted for bread production. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.gov/toxpro2.069) < LOD < LOD ..088-. ACGIH has developed workplace exposure limits for HCB.171 (. More information about external exposure (i.157 (.S.173) < LOD < LOD .156 (.186 (.145-.102) < LOD < LOD .060-.087 (.140 (.081-.114-.163 (.123 (.118) < LOD < LOD .091-.085-. reproductive and developmental toxicities.088-.126) . Biomonitoring Information Serum concentrations reflect the body burden of HCB.094 (.148-.095 (. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.S.127-.111) < LOD < LOD .095 (.079 (.092 (.160 (.099) < LOD < LOD .092 (.099) < LOD < LOD .118-.122) < LOD < LOD .155) < LOD < LOD .102 (.097 (.cdc. population from the National Health and Nutrition Examination Survey.225 (.143-.090 (.115 (. very high. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity. EPA at: http://www. Survey Geometric mean (95% conf.089-.086) < LOD < LOD .190 (. HCB interferes with normal heme synthesis. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.163-.086-.099) < LOD < LOD .174-.258) < LOD < LOD .090-. immunologic abnormalities.092-.092 (.109) * * .epa. thyromegaly.082-.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .123 (.111-. This condition.182 (.

111:349355. Jones KC.fda. but overall.. Hexachlorobenzene in the global environment: emissions. 2002. Organochlorines in Swedish women: determinants of serum concentrations. Chemosphere 2005. Barr DB.. Holland NT.135(4):400404. Dogramaci I.gov/~dms/ pesrpts. Bjerselius R. 1986. As a result of the lower limit of detection in NHANES 2003-2004.39(12):744-749. Link B. Otero R. Available at URL: http://www.71(6):1200-1209. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Seiwert M. Bertram et al. Muller C. the more recent values in these studies were similar to the lipid adjusted limit of detection in NHANES 1999-2000 and 2001-2002 (Dallaire et al. Atuma S. Fenster L. HCB levels were directly related to age. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. only 4. Lepom P. Gabrio T. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Sweetman AJ.110(8):835-838. more HCB levels were quantified. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. 4/21/09 Barber JL. Toxicological profile for hexachlorobenzene update [online]..cdc.. Biol Neonate 2002. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. 2006). Ozalla D. Bertram HP. Lackmann GM. respectively. J Assoc Off Anal Chem 1988. Paepke O. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. References Agency for Toxic Substances and Disease Registry (ATSDR). Available at URL: http://www. Arch Dermatol 1999. Lawrence River (Quebec. et al. 2005). 2003). Dallaire F. Jones D.html. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Schwartz JM.54(3):203-208. Cripps DJ. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. et al. Bradman et al. HCB detection in serum also was proportional to age. 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. Ayotte P. Kohli J. Environ Health Perspect 2003. Laliberte C. Biomonitoring of persistent organochlorine pesticides. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Gocmen A.44 mg/L. Lecha M.gov/ toxprofiles/tp90. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Bryan GT. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Gunderson EL. 2005).9% of participants had quantifiable levels (Stehr-Green. Becker K.html.81(2):82-85. Zoellner I..Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. 4/21/09 Glynn AW. Kaus S. Muckle G. September 2002. Granath F. In a representative sample of the 1998 German adult population.205:297-308. 2002. 1999). however. IARC Sci Publ 1986. Environ Health Perspect 2002. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. In the 1976-1980 NHANES subsample. Lackman. and other chemicals.. FDA total diet study. August 2008. April 1982 to 1984. dietary intakes of pesticides. Herrero C. Eskenazi B.349:144.17:388–399. 2002). distribution. Herrman T. Schulz C. Peters HA. Arch Neurol 1982. Dewailly E. Food and Drug Administration (FDA). Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. J Exp Sci Environ Epidemiol 2007. Darnerud PO.cfsan. Can J Biochem 1976. Canada).77:173182. The metabolism of higher chlorinated benzene isomers.. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. 2002) and among children (Link et al. Glynn et al. Kemper FH. Sala M. Int J Hyg Environ Health 2002. 2002. levels. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Reference values updated. Krause C.. Link et al. et al. Sci Tot Environ 2005.58:1185-1201. Piechotowski I. Bradman A. Over the past two decades.. Aune M. van Wijk D.atsdr. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Santiago-Silva M. and the geometric mean concentration of HCB in whole blood was 0. et al. 2005. In Spain. Safe A. selected elements. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 2002. trends and processes. 1989).. Lackmann.

J Toxicol Environ Health 1989.263:397-398. Barrot C. N Engl J Med 1960. et al. PA.Organochlorine Pesticides Schmid R. Demographic and seasonal influences on human serum pesticide residue levels. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Santiago-Silva M. Sala M.27:405-421. Environ Health Perspect 1997. Cutaneous porphyria in Turkey. To-Figueras J. Stehr-Green. Otero R. Fourth National Report on Human Exposure to Environmental Chemicals 103 . Rodamilans M.105(1):78-83.

In 2006.5) 67.20-16.5 (14.4) 901 1067 952 992 1224 1007 Females 11.1-27.9) 81.6-62.0 (<LOD-12.1-36.6) 16.3-85.9-81.7-166) 70.6-47.8) * * * * * * 15. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.1-32. Lindane has a half-life of about two weeks in soils and water.7) 18.9) 45.5) 14. particularly alpha and gamma have been detected widely in air. and 7.7-20. Technical grade HCH is a mixture of all four isomers. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.1 (21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.2-52.8-19. exists in several isomeric forms.6-37.2) 36.1 (12.6 (16.6) 18. including alpha. < LOD means less than the limit of detection.0 (37.1 (18.1-16.1-15.4 (12. the U.6 (22. EPA cancelled agricultural uses of lindane (ATSDR. formerly referred to as benzene hexachloride. See the section “What’s New” at the beginning of this Report for details.7 (53.0 (35. The gamma isomer.0) 7.5 (24. 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. commonly known as lindane.3) 14.5-29.0-21. and have been used either as fungicides or to synthesize other chemicals.50) 8.8) < LOD 10.S.9) 15. and 03-04 are 9.1 (27.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.8 (64.5) 29.3-38.4 (50.1 (11.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.9 (50.7) 32.4) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD 21.7 (29.5 (16.5) 16.6-18.6-135) 69.0) 41.1) 71.8-68.7) 73. **In survey period 2001-2002.7 (30.Organochlorine Pesticides Hexachlorocyclohexane CAS No.7 (<LOD-16.9 (40.1 (9.1 (9.4) 51.87 (9.90-8.5 (11.4 (16.9-51.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.8) 95th 68.9-21.0) 35.6) 653 758 589 1240 1533 1370 20 years and older 10.2-42.80 (6.7-26.8 (32. 01-02.4-73.0-34.8) 12.8) 52.80 (<LOD-14.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.6 (40.2 (31. 2005).4) 11.7-69.0) 17.8) 39.46-11.2-55.8 (17. HCH isomers.7-96. HCH isomers are lipophilic.4 (11. 319-85-7 gamma-Hexachlorocyclohexane CAS No.5) 22. gamma.8 (33.0-23.2-98.2-20.9) 17. containing about 64% alpha and 10%-15% gamma isomers.89 (<LOD-9.5-123) 49.4) 44.8 (9.6) 36.61-12.3 (26.6-20.4 (8.0-111) 70.2) 13.8-199) 134 (85. each result has been multiplied by 1.1-32.4-50.9 (9.0-70.0 (14.70-19.1 (30.7) 10. As pesticide applications of HCH were increasingly restricted or eliminated.36.2) 142 (99. interval) 9.70 (8. beta.60-13.1) 12.9 (32.1-49.4) < LOD 9.2) 9.5 (8.6 (33.2 (9.9 (62.6) 50. 104 Fourth National Report on Human Exposure to Environmental Chemicals .3 (62.7) 10.66-12.8-16.9-14.3) 37.6 (10.7) 27.1) 12.4) 21.7 (62.4 (52. The other isomers can be formed during the synthesis of lindane.7-96.3 (42.7 (13.0) 8.8-87. environmental levels declined. However. 608-73-1 beta-Hexachlorocyclohexane CAS No.5) 90th 42.3 (42.7) 23.8) 27.9-24. so they can accumulate in fatty tissues of animals.0-70. and sediment as a result of historic production and use.68 (<LOD-10. 6.1) 31.2 (48.3) 34. and delta.3) 25. 2005).5 (43.7-69. It is no longer produced or sold in the U.5528.30-11.4-45. water.4) < LOD < LOD < LOD 46.3 (13.0 (8.7) 97.9 (26.0 (33.6-14. soil.4) 27.6 (17.2-67.2-87.70 (6. see Data Analysis section) for survey years 99-00.8) 7.56-12.3) 51.2-17.6-89.0-20.9-56.9-178) 48.0) 71.S.6) 35.8 (21.7) 56.9 (11.7 (35.70-12. which may vary for some chemicals by year and by individual sample.S.6) 47.2 (34.6-42. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.76.5) 11.2 (50.9 (30.3-56.90-8.0 (19.8-54.8. respectively.4-111) 84.2-22.4) 10.43 (<LOD-9. 58-89-9 General Information Hexachlorocyclohexane (HCH).2-46.1 (16.2) 62.1-37. population from the National Health and Nutrition Examination Survey.8 (10.5 (37.5) 40.1) 13.8 (23.2 (18.7 (25.90) 7.2 (29.04-10.

400) .410) .410 (.300-.331 (.910 (.191-.360 (.080-.587) 653 758 589 1240 1533 1370 20 years and older . paresthesias.214) .260) . from 6% of samples in 1982-1984 to 2% in 1994 (FDA.308-. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.150) .120 (.190) . 1986).120-.191-.290) .260-.510) .120 (. ataxia.S.480 (.220 (.480 (.110-. or dermal exposure.412 (.290 (.096) .360-.100 (. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .840) .050) . for lindane.048 (<LOD-.254) 95th .221-.065 (.580 (. Rogan.125) < LOD < LOD < LOD .069) .070) . After dermal application of lindane 1% lotion.470 (.077) < LOD .661) 901 1067 952 992 1224 1007 Females .070-.103) 90th . 2008.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .220-. and nephropathy developed (IPCS.S.210 (. 1983).270 (.501) . 1996..290 (.287 (.200 (.260) .100-.120) . See the section “What’s New” at the beginning of this Report for details.372) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.250-.175 (.080) .062 (.081-.244-.090 (. tremors.110) . and memory loss (Nigam et al.297-.250 (.174) .118-. Fourth National Report on Human Exposure to Environmental Chemicals 105 .089) .S.190-1.103 (.090 (.180-.620-1.340) .080) * * * * * * .460 (.130 (. 1977).404) .057-.056-.. 2002).400) . hepatic enzyme induction.144 (.5528.450 (.160) .146-.160 (.098 (.092 (. **In survey period 2001-2002.250 (.350 (.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 .120-.680) .700) .120 (.130-.05) .130) .442 (.310 (.059-.051 (<LOD-.230-.070 (. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown. which may vary for some chemicals by year and by individual sample.200-.110) .119) .390-..234 (. When animals were chronically fed lindane at high doses.070-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.078 (.330-.140) .120) .100) .068-.310) . the serum half-life was about 20 hours among children (Ginsburg et al.167 (.32) .090-.570 (.040-.390 (.580-1.319) .047-.280-.. EPA has established a drinking water standard.083) .710) . population from the National Health and Nutrition Examination Survey.370-.140) .290) .050-.050-..210-. 1971.118 (.083 (. The U.050 (.080-.100 (.190) . 1981).350) .070 (.060) .620) .067) .057-.051-.280-.190-.170-. respectively. The beta isomer accumulates in fatty tissues and is metabolized more slowly. ingestion.050-.380 (.058 (<LOD-.080-. U. probably by blocking inhibitory neurotransmitters in the central nervous system.080 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.173-.220) .460) .073-.320 (.240 (.250) .281 (. resulting in a half-life of about seven years.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .305) .067 (.216 (.070-.410) .090 (.064) .170-.100-.077) < LOD .470) .150-.210 (.560) .120-. HCH isomers are absorbed after inhalation. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.450-.360) . interval) .150) . Distribution is mainly to fatty tissues. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.330 (. each result has been multiplied by 1. Workers who directly handled HCH have complained of headache.086) < LOD < LOD < LOD < LOD < LOD < LOD .240-.057 (<LOD-. Saxena et al.139 (.521 (.056-. enlarged livers.560 (. 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.140 (.064 (. and FDA has established a bottled water standard and food residue tolerances for lindane.294-. and seizures.420-.050 (<LOD-.210) .480) .103-.110) .Organochlorine Pesticides exposure to HCH is through the diet.600) .410-.340-.150 (. OSHA and ACGIH have established workplace standards and guidelines.250 (.124-.222 (.814) .065 (.372 (.160-.450) .091) .050-.100-.250-.100) .050 (<LOD-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.062 (.072 (.310) .37) 1.131-.290 (.01 (.140) .220-. Gunderson 1988).050 (.690) .089-.382-.080 (.200-.

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

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

Organochlorines in Swedish women: determinants of serum concentrations. The Great Lakes Consortium. Seiwert M. August 2008. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Biomonitoring of persistent organochlorine pesticides. Bjerselius R. Rivas A. Kutty D. Available at URL: http://www.gov/~dms/pesrpts. Siddiqui MKJ. Stehr-Green. August 2005.96:34-4Food and Drug Administration (FDA).205:297-308.57(4):315-320. 4/21/09 Kutz FW. et al. et al. Bull Environ Contam Toxicol 2004. Karnik AB. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Aune M.atsdr. Chemosphere 2005.120:1-82. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. selected elements. Int Arch Occup Environ Health 1986. Sturgeon SR. Kaus S.52(1):59-67. et al. Gabrio T.cdc. Needham LL. Nigam SK. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.9(4):417-424. Levels of DDT. Available at URL: http://www. Bhargava AK. et al. Olea-Serrano MF. International Programme on Chemical Safety (IPCS). FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. J Pediatr 1977. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Chemosphere 2004. Absorption of lindane (g benzene hexachloride) in infants and children.72:261265. Kulkarni PK. Kashyap R. Botella B. Astolfi E. Maass R. Wood PH. Placental transfer of pesticides in humans. Environ Res 2004. HCH.20(2):186-193. Pollutants in breast milk. Cancer Causes and Control 1998. Lepom P. and HCB residues in human blood in Ahmedabad.html. Lowry W. Angerer J. Darnerud PO. Bottimore DP. Potischman N. 4/21/09 Anderson HA.fda. gov/toxprofiles/tp43. India. Garrett N.106(5):279-289. Falk C. Demographic and seasonal influences on human serum pesticide residue levels. Bhatnagar VK. Int J Hyg Environ Health 2002. Exposure of women to organochlorine pesticides in Southern Spain. Crespo J. org/documents/jmpr/jmpmono/2002pr08. Brock JW. Paepke O. PA. Rothman N. Krishna Murti CR.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Needham LL. Rogan WJ. Olea N.inchem. J Toxicol Environ Health 1989. April 1982 to 1984. Link B. Bai KM. Olson J.58:1185-1201. Saxena MC. Radomski JL. Visweswariah K. Atuma S. available at URL: http://www. Saiyed HN.html.91:998-1000. et al. dietary intakes of pesticides.htm. children and newborn infants. Krause C. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. 4/21/09 Ginsburg CM. Arch Toxicol 1981. Occupational exposure to hexachlorocyclohexane. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Hanrahan L.111:349355. Rey AA. Becker K.cfsan. Cerrillo I. Majumder SK. Gunderson EL. et al. Toxicological profile for hexachlorocyclohexanes update [online]. Lindane. 2002.27:405-421. Burse VW. FDA total diet study. Ellis H.54:1431-1443. Buckland SJ. Zaidi SS. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Metabolism of gammahexachlorocyclohexane in man. Int Arch Occup Environ Health 1983. J Assoc Off Anal Chem 1988. Schulz C. Granath F. Glynn AW. Piechotowski I. Rev Environ Contam Toxicol 1991. Arch Pediatr Adolesc Med 1996. Patterson DG Jr. Deichmann WB. Needham LL.71(6):1200-1209. Environ Health Perspect 2003. Raju GS. Bates MN.150:981-990. Heinrich R. and other chemicals. VI.48:127-134. Zoellner I. Brinton LA. Toxicol Appl Pharmacol 1971. et al. Environ Health Perspect 1998. Herrman T. Reisch JS.

mirex was detected in human adipose samples. The most likely sources of human exposure to mirex are eating fish from contaminated water or living in areas with soil contaminated by historic mirex manufacturing.6 (<LOD-23.3 (15.2-230) 13.6) 9.7 (12.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.6 (<LOD-108) 9.1 (<LOD-65. where it has a half-life of 12 years. Mirex can cross the placenta and be excreted in breast milk.70-24.10-37. < LOD means less than the limit of detection. 10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. since 1977.8. where it was applied directly to soil and by aerial spraying. especially those from persons living in the southeastern U.6. disposal.5-82. water.8 (12. after which it is widely distributed in the body and stored in fat.10 (<LOD-15. Formerly.2) 51. 1991).S.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. Mirex is absorbed through the skin and from the gastrointestinal tract.8 (<LOD-73.S.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (14. it is a highly persistent chemical in the environment. see Data Analysis section) for Survey years 99-00.0-374) 11.Organochlorine Pesticides Mirex CAS No. 1995).3 (15.0 (<LOD-108) < LOD < LOD 50.6 (<LOD-31.7 (<LOD-47. 01-02. 2385-85-5 General Information Mirex has not been produced or used in the U.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. Survey Geometric mean (95% conf.3-225) 15.70 (<LOD-15.0) * * * 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 19.6-305) 15. and 03-04 are 14. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. sediments. 1985. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. Mirex is not metabolized in the body.5 (9.8) < LOD 15. and foods. (Kutz et al. Occupational exposure is limited to workers at sites where mirex contamination is present. resulting in exposure to newborns and nursing infants.4) < LOD 63. Mirex has been detected in air.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 16.5-425) 40.5 (<LOD-42. aquatic organisms.5-291) 11. which may vary for some chemicals by year and by individual sample.6) < LOD < LOD < LOD < LOD 71.40 (<LOD-13. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.2 (7. soil..90-29.1 (13. Some states and the U. population from the National Health and Nutrition Examination Survey.4) < LOD 15.0 (12. Mirex binds strongly to soil. In studies conducted in the 1970’s and 1980’s.70-40. and 7. animals.5 (<LOD-115) 153 (30.5. Fourth National Report on Human Exposure to Environmental Chemicals 109 . respectively.1 (8.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.S.7) < LOD 66.4-230) 18. 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. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.7) 8. or pesticide application..S.4 (8.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.

as well as in a subsample of NHANES II (1976-1980) participants. 1989).7 ng/g of lipid.79) .100 (<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 .102) < LOD < LOD < LOD < LOD . 1995.S. The geometric mean mirex levels of the Inuit mothers were 8.053-.92) .470) .02) .73) . The U.112 (. and 4. and NTP classifies mirex as reasonably anticipated to be a human carcinogen. serum mirex levels were generally below the limits of detection (Stehr-Green.170) < LOD . and 2003-2004 subsamples.430 (.220 (<LOD-. EPA has established environmental standards for mirex.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .470) .240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * 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 . 7.170-3. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.41) .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 .090-1.450) 1.610) < LOD < LOD < LOD < LOD .106) < LOD .062-.079 (<LOD-.html.635) < LOD .268) < LOD . Biomonitoring Information In the NHANES 1999-2000.08 (.064 (<LOD-. reproductive toxicity included decreased fertility and testicular damage.059 (<LOD-.atsdr..110 (<LOD-.077 (<LOD-.054 (<LOD-. 2004). and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue. which may vary for some chemicals by year and by individual sample.090 (<LOD-.093 (. population from the National Health and Nutrition Examination Survey.450 (.052-.220) .174) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.cdc.070-1. Fishermen in New York who consumed Great Lakes sport fish had median levels of lipid-adjusted serum mirex that were lower than the 95th percentile value among males the NHANES 2001-2002 subsample (Bloom et al.256 (.106 (.370 (. In addition.140 (<LOD-.410 (. environmental levels) and health effects is available from the ATSDR at: http://www. 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. 1991).690) .100 (<LOD-.gov/toxpro2. In samples obtained between 1994 and 1997. 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.37) . Survey Geometric mean (95% conf.090-1.215) 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 .S.470 (. 110 Fourth National Report on Human Exposure to Environmental Chemicals . 2001-2002.080-1.79) .e.089-. IARC classifies mirex as possibly carcinogenic to humans.090 (<LOD-.Organochlorine Pesticides exposures are unknown. 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.055-. More information about external exposure (i.090 (<LOD-.080-1.8..090-1.310 (.510) < LOD < LOD .108 (. 2005). Laboratory animals fed high doses developed liver enlargement and liver tumors..

Van Oostdam JC. Stehr-Green. Fourth National Report on Human Exposure to Environmental Chemicals 111 . and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Jr. Handbook of Pesticide Toxicology. Bottimore DP. hexachlorobenzene. Profiles of ortho-polychlorinated biphenyl congeners. Vena JE. Chlorinated Hydrocarbon Insecticides.330:55-70. Odland JO. Moysich KB. Olson JR. PA. J Toxicol Environ Health 1989. Dewailly E.atsdr. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. Wood PH.Organochlorine Pesticides effect. 2 Classes of Pesticides. Carra JS. Swanson MK. 1994-1997 organochlorine compounds. 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.120:1-82. Strassman SC. et al.27:405-421. Academic Press. Hansen JC. 4/21/09 Bloom MS. Jr and Laws ER. Stroup CR. Kutz FW. 731-915. Gilman A. Sci Total Environ 2004.97(2):178192. Toxicological profile for mirex and chlordecone [online]. Available at URL: http://www. 1991 pp. Circumpolar maternal blood contaminant survey. Inc. August 1995.15:385-394.html. Environ Res 2005. Eds.cdc. Vol. Kutz FW. Rev Environ Contam Toxicol 1991. Demographic and seasonal influences on human serum pesticide residue levels. Watts DL. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.gov/toxprofiles/ tp66. References Agency for Toxic Substances and Disease Registry (ATSDR). Smith AG. In Hayes WJ. Leininger CC. The human body burden of mirex in the southeastern United States. J Toxicol Environ Health 1985. dichlorodiphenyldichloroethylene. Chashchin V. New York.

but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.S. Occupational exposures.80 (2.40) < LOD 6.7.0) < LOD 11. however. < LOD means less than the limit of detection.4. including hexachlorobenzene and hexachlorocyclohexanes. hexachlorobenzene. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.0) 2.40) < LOD 4.50 (1.30-27.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.5-trichlorophenol.0 (4. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. Both chemicals have been detected in air.40 (1.50-63.31 (<LOD-9.0) 2.40 (.0) 2.0 (3.20-71.5-TCP) and 2.6-TCP).00 (3.20) < LOD 5.71 (<LOD-8. Such workers would probably Urinary 2.950 (<LOD-1. and polychlorinated benzenes (Kohil et al.0 (4.S. 1976).4.19 (<LOD-6.40-11.40 (.940-3. 2. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.03) 9.60 (2.30-11.42 (<LOD-12.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4. usually at herbicide production or waste incineration facilities.72) < LOD 1.80 (1. 1999).00-3.30) < LOD 4. population from the National Health and Nutrition Examination Survey.4.30-27.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR. 2. surface water. 2.60-18. 112 Fourth National Report on Human Exposure to Environmental Chemicals .57 (<LOD-15.20-36. 95-95-4 2. EPA.10-3.5-trichlorophenol (2.00-3.80) < LOD 1.0) < LOD 11.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1..0 (3.4.20 (4.0 (5. are metabolites of several organochlorine chemicals.S.40 (2.7) 24.920-3.0 (8.0) 2.0 (4.900-2. recent sampling of U.4. Historically. may occur by inhalation or dermal routes.0) 14.4.30-27.30-44.27) 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) < LOD 21.5-Trichlorophenol CAS No.30) < LOD < LOD < LOD < LOD < LOD 1.00-8.30-40.980-3.5TCP and 2.00 (2.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.40) < LOD 1.71 (<LOD-8.4.50-25.Organochlorine Pesticides 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .40 (2.6-trichlorophenol (2. 1999).60) < LOD 8. other organochlorines.42 (<LOD-8.4.9 (<LOD-121) 9.63) 18.0) 5.40 (2. public drinking water systems did not detect 2.8) 21.0) < LOD 5.50-16.0) < LOD 5. and sediments.3.40 (2.4.60 (4.6-TCP in any of the samples (U.0) < LOD 5. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.80-41.27) 696 661 521 696 603 939 Limit of detection (LOD.50 (2.40 (1. which may vary for some chemicals by year and by individual sample.60-8.9 and 0.4.9.40-18. 2006).0) 2. Survey Geometric mean (95% conf.60 (.30 (.50 (.6-TCP were used as intermediates in the production of certain pesticides.0) 2. Trichlorophenols are no longer manufactured commercially.6-Trichlorophenol CAS No.90-33.20) < LOD 90th 5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16. soils.4.20) < LOD 1. Exposure to trichlorophenols also may result from metabolism of lindane.50) < LOD 1. Formation of 2.30-3.980-3.

6-TCP as reasonably anticipated to be a human carcinogen..4.28-25.6) 4.html. 2003.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.02) < LOD 7.4. Survey Geometric mean (95% conf.00-19.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.cdc.9) 12. Urinary 2..4.50) < LOD 2.75 (<LOD-6.02-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.4) 5.44 (1.6-TCP.13-13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. However.5-TCP or 2.3 (5.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.37-11..2) < LOD 5.31) < LOD 2.4.57 (3. urinary 2. animals showed hepatocellular abnormalities.69 (2.24 (3.43 (2.69-18. Among 6-11 year old children in NHANES 1999-2000. 1995) were similar.4.73 (<LOD-8.53-3.4.8) 4.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.78) < LOD 1.6-TCP had increased rates of hepatic tumors.67 (1. Neither 2. 1989).19-4.60-3.64 (4. which includes trichlorophenols.82 (<LOD-32.33) < LOD < LOD < LOD < LOD < LOD 2.19-12.16 (.88-16. and other chlorinated compounds.00-29. environmental levels) and health effects is available from ATSDR at: http://www..67 (1.2 (2.0) 7. IARC classifies combined exposures to polychlorophenols.7 (4. leukemias. 1989).S.90 (4.9 (5.. 2004).62-20.Organochlorine Pesticides be exposed to mixtures of chlorophenols.5) < LOD 12.6) 4.4.4) < LOD 3.00) < LOD 4. furans.1) 2.57 (<LOD-7.980 (<LOD-1.20-6.05-17. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.5) 11.32) < LOD 4.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).37) 16.920-2.6-TCP levels at the 95th percentile were up to eight times higher than 3.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.86 (3.49 (1.atsdr.68-4.0 mg/L. population from the National Health and Nutrition Examination Survey.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.17) 9.4 (6. Human health effects from 2.8) < LOD 9.. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.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. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.5-TCP.8 (5.4.5-TCP and limited for 2.47-8.36 (1. In the same 2-6 year old children..2) 2.16) < LOD 90th 5.24) < LOD 1.24) < LOD 6.75 (3..29 (1. Fourth National Report on Human Exposure to Environmental Chemicals 113 .83-12. 2003).4. and lymphomas. The 95th percentiles for 2.11) size 1994 2496 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 2.78 (3.78-19.gov/toxpro2.1 (<LOD-58.4) < LOD 3.. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al. the 95th percentile urinary 2. the 95th percentile urinary 2.4. More information about external exposure (i.68 (<LOD-8.55 (4.74) 11.46 (1.24) < LOD 5. Laboratory animals chronically fed high doses of 2.24-11.79-4.53-3. 7. Radon et al.e. At lower doses. in addition to dioxins.6) 4.44 (.820-2.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.57 (<LOD-7.4.4. NTP classifies 2.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .5-TCP nor 2.43) < LOD 12. 1995) and up to 19 times higher than the 95th percentile value of 1.4.3 mg/L reported in German adults aged 18-69 years (Becker et al. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. as being possibly carcinogenic to humans.81 (<LOD-9.05-8.80 (1.15) < LOD 2.93-11.27-17. 2003).95 (3.

45-9.00 (4.30-2.68 (<LOD-2.4.70 (2.84) 2.90 (4.0) 9. similar to the limit of detection for this Report (Anderson et al.92 (2.4. respectively.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.8-24.10-2. was about six times lower than the median urinary levels for males in this Report (Radon et al.70) 3.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (3.9) 13.0) 15.0) 9.4. Survey Geometric mean (95% conf.80-20.66 (8.85) * 3.20-3.67) 4.70-3.90-8.00 (2.8) 32.4.32) * 3.8 (9. 2003).52 (2.40) 3..40 (2.53) 4.0) 12. for males in NHANES 19992002 (Agramunt et al.0-43.6) 21. Mean values of 2.2 (14.54) 6.65 (5.59-6.72-10.74-3.5-TCP or 2.70) 1.0 (7.98-7.10) 6.20-23.00-4.70-6.0) 11.2) 25.40-7.23-2.0 (6.78 (2.90) 2.9 (11.4.02) 2.7) 33.0) 13.95 (4.95-6. 2004)..95) 3.5-46.4.60-21.36 (1.00 (1.7-16.0-18.4.0) 7.40) 2.5 mg/g creatinine) were similar to the limit of detection for 2.4.0) 17. which may vary for some chemicals by year and by individual sample.80-7.0-68.0-44.24 (2.57 (<LOD-2.4.45 (2.5-TCP and 2.6-TCP than are found in the general population.8-15. Finding a measurable amount of 2.01-6.0-50.6-22.60-37.0) 10.70 (2.10-3.S.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.4 (10.67-12.20) 4.0 (6. 1998).40-4.10) 2.20-6.90 (3.4.3) 37.0-41.0) 13..4.0 (12.1) 16.0-38.18) Selected percentiles ( 95% confidence interval) Sample 95th 25. Urinary 2.40-14.5-TCP and 2.2-0.73-9.56 (3.0) 19.59) 4.6TCP values.7) 21.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.80 (3.30) 4.6-TCP level.6 (11.7-3.80 (2.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.75 (8.58 (1. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.0 (8.69 (3.80 (2.09-7.0 (16.50-5.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.63) 90th 15.28) 24. 0.91-4.9) 694 677 519 696 602 931 Limit of detection (LOD.3 (11. Urinary 2.0) 14.36 mg/g creatinine.4.80) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.4 (9.4 (17.48-26.0 and 1.10 (5.0) 17.45) < LOD 11.4.0 (14.40) 2.5-TCP and to the median 2.4.65) 15.32) 3.25-11.28) * 2.74 (2.78 (2.6-TCP in urine does not mean that the level of 2.40-32.6-17.60 (3.32-4.04) 2.31) * 2.3-17.18-3. Biomonitoring studies on levels of 2.0 (13.36-5.5-TCP (0.6-19.0 (14.4. < LOD means less than the limit of detection.70) 5.1 (8. Biomonitoring data will also help scientists plan and conduct research about 2.0-54.7 (9. the median urinary 2.0 (20.35-3.20 (3.6-TCP exposure and health effects.70-6.40-2.0 (8.5-TCP level of 0.60-3.85 (2.0 (11.14 (2.6TCP causes an adverse health effect.08 (2.6 (12.09) 15.89 (3.0) 13.0) 14.80-25.5-TCP or 2.53) 2.6 mg/g creatinine) and 2.33-4.0) 10. interval) 2.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.60 (3.0-38.8) 18.70) 5.3) 20.00-21.2) 12.60) < LOD 5.9) 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 2.52-3.1-25.98-11.60) 6.8-13.47 (3.0) 6.4 (8.4.07 (<LOD-3.4-17.60 (2.50 (2.4.89-6.40) 4.0) 13. population from the National Health and Nutrition Examination Survey. 114 Fourth National Report on Human Exposure to Environmental Chemicals .0) 7.40-2.44) 75th 4.4. In harbor workers exposed to chlorophenol-contaminated river silt.9 (13.87-14.0 (15.46-3.0 (9.79 (5.3) 23.3-26.5-TCP or 2.4.0 (15.30-2.3 (11.55-3.6-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.06) * 2.3.0) 19.10-3.0-37.76) 3.0 (6.0 (4.0) 11.30-33..0 (14.12) 2.23) 2.80-6.5-TCP or 2.30-11.7 (13.4.49 (6.40 (2.23) 3.26 (2.6-TCP (0.6) 26.0 (20.45 (5.51-12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.31 (3.7 mg/L.58-3.99) 6.1 (10. 1991).

9) 8.S.22-9.0 (11.40 (2.38) 22.53) * 2.88) 4.7 (14.9 (9.87) 2.0) 8.15 (6.02 (1.29-4.49) 4. interval) 2.7) 6.91-2.95-2.9) 19.8) 12.21-11.79-17.17) 13.00) 4.82 (8.5) 11.9) 7.33-2.68) 2.62-15.63) * 4.4) 9.00) 4.83-6.89-2.4 (12.42) 2.81-9.14-13.87-6.17-4.82 (3.76) 4.20-2.04-16.24 (1.38-5.1) 14.11) 10.Organochlorine Pesticides Urinary 2.5 (10.98) 10.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.9-64.88) 5.50-8.33 (7.0 (6.33) * 2.23) 4.23 (1.67-17.38 (2.02) 3.8 (7.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.52 (3.18-2.46-14.6 (12.25-17.63) 4.4) 8.70-9.2 (8.8) 11.25 (3.87-7.51 (2.30-2.43 (2.6 (9.83-6.19-5.88) * 2.6 (22.96) < LOD 4.58 (4.89) 10.32 (2.29-4.63-15.75) 75th 4.5) 11.88) 1.68) 2.33 (1.0 (9.76) 2.6 (5.05 (6.91 (3.06) 11.6 (9.87 (3.6 (10.47-5.63-13.65-21.54 (2.5) 12.78) 2.59 (2.6) 13.6) 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 2.66-4.72) 32.40 (7.7-36.83-5.76) 1.65) 2.2 (13.1 (13.78) 90th 12.1-21.56) < LOD 11.88) 4.38 (4.9 (9.91 (7.25-2.81) 2.60-2.10-9.22-2.05 (3.43-7.14-2.10) 4. Survey Geometric mean (95% conf.3-37.44 (3.56 (7.10 (6.22 (<LOD-2.53) 4.27-9.28-4.8 (8.35 (3.77) 2.6) 8.88 (2.2) 19.82-2.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.76-8.0) 10.83 (3.71 (3.7) 25.00 (2.17) 2.90) 2.63 (<LOD-2.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.87) * 2.77-4.99-2.52) 2.65) 18.8) 19.3-23.5) 9.2 (7.13 (1.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.01 (3.09-3.25-15.29 (6.5 (7.15 (1.94-13.92) 4.52) 2.3 (9.41 (3.5) 8.06) 4.98 (1.4) 4.4 (11.13-6.32-19.72-16.6) 12.60 (4.90 (1.08-2. Fourth National Report on Human Exposure to Environmental Chemicals 115 .82) 2.50 (2.49-3.06-2.2 (12.26 (6.8) 21.65-2.9-29.6-31.22 (1.26-13.25 (3.22 (3.9-32.51-21.42 (2.55-2.41-6.6 (6.3) 8.1 (8.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.51) 18.5 (8.63 (2.43 (<LOD-2.73-22.5-28.53-11.1-32. population from the National Health and Nutrition Examination Survey.00 (3.16-10.53 (3.56-5.88-7.1) 11.9-34.04-2.4.48-2.52 (5.9) 8.18-4.78 (2.73) 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

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

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

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

13 (2.623-1.52) 6.0 (7.33 (5.44 (2.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1. population from the National Health and Nutrition Examination Survey.56 (4.8 (8.5) 15.38-5.2 (7.80-24.1 (9.80) .86-15.98-5.830 (<LOD-3.26-6.7 (14.28) 1.68-7.00) 3.00 (5.9 (8.0 (6.9) 8.80) 2.6) 18.0) 11.36-4.26 (5.15-12.0 (5.01) * * 1.60) < LOD < LOD 4.4) 18.20-4.0 (7.0) 6.85 (3.63) 1.70-11.8 (14.60) .58 (5.20-7.10 (.80-22.70) < LOD < LOD 75th 3.9) 952 1187 928 997 1333 1003 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.750-1.3-15.07-10. interval) 1.80) .758-1.9) 14.30-4.90 (1.0 (6.05-7.74 (8.12-19.2 (7.08-2.1-23.15) 14.61 (3.55-6.08-15.93 (4.80) 4.0 (7.1) 13.80 (2.02) 4.5-16.0) 10.0) 6.0) 5.67) 3.96-3.20 (.8 (12.890 (<LOD-2.50-5. 01-02.99 (5.30 (4.32) 1.620-1.0) 5.80) 2.42-3.48-7.4) 20.4 (9.79 (5.91) 4.11 (.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.72) 5.0 (12.46) 10.43-12.19) 9.08 (<LOD-2.0-28.4 (9.20 (.2-20.S.27-3.21) 9.80 (4.35-11.23-5.13-2.1) 10.0-27.37 (3.0 (9.70-23.579-1.00-27.2 (7.8 (9.39 (8.70-19.76 (2.970-2.56 (6.8) 7.0) 10.2) 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 1.1-17.2 (14.66) * * 1.50 (2.20 (.8) 11.03 (.840-1.0) 20.32 (.00 (4.3) 14.60-11.0) 11.30 (2.0) 7.00-19.6) 7.98-12.00) 3.30 (2. and 0.70 (4.2 (14. which may vary for some chemicals by year and by individual sample.94) * * .44-3.02-5.2.40 (.490-2.22 (.44-38.51) 2.954 (. see Data Analysis section) for Survey years 99-00.52-11.57-7.73) * * .40-14.0) 12.70) < LOD < LOD 1.2) 16.2 (9.40-11.4) 17.17-3.0) 10.45 (2.5) 20.82-12.50-36.290 (<LOD-.56 (1.10) < LOD < LOD 4.40-1.10) < LOD .0) 10.53) 4.860-2.5 (8.80) 11. respectively.0 (8.2 (11.80-4.89) 9.35-16.70-14.7 (12.5-17.58 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.14) * * .0 (8.955 (.21 (.1) 95th 13.2) 16.79-7.600 (<LOD-1.47) 5.16 (2.60-25.2) 14.20 (2.0) 9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50 (.90) 3.97) 8. and 03-04 are 0.10-7.00 (1.981 (.47) * * 1.27-15.670-1.00-7. 0.70 (2.10 (2.740-2.93-24.12) 4.60-18.40-5.04) < LOD 1.74 (8.7) 11.0 (4.16) 4.8) 7.0) 15.29) * * 1.35-12.26-8.50 (4.34-3.55-8.8) 19.599-1.81) 11.60 (5.81) 1.2. 120 Fourth National Report on Human Exposure to Environmental Chemicals .95) 5.82) 10.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.40-19.3) 16. < LOD means less than the limit of detection.0) 5.90) 2.58 (2.81) 11.00-12.2) Sample size 1949 2520 1931 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0 (7.5 (11.9-18.56-13.0) 6.0 (9.1 (10.52) * * 1.34-7.00-27.13 (2.700-1.530 (<LOD-2.94) 3.70) .20 (.780) < LOD 3.00-12.80) 2.0) 10.90-5.71 (2.2 (9.1.39 (3.4 (7.0) 11.717-1.40-16.10 (.83 (5.757-2.60 (1.90-4.0) 11.290 (<LOD-1.3) 17.61) 4.33-18.54 (3.80) 3.97) 90th 7.4 (7.71-9.30-6.42) .50) 2.8-32.20-30.0 (8.10 (2.86 (1.810-1.

4 (4.68-4.83) 8.5 (4.9) 16.45-5.56) .66 (2.53 (6.2) 5.03) 2.80 (2.28 (5.57 (4.7 (10.87 (3.830-1.55-20.74) 4.38) .28) 10.88) 2.620-1.85 (6.23) 4.5-32.45-11.94-23.9 (9.8) 6.23 (4.35 (1.35) < LOD < LOD 3.76-4.93) 9.00) 8.95 (3.04-6.14 (3.66 (5.8) 12.820 (.01-2.883 (.53-11.960 (.0) 7.30) 2.75 (7.41) Selected percentiles ( 95% confidence interval) Total * * 50th .00 (4.98) .773-1.790 (.18 (.50) 7.13) 4.02 (7.29) * * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.66-34.4) 4.36) * * 1.60) * * .1) 4.4) 13.1) 4.47 (3.960 (<LOD-2.00-17.30 (1.40) 4.28 (4. interval) .6) 13.S.900 (.818 (.566-1.1 (7.5) 7.27) < LOD 2.24-3.37-5.996 (.47) 2.37-3.87-5.28-9.98 (3.1 (10.9) 11.54-11.21-23.8) 8.03 (2.98) .09-11.04 (1.82-14.0) 6.855 (.8) 16.6 (10.82-26.79-3.1) Sample size 1949 2519 1928 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.67) 4.47 (1.540-1.510-1.67-19.924 (.26) * * .34) * * .549-1.56) 7.1 (6.7) 12.430-1.57) 4.32-12.71) 10.51-5.3) 12.5) 11.80 (7.3) 16.710 (<LOD-1.00-19.61-29.54) . Fourth National Report on Human Exposure to Environmental Chemicals 121 .860 (.00 (4.92-2.440 (<LOD-2.7) 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 .870-2.03) 2.07 (.84) 7.56-13.6) 8.98-5.3) 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 1.69-10.4 (9.9) 12.780 (<LOD-1.2 (8.46-5.6) 11.2 (6.560-1.750 (<LOD-1.25) 6.62-5.41-12.03 (7.93-5.8 (10.37) 9.72) 11.3) 15.61-13.570-1.28 (2.02 (2.10 (3.19 (4.5-20.9 (9.57-10.05 (1.09 (.0 (8.650-1.1 (8.73 (1.76) < LOD .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.74) 90th 7.40-3.42 (3.2) 9.38 (1.500-1.5) 12.34) < LOD < LOD .2 (10.60-9.7 (8.10-13.43 (3.7) 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.7 (9.890 (<LOD-1.00-13.02-14.94 (4.2) 13.75-7.43) 2.7) 18.90-5.42) 12.34 (6.54-15.89-3.05) .77 (6.9 (5.25) < LOD .40) < LOD < LOD 75th 2.29 (2.920 (.69 (4.533-1.2) 95th 12.3) 5.98) 9.94-10.5) 8.8) 7.80 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20-8.98-22. population from the National Health and Nutrition Examination Survey.53) 9.93-9.2) 8.15-10.47) * * .81-5.94-22.40 (3.79-9.6) 9.47 (3.6 (9.06-2.94 (2.02-2.88 (5.88-10.64-5.58) * * 1.54-2.05 (.37 (5.5-16.46) 2.90-8.633-1.82-14.11-6.2) 7.45-5.75) 2.40-14.5) 7.69) 4.7) 5.09) 2.1-15.62) .67) 1.4) 4.44 (2.80) 9.61 (1.40-28.61 (1.95) 2.87 (1.60) 2.31-14.85) 2.84 (5.5-13.890 (<LOD-1.9-28.932 (.82-6.78 (2.608-1.83 (7.54-4.56) 4.89) * * 1.68) < LOD < LOD 3.69) 2.40-12.92-5.81 (1.94-9.1 (11.66 (1.88-15.34 (6.03-6.52) 4.66-15.574-1.31 (3.41) .39 (2.43 (.2) 5.1 (9.57 (6.75) 14.75 (3.37 (4.71-2.40-5.

7 (10.70 (1.30) 3.90) 4.67) 3.650-1.3) 20.680 (<LOD-1.4-17.70-8.70-5.0) 23.52 (6. 0.41) 3. which may vary for some chemicals by year and by individual sample.90-9.20) 3.90 (6.27 (7.16-1.0 (10.49-4.20) 3.88) 3.0) 12.6 (10.90 (6.3) 22.78) 5.61 (3.6) 14.90) 8.0 (10.910 (<LOD-2.6) 14.96) 3.4) 7.00) 3.70) 2.18) * * * * * * * * 1.88) 10.90-15.34-3.40) < LOD < LOD 75th 2.3 (11.3) 8. 01-02.9 (7.8-20.0) 11.17 (7.670 (<LOD-1.90 (6.80) .20) .67) 4.27) 4.7) 16.39 (5.0) 14.61-32.45 (3.970 (<LOD-2.00-4.10-10.06 (2.62-17.3 (9. 122 Fourth National Report on Human Exposure to Environmental Chemicals .7) 22.50) 5.7) 14.24 (2.95-9.97-4.20-8.740 (<LOD-1.60) < LOD < LOD 2.00) < LOD .27 (3.90 (2.3 (9.84-4.80-21.20 (<LOD-2.3) 10.50) 3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.18 (3.7-19.3 (7.00) 7.5 (8.80-12.67-10.96) 90th 7.35 (6.11-6.95 (2.0) 11.80) .0) 14.63-14.0) 12.S.00-16.01 (2.9) 95th 14.80-4.75 (3. and 03-04 are 0.58.29-4.6-19.41-5.9) 10.95 (5.670 (<LOD-1.0 (9.1) 11.72) 2.25 (2.6-41.9) 9.90 (1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .80-6.10-4.98-9.6) 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 * * * 1.60 (6.99 (3.0) 18.2 (9.0) 12.80 (2.2) 14.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0 (13.27) 9.81-6.90 (2.2 (7.34-10.0-24.15-6.47-6.70-9.9-14.73) 7.5-26.92-17.00-4.5.7 (11.34 (6. population from the National Health and Nutrition Examination Survey.50-4.0) 13.80-8.0) 9.20-18.00) 3.04 (3.89 (2.46-28.00-18.10-15.22 (6.60 (5.0 (14.1 (10. < LOD means less than the limit of detection.77-14.0-29. and 0.50) .00) 8.4 (10.39-13.50-5.70 (8.0 (8.10) 6.4) 11.51) < LOD 1.37) 2.5 (9.28 (7.31-12.53 (3. see Data Analysis section) for Survey years 99-00.00 (.7) 15.46-4.80) 5.90-31.30) 8.70-9.9-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-33.77-3.10 (<LOD-1.90 (2.670 (<LOD-1.5 (8.15-2.20-4.4 (10.89) 2.12 (4.8-17.8 (12.66-13.5.8) 8.34-5.80 (2.42 (1.6) 11.22-12.8) 9.1-23.0) 19.0-19.6 (10.4 (14.80-3.64) 10.22 (6.29) < LOD < LOD < LOD < LOD 3.40 (2.31) 1.790 (<LOD-1.9) 16.75 (2.31-7.00-9.0 (5.6) 18.90 (5.0-24. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3 (12.0) 7.82) 8.90-15.0) 9.33-11.60 (2.7) 10.35-3.92) 9.66) 4.670 (<LOD-1.59-3.22) 8.0 (15.3 (6.580-2.58 (1.5) 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 * * * * * * .37 (3.80-14.10 (.5) 21.8 (12.30) 3.74) * * * * * 1.30) < LOD < LOD 4.0) 6.35) 4.8-21.80 (5.8-20.86-10.40 (2.0) 13.27) .0 (7.3) 14.9-15.7-21.14 (6.00-18.30) < LOD < LOD .90 (6.24-5. respectively.9 (12.1 (10.0 (9.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.

96-11.16-14.89-3.67 (7.910 (<LOD-1.9-25.94 (5.63 (6.810 (<LOD-1.50-17.68-10.39-17.41 (7.6) 14.4-15.0) 14.3) 6.78) 4.3) 9.27-13.03 (6.34) < LOD < LOD < LOD < LOD 3.51-7.51-10.21) * * * * * 1.88 (1.86) 9.70-2.32) 2.6 (11.99) 2.27) * * * * * * * * 1.28-12.21-21.4) 7.2) 12.0-19.74-19.7 (10.7 (8.44-6.58 (4.04) 9.03 (2.3-21.97-4.5) 8.2-15.5 (11.87 (3.89-3.690 (.54 (7.67 (1.9 (9.4) 7.9 (9.0 (8.32-8.00) 2.54-5.5-17.6-19.28) 6.28 (1.50 (6.89-10.9-17.05-3.68-4.95 (2.09-11.47-9.0-21. population from the National Health and Nutrition Examination Survey.27) 1.7-23.85-17.5) 13.6) 95th 16.4) 7.620 (<LOD-.85-8.29 (5.93 (2.86 (3.75-3.4-18.1) 13.77 (2.4 (11.95) 90th 8.30) 2.3-34.29) 3.4-16.79-6.30) 8.9) 16.16 (3.91) 3.95) 3.11 (5.2) 16.75-3.89) 5.38 (.06) .6) 7.91-9.5 (15. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.09-11.8) 14.92) 3.42) 7.2 (9.890-2.6 (11.8) 16.94-14.5) 10.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.760 (<LOD-1.950) .7) 14.37) 3.86-3.45) 3.89-13.11-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.59-3.4) 16.5 (8.72) 4.7) 15.8) 11.2) 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.36 (2.6 (13.68-19.71) < LOD < LOD 2.72-4.8 (8.00 (3.3-15.1) 20.96-10.00) 8.78 (6.92 (5.69-11.25-9.29 (2.6) 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 * * * * * * .97) < LOD .80) 3.00 (2.27) 5. Fourth National Report on Human Exposure to Environmental Chemicals 123 .77 (2.06 (<LOD-1.1 (19.15) < LOD < LOD 75th 2.2) 8.7) 9.4-16.00 (<LOD-1.74-4.38 (2.55) 16.2-30.2) 12.61 (2.3 (7.1 (8.6 (12.6) 13.12) < LOD < LOD 4.7-19.93 (<LOD-2.00 (<LOD-1.12 (7.S.6 (10.78-10.20-3.37-5.70-35.7) 12.71 (1.63 (2.7 (11.15 (1.2 (9.33-10.7) 14.07) 2.55 (2.38) 1.2) 15.52-3.00 (7.42-19.68) .6 (13.42) 8.93-10.38-13.83 (7.0 (11.6) 6.07) 2.940) < LOD < LOD 1.3) 12.07-3.973 (.2) 19.30-5.6) 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 1.25 (4.23-3.99 (4.88-7.93 (6.530-1.0 (13.48 (2.43 (2.02-4.3) 8.9) 19.0 (10.33) 3.5 (9.64-11.83 (6.07 (5.2) 10.590 (<LOD-.34-18.780-1.4) 15.01-5.5 (10.81 (7.5) 22.27) < LOD .3-17.1 (13.82-8.53-8.6) 12. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .4) 9.89 (3.920 (<LOD-1.55) .850 (<LOD-1.89 (2.4) 6.54) 9.77) 3.2) 12.00 (5.14 (2.45) 6.29-2.38 (1.30) 7.3-17.79-9.78 (4.82-11.9 (9.18) 2.6) 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 * * * .03) 3.73 (5.19) 3.1) 10.7 (10.8 (10.

46-3.460-.01-1.03) 1.79) .11-3.780) .00 (1.69-4.710 (.449 (.30) 2.30 (.50-2.549 (.2.618) * .592) * 50th .50) 1.57 (1.388-.380-.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 * .398-.18 (.600-.380) .585) * * .336-.15) 2.950) 90th 1.65 (2.97 (2.08 (2.740 (.94 (3.13) 2.38) 1.690-.47 (1.700) .550 (.20) 2.940) < LOD .73 (1.730) .690) .83) 1.505 (.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 * .592-.08 (2.31) 2.584) .359-.75-2.70-7.970) 1.20-2.34) 2.70 (1.780 (.14 (1.20-1.467 (.76-6.10) 1.459 (.96-5.30-1.78) 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 * .800 (.31-3.83 (2.79) .710) .70 (1.89) 1.960 (.20 (1.49) .20 (2.50 (1.48 (2.00-2.930) < LOD .89) .45 (1.960) .303-.22-3.37-2.20) 1. interval) Selected percentiles ( 95% confidence interval) Total * .63 (1.510 (<LOD-.930-1.720 (.74) 3.29-2. 0.750) 1.750-1.20 (1.740 (.86 (1.340-.30 (.690 (.580-.20 (1.46 (1.64 (1.80) 3.42-2.50 (1.910 (.22-8.46) 1.94 (2.570-1.390-.670) .16) 2.17) 1.31) 95th 2.570 (<LOD-.490 (<LOD-.19-1.960) .04) .80 (1.45 (2.840 (. population from the National Health and Nutrition Examination Survey.20) 1.09.980) 1.440-.960-1.31-3.860) < LOD < LOD .83) 2.759) * .29) 1.34) 2.47) 2.50 (1.910-1.600 (<LOD-.77 (1.450 (<LOD-.570 (.30 (.22-2.90) 2.425 (.880) < LOD 75th .382-.59-2. see Data Analysis section) for Survey years 99-00.60) 3.30-3.949) .76 (1.930) 1.780 (.18 (1.592) * .30) 4.550 (.15) 2.96-3.40 (1.48 (1.740-.749 (.80) 3.54 (2.26 (2.26) . which may vary for some chemicals by year and by individual sample.210 (<LOD-.20-2.13) .45-4.587) * * .22 (1.10) 1.46 (2.160 (<LOD-.353-.880 (.455 (.570 (<LOD-.657) * * .89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.810) . 01-02.30-3.830 (.10-1.30) 4.60 (2.73 (2.820 (.60) 2.680-1.23-3.790 (.78) .25-1.27 (2.457 (.55 (3.80 (2.27 (3.910) 1.20) 2.09 (.850) < LOD .10) 3.60-4.14-1.36-4.50 (1.50 (1.95) 2. respectively.343 (.510 (.90 (1.350-.1.650-.33-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.260 (<LOD-.580-1.95-5.70 (1.98 (2.760 (.01) .30) 1.710 (.68-5.88) 1.05-2.59-6. 124 Fourth National Report on Human Exposure to Environmental Chemicals .930 (.61 (1.10-1.20) 3.35) 1. and 03-04 are 0.500 (<LOD-.620-1.05-3.597) * .01-3.11-3.45 (1.41-5.680-1.990-1.00) 2.32-1.560-.87-3.89-6.17-4.83) .740-1.20) 3.280-.40 (1.970) . < LOD means less than the limit of detection.57 (2.80) 2.54-2.201-.32) 3.49) 2.00-4.20-3.380-.95 (2.720-1.400) .350-.10) 1.80) 3.39) 2.570 (.98) .86) 3.720-1.453 (.960) 1.590-.90) 3.00) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240 (<LOD-.73-5.820 (.600-1.90-4.880) < LOD .77-2.570) * .74-5.94) .21) 3.83 (2.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.70-2.98-3.16-3.16) 1.41 (2.540 (.80) 2.80) 5.22-3.58 (1.700) .690-1.75 (2. and 0.90) 2.91) 2.54) .30 (1.32 (1.17) 1.50-2.S.04) 1.390-.

412-.73 (2.00-1.920) .42-6.02-3.23 (.470 (<LOD-.460) .57-2.310-.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.17) 2.07) 1.640 (.61 (3.07) 1.00-3.43) 2.850) 1.310 (<LOD-.870) .510 (.710 (.42) .45 (1.740) < LOD 1.58) 3.645) .71) .510 (.630) * . Fourth National Report on Human Exposure to Environmental Chemicals 125 .510-.330-.335-.58-6.60 (2.820) .350) .08-2.560-.24) 4.44) 2.08-3. interval) Selected percentiles ( 95% confidence interval) Total * .38-3.62 (2.75 (1.880) 1.67) 1.25-3.530 (.750 (.820) 1.49 (1.330 (<LOD-.64 (2.485) * * .730) .300-.45 (2.66) .87 (2.800-1.550-.42-8.305 (.840) 1.10) 2.800) < LOD .42 (.234 (.78) 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 * .370-.660-.17-2.28 (1.04) 95th 2.471-.50) 1.79 (1.57 (3.72-4.720 (.990-1.47 (1.33 (1.22) .180 (<LOD-.390-1.41 (.560 (.11) 1.32) 5.71 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67 (1.739) * .60) .08) 1.57 (1.368) * .19 (1.03-2.520 (.04-5.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.830 (.560-.380-1.99) 2.20-2.550-1.910) < LOD .590) * 50th .400) .82 (2.36) 3.89-3.80) 2.22-3.23) 2.32 (.830) 90th 1.22 (2.75 (2.250 (<LOD-.550) .16) 1.92 (1.77-4.490 (.75) 6.470) .02-6.23) 1.61) 2.22) 1.88 (1.22-2.380-.39) 2.08-2.38 (2.16-1.670 (.38 (1.43 (1.300 (<LOD-.61-3.840) 1.700 (.70 (2.550-.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 * .67 (1.480) .23) 2.08) 2.02-3.52 (1.535 (.62 (1.320-.320-.07) 5.05) < LOD .790 (.39 (1.270 (<LOD-.08-3.480-1.520-.310 (<LOD-.55 (1.43) 2.06) 4.97) 1.50 (1.90) 2.92-8.43) 1.680 (.08 (2.77 (3.285-.720-1.509 (.94) .400-1.597) * .30-2.06-2.32) 1.98) 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 * .930-1.98) 1.08 (.710 (.72 (2.05 (1.64 (2.13 (1.29-4.22) 4.71) 2.270-.318-.07 (.66 (2.18-2.590-1.55-3.372 (.67) .82) 2.58 (1.52) 3.72 (1.403) .84 (2.73-3.60 (1.11-2.348-.460-1.08-2.47-4.49-4.97 (1.32) 2.591 (.05-4.760) < LOD 75th .07) 1.75-3.790) .31-1.47 (1.270-.14 (2.60) 1.05) 1.688) * .97) 2.07-3.30) 3.280 (<LOD-.136-.580) .700 (.500-.97 (1.22-3.580-.67-3.742) * * .750 (.81) 2.447 (.92) 3.69 (1.89 (1.23) 3.76) 1.03-1.580 (.99) 1.09) .840) .700 (.33) .740) .00 (3.540-.08-3.34 (1.61-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.640 (.440-1.444-.20-7.79) 1.08-3.710 (.88) .95) 1.S.448 (.900) 1.870 (.20) 1.640 (.72) 1.390) .980-1.515) * * .44-2.380) .07-2.940-1.460 (.65) 2.552 (.63 (1.53) .11 (.393 (.69 (3. population from the National Health and Nutrition Examination Survey.17) 2.57-4.250 (<LOD-.84-6.05-2.453 (.32-1.950-2.77-3.760) .230 (<LOD-.253-.690) < LOD < LOD .590 (.377-.04-1.16-2.70 (3.91 (1.

19) 2.87-7.44) 3.4 (19.91 (4.96) 5.40) 50th 2.1-25.0) 31.2-27.2) 16.8 (12.85) * 2.4-76.600-2.4-22.07-5.0 (13.21 (3.14) 5.90 (1.30) 4.0 (37.1) 95th 48. 01-02. < LOD means less than the limit of detection.0) 28.52 (4.99 (2.44) Selected percentiles ( 95% confidence interval) Total * 2.0) 15.60 (2.50-20.90) 11.41) 1.7 (12.0 (38.9-51.0-47.0-29.9 (10.9 (19.11 (4.1 (25.67 (1.0 (38.0-58.60) < LOD 1.30 (.29) 2.06) * 2.0) 32.77) 38.41) 5.9 (19.27-6.53) 40.0 (33.53) 1.610 (<LOD-1.10 (1.11) 2.05) 1.0) 5.9-21.3) 28.0-230) 35.5-27.0-41.82 (1.0) 28.0 (38.0 (11.9) 48.81-3.98 (1.41-4.58-2.830-3.83 (1.6 (9.0) 30.30) 11.12) 1.46 (.6-22.8) 41.0 (21.53 (1.70) 1.26 (.17-2.0) 3.94 (1.6 (26.18.6 (15.0-110) 42.70 (7.50-5.05) * 2.2-33.70 (1.90-8.36-2.0 (6.6-27.8-24.45) 2.0-50.45) 2.0-260) 34.0) 3.83-2.23) 9.86-3.0 (7.98) * 2. which may vary for some chemicals by year and by individual sample.1) 38.21 (1.59 (1.31-6.0 (20.46-6.3 (12.90 (1.40) < LOD 2.80) .9) 18.3 (10.8-21.79 (1.00-24.53) * 2.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.23-2.66-5.0 (20.0 (17.72 (1.0-39. and 0.00 (.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5 (24.0 (8.13 (1.4 (10.2 (12.30-14.21 (4.0 (24.2-62.5-20.8) 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 1.1 (11.0) 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 2.06 (1.0) 17.5-40.54 (1.58) 16. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0 (32.18) 14.43-7.10) .0 (8.690-3.5) 69.41) 1.48-2.470 (<LOD-1.0-41.64-3.0 (40.4 (15. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0-53.0) 3.2 (19.05-3.830-4.1-19.0) 20.0) 4.0) 13.40) < LOD 1.64-8.65 (4.2-47.4) 38.1 (22.76 (2.0 (26.88) 1.0) 15.16) 2.8) 62.0) 4.74-2.2-26.0) 33.4.5-45.12 (3.13) 12.40-4.0) 20.83 (3.48-2.S.42) 1.3 (24.3 (12.0-53.70-17.2-39.92-5.0 (19.29-4.10 (1.10 (7.70 (1.16) * 1.530-4.50-7.10) 39.95 (5.61-2.0-110) 34.57-2.9) 38.50-17.04) 3.8) 39.19-2.71-2.0) 19.6-45.8 (22.1) 38.69) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.44-7.88) 3.0 (8.80) < LOD 1.20 (2.71) 5.0-69. respectively.6-54.10-4.25-3.23-2.0 (38.77 (1.7-22.78) 9.20-4.70) 5.02 (2.41 (1.1-40.0-41.7-41.09 (4. see Data Analysis section) for Survey years 99-00.50-2.33 (5.8 (26.35-6.04-8.660-2.5) 30.3) 31.3) 33.48) 5.7 (12.1-47.63-6.0) 45.8) 32.20) 1.7) 20.00 (.0-43.0-92.0 (38.18) 6.8 (12.10 (1. 0.76 (2.3 (14.3 (23.2) 31.46-2.0-31.2-80.32 (2.80) 90th 38.83-2.13 (1.80) 1.0) 3.59 (1.6 (11.0-49.10 (1.93-3.9 (27.0) 6.79-2.54 (3.1-20.7) 47.5-74.40-16.0) 42.1 (10.70 (.0 (38. population from the National Health and Nutrition Examination Survey.0-58.0-39.75-14.70) 1.0) 17.1) 18.0-62. interval) 1.7 (28.29-9.50 (2.97) 6.44) 2.79 (2.26) 75th 11.1-46.0) 8.0-52.57-2.0) 16.61 (1.9) 17. and 03-04 are 0.10-13.0) 4.81-2.0-62.1) 140 (46.78 (1.5.0) 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 2.4) 19.71 (4.49-2.0 (25.2-27.3) 38.0) 18.0) 16.70-6.18) 20.04 (<LOD-2.80-2.9 (23.80-18.1 (26.85 (1.6) 52.1 (25.3) 26.0 (38.86 (1.92) * 2.

00-16.0) 13.88 (4.0 (25.0-118) 29.02 (.4-34.52 (1.86) * 3.19 (1.57 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4 (25.69-18.40-7.9) 24.3 (8.2-47.83) .7) 95th 51.6-49.07-2.1-22.75 (1.30) 28.2 (8.61-22.32-3.3 (10.36) 10.0-40.08) 1.0 (17.4 (11.52-4.5 (41.25-3.43-2.680-4.93) 5.59-2.6-38.4) 3.63-5.38-5.68) 47.4-39.8) 31.09 (5.32 (3.17) 2.0 (14.94) 19.51) < LOD 1.7 (18.19) 5.17-3.75) * 1.80 (1.8 (7.71) 8.7) 34.870-3.6) 19.23-1.86) * 2.1 (25.24 (1.27) 50th 2.9 (39.2) 4.930 (<LOD-1.7) 26.38) 5.0 (6.61 (1.88 (1.0 (39.9) 3.18) 3.7 (18.6 (11.02) 1.28 (1.39 (1.02) * 1.7 (10.94-20.0 (19.12 (1.670-1.9-52.1) 52.22-2.3) 13.8) 32.2) 36.3-22.2 (22.5 (15.58-17.0) 3.46-5.2-28.2-70.1) 36.2-34.19) 5.9 (26.6-51. Fourth National Report on Human Exposure to Environmental Chemicals 127 .26-2.33) 1.67 (1.60 (.1-60.899-2.7) 15.7-20.34) * 1.4) 14.54-15.9 (13.82 (2.3) 28.0) 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 1.1-63.00 (4.4) 12.6) 3.1 (12.23) < LOD 2.33) < LOD 1.9-18.0) 10.7-19.7-109) 22.26-4.750 (<LOD-1.66) 8.95-16.0) 25.44) 9.S.2 (21.75 (1.67 (1.4-21.4) 12.71-2.40 (5.97 (1.33) 2.18-1.36 (4.64 (1.1) 25.06) 1.41 (2.2 (16.3 (9.21 (4.95) 90th 32.8) 23.1) 27.82) 1.6 (27.6 (7.8-26.5 (15.79-17.2) 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 1.62 (2.95-16.3-27.58-2.9) 12.43-12.69-5.57) 4.40-4.55 (2.16 (1.14-8.0) 30.35) 1.8-45.7-43.88 (4.22-3.61-2.2) 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.23) 37.1) 25.22 (.29-5.9 (7.0-70.2-38.5-97.14 (.6) 112 (40.45-1.7-38.75-6.0-71.4 (12.47 (1.3 (10.7) 23.7) 30.3 (20.0) 48.2) 41.59-2.01 (.53) 1.19-14.54-2.11) < LOD 1.67-16.08 (1.0) 47.4 (21.79 (2.84-13.4 (19.9) 3.5-190) 30.27 (6.0 (32.4 (5.88 (1.8) 3.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.43) * 2.1) 13.94) 1.1 (33.46-6.5 (13.888-1.68 (1.72) 2.33-5.6) 11.11-2.9-36.8-37.8) 11.48) 1.2 (9.890-4.03-2.7 (24.16 (1.8) 15.00) 1.06) 1.2 (15.7-47.9 (19.56 (2.8-34.9-95.16 (1.51) .15 (.1) 13.31) 2.90 (.7) 66.5-36.870-3.45 (1.99-4.5 (8.6) 7.5) 27.6 (24.38 (3.6) 23.37-2.0 (23.4-67.4 (25.06) 75th 9.1 (50.7) 61. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.95 (2.0 (23.76-2.9 (10.5-43.46-22.1 (39.7 (11.80-8.18) * 2.06-1.66 (1.16-2.03) 1.8-43.28) 1.70-4.35 (2.56) 1.07) 9.48 (4.12) 3.2) 13.2) 33.47-17.9) 54.71 (1.96-16.67-3.4 (9.83 (.46) 1.5 (6.00) 6.66 (1.59-15.40 (2.860 (<LOD-1.22 (2.1 (34.07-2.6) 3.1) 27.38-1.5 (34.7-37.37 (1.20) Selected percentiles ( 95% confidence interval) Total * 1.60) 4.96) 2.50-5.20-5.2) 13.70 (1.91 (6.5 (17.9) 24.9-37.1) 17. population from the National Health and Nutrition Examination Survey.27) 10.9-41.47 (3.50 (2.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.19-6.870-3.3-19.4-71.6-32.3-42.35) .91-2. interval) 1.1) 15.27-3.5) 70.62) 4.36-13.

610-.650-1.700-1.210 (.680-1.990) .660 (.770 (. see Data Analysis section) for Survey years 99-00.117 (. respectively.690-1.530-.350) < LOD < LOD < LOD < LOD .12 (.100 (.450 (.770) < LOD 95th .090 (<LOD-.410-.650 (.990 (.36) .130) .300-.200) < LOD < LOD .630 (.05.760) < LOD .720 (.090 (<LOD-.190 (.430 (.290 (<LOD-.560 (.900 (.310) < LOD < LOD < LOD < LOD .210 (.540 (<LOD-.160) .150) .840) .120-.320 (. < LOD means less than the limit of detection.380-.720-1.360-.S.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.740) < LOD .850 (.370-.470 (.160-.870 (.230-.940 (.40) .640) .680 (.620 (.410-1.13) .140-.380-.130-.730) . and 0.110-.850) < LOD .550) .860) .140) .120 (<LOD-.860-1.360-.730-.280) < LOD < LOD < LOD < LOD .350) .610-1.090 (<LOD-.640 (.42) .170-.600 (.640) .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 * * * * * * * * * . and 03-04 are 0.190 (.1.30) .700-1.470-1.180) .490 (.830 (.640-1.320-.830 (.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 . 01-02.560 (.58) .03) .830) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130-.870 (.700-1.780) < LOD 1.630 (.370-.60) 1.410) < LOD < LOD < LOD < LOD .140-. 128 Fourth National Report on Human Exposure to Environmental Chemicals .160) .820 (.990) .171) * * .410-.120-.10) .570) .720) .190 (.870 (.240 (<LOD-.260 (.450 (.390 (.830) .130 (.42) .090 (<LOD-.1.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.850 (.290) < LOD < LOD < LOD < LOD 90th .820 (.220 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .540) .15) .084-.300-1.460 (.090 (<LOD-.230) .840) .510-1.400-.460-.650) .680) .220 (.270 (.330-.090 (<LOD-.440-1.20) .10) .870 (.870) < LOD .310) < LOD < LOD < LOD < LOD .30) .30) .310 (. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.130-.310 (.930 (.430-.10 (.150 (<LOD-.580) 471 576 310 664 822 717 814 1118 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .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.450 (.310-.162) * * * * * .650) .140-.050-.32) . 0.870 (.380-.680-1.080 (<LOD-.390) < LOD < LOD .290) < LOD < LOD < LOD < LOD .099-.00) .610 (.130) .650-1.080 (<LOD-.540) .700-1.420-.10) .610 (.

330-.700 (.60) .270) < LOD < LOD < LOD < LOD .03 (.200 (.240-.440 (.12) < LOD .860 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .230-.570 (.170 (.19 (.940) .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.580) .161) * * .360-.780 (.460 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.780) < LOD 1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .700-1.140-.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 * * * * * * * * * .580 (.580 (.940) .720 (.740 (.450) .500) .730) .220 (.380-1.140) .550 (.880-1.140-.02-1.870) .S.24) .38) 1.070 (<LOD-.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00) < LOD .360 (.700 (.960) .810 (.400 (<LOD-.29 (.720 (.116 (.170 (.970) .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 * * * * * * .730) .410) .140-.250-.070 (<LOD-.260-.03 (.190-.380 (.760) .057-.110) .670-1.111) * * * * * .300-.670 (.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .470 (<LOD-.580) < LOD .540 (.650) < LOD .450 (.14) 1.730 (.330-.110) .24 (.190 (.190 (.500-1.060-.110-.050 (<LOD-.180-. population from the National Health and Nutrition Examination Survey.120) .740) < LOD 1.400) .01 (.270 (.410 (.330-.640-1.990) .140-.650-1.03) .02) .340-.410-.230 (<LOD-.09) .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 .150-.310) < LOD < LOD < LOD < LOD .330 (.490-1.200 (.220) < LOD < LOD < LOD < LOD .510-.86) .20) 1.260) .330 (.850 (.380-.370 (<LOD-.170) < LOD < LOD .570-.62) 1.86) .080 (.43) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.550 (.700) .860-2.610-1.03 (.58) 1.660-1.580-1.750) < LOD 95th .410 (.080) .390-.560 (.890 (.360) < LOD < LOD < LOD < LOD .410-.66) 1.230) < LOD < LOD < LOD < LOD .860 (.500 (<LOD-.090 (.710-1.360-.110) .880 (.100 (<LOD-.730) .600) .78) .990) .380-.070 (<LOD-.36 (1.440-1.390-.670 (.540 (.084-.410) < LOD < LOD .570-1.280) < LOD < LOD < LOD < LOD .210 (.070 (<LOD-.800-1.600-1.290) < LOD < LOD < LOD < LOD 90th .520-.120) .380-.140-.080 (<LOD-.300-.320 (<LOD-.090 (<LOD-.67) .110) .100-.540) .300 (.

90-20.52) 5.49 (1.750-2.14) 2.0) 2.26 (2.0 (5.0 (4.690 (.0 (16.39) .0 (5.S.61 (1.97) 20.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.55-4.40 (1.0-39.0 (5.53-7.620-1.42) .07 (3.00-17.14-5.21) 3.65) 1.08.18) 1.99) 11.48) 13.0) 4.800) 17.40) 2.52 (1.28-9.45 (2.350-.90 (2.170-1.0-40.0-38.67 (2.360-1.12) * * * * * * * * .83) 2. 01-02.70) 2.59-5.32 (1.52 (1.01) 5.47 (3.0) 5.0 (13.38-3.3) 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) 2.20-4.10-3.0) 2.87) 5.0) 3.35-10.33 (4.740 (.70-50.610 (.10 (3.86) 4.0 (17.05 (3.830 (. see Data Analysis section) for Survey years 99-00. population from the National Health and Nutrition Examination Survey.10-3.83-3.30) 95th 19. respectively.0) 5.00-17.14) .480-.400-1.610) < LOD < LOD < LOD < LOD < LOD 2.30 (1.840 (.250 (<LOD-.82-4.21-3.0 (5.35) 11.30 (1.94 (1.99) 19.40 (1.0) 7.20 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (6.0 (4.800-4.29-10.840-3.60) 1.63) 32.1.97) 20.49 (1.48 (2.580 (.910) 2.960 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.0 (17.770) 2.90) .66) 4.0 (17.0-40.0) 2.96 (1.70-7.16) 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 .46 (1.55-8.00) 1.15) 19.42) 2.30 (1.6) 5.30) .110 (<LOD-.30 (2.40-8.11) 13.10 (.40-7.68) 2.0-38.40-4.00 (1.07 (3.11 (1.20-17.0) 4.380-.210-1.0-38.30 (.07-3.28) .31-10.90-28.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.43-4. and 03-04 are 0.67 (1. which may vary for some chemicals by year and by individual sample.0 (3.00) .39 (2.07) 1.691 (. 0.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.00) .40) 1.590 (.74 (3.370-.05 (2.70-17.94-8. < LOD means less than the limit of detection.90) .94-3.880) 5.30-7.37) .13 (3.53 (2.0) 2.53) 20. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20) < LOD < LOD < LOD < LOD < LOD 1.51 (2.30-3.36-3.67) .330 (<LOD-1.0 (17.260-.0) 5.960 (.350-.800) 90th 13.32-9.90-37.190-1.74) 5.425-1.90-9. 130 Fourth National Report on Human Exposure to Environmental Chemicals .07 (1.20-4.90 (1.00 (.890 (.80 (4.850) 16.0 (7.88-3.51-8.10 (3.750-1.60) .0-44.70-30.63 (3.900 (.15) 14.03 (.62-8.11) .99 (1.62) 471 575 306 664 821 699 814 1122 925 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .0) 2.05-3.50) 2.50) .36-3.28) 1.24-7.90) . and 0.85-3.0 (5.23-6.35) 5.720) 2.83-3.31) .49) 17.1.0) 5.10-9.0) 2.87) 12.870) < LOD < LOD .0 (17.640 (.600 (.76 (1.730 (.40-20.07-3.30-6.70-3.640 (.770 (<LOD-1.840 (<LOD-1.510-.0) 4.080-1.12-1.0) 4.20 (1.

92 (2.22) 2.69) 2.27 (2.730-3.82-11.62 (1.04-16.270 (<LOD-.96) 2.25-38.47) .88) 17.31) .35 (.3) 3.66-47.1) 2.02-4.44) .10) 2.33 (3.29-4.7) 5.7) 4.09-3.56) 2.710 (<LOD-1.57) 1.83-11.49-2.9 (11.57-40.85-3.00-19.580) 16.33-5.69-7.11) .64-4.50) .17 (1.88 (.820 (.7) 6.04 (1.51-4.86 (3.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.9) 5.40-12.560 (.7 (6.33 (1.S.8) 2.36 (.40 (.51-44.62-17.32-6.580) 1.01 (1.10-3.41) 18.8) 1.690-5.67-6.17) 5.580-1.71 (.75) 5.5) 2.360 (.80) 3.650) 90th 10.77 (.5 (8.840-3.60 (1.5 (11.50 (4.18) * * * * * * * * .430) 1.14 (1.57 (.660) < LOD < LOD .890 (.10 (2.44-11.56 (1.700) 6.47-10.57) 8. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.84) 9.47) 5.52 (.45 (1.8) 7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.340 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30 (4.0) 4.24) 3.8) 2.590) 2.780-4.820) .28-6.25 (1.07 (2.4-34.340-.38 (2.67 (2.90-6.31) .55 (3.02) .12-4.8) 7.65 (2.59 (1.4 (4.07-21.05) .9) 6.600 (<LOD-1.860-2.930) .5) 2.670 (.630-1.1) 471 575 306 664 820 697 814 1122 924 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .2-38.740-1.12 (4.320-1.98 (4.96-25.67) 1.18) 95th 21.02 (1.830-3.91-4.580 (.240-.48 (4.260-.00) .41 (4.33-3.40-2.23-7.02 (.0 (4.6) 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 * * * * * * * * * .700) < LOD < LOD < LOD < LOD < LOD 1.748 (.08) .4) 2.450 (.790) 11.73 (4.22-27.470 (.370 (.970-3.96-8.960 (.40) 1.370-1.8) 4.390-.500 (.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.71 (2.53) .48-42.37) 4.32) 9.79 (.940-4.55) 21.340-.850-3.83 (4.64) 30.8 (20.330-1.21-3.260-.50 (2.790 (.14-6.770) .540-1.85 (1.31-18.06 (.8-33.53) 27.190-1.29 (4.540 (.11-5.25-9.88 (2.800-2.5) 7.250 (<LOD-.56) .2 (8.150 (<LOD-.5 (9.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.7) 3.620-3.18) 1.430 (<LOD-.270-.474-1.74 (2.830 (.86) .13 (2.0 (9.03) 16.48-7.33-4.39) 20.3) 2. Fourth National Report on Human Exposure to Environmental Chemicals 131 .97) .650 (.1 (5.370) < LOD < LOD < LOD < LOD < LOD 1. population from the National Health and Nutrition Examination Survey.31-7.88-3.43) .55) 21.89 (2.340-.91) 2.03) 2.67) 2.50) 11.61) 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 .80 (.310-.81-17.7 (12.1 (7.47-10.15) 9.5-40.

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Weisskopf C. Irish RM. Muniz J.12(2):134-141. National Research Council (NRC). Rosenstock L. Salvini S. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Keefe TJ. London L. Office of Prevention Pesticides and Toxic Substances. Johnson C. McConnell R. Bradman A.52(10):648-653. Lancet. Environmental Protection Agency (U. Am J Public Health 1994. Frasca G. Thompson ML. Bull Environ Contam Toxicol 1994. Terry AV Jr.php?record_id=2126&page=1. et al. Neurotoxicity among pesticide applicators exposed to organophosphates. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Saieva C.44(4):352-357. Kidd M. EPA). Myers JE. Calvert IA. Gillham R. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Occup Environ Med 2001. Seiber J. National Academy of Sciences. Available at URL: http://www.338(8761):223-227. Scand J Work Environ Health 1998. Stark A. and cholinesterase status of date dusters and harvesters in California. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Neurotoxicol Teratol 1998. Spurgeon A. Smit LA.38(4):546-563. J Occup Environ Med 2002. Rohlman D. 2004. Chrislip D. Steenland K.epa. Washington (DC).84(5):731-736. Stokes L. Stephens R. Lambert WE. Hansen S. Scherer J. Masala G. Lewis JA. 1993 [online]. vibration sense and tremor among South African farm workers. Burcar PJ. et al. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Occup Environ Med 1995. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Russo J.nap. Visuthismajarn P. Wickremasinghe AR. Takamiya K. 4/7/09 Young JG.52(2):190-195. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Effects of chronic. Pesticides in the Diets of Infants and Children.24(1):18-29. Rothlein J. Lasarev M. Available at URL: http://books. Int J Occup Environ Health 2006. metabolite clearance.12(2):153-172. Lancet 1995. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Gladstone EA. Ruberu DK. Buccafusco JJ.43(1):38-45. Muniz J. Environ Health Perspect 2005. et al. A behavioral evaluation of pest control workers with short-term. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Keifer M. Savage EP. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Am J Ind Med 1987.114(5):691-696. Caltabiano LM. Ames RG. Barr DB. O’Malley M. Arch Environ Health 1988. low-level exposure to the organophosphate diazinon. S. low-level organophosphate exposure on delayed recall. et al. U. gov/oppbead1/pestsales/01pestsales/market_estimates2001.2000 and 2001 market estimates.S. Mounce LM. Buchanan D. Aprea C. Bravo R. 1991. Robson MG. Jamal GA. Claypoole K. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. discrimination. Arch Environ Health 1975.S. Lasarev M. Lu C. Phillips J. Pilkington A. Hore P. Malathion deposition.345(8958):11351139. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Heaton RK. Santana J. McCauley L. Beach J.pdf.113(4):504-508.68(3):209-227 Maizlish N. Samuels S. Sci Total Environ 2004. Eskenazi B. Chronic neurological sequelae to organophosphate pesticide poisoning. Schenker M. Washington (DC): U. Berry H. 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. Effects of long-term organophosphate exposures on neurological symptoms. Prendergast MA. Tumino R. Petchuay C. Nell V. Environ Health Perspect 2006. Jenkins B. 1/12/09 Peiris-John RJ. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Pesticide industry sales and usage . Arch Environ Contam Toxicol 2000. van der Hoek W. Narang A.30(2):98-103. J Toxicol Environ Health A 2005. Rodnitzky RL. EPA.58(11):702710.26(2):199-209.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI.332(1-3):71-80.20(2):115-22. The Pesticide Health Effects Study Group. Vitayavirasak B. Daniell WE. Pedersen L. Neurotoxicology 2005. et al. Levy LS. May. Rothlein J. Marshall E. Dinoff TM. Weerasekera G.edu/ openbook. and spatial learning in monkeys and rats.

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

63 (8.7-23.15 (1.32-1.0) 7.47-13.90 (1.0 (13.10-17. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.20 (4.5) 7.25) 1.70 (1.09 (3.3 (8.40) 9.50-14.90 (2.0) 18.90 (1.35) 2.90) 7.60 (5.70-15.71 (6.77 (1.90 (3.0) 10. and on plants for days to several weeks.4 (10.and post-construction structural applications for termite control were to be phased out by 2005 (U.88 (1.0) 11.30-9.0) 12.31-2.52-12. For instance.67 (2. 2007).27 (7.20) 2.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40-13.13-3.30) 4.7) 9.40) 2.90-8.50 (1.0) 12.99-4.81-2.3 (10. 2005).30 (2.0 (9.8) 9. in 142 urban homes and preschools in North Carolina.51 (1.90-7. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.72) 2.32) 2.0) 9. It has low leachability.21) 3.30 (4.90) 3.70-11.00) 3.00-8. applied to structures to kill termites.4 (8.74-9.29-1.9-18..47-9.0 (7.5 (8.60-3.94 (4.9 (9.0) 6.84) 1.0 (7.10) 6.00-24.03) 1.64) 3.70-17.0 (7.0 (7.55-5.30-5.28-3.20-2. but can be detected in streams receiving runoff from application sites.50-8.50 (2.EPA.63 (2.72-4.38 (3.90-2.00) 2.25) 3.20) 4. 5598-13-0 General Information The chemical 3.92 (1.70 (1.1-16.20) 2.60-4.50 (1.3) 8.34) 1.40-10.97) 2. USGS.10 (4.51) 1.8-15.30) 5.59-2.30) 4.40 (5.0 (7.31-2.01) 1.EPA.5.95) 7.50 (2.50 (2.05-5.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.70-5.60-2.50-4.37 (4.30-2.0) 10.5-24.66-15.6) 7.97-7.28) 2. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.60-3.9 (10.45 (1.10 (1.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.68-2.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.S.0) 12.4-15.71 (1. and inhalation routes. 2921-88-2 Chlorpyrifos-methyl CAS No.0) 14. dermal.67 (1.22 (1.80 (7.S. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.26) 7.47) 1.60) 5.9) 697 660 521 701 602 947 Limit of detection (LOD.19-3.04-10.71 (2. 1999.51-2.80) 2.0) 8. Estimated intakes from diet and water have not exceeded recommended intake limits.000 pounds are used per year.2 (10.44-5.60 (2.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.20-16.78 (7.20 (2.46-2.29) 90th 7.61) 75th 3.79-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.00) 1. chlorpyrifos was no longer registered for indoor residential uses in the United States.67 (2.30-11. 2002).9 (7.77) 1.40-2.30-1.19 (1.70-16.80-8.87-6.3) 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. and sprayed to kill mosquitoes.1) 5.57 (2.10 (5.02 (7.24-1.39) 4. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.74 (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. pre.10) 2.52-2.91 (1.53 (1.80) 1.4 (9.66-4.16) 2.37) 5.37 (1.97) 2.44 (3.80) 4.86) 4.04-10.50-5.5.43-2.80-10.13 (1. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.83) 1.40-26.62-2.10 (3.0) 15.76 (1.3 (11.20-14.95 (4.40 (5. Fourth National Report on Human Exposure to Environmental Chemicals 135 .0-28.24-3.89 (2.91) 16.77-6.98-15.60 (4.8) 10.63 (1.17 (1.47-11.61-7.89-2.90 (6.0) 12.20-4.4.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.97) 7.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.35) 1.0 (10.02 (1.22) 2.30 (2. population from the National Health and Nutrition Examination Survey.90-4. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.40 (6.80) 12.80 (1.20-3.S.0) 10.59) 2.50-2.02) 1.44-2.30-12.68 (7.0) 12.20-11. Approximately 21-24 million pounds per year were used domestically from 1987-1998.4 and 0.0) 8.39-2. interval) 1. After 2001.70) 1.7) 8.20) 10. The general population may be exposed to chlorpyrifos via oral.7) 13.05) 1.09 (2. and dust. air.50-2. and is infrequently detected in ground water (IPCS.76 (1.47 (4. 2002).36 (4.43-2. Approximately 80.97) 4.77-15. It also has been applied directly on animals to kill mites.61 (1.9) 11. Exposure can also result from contact with contaminated surfaces.50-4. Chlorpyrifos is Urinary 3. staying bound to soil particles.96) 3. Survey Geometric mean (95% conf.

69 (1.31-4.3) 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 1.91-4.9 (12.1 (7.32) 1.64-2.S.93 (2. paralysis.90-9.68) 1.87-3.24-1. and producing acute symptoms such as nausea.85 (3.66 (1.29 (3.93) 5. Survey Geometric mean (95% conf.5) 5.35-1.82 (2.47-2.48 (1. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.09 (1.79-13.19) 6.78 (1.1 (10.94-14.77) 1. 2005. interval) 1.02 (5.16 (4. neurotransmission.16) 6.38) 3.45-1.24) 75th 2.1-38.24 (1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.60 (1. Urinary 3.62) 1.46 (2.92-2.05-4.97) 3.05-3.50 (4.14-8.05-1.56) 5.19-1.57) 9.22 (4.07) 1.27-1. 2006a.31) 1..46 (1.21-6.86 (3. vomiting. 2005.88 (1.34-1.01) 3.57-2. cholinergic effects.93 (4.11 (2.80) 3.19-2.15 (4.09-2.0) 6.06 (1.39 (4.88-9.94-12. Once absorbed.. Howard et al.06 (5.66) 1.49-2.85) 4. 2005.23-1.41 (1. Two observational studies of pregnant women and their offspring exposed to chlorpyrifos at environmental levels have found inconsistent relationships with birth outcomes of weight and length (Eskenazi et al.14) 1.95 (3.35) 2.42-2.00 (7.0) 12.58) 1.49-2.28) 2..6-Trichloro-2-pyridinol (creatinine corrected) Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..99) 1. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.88 (1.31-1.20 (2.88-8.27-7.12-3.57) 2.97) 3.3) 8. Betancourt et al.58 (4.52 (5.56 (1..75) 6. 1984).76 (2. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.88-10.85-4.85) Selected percentiles ( 95% confidence interval) Sample 95th 8. 2006.33 (.11-9. TCPy can also occur in the environment from the breakdown of the parent compounds..74) 1.64 (1. weakness.85) 1.21-1. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.63-2.45 (1. TCPy is more persistent in the environment than chlorpyrifos itself (U.89) 4.33) 2. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.47 (5.80-6.42 (6.97 (3.53 (2.63 (5.58 (1.8) 9.39) 6.09-1. resulting in excess acetylcholine at nerve terminals.44-6.00-13.06-4.85 (2.5.33-7.7) 7.84-6.60-3.6) 10.00) 1.66-11. and other metabolites.71) 3.88-8.22-6.70-4. Roy et al.55 (1. population from the National Health and Nutrition Examination Survey.44 (5.6) 9.92 (1. Slotkin et al. 2006.12) 1.72) 1.17-4.39 (2.33 (5.80-4. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.82) 8. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Ricceri et al.91) 10.82-4. Thus.42 (5.11) 7.26-14.33 (1.91 (3.24-5.58-5.25-12.09-3.47 (1.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.91-13. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.72) 2.86 (1.80-11.940-1.02) 7.4) 4.43-10.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .54 (2.35) 1.30-1.05) 3.99-8.56-2.05-8.24-4.97 (2.83-2.44 (5.2) 6.68) 6.25-11. In pesticide applicators.11 (2.28) 2.76 (3.82 (3. Metabolic hydrolysis leads to the formation of TCPy.75 (1.49-2.48 (2.44 (1.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.08) 6.86 (1.49 (1.36) 1..55 (4.91) 1.17-4.S.93 (1.92) 3.47 (1.65-11.24) 5.95 (1.40) 1.07) 5.56) 2..19) 3.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.56 (4.25-1. 2006b).62) 90th 5.01) 3.58) 5.30-4. and seizures..83) 1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).63 (4.03) 1.91 (4.0) 16.81) 2.12-1.22) 1.44 (6.62-7.01) 1.91) 2.81 (3.64-7.98 (7.5 (6.53-5.73 (1. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.3 (7.71 (1.22 (6.58 (1.23) 14. Based on animal data and human cholinesterase monitoring during occupational exposure.59-2.98 (6.0) 10.43 (4. 2000).55) 1. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.39-1.2 (7.97-3. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.57-2.3) 8.93) 2.65-15.00-8.24-24.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.88) 6.1-21. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.20-1.37 (1.96) 3.44 (1.59) 3.54) 5.72-2.51 (1.91) 1.EPA. 2002).83-11.3) 9.

Perera et al. 2005). Of 482 pregnant women living in an agricultural community. Aldridge JE.gov/toxpro2. Catenacci G. Lioy PJ. 2005... Aprea C.S. 2007).. Whyatt et al. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al.109(6):583-590. Freeman NC. 2005. In a probability-based sample of 102 Minnesota children aged 3-13 years. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. MacIntosh et al. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. environmental levels) and health effects is available from ATSDR at: http://www. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. 2004). representative subsample of NHANES 19992000 (CDC. EPA at: http://www. Eberly LE. 2003. U. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP.Reference values of urinary 3.. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. Berent S.e.. Carr RL. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. Seidler FJ. population (CDC. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. Burgess SC. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. Albers JW. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.. Fourth National Report on Human Exposure to Environmental Chemicals 137 . 2002).Organophosphorus Insecticides: Specific Metabolites 2004. et al.113(8):1027-1031.82(2):305-312.. Haidar S. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al.epa.S. 2004)...cdc. In Iowa farm families using several different pesticides. 1992. Occup Environ Med 2006. Chlorpyrifos exposure and biological monitoring among manufacturing workers.. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain.92(2):500-506. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Giordani B. 2001) and Italy (Aprea et al. Betta A. 2005). 2001). 2006). Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Biomonitoring studies of TCPy provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of chlorpyrifos or chlorpyrifos-methyl than are found in the general population. Additional information about external exposure (i.atsdr.EPA. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy.63(3):218220. Following crack-and-crevice application of chlorpyrifos in their homes. the geometric mean urinary TCPy levels were similar in parents and children. 2005).. 2005.S. Lotti A. Betancourt AM. et al. Environ Health Perspect 2005. Levels of TCPy in the U. 2005)..5.html and from U. et al. Slotkin TA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In Minnesota and South Carolina farmers who used chlorpyrifos. J AOAC Int 1999. Meyer A. Barisano A.. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Garabrant D.S. 2005). but levels were roughly four to six times higher than the geometric means in the U. Toxicol Sci 2006. but not chlorpyrifos. Burns CJ. urinary TCPy levels in children were reported not to have increased (Hore et al. Curwin et al. Clayton CA. 1999). Biomonitoring Information Urinary TCPy levels reflect recent exposure. Barr DB. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. Magnaghi S.. Environ Health Perspect 2001. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. 2005). Koch et al..gov/pesticides/. CDC.. 2000). References Adgate JL.S.

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Neurologic function among termiticide applicators exposed to chlorpyrifos. National Toxicology Program (NTP). Exposures of preschool children to chlorpyrifos and its degradation product 3.73:8-15. Levin ED. 4/7/09 Koch HM. Environ Health Perspect 2005. Freeman N. February 5. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Bennett DH. Hein MJ. J Expo Anal Environ Epidemiol 1999. Ryan L. EPA). mothers and fathers living in farm and non-farm households in Iowa. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. et al. Ryde IT. Slotkin TA. Hore P. Available at URL: http://www. Seidler FJ. Mandel JS. Striley C. Ricceri L. Environ Health Perspect 2004.S. et al. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Environ Health Perspect 2006a. et al. U.6-trichloro-2-pyridinol. Acquavella JF. 2005. Rauh V. MacIntosh DL. Urinary pesticide concentrations among children. Third National Report on Human Exposure to Environmental Chemicals. Ann Occup Hyg 2007. Executive summary of safety and toxicity information. Lu C. Robson M. Baker BA. et al. Zhang J.15(3):271-281. Bradman A. Nolan RJ.5.

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

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

560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. < LOD means less than the limit of detection.S. * 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 141 . Survey Geometric mean (95% conf. 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.200 (<LOD-.670 (<LOD-1. population from the National Health and Nutrition Examination Survey.S.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 .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. 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 .2.27) < 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 . Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-. 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. which may vary for some chemicals by year and by individual sample.380 (<LOD-. see Data Analysis section) for Survey year 01-02 is 0.

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

It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. 1998). 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.S. and particularly when it was ingested in granular form. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. USGS. population from the National Health and Nutrition Examination Survey. in some pest strips. since 2004.45 (<LOD-3. vegetable. It is also used for cattle ear tag applications to control flies and ticks and. see Data Analysis section) for Survey years 99-00 and 01-02 are 7.49 (<LOD-2. Inhalational and dermal routes of exposure can be significant for pesticide applicators. seed and foliar applications are planned to be phased out (U. diazinon produced wild bird kills before use restrictions were in place. which may vary for some chemicals by year and by individual sample. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine.EPA. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1842 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. 1998. Survey Geometric mean (95% conf. diazinon was widely used in residential and garden application. Once absorbed.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. Most granular formulations. but is rapidly absorbed orally (IPCS. diazinon cannot be sold for residential use. 2007).7. 2004). about 13 million pounds of diazinon were used annually on agricultural sites in the United States. and forage crops. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. an organophosphorus insecticide that is used to control insects on nuts. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. 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.S. in the past. Estimated intakes from diet and water do not exceed recommended intake limits (U. It is toxic to birds.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. Before these restrictions.S.EPA. Diazinon is not well-absorbed through the skin. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. aerial. < LOD means less than the limit of detection. and other metabolites. Prior to 2000. fruits. 2004).2 and 0. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. Fourth National Report on Human Exposure to Environmental Chemicals 143 . but these uses have been phased out.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No.

Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure.EPA considers diazinon unlikely to be carcinogenic in humans.e. Survey Geometric mean (95% conf. and producing acute symptoms such as nausea. In animals.S.45) < LOD < LOD < LOD < LOD 454 580 632 828 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. 1986 Rajendra et al.49 μg/L.atsdr. 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.gov/pesticides/.S. respectively (Baker et al.. At high doses. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. paralysis. Diazinon has moderate acute toxicity in animal studies. 144 Fourth National Report on Human Exposure to Environmental Chemicals . animal carcinogen. Olsson et al. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. 2000. and indoor applications have been documented. or reproductive toxicant (IPCS.. 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. In the U. respectively.. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants. In two nonrandom samples of United States adults and children.S. Additional information about external exposure (i. diazinon does not accumulate in tissues (IPCS. Intoxications in humans from intentional overdose.76 (<LOD-3.cdc. and seizures. cholinergic effects. 1992)..72 (<LOD-4.S. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. in the 2001-2002 subsample (CDC.. The U. resulting in excess acetylcholine at nerve terminals. vomiting.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. agricultural. teratogen.epa. environmental levels) and health effects is available from ATSDR at: http://www. Diazinon is not considered to be a mutagen. 2003). Thus.gov/toxpro2. 1998). EPA at: http://www. population from the National Health and Nutrition Examination Survey. 1986. subsamples of NHANES 1999-2000 and 20012002. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown.html and from U. Seifert and Pewnim. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. weakness. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound.. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. 2002).45 and 1. In addition to being a human metabolite of diazinon. 1998). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

et al. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Study for Future Families Research Group. Drobnis EZ. Centers for Disease Control and Prevention (CDC). Environmental Health Criteria 198. 2006). Toepel K.usgs. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Available at URL: http://www. Baker SE. Barr DB. Bull Environ Contam Toxicol 1986. In 23 children. Swan et al. Available at URL: http://pubs.50(5):505-515. Liu F.htm. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. The Quality of Our Nation’s Waters.37(4):501-507.114(2):260-263. Available at URL: http://www.S. Barr DB. Pesticides in the Nation’s Streams and Ground Water. Third National Report on Human Exposure to Environmental Chemicals. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Beeson MD.9(2):117-131. Environ Health Perspect 2003. 1992-2001. Barr DB. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Barr DB.376(6):808-815. 2005.org/documents/ehc/ehc/ehc198. Geological Survey (USGS).S. Driskell WJ. Oloffs PC. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Ann Occup Hyg 2006. Garfitt SJ.111(12):1478-1484. 2007 [online]. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon.Organophosphorus Insecticides: Specific Metabolites 2005). Rajendra W.gov/ oppsrrd1/REDs/diazinon_ired. Brunet RC. International Programme on Chemical Safety-INCHEM (IPCS).44(11):2243-2250. Oloffs PC.10(6 Pt 2):789-798. Diazinon.pdf. Semen quality in relation to biomarkers of pesticide exposure. Biochem Pharmacol 1992. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Dumas P. March 2006.inchem. 2006). EPA 738-R-04-006. EPA). 1/14/09 U. 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. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Banister E. Jones K. J Expo Anal Environ Epidemiol 2000. Drug Chem Toxicol 1986.gov/circ/2005/1291/. Diazinon. Cocker J. Environmental Protection Agency (U. Bravo R. Sadowski MA.134(1-3):105-113. Environ Health Perspect 2006. Bouchard M. Olsson AO. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Mason HJ. Toxicol Lett 2002. 4/7/09 Lu C. 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. Nguyen JV. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Carrier G. Banister EW. Atlanta (GA). Redmon JB. Seifert J. Noisel N. U.S.. May 2004. In 54 Canadian greenhouse workers. Fenske RA. Irish R. In a small number of men visiting fertility clinics in Missouri and Minnesota.epa. Swan SH. Interim reregistration eligibility decision (IRED. References Anthony J.. Needham LL. Kruse RL. Effect of sublethal levels of diazinon: histopathology of liver. Pewnim T. Anal Bioanal Chem 2003. 1998. revised February 15.

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

2006).S. 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. Pluth et al.S.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. but cholinesterase activity was not affected.. Flessel et al.atsdr.gov/pesticides/. 2001. Lu et al..74 (<LOD-5.gov/toxpro2.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. 1999). Malathion itself has not been considered genotoxic (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. 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.cdc. 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. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al.EPA. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample.5 and 5. and it is not considered an animal teratogen or a reproductive toxicant... Giri et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. EPA at: http://www. but isomalathion. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid.. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. 2002. 1999. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. IARC considers malathion not classifiable as a human carcinogen. 2004). Thomas et al. 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. Survey Geometric mean (95% conf.EPA. 1987.S. 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. 1996. 2000). 2005).S. Human studies of single oral doses between 0. 2003). Fourth National Report on Human Exposure to Environmental Chemicals 147 . Toxicity from unprotected bystander exposure during applications is rare (U. 2005.50) < 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.. 2005). Of 382 pregnant women living in an agricultural community. population from the National Health and Nutrition Examination Survey. Additional information about external exposure (i.. 2006). representative subsample from NHANES 19992000 (Adgate.e. 1990). 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.epa.S. 2006). CDC. environmental levels) and health effects is available from ATSDR at: http://www... median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC.html and from U.. 1993.

Dumoulin MJ. Ryan PB. and cholinesterase status of date dusters and harvesters in California.inchem. Prasad SB. EPA 738-R06-030. Environ Health Perspect 2001. 1992-2001. metabolite clearance. Lioy PJ. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. et al. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Eskenazi B.S. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Giri S. Dinoff TM. Toxicol Sci 2003 May. Bradman A. J Expo Anal Environ Epidemiol 2005. Giri A. Jewell NP. Mutat Res 1999.445(2):275-283. Lu C.56(10):2393-2399. Atlanta (GA). Environ Health Perspect 2006. Quintana PJ. Pluth JM. 2005. Harley K. Bravo R.9(5):494-501. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Grether JK.pdf. Toepel K. J Expo Anal Environ Epidemiol 1999. Am J Epidemiol 1990. Szyfter K. Goldhaber M. Hertz-Picciotto I.S. et al. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Samuel O. Griffith W. Freeman NC. 4/7/09 Kissel JC.109(6):583-590. March 2006. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Arch Environ Contam Toxicol 2000. Lu C. U.77:1009-1010. Environmental Protection Agency (U. Reproductive outcome in women exposed to malathion. International Programme on Chemical Safety-INCHEM (IPCS). Eberly LE. Hooper K.73(1):182-94.38(4):546-553. Petitti D. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Irish R. EPA). Jaloszynski P. Malathion deposition.132(4):794-795.514(1-2):223231. Trzeciak A.15(2):164-171. Pesticides in the Nation’s Streams and Ground Water. Blasiak J. Environ Mol Mutagen 1993. revised February 15. Hammerstrom KA. Barr DB. Centers for Disease Control and Prevention (CDC). et al. MacIntosh DL.gov/oppsrrd1/REDs/ malathion_red. Gosselin NH.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Albertini RJ. Am J Public Health 1987. Carrier G. Fenske RA.epa.S. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. O’Neill JP. Needham LL. Curl CL. Malathion (addendum). Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. 2007 [online]. Genetic toxicity of malathion: a review. Barr DB. Mutat Res 2002. The Quality of Our Nation’s Waters. Krieger RI. July 2006. Flessel P. Kedan G. Geological Survey (USGS). Swan SH.usgs. Clayton CA.22(1):7-17. Rappaport E.gov/circ/2005/1291/. Bouchard M.74(2):following table of contents. Reregistration eligibility decision (RED) Malathion. Harris JA. Barr DB.112(10):1116-1124. Barr DB. Sharma GD. A longitudinal investigation of selected pesticide metabolites in urine. Thomas D.114(2):260-263. Brunet RC. Environ Health Perspect 2004. Available at URL: http://www. 6/1/09 U. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Cancer Res 1996. Neutra R. Erratum in: Toxicol Sci 2003 Aug.org/documents/jmpr/jmpmono/v2003pr06. Available at URL: http://pubs. Nicklas JA. Weltzien E. htm. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://www.

70) 2.09-1. 1977).37) 2. It had been applied to cotton. first registered in 1948.50) 2. Estimated intakes from diet and drinking water have been below recommended limits. on cereal grains.45 (1. < LOD means less than the limit of detection.48) 90th 2.70 (2.41-4. and to a lesser extent.40-3.36-1.10-1.18-3.01) 4.790 (<LOD-. Once absorbed.44) 2. Methyl Parathion.EPA.50 (1. but by 2003.02-6.60-19. which may vary for some chemicals by year and by individual sample.10) 4.50) 1.40-4.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .60-5.26 (1. Ethyl parathion.910) < LOD .70 (2.60-36.300-.40) 1.S.67) < LOD 1.910) < LOD < LOD < LOD 1.22-3. In the 1990s.730 (<LOD-.20) 5.70 (<LOD-3.60) 1.67 (1.69) 4.90-9.0) 4.0) 3. Survey Geometric mean (95% conf.70) 2.60-24.20 (<LOD-2.50) 3.30 (1.16) < LOD 1.770 (.0) 3.00 (2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. all registered uses were voluntarily cancelled (U.11) 2.80 (1. Morgan et al.01) 695 660 518 679 603 941 Limit of detection (LOD.70-3. was once a restricted-use insecticide with limited applications on certain agricultural crops.70-6.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.80) 2.50 (2. ethyl parathion.30 (2.46 (3. and aquatic invertebrates. Many previous registered agricultural uses of methyl parathion have been cancelled (U.69 (2.298-00-0 Ethyl Parathion CAS No. and has a short half-life in soils and on plants.58) 3.34 (3.60 (4.92) 5. pulmonary.32-1.12) < LOD < LOD 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.85 (2.37-4. 2002.66 (2. peak domestic use was as high as 5-6 million pounds per year.71 (2.10 (<LOD-6. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.47) 2.32-1.28 (1.20 (2.0) 2.70-6.15-3.90-11. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion. and of the chemical nitrobenzene.30-16.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .00 (2. Fourth National Report on Human Exposure to Environmental Chemicals 149 .70-3.0) 3.61) < LOD 1. population from the National Health and Nutrition Examination Survey. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.89 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.72 (3.940 (<LOD-2.21-1.33 (1.13-1.40-4. binds tightly to soils resulting in low leachability.40) 2.21 (2.19 (.92-2.05) 4. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.EPA.28 (1.30-3.37-2. Methyl parathion is not registered for residential use in the United States.11-4.80 (2.32-3.80 (2.45) 5.1.90 (1..10-11.50 (1.. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.50 (1.70 (2.50-14.91-3. fish.40 (1.37-4.S.28-4.10 (3.0) 3. methyl parathion was rapidly absorbed after ingestion.10 (3. and oral routes can occur in pesticide and agricultural workers (Muttray et al.30-5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. Methyl parathion use is highly restricted.700 (<LOD-.40) 4.57-4.33) 2.00) 3. 2003).20-5. with limited applications in agriculture.910) < LOD < LOD .74) 5. Methyl parathion has low water solubility. more slowly absorbed through the skin.27) 2.50 (2. Given its limited use.50 (1.62 (1. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.10) 22.71 (3. 2000). Increased risk of exposure via dermal.50) 3. In animal studies..50-9.70-6.32 (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 1.79) 4.8 and 0. and eliminated rapidly from the body after absorption (Kramer et al. Both are toxic to birds. 2006).70 (3.990-1.01-4.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .S. 2007).850) < LOD .860 (<LOD-1.57) 1.70) 2.49 (1.0 (3.0) 3.61) < LOD 1.

26) 17.cdc.440 (<LOD-.. ethyl parathion.37-1.930 (.91) 1.370 (<LOD-.15-10.S.1) 2. Survey Geometric mean (95% conf.94-47.70) 3.88) 1.78-2..S.57) 6. and producing acute symptoms such as nausea.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .3) 2.97 (2.25 (2. At high animal doses of methyl parathion.55 (<LOD-3.89 (2.e.08 (1.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.90 (1.82) < LOD . gov/pesticides/. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.07) 2. accidental exposure.14-3..21) 1.01 (.720-1.2) 2.67 (3.59 (1.870) < LOD .60 (1.840 (.atsdr.html and from U. and other metabolites.13-12.20 (3.4 (3.680 (<LOD-1.56-2.33-6.30-1.930 (.39) 1. Methyl parathion is not considered genotoxic.83 (1.15) 3.96 (1. Orsorio et al. 2006.30) 3.Organophosphorus Insecticides: Specific Metabolites Metabolites”).26 (1.01 (2.29) 1.48-4. paranitrophenol.800-1. WHO.60-2.20) 3.. 2003. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. 1990.790-.940 (<LOD-1.9) 1.76-14.690-1.11-4.95) 1.38-3.880 (. 150 Fourth National Report on Human Exposure to Environmental Chemicals .540) < LOD . 2004). 2004). weakness.77-7.88 (1.29) 2.44-3.05) 4.25) 1. resulting in excess acetylcholine at nerve terminals.80 (1.87 (1. does not inhibit acetylcholinesterase enzymes. and unintentional acute or chronic high-level occupational exposure (Hill et al. Parathion and methyl parathion have high acute toxicity in animal testing. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.430 (. EPA at: http://www. Zurich et al.850-1.97-10. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.57-7.61) 4.29 (2.31-3.epa.72-2. In addition to being a metabolite of methyl and ethyl parathion.730-1.82 (2.91 (1.08) < LOD ..55) 2.S.01-3.530) < LOD < LOD < LOD .720 (<LOD-.33-3.830-1.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Lores et al.970 (. In large doses.79) 1. 1978. 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.07 (1.00 (1. 2006. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.950) < LOD .. teratogenic. Jaga and Dharmani.13) 4.20) .31) < LOD .86 (2.78 (2.640) < LOD < LOD 1. 2005. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.04) 1.980 (.7) 3.73 (1.10 (1.08-3.43) 4.79 (1.790-1.00 (1.500) < LOD < LOD . population from the National Health and Nutrition Examination Survey.23) 1. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.89 (2. Karanth and Pope et al.78-2.41-2.17) . Additional information about external exposure (i.57-2..11) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. gov/toxpro2.23) 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 .17-4. methyl parathion.04 (2.44-3.33-3. The metabolite. 1995).310-.. Slotkin et al.93 (2.80 (1.94-4. 1991).96 (1.92 (2.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . environmental levels) and health effects is available from ATSDR at: http://www.39 (1.98-7.10) 90th 2.67-2. but lists ethyl parathion as a possible human carcinogen. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS. Methyl Parathion. paralysis. U.21-21.00) 2. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS. cholinergic effects.84) 3. and seizures.71 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4. Thus.78) 2.EPA considers methyl parathion unlikely to be carcinogenic to humans. 1995.2) 2.400 (<LOD-.71) 1.35-3.97 (<LOD-4.16-4.09) 2.970 (. vomiting.60) 2.35-3.

Lewalter J. Chicago area methyl parathion response. Kramer RE.. Ashley DL. et al. et al. Harley K. Cline RE. Rubin et al. Barr DB.110 Suppl 6:1085-1091. Curl CL.S. Barr DB. Moomey CM.110 Suppl 6:1075-1078. Hill RH Jr. Arch Environ Health 1978.15(2):164-171.5 mg (500 µg)/g creatinine for workers at the end of shift. Laboratory investigation of a poisoning epidemic in Sierra Leone. a range of values several hundred times higher than levels found in the U.. Needham LL. 4/7/09 Jaga K. McCann KG. Environ Health Perspect 2002. general population (CDC. Dharmani C. Gregg M.. 2002. et al. Occup Environ Med 1999. Leng G. 1995). Third National Report on Human Exposure to Environmental Chemicals. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation.215(3):182-190. Head SL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Rev Environ Health 2006. McClure PC. Slach EF. oral or dermal administration. Barr DB. Centers for Disease Control and Prevention (CDC). Pharmacokinetics of methyl parathion: a comparison following single intravenous. 1995. DiPietro E. Bailey SL. 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. Guizzetti M. 2002). Head SL. and levels were similar or slightly lower that those in a small convenience sample of the U. McCann et al.21(1):5767.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure.112(10):1116-1124. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Atlanta (GA). Moseman RF. Alley CC. Levels of para-nitrophenol in the NHANES 1999-2000 and 2001-2002 subsamples were similar or slightly lower than those in a nonrandom subsample of NHANES III (19881994) participants (CDC. J Anal Toxicol 1990. Wellman SE. Rockhold RW. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Jewell NP. Neurotoxicol Teratol 2003. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects.inchem. Pesticide residues in urine of adults living in the United States: reference range concentrations. In a study of workers who handle parathion. Lin LI. Turner WE. Pathak S. Baker RC.. Methyl parathion: an organophosphate insecticide not quite forgotten. Available at URL: http:// www. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. J Biomed Sci 2002. Arch Environ Contam Toxicol 1977. Clark JM. Lores EM. Pope C. Runkle KD.71:99108. 2004). 2002. 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. and many residents were symptomatic (Barr et al.56(7):449553. Morgan DP. Hetzler HL. Pesticide workers may have much higher levels following pesticide applications. Role of individual susceptibility in risk assessment of pesticides. Toxicology 2005.S. et al. Kissel JC. Giordano G.. Environ Health Perspect 2002.. et al. International Programme on Chemical Safety-INCHEM (IPCS).org/documents/jmpr/jmpmono/v95pr14. Shealy DB. Bradway DE.. Hill RH Jr. Baker S. ACGIH recommends a BEI of 0. Lu C. 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. population (Olsson et al. Hill et al. 2005). 2005. 2005). Baker SE. Karanth S.33(5):270-276. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Hryhorczuk DO. 2005. Bradman A. Environ Health Perspect 2004.6(2-3):159-173. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al.14(4):213-216. Costa LG. 1999). CDC. J Expo Anal Environ Epidemiol 2005. References Barr DB. Eskenazi B. Parathion-Methyl (addendum). Environ Res 1995. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Kedan G. Weltzien E.htm. 2005. Barr JR. Griffith W.25(5):599-606. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.9:311-320.

162(2-3):219-224. Letzel S. et al. Slotkin TA. Environ Health Perspect 2006. Olsson AO.201(2):97-104.int/water_sanitation_health/dwq/chemicals/ methylparathion. 1/14/09 U. 5/19/09 Zurich MG. EPA-738-FOO-009.epa.S. Backer G. Facts. 0153. Available at URL: http://pubs. Seidler FJ. revised February 15. External and internal exposure of wine growers spraying methyl parathion.usgs. Mengle DC. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.E. Hill RH Jr. U. Ethyl parathion. Available at URL: http://www. Environ Health Perspect 2002. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Schilter B.gov/oppsrrd1/REDs/factsheets/0155fct. 2004. Environmental Protection Agency (U. Osorio AM. Kieszak S. Investigation of a fatality among parathion applicators in California. March 2006. Am J Ind Med 1991. Jung D. 1992-2001. Ryde IT. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Methyl parathion in drinking water. 1/12/07 U.S. Monnet-Tschudi F. Available at URL: http://www.who. Levin ED. 152 Fourth National Report on Human Exposure to Environmental Chemicals . EPA).20(4):533-546. Anal Bioanal Chem 2003. WHO/SDE/WSH/03. Rosenberg J. Hill G. Ohio.376(6):808-815. Nguyen JV. EPA).S.gov/circ/2005/1291/.pdf. Tate CA. Rubin C. Yacovac R.S. pdf. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. 6/1/09 World Health Organization (WHO).110 Suppl 6:1047-1051.114(10):1542-1546.pdf. Pesticides in the Nation’s Streams and Ground Water. gov/oppsrrd1/REDs/methylparathion_ired. 1995-1996. 2007 [online]. The Quality of Our Nation’s Waters.Organophosphorus Insecticides: Specific Metabolites Muttray A. September 2000. Ames RG.S.04/106. Costa LG. Available at URL: http://www. Toxicol Lett 2006. Dunlop B. Environmental Protection Agency (U.epa. Geological Survey (USGS). Case No. 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. May 2003. R.D. Esteban E. Sadowski MA. Barr DB. Toxicol Appl Pharmacol 2004. Honegger P.

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

670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .17 (.850 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 . see Data Analysis section) for Survey year 01-02 is 0.470 (.27) .210-1.840) 669 687 929 Limit of detection (LOD.200-.780 (<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 .500 (.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .300-1.610 (<LOD-1.94) .820) < LOD < LOD .Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.410 (<LOD-1.780 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.840 (.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .210 (<LOD-. Survey Geometric mean (95% conf.55) .07) . population from the National Health and Nutrition Examination Survey.210-.21) < LOD .430 (<LOD-.760 (<LOD-.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.740 (.S. which may vary for some chemicals by year and by individual sample.670 (<LOD-1. 154 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf.580-1.700-.15) < LOD . < LOD means less than the limit of detection.740-1.950) < LOD < LOD 1.2. interval) Selected percentiles ( 95% confidence interval) Sample 95th .680 (<LOD-.S.31) .780 (.700-1.64) .250 (<LOD-. population from the National Health and Nutrition Examination Survey.780 (.

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

Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers. such as piperonyl butoxide. They are ranked as having moderate acute oral toxicity. and sumithrin) are also registered for use in mosquito-control programs in the United States.S.S. 2002). bind to soils. and greenhouses. Soderlund et al.. and deltamethrin have been used frequently on cotton. and are rarely detected in ground waters (USGS. 2002. 2003. or carbamate pesticides.. Outside the U.2-Dibromovinyl)-2. by either ester hydrolysis or hydroxylation. About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U.2-Dichlorovinyl)-2. 1992). 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-(2.2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. Unmetabolized pyrethroids have been measured in breast milk. resmethrin. After absorption from inhalation or ingestion. Woollen et al. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides. solvent oils.. The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. but pyrethroids are highly toxic to fish and some aquatic invertebrates. 1999. EPA. 2007). but may be poorly transferred across the placenta (ATSDR. and synergists. 1992). where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al. 2003. Leng et al. 2002). Certain pyrethroid insecticides (such as permethrin. Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. Pyrethroids are not well absorbed through the skin (ATSDR.EPA.2-Dichlorovinyl)-2. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings.. Woollen et al. agricultural fields. cyfluthrin. Generally. This class of pesticides has low toxicity in birds and mammals. pyrethroids are rapidly metabolized..S. and then eliminated over several days in urine and bile (Kuhn et al. deltamethrin has been used for indoor protection against mosquitoes that carry malaria. they are not persistent in the environment due to their rapid degradation within days to several months.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals . There are about 30 different pyrethroid pesticides in use. 2005. cypermethrin. in some situations replacing the use of DDT. 2005). Compared with other classes of insecticides such as organochlorines. The table shows the urinary pyrethroid metabolites measured in this Report. warehouses. They are also applied on livestock to control insects. organophosphorus. 2006a. 1997. Soderlund et al. WHO. pyrethroid pesticides have less acute toxicity in animals and people. animal facilities. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies.. Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown.Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins. In agriculture.2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations. which are natural chemicals found in chrysanthemum flowers.. Adverse effects from large doses are related to the action of pyrethroids on the nervous system. 2006b). Estimated intakes from diet and drinking water are below recommended limits. Pyrethroid pesticides have low volatility. so usage is restricted near water (U.. followed by conjugation.

In developing rodents.atsdr.S. fenvalerate. hypersensitivity. Caudle WM. Song L. Xenobiotica 1997. Bull Environ Contam Toxicol 1999. Estrogenic and antiprogestagenic activities of pyrethroid insecticides.html. Shukla Y. Pogo BG. Elwan et al.. salivation. Leng G. Thomson BM.211(3):188-197. Shaw IC. Lewalter J. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Kim IY. 2001. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. et al. Berger-Preiss E. and permethrin) in the Hershberger and uterotrophic assays. Toxicol Appl Pharmacol 1991. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. 1998.27(12):1273-1283. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002.62:101-108. Eriksson and Fredriksson. Salzgeber SA. Shafer. 2003. Leng G. bioallethrin and deltamethrin. Okuno Y. and striatal dopamine levels in male and female rats.cdc. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays.. Int J Hyg Environ Health 2002.8(1):197-202. WHO. Garey and Wolff. Neurosci Lett 2001.. Bernardi MM. 2005). Seth PK. Chen JH. Wieseler B. Additional information about pesticides is available from U. 2000. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Yang J. References Agency for Toxic Substances and Disease Registry (ATSDR).html. Estrogenicity of pyrethroid insecticide metabolites. Neurotoxic effects of two different pyrethroids. Hu JY.gov/toxpro2. Ose K. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Hu et al. Elwan MA. Moniz et al... Fourth National Report on Human Exposure to Environmental Chemicals 157 . Ranft U.gov/toxprofiles/ tp155. 2003. 2001. Varoli FM. 2004. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. 2002.27(4):609-614. Soderlund et al. Wang SL. dopaminergic. Idel H. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR... Regul Toxicol Pharmacol 2002. September 2003. cdc.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Garey J. EPA at: http://www. Yamada T. Lee SJ. Biochem Biophys Res Commun 1998. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate.50(2):245-255.23(6):665-673. Kang IH. Neurotoxicol Teratol 2005.35(2 Pt 1):227-237. and seizures (ATSDR. Eriksson P. Kunimatsu et al. Environ Health Perspect 1999.. Toxicological profile for pyrethrins and pyrethroids.. Indoor pyrethroid exposure in homes with woollen textile floor coverings. on immature and adult mice: changes in behavioral and muscarinic receptor variables.gov/pesticides/ and from ATSDR at: http://www. 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. Lazarini et al. Shin JH.1/15/09 Aziz MH. 2005). tremor. Toxicol Appl Pharmacol 2006. Kuhn K. Spinosa HS. neurochemical changes in cholinergic. In California. 2005). Agrawal AK.205(6):459-472. Abell AD. Available from URL: http://www. Florio JC. Kuhn KH.. Leng G. J Environ Monit 2006. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. McCarthy et al. Kunimatsu T. 2005). 2006). choreoathetosis. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR.. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Generally. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Garey J. 1991. Neurotoxicol Teratol 2001. et al. Kim HS. Lemonica IP. Bernardi MM. Leng A. et al. 2006. Lazarini CA.300(3):161-165. Idel H. Sunami O. 1999.108(1):78-85.atsdr.. 2006. Kim TS. McCarthy AR. Wolff MS.. Go et al. Moniz AC. 2002). Adhami VM. Effects of prenatal exposure to deltamethrin on forced swimming behavior.107(3):173-177. et al. Levsen K. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Zhao RC. Pauluhn J. Guillot TS. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Fredriksson A. Go V. epa. Pyrethroid pesticide-induced alterations in dopamine transporter function. 2002). Ray et al. Kim et al. Wolff MS. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Cruz-Casallas PE. 2003. 2003. Sugiri D. J Reprod Dev 2004. Kamita Y.251(3):855-859.8(1):18-21. Miller GW. Richardson JR. motor activity.

S.10.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005.22(8):983-991. Available at URL: http://www. Available at URL: http://whqlibdoc. 5/26/09 Woollen BH.S. Rev Environ Contam Toxicol 2006. sumithrin synthetic pyrethroids for mosquito control. Available at URL: http://pubs. Environmental Protection Agency (U. June 2006b. Safety of pyrethroids for public health use.Pyrethroid Pesticides Ray DE. J Toxicol Clin Toxicol 2000.186:57-72. Piccirillo VJ. Soderlund DM. Pesticides in the Nation’s Streams and Ground Water. Revised February 25.S. 5/26/09 U. EPA).htm.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. 2005. Spencer J.epa. Forshaw PJ.171:3-59.who. Meyer DA.htm. Lesser JE.S. Mullin LS.S. EPA). pdf.S. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. Available at URL: http://www. synergies. et al. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Xenobiotica 1992.pdf. 19962002. Environmental Protection Agency (U. 5/26/09 U. U. Pesticide and Evaluation Scheme. Permethrin. 2007. Pyrethroid illnesses in California. Sheets LP. Laird WJ. Crofton KM.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Marsh JR. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . 1992–2001. O’Malley M. June 2006a. resmethrin. Geological Survey (USGS). Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).gov/ circ/2005/1291/. Shafer TJ. Reregistration Eligibility Decision for Cypermethrin.113(2):123-136.gov/oppsrrd1/REDs/cypermethrin_red. Available at URL: http://www. Pyrethroid insecticides: poisoning syndromes. Toxicology 2002. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs.epa. Sargent D. 5/26/09 U.38:95-101. Environmental Protection Agency (U. EPA). World Health Organization (WHO). Clark JM.usgs. April 2002. and therapy.S. Environ Health Perspect 2005. March 2006.epa.

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

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.2. 160 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.S.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. Survey Geometric mean (95% conf.2 and 0. 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. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.

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

Williams RL.186:57-72.206(2):85-92. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Int J Hyg Environ Health 2006. Int J Hyg Environ Health 2006. Human exposure to indoor residential cyfluthrin residues during a structured activity program.209(3):221-233.77(1):67-72. Environ Health Perspect 2001.Pyrethroid Pesticides References Baker SE. Ball M. Angerer J. Hadnagy W. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.109(3):213-217. Angerer J. Heudorf U. Int J Hyg Environ Health 2003. 19962002. Sugiri D. Angerer J. Hoppe HW. Heudorf U.13(2):112-119. Rev Environ Contam Toxicol 2006. Ranft U. Arch Environ Contam Toxicol 2004. Leng G. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Seiwert M. Kolossa-Gehring M.46(3):281-288. Olsson AO. Angerer J. Schulz C. Atlanta (GA). Becker K.209(3):293-299. Heudorf U. Centers for Disease Control and Prevention (CDC). O’Malley M. Third National Report on Human Exposure to Environmental Chemicals. et al. Butte W. Spencer J. Berger-Preiss E. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Idel H. Bernard CE. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Krieger RI. 2005. Pyrethroid illnesses in California. Barr DB. J Expo Anal Environ Epidemiol 2003. Int Arch Occup Environ Health 2004. Drexler H.

120-.380-.470 (.210-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-Dichlorovinyl)-2.870) 1.11) .110 (<LOD-. 52315-07-8 CAS No.920) 1.490-1.28) 671 680 518 701 591 957 Limit of detection (LOD.210) .200) .140 (.180) .270 (.740-1.54) .530 (.120-.610) .50) . trans-permethrin.570 (. Biomonitoring Information Urinary levels of cis.13 (.820 (.370 (.500 (.300 (.740 (.570-.880 (.500 (.680 (.160 (.580) 1.120-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 1985.220-.220-. Kuhn et al.2-dichlorovinyl)-2.740-2.44 (.710-1.370-.08) .200-.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.260 (. but it can also reflect exposure to cis-3-(2.68 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .300 (.262) * * * < LOD < LOD .170 (.12 (.600 (.2-dichlorovinyl)-2.280-.950-2.430-. and trans-cyfluthrin.410) .270 (. cis-permethrin.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.790-1. Survey Geometric mean (95% conf. 1985.420-.or trans-3-(2. Kuhn et al.68) .15) .770) .310) .380 (.24) 1.210) 90th . The presence of cis-3-(2.790) .07 (. 1999). The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.47 (.53) .300-.670-1.470-1.68359-37-5 Cypermethrin Permethrin CAS No.110-.690) .2-dichlorovinyl)- CAS No.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.220-.650-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.32) .610) .200-.710) ..1.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.200) .510 (.790 (.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .490-1.410) .280 (.380) .770-1.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George. the presence of trans-3-(2.230) .630-.730 (.200-.150 (.160 (.202 (.68) .380-.. and ciscyfluthrin.330) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.220-.43) . more of the trans-metabolite than Urinary cis-3-(2.910-5.220) . Cyfluthrin. population from the National Health and Nutrition Examination Survey.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 .200 (.2-dichlorovinyl)-2.780) .160 (<LOD-.340) .670 (. Generally.640 (.80) .140 (<LOD-.600) .960 (.890 (. In the body.730 (.890 (.630) .35) 1. < LOD means less than the limit of detection.700) .670-1.250 (.1 and 0.490-.35) . which may vary for some chemicals by year and by individual sample.240) .850 (.380-. Similarly.630 (.670-2.2dichlorovinyl)-2.155-.21) .2dichlorovinyl)-2.520) .490-.630) . transcypermethrin and trans-cyfluthrin.340) .77 (.250-.and trans-isomers. The chemical trans-3(2. ciscypermethrin and cis-cyfluthrin.730 (.2-dichlorovinyl)2.600-1.400-.740) 1. but can also reflect exposure to trans-3(2.300-.680-3.580-1.110-. trans-cypermethrin.270-.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.S.350) .28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . cis-cypermethrin.460-.120-. Fourth National Report on Human Exposure to Environmental Chemicals 163 .240) .510 (.200) < LOD < LOD < LOD .460 (.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.340-.330 (.110-.790-1.180 (.510 (. cis-3-(2.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.550) .900 (.270 (.460-1.440 (. 1999).

138 (. Survey Geometric mean (95% conf.640-1.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC. 2005).420 (.190) .340) .33) .08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .67 (..640 (.270 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.750-1.700-2.300) .300) ..640-1.59 (1. 2005).520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .and trans-3-(2.410) .2-dimethylcyclopropane carboxylic acid did not increase.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.450-. 2006.2-dichlorovinyl)-2.710-3. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.440 (.550 (. In a study of volunteers. Cyfluthrin.190) .780) 1.49) .11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .220) .14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.130-..440-.21) .680-1.S.2-dichlorovinyl)-2.700) .2dichlorovinyl)-2.Pyrethroid Pesticides 2.390-.250) 90th ..2dichlorovinyl)-2.120 (. In the same residents. 2006) and 1177 urban adults and children (Heudorf et al.230-. 2002).430-.12 (.470-1.230 (.170 (.390 (.260-.200-.400-1.350 (. 2003).340) .450 (. 2005). urinary trans-3-(2. urinary levels of cis-3-(2.320-.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.370-.280-. Other studies have provided evidence that urinary levels of cis.390-. population from the National Health and Nutrition Examination Survey. Lu et al.170 (.440 (.250-. In these volunteers. post- Urinary cis-3-(2.540) .640-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.170) < LOD < LOD < LOD ..680 (.80) .550) .2-Dichlorovinyl)-2.580-1.11 (. 2002).150-.450-1..680-1.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al. the median and 95th percentile of urinary levels of cis-3-(2.29 (. 2001) showed urinary levels of cis.570) .2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.2-dichlorovinyl)-2.380 (.200) . median urinary levels of trans-3-(2. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.560) 1.340-.104-.160 (<LOD-.430 (.320) .430-1.230-.560) .640) 1. 2004).590) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.250 (<LOD-.59) .300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.530 (.200 (.750 (.150-.880) ..12-2.11) .220 (.440-.11) .540 (.180 (.. 2004.810 (. 2006).. In a study of urban residents in Germany (Berger-Preiss et al.280 (.900 (..540 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.510-1.290-.580) . Studies in Germany of 396 children and adolescents (Becker et al.550-1. 2005).240 (<LOD-.250-. Schettgen et al.150-.250-.800 (.200-.370-.350) .080-.260 (.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 .290) .530 (.780 (.290) . 2001.380-. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.300 (.890) .290 (. 164 Fourth National Report on Human Exposure to Environmental Chemicals .182) * * * < LOD < LOD .11) 1.600 (.700) .300-.140-.400 (.and trans-3(2.31) .270-.24) . 2006.260) . representative NHANES 2001-2002 subsample (CDC.S.03) 1.250) . 2003).690-1.230-.370-.830) .590 (.220 (.33 (.380) .890 (..180-.210-.360-1.260 (.500 (.840 (.550-1.840 (.260 (.270) .710 (.270) .59) .920 (.250) . 2005) In a small group of indoor pest-control operators.67) .190 (.37) .2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.550) .2-dichlorovinyl)-2. 2006).2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.

780 (. Biomonitoring studies on urinary levels of cisor trans-3-(2.69) 1.56) 2.410 (<LOD-.4 and 0.90) 1.20 (.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .95) 3.910-1.68) 1.470 (<LOD-.68-3.420 (<LOD-. < LOD means less than the limit of detection.2-dichlorovinyl)-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.920-1.4.54) 4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.530) .470 (.500-.11-2.490 (<LOD-.480-.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .60) 1.08-6.89 (2.70) size 1976 2525 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin. trans-Cypermethrin.49-3.560 (.41 (1.500 (.40 (1.2dichlorovinyl)-2.S.48) 4.and trans-3-(2.560 (.400-.87 (1.700-1.97-11. Fourth National Report on Human Exposure to Environmental Chemicals 165 .68-2.20 (.76-3.670) .39-5.62 (1.77) 2.680-1.800-1.17-1.25-3.77 (1.5) 2.11-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.41-14.850-1.50 (1.01 (1.17 (.85) 4.54 (1.56) 2.Pyrethroid Pesticides application median urinary levels of summed cis. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.03-1.20 (.660) 1.63) 1.12-6.07 (1.19 (2.14-6.56 (1.56 (1.43) 2.860) .14-2.16) 1.400 (<LOD-.08) 1.03-1. which may vary for some chemicals by year and by individual sample.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer. 2005).28 (2.2-Dichlorovinyl)-2.500) .460-.23) 2.27 (1. Survey Geometric mean (95% conf. however.39 (1. 2005).940 (.55-5.810-1.60-4.7) 2.13) .550 (.560 (.19) 1. Finding a measurable amount of cis.440 (<LOD-.76-4. The maximum post-application urinary levels.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.66) 691 680 518 690 595 954 Limit of detection (LOD.410-.55-3.2-dichlorovinyl)-2. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.910-1.17 (.68) 2.91 (1.610) 1.410-.520-.64-4.23 (.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.830-1.77) 1.35) 1.620) < LOD 2.07-3.820) .410 (<LOD-.10) 2.08-4.55-4.59 (1.670) .570) 90th 1.14) 1.580 (.19 (3.94 (1.63) 1.84 (1.460-.or trans-3-(2.520) .68) 1.42) 1.750) .37 (1.69 (1.49-5.710 (.60) .730) .09 (.49-3.840-1.01) 4.760) .81) 2.25 (1.42 (2.22 (1.26 (.700) .2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.28 (1. population from the National Health and Nutrition Examination Survey. Urinary trans-3-(2.66) .970 (.490-1.95) 2.

86 (2.47 (1.530 (<LOD-.700 (.610-.900 (<LOD-1.08 (.540) .S.27-2.98 (1.75 (1.720-1.00) 5.560 (.48 (1.44) 2.39 (1.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.470-.55 (2.740) .580) .28) 2. 166 Fourth National Report on Human Exposure to Environmental Chemicals .19 (1.07-1.19) .55 (2.970 (.800-1.42 (.40-2.3) 2.48-2.35) 1.520 (<LOD-.67 (2.60 (1.13) .660) .56 (1.37 (1.60) 2.07) 2. population from the National Health and Nutrition Examination Survey.89) 2.15-3.640) .00 (1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.730) .08 (.700-.530 (.87) 1.2-Dichlorovinyl)-2.480-.720-1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .770) < LOD 2.91 (1.700 (.29) 1.57 (1.07-3.47-2.22-2.800-1.68) 3.12 (.33 (1.56-5.15) 3.02-1.Pyrethroid Pesticides Urinary trans-3-(2.00) 1.930-1.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .750) .45-2.65) 1.31 (2.31) 1.27-2.15 (1.13) 1.36) 2.87) 1.410-.33-1.12-1.570-.33-2.30-3.15) 2.64 (1.500-.87-3.880-1.22) 1.60) 2.91-11.880 (<LOD-1.22-1.47-2.780 (<LOD-.580 (.570 (<LOD-. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00-5.850-3.36 (1.57) 3.20-2.780) .880 (.74) .07) 2.850) 1. trans-Cypermethrin.61) 1.34-4.91) 1.35 (1.74) 2.34-3.81 (2.850) .19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .30-6.87-8.16 (1.41) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.15-3.56-2.780) 90th 1.15-3.20 (1.39) 1. Survey Geometric mean (95% conf.55 (2.65 (2.720 (<LOD-.760 (.820-2.45 (1.70 (.80) 1.87 (1.31 (.42) 1.440-.11) .07-2.26 (1.00) 1.670) .470 (.570 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides.134(1-3):141-145. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int J Hyg Environ Health 2006. Int J Hyg Environ Health 2006. Bravo R.209(3):221-233. Berger-Preiss E. Leng G. Int J Hyg Environ Health 2002. Angerer J.77(1):67-72. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Schulz C. Environ Health Perspect 2001. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Heudorf U. Angerer J. Bartell S. Angerer J. Wieseler B. Angerer J. Berger-Preiss E. Drexler H. Schettgen T. J AOAC 1985. Levsen K.Pyrethroid Pesticides References Becker K. Sugiri D. Angerer J.209(3):293-299. George DA. Barr DB. Hoppe HW.62:101-108. Idel H. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Idel H.114(9):14191423. Heudorf U. Kuhn K. Leng G. Ball M. Biological monitoring of workers after the application of insecticidal pyrethroids. Int Arch Occup Environ Health 2004. Ranft U. Hadnagy W. Int J Hyg Environ Health 2003. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.76(7):492-498. Hardt J. Angerer J.109(3):213-217.205(6):459-472. Environ Health Perspect 2006.206(2):85-92. Seiwert M. Heudorf U. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Int Arch Occup Environ Health 2003. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. et al. Lu C. Kolossa-Gehring M. Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals. Pearson M. Leng G. Ranft U. Drexler H. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Centers for Disease Control and Prevention (CDC).68(6):1160-1163. Heudorf U. Bull Environ Contam Toxicol 1999. Sugiri D. 2005. Butte W. Permethrin and its two metabolite residues in seven agricultural crops. Idel H.

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

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 169 . Survey Geometric mean (95% conf.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-Dibromovinyl)-2.1 and 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Pyrethroid Pesticides Urinary cis-3-(2.1. < 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. which may vary for some chemicals by year and by individual sample.S.

Survey Geometric mean (95% conf. 170 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.2-Dibromovinyl)-2. * 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 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.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.Pyrethroid Pesticides Urinary cis-3-(2.

Batres LE. Drexler H. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Heudorf U. Angerer J. Kolossa-Gehring M.htm. International Programme On Chemical Safety (IPCS). [online] 1990. Deltamethrin. Angerer J. Hoppe HW. Environmental Health Criteria 97. Carranza C. Environ Health Perspect 2001. Atlanta (GA). and genotoxicity in exposed children. Angerer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Third National Report on Human Exposure to Environmental Chemicals. Heudorf U. Int J Hyg Environ Health 2006. et al.113(6):782-786.77(1):67-72. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. et al. Grimaldo M. Available at URL: http://www. 5/26/09 Ortiz-Perez MD.209(3):221-233. Int Arch Occup Environ Health 2004. Seiwert M. Environ Health Perspect 2005.org/documents/ehc/ehc/ ehc97. Heudorf U. Ball M. 2005.inchem. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Int J Hyg Environ Health 2006. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Schulz C. Torres-Dosal A.109(3):213-217. Angerer J. toxicokinetics.209(3):293-299. Lopez-Guzman OD.Pyrethroid Pesticides References Becker K. Centers for Disease Control and Prevention (CDC). Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Butte W.

52315-07-8 CAS No. CDC. representative NHANES 2001-2002 subsample (CDC.S. Thus. 2005). Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. (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. 2003). In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. 2005). Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. In a small group of indoor pest-control operators. 2005).. CDC. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the 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.. 2005). Fenpropathrin Permethrin CAS No. Following residential spraying with deltamethrin for malaria protection in Mexico. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. 68359-37-5 Cypermethrin Deltamethrin CAS No.. 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. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 2005).. Saieva et al. 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. Hardt and Angerer. Baker et al.. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. In one study of 145 urban residents in 80 private homes in Germany. 2006. 52645-53-1 Tralomethrin CAS No. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In the New York City study. 2006). 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. CDC. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides.Pyrethroid Pesticides Cyhalothrin CAS No. 2005). Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. 39515-41-8 CAS No. 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. 52918-63-5 use and house dust levels (Lu et al. 2005. 2004). Becker et al. mean peak urinary levels of 3-phenoxybenzoic acid in children increased at least sixtyfold over non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (OrtizPerez et al.. 2003... 2002. 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 . 2003. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. A study of 396 German children (Becker et al.

62) 5.18 (1.680 (.550-.16) 1.69) 3.440) .387) .364) .271-.340) 75th .710 (.227-.570-1.34) 8.297 (.750) .260-.273 (.210-.23 (2.520 (.250 (.30) 3.800) 1.370) .35 (1.820) .89-71.34-6.79) 3.295) .330) .670 (.12 (.260 (.49-2.320) .373) .270 (.230-.510-.233-.406) .200-.311 (.86 (1.350-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.266-.1) 3.1 and 0.830) 90th 1.384) .740 (.490-.25-7.27-2.265-.25-4.830-2.700 (.240 (.41-3.73) 1.02-6.200-.13 (.21 (2.62-8.630) .35) 2.190-.434) .32 (2.321 (.560-.288-.374) 99-00 01-02 99-00 01-02 99-00 01-02 .230 (.43) 3.330) .75 (1.14-6.76 (1.34 (2.1.600 (.25 (2.8) 3.230-.90) 1.300) .12) 4.292-.570-.33 (1.38 (2.04) . Fourth National Report on Human Exposure to Environmental Chemicals 173 .81 (1.29-1.27-2.38 (2. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.16-1.250 (.288 (.25 (2.325 (.46) .160-.454 (.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .26-2.33) .190-.72 (1.260 (.41-2.601) .45 (2.18 (2.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.71 (1.49-2.52-4.470-.32 (1.780) 4.810) 1.369) .64) 697 680 524 701 603 957 Limit of detection (LOD.78) 1.990) .49 (1.33 (2.230 (.430-.250-.360) .35 (2.32-21.490) .48-2.05) 1.298 (.940) 1.260 (.S.560-1.78 (1.83-11. interval) .54) 1.620-1.700-1.220-.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 .427) .27-11.292 (.246-.42-2.60) .63-3.340) .586) .226-.12) .362) .44) 5.53-3.270) .510-.35) 1.25-1.05) .01 (1. population from the National Health and Nutrition Examination Survey.740 (.51-6.49 (1.238-.50 (2.52-5.314 (.35) 2.230-.595) .417 (.590 (. Survey Geometric mean (95% conf.315 (.280 (.300 (.320) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.36) 1.353 (.320) . Deltamethrin.530-.730 (.26) 2.352-.190-.41) 3.850) .870 (.250 (.530-.640 (.78) 6.240 (.430-.820) .160-.328 (.750-1.45-5.277-.290 (.355) .390) .960 (.276-.62-6.320) .800 (.65-2.1) 3.750) .336 (.610) .63 (3.55 (1.710 (.428-.51-3.03 (3.190-.30 (.850) .28) 1.65 (1.314) .340) 1.760 (.253-.450 (.53) 1.560-.247-.267 (.04-5.210-.1) 3.300 (.320 (.13) .26) 2.30 (1.590-.46) 2.420) .300 (.92-3.56-5.78) 1.48-2.200-.39) 2.507 (.840-1.650 (.41 (1.69 (1.93 (1.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .180-.

48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .400-.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.446) .216-.640 (.270 (.17 (.534) .200-.53 (1.80) 4.290-.22 (1.310) .420-.36-6.234 (.220 (.500) .370-.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .250) .13-1.270-.309) .48 (1.62) 1.49 (1.40) 2.275 (.437) .41-4.88) 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 .13 (.83 (1.280) .330) 1.590) .05-3.27) 1.253) .280 (.04 (.10 (2.41) 1.930) 1.160-.240-.362 (.88-5.44 (1.210 (.67 (1.840-1.274 (.240-.580) .400) .730-1.328) .25-5.264 (.75-8.240 (.84 (1.490 (.04 (3.64-5.590) .43 (1.380-.270) .230) .11 (.280) .03-1.860-1.83) 1.590) .63-3.240 (.330) .490-.378 (.410) .750-1.350) .390-.240-.400-.49-2.230-.190-.329) .280 (.720) 90th 1.309 (.95) 1.299-.200-.530-.810) 1.490 (.00) 1.329) .S.178-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.52) 2.240-.44) 2.36 (1.460-.210-.67) 1.300-.37 (1.670) 3.380 (.16-4.91 (2.387) .60-4.650) .290) .590-1.00) 5.730) .94 (1.74) 3.02-1.86 (1.261 (.40 (1.630) .220-.357) .73-4.25-2.560 (.440-.00) 1.91-4.190 (.17-1.229-.32 (2.510 (.261-.330) 75th .19) 2.300-.320) .550 (.246 (.81 (1.270) .321-.21-4.250 (.330) .0) 3.640 (.73) 1.540 (.316 (.90) 3.610 (.96 (1. population from the National Health and Nutrition Examination Survey.330 (.760) .37) 1.91) 9.06-3.63) 1.202-.370 (.43) 1.460-.480-.09-2.61-2.55 (1.21 (1.39) 1.440-.860-1.930) .240 (.02 (2.238-.335-. Survey Geometric mean (95% conf.49) 1.423 (.200-.210 (.13-1.72 (1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.272) .677) .09) 3.190-.35-3.365) 99-00 01-02 99-00 01-02 99-00 01-02 .09 (.510 (.35) .224-.43 (2.450 (.200-.700-1.09-2.35) 1.960-1.480 (.440-.550 (.372) .720 (.323 (.271-.49) 3.225-.580 (.11 (.67 (1.173-.52 (1.227 (.670) .230-.55) 3.19-6.272 (.311 (.07) 2.530-.35 (1.15-2.510 (.280-.240 (.51-7.07-5.60) 1.150-. Deltamethrin.54 (1.410-.270 (.550 (.350 (.290) .860 (.280 (.274-.278) .312 (.91) .570) .730) .25) 2.19 (2.62) . interval) .226-.250 (.401) .03 (.740) .43-64.

Barr DB. Becker K. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Carranza C.46(3):281-288. Sugiri D.111(1):79-84. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Lapinski R. Obel J. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. urban cohort. Exposure to indoor pesticides during pregnancy in a multiethnic. Pearson M. Godbold J. Idel H. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Arch Environ Contam Toxicol 2004. Lu C. Int J Hyg Environ Health 2002.205(6):459-472.206(2):85-92. Environ Health Perspect 2005. Barr DB. Ranft U. Seiwert M. Ortiz-Perez MD. Leng G. Idel H. Sugiri D. Int J Hyg Environ Health 2003. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Berger-Preiss E. Int J Hyg Environ Health 2006. Bravo R. toxicokinetics. Liu Z.113(6):782-786. 2005. Hadnagy W. Int Arch Occup Environ Health 2003. Angerer J. et al.Pyrethroid Pesticides References Baker SE. Bartell S. Hardt J. Torres-Dosal A. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Lopez-Guzman OD. Berkowitz GS. Deych E. Centers for Disease Control and Prevention (CDC). Kolossa-Gehring M. Grimaldo M. Batres LE. Biological monitoring of workers after the application of insecticidal pyrethroids. Levsen K. Leng G. Environ Health Perspect 2006. et al. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Ball M.76(7):492-498.114(9):14191423. Angerer J. et al. Atlanta (GA). Hoppe HW. Environ Health Perspect 2003. Berger-Preiss E. Third National Report on Human Exposure to Environmental Chemicals. Ranft U. Olsson AO.209(3):221-233. and genotoxicity in exposed children.

see Data Analysis section) for Survey years 99-00.150) .250 (.100 (.095-.300-.175 (.190 (. and 03-04 are 0.210-. It is also used in paints. Stibine is a metal hydride form of antimony used in the semiconductor industry.126-. enamels.240) .160 (.400 (.210 (.280-.290-. People are exposed to antimony primarily through food and.320 (.360 (.135) * .146 (.160-.510) .109-.330) .180-.169 (.210 (.330-.158 (.270) . storage batteries.260-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.157) .490) .154-. and pewter.170) .130 (.154) .200 (.140) .310) .130) .230) . fireworks.190 (. Workplace exposures can occur at smelters. It is used in metal alloys.130-.400 (.160) .230 (.330) .240 (.130 (.360 (.220-.200 (.130-.080) .220-.310 (.100) .180-.220 (.350) .190) .080-.230 (.230-.120 (.160-.170-.150 (.095 (.04.130 (.350) .400) .150 (.160 (.350 (.350) . distribution.390) .100 (.500) .090 (<LOD-.128 (.280-.270) .130-.136-.108 (.079-.100-.240 (. water.320) Total .190 (.240-.200-.210) .200 (.710) .200 (.170-.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 . ammunition.100-. castings.110-.180-.120-.290 (.250-.230-.170 (.420) .250 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.S.180-. < LOD means less than the limit of detection.210) .180) . solder.142 (.390) .176 (.080) .210) .115-.090) 75th .128 (.330-.230-.190) .470 (.200) .130 (.150-.360) .190 (.190-.148-.430 (.390 (.117-.350 (.150 (.220) .120-.160 (.180 (.320-.330) .440) .120 (.Metals Antimony CAS No.350 (. and refuse incinerators that process or release antimony.087-.141-.320-.260) .390-.320 (.108-.110 (.088-.130) .140) .132 (.350 (.150) . often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.110-.130) .260 (.290-.197) .310-. and +5.280 (. interval) .490 (. sheet and pipe metal.140) .090 (.440) .340 (. and excretion of antimony vary depending on its oxidation state.125 (.300) . 0. and glass.600) . metal bearings.200 (.190 (.098-.130-.280-.140) .145 (.160) .230) .143 (.410-.150) 90th . coal-fired plants.137) .130) < LOD .220-.07. which may vary for some chemicals by year and by individual sample.560) .220-.120) .190) . and 0.112-.230 (.260 (.140 (.180) .310) .140) .160) .180 (.260-.390) .156-.250) . The absorption. or other substances containing antimony is another means of exposure. 7440-36-0 General Information Antimony is found in ores or other minerals.140 (.220) 95th .130-.103) .360) .330 (. +3.144) .390-.115) .070 (<LOD-.190) .390) .200) .180 (.160-.130 (.530) . and as a fire-retardant in textiles and plastics.240 (.340) .117-.280) .470) .154) .120) .184) .170-.270 (.142) * Sample size 2276 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .250-. 0.260) .320-.122 (.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.390-.140 (.360-. 01-02.140 (.119) .170-.250-.230-.310 (.130-.150-.099 (.123 (.350-.130 (.120-.130 (.120 (.110) .200) .114) .350 (.350) .260) .270-.161) .133) * .400-.134-. Antimony can exist in one of four valences in its various chemical and physical forms: -3.340 (.310 (.310-.190) .400) .200-.140) .190-. population from the National Health and Nutrition Examination Survey.460) .160) .131-.280-.120-.160-.430 (.090-.410) .280-.160) .270 (.120-.105 (.070 (<LOD-.200-.240-.250 (.460 (.180-.300) .120-.170 (.370) .137) .190-.180 (.400) .080 (<LOD-.320) . ceramics.180 (.300 (.120-.093 (.220) .210-. 176 Fourth National Report on Human Exposure to Environmental Chemicals .500) .300) .200-.120) .370-. respectively.250-.310 (. to a lesser extent.280) .136) * .220) .120-.200 (.220-.570) .145) Selected percentiles ( 95% confidence interval) 50th .119-.330 (.280) .150-.320-.460 (.430 (.126 (.210) .200) . Dermal contact with soil.170-. Antimony enters the environment from natural sources and from its use in industry.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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.132 (.160) .210) .230) .240 (.330) .230-.220-.140-. from air and drinking water.400 (.180 (. 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.330 (.164-.04.270 (.070-.350-.470) .120-.440 (.350-.150-.130-.150-.260 (.300 (.150) .410) .110-.130 (.190-.240 (.220 (.120 (.300-.280 (.300-.134 (.207) .110-.120 (.178) .090-.270 (.190-.120) .460 (.

171) .111-.163 (.338) .250-.068 (. Ming-Hsin et al.121 (.120 (.199-.250) .204-.417) .159-. 1954). diarrhea.085) .087) .203) .108 (. resulting in hemolysis with abdominal and back pain (Dernehl et al.140) < LOD .250-.123 (.277 (.194-.222 (. 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.228 (.150-.228 (. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.178-.143) .153 (..170 (.228-.156 (.209) .132 (.108-.135 (..321) .147-.380 (. 1988.149) .127) .247) .471 (.138-.235-.265-.253-.167 (.230) 95th .333-1.152) .081) .128-.069-.138) * .129 (.429 (. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.109 (.150-.310 (.109 (.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 .125 (.175 (.115 (.239-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al. and gastrointestinal symptoms such as vomiting.126 (. 1962).187) .385 (.117-.191 (.075 (.152) . species. and kidney have been demonstrated in high dose animal studies depending on the dose.149-.125-.118 (.154-. interval) .119-.179-.271-.103-.238) .098) .238) .417) .317) .217 (.161) .098-.338 (.250 (.099-.229-.173-.181) .333-.112-.109-.173 (.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 .112 (.104-.192 (.099-.208-.225 (.280 (.421) .162-..259 (. 1973).159-.143) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.444) . liver.250-.357-.120 (. 1986).227-.137 (.189 (.278) .107-.138-.144-.116-.113-.391) .266 (.391) . 1986).153-.500) .148-. abdominal pain.080 (.167 (.320 (. Acute antimony poisoning may cause a metallic taste.115-.195-.078 (.315) .414) .119 (.167-.148) * .104-.146) .126-. Inorganic antimony salts irritate the mucous membranes.075 (.333-.183) .122 (.151) .245) .248-.313-.364 (.086) 75th .357) . 1944).352 (.741 (.176 (.069-.310) .265 (.181) .S.071-.226 (.220) .Metals than for trivalent compounds (Elinder and Friberg.230-.122 (.131 (.200-.233-.198) .320-.079 (<LOD-.146-.118 (.113) .281-. myocardium.167 (.317) .129) * .077) .236 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.438) .176-.188-.430) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.196 (.107-.207) .136) .108-.320-.173) .143) Selected percentiles ( 95% confidence interval) 50th .089) .185 (.318-. 1995).134) .127) .076-. and route of exposure (Elinder and Friberg.130) .074 (.200-.130) .333 (.115 (.241-.113-.225) .214) .126) .102-.138 (.288 (.135) .139 (.209) .120 (.132) .117-.364 (.300) .159-.333 (.343 (.161) .108-.092) .295 (. 1958) and occupational exposures (Briegner et al.105-.164-..267) .471) .318-.146-.278 (.115-.176 (.135 (.261) .257) .115 (.124-.114 (. Fourth National Report on Human Exposure to Environmental Chemicals 177 .425) .276 (.107-.480) .185-.255) .320 (.082) .188) .209-.068-.164 (.102-.080 (<LOD-. and ulcers (Werrin.213 (.103-.193) .263 (.095-.146-.156-.206-.127) .164) .211) .242-.084) .123) .096-.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.195-.310) .127 (.333 (.300 (.203) .272) .116 (.338 (.250-.30) .269 (.280-.121 (.200-.092-.130 (.208 (.124 (.429) .405) .143) 90th .233 (..163 (.135) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.294) Total .267 (.081 (<LOD-.082 (<LOD-.114 (.485) .268) .106-.160 (.253 (.120 (.129 (. skin.185 (.186) .238 (.076-.086 (. population from the National Health and Nutrition Examination Survey.241-.097-.233) .182 (.143 (.061-.115) .727) . 1953).333) .140) .286 (.130) .145) .135) .244-.192) .263-.195 (.098-.209 (.371 (.181) .373) .119-.127) .193 (.178 (.111 (.124) .250 (.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 .133) . Histopathologic inflammatory and degenerative changes in the lung.256 (.139 (.172-.082) .352) .117-.308-.131) .320) .192-. and eyes.106-.333-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.114 (.131-.147) .173 (.224 (.267-.100 (.248) .095-.255-.300) .444) .124-.205-.112 (.129) .741) .148-.121) .298 (.200) .400 (.317) .447 (.308) .

Yu H-S. EPA. Apostoli P. Hamilton EI.. Gallorini M.e. Kiberd B. Yang C-Y. Costeloe K. Iavicoli et al. and future strategies. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals .atsdr. 1997). eds.. Chemotherapy for leishmaniasis: Biochemical mechanisms. Biological monitoring of exposures to aluminum. Dezateux et al. Bailly R. 2005. clinical efficacy. Nordberg GF. Atlanta (GA).. Industrial Medicine 1944. Dunkelberg. Semisch CW. 1986.S. Delves HT. J Clin Pathol 1998. Ju-Sun P. even when exposure levels were below workplace air standards (Bailly et al. Pilgrim L.59:469-474. Environ Health Perspect 1998.. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Third National Report on Human Exposure to Environmental Chemicals. 1998) or compiled reference ranges (Hamilton et al. population. Int Arch Occup Environ Health 1987. Centers for Disease Control and Prevention (CDC). Antimony in blood and urine of infants. Konings J. 1995. Ming-Hsin H. Urinary antimony in infancy. Rev Infect Dis 1988. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Mayer P.48:93-97. Arch Dis Child 1997.. Cullen A. J Occup Environ Med 2004.16: 33-39. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Int Arch Occup Environ Health 1995. Lauwerys R. Pietra R. Sabbioni E.. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Ho C-K. Stocks J..)1954. Industrial antimony poisoning. Stone FD. Mayne P.html. Dezateux C.158:165-190. et al. et al. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. References Berman JD. Ludersdorf et al.13:361-362. et al. and hydrogen sulfide. gallium. which may be due to methodologic. 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. Stead FM. Liao Y-H. 1991.. Gebel TW. VI. Sci Total Environ 1994. and a drinking water standard has been established by the U.. Trace element reference values in tissues from inhabitants of the European community I. Schacke G. respectively. Carelli G.106:33-39. 1990. Buchet JP. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000.. Biological assessment of exposure to antimony and lead in the glass-producing industry. Vouk VB. Roland H. Pozzoli L. gov/toxpro2.76:432436. Iavicoli I.67:119-123. Br J Ind Med 1991. Chia-Yu H. Dernehl CU. New York: Elsevier. Delves HT. Nau CA. HH. In: Friberg L. Leinemann M.Metals to antimony have been established by OSHA and ACGIH. Industrial Medicine and Surgery (Dec. Bolten C. 2002. Fuchs A. Paschal et al. 1994) have reported values slightly higher than those in this Report. or exposure differences. Kentner et al. O’Regan M.. Skulsukai G. arsenic. Matthews T. Pulmonary edema of environmental origin.76(2):103-115. Biomonitoring of a worker population exposed to low antimony trioxide levels. Minoia C. Element reference values in tissues from inhabitants of the European community. Liao Y-H et al. Handbook on the toxicology of metals. Shao-Chi C. Suchenwirth R. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Wu M-T.64(2):182-185. 2004. Chest 1973. External and internal antimony exposure in starter battery production. Arsine. and 2003-2004. indium. and antimony in optoelectronic industry workers. Review of elements in blood. pp. J Trace Elem Med Biol 2002. Antimony.51:238-240.46:931-936. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Kuo-Juie Y. Cordasco EM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Mahieu P. 1998. Antimony trioxide is rated by IARC as a possible human carcinogen. 1998). Chen J-R. Sabbioni E. Chin Med J 1958. Briegner H. Petrucci F.10(3):560-586. 2nd ed. Piatnek DA. Information about external exposure (i.521-523. Lenert G. Alimonti A. Wade A. Elinder CG. Van der Venne MT. 1987). 26-42. Caroli S. Weltle D. stibine. Stasney J. Schaller KH. Friberg L. Kentner M. Cheng-Wei L.. 20012002. Luedersdorf R. Earlier measurements in general populations (Minoia et al. environmental levels) and health effects is available from ATSDR at: http://www.cdc.

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

1) 1281 1276 03-04 03-04 03-04 9.74.8) 29.4) 60.6-43. and indium arsenides are used in the semiconductor industry.1-18.10) 10.8) 30.8) 7. gaseous hydride manufactured in small quantities for use in the semiconductor industry.Metals Arsenic CAS No.34-9. arsenic compounds. such as arsenopyrite (FeAsS) and realgar (As4S4).02-8. lead hydrogen arsenate. semiconductors.50-14.7-83.70 (6.4) 13. population from the National Health and Nutrition Examination Survey. arsenocholine.90-8.4 (24. aluminum. and as a cosmetic to lighten complexion. though in some locations arsenite may be prevalent (WHO.3-15.10 (6.2-17. and foods.0 (15.77) 6.4) 40. Since the 1940s.5) 66.4 (26.5) 95th 65. lead.97) 8.0-60. In the last century.1 (38. cancers. arsenic as elemental metalloids may be used in some ammunition.57) Selected percentiles ( 95% confidence interval) 50th 7. 2001).84) 8. Also. and arsenosugars. Before the 20th century.8-77. 2005).5 (36.41 (7. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.19-9. interval) 8. pesticides.10-10.5) 43.0 (43.9 (17.90) 16. Water sources contain mostly inorganic arsenate.10-7. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. and gray forms). particularly arsenic trioxide.40) 7.S.34-10.5-19.1-40.7-95. and.7 (11. grain. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. Gallium.13-8. and as homicidal poisons.2 (12.70) 8. alloys.0 (22. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. from coal burning. General population exposure to inorganic arsenic can occur through consumption of drinking water and.8) 34.90 (7.9) 68. ocean and fresh waters.30) 17.8) 7.2-93.90-7.70-9. see Data Analysis section) for Survey year 03-04 is 0.5 (14.90) 75th 16.4 (7. retaining walls.00 (6.0 (11.5-41.5) 41. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. and play sets. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.5 (23.55 (7. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.3-19.6) 618 722 1074 Limit of detection (LOD.4 (31. to a lesser extent. Survey years 03-04 Geometric mean (95% conf. +3 and +5).90 (7.66-8.3-111) 78.1) 290 725 1542 03-04 03-04 9.00-9. to a lesser extent.000 metric tons annually.30 (7.8) 33.0-19.50 (8.84) 8. sodium arsenite.4-65.1) 7. Arsine (AsH3) is a reactive.27) 9.2 (41. Arsenic trioxide is approved to treat acute promyelocytic leukemia.6-35.08 (5. copper arsenates. psoriasis.30 (6. Arsenic trioxide (As2O3.90-14.1) 15.2 (51. 180 Fourth National Report on Human Exposure to Environmental Chemicals .5 (40. and arsenates (oxidation states of -3.90-8. Arsenic is measurable in most soils. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. or rarely as elemental metalloids (yellow.5 (34. referred to as inorganic arsenic compounds.90-11.12 (6.9 (8.29 (8.2) 15.7) 24. In nature.9) 21.6 (15. solders.6 (13. and other metals.0 (14.6) 11.80-9. The United States no longer produces arsenic from mining but imports about 22.4 (48.3) 10. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. black.5-52.8-61. and produce.12-10. the smelting of copper.9-34.3) 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 7.6 (32. meats.20 (8.1 (32. as alloy in metal bearings.7) 65.5-178) 46.9-62.2) 46.2-61. mostly for use in wood preservation (ATSDR.6-141) 53. and in lead-acid storage battery grids. Although it is still widely used in the United States. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.80) 6. Arsenic and its compounds have had many uses in the past and present as medicines. cacodylic acid. mental disorders.8 (48. arsenites.80 (5.2 (13.6 (9.2-20. it is found in over 200 crystalline or mineral forms. were used as treatments for syphilis. trimethylarsine oxide.25-9.9-46. Various arsenic compounds were used in paint pigments and for tanning animal hides.90 (5.8) 17.7) 90th 37.

2 (12. WHO.96) 12.38-10. 2007.33-10.07-9.9 (45.1) 6. 2007.11 (5. 2001).. In aquatic sediments. NRC.8) 27. as observed in Bangladesh where millions of people have been exposed. 2003.4-64.47-6.58-10.12-10.31 (6.86-17. Inorganic forms of arsenic demonstrate high acute toxicity. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.9) 53. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. Children may have additional exposures from ingestion of contaminated soils (e.7-188) 27. gallium arsenide and indium arsenide.3-41.1) 24.5 (9. Steinmaus et al.25-9.1) 58.59) Selected percentiles ( 95% confidence interval) 50th 7.5) 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. and folate status (Chen et al.0) 26. interval) 8.4 (12.13) 8. arsenocholine.6 (17.51) 75th 14.10-16. cacodylic acid and monosodium methyl arsenate. Fish.10-8. Extremely high groundwater arsenic levels. 2001). Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.5) 17. arsenic does not show biomagnification in the food chain (WHO. 2001).1-36.2) 90th 30.04) 7. Arsenate is reduced in the body to arsenite (oxidation state +3).4 (24.. In aquatic organisms.4 (42.75 (5. 2001.S. WHO.g.1) 7. Though modest bioconcentration occurs in some aquatic life. but is poorly absorbed dermally (WHO.6) 45. 2006.3-53.3) 6.25 (6.8-62. though some reduction may occur in the gut prior to absorption.44-11. dose level. have caused clinical arsenic poisoning.76 (6. Chowdhury et al. selenium.45) 5. and arsenosugars.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.75) 13. EPA’s maximum contaminant level (Hughes..47 (7.93-8. shellfish.00 (6.23-7.47 (6.4 (26.9-56..0-26.1 (14.7-18. dust.6 (35. age. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. 2001).4) 32.0) 12. so exposure to the general population is extremely limited.5) 290 725 1542 03-04 03-04 8.66-8.2-46.40) 8.8-75.3-64. 2001).01) 11. 2007. 1988). After absorption.7 (25.0-69.5-120) 40.0) 33. U.0) 1281 1276 03-04 03-04 03-04 8. trimethylarsine oxide (TMAO). mine tailings)..99-9.8 (20. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.4 (11.4 (40. Direct exposure to DMA and MMA may result from use of the two pesticides. kelp.0-18.7 (11. inorganic arsenic is widely distributed within the body.61 (7.88 (5.8 (21. and contact with CCA-preserved wood structures.4) 54.64 (7.8-32.2) 15.0 (31.0 (17.66 (7.1) 8. and some other seafood can contain organic forms of arsenic including arsenobetaine.3) 9.8 (27.41) 6. are used in enclosed ultraclean operations within the semiconductor industry. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. population from the National Health and Nutrition Examination Survey. 2001.7) 95th 50. Smoking tobacco is also a source of inorganic arsenic. EPA.18 (5. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.20-9. 2006. 2001).0) 14.3 (27. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al. Survey years 03-04 Geometric mean (95% conf.S.6-17..7) 28.04 (5.7-17.01) 7. The semiconductor dopants.88) 7.93-9.7 (9.06 (4.44) 6. 2001).Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.1 (11.50 (6.33 (6.35) 7.32 (5. organic arsenic can be converted back to methylated and inorganic arsenic. Tseng.9) 13.8 (11. 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.0) 42.66-8.28-7.0-38.8) 22. 2001).8 (12.24 (7. 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.5-17.7-35.S.81-9.3-62.6 (10.2-15. Gamble et al.7-34.2) 40.30-9.3 (24.

peripheral vascular disease.20 (<LOD-1. and DNA repair inhibition (Cohen et al. Studies of arsenic at levels typical of U. 2006. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 1.. 2006.60) 1.50) 621 725 1078 Limit of detection (LOD. WHO. Cohen et al.S.. NRC. Bangladesh.g. Chronic arsenic exposure in humans is considered to be a cause of skin. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. food residue. renal failure. Survey years 03-04 Geometric mean (95% conf.10 (<LOD-1. drinking water have not been associated with increased cancer rates (Schoen et al. 2007.10 (<LOD-1. lung. gluconeogenesis. Chronic elevated arsenic intakes have been associated with diabetes. and it also will inhibit succinate dehydrogenase. NRC. see Data Analysis section) for Survey year 03-04 is 1. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. and childhood neurodevelopmental effects in observational human studies. 2001)..g. 1998. Chronic human intake of arsenic at less than acutely toxic doses. hematocytopenias. 182 Fourth National Report on Human Exposure to Environmental Chemicals . and production of glutathione may be affected as well. U. population from the National Health and Nutrition Examination Survey. cytotoxicity. The U.10 (<LOD-1. Cellular glucose uptake. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al.50) 1.20 (<LOD-1.EPA. 2006. Taiwan. Cardiac arrhythmias. 2001). 2000. can cause peripheral sensorimotor neuropathies. vomiting.0. 2001). Such actions may lead to decreased energy production. fatty acid oxidation. substitution in phosphate metabolism. Raml et al. including drinking water sources with elevated arsenic levels (e. 2004). WHO. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. 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. and diarrhea. 2007)..20 (<LOD-1.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. and by uncoupling oxidative phosphorylation (NRC.10 (<LOD-1..S. Although arsenate is reduced in the body to arsenite.EPA has established drinking water.. 2001). OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. noncirrhotic portal hypertension. increased oxidative stress.60) 1. Bredfeldt et al. 2004.10 (<LOD-1.S. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. Arsenic has many actions demonstrated in cellular studies. hyperkeratosis. 2004).30) 1..S. and endothelial injury (Kumagai and Sumi. arsenic trioxide) includes hemorrhagic gastritis with nausea. With chronic exposure. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. WHO..50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. leading to a decrease in adenosine triphosphate energy production.20 (<LOD-1. 2006) or when exposure occurs in smokers (Chen et al.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. apoptosis. hypertension. interference in signal transduction pathways. WHO. 2007. 2001). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. some of these effects may take years to develop. Laboratory studies using inorganic arsenic have shown chromosomal aberrations.. 2001. which can lead to dehydration and shock. < LOD means less than the limit of detection. but additional or confirmatory research is needed (Kapaj et al.80) 1. 2001.. respectively. 2001). cell transformations. and bladder cancer (IARC. and altered gene expression.. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. Chile). including inhibition of numerous enzymes. The organic forms of arsenic occurring in seafood have little known toxicity. and hyperpigmentation of the skin (NRC. hepatotoxicity. Acutely..

Compared with this Report.00) 1.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2.18 (<LOD-3. 2006). WHO. Shalat et al. In the German Environmental Survey III of 1998.75 (<LOD-2. median urinary total arsenic levels in 4052 adults varied with seafood intake.. 2006). Pellizzari and Clayton 2006).S. Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al.. 1999.69 (<LOD-3...e.S. 2008.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 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.04 (<LOD-3..cdc.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2000. Josyula et al. Calderon et al. 2007. urinary arsenic levels have been accepted as a good biomarker of dose (WHO.18) 3. Fourth National Report on Human Exposure to Environmental Chemicals 183 . population from the National Health and Nutrition Examination Survey. Caldwell et al. 1999)..33 (<LOD-3. 2001). 2008).... In animal studies. 1999.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2001)... 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Caldwell et al. had decreased since the prior 1990– 1992 survey. Shalat et al. Meza et al... 2001). 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.75 (<LOD-2. 2006. Pellizzari and Clayton.19) 3.. Additional information about external exposure (i. DMA produced bladder cancer in some chronic rat studies (Cohen et al. 2006).80 (<LOD-4. 2007. and were about two-fold lower than those for the U..atsdr. gov/toxpro2. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. 1986). Pellizzari and Clayton. Valenzuela et al. population in NHANES 2003–2004 (Schulz et al.. 2004. Offergelt et al.. 2006. environmental levels) and health effects is available from ATSDR at: http://www. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. 2008). 2004.33 (<LOD-3. Vahter et al. Several studies have shown that urinary arsenic levels are not correlated with low levels of arsenic measured in house dust or in washings taken from hands (Hysong et al. Consequently. 1992. 2006..html.61 (<LOD-3.. 2000).41) 3..50) 1. In a Nevada town where groundwater levels were naturally elevated. 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. 2003.. Levels of total urinary arsenic in the U. population (Rubin et al.S. 2006).S. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.. Survey years 03-04 Geometric mean (95% conf. 1998. but generally only at maternally toxic doses (WHO. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. and the FDA has established a bottled drinking water standard. arsenic has been fetotoxic and teratogenic.Metals compounds.. although urinary arsenic levels were not associated with CCA contact (Shalat et al. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.

9-23.5) 292 728 1548 03-04 03-04 1.1) 18.00-6.3) 1284 1284 03-04 03-04 03-04 1. In the late 1980s.80) 1.800-1.2 (6. population from the National Health and Nutrition Examination Survey.62) 2.0) 29. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.S. After recent seafood ingestion.70 (5.800) 1.40-6. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (2. 2005. arsenobetaine.10 (4.4-35.50) . as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.8 (12..400-.5 (14. and other factors such as nutrition. Measurable organic arsenic species in this Report are three biologically generated environmental forms.8 (17.31-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) 2. Also. Caldwell et al. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.8-50. which may vary for some chemicals by year and by individual sample..29 (1.00 (1.43-1..60) 1.80 (.900-1. and TMAO.7-22.900 (. 2008). and TMAO were detected in only 7. 2007). 2006). 1.40) 5.10) 8.30) 10.37 (1.90-29.80 (4. 1985.6 (11. Valenzuela et al. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. population (Ahsan et al.1-51.0-23.50) 90th 16.9 (6.7 (21. population (Sun et al.7 (13.2-35.800 (. These associations are stronger at higher urinary levels. geometric mean levels were about 70-fold higher than for the U.. Aposhian et al. DMA and MMA.500-1.7) 15.05) < LOD .17-1.66 (1.70) 6. respectively.1-25.871-1. Arsenate. 2003)..0) 4. Median and mean total urinary arsenic levels for residents in some districts in Bangladesh were reported to be about 50-fold higher than respective levels in the U.S.90-7. < LOD means less than the limit of detection.00 (.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. 1996. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. For residents of Inner Mongolia. population in the NHANES 2003–2004 subsample.48-2..800 (.. 2008.5 (26. Pellizzari and Clayton. Caldwell et al.4) 23.0 (26.50) .2-38. China. dermal keratosis. 2005. Individually measurable species resulting from inorganic arsenic exposure are arsenate.7) 13.11-1.. Caldwell et al. 2007) with higher levels of arsenic in the drinking water.800-4. 2000.8-40. Chowdhury et al. 2001.50-6. arsenite.600 (. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. 2008.5) 29. 2005.20 (1.9) 13..5) 32.6 (13.9 (7..4. arsenocholine.20) 3.Metals other areas of the world (Ahsan et al.70-21.20-25.20) 7.700-1.S. 2008)..68) . and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. 2000. in NHEXAS 1995–1996.8) 35.6-44.00-1. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. Caceres et al. with DMA.S.3-39.80 (3.93) 1.4 (16. interval) 1.6. Tseng et al. when seafood organic arsenic is subtracted). The higher percentiles of total urinary arsenic levels in the U...40-7. 2008). and duration of exposure are also considered important. Some noncancer effects of arsenic (e.74 (1. Sun et al. population showed a higher contribution of arsenobetaine (Caldwell et al. 4.3) 95th 35.. see Data Analysis section) for Survey year 03-04 is 0.20-190) 31.. arsenite.80-5.60-3. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.. WHO.45 (1. In most human studies.700-1. 2000...0 (27.83) Selected percentiles ( 95% confidence interval) 50th 1.19 (. 184 Fourth National Report on Human Exposure to Environmental Chemicals .70-21.1-94. vasospasm.20) 18.28) 1.3) 35.30 (1. arsenocholine.6. Survey years 03-04 Geometric mean (95% conf.00-4. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.00) 3.8. and two methylated metabolic products.. In the residents of a Chilean town who consumed water with high levels of arsenic.S.10) 4.3% of a representative sample of the U.00-12.55 (1..5) 621 725 1078 Limit of detection (LOD.20 (. 1990.1) 45. When seafood intake is avoided.20-3.3 (9. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic. MMA.e.g. 2008).70 (3. 2001). and 0.6 (25.40) 75th 5. Blom et al.30 (2.20 (4.3 (21.4) 31. methylation capacity.

3) 1284 1284 03-04 03-04 03-04 1.S.6) 19.37-2.4-28.05 (.1) 26.43) 75th 5.00 (3.Metals as with DMA.3 (10.938-1. 1986.1-36.83) 2.83) 8.00 (1.4-82.7) 9.79 (1.833-1.64-29.18-1.2 (12.30-1.1-18.S.29-14.05) 1.0) 621 725 1078 < 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 185 .5) 26.6-46.67) 4.30) 1.4) 32.51-2.612-1.88) 2.4-21. Vahter et al.3-24.39-3.51) 5.58 (3. In recent years.65 (1.2 (4. The 95th percentile of the U.2 (13.11 (..15-4. WHO.82) Selected percentiles ( 95% confidence interval) 50th 1.5-20.19-2. 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. 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.3) 95th 29. interval) 1.12) < LOD . 2008). 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.4) 292 728 1548 03-04 03-04 1.78-5. 2001).1 (26.5 (18.4) 13.53 (.901-2.959-1.40) 1.4 (24.. 2001).15-1..72) 12.6 (9.9-18. 1992.88 (5.80-153) 17. Timber treatment workers had median urinary DMA levels that were about 15-fold higher than the general adult median levels reported in NHANES 2003–2004 (Morton et al.7) 30.5 (18..4 (11.62-6.9 μg/L.786-1. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0 (9.9) 32.40 (1.70) 5.10 (. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. not to imply a safety level for general population exposure.638) 1.3 (10. 1998. Information about the biological exposure indices is provided here for comparison. population for the sum of inorganic related species was 18. Survey years 03-04 Geometric mean (95% conf.6-32.13-39.0-36.76-27.36) 2.82) 4.4) 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. 2007).68 (1. Biomonitoring studies of urinary arsenic can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of arsenic than are found in the general population.67) 1.9 (25. Sun et al.28) 1.50-15.909-1.44 (1.7) 17. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.50-7.54 (1.78 (3.93 (1.47 (1..6-29.2 (12.9 (13.29 (4.73-6.43) 14.14 (1..400-.6 (6.32-7.9) 14. population from the National Health and Nutrition Examination Survey.21) 5.47 (2. Caldwell et al.8) 29.81 (4. 2008).55) 1.25 (. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect..877 (. 2003.91) 90th 16.15-1. 2006.45) 1.16 (. which is below the ACGIH BEI (Caldwell et al.5) 17.91 (4.80) . Offergelt et al.61-6.531 (.25-7.

population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf. Urinary Arsenocholine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.Metals Urinary Arsenocholine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. 186 Fourth National Report on Human Exposure to Environmental Chemicals .6. see Data Analysis section) for Survey year 03-04 is 0. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < 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. * 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.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) 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.

Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. < LOD means less than the limit of detection.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.40 (<LOD-1.00) 1.80) < LOD 621 725 1078 Limit of detection (LOD.44) 2. which may vary for some chemicals by year and by individual sample.S.00 (<LOD-3.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3.00 (<LOD-2. population from the National Health and Nutrition Examination Survey.20 (<LOD-1. Survey years 03-04 Geometric mean (95% conf.08 (<LOD-4.2. population from the National Health and Nutrition Examination Survey.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Fourth National Report on Human Exposure to Environmental Chemicals 187 . 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.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.95 (<LOD-2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Survey years 03-04 Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 1.

00-5.48 (3.12 (3.44) 5.14) 3.90) 2.24) 3.00-15.00) 6.18 (6.80-5.0) 13.00 (6.00) 6.9 (11.95 (4.92-12.0-12.00-22.00-3.00) 9.27-5.67) 8.0) 13.82-5.71-4.10) 3.4 (7.70-3.05) 3.19) Selected percentiles ( 95% confidence interval) 50th 3.20-4.70-4.32 (4.7-16.97-3.67) 9.45) 3.0 (13.12-4.91) 75th 5.1-22.0) 16.95-4.14) Selected percentiles ( 95% confidence interval) 50th 3.00 (5.78 (4.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.33-4.9 (7.70) 5.71 (4.57 (3.34-4.00) 6.45) 8.16-11.00-15.69 (3.39-3.84-8.85 (3.7 (10.00) 5.5 (11.00) 4.60-3.00) 90th 11.37 (2.7) 1284 1284 03-04 03-04 03-04 4.78) 4. Survey years 03-04 Geometric mean (95% conf.69-6.57-5.0) 11.11) 4.0) 17.0 (11.00 (5.60-7.1-15.6-18.28) 2.80) 7.00-9.0-19.5) 12.52) 3.0) 292 728 1548 03-04 03-04 4.82-9.34 (3.71) 3.6) 292 728 1548 03-04 03-04 3.0) 9.0-17.0 (14.0 (8.1-18.03-6.00 (6.00 (6.8) 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. population from the National Health and Nutrition Examination Survey.00 (3.34 (3.00 (3.74) 90th 9.00) 3.34) 3.9) 13. see Data Analysis section) for Survey year 03-04 is 1.27 (2.69 (3.77 (3.00-4.S.17-6.9) 5.00) 12.0) 11.7) 12.00-4.05) 5.00-7.50 (4.S.60-4.0-16.59 (6.00 (5.00) 7.00-7.3 (8.00 (5.5) 95th 13.27 (3.0) 16.27-2.80-3.16 (2.74 (2.89 (3.49) 10.17-4.50-15.90 (3.81 (5.44 (2.86-7.30) 3.70 (3.70-12.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .00) 6.00 (7.73 (3.00-4.00-7.69-3.16 (4.0-16.3 (7.0) 10.00-4.3 (8.17 (2.0) 9.49-4.0 (12.45 (8.00-11.00) 75th 6.2) 10.50-5.55 (2.0 (13.09 (7.60-6. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.32-10.72 (4.6) 1284 1284 03-04 03-04 03-04 4.13-4.00 (3.80) 2.94-3.7) 13.20-12.0) 14.6 (9.8) 7.00-3.82) 3.29-4.62) 4.48 (2.0-17.8) 7.00 (3.00-11.0-25. interval) 3.00 (3.00-7.9) 11.31) 4.46 (4.00-11.05) 10.32 (8.61-16.86-21.9) 12.00-12.42) 3.22) 4.1 (8.00) 3.00-8.98) 4.00-10.00 (3.34-4.0 (9.37 (3.65-6.0) 9.00-13.00-4.30 (7.0 (10.00 (7. Survey years 03-04 Geometric mean (95% conf.0 (8.0 (10.20) 11.0 (12.95-3.61-11. interval) 3.31-4.00-15.7.15) 4.11 (3.08 (2.25 (4.00-12.79 (3.80-6.80 (4.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.0 (9.0) 95th 16.65-8.0) 12.38 (3.24-4.00-4.0) 17.94) 3.92) 3.88 (4.0) 621 725 1078 Limit of detection (LOD.0 (9.73) 6.0 (10.33) 3.95-6.03 (3.00 (5.0-18.84-18.00) 4.90) 5.86 (2.71 (3.10) 6.0 (10.00 (4.06) 5. population from the National Health and Nutrition Examination Survey.

53-2.20) 2.30 (1.88 (1.40) 2.50) 621 725 1077 Limit of detection (LOD.30 (1.70-2.61) 2.90 (2.40-2.62) 2.28 (1.00 (2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.22) 3.50) 1.86) 2.40) 1.30) 1.00) 1.57) 95th 2.816 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.96-2.84-3.00-2.10-1.07-3.40-3.60) 2.90) 2. see Data Analysis section) for Survey year 03-04 is 0.20-3.00 (1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.46-2.07) 2.30) 1.90 (1.S. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.80 (1.30 (1.20 (1.00) 2.52 (2.45) 3.20 (1.80) 1. Survey years 03-04 Geometric mean (95% conf.71-2.00 (<LOD-1.77) 1.50 (2.50 (1.40 (1.33 (1.50 (<LOD-1.58) 2.10 (.30-2.00 (<LOD-1.54) 90th 2.22 (1.05-1.15-1.70-2.20 (1.79) 2.40-2. < LOD means less than the limit of detection.14-1.63 (<LOD-1.20 (1.23) 1.07 (1.35-3.88 (1.31 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.18-1.9.10) 95th 2.36 (1.80-2.16 (2.00) 2.10-3.20 (1.61-3.70-3.900-1.60) 2. population from the National Health and Nutrition Examination Survey.10 (1.28 (1.53 (1.20-1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.40) 1.82-2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .10 (1.86) 3.93) .00) 1.70) 2.31-3.46 (1.11-1.73-2.853-1.00) 1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.30) 2.86 (2.10) 2.20 (1.10 (<LOD-1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00-4.30 (2.30) 90th 1.S.985) 1.00-1.85) 1.50-2.60-2.86 (2.80-2.80 (1.81) 1.00-2.80 (1.60) 1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.30-1.34) 2.90) 2. Survey years 03-04 Geometric mean (95% conf.50 (1.90) 1.33 (1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.37 (1.60 (2.40 (2.70-2.17) 2.88-2.40-3.00 (2.36) 1.18-1.60 (1. which may vary for some chemicals by year and by individual sample.85) 2.82-2. population from the National Health and Nutrition Examination Survey.30-1.70-2.80 (2.43-3.80 (1.10 (.10-1.00-1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.80) 1.

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

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26) 2.40 (1.11 (3. Barium compounds are also used commercially in paint.60 (1.93 (4.49) 4.00-76.64 (1.51) 1.54) 1.06-1.70) 1.72) 75th 3.36 (1.15-11.35 (3.86) 6.56 (1. fireworks.91) 2.20 (1.15 (6.20-6.53) 2.76-2.78) 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 1.70) 4.31 (2.82) 1.91 (2.15 (1.50 (2.65 (5.18-1.64-3..50 (4.29-1.32-7.31-2.30-1.36-1.08 (6.64) 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 2.20 (3.35 (1.04-6.55-3.20-8.40 (1.80-3.40 (1.63) Total 1.77-3.30-5.90 (6.30-2.50) 1.63) 1.70-2.66 (4.96-2.53-5.60) 4.26-1.68 (1.48-4.60) 3.47-1.00 (2.33 (1.90 (4. bricks.39 (1.61 (1.19) 2.50 (4.48 (6.61 (2.8 (6.76-3.15-1.21 (1.29-5.73 (6.30 (2.80 (1.50 (1.24-1.20-5.54 (6.92) 2.80) 1.56) 1.15) 5.00 (1.36-1.86-5.8) 9. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.57-7. Barium salts have also been available as rodenticides.70) 1.37) 1.01 (4.81-2.47-1.10 (4.10-4.36) 5.32-1. respectively.38 (1. whereas others are practically insoluble (e.45) 7.48) 1.22-1.20) 2.75-3.80) 7.69 (1.30) 5.37-8.80) 6. soluble forms of barium.44 (1.38) 8.20-1.87-9. and 0.10 (3.12 (2.12 (2.49-1.12.g.10 (2.28-1.93-2.39) 4.43) 2.71 (2.60-3.46-1.70) 3. are high in barium (Genter.34 (2.93-8.72) 1.87) 7.20-1.50 (3. 2001).25-1.80 (2.65-1.54-1. such as barium chloride.56 (6.30) 2.28) 90th 5.10) 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 1.27 (1.81-3. In single dose animal studies.70 (1.41-1.59-11.90 (1.40) 7.51 (1.05% of the earth’s crust.40 (5.35) 5.40) 7.27) 2.50 (1.18) 3.42 (1.14 (6.90-9.12) 6.61 (5.59) 3.90) 1.65-5.19-1.78-3.25-11.56 (1.56) 4.70-6.20-8.15 (2.30 (5.27 (1.35-1.73-5.44-5.30 (1.12.24 (4.49-9.21-2.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.71) 95th 6.4) 9.90-2.48-4.24-1.87 (6.21 (1.80-7.85 (2.00) 1.87-7.76) 1.71) 1.99 (4.22) 6.74-3.49) 2.85) 1.40 (5.50) 2.39-1.1) 9. Fourth National Report on Human Exposure to Environmental Chemicals 193 .54) 1.30) 4.38) 2.12-1.65) 1.03 (1.32) 8. The general population can be exposed to low amounts of barium in air.15-1.63) 1.77 (3.60-6.85) 1.29) 5.40-13.22-1.02 (7.S.50) 4.80 (2.90-13.14-6.4) 7.80 (1.76-7.45 (1.39 (1.50-6. water.90) 4.54 (2.63 (1.61 (1.30-3.91) 6.30-2.30 (3.26-7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50 (1.98) 1.88 (5.20-1. and ceramics.84) 5.09 (2. such as brazil nuts.50-6.11-1.87-3.80 (1.50 (4.71-9. 0.60 (2.51) 7.95-6.00) 4. 01-02.37 (4.88) 1. Workers employed by industries that make or use barium compounds can be exposed to barium dust.49) 11.21-8.73) 1.78-2.49 (1.86 (4. tiles.34) 2.62 (1.11 (3. see Data Analysis section) for Survey years 99-00.41) 1.08-8.12) 7. depilatories.52 (4.60-10. Certain foods.80-2.34 (1.67) 6.44-2. interval) 1.46) 1.99-5.52 (1.87 (5. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.17-1.35-1. and food.00-3.60) 1.82) 2.05-2.50 (5.71) 2.70-2.94-6.60-6.30) 8. barium sulfate and barium carbonate).77) 1.25 (1.50-1.51) 2.41-3.4) 6.70-5.30-1. glass.75) 2.80 (5.70 (5.09 (1.70-8.86-4.82-6.72) 4. Some barium salts are freely soluble in water.43 (1.50-1.26) 5.74) 3. 7440-39-3 Medically.40 (5.16 (1.55-7.35-4.04-2.86 (4.49) 8.37-1.39) 1.70-3.06-2.63 (5.50 (6. Small amounts of barium can be released into the air during mining and other industrial processes.97 (1.70) 5.81-2.40 (4. rubber.31.30) 5.73) 3.43 (5.62) 1.35 (2.73 (5.90) 2.18 (6.00) 1.76 (3.54-1.95 (4.88) 4.43) 6.00) 6.14-1.61-8. and 03-04 are 0.56 (2.63 (2.80-5.2) 6.74-2.9) 5.16) 5.50) 2.63 (8.47) 4. In nature.20-8.8) 5.60-2.66) Selected percentiles ( 95% confidence interval) 50th 1.01-7.65-8.65) 3.20 (4.30 (5.38 (1.53) 1. it combines with other chemicals such as sulfur or carbon and oxygen.70) 7.10) 3.62) 1. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).40) 3. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.62 (1.88) 7.00-8.50 (1.65) 1.37) 5.30) 5.10) 5.Metals Barium CAS No.87-14.34 (1. Barium compounds are used by the oil and gas industries to make drilling muds.61 (3.57 (5.48) 1. population from the National Health and Nutrition Examination Survey.78) 1.57) 3.54) 2.46) 1.11 (2.07 (2.43 (1.30) 3.10-5.90) 2.50 (1.60) 1.54-8.36 (4.20-1.

00 (2.90-2.2) 6.25) 4.08-2.37-2.40 (1.3 (6.39 (2.92 (4.10) 6.91 (3.38) 1.68-3. NTP.26-4.11-2.33 (5.27 (2.61 (4.28-7.67-6.05-1.25 (1.12) 2.39-1.28 (1.4) 5. 1989). a benign condition that may occur among barite ore miners.88 (6.55 (5.50) 1.24 (5.31 (1. The health effects of exposure to barium compounds depend on the dose.49 (1.46-22.77) 1.96 (4. and cardiac dysrhythmias.13-3.48) 2.86) 5.75) 2.43-6.47) 1.22-1.06) .73) 2.47 (5.40 (1.02-5.48-1.03) 3.38-7.14-2.30 (1.38) 4.80) 4.81-6.00) 4.16 (1.26-1.80-6.36 (1.710-1.3) 6. are not absorbed when administered.Metals was eliminated primarily in feces and to a lesser extent.48-5.56 (1.57-5.84-2.76 (4.87) 1.905 (.75-22.39 (2.58 (2.56 (1.24-1.98 (2. Following intravenous injection in animals.33) 6.86 (2.27-1.97) 1..20) 4.11) .36-1.62 (2. in urine.68-3.19-1.01 (5.09) 6.49-1.23-1.27-3.00 (3.65 (5.29-3.15-4.33-1.24-1.51 (3.59) 1.31 (4.71 (5.75) 1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter. Perry et al.41 (1.55 (1. 2001).02) .48 (1.00-1.54 (1.91) 2.915 (.16-1.38-1.52-10.97 (5..45 (1.777-1.52 (3.77) Total 1.19-2.46) 1.56) Selected percentiles ( 95% confidence interval) 50th 1.04) 5.16) 11.96) 7.S.33 (1.85-5.89) 90th 4.40 (1.00) 4. chemical form.36 (5. Wones et al.81-7.24) 3.59) 1.45) 95th 6.26) 4.44-2.92) 2.42) 1.82) 1.97-3.47) 10. 1990).00 (5.27) 7.26-1.832-1.79-5. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.47) 1.20-1.47-8.76) 1.64) 7.55-6.83) 3.963 (.54) 2.36-2. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.32) 2.29-4.41 (2. water solubility.41) 4.64 (1.50) 2.29 (3.29) 1.45-1.73-2.30) 2.54) 1.58) 4.61) 2.96) 4.79) 1.891 (.10) 3.51) 4.39-5.65 (2.59-7.60 (1.22-1.68 (3.76-3. weakness. hypertension.84-5.99 (2.48 (1.41) 5.29 (1.26-1.51) 4.33) 1.31-1.46 (2.24-3.38 (1.8) 4.33-4.19-1.91 (3.91-2.56) 4.0) 5.22-2.82) 1.25-11.00 (3.00) 6.32 (1.34-5.69 (5.40-1.32 (1.60 (5.08-1.45) 1.96) 4. and route of exposure.45-6.10-1.42 (4.5) 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 1.59) 2.84 (3.23-5.2) 5. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.63) 1.70) 10.58-6.58 (4. Symptoms following acute high dose include perioral paresthesias.03) 1.36-1.38) 1.64 (1.68) 1.57-10.32) 2. Chronic high doses in animals resulted in kidney damage (McCauley et al.76 (3.53-21.62) 2.56-3.31-1.03) 2.80) 3.36 (1.29-4.04 (2.37 (1.59 (1.64 (1.97 (4.76) 2.78 (2.53) .64 (1.86-7.34 (1.77-5.20-8.31-1. 1984.34-3.35-1.77) 1.68 (2.04) 1.72) 6.42) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60 (2.48-3. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.74) 1. diarrhea.20-2.02) 4.00-7.49-1.30 (1.21 (1.58) 75th 2.52) 7.45-8.68 (3. interval) 1.64) 7.34-1.57) 2.32 (2.69-9.72) 4.28-1.50) 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 1.01 (4.24-6.84) 2.38 (4.03-1.50 (4.49 (1.44-2.99 (4. such as those used in medical radiographic procedures.51-3.22-4.75-3.76) 2.55-5.57-7.11) .39-10.45 (3.60 (2.47) 4.28) 5.99) 1.70) 1.35-3.88 (2.23-2.60) 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 2.01) 1.59 (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 .18 (1. Toxicity from soluble barium salts is rare.37 (1.26-1.57 (6.62 (4.72 (2.96 (4.89 (2.31) 5.74) 1.38-5.66 (1.50) 1.60 (1.70) 4.47 (2.34) 1.96-6.4 (5.10 (6. 1985.0) 6.63-4.10-2. population from the National Health and Nutrition Examination Survey. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.43) 1.77) 1.24-11.51) 6..881 (.41 (1.54 (2.06) 2.19-1.51 (1. paralysis. 1986). Insoluble barium salts.55 (1.38 (1.33 (1.81-6.97-4.73-4.29-1.703-1.36 (3.74 (5.75) 1.39 (2.52) 2.24-6. 1994.83) 2.20 (1.49-1.96) 4.39-1.46) 2.03-1.24 (3.58) 1.00) 1.28-6. vomiting.44 (1. Barium is not rated for human carcinogenicity.39 (3. 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.55) .921 (.0) 7.754-1.2 (3.55 (4.75) 2.13-2.62 (1.18 (1.48 (1.880-1.35-1.45-1.37) 2.28-11.36 (3.37-1.46) 3.02 (3.51 (1.39) 4.38 (4.52) 1.76 (2.52-4.29-7.77) 5.68) 3.53 (2.

gov/toxpro2.. Zschiesche W. [online]. Inc. Barium. and radium In: Bingham A. J Toxicol Environ Health. Frohman.atsdr. Pirkle JL. Atlanta (GA).pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. Minoia C.. Trace metals in urine of United States residents: reference range concentrations. 1998). Cohressen B. Clin Chim Acta 2000. 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. eds. strontium. Gallorini M. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. Environ Res 1998. 2nd Ed. and 2003-2004 (CDC. In: Inorganics in drinking water and cardiovascular disease. In: Calabrese EJ. 2005. environmental levels) and health effects is available from ATSDR at: http://www. patient population and literature reference intervals for urinary trace elements. and a drinking water standard has been established by U. barium. p. 4/8/09 Paschal DC. 1994. Powell C. and serum of Italian subjects. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. Morrow JC.197210. Costa R. Princeton (NJ): Princeton Scientific Publications. Nordberg GF.. calcium. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. Sampson EJ. Available at URL: http://ntp. ed. Pozzoli L.. 2001.. Schaller KH. Handbook on the Toxicology of Metals.niehs. 84-94.85:355-359.296(1-2):71-90. Pietra R. Exposure to soluble barium compounds: an interventional study in arc welders. 1992). Lack of effect of drinking water barium on cardiovascular risk factor. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report.. Fourth National Report on Human Exposure to Environmental Chemicals 195 . p. 2001-2002. 5th ed.95:89-105. Vol 2: Specific Metals. LA.nih. EPA. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Stadler BL. 231-249. ed. Jr. pp. the welders had no obvious adverse clinical effects (Zschiesche et al. eds. Perry EF.. Ash KO. 2000) to levels in NHANES 1999-2000 and 2001-2002.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA.cdc. Jackson RJ. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al.64(1):13-23. Genter MB. In Friberg L. 1990. Wones RG. Weltle D. Environ Health Perspect 1990. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). Sci Total Environ 1990. Epidemiological study of barium in Illinois drinking water supplies. 221-252 Komaromy-Hiller G. 1984. et al.nih. NTP. Trace element reference values in tissues from inhabitants of the European community I. Sabbioni E. 1985.S. Advances in modern toxicology. Princeton NJ: Princeton Scientific Publications. Vouk VB.. Third National Report on Human Exposure to Environmental Chemicals. Int Arch Occup Environ Health 1992. McCauley PT. blood. Laurie RD. References Brenniman GR. Minoia et al. 2005.gov:8080/cs.S. Perry HM. National Toxicology Program (NTP). Douglas BH.28(3):373-388.html?charset=iso-88591&url=http%3A//ntp. Howerton K. Comparison of representative ranges based on U. Apostoli P. et al. p. Calabrese EJ. Reeves AL. et al. Magnesium. 1989. 1986. New York: John Wiley & Sons. Ting BG.76(1):53-59..e.html. Patty’s toxicology. Centers for Disease Control and Prevention (CDC). Levy. A study of 46 elements in urine. Kopp SJ. Paschal et al. New York: Elsevier. Investigations into the effect of drinking water barium on rats.gov/ntp/htdocs/LT_rpts/tr432. Biomonitoring Information Levels of urinary barium reflect recent exposure. PS.niehs. 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.

13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . the lightest of all metals. and from breathing tobacco smoke. and 03-04 are 0. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. computer.13. which may vary for some chemicals by year and by individual sample. Beryllium compounds are commercially mined. 7440-41-7 General Information Pure beryllium is a hard gray metal. and volcanic dust. < LOD means less than the limit of detection. In studies of laboratory animals. beryllium is used in instruments. aircraft. 196 Fourth National Report on Human Exposure to Environmental Chemicals . and machine-parts industries. Exposure to beryllium occurs mostly in the workplace. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. and can be found in mineral rocks.130 (<LOD-. Two types of minerals.13. population from the National Health and Nutrition Examination Survey. nuclear. x-ray machines. 01-02. are mined for commercial recovery of beryllium. and 0. coal. and refined beryllium is used in mirrors and special metal alloys for the automobile. near some hazardous waste sites.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. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames.Metals Beryllium CAS No.S. see Data Analysis section) for Survey years 99-00. and dental bridges.170) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . respectively. In medicine. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. or drinking water containing the metal. electrical. 0.150) < 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 .130 (<LOD-. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. eating food. Low-level beryllium exposure in the general population can occur through breathing air. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. bertrandite and beryl.140 (<LOD-. soil.

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

1990. Sci Total Environ 1994. less than 0. and the fact that most NHANES participant levels were undetectable. Gallorini M. A study of 46 elements in urine.. Minoia et al. 2001). Sci Total Environ 1990. et al. 0. Howerton K. Van der Venne MT. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. VI. Ash KO.95:89-105.e. 20012002. References Apostoli P.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Centers for Disease Control and Prevention (CDC). Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Environ Res 1998. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al.. Minoia C. Sabbioni E. Maier L. Atlanta (GA) 2005. 2000.1 μg/L). 198 Fourth National Report on Human Exposure to Environmental Chemicals . They reported urinary beryllium levels ranging from 0.. which approximate this Report’s limit of detection.296(1-2):71-90.S. Paschal DC. Costa R. Trace element reference values in tissues from inhabitants of the European community I. Environmental Health Criteria.gov/toxpro2. Comparison of representative ranges based on U. 106.76(1):53-59. In other studies..atsdr. patient population and literature reference intervals for urinary trace elements. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. et al. Clin Chest Med 2002.158:165-190. Third National Report on Human Exposure to Environmental Chemicals.inchem.157:388-398. Andrew M. plasma and urine and a critical evaluation of reference values for the United Kingdom population. blood.Metals (i. environmental levels) and health effects is available from ATSDR at: http://www.. Trace metals in urine of United States residents: reference range concentrations. 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.S. 3/27/08 Komaromy-Hiller G.org/documents/ehc/ehc/ ehc106. Hamilton EI. Morrow JC. 1990. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. it is likely that urinary beryllium levels in the U. Weston A.html. Ting BG. Levels of beryllium in urine for the U.S. HLA-DPB1 and chronic beryllium disease: a HuGE review. Sampson EJ. Given these results. Available at URL: http://www.74:162-166. International Programme on Chemical Safety (IPCS). Jackson RJ. and 2003-2004. 1998). Paschal et al. Am J Epidemiol 2003.13 μg/L. Hamilton et al. Pozzoli L. Beryllium [online]. Sabbioni E.e. Genetic and exposure risks for chronic beryllium disease.cdc. McCanlies EC. population are lower than levels in workers. Schaller KH. Review of elements in blood. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. population were generally undetectable in NHANES 1999-2000. and serum of Italian subjects.12 to 0.htm. Element reference values in tissues from inhabitants of the European community. Pietra R. Kriess K. and the 95th percentile for males in NHANES 2001-2002. Apostoli P.23:827-839. Int Arch Occup Environ Health 2001. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Pirkle JL. Clin Chim Acta 2000.

00) .40 (1.300-.300-.300-.10) 1.10 (1.900-1.400) .300 (.200 (.300 (.400-.255) .700 (.600 (.500-.10) 1.10) 1.300) 1.20) 1. and 0.300 (<LOD-.600) . bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.400-.300 (.500-.S.500-.400-.500 (.326 (.300-.30-1.10 (.500-.300 (.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .300) .70) 1.700-1. < LOD means less than the limit of detection.20-1.00-1. and 03-04 are 0.400) .400 (.216-. U.300-.60 (1.300-.900 (.378 (.900 (.296-.500-.600) .300) .60 (1. 01-02.500-.300-.80 (1.900-1.266-.20 (.200 (.300-.500-.500 (.300) .700-1. 7440-43-9 General Information Cadmium is a soft.344) .400) .30-1.700) . and nonferrous alloys.600 (.300) .400 (.40) 1.00-1.400) < LOD . cadmium use has declined in response to environmental concerns (http:// minerals.600-.300-.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00 (1. The predominant commercial use of cadmium is in battery manufacturing.400 (.400 (.20-1.900-1.395 (.600) .283 (.300) .500 (.304 (.500 (.426-.200 (<LOD-.300-.300) .200-.300-.500-.400 (.300-.900-1.300 (.362-.600) 1.400) .441) * .400 (.500) .200-.00 (.400 (.600) .500) .700) .10 (1.S.40 (1.600 (.600 (.20-1.800-1.300) .300-.700) .304-.700) 1.700) .500-. Other uses include pigment production.500 (.500-.468 (.30) .30) 1.403 (.70) 1.300-.00-1.400-.500) .20) .500-.500-.20) 1.600-.378-.80) 1.382 (.300) .470) * .70) 1.600 (.400) .400 (.40 (1.300 (.300-.30-1.40-1.600-1.300-.800) .14.400-.300-.00-1.800 (.900-1.400-.S.500-.00 (1.10 (1.420 (.600) .20-1.398) < LOD < LOD < LOD < LOD < LOD < LOD .20) 1.304 (.600-.60) 1.300) 75th .Metals Cadmium CAS No.300 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.376-.500 (.50 (1.600) 90th 1.800-1.300) .10) 1. respectively.20) 1.600) .300 (<LOD-.50-1.449) Selected percentiles ( 95% confidence interval) 50th .400) .40-1.900-1.600 (.289-.333 (.50-1. plastic stabilizers.313 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .400 (. see Data Analysis section) for Survey years 99-00.00 (.50-1.800) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500-.80) 1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.400) .00-1.600 (.00 (.20-1.403) .800) .600 (.40 (1. during refining of lead and copper from sulfide ore.50) 1.00) .300-.500 (.500) .500-.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 .20) 95th 1.10 (1.10) 1.30-1.50 (1. which may vary for some chemicals by year and by individual sample.600 (.60) 1.427) * . interval) .400 (. coatings and plating.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 .700) .400) .300 (.400) .600 (. Cadmium also may be emitted into the air from zinc.500-.400-.20) 1.40 (1.300 (. malleable.60) Total * .600 (.00 (.700) .10) 1.452) .400) .500-. Since 2001.00 (.30) 1.400) < LOD .400) .200-.500) .600 (. EPA.400 (.400 (.200-.386-.10 (1.20-1.400) < LOD .40 (1.00 (.400 (.900-1.20-1.20 (1.30) 1.300) .200) .90) 1.400-.400) < LOD < LOD < LOD .359-.400-.3.300) .421 (.10 (1.300-.900-1.500) .30 (1.20) 1.40) 1.600) .60 (1.400 (.10) 1.00 (.500 (. as zinc sulfide) and to a lesser extent.460) .400-.361-.400) .50) 1.235 (. population from the National Health and Nutrition Examination Survey.200 (.300-.600) .400 (.200-.500) .200 (<LOD-.300 (.3.800 (.300 (.367-.400) .368-.00 (.600) .400 (.300 (.50 (1.700) .20) 1.600 (.60 (1.393 (.300) .900-1.412 (.366) * * . 0.400-. and incineration of municipal waste materials.00-1.309-.425 (.00-1.500 (.00 (.424) * .300-.60) 1.300) .70) 1.20) 1.331) .200) . lead.513) .500-.700-1.40 (1.300 (.10) 1.usgs.50-1.00 (.900-1.60-1.10 (1.gov/minerals/pubs/commodity/cadmium).300 (<LOD-.400 (.300 (.700) . Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.275-.20) .300-.300 (<LOD-.337) .50) 1.30-1.60 (1. or copper smelters (U.50 (1.00-1.600 (.00-1.400) .

.430-. Inhalation of cigarette smoke is a predominant source of exposure in smokers. Diamond et al.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 . wheat.229) .239 (. 1999.06.633-1.220-.255) .221) . 2004a.366-.479) .806) .17 (.187 (.320) .388-.640) .713) .148-.455 (.260 (.282 (.440 (.445 (.220-.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 .394-.230) 75th . The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al. 0.204 (.280 (.100-.09-1.219 (.249) .858 (.281 (.705-.179-.623) .748-1.195-.820 (.157-.530 (. 2001).150-.192-.520-.06-1.41 (.061-.540) .090) .220) .530) .28 (1.480) .839 (.231) .246) .115-.229) .763-.067-.302 (. For nonsmokers who are not exposed to cadmium in the workplace.892 (.210 (.262) .Metals 2000).157) .38) 1.83) 1.20) 1.203 (.13) .150) .206 (.445 (.233) . respectively.07-1.730-.060-..450 (.596) .160 (.210) .140 (.273 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.235) .551) . Renal tubular and glomerular damage.20-1.194-.230) .550 (.203) .72) 1.855-1.686-.13 (.322 (.253-.234 (. ingestion through food is the largest source of exposure.169-.24) 1.19) 1.181 (.476-.170 (.860) 1.433-..48 (1. With chronic exposure.092 (.04 (.** Survey Geometric mean (95% conf.216 (.193-.817 (.308) .790 (.430) .257) .38) .189-.191-.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .192-. Cadmium in soil is absorbed by plants.15 (.790 (.918-1.S.500) 90th . 01-02.607) .223 (.700-.210 (. Cadmium is absorbed via inhalation and ingestion. whose body burdens of cadmium can be approximately twice that of nonsmokers.208-.977) .160-.481) .372) .199 (.077 (.211-.180 (.316 (.200-.820) 1.766 (.545 (.109 (.390 (.241) .237-.210 (.423-.201 (.210 (.170-.. Kikuchi et al.243-.173) .130 (.306 (.200 (.989-1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR. see Data Analysis section) for Survey years 99-00.400-.326) .890 (.700-.462 (.500) .381-.238) .255) .466 (.109-.160) .261-.36) 1.151-.077 (.198) .452 (.20 (1.47) 1.733-.366-.980) .366) .393-.559 (.090) .510) .277 (. To a lesser extent. 2003).310) .22 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.329 (.226) .270 (.38) .880) .980 (. and 0.191 (.800-.265) .200-.255) .295) .817 (.836-1.221 (.300 (.886) .813 (.219 (.82) 1.110-.919) .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.493-.01) .279 (.175 (.265 (.456-.551 (.03) .141 (. 2003).339) .580) .261-.490) 1.436-.390-.980-1.498-.336) .257-.232 (.15) .220) Selected percentiles ( 95% confidence interval) Sample 95th 1.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * . cadmium accumulates in the liver and kidneys where it is bound to metallothionein.519) .458 (.299) .04 (.272-.121 (.175 (. drinking water is a source for cadmium intake.270 (.190-.350 (.232) .327 (.890-1.51 (1.12 (.06) .28) 1.440-. 200 Fourth National Report on Human Exposure to Environmental Chemicals .206) .680 (.848 (.01-1.52 (1.354) .507) .300) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.193 (.426 (.17 (.240-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.06.160) .980) .25) 1.06-1. interval) .633 (.260-.189-.17) .820-1.717-.32 (1.135 (.170-. 2003.061 (<LOD-.940-1.190-.30-1.165-.310 (.219 (.153-.800 (.240) .12-1.078 (.539) .589 (.875 (.57) 1.183-.209 (.220 (.189) . individual values vary and are affected by factors such as dietary intake of essential nutrients (iron. and various seeds.10 (1.191-.700-.081) .22 (1.440 (.283 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. an inducible metal binding protein. 2003).229-.960) 1.202 (.065-.210 (. population from the National Health and Nutrition Examination Survey.251) .351-.092) . Cadmium absorption may be increased with iron deficiency (Berglund et al.233) .285-. 1994).870) .128 (.238-.875) .135-. potatoes.134) .990) . copper) and protein.892-1.101) .387) .177-.087-.360) .067-.519) .17 (.25 (1..02-1.178-.886-1.249-.390-.13-1.222) .207-. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.126) .980-1.28-1.20 (1.247) .184-.470-.01 (.362) .753-.38) 1.972 (.20 (1. and 03-04 are 0.741-1.74) 1.843-1.818 (. rice. calcium.450 (.810-1.714-1.313) .167-.06.447 (.107-.260-.475 (.492 (.227 (.114-.34) 1.200 (. zinc.610) .230 (.733) .400-.15) 1.482) .214-.963-1.112-. Horiguchi et al.210) .202-.136) .43) 1. including many food crops such as cereal grains.263) .171-.290-..120 (.211 (.080 (.190-.960 (.490) . however.196-.289-.330-.412) .148) .510-.284) .

02 (.219 (.187-.387 (.962) .205 (.078 (.927-1.909-1.668-.078-.281) .212 (.364) .769 (.719 (.876-1.234 (.236-.096) .229) .414 (.663 (. Fourth National Report on Human Exposure to Environmental Chemicals 201 .318 (.08) .090 (.617 (.440) .202 (.136-. Horiguchi et al.830) .245 (.184) .067-.189-.266) ..630-.166 (.688-.222-.209) .173 (.181 (..541) .157-.208-.263-.238) . can result from high dose chronic exposure.232) .247-.350) .470) .130-.182) .150-.292) .479 (.414-.826-1.559-.140-.077-.178-.270 (.289) .091 (.183 (.490 (.219 (. Olsson et al. 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.473 (.674-1.481 (.196 (.206-.338 (.289) .177) .250) .426-.191-.828) .163 (.252 (.168 (.421 (.304-.09 (.484 (.806-1.308 (.218) .183) .163) .850) .154-.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.444-.084-.07) .300-.17) .175 (.170 (.187) .147-.340) . 2004b). 2000.941 (.303) .691-.412 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.184-.438-.122 (.446) .161-.288-.16) 1.865 (. 2002.388-.182) .818) .247-.13) .253) .234) .234-.071 (.562-.086 (.104) .614) . interval) .143-.104) .434 (.293-.839) .533) .826-1.827) .331 (.216-.148 (.278) .256-.210) .075 (<LOD-.667) .233 (.100 (.209) Selected percentiles ( 95% confidence interval) Sample 95th .850) .440) .168-.716) ..931 (.335 (.538) .253 (.607) .297) . 1999).261-.441-. 2003.111-.215 (.267 (.818) .207-.693 (.156-.686 (.622 (.712 (.940-1.792 (.308) .560-.423-.283 (.085-.687 (.123-.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 .051-.884) .242) .551) .266-.12) 1.210 (.274) 1..220 (.281) ..833-1. Jarup et al.653) .784) .112) . 2002.147 (.176 (.472) . Whether the markers of renal tubular effects found in populations with low environmental exposure are likely to progress or predict an increased risk for developing clinically evident renal dysfunction is unknown (Hotz et al.678-.501 (.873 (.718 (.325 (.696-.690-.830-1.131-.170-.767) .063-.311) .950) .545) .700) .336-.091) .282 (.098) .197-.700 (. 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.191) .537-..107) .140-.123-. population from the National Health and Nutrition Examination Survey.381-.144-. 1999).729 (. 1999).757 (.418) .171-.097) .722-.190 (.135) .085 (.591 (.783 (.211 (..998) .280 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.241) .874-1.199 (.101) .227-. 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.476) .449) .415) .136-.204-.07 (.221-.404 (.802 (.727-.690-.917) .208 (.261) .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.795) 1.919 (.157-.779 (. At lower environmental exposures.631) .343-.536 (.174-.391-.154 (.240) .767 (.106) .228-.240) .162 (.221 (.113-.740 (.239-.084 (.181) .418-.470) .268 (.404) .316) ..650-.143) .304) .813-.184-.500-.708-1.S.074-.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .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 .190 (.387-.247-.181-.789 (.083-.398-.185) . 1996.329 (.288) . During the 1950’s and 1960’s.979 (.192) .678 (. Staessen et al.178) .813-1.191 (.906) .917 (.352) .159 (. 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. most often a result of occupational exposure (Roels et al.255-.296 (.518) .531 (.507-.382-.05) 1.137-.199-.126 (.175-.** Survey Geometric mean (95% conf.223) .091 (.198) .647-. 2002.16) .757) ..238-.137 (.094) .382) .10) 1.224 (.147-.210 (.200 (.075-. However.158-.143-.146-.432 (.181 (.225) .225) .00 (.687-.182) .263 (.433-.377-.232) .159 (. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.06 (.185 (.321) .940 (.491-.645-.725-1.156) .783) .288 (.929) .156 (.716-.207) .516-.168-.093 (.754) .201-.856) .04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .194-.666-.856 (. 2004).226) 75th .316 (.173-.273 (.175 (.00 (.176 (.423 (.438) 90th .267 (. Noonan et al.431) ..261 (.690 (.487 (.235) .985 (.38) .

2004b). intermediate in former smokers and lower in never-smokers (Becker et al.... pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Moriguchi et al. as may occur from welding cadmium-alloyed metals. In adults aged 60 years and older. 1996)... Animal studies have demonstrated reproductive and teratogenic effects. environmental levels) and health effects is available from ATSDR at: http://www. Ezaki et al.S.. 2002).S. 2006).. Jin et al... Staessen et al.. 2003. respectively.S. Wilhelm 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. Zhang et al.cdc. Salpietro et al. 1996. 2002). 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).. 2002. CDC. Horiguchi et al. 2003. Friedman et al.... Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. For NHANES 19992000. 2002.. 2005. 2002). Wennberg et al. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al.. not to imply a safety level for general population exposure. Jarup et al.. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al... Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. In the typical environmental exposure.. Olsson et al. 2002. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals .. 1999). 2002).atsdr. 2004. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. 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. Cadmium can produce lung. Komaromy-Hiller et al. 2003).html.. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC.26 and 3. 2003. 2003... with peak values observed in the fifth to sixth decades (CDC. 2004). urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.1 mg/L (Alfven et al.. 2006. Acute and heavy exposure to airborne dusts and fumes.gov/ toxpro2. 2003. 2000). 2006. 2004b. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. Suwazono et al.. Further research is needed to address the public health consequences of such exposure in the United States.. Noonan et al. 2002.46 mg/gram of creatinine) (Ezaki et al. Becker et al. However. Horiguchi et al. Several studies of populations residing in areas with higher cadmium soil concentrations or with frank cadmium pollution have reported mean blood and urine cadmium levels considerably higher (as much as 10 times higher) than control groups or representative U... approached these values associated with subclinical changes in renal function and bone mineral density. Olsson et al.. 2005). Jarup et al. Becker et al. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles.. In postmenopausal women.. 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... Ezaki et al. 2004. Occupational standards are provided here for comparison only. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. 1999). data (CDC. 1999. Both IARC and NTP consider cadmium a human carcinogen. 2005.. 2005.. 2003.. potentially fatal pneumonitis (Fernandez et al.. Staessen et al. 2002) and length at birth (Nishijo et al. 2000. Women had higher blood and urine cadmium levels compared to men of similar ages. and drinking water and environmental standards have been established by U. 2004. 2002). 1988). respectively. Becker et al. Staessen et al. 2002. Wennberg et al.e. 2000. 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. 2002. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. Creatinine-corrected urine cadmium values in U. 2005. 2004. Mannino et al... has resulted in severe. Information about external exposure (i. maternal blood or maternal urine and birth weight (Nishijo et al.. 2000. 2006). EPA. Olsson et al..

Lidfeldt J. Lepom P. Venables KM. Chislovska NV. Gadea E. Kikuchi Y. Ezaki T. Fukui Y. 4/8/09 Alfven T. Machida M.S. Jin T. et al. 102:10581066. Greves HM. Nordberg G. Bellerup P.102:83-89. Fukui Y. Kundiev YT. Third National Report on Human Exposure to Environmental Chemicals.57:668-672.45:43-52. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Int J Hyg Environ Health 2003. Lancet 1999. Jarup L. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Mannino DM. Vahter M. Bernard A. Thayer WC. Mascagni P. Uemura T. Fourth National Report on Human Exposure to Environmental Chemicals 203 . et al. Sasaki S. environmental.205:297-308. Bo M. Olfactory function in workers exposed to moderate airborne cadmium levels. Palomar M. Krause C. 196:114-123. patient population and literature reference intervals for urinary trace elements. Ash KO. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Schulz C. J Toxicol Environ Health 2003. Comprehensive study of the effects of age. Howerton K. Available at URL: http://www. Tsukahara T. Bregante G. Agency for Toxic Substances and Disease Registry (ATSDR). Fayers PM. Consonni D. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Berglund M.76:186-196.S. Hellstrom L. Schulz C. Vahter M. Chiappino G.59:194-8. Tsukahara T. Int Arch Occup Environ Health 2003. Lauwerys R. Taylor AJ. Seifert B. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. population. diabetes mellitus. Costa R. Ye T. Lancet 1988. Stock AL. Lison D. Buchet JP. Savage-Brown A. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Cadmium fume inhalation and emphysema. Anthropometric.59:497]. Nermell B. Becker K.html. Furuki K. Nomiyama T. et al. Miyamoto K. Seiwert M.atsdr. Oguma E. et al. Fernandez MA. Thorax 2004. Takebayashi T. Seiwert M. Toxicological profile for cadmium update. Comparison of representative ranges based on U. 2005. Darbyshire J. Friedman LS. Sasaki S.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.354:1508– 1513. et al. References Akesson A. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Environ Health Perspect 2005. Sanz P. et al. Atlanta (GA). Moriguchi J. Environ Health Perspect 2002. Becker K. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Moriguchi J. et al. Ikeda Y. Occup Environ Med 2000. Akesson A. Ezaki T. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Mucha A. Clin Chim Acta 2000. J Occup Health 2003. Komaromy-Hiller G.1(8587):663-667. et al. Environ Res 2004. iron deficiency. Grubb A. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Ikeda Y. et al. Lundh T. Diamond GL. Toxicol Lett 2004.13(11):1627-1631. et al. Persson B. Horiguchi H. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Jarup L. Alfven T. Jones RL. Dekio F. Oguma E.24:717-724. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Environ Res 2004b. 1999 [online]. Kumagai N. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.96:353-359. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Ukai H.110:699-702.46:372-374. Pickering CA.148(1-2):11-20. Fatal chemical pneumonitis due to cadmium fumes.000 women in the Japanese general population: a nationwide large-scale survey. 206:15-24. Holguin F. Okamoto S. Neurotoxicology 2003. et al. Carlsson MD. Environ Health Perspect 1994. Furuki K. Nerbrand C. Int J Hyg Environ Health 2002. Hotz P. Toffoletto F. Kaus S.cdc. Miyamoto K. Horiguchi H. Zhu G. Kaus S. Serra J.gov/toxprofiles/tp5.95:20–31. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Lukyanova EM. ShkiryakNizhnyk AZ. Environ Res 2006. Davison AG. Occup Med 1996. Elinder CG. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Machida M. Toxicol Appl Pharmacol 2004a.66(Pt A):2141-2164. Centers for Disease Control and Prevention (CDC). possibly better than b2microglobulin.296(1-2):71-90. Wang H. Choudhury H.

Environ Res 2000. Usefulness of biomarkers of exposure to inorganic mercury. et al. J Cardiovasc Risk 1996.S. Wennberg M. In: Clarkson TW. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. 2001. Lison D. Stelitano A. Gallmans G. Nishijo M. United States Environmental Protection Agency (U. pp. cadmium. Kobayashi E. Ottosson H. Honda R. Zhao YC. Vangronsveld J. Nakagawa H.59:394-397. Lijnen P. Cadmium compounds. Roels H.30(5):395-399. Tawara K. Bensryd I. et al. Int J Hyg Environ Health 2006. Lundh T. Nordberg GF. Noonan CW. Environmental exposure to cadmium. and risk of fractures: prospective population study. Schwenk M. Nakagawa H. 2004. Mutat Res 2003. Environ Health Perspect 2002.39:2507-2515. et al.gov/ttn/atw/ hlthef/cadmium. Wang JX.533(12):107-120. Suwazono Y. Sarasua SM. Environ Health Perspect 2002. age. Cadmium in blood and urine – impact of sex. Roels HA. dietary intake. Tanebe K. Nordberg GF. Hazard Summary. Olsson IM. et al.100:330-338. Lybarger JA. Ren Fail 1999. Occup Environ Med 2002.59(1):22-25. Jansson J-H. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. Biological monitoring of toxic metals. Fan YG. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Stegmayr B. et al. Schultz C. Bruiglia S. Staessen J. J Environ Sci Health B 2004. eds. Cadmium carcinogenesis. New York: Plenum Press. Campagna D. Arch Environ Health. Honda R. and mercury in the population of northern Sweden.html. Minciullo PL. Sager PR. Oskarsson A. Bergdahl IA. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Saito S. Revised and new reference values for arsenic.84 (Section A):4455.Metals Nishijo M. Time trends in burdens of cadmium. et al. Salpietro CD. Emelianov D. Thijs L.21(3-4):251-262. 151-168. Nogawa K. created 1992. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Tanebe K.epa. and former smoking – association of renal effects. Lauwerys R. Toyama. Nakagawa H. lead.353:1140-1144. forearm bone density. lead. Environ Res 2006. Roels HA. Buchet JP. iron status.209:301305. Lundh T. Japan. Ginucchio G.3:26-41. Nordberg M. Available at URL: www. J Perinat Med 2002. Kido T. Merlino MV. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Revised 2000 [online]. EPA). Biological monitoring of cadmium. Kathman SJ. Gangemi S. Liu QF. 204 Fourth National Report on Human Exposure to Environmental Chemicals .110:151-155. Wilhelm M. Skerfving S. Zhu HD. 2000.110:1185-1190. Lancet 1999. lead. Mueller PW. Staessen JA. Okubo Y. Kuznetsova T. Effects of exposure to low levels of environmental cadmium on renal biomarkers. 4/8/09 Waalkes MP. Friberg L. Hoet P. Relationship between newborn size and mother’s blood cadmium levels. Zhang YL.

2 (9.40-5. photographic emulsions.93 (4.98 (7.55-11.54-11.08 (6.0) 11.23-4.99) 7.4 (10.12) 5.62 (5.55 (4.25-5.31-8.09) 5.30-10.36) 3.07) 4.S.64) 4.1 (9.16-6.40-5.94-4.9 (11.8) 12.90-12.2-12. population from the National Health and Nutrition Examination Survey.40 (4. and high-power gas-ion devices.60-12.35 (4.70-5.52-9.09-5.33 (5.87 (4.1) 11.71-9.17-6.05) 5.9) 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. see Data Analysis section) for Survey years 99-00.00-10.7 (11.1) 9.81 (4.20-7.3-13.7 (9. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.90-10.81) 4.4) 11.6) 11.30) 5.72-7.73-11.12 (4. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.7-14. scintillation counters. 01-02.62) 4.00-8.70) 5.74 (4.00) 6.03 (4.60-7.32 (3.0-13.34 (4. and cardiac arrhythmia (ATSDR.77-8. diarrhea.82) 5.27-5.80-11. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.70 (8.08) 7.81) 4.3) 10.20 (6.49) 4. Little is known about the health effects of this metal.9) 12. and as polymerization catalysts.2-13.1-12.95-4.08-5.71 (4.3) 10.9 (10.39) 7.67 (4.2-13.79 (4.0) 9.60) 5.55 (7.4 (9.6) 10.4) 9.05) 5.71-5.89) 5.86 (7.70 (6. and clay.52) 7.64) 5.6 (9.97-7.64 (4.89-5.7 (10.35-5.32-5.1 (10. Whether cesium compounds are carcinogenic is unknown.90 (6.99-11.62 (5.17 (6.83) 6.40-5.73-5.80 (4.2-14.4) 10.83-4.01) 7.59-5. 0.3 (8.56-11.1 (11.57-5.50) 9.61) 7.10 (8.68 (7.32) 4.3-13.50 (4.8 (11.3) 10.9 (11.59-5.56 (4.20) 7.20 (4.Metals Cesium CAS No. Radioactive 137Cs has been used medically to treat cancer.0) 11.13-8.0-15.54) 4.01-6.05-5.80 (8.15-8.25) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.56) 5.92-13.70 (5.4 (9.17) 4.42) 7.71 (8.59) 7.80 (8.21 (4.40-11.8) 11.81) 9.74) Selected percentiles ( 95% confidence interval) 50th 4.26) 7.30 (6.5-14. Fourth National Report on Human Exposure to Environmental Chemicals 205 .77 (9.9) Total 4.70 (4.38) 5.10 (6.1-13.94 (4.40-11.63) 6.02 (4.60-6.8 (10.80) 7.03-4.90) 4.70) 7.84-5.00-8. Most human exposure to cesium occurs through the diet.24) 4. interval) 4. However.14.20-8.3-15.5-16. 2004).00) 4.97 (7.4) 12.80-10.53 (6.10 (6.0 (10.91-8.63 (4. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.40-5.47-4.94) 4.14.35 (4.40) 5.7) 11.8) 12.90) 5.10-8.2) 11.5 (10.60) 7.04) 7.3) 9.90-10.94 (4.70 (8.74-5.49) 75th 7.12-11.40) 5.80 (8.25 (3.90-10.98 (7.0) 10.7 (10.84) 8.90 (4.40) 7.69-6.71-8.70 (9.64-10.90) 9.49 (5.10-5.6 (11.3) 10.22-4.7) 10.08-5. respectively.50) 5.60 (8.68) 9.7 (9.4) 12.99-6.37) 7.4) 10.42-7.26-11.43-8.13 (8.97) 4.9 (11.87-7.22 (4.01-8.21) 90th 9.3) 12.88 (8.45-8.50-7.2 (9.37) 5.27) 4.60) 7.00-4.8) 11.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.33-5.60-7.07-11.03 (4.00 (7. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.20) 5.80-10.00) 7.8) 12.90) 5.36 (3.59 (5.29 (4.6 (9.20) 8.1) 9.14 (4.99-11.89) 4.5) 9.6) 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 4.4-13.87) 5.9) 8.0 (9.91 (7.97) 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 4.50 (7. For absorbed cesium salts.20) 4.1-12.80-6.2) 12.8) 9.13 (5.12-5.0) 12.39-4.80-13.84 (4.70-8.0) 12.76-6.10-7.27 (7.60-6.82-4.81-14.5-14.36 (6. infrared lamps.16-6.90-12.6 (11. soil.2.47-8.50 (4.86-11.5 (8.60-5.40-7. and 03-04 are 0.99) 9.4) 95th 11.80 (4.30) 7.84) 5.23) 9.00-9.0) 12.34) 9.13 (7.1) 11.61-6.77 (9.5) 12.80-10. nausea.72) 4.71) 4.44 (8.60 (7. semiconductors.7 (10.7) 10.77 (4.90) 7.5-13.26) 4.8 (10.64-5.30-5.84-9.30 (6.59-5.7 (8.3 (8.29) 4.86-12.33 (6. the body half-life is estimated to be 70-109 days based on 137Cs exposures.64) 5.8-13.9 (11.9) 11.90-8.87 (4. although cesium was generally of low toxicity when given to animals.43 (5.50 (4.42) 6.95) 5.7 (9.70 (6.7) 11.9 (10.5) 10.46) 7.95 (3.96 (6. and 0.80 (4.6 (9.50 (6.10 (8.87 (4.70) 5.1) 10.20-4.6 (9.10-9.53-11.05-5.45-5.20-5.08 (7.66 (7.04 (4.8) 9.49 (4.56 (4. cesium hydroxide is corrosive and irritating at high concentrations.2-13.63-4. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.26 (3.

79) 9.3) 9.68) 4.46-8.63-6.13-9.4) 10.48) 7.57) 3.16-8.81 (4.30 (3.7) 10.89-4.00) 6.27-4.85-4.53) 3.31-6.15-4.97-4.03) 5.85) 4.35) 3.49) 3.30) 10.96 (4.2) 11.38-12.9) 10.55-5.5) 9.08) 3.65 (6.98) 5.51 (4.23 (7.62-8.43 (4.63) 6.41) 9.51 (7.83-6. population.00-8.64) 9.17-4. Komaromy-Hiller et al.38-7.81 (4.43-11. population results shown in this Report (Alimonti et al.25) 4.47) 7.50 (5.13) 7.78 (3.7) 10.53 (4.95-12.91-6.42-4.00 (8.50) 8.79) 6.95) 10.42 (4.77 (6.83) 8.31 (4.66 (5.8) 6.99-9.05) 6.67 (5.95 (3.74) 75th 5.21-4.82-4.20-4.98) 5.06 (5.3 (10.18) 8.54 (4.38) 10.33 (5.2 (8.12) 3.94) 7.02 (5.56) 4.03) 6.41 (8.72-5.58 (6.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.20) 5.75-11.13-9.S.05-4.08 (6.65-3.74) 3.00-4.27 (8.48) 90th 7.59) 4.60-10.46-4.52-5.43-6.45 (4.21 (2.73-4.38 (3.51 (3.87-4.60 (3.65-4.28) 8.40-5.50) 4.S.15) 95th 8.02-4.78) 4.25) Selected percentiles ( 95% confidence interval) 50th 4.30-4.91-7.44 (4.66 (5.50) 4.17 (6.53) 6.16-8.21-3.10 (5.06) 4.46 (7.08) 4.79 (5.68) 3.27-6. interval) 4.30 (7.18-6.95-6.18-7.60-20.14) 4.92 (5.56) 3.54 (5.84-11.12 (3.29) 5.91) 4.33-3.90-8.84-9.30-4.3 (9.14-7.5) 7.47 (7.61 (7. 2004).79-5.14 (6.71) 6.40) 7.51 (4.68 (4. population from the National Health and Nutrition Examination Survey.95) 4.64 (4.99-9.31 (4.04-5.04) 6.26-6.44 (8.64-6.22 (3.67 (6.51 (3.41-7.33 (5.66-6.22-11.00-9.93-7.41 (5.00-5.21-5.47) 4.19-6.77-5..60) 3.19-3.07) 8.62) 5.07) 8.31-4.11 (5.26 (3.16-5.61-3.S.83-7.0 (7.53 (6.6 (9.82) 7.05-3.04-11.29-3.3-15.12-6.73 (3.05) 3.3 (8.46) 6.33-8.87 (5.35-11.91) 5.20-4.99-4.30) 10.15 (7.84-7.90-3. (2000) found urinary cesium levels that were slightly lower than those reported for the U.68-11.28) 7.63 (6.9 (9.10-4.04) 5.39) 5.29-3.07-4.84-9.95 (5.78) 4.29) 4.43) 8.27 (6.39) 8.93-9.03-6.88-4.67) 5.35 (3.96) 4.10 (3.08) 4.76-9.84-7.97) 8.71 (7. Two small studies of European populations reported urinary cesium levels similar to U.2 (8.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.05 (4.24-10.13 (3.70) 6.80) 6. 2005.06 (3.7-12.85) 5. Biomonitoring studies on levels of cesium can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cesium than are found in the general population.27) 4.77 (7.43 (8.74-11.36-6.03-5.77 (4.98 (7.28 (4.64 (8.29) 4.14-6..88-10.0) Total 4.47) 6.44-9.24 (3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.37) 4.74 (5.47) 6.58 (4.99 (3.09 (4. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.0) 7.39 (5.41) 4.40) 6.14) 4.8) 10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10 (3.27 (6.35-7.90 (7.70) 7.30 (4.07 (5.47 (4.58) 8.76-6.42-4.08-7.00-5. Using clinically submitted specimens.36-10.50 (7.56-10.41-4.55) 4.06) 5.6 (9.72) 4.08-3.96-4.3) 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 3.58-5.63 (7.09) 8.60 (5.26 (4.72 (4.68) 6.99) 4.50-5.15-11.94 (5. Minoia et al.44-5.79) 4.87) 5. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.90-8.63 (4.17) 9.00-10.45-6.74 (4.17) 4.01-8.14-4.48-6.86 (4.11 (5.8 (9.41 (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 .54 (3..63-6.36-3.10) 7.91) 5.28 (5.50 (6. 1990).22) 6.5 (9.43 (4.05-3.97-5.91 (5.75 (6. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.16) 5.18 (7.92) 3.24-4.5) 9.54 (4.96-4.95) 8.38 (3.08 (3.78 (3.6) 6.37-3.98 (6.3) 11.35 (4. and were also roughly similar to those in this Report.77) 4.43 (3.51) 4.1) 11.96) 4.42-6.44) 3.56 (4.34 (5.42 (5.66 (6.58) 3.64) 4.20-8.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.64) 5.91-9.70 (7.50) 4.91 (5.20-4.9 (10.56) 4.08 (5.75 (7.55 (3.46 (8.8) 5.59-8.09) 4.

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

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.285 (.22-1.294 (.940-1.410 (.21) 1.900) .450) .68 (1.670 (.810-.17 (1.308-.367 (.610) .65) 1.660-. diamond-polishing wheels.369 (.08. and 0.46 (1. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.470) .374 (.431) .03 (.463-.33-1.770) .270-.16 (.460 (.23) .620-.47) 1.520 (.313) .270-.32 (1.410) .550) 90th .540-.37-1.73) 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 . interval) .640) .16) 1.620-. 01-02.520) . 208 Fourth National Report on Human Exposure to Environmental Chemicals .434 (.48) 1. respectively.740 (.450-.04 (.960-1.300 (.380 (.331-.327-.06-1.364-.900) .420 (.427-.600-.430 (.530 (.53) 1.820 (.08) .480-.380 (.940-1.06 (. Cobalt compounds are used as catalysts in producing oil and gas.03) .490-.680) .499 (.05 (.610-.39) 1.334) .870 (.01-2.660) .530-. Cobalt occurs naturally in airborne dust. It is also a component of porcelain enamel applied to steel bathroom fixtures.336-.410 (.583) .890) 95th 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 .386) .370-.270-.23-2.920) 1.372) .04) 1.540-.81) 1.410 (.373) .S.410-.590 (.370-.810) .371 (.03) 1.419) Selected percentiles ( 95% confidence interval) 50th .790 (.890-1.03) 1.480 (.760) .73) 1.790-.355-. and inks.310-.430) .291-.04-1.340-. large appliances.25-1.20 (1.540-.730) 1.01 (.660) .310 (.610) .50) 1.750 (.490-.460) .375 (.431) .370) .22) 1.390-.800-.850) .399) .890-1.840) .670 (.380 (.379 (.28 (1.920-1.48) 1.06 (.950-1.350-.47) 1.Metals Cobalt CAS No.581) . blue-colored pigments.570-.290-.469-.14) . Usual human exposure is from food sources.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Cobalt compounds are also used in manufacturing battery electrodes. steel-belted radial tires.520-.14-1.350 (.520-.370-.340 (.64) 1.820 (.26) 1.850-1.418 (.09 (.08-1.800) .460 (.630 (.523) .32-2.750 (.28 (1.452 (.16-1.680 (. population from the National Health and Nutrition Examination Survey.670-.640) .17-1.28-2.620-.01-1. The cobalt used in U.390) .519 (.360-.12) 1. hard metal or in combination with other elements. varnishes.430 (.12) 1.404) .280-.01 (.81) 1.348-.680) .339 (.710 (.16-1.50 (1.17 (1.60 (1.870 (.348-.393-.890-1.26-2.44) 1.630 (.740-.388-.340) .19) .800-.377-.750 (.461 (.496) .420) .460) .99) 1.950-1.630-.00) . hard metal (alloys of cobalt and tungsten carbide).950 (. seawater.940 (.460) .42) 1.950) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.05 (.47 (1.09) .520 (.590-.301 (.550-.570) .550 (.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 .350) 75th .03-1.333-.890) .398 (. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray. and soil. automobile airbags.670 (.600) .370 (.740-.880 (.67) 1.600 (.710) 1.530) .950 (.454 (.450) .690-.390 (.420) .540-.430) .07 (.359 (.05) 1.860 (.580 (.352 (.379 (.26-1.330) .930-1.610 (.400-.13) 1.414) .500) .450) .900-1.330 (.360-.03 (.570) .750-.333-.450-.33 (1.17 (.24 (1.07-1.398) .92) 1.07.16 (1.316-.45 (1.32) 1. 0.16 (1.435 (.700) .670-.430-.16) 1.620) .410) .543) .980) .350-.790) .15-1.520 (.350-. see Data Analysis section) for Survey years 99-00.47 (1.930) .520) .910-1.690 (.590) .373-.520-.570-. Cobalt is used as a drying agent in paints.338-. industry is imported or obtained by recycling scrap metal that contains cobalt.36) 1. and kitchenware.580 (.540) 1.930 (.430 (.02-1.405-.305-.417) .650 (.390 (.390 (. and 03-04 are 0.04-1.650-.410 (.590-.32 (1.570 (.343 (.880-1.502) .75 (1.520 (.424) .59 (1. shiny.316 (.410-.440-.460-.360-.28 (1.640) .515 (.380-.380-.810) .650 (.340) .330-.450) .07-1.580 (.52 (1. It is emitted into the environment from burning coal and oil and car and truck exhaust.520-.510) 1.830-1.900) .259-. and magnetic recording media.26) Total .320 (.710) .07.900-1.15 (1.04-1.300-.820 (.465) .410 (.690-.680 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.980-1.564) .760 (.340-.470 (.410-.319) .416) .700) .870-1.487) .428-. and in synthesizing polyester and other materials.56) 1.22 (1.09 (. and fertilizers.32) 1.394) .S.480 (.500 (.24 (.560 (.850-1.29 (1.850) 1.

refining or processing alloys.313-.49) 1.27) 1.733-1.50 (1.821 (.346 (. population from the National Health and Nutrition Examination Survey.Metals fabricated from cobalt alloys (Lhotka et al.215-.543) .12-1. using hard metal cutting tools.237-.428-.963-1.73) 1.317 (.342-.756 (.781) 95th 1.290 (.248-.609) .30 (1.358 (. Cobalt is absorbed by oral and pulmonary routes.386 (.513 (.33) .500 (.700 (.562) .29 (1.634-.277-.842) .28) 1.753) 1.937 (.857-1.378-. 1979).11-1.14 (..380-.24) .547 (.35) 1.429) 1.644 (.826-1.975 (.328 (.00 (. cobalt is excreted predominantly in the urine.449-.737 (.29 (1.273 (.500-.333-.508-.319-.29 (1.290 (.523 (.792 (.352 (.938) .554 (.313-.25 (. A portion of cobalt retained for long periods is concentrated in the liver.475 (.560-. or using diamond-polishing wheels that contain cobalt metal.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 .396) .280-.327 (.694) .00 (.667-1.976 (.06 (.328 (.963) .33) 1. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.394) .563-.02 (.522) .16 (..243-.361 (.294-.955) .03-1.781-1.339-.983) .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 .417) .00) .594) .785) .03 (.911-1. 2003).703-.905) .952 (.552 (.316 (.281) .606 (.630-. Exposure in the workplace may come from electroplating.626-.582-.900-1.435-.50) 1. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.329 (.630-.304) .10-1.463-. 1972).368 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.309) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.476-.562) .313-.990-1.471 (.738 (.407 (.396) .290 (.10) .407) .523 (.879-1. in the feces.381) .251-.898 (.306 (.239-.334) .550-.36) 1.00) .29) .457) .434-.275-.425) . Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).829-1.462) . Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.352 (.27) 1.616-.638-1.271 (.333 (.611) .324) .303-.679-.355) .728) .348) .647) .467-.738 (.829) .257 (. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.387) .662) .895-1.302-.615) .861 (.963-1.297) .278-.513-.306) 75th .425-.343-.689 (.29) 1.378-.669) .598 (.548 (.895-1.708) .585) .740-1.293 (.513) .960 (.487-. respectively.581) .404-.323) .328) .314 (.297-.353 (.04 (.683-.955) .964 (. 1994).595) .667-1.282-.850-1.704-.830 (. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.369 (.376 (.278 (.821-3.313 (. and to a lesser extent.363) .362 (.327-.10 (.691 (.44 (.442-.368) . an essential human nutrient.537 (.750) . Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.362-.774 (.247 (. interval) .461) .707) .591 (.337 (.250) .611) .861-1.917) .848 (.593) .833-1.60) 1. Smith et al.391) Selected percentiles ( 95% confidence interval) 50th . Once absorbed and distributed in the body.268 (.872 (.361-.777-.296-.455 (.435 (.09) 1.365) .361 (.272-.298 (.361-.640) .438) .753-.600-.542 (.301) .632-.561) .760-1.393 (.36) 1.259) .256-.844 (.736-.393-.457 (.488) .17) .599) .335 (.378 (.00 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.11-1.421) .282 (.757-1.824 (.259 (.15 (.55) .344-.449) .313-.400 (.384) .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 .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 .426 (.417 (.234 (.15) 1.257-.279 (.457-.388 (.00 (.54) 1.481) 90th .83) 1.574-.673-.391 (.786-.248-.534-.479-.469-.16 (1.963) ..608 (.929) .503-.534 (.505) .372) .444 (.57) 1.333-.500-.368) .479) .471-.529 (.25 (.728 (.329-.296) .362) .635 (.16 (.723 (.50) 1.259-.533 (.932-1.365-.360) .487-.402 (.286) .301-.313-.727 (.439) .419) .433) ..353-.744) 1.12 (.04-1.847) .382-.60) 1..275-.750-.279) .310) .850 (.660-.408 (..304-.388 (.554 (.851 (.409) . 1972).452-.274-.337) .700 (.983-1.10) Total .792-1.392 (.S.990) .23 (1.515 (.35) .378-.352) .19) .838 (.324-.495 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.326-.343 (.804) 1.331-.333-.300) .349) .471-. 1994.468) .289) .00-1.938-1.949) .291 (.16) .

1993). 210 2006. 1994). The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. 1955). Am J Med 1972.. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda.. Linnainmaa and Kiilunen. Swennen et al. 2005. Information about external exposure (i. 2005 [online]. Cobalt was once added as a foaming agent to beer.. Perkins DG..S. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect.. “Hard metal” disease. has been associated with exposure to dusts that contain cobalt.Metals Toxic effects of cobalt have been encountered in workplace settings. with mean levels that were about 15-20 times higher than in the general U. Dunstan et al.e. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al.gov/ exposurereport/. 2003. 4/3/08 Christensen JM. 1998). Toxicol Sci 1999. Lison et al. Lauwerys and Hoet... IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. 2005.gov/toxpro2.. 1998). Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al.atsdr. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. 2001. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al.. Cobalt-beer cardiomyopathy.43(4):299-303. Cugell DW. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al.... 1997. 1997). Atlanta (GA). Grumbein SL. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al.. population (CDC. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . 1999). MacDonald et al.. Lisi. 2003. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 1988).53:395417.cdc.. Arch Environ Health 1988. 1992). not to imply that the BEI is a safe level for general population exposure. environmental levels) and health effects is available from ATSDR at: http://www. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. usually in combination with tungsten carbide (Cugell et al.. 1989). Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. Poulsen OM. 2001.50(13):95-104. Hailey JR. Iavicoli et al..html. Haseman JK. Available at URL: http://www. 1988).cdc. 2001). Morgan WKC. Information about the BEI is provided here for comparison. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. 1985. A 1982-1992 surveillance programme on Danish pottery painters. 2001. A clinical and pathological study of twenty-eight cases. although substantial occupational exposures have produced elevated urinary levels for many weeks.. Blood and urinary concentrations as estimators of cobalt exposure.. Sills RC. 2006. Daniel et al. Shirakawa et al. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. 1994. population results in this Report (Kristiansen et al. 2003).. 1994. 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. Rubin A. White and Sabbioni.S... 1993).. Urinary measurements mainly reflect recent exposure. Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. 1990). For workers exposed to cobalt in the air. Alexandersson R. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis. 1972). Bucher JR. References Alexander CS. Centers for Disease Control and Prevention (CDC). et al. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. Sci Total Environ 1994. Third National Report on Human Exposure to Environmental Chemicals. Krause et al. Thomassen et al.. Roycroft JR.49:56-67.

Science 1988. Ziaee H.22:359367. Heki S. Kirsch-Volders M. J Bone Joint Surg Br 2005. Int Arch Occup Environ Health. 1985.95:29-37. Vitali MT.50(9):835-842. et al. Lhotka C. Cresti R. Leghissa P. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Jarvis JQ. Occup Environ Med 1994. Sabbioni E. Kato M.533:135-152. Sabbioni E.58(10):631-634. Roto P.150(1-3):167-171. Mosconi G. McCalden RW. Occup Environ Med 2001. Boca Raton (FL): Lewis Publishers. Blunn G. Biological monitoring of workers exposed to cobalt metal. Outcome of occupational asthma due to cobalt hypersensitivity. salt. Iavicoli I. Sci Total Environ 1994. Thomassen H. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Kriss JP. MacDonald SJ. Lisi P. J Rheumatol 2001.21(2):189-195. Cobalt cardiomyopathy. Trace element reference values in tissues from inhabitants of the European Union. Goto S. et al. and hard metal dust. Weyher I. J Occup Med 1992. Angerer J. Mutat Res 2003. Health Phys 1979. Romazini S. A report of two cases from mineral assay laboratories and a review of the literature. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Sanghrajka AP. Co-sensitivity between cobalt and other transition metals. Hoet P.69(3):193-200.148:241-248. Kiilunen M. Alessandrelli M. Radulescu M. Christensen JM. Linna A. Hoher T. Uitti J. Buchet JP.28(5):1121-1128.88(4):443448. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Wild P. Zhuber K. Ghat IS. Hammon E.34:620-626. Health Phys 1972. Zedda S.” Contact Dermatitis 2001. Goldberg MA. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. et al. Thakker DM. Lauwerys R. Bunn HF. Kristiansen J. The release of metals from metal-onmetal surface arthroplasty of the hip. Fujimura N. Chest 1989. Shirakawa T. Lauwerys RB.150:177-183. White MA.204:147-160. Rorabeck CH. Lung cancer risk in hard-metal workers. Dunning SP. oxides. Absorption and retention of cobalt in man by whole-body counting. Molders J.45:246-247. Sci Total Environ 1997.48:172-173. Sci Total Environ 1998. Meier R. 3rd ed.20(1):25-31. Sci Total Environ 1994. J Trace Elem Med Biol 2006. Falcone G. X. Epidemiological survey of workers exposed to cobalt oxides. Weber A. DeSantis V. Unwin P. and cobalt metals. Smith T. Buchet JP. Robinson C. Hedge AG. Lison D. Pisati G. Cannon SR. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Cleland D.242:1412-1415. et al. Zobelein P. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Lauwerys R. Meyer zum Buschenfelde K-H. Int Arch Occup Environ Health 1997. Daniel J. De Boeck M. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial.87(5):628-631. Salama A. Sabbioni E. Lison D. Clin Orthop Relat Res 2003.150. Dunstan E.44:124-132. Respiratory health of cobalt production workers. 2001. Kuska Y. Long-term clearance of inhaled 60Co. Chess DG.55(4):269-276. Lison D. Lasfargues G. Br J Ind Med 1993. Barnaby CF. Kusaka Y. Gross RT. Swennen B. Schaller KH. Schank M. Bacis M. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Thabe H. Tilley S. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Iversen BS. Arch Intern Med 1990. cobalt salts. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Zweymuller K. Edmonds CJ. Moulin JJ. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Linnainmaa M. Ichikawa Y.157:117121. Contact Dermatitis 2003. a study of 13 elements in blood and urine of a United Kingdom population. Szekeres T. Carnes WH. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Stanescu D.216:253-270. HoffmannB. Steffan I. et al. Dickel H.51(7):447450. Kraus T. McMinn DJ. Swennen B.Metals effects of cobalt. Peltier A. Am J Epidemiol 1998. Diepgen TL.406:282-296. Cobalt and antimony: genotoxicity and carcinogenicity. Palmroos P. Salvatori S. Industrial Chemical Exposure: Guidelines for Biological Monitoring. J Bone Joint Surg Br 2006. Pradhan C. Laippala P. Bourne RB. Occupationallyinduced “isolated cobalt sensitization. Schramel P. Goto S. et al.(1-3):133-139. J Orthop Res 2003. Bozec C.36:732-734. Oksa P. Am J Ind Med 2003.

90-3.90-2.40) 5.20-4.50-3.60) 1.50 (3.80 (2.60) 2.80 (5.20 (3.00-4.52 (1.00) .10-8.20-3.20 (2.10) 2.20-3.30 (3.60) 1.20) . interval) 1.90) 2.70 (2.40 (4.60 (2.40-1. bronze).60 (1.60 (1.60-4. 01-02.60-1.899-.10-2.70) 1.50) 75th 2.60-1.90) 2. Lead has a variety of uses in manufacturing: storage batteries.80 (1.40) 2.60) 1.60) 3.00) 4. Elemental lead can be combined with other elements to form inorganic and organic compounds.60 (4.00 (4.50) 7. antique-molded or cast ornaments.81) 1.40-6.90 (2.30) 2.40) 1.69) 1.60) 2.10-3.80 (1.80 (1. ceramic glazes.00 (2.986) .70-2.30 (1.60) 2.10-3.40) 3.60-1.37 (1.942 (.49-1.60) 3.00-1.56 (1.20 (3.80) 2.60 (2.75 (1.37-1.39-1.50 (2.90-2. and 03-04 are 0.60 (3.10 (2. 212 Fourth National Report on Human Exposure to Environmental Chemicals .40) 2.900 (.20 (1.00) 2.900-1.20-1.S.80 (2.60 (3.02) 1.45 (1.10) 1.40-1.55-1.40) 2.50-4.70-4.00 (5.10 (1.30 (2. malleable.90-4.50-2.10) 1.91) 1.30 (2. metal alloys (e. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.50 (3.80-4.80) 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 1.00) 2.20-1.40-2.09) 1.68-1.32-1. respectively.00) 1.70 (3.30-2.70 (3.10 (3.50-2.66 (1.80 (1. plastics.878-1.90-4.80 (5.52-1.90 (3.946 (.70) 1.80-2. population from the National Health and Nutrition Examination Survey.10-2. and 0. see Data Analysis section) for Survey years 99-00.50-1.60-3.80) 1.40 (3.10 (2.10) 2.70 (1.30-5.30 (4.90 (4.50) 1.12-1.93-2.60-1.00 (3.00-6.30 (4.14-1.10) 1.04-1.83 (1.80-5.90) 2.20) 90th 3. the main source of lead exposure for the general U.3.00-4.60-2.86) 1.50 (4.37 (1.60 (2.80-3.60 (2.20 (3.30-1.50-5.50-2.60 (1.10-2.70 (1.40-3.10-1.60 (3. such as lead phosphate and tetraethyl lead.90-4.40) Total 1.89) 1.80) 2.80) 1.50) 4.60) 2.30 (2.36) 1.70-1.00-1.70) 1. dense.60-4.50 (2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.60 (2.00) 2.30-1.43) 1.00-2.50-1.40-1.S.70-1.77 (1.90 (3.70 (1. 7439-92-1 General Information Elemental lead is a soft.10-3.90) 1.71-1.20 (3.80 (4.20 (1.25 (1.40) 1.g.75-2.20) 2.00) 3.01 (1.50 (1.10-4.40-4.40 (1.50) 1.10-4.50 (2.30-4.50) 4.80 (2. Lead is most often mined from ores or recycled from scrap metal or batteries.48) 1.69 (1.50) 2.40-3.10) 4.90-4.60) 5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00) 3.10-1.70) 4.90) 2.10) 3. blue-gray metal that occurs naturally in soils and rocks. lead was added to gasoline and residential paints and used in soldering the seams of food cans.69 (1.40 (1.60 (1.62 (1.90 (3.30) 2. 0.60) 4.70) 1.10) 3.70-3.90-2.80) 1.40 (1.95) 1.70) 4.900 (.00) 4.70-5.20) 4.70) 4.46 (1.70 (1.10-6.50-6.60 (1.60) 3.20-3.80 (4.50) 5.90 (3.40) 4.30 (1.30-6.30) 1.00-5. brass.23 (1.90 (3.60 (3.90 (2.30-2.60) 3.00) 1.40) 1.50-1.Metals Lead CAS No.40-2.30 (2.80) 2.40-1.30 (2.96-2.60) 4.00) 5. Since lead has been eliminated from gasoline.45-1.70-2.00 (1.43) 1.70 (2.80) 1.51 (1.00) 1.75-1.19 (1.78 (1.40-1.10 (4.40 (1.50 (1.90) 1.90 (1.50-1.20) 4. solders.800-1.80-3.10 (1.10-2.70) 3.10 (1.30-2. population was aerosolized lead emitted from combustion engines that used leaded gasoline.20 (4. Before the 1980’s.20 (1.10-2.30 (1.43 (1. leaded glass.55-1.80 (1.80) 1.55 (1.50 (2.70 (2.40-2.10-1.30-1.70) 3.00 (1.25 (1.65 (1.20) 3.20) 3.62) 1.70-2.60) 4.50) 5.50-3.10) 5.60) 1.87 (1.80 (3.70) 3.34-1.50) 2.90 (1.20 (3.51) 1.50-2.30 (2.20) 5.90) 5.30-1.10) 3.30-1. and for radiation shielding.30 (4. ammunition.40-1.70 (5.10-3.53) 1.69) 1.60) 1.50) 3.72) Selected percentiles ( 95% confidence interval) 50th 1. In the past.50 (4.90-2. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.50 (2.14-1.00) 1.36-1.30-2.20 (3.50-5.60 (1.60-6.10-6.50) 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. Lead was used in plumbing for centuries and may still be present.20) 3.20 (2.40-6.60) 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 2.90) 3.10-2.31) 1.87) 1.80-4.36-1.25) 1.39) 1.00-4.20-2.70-6.17) .10 (2.00 (6.50-1.70-1.70) 4.22 (1.30 (2.20-2.00) 1.43 (1.62-1.20 (3.66) 1.70) 1.70) 2.40 (5.50) 1.60 (1.14-1.50-4.50 (1.40 (2.30) 5.80) 2.3.40 (2.43-1.80) 3.75) 1.32-1.00 (4.20-6.20 (1.00) 2.40-5.20-3.30 (1.80-3.90) 1.40) 2.80 (1.60) 4.80-3.60) 2.60-2.60 (2.30) 2.20) 1.30) 95th 5.52-1.90) 3.20) 3.28.90-6.50 (1.30-1.60) 5.90) 2.20 (1.50) 1.80-4.00) 6.40-3.

10 (.600-.91) 2. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.00) .923 (.50 (2.80 (2.970-1.920 (.677 (.33 (2. interval) .540-.579-.80 (1.700 (.03-2.10 (1.00-2.Metals occupational (e.59-2.50) 1.70 (2.731 (.78-2.20-2.50 (1.14 (1. 2007.30) 2.12) 90th 2.70 (2.60 (1.708-.30) 2.60 (1.90-2.30) 1.52 (1. imported children’s trinkets and toys.604 (.00-1.10-3.795 (.595-.616) .900) .600) .80) 1.90-3.10 (1.506-.g.700 (.14 (1. and contact with soil. lead-based painted surfaces undergoing renovation or demolition.10-1.13-3. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20) .97) 4.573 (.40) 1. 1991).20 (3.700 (.800-1. 01-02.572-.90-2.30) 1. stained glass framing.07-1. lead-containing folk remedies and cosmetics.30) 1.600-. bullet fragments retained in human tissue.700 (.70) 1.40) 1.642 (.80-2.90-3.50 (1.790 (..10 (1.50) 3.23-4. In the blood.857) .60-1.00) .900-1.23) .72) 1. and 03-04 are 0.30-5.10-1.671-.935) 1.900) .800) .11 (1.62-4.82 (2.745-.579-.60-3.20 (2.80) 2.941) .60-2.1.60 (2.641-.06) .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 1.900) .00-1.09) 1.40 (1.773) .848 (.90 (2.60-2.960-1.800 (.50-1.40-3.80) 1.730 (.10) .526-.580-.00 (2.90-4.41) 2.03 (1.82 (1.20) . the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.80 (1.570-.710-.50) 2.20 (1.50 (2.86) 95th 2.78-2.850 (.90 (1.900-1.30) 2.986) .44-2.10) .00) 1.40) 1.591 (.30-1.700-.00 (1.910-.04 (.00 (1.40 (2.20) 1.40 (1. pewter utensils and drinking vessels.75) 4.31 (1.00) .20) .20-1.700-.757-.600-.833-1.800 (.800) .1.480-.11) 2.900 (.30 (2.60 (1.10) 1.80) 2.40 (1. dust.600-.800-1.50-2.33-2.800 (.40) 1.628) 1.00-2.20 (1.637-.90) 1.40) 2.80-3.04-2.20 (2.700-1.20-1. Approximately half of the absorbed lead may be incorporated into bone.78-2.600 (.70 (1.27 (1.40) 2.990) 2.90) 2.50) 1.04) .66 (2.766 (.640-.40-1.558 (.688 (.. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.80) 2.30-1.80-2.35 (.820-1.800-. However.900-1.90 (2.10 (.40-2.752 (.70 (2.86 (1.50) 1.27) 1.29) 2.10-1.30-1.800-.07 (.610 (.900) .30 (1.10-1.60) 2. population from the National Health and Nutrition Examination Survey.800) .700) 1.80) 2.700-. 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.75) 3.600 (.560-.80) 1.651) .40 (1.20-2.70 (2.02 (.80) 3.30) .590 (.900 (.815 (.02) 1.40 (2.18-1.90) 2.828) Selected percentiles ( 95% confidence interval) 50th .30) 1.31-3.990) 1.931) . older plumbing systems with leaded pipes or lead soldered connections.625 (.00) 2.700-.80) 3.40) 3.808 (.30-1.20 (1.800) .862) .30-3.540 (.20) 1.50-3.10-3.710-1. respectively.613) .915-1.33.749) .10-3.90 (2.10-1.90-2.13) .600-.900) .625-.660) .00 (.800) .19 (1.50 (2.718) .701) . Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.500-.661-.70) 2.50) 2.785) .17 (1.20 (2.753 (.40 (1.52-1.24-1. Fourth National Report on Human Exposure to Environmental Chemicals 213 .700 (.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 .960 (.90) 2.30) 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 1.50-2.700) .695 (.630 (.955-1.553-.818) .60-3. or water contaminated by mining or smelting operations.21 (2.900) .40) 2.810-1.840 (.659 (.40 (2.700 (. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.20-1.90-2.00) .40) 1. 0.636 (.564 (.90 (1.10-5.650) 1.10 (1.940 (.690) 75th 1.70) 1.20) 1.60 (1. or after soluble lead compounds are ingested.86-2.960-1.40-1.00) 2.40-5.30-2.40-1. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.49 (1.30 (3.00 (1.04) 2.90 (1.729-.800 (.89) 2.620) 1.50-2.833 (.900 (.20 (1. 2000).700-.70-2.674) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.620 (.738) .10 (.29 (2.86) 1.40) 2.70) 3.00 (1.680-.680-.70) 1.535-. CDC.920 (. and 0.70) 3.04 (.00-2.600) .40-1.64) 2. see Data Analysis section) for Survey years 99-00.40 (2.680) .691-.10) 2.66 (2.62) Total . battery and radiator manufacturing) and recreational sources.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.22) 1.822-1.32 (1.70-3.640 (.20 (1.30) 1.10) 2.00-1.S.14-1.605) . lead-contaminated dust in indoor firing ranges.556-.20) .589-.59) 1.900-1.52-1.20 (1.80) 2.73 (1.

753) .710) .712 (.810 (. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.03) .20) .920-1.914 (.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 .681-.670) 1.02) 1.938 (.31 (1. scant amounts are lost through sweat.39-1.23 (1.11 (.594-.618 (.33 (1.667-.862-.22-1.992-1.62-3.44 (1.85-2. 1993.50-2.85) 1.97-18.742) Selected percentiles ( 95% confidence interval) 50th .74 (1.10) 1.00) .00 (1.38 (2.383-.828) .408-. zinc.551-.Metals 90% of the body lead burden in most adults. and paralysis.731-.61) 1.561-.43 (2. Large amounts of lead in the body can cause anemia.404 (.841-1.667-.14) 1.657) 1.97) 1. Staessen et al.812-1.44 (1.10 (.96 (1.709 (.10 (1.20-3.718) .608 (. BLLs and associated toxic effects differ in children and adults.703) . 2003.658 (.992-1.41-1.900 (.609 (.55 (1.639 (.11 (1.688) .41 (1.47 (2.622 (.977) 1.43) 2.63) 4.659-.11 (.61) 3.06) 1.78 (2.380-. and nails (Leggett.31 (2.725) .94-2.781-1.559-.962 (.682) .03 (1.625 (.62-2.88) 1. encephalopathy.56-3.59-3.08) .404-.36-2.06 (1.38 (2.43) 1.648 (..S. CDC.607-.52) 1.608-.851) .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 .707 (.33) 2.82) 1.893) .793-1.31) 1.53-1.03 (.33-1.29 (1.604-.64 (1.66 (1.15-2..68 (1.718) 1.644 (.508) .725) .701) . O’Flaherty.53) 1.73) 2.645-. In 1991.765) .61) 1.639) .882-1. through the inhibition of certain enzymes.07 (.72) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.957-1.838) .342-. 1996). Approximately 70% of lead excretion occurs via the urine.583-.28) 2.03) .677) .24 (1. For instance.375 (.50-2.18) .79) 2.971 (.62-1.64-2.97 (1.654) .460-.914 (.721 (.722 (.988-1.758) .19) 1.997-1.06) .926 (. and iron.981-1.587-.796-1.18) 2.66) 2.88) 2. abdominal pain. Schwartz.655) 75th 1.677 (.633 (.92) 2.03 (.17-1.623 (.720 (.09) 1. with a half-life of years to decades.655) .681-.11) .606-. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.0) 3.85 (1.623 (.58) 1.66 (1.702) .18) 1.25-1.720 (.25-1.19-5. 1991.22) .603-. hair.01 (. based on prospective population studies.569 (.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 .65 (1.44) 1.08) .898) .18 (1.529-.22-2.790) .37-1.914-1.78-4.97) 1.701 (.71-2.98) 2.742) .07) .683-.52 (1.56 (1.722 (.975-1.887 (.603-.734) .61) 1.85-2.876-1.698) .28-1.48 (1.50-1.04-3.47 (1.686) .03) 1. and through binding to ion channels and regulatory proteins.83) 1.693 (.918-1.22) 1.05-1.31) 1.64) 95th 2.64) 2.34-1.31 (1. population from the National Health and Nutrition Examination Survey.83 (2.700-.615 (.72-2.18) 1.588-.63) 1. 1993). BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger. kidney injury.641 (.746) .50 (1.02-1.35) 2.72-2.89-2.917-1.644) .668-.870 (. 2004.645-.469 (.579-.739) .702) .15-2.56-2.98 (1.461) .432 (.05 (1.38 (2.09-1. the Centers for Disease Control and Prevention (CDC) established a BLL of 10 Urinary Lead (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. with lesser amounts eliminated via the feces.673) .73-2. 1995.730) 1.41) .918 (.06 (.55 (1.774 (.89-5.615 (. The toxic effects of lead result from its interference with the physiologic actions of calcium.49 (1.12-1.639 (.09-1.510-.940 (.933) .28) .88) 2.496 (.586-.07-1..77) 2.65-2.88-2.47) 1.05-1.655-.17 (.37-1.45 (1.621 (.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 1.62) 2.51 (1.755 (.26) Total .571-.22) 1.639 (.676) .75 (2.679) 1.828-1.696 (.436) .98-2.933-1.04) 2.11 (1. The skeleton acts as a storage depot.652 (.963-1.632 (.400) .01) .800-.46 (2.14 (1.592-.86 (1.69 (1.46 (1.71 (1.601-.603 (.61) 1. Nash et al.87) 1.638 (.990 (.09-1. seizures.27 (1.03) 90th 1.00 (1.988 (.03) 1.946-1.617-.708 (.50) 1.03 (. Lead can cross the placenta and enter the developing fetal brain.15) 1.605-.612-.428) . Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.20) .404 (.679-. interval) .03-2.00 (.11-1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.11) 1.677-.15) 1.571-. 1995).56) 3.05 (.33) 1.588-.70 (1.51) 1. 2007).79) 1.671 (.938-1.88 (1.75-2.979 (.541-.492-.698) .594-.535) .43 (1.40-1.667) .26) 2.67-4.08-2.702-.593 (.43-1.763) .649 (.635 (.853-1.03) 2.03) 2.15-3.79 (1.00 (1.94 (1.50-2.

S. 1991.. respectively.cdc. state childhood lead programs also show a decline in the percentage of children younger than 6 years of age who had BLLs of 10 mg/dL or higher.. 2003). Muntner et al.07 µg/dL (Becker et al. 2005b. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. usually with BLLs greater than 40 mg/dL.. EPA. approximately 11. 2005a). 2000). the geometric mean BLL was 3.5 per 100.6%) were lower than those from NHANES 1991-1994.6% in NHANES 1988-1991 to 1.html.e. For example. The U. 1996.atsdr.. which is an 84% decline.0 µg/dL in females (Soldin et al.2 µg/dL in males and 3. including minority race or ethnicity. Lanphear et al. and peripheral neuropathy generally occurring at much higher levels (e. At low environmental exposures. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. 1999). particularly in the skeleton. Information about external exposure (i.21% of approximately 3. 2009).75 µg/dL in U.. 1994).. higher than 100-200 µg/dL).. adults in the 1999-2000 NHANES sample.. 2003. 2003. 1987. 2006)... Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. CDC. 2002a).. Fourth National Report on Human Exposure to Environmental Chemicals 215 .S.. adults in the 19992000 NHANES sample (Apostoli et al. 1999). 1998).S. Schwartz.7 µg/dL and 4. In NHANES 1999-2002 in children 1-5 years old. urban residence. 2003. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. In occupationally exposed adults. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. and decrease fertility (Alexander et al. when the geometric mean BLL was 2.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006.3 million children tested had BLLs of 10 mg/dL or higher (http://www. lead in women may be associated with hypertension during pregnancy. Bellinger 2005. 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.gov/toxpro2. Schwartz et al. seizures.S. 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. BLLs reflect both recent intake and equilibration with stored lead in other tissues.. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. 2002. and organic lead compounds not classifiable with respect to human carcinogenicity.. 1996. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. 1996.xls). 2007).S. Korrick et al... adult residents. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.4% in NHANES 1999-2004.. Overall. Surveillance data reported by U.. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. premature delivery. However. and spontaneous abortion (Baghurst et al. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. may alter sperm morphology. though there is greater individual variation in urine lead than in blood and greater potential for contamination. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. 1984. Payton et al.. 2001).. with overt encephalopathy.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.. 1995. IARC considers inorganic lead compounds probable human carcinogens. and low family income (CDC. 2000). both the geometric mean (1. 2006). Telisman et al. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. Both drinking water and ambient air standards for lead have been established by the U. Urine levels may reflect recently absorbed lead. Jones et al.g. Data submitted through state public health programs from 2006 showed that 1. 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. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. residing in housing built before the 1950’s. the prevalence rate has declined annually since 1994 (CDC. Pirkle et al.000 adults. Borja-Aburto et al. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U.. High dose occupational lead exposure. almost double the geometric mean of 1.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 2005b).4% of children had BLLs of 10µg/dL or higher (CDC.Metals µg/dL or higher as the level of concern in children.S.cdc. environmental levels) and health effects is available from ATSDR at: http://www. reduce sperm count. 2002). Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. More recently. Staessen et al..

Blood lead reference values: the results of an Italian polycentric study.123:e376-e385.gov/mmwr/preview/mmwrhtml/ mm5532a2. Caldwell KL. Pirkle JL. Hernberg S. Available from URL: http://www. Hu H. Lanphear BP. Cox C. Brody DJ.89:330-335. Leggett RW. Sparrow D. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Available at URL: http://www. Homa DM.205:297-308. Rios C. Centers for Disease Control and Prevention (CDC). gov/mmwr/preview/mmwrhtml/mm5420a5.htm. et al. Becker K. Available at URL: http://www. 2005b. Pediatrics 2004. McMichael AJ.115:521-529. Lanphear BP. Meyer PA. Wager C. Cory-Slechta DA. Bellinger D. Hu H. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Ronchi L. Mantere P. Muntner P.87:1-471.54(20):513-516.cdc. Pediatrics 2009. Jones RL. Dietrich K.cdc.73:409-420. MMWR Morb Mortal Wkly Rep 2005a. Neri A. 4/14/09 Alexander BH.8(3):395-401. Rotnitzky A. Korrick S. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. 4/14/09 Centers for Disease Control and Prevention (CDC).gov/nceh/lead/ CaseManagement/caseManage_main. Muller CH. Seiwert M. Farias P. Borja-Aburto VH.26:359-371.55(32):876-879. Henderson CR. Preventing Lead Poisoning in Young Children. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Age-specific kinetic model of lead metal in humans.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. Baghurst PA. Hu H.53:411-416. Reese YR. et al. Aug 2007 [online].html. Angle CR. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. doi:10. Hunter DJ.gov/nceh/lead/publications/ books/plpyc/contents. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. 1999-2002. Public Health Rep 2000. 1988-2004. Teratogen update: lead and pregnancy. Baj A. et al. Aro A.1542/peds:2007-3608. Sci Total Environ 2002. CDC. Bellinger D. Luukkonen R. Lepom P. Int J Hyg Environ Health 2002. Rojas LM. Blanco J. MMWR Morb Mortal Wkly Rep 2006.287:1-11. Scand J Work Environ Health 1984.275(15):1171-1176. Manton WI. Rotnitzky A. References Agency for Toxic Substances and Disease Registry (ATSDR). Batuman V. Available at URL: http://www. N Engl J Med 2003. Vupputyuri S. Hänninen H. Robertson EF. Am J Epidemiol 1999. Semen quality of men employed at a lead smelter.150(6):590-597. 1991 [online]. Korrick SA.cdc. Kaufman JD. Third National Report on Human Exposure to Environmental Chemicals.htm. Neurodevelopmental effects of postnatal lead exposure at very low levels.10:43-50. Auinger P. IARC Monogr Eval Carcinog Risks Hum 2006. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Atlanta (GA). et al. Wigg NR. 2002 [online]. Jusko TA.101(7):598-616. et al. Coresh J. van Netten C. JAMA 1996. Apostoli P. Kaus S. Ganzi A. Jacobson JL. Adult blood lead epidemiology and surveillance—United States.htm. Weiss ST. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development.cdc. Acquisition and retention of lead by young children. 2005. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Chiodo LM. Environ Health Perspect 1993.atsdr. Occup Environ Med 1996. Weiss ST.275:1177-1181. Neurotoxicol 1987. Managing Elevated Blood Lead Levels Among Young Children. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Am J Public Health 1999.cdc. Lead. Kim R. Neurotoxicol Teratol 2004. Atlanta (GA). Hertz-Picciotto I. Schulz C.82:60-80. Environ Res 2000. Vimpani FB. Payton M. Checkoway H. Blood lead levels—United States. Atlanta. Bavazzano P. Roberts RR. The relationship of bone and blood lead to hypertension. Canfield RL. 4/14/09 Centers for Disease Control and Prevention (CDC). Ga. Blood lead levels measured prospectively and risk of spontaneous abortion.gov/toxprofiles/tp13. Ewers TG. Available at URL: http://www. Speizer FE. Stanek KL. Sparrow D. Inorganic and Organic Lead Compounds. Kuehnemann TJ. Toxicological profile for lead. Lead and hypertension in a sample of middle-aged women.348:15171526. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Krause C.113(4):1016-1022. Jacobson SW. Cox C.htm. JAMA 1996. Birth Defects Research (Part A). 4/14/09 Centers for Disease Control and Prevention (CDC). 2003-2004. 4/14/09 Centers for Disease Control and Prevention (CDC).

J Hum Hypertens 1995. Gunter EW. Arch Environ Health 1995. and tibia lead with neurobehavioral test scores in South Korean lead workers. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Paschal DC. population to lead: 1991-1994.140:821-829. Wilhelm M.327:109-113. Soldin SJ. and copper in men. JAMA 2003. Nash D. Am J Epidemiol 1994. Lustberg M. Exposure of the U. Association of blood lead. Gavella M.106:745-750. Blood lead. blood pressure. stable lead isotopes to determine release of lead from the skeleton. Int J Hyg Environ Health 2006. Amery A. Lee GS. Schwartz J. Hwang KY. Staessen JA. Magder L.108(1):45-53. Stewar WF. Toxicol Appl Pharmacol 1993. Environ Health Perspect 2000.Metals results from NHANES III.9:303-327. Kinetics of lead disposition in humans. and hypertension in perimenopausal and postmenopausal women. Kaufmann RB. Payton M. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Brody DJ. Pizent A. Low-level lead exposure and blood pressure. Smith DR. Kaufmann R. blood pressure and cardiovascular disease in men. Rubin R. Soldin OP. Clin Chim Acta 2003. Use of endogenous. Schulz D. IV. Telisman S. cadmium. et al. Am J Epidemiol 2001. Kidney Int 2003. Physiologically based models for bone-seeking elements. Rocic B. Roels H.S.63:1044-1050. Flegal AR. dimercaptosuccinic acidchelatable lead. et al. Low-level lead exposure and renal function in the Normative Aging Study. Weiss ST. Osterloh JD. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Hanak B. O’Flaherty EJ.153(5):453464.289(12):1523-1531.209:301305. Environ Health Perspect 1998.104(1):60-66.118:16-29. Schwartz BS. Lee BK. lead. Environ Health Perspect 1996. Sparrow D. cadmium. zinc. Jurasovic J. Hu H. Hickman T. Sherwin R. Lauwerys RR. Revised and new reference values for arsenic. Pirkle JL. Schwenk M. Lee SS. Blood lead concentrations in children: new ranges. Cvitkovic P. 50:31-37. Lead.

363-.60-2.50-3.563 (.600 (.50) 5. After elemental mercury is absorbed. an organic form of mercury.00 (.927) . thermostats and switches). Other major uses include electrical equipment (e. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.20-3. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.753-1.12) ..500-..500 (. Atmospheric elemental mercury can be deposited on land and water.60-5.800-1.30-5.372) .60 (1.60 (1.60-6.. Also.00 (.90) 95th 4.40 (3.700) .781 (.90 (1.30) 3.574) .60) 2085 2293 3478 Limit of detection (LOD. Kingman et al. which create an episodic potential for volatization and inhalation of mercury vapor.70) 911 856 2081 4525 03-04 03-04 .40) 3. thermometers. to form inorganic mercury compounds or salts. and dental amalgam.80 (1.g.40-1.70 (4.979 (.877 (.Metals Mercury CAS No.30) 1.80) 4. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges. electrical lamps.80 (1.500) .S.490 (.00 (2.900) 1.800 (.S. sulfur. Survey years 03-04 Geometric mean (95% conf.814 (. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. Woods et al.50-2. IARC.00) 3. Some cosmetic skin creams from countries other than the U.860-1. Accidental spills of elemental mercury. have often required public health intervention (Zeitz et al.80) 3.30 (1.700-. 218 Fourth National Report on Human Exposure to Environmental Chemicals .800-1..500-.30) 1. thimerosal.60-6. see Data Analysis section) for Survey year 03-04 is 0.60) 1.400-.02) . merbromin).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 .797 (.30 (2.90-3. which can bioaccumulate in aquatic and terrestrial food chains.g. solid-waste incineration. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).20-4.30) 5.714-.903) Selected percentiles ( 95% confidence interval) 50th .500 (.00-5.50) 4.90) 3.700-.g.g.326 (. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.472-. The ingestion of methyl mercury. 1980.900) 1.90 (1.00) 4. 1998. may contain inorganic mercury. inorganic.70 (1.00-1..50) 1. phenylmercuric acetate) or topical antiseptics (e.776 (.40-2.300 (.30-4. Elemental mercury is a shiny.2. Poorly absorbed from the gastrointestinal tract.10-3. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.00 (.40-3.700 (.40 (4. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach..703-.400-.800-1. with the highest concentrations occurring in the kidneys (Barregard et al.418-.00 (2. Apart from methyl mercury.00) 1.70 (3.. constitutes the main source of dietary mercury exposure in the general population.285-. such as chlorine (e.655-.00 (.40-2.40-1.10) .800 (.700-.800-1.919) .40) 1.900) 75th 1. The kinetics of the different forms of mercury vary considerably.50) 2.700-. and organic forms.900) . Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.419 (.484) . and mercury compounds are still used as preservatives (e. 1999 . In addition. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. elemental mercury is absorbed mainly by inhaling volatilized vapor. predominantly from fish and other seafood. and is distributed to most tissues.700) .30-2.. Hursh et al.60-3.400 (.20 (2. synthetic organomercury compounds were once used in pharmaceutical applications.80) 1.30) 4132 4241 03-04 03-04 03-04 .00) . sphygmomanometers and barometers..40 (3.60) 1.00 (2. 1993).800-1. population from the National Health and Nutrition Examination Survey.886) .70-2. and mining and smelting.50-1.689-. 2002).900 (.80 (3.672) .00) 1. or oxygen.70 (1.800 (. interval) .700-. 2007).20) 2. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).80 (1.90 (4.40 (4.60 (2.900) 1.20-4. mercuric chloride).00 (1.800 (.600) 1.300) .30-6.30) 3.90) 90th 3. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.300-. 1994.

407) .30-11.70-6.30-2.20) ..800) 75th .900 (.70-5.200-.825-1.60 (3.70) 4.900-1. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.00) 2.500-.60 (1. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .600) . 1991.307 (.40) 2.00-3.300) . 1999-2002..06-1.800) 1. Myers et al.27) .400-.70-3.29) .475) ...7) 4.00) 6.820 (. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury. Suzuki et al.20 (.00) 1. 2005).833 (. Sandborgh-Englund et al.40-2.30-4.20-3.70 (1.600) . Jonsson et al.90) 2. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.500-1.200-.10) 1.50) 95th 2.90 (1.40-1..200 (..600 (.14 and 0.70-3.10) ..329 (. Geometric mean Survey years (95% conf.00 (3.30-6.300) .500 (.80-3.500-. Methyl mercury enters the brain and other tissues (Vahter et al. 1993).60) 1.50-2.90) 5. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.343 (. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.268-.10 (1.700 (. 1969.377) .30-6.90) 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 ..30 (1.500-.. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.40 (1.70) 1.30-3.70) 4.30 (1.00) 1. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.40) 1.00) 4.00 (1.265-.900 (.01) .800 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Smith and Farris.200 (.30 (1.Metals the tissues to mercurous and mercuric inorganic forms. 1971). 1993).871-1.256-.200-.800) . 1984.00-6. 1996). and a useful marker of exposure in epidemiologic studies (Grandjean et al.00 (2.80) 579 527 370 436 588 806 Limit of detection (LOD. Excretion occurs by renal and fecal routes.919) . for both acute and chronic exposures.20-3.. 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.60 (1.00 (2.900-1.300 (. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.395) . 1995.700-.940) Race/ethnicity (females.10 (3.02 (. 2003).80) 1.50) 1.700 (.60) 2.700) 2.374) .30) 3.200-.60 (1.S.20 (2.726-1.80 (1.00) 7. 1994) and then undergoes slow dealkylation to inorganic mercury.300 (.10 (.800 (. with most elimination occurring through in the feces (Sherlock et al. 1973)..377 (..700 (.664-1.200-.23) .300 (. thereafter.70-5.500-.50) 2.10) .318 (. interval) Selected percentiles (95% confidence interval) 50th . 2004. Miettinen et al.90 (4.50-12. 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. 1990).90 (4.00 (2.30-6.738-.60 (3.10 (1.20-3. a measure of accumulated dose (Cernichiari et al.00-2. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.60 (2.90) 3.90) 2.0) 4.70 (1.60) 3.60) 1.50 (2.30) 1.10-1.40-2..00-1. 1992 and 1999.3) 4..00-2. 1992.30 (. 1999). After exposure to elemental mercury.500 (.35 (1.14...20-2.697-. National Health and Nutrition Examination Survey.700-1.20-11.. Vimy et al.50 (1.30-5. population. 1998). urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.90) 90th 1.20) 1.300) .10-3. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.10 (1.50) 1..300) .70 (1.369) 1.297-.700-.800) 1. 1992).800) .40 (1.73) 1.800-1.700-1.. Methyl mercury is incorporated into growing hair.500-.90 (3..40) 5.10 (. 1994.50) 3. Smith et al.300) .90 (1.06 (.800-1.200-. Vahter et al.800-1. 1998). Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.00-2. 2003). 1994).800 (.300) . McDowell et al.30-4.944 (..300 (.541-.667 (.80 (3.50-3. Fourth National Report on Human Exposure to Environmental Chemicals 219 .10 (5. 1996.30) 1.20) . The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.900 (.299-.269-.700 (.824) 1. 1975..317 (.00) .

In recent epidemiologic studies. 2002. The constellation of findings may include anorexia. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. fatigue.600 (.600 (. and progressive constriction of the visual fields. Smith et al... dysarthria. 1998. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.700-. causing parasthesias. Once absorbed.800) . hypertension. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.600) .600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500-. Inorganic mercury exposure usually occurs by ingestion.500 (. which may vary for some chemicals by year and by individual sample.800) .600 (.600-.500-.700 (. Overt poisoning from methyl mercury primarily affects the central nervous system. Rice. 1995.500-.600) .500-. Stern 2005. 220 Fourth National Report on Human Exposure to Environmental Chemicals . and sleep disturbance (Bidstrup et al..700 (. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. 1996). high-dose exposure to elemental mercury vapor may cause severe pneumonitis. overt signs and symptoms of chronic inhalation may include tremor. 2000).700 (.600) . 1970. 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) ..600) .. 1951.... anorexia. Factor-Litvak et al. and neurocognitive and behavioral disturbances. 2003).600 (. limb deformities. gingivitis. DeRouen et al.700) 2007 2240 3406 Limit of detection (LOD. 2004. 1995. 2000.Metals may be more efficient for inorganic mercury (Grandjean et al. depression.600 (. Sakamoto et al. Acute. and cerebral palsy (NRC. and pinkish discoloration of the hands and feet (Tunnessen et al. 1963). High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.600 (. 1993).. see Data Analysis section) for Survey year 03-04 is 0. typically after a latent period of weeks to months.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .700 (. Vupputuri et al.S.600) . population from the National Health and Nutrition Examination Survey. insomnia. 1983).600 (. Bellinger et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004. particularly irritability. 1987). 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.. 2004).600) .500-.600-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . maculopapular rash. Sakamoto et al. Drexler and Schaller. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.500 (<LOD-.600-. Oskarsson et al. cerebellar ataxia.600) .500-.. 2004).700-. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. Smith et al. Rissanen et al. 2006.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .500-.700-. 2005.600-.500 (<LOD-..500 (.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 .42. sensory impairments..500-... dysarthria. 2000..700 (. hearing impairment. < LOD means less than the limit of detection. At levels below those that cause acute lung injury.. the existence of a causal relation is unresolved (Chan and Egeland. altered physical growth. irritability. 2005).600 (.700 (. pain in the extremities.500-. Survey Geometric mean (95% conf. 2006. ataxia. short-term memory loss.500) ..600) . Salonen et al.

530-.396-.39-3. However.01 (.60 (1.60-2.97) 2. 1995.90) 2.447 (. Survey years 03-04 Geometric mean (95% conf.430) . Grandjean et al..480) 75th 1.460) .476 (.24 (2. interval) .93 (1. adult women in several ethnic subgroups (Hightower et al.58 µg/L for 4645 adults.509) .42) 95th 3. Biomonitoring Information In the general population.460 (.78 µg/L for adults and 0.77-2. EPA. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.382-.890 (. 2000).9 years). Total blood mercury levels increase with greater fish consumption (Dewailly et al.68 (2..406-.442-.213-.416 (.930-1.330-.26 (1.254 (. and the age-related changes differed across the groups (Caldwell et al.34-3.509) .340-. From 1996 through 1998.330-.430 (.420 (.23) .88) 287 722 1529 03-04 03-04 . 2001..400 (..534) .413-.530) .05) 3.89) 3.940 (.405-.96 (1.14) 90th 2.700-1.85-2. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.54 (2. 2003).19 (2.61) 1.30) 3.03-4. Benes et al.76-3..05) 1.96 (1. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.76-4.16 (. the total blood mercury concentration is due mostly to the dietary intake of organic forms.440 (.530) .410-.408) .33 (2.13-2.330 (. 1997.8 years.430 (.313-. 2009). military veterans (mean age 52. 2009).520) . 1998).gov/mercury and from ATSDR at: http:// www.610-1.24) 1.55) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2538 03-04 03-04 03-04 .Metals standard for inorganic mercury has been established by U.08 (1. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.549) .463) .330-. 1998). the median concentration of blood mercury was 0.420 (.gov/toxprofiles. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.160-. Among the three racial/ethnic groups.960 (.60) 619 713 1066 Limit of detection (LOD.67-2.46) 3.67-3.. A cord blood mercury level of 85 µg/L (lower 95% confidence bound = 58 µg/L) is associated with a 5% increase in the prevalence of an abnormal Boston Naming Test (NRC.00) 1.480 (. A cohort of 1127 U. Over the NHANES 1999-2006 survey periods.870-1. total blood mercury geometric mean levels in females aged 16-49 years did not change.14-2. and increased slightly in non-Hispanic white children (Caldwell. Kingman et al.07 (. Sanzo et al. range 40 years to 78 years) had an average total blood mercury concentration of 2.250) .360-. 2002).290-. particularly methyl mercury.304) . Urinary mercury consists mostly of inorganic mercury (Cianciola et al.29) 1.570) .e.360 (. average age 33 years. 2004.. Fourth National Report on Human Exposure to Environmental Chemicals 221 .S.31) 1266 1272 03-04 03-04 03-04 . Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning. see Data Analysis section) for Survey year 03-04 is 0.580) . EPA at: http://www.atsdr. aged 18 to 69 years.700 (.52) 2.840-1.66) 3.. Schober et al. slightly higher total blood mercury levels were found in U.88 (1.280-.350-.. Mahaffey et al.09 (2.63-2.55 µg/L.870-1..19 (1. Information about external exposure (i..S.65) 1.18) 2. total blood mercury increased with age.492) Selected percentiles ( 95% confidence interval) 50th .770-1. In NHANES 19992002.433 (.14.358 (.cdc.370) .12 (.495 (. who participated in a 1998 representative population survey (Becker et al.200 (. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females. 2006). population from the National Health and Nutrition Examination Survey.. In Germany the geometric mean for blood mercury was 0. These distinctions can help interpret mercury blood levels in people. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.. During the same survey periods.46 µg/L for children. environmental levels) and health effects is available from the U. et al. 2001.00 (. 2003).840-1.99-6.840) 1.S.epa.88-3.S. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.441 (.28) 1.555) .16 (1..23) 2.360-.78-2.20 (1.08 (1.S.31) 2.76-3. average age 9. 758 children.

620-..343 (.67 (1.1 µg/L.255 (.40 (1.40-1. 2003).443 (.455-.455) .28 (. 2006).289) ..11) 1.417) . the urine mercury increased by approximately 0.01) 2. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.619-.391) .476 (..87) 2.447-.404-.35 (1.S.362 (.535) 1.400-. not to imply a safety level for general population exposure.31 (1.545 (.30) 2. military veterans with dental amalgams.800-1.785-1.62 (1.365 (.39) 1.376-.667-1. 2005).400) .306 (.599) .03) 2.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .297 (..990) .522-. DeRouen et al.472-.S.13 (1.714-1. 2002) adult population surveys were similar to those in a U.768 (.508 (..480) .51-2. reversible increase in urinary N-acetyl-glucosaminidase. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.76 (1.06 (.276 (.532 (. An expert-panel report recently prepared for the U.. Czech (Benes et al. 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. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.67 (1. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.616) .486) Selected percentiles ( 95% confidence interval) 50th .S.498) 75th . 1992). 2002).275) .347) .463 (. et al.78-4.30) 1.61) 1.Metals 2000).265-.687) .196-.485 (.18-1. Survey years 03-04 Geometric mean (95% conf.23-2. and Italian (Apostoli et al.587 (.464 (.. 1988.875-1.63) 1.652) .225-.969-1.208-.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 . 2006.41-2. Biomonitoring studies provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of mercury than are found in the general population.358) .00) 286 722 1529 03-04 03-04 .06 (. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine. 1998).56) 1266 1271 03-04 03-04 03-04 .384 (.79 (1.1 µg/L for each surface with a dental amalgam (Kingman et al.11-2.455-.307-.217 (.909 (.333-. Urine mercury and the number of dental amalgams were correlated.970 (.44) 1. 2009). mean urinary mercury was 3. Information about the biological exposure indices is provided here for comparison.32-2.S.630) .87 (1.280-.46-2.77 (2.566) .391-.525 (. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.16) 1.784) 1. and on average.65 (1.385-. Department of Health and Human Services noted that several studies have observed a modest. women of childbearing age have generally been much lower than these levels (CDC.537) . Urinary mercury levels in recent German (Becker et al.964-1.00) 90th 1.. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L. Langworth et al.12-3.88-2.309-.11) 2.368) .246-.365 (.301-.588) .79) 1.86) 95th 2. population from the National Health and Nutrition Examination Survey.09) 1. Levels in U. 2009). In the study of U.392-.13-2.21) 1.447 (.54 (2.64-2..88 (1..88-2.S.04-3.25 (.696 (. et al. interval) .32 (1. a biomarker of perturbation in renal tubular function.07) 1.00 (.

00 (2.966) .84 (2.52) 3.706 (.59-5.68-3.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .79) 3.32-3.45) 2.30 (2.14-1.42-3.592 (.35 (1.664) .98 (5.526-.65-4.62 (3.18 (3.831) .650 (.51 (3.656-.580 (.833) .97) 2.31-1.24) 6.10-4.50-4.31 (1. population.09-1.540-.47) 1.56) 4.685 (.76-5.97 (1.70 (2.24-1.56 (1.14-2.55) 90th 3.32) 2.14) 3.45) 2.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.69 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.06 (.710) 1.650 (.520-.35) .46 (1.30 (2.77) 2.637) .Metals Urinary Mercury−Females Aged 16-49 Years Old.16-5.582-.501-.79) 1. 16-49 years) 99-00 01-02 .61) 1.72) 1.97) 2.30-2.68 (3. Geometric mean Survey years (95% conf.740 (.624-.710 (.00 (3.27 (2.81 (3.709) 75th 1.610-.14.846) .28 (1.55-3.09-1.565 (.799) .23-1.508-.91 (2.831) .605-.620 (.41 (1.41-6.742-1.07-5.892) .691) .03 (.450-. 1999-2002.616-.62 (4.42) 2.92) 4.76) 2.45) 95th 3.721 (.03-2.18) 3.84 (2.99) 1.91-7.85-3.41 (1.04-1. 16-49 years) 99-00 01-02 .27 (1.23-1.387-.07-2.21-3.650) 1.475-. interval) Selected percentiles (95% confidence interval) Survey years 50th .636-.47) 1.600 (.00) 2.99 (2.45-2.909-1.3) 5.50 (1.553-.809) . National Health and Nutrition Examination Survey.15-1.53-3.560-.95 (2.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .97) 2.41 (2.930) .596 (.25) 2. Geometric mean (95% conf.13 (2.500-.870) .10-2.622-.45-3. 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.89 (2.665) .92) 3.99-2.87-4.39-3.14 and 0.772 (.420-.17) 95th 5.709) .540 (.760 (.83-3.774) .04-10.85) 4.502-. National Health and Nutrition Examination Survey.77) 1.578-.51) .719 (.92) 2.27-1.557-.46) 3.43-1.22-3. population.30 (1.806) .580-.579-. interval) Selected percentiles (95% confidence interval) 50th .686) .45 (1.03 (.810) .46-4.15 (2.910) .658 (.68) 3.615 (.57-4.631-.657 (.723 (.22 (.94) 1.16) 5.724 (.21 (1.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.38) 4.65) 1. 1999-2002.99 (3. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.560 (.13-4.832-1.42) 90th 2.569-.37) 1.516 (.426-.699) 1.76 (1.710 (.05 (2.522 (.S.824) .744) 1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.62 (1.48 (2.655 (.520-.05 (3.606 (.03) 1.44) 3.37 (1.670) 75th 1.21 (2.56) 3.81-6.61-6.410-.32 (1.69-3.54) 595 531 381 442 594 826 Limit of detection (LOD.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .850-1.50 (2.632 (.S.790) .07) 1.639 (.

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Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Bernardo MF. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Vorwald AJ. Arch Environ Health 1993.258(4 Pt 2):R939-945. Fisher HL. Nakazawa M. Smith RG. Smith JC. Environ Health Perspect 2007. Schober SE. Vimy MJ. Whittle K. Amiano P. Stern AH. Patil LS.111(12):1465-1470. Blood mercury levels in US children and women of childbearing age. Shen DD. Suzuki T. Mooney TF. Lorscheider FL. Aguinagalde FX. Sherlock J. Friberg L. McMahon KJ. et al. Effects of occupational exposure to elemental mercury on short term memory. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Most B. 1999-2000. Yoshinaga J. Sinks TH. Stern AH.4(5):981-988. Allen PV. Farris FF. Smith AE. Tunnessen WW. 1993-1998.124:221-229.115(10):1527-1531.289(13):1667-1674. Br J Ind Med 1983. Effects of exposure to mercury in the manufacture of chlorine. Hum Toxicol 1984. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Smith PJ. The contribution of dental amalgam to urinary mercury excretion in children. Mottet NK. Amurrio A. Baser M. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Newton G. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Zeitz P.97(2):195-200. Lind B. Bolger PM. Daniels JL. Vahter M. Burbacher T. Woods JS. Kaye WE.128(2):25125-25126. Public Health Nutr 2001. Toxicol Appl Pharmacol 1994. Hongo T. McDowell M.31:687-700. Hislop D. Am J Physiol 1990. et al. Methyl mercury pharmacokinetics in man: a reevaluation. Matsuo N. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Toxicol Appl Pharmacol 1994.37:245-252. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. JAMA 2003.40:413-419. The kinetics of intravenously administered methyl mercury in man. Hall LL.48(4):221229.110:129-132. Topping G.2:117-131.Metals Sanzo JM. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Leroux BG. Am Ind Hyg Assoc J 1970. Goldberg J. The hair-organ relationship in mercury concentration in contemporary Japanese. DeRouen TA. Azpiri MA. Acrodynia: exposure to mercury from fluorescent light bulbs. Sandler DP. Guo S. et al. Environ Health Perspect 2003. Imai H. Orr MF. Vupputuri S. Environ Res 2005. Smith JC. Jones RL. Martin MD. Langolf GD.98(1):133-142. Toxicol Appl Pharmacol 1996. Takahashi Y. Leitao JG. Pediatrics 1987. Environ Health Perspect 2002. Osterloh J. Longnecker MP.79:786789. Turner MD. Dorronsoro M. Environ Res 2005.

2) 48.7-73.8) 46.6) 93.7 (71.3) 47.6 (43.5) 44.7) 75th 84.3) 37. 1996).0) 39.3 (79.6 (40.2) 52.1-52.8-49.7) 86.2 (56.9 (44.8-90.0) 55.5 (37.2 (61.0 (42.9-55.7) 45. aldehyde dehydrogenase. and paints.1 (71.3) 41.0-53.7-51. and 1.2-37.3 (55.5 (67.0 (46.6 (73.7-47.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.3-44.0-71.7 (36.0 (76.7-92.3-75.5 (41.3 (64.8 (42.6-96. urinary excretion over six days CAS No.6) 53.7-41.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.2-70.0-85.2 (55.9-83.5.9 (78.3 (47.6-82.5-52.6 (55.4-75.6-62. In humans. WHO.9 (34. lubricants.1-63.5-65.9-109) 97.8) 75.0 (43.0-56.1) 46.1 (34.2-59.8 (67.5 (81.6-72.3) 83.4 (34.4 (80.9) 67.2 (38.9 (73. respectively.0-100) 63.4 (48.1-51.5) 80. 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.7) 57.9) 34.3 (84.1-52. chemical reagents in hospital laboratories.7 (44.3 (46.3 (37.1) 82.4-61.8.7 (51.2) 41.6-42.4 (79.8-106) 88.0-62.7 (73.6-111) 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 52.9 (33.9-56. hydrogenation catalysts.5-41. Excretion occurs predominantly via the kidneys.5-46. Fourth National Report on Human Exposure to Environmental Chemicals 227 .8) 39.8) 44.5-91.3 (55.2 (40.6 (55.4) 56.9-55.3 (71. 01-02.6) 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 (99.8) 40.6-58.4-82.0-110) 90. and in pigments for ceramics. More recently.0) 45.2-91.0 (81.0-38.0) 84. population from the National Health and Nutrition Examination survey.4-52.9 (37.7) 51. At a daily oral molybdenum dose of 24 µg.2-79. which exert homeostatic regulation over molybdenum balance.0) 97.6) 71.7-96.9 (52.0 (42.7) 78.1) 35.6) 51.2-53.3) 65.5 (48.5) 80.7-122) 93.5 (43.7-50.0) 60. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.0-101) 82.4) 76.5 (74.1-48. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.7 (37. semiconductor and battery industries have begun to use molybdenum.2 (49. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.7-60.5 (41..7) 46.3-91.9 (32.3 (73.6-46.7 (45.3 (38.1-44.6-55.0-77.2) 53.4) 41.2 (83.7) 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 78.7-91.7 (58.7-39. Compounds of molybdenum are also used as corrosion inhibitors.1-55.9-85.3-47.8 (85. molybdenum is a cofactor for three enzyme classes— sulfite oxidase. 0.1) 60.1-88.7 (50. 2001.1) 126 (106-147) 109 (94. 1997).3) 85. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.4) 52.5-66.0 (48.Metals Molybdenum or ore deposits.1-59.2-42.1) 59.4) 49.8-94.3-115) 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.4 (48.7-68.7-84.4) 45.6) Selected percentiles ( 95% confidence interval) 50th 50.0) 62.8-108) 87.0 (41.7) 77. and xanthine oxidase (Kisker et al.8-46.9-82. 7439-98-7 General Information Elemental molybdenum is a silver-white.1) 57. see Data Analysis section) for survey years 99-00.7) 78.4 (72.1 (91.2) 178 (147-259) 169 (138-197) 138 (127-152) 146 (112-171) 145 (129-159) 118 (105-125) 126 (114-134) 114 (103-124) 105 (98.6) 71. and 03-04 are 0.5-124) 108 (92.5) 60.8.2 (49.2-59.5) 85. inks.4) 42.3) 54.1 (38.7-105) 69.S.8 (82.3 (53.5) 47.9) 62.5-68.9 (40.3-108) 215 (161-278) 169 (145-194) 148 (136-163) 154 (132-180) 158 (130-177) 127 (114-139) 1121 1335 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 47.2 (63.2) 79.0-65. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5 (49.8) 48. interval) 45.2) 40.5-52.6 (40.0) 54.2) 37. hard metal widely used to add strength and hardness and retard corrosion in metal alloys. 2001).2 (69.6 (52.

1 (38.5 (79. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.2) 39.2 (36.3-141) 109 (81.8) 37.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.8) 39.0 (58.4-76.4-41.6) 43.4) 89.8-65.2) 43.8) 79.7) 115 (93.8 (57.9) 40.4) 122 (107-133) 109 (99.5-50.4-120) 101 (84.0) 39.6) 36.9) 41.8 (56.9-42.1) 65.9-68.8) 38.3) 41.2) 42.6-63.1) 101 (83.5-92.1 (49.3 (36.1 (82.2-41.7-44.1 (30.3-59.3-52. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.0-120) 85. at daily oral doses of 95 µg and 428 µg.8-46.5-48.1 (33.1-43.6-88. respectively.8) 71.1) 37.3) 56.1-39.5) 90th 108 (97.0-56.5 (39.5 (50.6-63.3) 40.2) 55.1 (38. 1961.5-69.2) 58.0) 33.9 (39.5 (38.2-65.1 (44.8-67.0 (35.5 (54.5-44.2-96.5) 63.5 (41.5-60.7) 62.9-61. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.9) 44.7) 53.8 (37. Molybdenum is generally considered to be of low human toxicity.5 (37.7) 57.0-133) 119 (88.4) 60.1 (54.3) 37.6-61. 1997).7) 75th 63.2 (43.Metals was 18% of the ingested dose.6-45.2 (69.1-43.0) 39.8) 45.6) 48.2 (33.9) 31.03 mg/kg/day in humans (IOM.3) 44.5 (40.6 (57.4) 47.1-45.0 (80.2 (50. Biomonitoring Information Molybdenum is an essential element for health.4 (67.2 (73.4) 61.7-43.5 (65.2-47.3 (53.1-127) 90.2) 39..6-76.5 (39.2-96.4 (44. population from the National Health and Nutrition Examination survey.3-115) 98.0) 88.2-80.2 (40. but available epidemiologic data are scant.1-81.6-41.1) 56.0-46.7 (75.1-109) 89..1-79. Based on studies finding adverse reproductive effects in rats and mice.5 (83.1-34.3 (83.3-43.5-46.5-62.4 (37.9 (49.7-100) 77.9-118) 91.4) 48.3) 61.9 (64.3) 43.9-117) 57.9-87.5 (80.2) 38.9 (64.1-40.4) 58.6) Selected percentiles ( 95% confidence interval) 50th 41.4 (78.3-44.4-118) 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 .7) 45.2-46.5-70.8) 62.3 (71.7) 41.5 (65.8-52.4 (56.4) 77.1-100) 86.5 (36.S. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0-46.3 (51.1) 40.6) 39.4-185) 106 (94.6 (42. U.7) 112 (95.7-120) 87.9-40.3) 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. urinary excretion over six days rose to 50% and 67%.0) 53.7-93.9 mg/kg/day and established a tolerable upper intake level of 0.2) 37.8-42.1-67.6-61.3 (37.5-97.8-118) 81. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8-66.1-112) 78.2 (52.0-38.3-45.1 (39.7-52. and urinary levels reflect intake from all sources.2 (40.7-38.4) 44.5) 73.0-41.8-47.4-107) 85.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.1) 43.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.1-39. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.7-137) 129 (109-155) 112 (97. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.6) 39.0) 62.9-96.4-66.4 (55.9-45.9 (73.9-71. interval) 43.8) 61.4-106) 85.8-84.8 (75.9-45.5 (35.0-103) 103 (90.8-47.2) 42.3) 57.5 (37.2-49.2-40.6 (36. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5 (41. of the ingested dose (Turnlund et al.2 (40. EPA.8 (36.3-102) 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. 2001).6 (71.9) 92.5-99.9) 79.5) 71.5 (34.S.3 (58.7 (30.4-39.3) 64.9 (35.4-42. 1993).3 (55.3 (37.7-40.5-35.7-62.0) 36.1-41.3-68.5-119) 90. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.9 (36.3 (71.5-45.5) 72.0 (74.2) 37.2 (37.5) 60.9 (39.9-41.4) 116 (101-126) 104 (88.4) 40.4 (53.9 (40.2 (57..2-121) 107 (92.8) 38.3-46.5 (40.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42. 1995).5 (35. 1999). and clinical or epidemiologic evidence of adverse effects is limited.6 (38.5 (59.5 (78.0) 38.4 (40.0) 72.1-38.6-78.6 (36.1 (40.3 (36.6 (59.1) 37.1 (37.7 (66.7 (77.1 (42.4 (59.9 (79.0) 44.3-56. In industry.7) 42.8 (90.

(DC): National Academy Press. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. chromium. iron. Molybdenum in infancy: methodical investigation of urinary excretion. nickel. 1996. Yarovaya GA. TR-462. Molybdenum absorption. Sci Total Environ 1998.gov/index. Rees DC.php?record_id=10026&page=420. Peiffer GL. Weyler JJ. van Sprundel MP. copper. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Institute of Medicine (IOM). Menne C. 2002. 2005.S.15(2-3):149-154. Zhurnal Obshchey Biologii 1961.Metals in urine for the U. References Centers for Disease Control and Prevention (CDC).nih.123(1):81-85. and zinc: a report of the Panel on Micronutrients. Minoia C. World Health Organization (WHO). molybdenum.62(4):790-796. Minoia et al. Sabbioni E. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Environmental Protection Agency (U.S. Available at URL: http://www. Shmavonyan DM.22(3):179-191. White MA. 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.gov/iris/ subst/0425.nap. 1998. Keyes WR. Sabbioni E. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No.. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. excretion. Vermeire PA. et al. Turnlund JR. Geneva: WHO. Rapid Comm Mass Spectrom 2002. Kristiansen J. vitamin K. A study of 13 elements in blood and urine of a United Kingdom population. pp. J Trace Elem Med Biol 2001. 2005).216:253-270. silicon. Christensen JM. Occup Environ Med 1999. X. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Turci R.htm. 144-154. Schaub J. 4/14/09 White MA. pp. 420-441.. National Toxicology Program (NTP). Droste JHJ. Occupational risk factors of lung cancer: a hospital based case-control study.niehs. 56:322-327.S. Koval’skiy GA. 1998). iodine. Trace element reference values in tissues from inhabitants of the European Union. White and Sabbioni. 4/14/09 Sievers E. Dietary reference intakes for vitamin A. Aprea C. 2001). Molybdenum 1993 [online]. Molybdenum. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Ronchi A.epa. Food and Nutrition Board. Third National Report on Human Exposure to Environmental Chemicals. Washington. Atlanta (GA). these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. vanadium. Molybdenum-cofactorcontaining enzymes: structure and mechanism. boron. Schleyerbach U. 16:1313-1319. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. edu/openbook. Analyst 1998. EPA). Ann Rev Biochem 1997. arsenic. 4/14/09 Iversen BS. Available at URL: http://books. Van Meerbeeck JP. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. manganese. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. 2001. Am J Clin Nutr 1995.66:233-267. Gatti A. U. Sciarra G. Available at URL: http://ntp. In: Trace elements in human nutrition and health. Kisker C. Schindelin H.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. cisplatin. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.. Platinum compounds are used in electrodes. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel.. respectively. carboplatin) in the treatment of cancer. strength at high temperatures. however. and as drugs (e. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00.S. 230 Fourth National Report on Human Exposure to Environmental Chemicals . as oxidation catalysts in chemical manufacturing. 7440-06-4 General Information Platinum is a silver-gray. 01-02. thick-film circuits printed on ceramic substrates.04. Important properties of platinum are resistance to corrosion.Metals Platinum CAS No. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. and 03-04 are 0. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. jewelry. 1998).07. population from the National Health and Nutrition Examination Survey. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. copper. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. dental alloys.g. 0.04. the ambient air concentrations of platinum associated with its use in automotive engine catalytic converters are estimated to be thousands of times lower than occupational exposure limits. and 0. and high catalytic activity. and iron.

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

Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Ensslin AS. Parrot JL.76(1):5-10. Ewers U..10:63-71.207(1):69-73. Begerow J. palladium. Urinary excretion of platinum from platinum-industry workers.. Thornton I. eds. Petrucci F. Saindelle A. Nickel. Hysell D. Powell CH. Wilhelm et al.4(1):27-36. Patty’s Toxicology. Kavanagh P. Ruff F: Histamine release by sodium cholorplatinate. Bocca B. Herr CE. Ruff F: Platinum and platinosis. Herr et al. rhodium. Biomarkers 1999. Iavicoli I. Fruhmann G. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. 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. Raab W. Schierl. Analyst 1998. New York: John Wiley & Sons.61(7):636-9.123(3):451-454. Gromiec JP. Kelly J.inchem.. 2003. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Arch Environ Health:1969.. Gieler U. Kulka U. Neuendorf J. Environ Health Perspect 1975b. 2004). Int Arch Occup Environ Health 2003. 2003. et al. Urinary platinum levels associated with dental gold alloys. Pethran et al. Kaus S. Biomonitoring of traffic police officers exposed to airborne platinum. Moore W Jr. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. 2003. Seifert B. 1991 [online]. Angerer J. Arch Environ Health 2001.01 µg/L (Becker et al. Saindelle A. 2004. In: Bingham E. 289-380. Huber R. Herr et al.org/documents/ehc/ehc/ehc125. 1998). Wilhelm M. ruthenium. Campbell K. 232 Fourth National Report on Human Exposure to Environmental Chemicals . J Expo Anal Environ Epidemiol 2003. Grimm CH.S. 1999. Cohrssen B. Several studies have shown that background concentrations in general populations were usually less than 0.. Levels of platinum in urine for the U. Hall L. Platinum concentrations in urban road dust and soil. 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.Metals the International Programme on Chemical Safety at http:// www. Duneman L:Long-term urinary platinum. International Programme on Chemical Safety (IPCS). Int J Hyg Environ Health 2004. References Becker K.55(2):138-140. 2004) or less than 0.9:152-158. Hebert R. which elevate urinary platinum by five to twelve-fold (Begerow et al. 1997. Farago ME. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Senofonte O. Pethran A. Biomonitoring Information Urinary platinum levels reflect recent exposure.. Schierl R. osmium.005 µg/L (Iavicoli et al. 2000.. Occup Environ Med 1998.. population were below the limit of detection (0. Environ Res 1975a. 2003). Rommelt H. pp. Crocker W. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Int Arch Occup Environ Health 1997. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum.70(3):205-208. International Journal of Hygiene and Environmental Health 2003. van de Weyer C. Kazantzis G. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Schierl et al. Kuster W. Part 1: monitoring of urinary concentrations. and gold excretion of patients after insertion of noble-metal dental alloys.35:313-321. Schulz C.htm. Turfeld M. Seiwert M. 206:15-24. 1998)..inchem. Nowak D. et al. Blanks R. palladium. 5th ed.. Schierl R.56(3):283-286. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Br J Pharmacol 1969. Occup Environ Med 2004. Hauff K.org/documents/ehc/ehc/ ehc125. Stilianakis NI. Allergy and histamine release due to some platinum salts. 3/31/08 Moore W Jr. 2001). Schierl R.13(1):24-30. Schierl R. Pethran A. Alimonti A.19:685-691. Environmental Health Criteria 125. Schulz C. and platinum. Czerczak S. Hysell D.. Boos KS. Carelli G. Influences on human internal exposure to environmental platinum. et al. Fries HG. Platinum.htm. Jankofsky M. and in blood and urine in the United Kingdom. et al. Uptake of antineoplastic agents in pharmacy and hospital personnel.04 µg/L) in this Report. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Available at URL: http://www.

440-.310 (.520) .480) .160 (.290 (.310 (.230-.400-.460-.360 (.270 (.220) . Thallium disappears from the blood with a half-life of several days.400-.230) .180) 75th .160-.160 (.440) .480) .183) .270-.330-.590) .185 (.210-.290-.500) . interval) .290 (.280) .300 (.147-.640) .240-.350 (.350-.170-.200-.410 (.163) .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.02.430) .260) .215) . see Data Analysis section) for Survey years 99-00.300) .190 (. From these and other sources.220 (.430 (.520) .150-.250-.270 (.153-.450 (.200 (.410 (.218) .400 (.320 (.140-.420 (.420) .520 (.S.202 (.470 (.162-.165 (.490 (.320) .330-.180-.320) .200) .350-.430-.220) .360 (.440 (.360-.550 (.260-.190 (.175) .160-.146 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.260-.200) .180 (.340 (.230-.170) .370 (.144 (.370 (.420-.154-.370) .202) .470 (.220 (.243) .360-.155 (.280) .430 (.170-.340-.460 (.200-.280 (.190 (.170 (.380 (. representing distribution into other tissues.480) .370) .200 (.150-.420) ..183) .330-.420-. and 03-04 are 0.480) .450 (.159 (.320-.200) .400-.191 (.197 (.137-.167-.270) .460) .400 (.290 (.134-. respectively.170) .250 (.225) .148-.400) 95th .160-.180) .Metals Thallium depilatory cosmetics.196) .490) .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 .300-. 2005).400 (.440 (.290) .340-. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.180-.420) . thallium readily crosses the placenta and also distributes into breast milk. it has not been specifically mined or refined in the United States since 1984.172 (.210 (.450) .170 (.380) .330-.310 (.220-.220 (.145 (.280-.410-.210) .192) Selected percentiles ( 95% confidence interval) 50th .239) .218) .390) .400) .290) .490) .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 .370-.340-.410-.178) .330-.260 (.280 (.390 (.220) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.170-.590) .390) .188) .320) .200-.172 (.440 (.410 (.390-.220 (.150-.370 (.410 (.400-. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 233 .240) .160-.190 (.290 (.147-.410 (.480) .490) .184 (.290) .420) .420) .370-.440 (.180 (.157-.149 (.150-.260-.420-.290-.450 (.170-.430-. 0.240) .187-.390-.490) Total .250-.220) .181-. 01-02.197-.170 (.260 (.270) .400) .350-.300) .170) .02.133-.220) .200) .250-.270-.450 (.390) .400 (.260-.410-.340) .240) .370 (.370 (.240-.200 (.170-.420) .440) .250-.210 (.510 (.310-.310) . In the United States. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.160 (.330) .450 (.167 (.350-.230 (.250-.430 (.170-.560) .159 (.250-.370-.300) .450 (.160 (.390 (.270 (. In addition.182-.370 (.420) .220) .158) .200) .230-.500 (.290 (.220 (. 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.270 (.270-.400-.350 (.240-.217) .520) . thallium was obtained as a by-product of smelting other metals.400) .145-.290) .330) .171 (.630) .200 (.190 (.290 (.160 (.410) .350-.370 (.280) .156) .360-.360-.360-.440) .159 (.250-.173-.300 (.350) .420-.270 (.150-.180-.202 (.150-.200-. the latter being the current major industrial consumer of thallium in this country.201 (.250 (.450 (.410 (.330-.410-.201 (.167-. however.185-.450 (.173) .350) .330) . Human health effects from thallium at low environmental CAS No.430) .300 (.156) .156-.360) .135-.340-.02.200) .390-.180-.390) .410-.250) .290) 90th .340) .360 (.172) .470) . 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.510) .380-.370-.500) .230) .206) .230) .380-.260 (.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 .196) .217 (.200 (.173) .330-.200 (.470) .390-.250-.400) .160-.400 (.260-.176 (.190-.470) .350-.450 (.145-.280-.230) .330) .500) .410-.179-.380 (.430 (.430-.190 (.690) .280 (.147-.300) . and 0.180 (.360 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.170-. In the past.177) .

143-.297 (.gov/toxpro2.153 (.160) .217) .274-.348) .282 (.203-.149-.167) .286-. interval) .173) Selected percentiles ( 95% confidence interval) 50th .250) .258-.192-.144-.230) .176) . respectively.287-.333-.atsdr.161 (.217-.234-.212) .144-.286 (.208) .128-.140-. although additional mechanisms of action are possible.349 (.206 (.157 (. neurologic injury.324) .313-.156) .278 (. Severe accidental thallium poisonings from ingesting of rat poisons that contained water-soluble thallium salt have occurred.187-.283 (.323 (.167 (.162) .366) .207) .142 (.532) .300) .218 (. population from the National Health and Nutrition Examination Survey.380 (.256 (.153-.161) .361 (.162) .133 (.167 (.350 (.318-.128 (.180) .317 (.243) .154 (.185 (.224 (.364 (.153) .204 (.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 .159-.300-.389) .137-.171) .131-.350) .215 (.214-.159 (.170) .135-.338 (.155-.369) Total .221) .156 (.208-.153) .291-.307) .200) .258 (.306-.226-.271-.362) .333-.153 (.286 (.306 (. population have been well characterized in NHANES 1999-2000 and 2001-2002 Urinary Thallium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.273 (.146-.207-.259) .221 (.169-.600) .254 (.135-.313 (.S.208-.170-.299-.164) .200-.254-.204) .269) .216 (.210 (.278 (.152) .278-.196 (.133-.365) .166 (.122-.150) .159) .343 (.343 (.304) .196-. EPA.167 (. and polyneuropathy.153-.160-.271-.140 (.172) .456) .148 (.202 (.375 (.html.146-.194 (.265-.333-.287 (.387) .333 (.135-.157-.231-.147-. Information about external exposure (i.148-.177) .321 (.271-.246-.169 (.149 (.221) .145) .154 (.462) .240) .142-.146 (.304) .167-.182 (.184-.171) .145-.211 (.340-.214 (.167-.462) .166 (.205 (. Chronic high-level exposures have been associated with weight loss.333 (.317 (.155-.271-.147-. environmental levels) and health effects is available from ATSDR at: http://www.325-.293) .164) .125-.157) .194 (.238) .152) .191-. IARC and NTP consider the evidence for the carcinogenicity of thallium as inadequate or unclassifiable.402) .189) .148-.278) .198) .286) .184-. and a drinking water standard has been established by U.155 (.cdc.S.328 (.326-.458) .278) .147-.329) .328-.278) .146-.369 (.188 (.160 (.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 .138 (.151-.306-.162-.156 (.155) .145-.180-.280-.313 (.307 (.250-.176) .152) .282-.154 (.235-.244-.289) .158 (.143) .142 (.156 (.304) .146) .200 (.153-.148 (.292 (.222-.321) .S.173) .342) .301-.222 (.402) .317) . (ATSDR.300) .412 (.364) .161) .260 (.248) .333) .223 (.233 (.263-.304) 95th .469) .387) .207 (.146) .198-. arthralgias.422) .229-.233) ..241) .330-.148-.226) .171-.297) .184-.214) .319) .237-.348 (.272 (.266-.333) .389-.168 (.176) .312 (.219) .143-.346) .364) .400-.222 (.162-.346-.141-. 1992) Workplace air standards and guidelines for external exposure are established by OSHA and ACGIH.173 (.192-.153 (.149) .198-.297 (.149-.153 (.119-.278-.286 (.300 (.143 (.366 (.272-.356) .222) 90th .327) .370 (.383 (.146 (.167) .213 (.424) .217-.273-.154 (.214 (.286 (.162) .178 (.192 (.198-.179) .160) 75th .286-.458 (.250-.280) . Relatively high-dose intentional or accidental ingestion can result in gastrointestinal symptoms followed by multiorgan failure.389) .273-.236) . Peripheral neuropathy and alopecia are well-documented effects of acute and chronic exposures.134-.151) .197-.136 (.197) .162 (.145 (.161 (.383) .169) .191-. and death.377) .368 (.260-.200-.235 (.313-.Metals doses or at biomonitored levels from low environmental exposures are unknown.222) .167 (.179-.140 (.227 (.223) . Biomonitoring Information Urinary thallium levels reflect recent exposure.304 (.293 (.153 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.264 (.215) .348-.237) .244 (.378 (.412 (.160) .281-.377) .211 (.238-.338-.267-.181) .364 (.158-.215-.255 (.143 (.229) .e.148-.156 (.214) .231) .200-.269 (.170) . Levels of thallium in urine for the U. Thallium produces toxicity by replacing intracellular potassium in the body.176) .129-.424 (.150) .289) .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 .337-.356-.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 .

. Raithel HJ. 1985). Paschal et al. A study of 13 elements in blood and urine of a United Kingdom population. Investigations of thallium-exposed workers in cement factories. Pietra R. Ewers U. 1990. White MA.47(3):223-231. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U.95:89-105. Sci Total Environ 1998. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. References Agency for Toxic Substances and Disease Registry (ATSDR).Metals (CDC. Valentin H. Centers for Disease Control and Prevention. Sabbioni E.. Int Arch Occup Environ Health 1980. 1992 [online]. Paschal DC. J Soc Occup Med 1985. Trace metals in urine of United States residents: reference range concentrations. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Manke G.76(1):53-59. Third National Report on Human Exposure to Environmental Chemicals. Sabbioni E. Int Arch Occup Environ Health 1981. Sci Total Environ 1990. A study of 46 elements in urine. Boisson P. Investigation of a working population exposed to thallium.html. 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. Brockhaus et al. Radiat Prot Dosim.113(1):47-53. 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. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Brockhaus A. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1980. Environ Res 1998. Dolger R. 1998). Available at URL: http://www. Sampson EJ. Trace element reference values in tissues from inhabitants of the European Union. Schaller et al. Wiegand H.cdc. Marcus RL. Atlanta (GA). Trace element reference values in tissues from inhabitants of the European community I. blood.gov/toxprofiles/tp54. Minoia C. et al. 2005. Buhlmeyer G.265 people living near a thallium-emitting cement plant in Germany. Celier D. Kramer U. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Gallorini M. Jackson RJ. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging.5 μg/L. with concentrations ranging up to 76. Martin J-C.atsdr.48(4):375-389. Minoia et al. Toxicological profile for thallium.. population) are thought to correspond to workplace exposures at the threshold limit value of 0. 2005. Schaller KH. X. Challeton-de Vathaire C. Schmidt M. Morrow JC. White and Sabbioni. 7/15/09 Blanchardon E. Soddemann H. Pirkle JL. Ting BG. 1998. et al. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Pozzoli L. 1981.. 2005) and are shown with results from NHANES 2003-2004 in this Report. et al. Apostoli P. and serum of Italian subjects.S.216:253-270.1 mg/m3 (Marcus. Cassot G. (1981) studied 1.35(1):4-9.

570 (.550) .133) .310-. which are used in rock drills and metal-cutting tools.470 (.510 (.310) .120-. bronzes in pigments.086 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .520) .530 (.080 (.130) .120-.090-.430 (.430 (.190-.080) .170-.530 (.110 (.150 (.250-.084) . and 0.100 (.290) .670) .113 (.580) .400-.300) 95th . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).126) . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.510-.073 (.071-.500 (. interval) .120-.570 (.300 (.120) .410-.180-.160) .050-.470) .220 (.300 (.104) .069-.290 (.062 (.800) .105) .240 (.070-.230-.290-.200-.250) . population from the National Health and Nutrition Examination Survey.270 (.590) .140-. 0.290-.300-.109) .360-.092 (.500 (.190 (.350) .270-.490 (.280-. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.113 (.100-.950) .080 (.058-.180) . and 03-04 are 0.220) .210 (.270 (.080 (.110 (.077-.140-.062 (.53) .400 (.096-.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.100) .080-.340-.280 (.101-.160-.090) .370 (.090) .110-.090-. mainly as scheelite (CaWO4).070-.065 (.095-.080-.060 (.490) .073-.068) .360-.650) .130-.110-.093) .460 (.090 (.460 (.390 (.130 (.520) .250-.070) .060-.096 (.100) . Little information is available on the toxicity of tungsten. filaments for incandescent lamps.360 (.450-.480) Total .380-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.350 (.420-.170 (.160 (.070 (.140 (.123-.180) .360 (.160 (.400 (.140 (.180) .370 (.220) .230-.090-.230) .160 (.380 (.260) .310-.360 (.100) Selected percentiles ( 95% confidence interval) 50th .070-.105 (. see Data Analysis section) for Survey years 99-00.180) .430 (.350) .107 (.100) .560 (.460) . Tungsten is used mainly for producing hard metals.100 (.110) .410 (.790) .100 (.093 (.390) .130-.088 (.074-.460 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.090-.073) .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 .330-.113 (.160-.060 (.210 (.190) .320) .170) .064-.180 (.060 (.082 (.300 (.084-.250) .060-.180-.130) .470 (.810) .330 (.Metals Tungsten CAS No.550) .090-.250) .270-.150 (.180 (.210-.260-.120) .430) .090) . respectively.050-.070-.270-.470) .120) .100 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.097-.250) .170 (.320-.110-.092 (.070) . their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.04.430-.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 .170) .130) .090) .073-.082) .076 (.190-.04.370-.140) 90th .270 (. Tungsten compounds are used as lubricating agents.060 (.060 (.070-.550 (.250) .150 (.260-.130) .080 (.071 (.620) .560) .400) . and for producing ferrotungsten.180-.100) .080-.550) .370-. 01-02.290) .120) .310 (.520) .380) .081 (.091) .066-.770 (.130-.082 (.420-.350-1.078-.056-.160 (.280 (.440) .204) .060-.330) .113 (.137 (.800) .200 (.150-.087) .150) .310-.120-.630) .130) .330-.090-.230-.00) .210 (.100) .050-.240-. Evidence is lacking for the carcinogenicity of tungsten.190-.050-.320 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.380-.370 (.620) .230) .460) .158 (.400 (.122) .160-.260 (.200) .04.111-.090-.690) .340) .310-.095-.120) .230 (.080 (.101 (.360) .500) .340-.310-.330) .110) .160) .132) .260-.130 (.220-.380-.210 (.140 (.080) .070) .350) .220) .151) . and as catalysts in the petroleum industry.090-.830) .076 (.060-.087-.510-1.170) .170) .230-.370) .060-.250) .380 (.130-.260 (.560) .088) .400 (.060-.116) .070 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.090 (.120) .340-.080) 75th .210) .640 (.060 (.380-.210 (.065-.160-.092) .450 (.S.530 (.110 (.320-.560) .082-. which is used in the steel industry.080) .120-.180-.190-.120-.470-.120 (.110 (.620 (.270-.090 (.110 (.084 (.160 (.100-.135) .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 .430-.300) .069) .056-.070 (.290-.190 (.070) .093-.100-.140 (.320 (.560) .

179-.121-.084 (.880) . Patients with medically-inserted tungsten found at increased levels in drinking water.116 (.087 (.073 (.339 (.146) .197-.308) .100 (.360 (.267-.107-.253 (. interval) .383 (.122-.199 (.065-.215 (.088) ..080 (.301) .136-.064-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.333 (.069 (.061-.094) .200-.267) .098-.091 (.302-.157) .083 (.125) .431) . Using neutron activation analysis to 2000.075) .083) .105 (.412 (.146 (.201 (.065 (.111 (.359 (.120) .139) .174) .237) . (1987) found possibly due to methodologic.144 (.341 (.136 (.279 (.154) .317-.459) .381) .452-.151 (.084) .165) .237) .222) .068 (.063 (.077-.261-.094-.085 (.179-.347 (.058-.090-.167) .067 (.104-.063-.078 (.093-.300 (.063 (.329 (.096) .275 (.063-.072-.306) .070 (.414) .078) .333 (. and 2003-2004 (Paschal et al.108-.116) .074-.317) .379 (.064-.255-.103-. population from the National Health and Nutrition Examination Survey.339 (.066 (.216-.231-.284) .061-.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.067 (.090-.605) .354) .133) .279 (.333-.139-.085) .130-.071-.116-.075-.119-.145 (.554) .062 (.197) .057-.206-.344-.214) .049-.237-.186 (.375) .060 (.158) .136-.065-.190) .386) . population.294 (.079 (.154) .105 (.081) .164 (.176-.068-.054-.086) . 2001-2002.078) .265 (.069 (.073 (..060-.209-.270 (.333 (.217-.087) . 2001).217-.538) .823) .084) .136-.066 (.158 (.439 (.089 (.333 (.208-.075) . or exposure that a control group of non-metal workers had mean levels differences.358) .095-.075-.065 (.300-.258-.073 (.117) . measure urinary tungsten.124-.727) .070 (.086-.056-.150 (.203-.326) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.133) .436-1.497 (.067-.301) .098) .333) .436) .082) .582) . 2003.130 (.084 (.083) .431) .091) .069-.077) .079) .250-.500) .279 (.198) .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 .184 (.667) .059 (.100) .086) .083-.138) .122 (.081 (.170-.216-.133) 90th .126-.078-.293 (.091) .098-.074) .106 (.148 (.797) .150-.094) .385 (. Nicolaou et al.109 (.278-.079) .174 (.074) 75th .211 (.093) .085-.340 (.091 (.053-.410-.245-.198-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.222-.216-.117 (.667 (.075 (.215) .152-.333-.054-.(Kraus et al.063-.055-.555 (.081-.205-.121 (..201) .077) .098-.301) .059-.240-.180-.28) .255 (.169) .465) .359 (.071) .074 (.139 (.634 (.331-.065-.092) .250 (.108) .083 (.153-.176-.167-.072 (.144-.392) .071 (.426) .255 (.158) .080 (. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.197) .072-.283) .120) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.138 (.300-.143-. similar to those in this Report (Schramel et al.124 (.231 (.077-. 1997).095) Selected percentiles ( 95% confidence interval) 50th .484 (.S.075 (.071 (.091) .299 (.080-.188-.218 (.167-.131-.122-.272-.329-.333) .482 (.079) .099-.216 (.462) .S.197 (. 1998).302-.453) .224) .061-.098 (.161) .059-.426) .088) .074-.465) .086) .169 (.317 (.136-.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 .431) .353 (.158) .286-.079 (.079) .146 (.739) .078 (.125 (.285) .168 (.214-.258 (.100) .082 (.081 (.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 .089) .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 .091) .439) Total .143 (.153) .199 (.187) .059-.287) .057-.071) .150-.167) .364 (.253) 95th .S.315-.073 (.200-.063-.439 (.300) .071) .181 (.233-.155-.216 (.056-.071 (.109-.484) . Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.119 (.060-.065) . 2005).353 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999. population (CDC.082) .080-.250 (.253-.148) .308) .354-.

Environ Res 1998. bismuth. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. palladium. Morrow JC. [online] 2003. Mosconi G. Paschal DC.58(10):631-634. 2005. The determination of metals (antimony. lead. Manke C. Pirkle JL. Third National Report on Human Exposure to Environmental Chemicals. 4/15/09 Centers for Disease Control and Prevention. Lenhart M. Schramel P.. Wendler I. et al. Sabioni E. Weber A. Kraus T. Angerer J. Link J. Paetzel C. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Angerer J. Cassina G. 2004). Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Nicolaou G.62:380-384. urine. Catheter Cardiovasc Interv 2004. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. cadmium. Schaller KH. Pietra R. 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.gov/nceh/clusters/Fallon/study. Ting BG. Jackson RJ.cdc. platinum. Available at URL: http://www. 238 Fourth National Report on Human Exposure to Environmental Chemicals . Schramel P. National Center for Environmental Health. Occup Environ Med 2001. Feuerbach S. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. mercury. References Bachthaler M. thallium. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect.Metals blood. Int Arch Occup Environ Health 1997. Cancer Clusters. Centers for Disease Control and Prevention. Trace metals in urine of United States residents: reference range concentrations. J Trace Elem Electrolytes Health Dis 1987.76(1):53-59.htm. tellurium. Seghizzi P. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Zobelein P.69(3):219-223. Nevada Exposure Asssessment.(2):73-77. Churchill County (Fallon). Atlanta (GA). Sampson EJ. and hair (Bachthaler et al.

037) .007) .034) .040 (.047 (.023-.018) .012 (.037-.012) .007-.030 (.039-.016) .007-.020 (.008 (.009-.008 (.010-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).015) .009 (.006-.008) .009) .010) .017 (.011) .011-.279) .035) .026 (.013-. and 0.015 (.008) .013 (.018) .037 (.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 .038 (.031 (.007 (.027 (.042) .007-.027 (.030 (.006 (.018-.016) .028 (.013 (. interval) .S. nuclear fuel.009 (.009) * .009 (.027) .008-.011-.006-.040) .009 (.010-.017-.029-.018 (.023-.014 (. In workplaces that involve uranium mining. 01-02.026-.008 (.014 (.020-.010 (.007) .023) .009) .040-.023) .006-.020) .007-.016-.010-.007 (.027-.049) .048) .127) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.009 (.008 (.033) .015-.009) .007-.013-.005-.009 (.023 (. in some ceramics.011) .034-. Fourth National Report on Human Exposure to Environmental Chemicals 239 .018) .016-.012) . respectively.055 (.009-.010 (.035) .009-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.008 (.011) .021 (.010-.009 (.007 (.011-. or processing.015) .066) . and 234U.054) .007 (.009-.010 (.026 (.007-.022-.012-.065) .045) .026-.052 (.024-.008 (.009 (. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.027) . Since the 1990’s.016) .043 (.008 (.046 (.021) .053) .026 (.015 (.012) .016) . Variable concentrations of uranium occur naturally in drinking water sources.012-.007) .027 (.017) .007-.012 (.019-.026) . 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.023) .008 (.037) .008-.007-.037) .033 (.009) .011) .030) .009) .010-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.007-.009 (.006-.014 (.020-.017-.013) 90th .006 (.72%). and as an aid in electron microscopy and photography.017) .029-.005-.008-.017-.009 (.005-.039) .007 (.013 (.015 (.005-.007 (.024-. 235U (about 0. and 03-04 are 0.016 (.016) .007) .006-.010) .009) .036) .016-.027 (.006-.064 (.021-.006-.017) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.054) . population from the National Health and Nutrition Examination Survey.072) .040-. Thus.012 (.008 (.037) Total .027-.036 (.046-.035-.007-.027) .020-.008 (.007-.007) 75th .004.030-.011 (.014 (.008) .009) Selected percentiles ( 95% confidence interval) 50th .009-.069) .010) .027) .019-.032 (.046 (.008) .006-.007-. 0.036-.028 (.009-.067) .023 (.006-.008 (.067) .010) . human exposure occurs primarily by inhaling dust and other small particles.044 (.010 (.021-.020-.022-.021 (.012-.008 (.006 (. see Data Analysis section) for Survey years 99-00.010-.062) .022-.017-.Metals Uranium CAS No.008 (.050) .050) .039) . milling.020) .041 (.029 (.033-.026) .010) .013-.027-.017-.040) .008) .007 (.042 (.009) .007) .008 (.031 (.019 (.051) .017) .007-.021) .053 (.017-.010) .008 (.026) 95th .018 (.008 (.007 (.005-.013 (.048 (.056) .033 (.006-.028 (.060 (.006-.014 (.021 (.073) .009) .028-.021) .009) .005.045) .040 (.008-.011) .011-. Exposure to DU may occur in military personnel from retention internal shrapnel that contains DU or exposure to dust generated from ammunition Urinary Uranium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.030 (.036) .007-.031-.013) .046 (.009-.023 (.011-.034-.063) .011 (.009) . including nuclear weapons.046 (. Uranium has many commercial uses.049) .008-.006-.041 (.054-.013 (.009) .019-.007 (.008 (.031 (.011) .012 (.019-.016) .046) .011) .007-.043) .025-.012) .011-.007-.011-.028-.158) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.013 (.010) .022) .008-.024-.007-.007 (.009) .004.017 (.022 (.056) .012 (.088) .024 (.036 (.031 (.014 (.009-.114 (.006-.023-.038) .009-.007 (.010) * .020-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.012-.023-.009) .031 (.065) .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 .008-.013 (.036-.008-.006 (.015 (.012 (.017) .010) * .009-.012-.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 .018) .012-.010 (.007-.

007 (.018-.005-.009-.021 (.012-.008 (.006-.009 (.033) .013) .007-.025) 95th .009-.006-.012 (.019) .056) .012 (.007) .028-.012 (.009 (.011 (.048) .006-.013 (.013 (.034 (.008 (.1%-6% of an ingested dose may be absorbed.014 (.009) Selected percentiles ( 95% confidence interval) 50th .005-.011-.030) .008) .021 (.014-.007-.030 (.011-.009) * . Health effects from uranium exposure result from chemical toxicity to the kidney.006-. which can occur occasionally from high occupational exposure.011-.009) .007 (.019-.008 (.014-.004-. In cases of retained DU shrapnel.024 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.027) . 2003).007-.034 (.007 (.010-.020 (.006 (.025-.017-.030 (.011) * .012 (.024-.024 (.020-.014) 90th .020-.026 (.029 (.029 (.007 (.006) .013) .008-.018-.009) . 240 Fourth National Report on Human Exposure to Environmental Chemicals .077) .015-.007 (.039) .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 . the shrapnel acts as a source of chronic. Depending upon the specific compound and solubility.024) .040) 883 682 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites * Not calculated: proportion of results below limit of detection was too high to provide a valid result.008-.008) .007) .026) .010-.053) .006-.016) .007 (.039) Total .006-.010 (.005-.050) .018 (.018) .047) . Radiation risks from exposure to natural uranium are very low.010) .016) .020) .024 (.033 (.022 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.011-.. 1992).026 (.008 (.010 (. 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.022 (.029 (.027-.032) .009) .017-.016-.029) .015) .006-.006-.008 (.007 (.008) .009) .010-.006-.021 (.008) . Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.044) .025 (.008) .010) .030 (.019-.008) .048) .016) .007 (.006-.010-.019 (.006 (. with much slower elimination from bone.028 (.020 (.007-.045 (.018-.020-.007-.018-.009 (. kidneys.006 (.067) .016) .011-.054) .015 (.016) .061) .050) .006-.010) * .005-.030) .051) .034 (.009 (.031-.009) .027-.018-.022-.008 (.008-.024) .007 (.014 (.017-.009) .010-.042-.033 (.024) .015-.006-.008) Sample size 2464 2689 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .010-.022) .013-.007-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.029) .008 (.006 (.006-.015 (.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 .006-.007-.037 (.010) .009-.026-.006 (.027) .016) .011-.009) .027 (.034-.012) .009-.008 (.006-.014) .008) .027-.058) .009-.006-.006-. Uranium is eliminated in feces and urine.039) .007 (.015) .080) .007 (.024-.022-.042) .019 (..016 (. low level exposure.015-.032) .016) .006) . 0.006-.058) .039) .016) .035 (.007 (.034 (.053) ..015-.043 (.034-.024-.015 (.012) .028) .017-.013 (.027 (.007 (.015 (.010-.019-.006) .027-.012-.005 (.007 (.Metals impact.006-.007 (.017) .011-.015) .022-.012) .035 (.016-.008) .010) .006 (.008 (.011 (.019-.021-.030-.051 (.009-.011) .005 (.007-.050 (.146) .011) .005-.010 (.011-.024) .011) .015) .025-.008) .025 (.005-.017 (.270) .009) .014) .006-.019) .007 (.008) 75th .009) .013) .028) .017 (.034 (. population from the National Health and Nutrition Examination Survey.010-.020-.004-.007 (.051) .010) .021 (.033 (.013 (.007 (. liver.013 (.014) .013 (.006) .024) .008-.008-.100 (.019 (.031 (.051) .010-.007-.074) .028) .034) .025-. Inhaled uranium-containing particles are retained in the lungs.028) .006-.006-. which represents distribution and excretion.008) .007) . about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.013 (.026 (.021) . After inhalation.013 (.005-.010) . interval) .027 (.009) .029) . the initial half-life of uranium is about 15 days (Bhattacharyya et al.009 (.007 (.042) .010 (.006) .016-.033 (.012 (.010 (.007-.011-.017) .030-.019-. 2005).006-.040 (.029) . After long term or repeated exposure.059 (.025-.005 (.007 (.063) .006-.022 (.013 (.007 (.010-.017) .005 (.S.023-.041) .009) .016-.028 (.012 (.020 (. where limited absorption occurs (less than 5%). the half-life of insoluble uranium in the lungs is several years (Durakovic et al.014-.008-.012 (.008 (.010-.008) . After exposure to soluble uranium salts.015-.013 (.

. Dietz LA. in that the levels were below their respective detection limits (Byrne et al. and 2003-2004 (Dang et al. Kent (England): Nuclear Technology Publishing.. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.55 μg/L (median 0. Health Phys 2000. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU.. 2006).html. 1978).107:143-157.S. Durakovic A. Dang HS. population. 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. NRC. had a mean urinary uranium concentration of 0. In 17 U.. ingestion. eds. Sci Total Environ 1991. 1-49. Radiation protection dosimetry. 2002).078 μg/L (ranging up to 5. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. 1994. 1992. Boyd P.. 2002. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population.e.162 μg/L) (Orloff et al. (May et al.. respectively.S. Atlanta (GA). In two studies of a Finnish population with high natural uranium concentrations in their drinking water.S. et al. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. urinary levels of uranium were as high as 9. McDiarmid M. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. 2004).1992. and no consistent effects on multiple endpoints of kidney function were found. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al.cdc. the median urinary concentration was 0. 2000). Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.. 1991. 2004). 41 (1). In the same study. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Benedik L. pp. Fourth National Report on Human Exposure to Environmental Chemicals 241 . Squibb K. A cohort of 46 U. Volf V. Mil Med 2003. IARC and NTP have no ratings for uranium human carcinogenicity. In a study of 105 persons exposed to natural uranium in well water. the median urinary uranium concentration was 2. 2004).. Tolmachev et al. Breitenstein BD.gov/ toxpro2. Uranium content of blood. 2004). Byrne AR. Galletti. McDiarmid et al.. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Hamilton et al..Metals injury associated with elevated urinary uranium levels (Kurttio et al.. Carmichael AJ.. Ejnik JW. Metivier H... 2005. the geometric mean urinary uranium concentration was 0. with emphasis on quality control. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.61 μg/g creatinine. although slightly increased during and after deployment.. References Bhattacharyya MH. Drinking water and other environmental standards have been established by U. 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.066 μg/g creatinine (Gwiazda et al. Information about external exposure (i. soldiers who had been injured and had embedded DU shrapnel for as long as eight years.011 μg/L (McDiarmid et al..62:562-566. Pillai KC. 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. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Vol. but in whom no shrapnel was embedded. The U.. In: Gerber GB. soldiers evaluated before.S. Horan P.atsdr.. Centers for Disease Control and Prevention (CDC).65 μg/L).S. 2001-2002.1996.78:143-146. Zimmerman I. Komaromy-Hiller et al. Third National Report on Human Exposure to Environmental Chemicals. 2006).110 to 45 μg/L (Ejnik et al. or wound contamination. 2006). Health Phys 1992. 28 soldiers who may have been exposed to DU by inhalation. Hamilton MM.168(8):600-605. 2006). Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. Pullat VR. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. Muggenburg BA. environmental levels) and health effects is available from ATSDR at: http://www. during. 2000). Six workers in a depleted uranium program showed concentrations of 0. Thomas RG. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2006. Karpas et al. and after deployment had geometric mean urinary uranium concentrations that were less than the NHANES 1999-2000 and 2001-2002 geometric means at all three time periods.S. EPA. 2003. Stradling GN. (Kurttio et al.

Biokinetic modeling of uranium in man after injection and ingestion. Uranium daily intake and urinary excretion: a preliminary study in Italy. Jarrett JM.Metals Galletti M.82(4): 527-532. Smith D. Health Phys 2006. Noguchi H. Mistry K. concentration and daily excretion of uranium in urine of Japanese. et al. Howerton K. Comparison of representative ranges based on U. Renal effects of uranium in drinking water. Lewis BM. Hollriegl V.S. May LM. Hamilton EI. Katorza E. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Hancock RG. Karpas Z. Am J Kidney Dis 2006. Wahl W. D’Annibale L. Nuclear Regulatory Commission (U. Sampson EJ. plasma and urine and a critical evaluation of reference values for the United Kingdom population. U. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Gucer P. patient population and literature reference intervals for urinary trace elements.S. Marko R. J Toxicol Environ Health A 2004. Human exposure to uranium in groundwater. Makelainen I. Wilson PD. Health Phys 1996. Gwiazda RH.158:165-190. Komaromy-Hiller G.85:228-235. Environ Res 1999.S. et al. Sabbioni E.22–Bioassay at uranium mills. Andrews WS. Jackson RJ. Marino R. Salonen L.86:12-18. et al. Shelly T. Environ Health Perspect 2002. Int Arch Occup Environ Health 2006. Kuwabara J. Van der Venne MT. Review of elements in blood. Paschal DC. Saha H. Oberbroekling KJ. Paretzke HG.296(1-2):71-90. Oeh U.110(4):337-342. Costa R. Saha H. rapid. Health Phys 2002. Pekkanen J. Li WB. U. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Biologic monitoring for urinary uranium in Gulf War I veterans.87:51-56. et al.91(2):144-153. McDiarmid M. July 1978. Orloff KG. Squibb K. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Auvinen A. Komulainen H.81:45-51. Washington (DC): NRC. Englehardt SA. Oliver M. McDiarmid MA. Kurttio P. Radiat Environ Biophys 2005. Karpas Z. Ejnik J.44:29-40. Roiz J. Nuclear Regulatory Commission (NRC) Guide 8. Heller J. McDiarmid MA. Engelhardt SM. Clin Chim Acta 2000. Scott K. Lorber A. Cremisini C. Kidney toxicity of ingested uranium from drinking water. Charp P. Bennett LG. Auvinen A. VI.47(6):972-982. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Sci Total Environ 1994. Inductively coupled plasma mass spectrometry as a simple.S. Halicz L. Health Phys 2003. et al. Ough EA. Cordero S. Kurttio P. Ash KO. Roth P. Squibb K. Health Phys 2004.94:319-326. Kalinsky V. NRC). Harmionen A. Pirkle JL.67(8-10):697-714. 242 Fourth National Report on Human Exposure to Environmental Chemicals . et al. Uranium and thorium in urine of United States residents: reference range concentrations.71(6):879-85. Health Phys 2004. Pinto V. Tolmachev S. Ting BG. Salonen L.79(1):11-21. Metcalf S. Kane R. Environ Res 2004. Element reference values in tissues from inhabitants of the European community.

20 (4.40 (4.0-29.0) 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. 2002).40 (3. and reducing agents.10 (6. 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 10. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.00) 3.S.80 (3.90-12.5 hours and has a small estimated volume of distribution (Crump and Gibbs.88) 3.80) 75th 6.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.0-17.93-4.20-4.00) 7.20 (7. Drinking water.50-4.20 (4.70-7.60) 8.30) 6.0) 10.S.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0 (11.90-3.40 (5.40) 3.0-17.10-12..20 (5.60) 3.0 (9. Perchlorate was added to the U.22-5.30-19.38) 5.70-12.10 (5.0 (11. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .90 (3.68) 4.10-11.0-18.70-9.30) 6. In addition.40) 3..0) 9. and electroplating.0-20.0 (11.39-4.80 (7.0 (12.50 (5.0 (11. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.00) 5. fabric dyeing.50-4.0 (12. interval) 3. laboratory analysis.62 (3.70 (3.90-11.50 (8.60-7.60 (7.10 (6.0 (9.16) 3.81) Selected percentiles ( 95% confidence interval) 50th 3.20 (6.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.0) 13.0-19.0-15.0) 13.67-5.20) 4.80-6.70-11.0) 11.22 (2.20-4.70 (3.90-6.0 (9.0-23.54 (3. Other manufactured uses include fireworks. lettuce) can be the main sources of intake for humans (FDA.0) 12.31) 2.30-6.0 (12.0-17. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.50-11.40-7.90-11.0) 11.50-3.0) 8.40-5.46) 3.00-6. 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.02 (3.20-11.40 (5.10 (7.18-3.40-4.00) 3.79 (2.07-4.96 (3.60 (4.20 (2.60) 5.10) 12.74-3.0 (11.0) 708 617 681 652 1228 1092 Limit of detection (LOD.0) 13.80-12.0) 15.75 (3. potassium.0 (11.00) 4.0) 13.10 (2. certain catalytic metals.0 (12.90 (5.80) 12.0 (9.0 (11.0 (11. population from the National Health and Nutrition Examination Survey.56) 3.66) 3.89-3.20) 3. It is normally found and produced as the anion of a sodium.20-12.10) 3.0) 14.50-7.0-18.90) 5.0) 9.10) 3.90-9.05 and 0.0 (10.40 (5.80 (6.40) 2.76) 4. or ammonium salt.0 (8.10) 5.40-4.0) 13.0) 13.Perchlorate Perchlorate (Urbansky. but has strong oxidant properties in the presence of concentrated acids.05. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.20-3.80) 3.70) 3. 2007). 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.00-6.93 (4.21 (2.40) 6.40 (4.0 (9.0) 16. 2005).0 (8.90-9.0-18.80-4.10-11.01 (2.30-7.0) 9.20) 7.70-6.87-3.0) 9.70-3. matches.00-5.30 (2.65) 3.11) 4.70-5.76 (3.0) 13.90 (5. and certain plants with high water content (e.11) 3.0) 11.60 (4.30 (2.0 (11. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.EPA.09) 3.0) 15.29-3.45-4.40-6.51 (3.26 (2.90 (4.0 (8.30-17.0-15.40 (8.g. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.51 (3.40) 3.0) 19.32 (3. Perchlorate is stable under most environmental and physiological conditions.40) 90th 10.80) 7.80-4.0 (8.0 (9.80 (3.20 (8.0) 9.40-13.0) 14. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.93-3.84) 14.44-4.05 (2.70-3.30 (5.0 (9. milk.90-3. leather tanning.20 (2. 2005).08-3.50) 3.0-14.50 (3.19 (3.0 (8.60-6.0-17.0) 14.40-11.30-7. 1998).0 (13.47-4.80-15.30 (5.75-3.10-7.80-8.50) 5.0-17.90 (5.50) 11.10) 5.90) 6.S.70 (3.19-4.35 (3. and limited applications in pharmaceutics.90-10.40 (3.50) 5.49-3.0 (11.0) 9.10-4.0) 10.03) 3.0-17.0) 13. Survey years 01-02 03-04 Geometric mean (95% conf.81-16.0) 8.0) 95th 14.50) 6.12) 3.40) 4.90 (2.

33-6.50) 2.66) 3.10 (1..60 (3.EPA.41-9.90-9.30 (3.37-13.35 (4. Greer et al.60-6.82 (5.2) 8.90-15.0) 10.93-5.0) 7.19-6.83 (5.87) 2.76 (3.0) 11.33 (7.00 (2.87) 7.0 (9.50) 9. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.7 (11.90-11.00-3. interval) 3.25) 5.00) 9.20-10. 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. NAS.0-44.99 (5. 2002.30) 75th 5.19-10.20 (7.5 (13.42 (3. 1999.16-3.Perchlorate inhibition (RUI).80 (4.30 (6..00) 4.10-3.25) 5.70 (2.22-4.93) 3.44-6.90 (2.73) 3.45) 3. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.S.77 (3.0) 9.60-3.90 (2.70 (4.64-3.61-10.86) 4.22 (2.4 (11.07 (2.52 (8.90) 5.0 (10.30 (5.10 (6. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.3-14.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.0-17.00 (6.08 (3.52-9. Many factors may be important in consideration of perchlorate action on the thyroid: dose.56-3. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al. 2000). Li et al.40 (3.80 (7.3 (10.99-3..70-15. age.50) 5.1-13.0 (8.25 (3..70-5.10 (2.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3. In the U.71 (5.30-10.1 (8.0) 6. 2005).60-15.0) 12.26) 4.6-17.50-3.84) 2. levels.67) 5.0) 12.95 (2.34-3.3) 8. population from the National Health and Nutrition Examination Survey.6) 12.10) 3.0-14.15-12.51 (3.5) 8.51-4.50 (3. women with urinary levels of iodine less than 100 micrograms per day. 2005. 2002. Lamm and Doemland.29) 2.60-8.37 (4.0) 14.76-3.1-14. 2003.20-9.72 (3.1-16.20-3.30-5.70-3.35) 3.4 (8. 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.87 (5.S.S.60) 8.50) 2. 2005).10) 4.S.0-14.4-16.46 (3.24 (4.00) 3.21 (2.70-4.S.3) 12.20-4. perchlorate is negative in most genotoxic assays (U.70 (2.04-3.80) Selected percentiles ( 95% confidence interval) 50th 3.. medications).54 (2.1 (11.50-9.20 (3. 2001.0 (8.50 (6. and the presence of other substances known to affect thyroid function (e.90 (7.60-5.93-5.1-22.90 (4. Lawrence et al.61-5.09) 3.12 (6.30) 5.24-2.74) 7.46-4.36 (8.96) 2.40 (4. levels and sufficient in most participants (Tellez et al.0 (11.EPA.03 (2.20 (4.0) 12.0) 12.53 (2.6) 20. Steinmaus et al. 2007).60) 3.S.05 (4.25) 5. thiocyanate.75) 3.80-3.4 (10.50-5.56 (3. Also.0) 4.44) 3.40) 17.18-3.93-8. 2002).0) 13.40 (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 3.0) 13.20 (2. During gestation and infancy.39) 2.32) 5.64) 5.35 (2.10-7.0 (9.60) 10.39 (3.40-10.26 (3.30) 3.10 (4.45-2. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.70) 10.60-8. Survey years 01-02 03-04 Geometric mean (95% conf.g.02) 3.0 (11.4) 8.60-11.80-3.90-3.12-2..87 (7.70) 2.40 (7.89 (2.20) 3. nitrate.98) 3.90-20.54 (3. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al. gender.00-2.S.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 .60-5.0 (11.81-3.47) 2.89-3.8 (11.40) 3.60-11.1) 8.87-3.40) 5.61 (5.20-3.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3. up to 68% RUI has been demonstrated.50) 6. menopausal status..20) 8. 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. dietary iodine intake. chronicity of exposure.4) 13.80 (7. 2005).90-2.10) 6. although iodine intake was higher than U.0 (9.02-4.59) 3. in a representative sample of U. U. 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.39-4. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.93-7.00 (4.09 (7.30) 90th 9.3) 11.10) 13.04-3.22-6..14 (2. However.00-11..50) 95th 12.20 (6.58) 2. 2006.10 (4.46-13.4 (11. 2005.29-6.91) 4.08) 3.97-5..43) 6.0) 9.22-4.0-19.30-5.33-12.2) 8.

Skeels MR. Lamm S. Barnard JC. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans.110(9):927-937. Osterloh JD. Lamm SH. and environmental perchlorate exposure among residents of a Southern California community.10(8):659-663. Thyroid 2000. et al. Lawrence J. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002.EPA at: http://www. et al. Landingham CB.S. CFSAN/Office of Plant & Dairy Foods.fda. J Expo Sci Environ Epidemiol 2007. Environ Health Perspect 2002.html and from ATSDR at: http://www. He X. Food and Drug Administration (FDA).html. Environ Health Perspect 2006. Cross M.. Osterloh JD. 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. most of the population is considered to be below the U. Neonatal thyroxine level and perchlorate in drinking water. Page Last Updated: 05/28/2009. Primary congenital hypothyroidism. 2005. Goodman G. epa. Sesser DE.46(5):509. Greer SE. et al. Lau EC. Blount BC. National Research Council of the National Academies. National Academy of Sciences (NAS). Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.cdc. Li FX. 2001-2002. newborn thyroid function. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Miller MD.gov/toxpro2.115(9):1333-1338. 2005). Steinmaus C.S. Caldwell KL. Benchmark calculations for perchlorate from three human cohorts. Mauldin JP. Pirkle JL. 6/2/09 Greer MA. Available at URL: http://www. Valentin-Blasini L. J Clin Endocrinol Metab 2005.. Dyke JV.114(12):1865-1871. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Blount BC. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. The effect of perchlorate. Dasgupta PK. May 2007. Erratum in: Environ Health Perspect 2005. Li Z. Kirk AB. Valentin-Blasini L. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. 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. thiocyanate. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data..42(2):200-205. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 .113(11):A732. Also. Blount 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. Gibbs JP. 2007). Richman K. and nitrate on thyroid function in workers exposed to perchlorate long-term.gov/safewater/ccl/perchlorate/perchlorate.S. Environ Sci Technol 2006.113(8):10011008. Lamm SH. Byrd D. Washington (DC): National Academy Press. Lamm SH. Buffler PA. et al.40(21):6608-6614. Environ Health Perspect 2005. Analysis of relative source contributions to the food chain.17(4):400-407. Deyhle GM.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Perchlorate Exposure of the US Population. Pirkle JL.90(2):700-706. Additional information about exposure and health effects is available from the U. Chacon PM. The effect of short-term low-dose perchlorate on various aspects of thyroid function.45(10):1116-1127. Health Implications of Perchlorate Ingestion. population.11(3):295. Pino S. Braverman LE. J Occup Environ Med 2003.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. EPA reference dose (Blount et al. Erratum in: J Occup Environ Med 2004. Rutherford GW. Jackson WA. Pleus RC. Perchlorate in the United States. Environ Health Perspect 2007. (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. Braverman LE. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Crump KS. References Blount BC. Thyroid 2001. Daaboul JJ.atsdr. Abarca CR. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Doemland M. Braverman LE.41(5):409-411. J Occup Environ Med 2000. Crump KS. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Magnani B. Howd R. Tellez RT. Low dose perchlorate (3 mg daily) and thyroid function. 2005).htm. Kelsh MA. Pino S. Lawrence JE.

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

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

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

400-1.S.400-1. and humans.00) . the median PFCs values tend to be roughly similar in these age categories (Olsen et al. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. 2004b).. thyroidal). Cook et al. PFOS. PFOS.800 (. 2004.S. 2003a).400 (<LOD-.80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th . EPA. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. monkeys.400-1.800 (. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. 2003a. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. Survey Geometric mean (95% conf.00 (.500) .300 (<LOD-. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.. PFOA.500 (<LOD-1.800) 1. 2007b. 2003. 2007b).300 (<LOD-. perfluorohexanesulfonate (PFHxS).600 (. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.108 times higher than background serum levels in humans (Butenoff et al. 2003a.500-1..500-1.. EPA. 2004. which may vary for some chemicals by year and by individual sample.800) 1. 2001..900 (. Olsen et al.500) .. hepatotoxicity. 2003). and there was no clear evidence of excess all-cause or diseasespecific mortality.500-. 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. In comparing three separate reports on adults.600 (..800 (. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al..300 (<LOD-. Animal studies of PFOS have demonstrated weight loss.S.900 (.20) . and no substantial age trends were seen within adults ages 20-69 (Olsen et al. 2004a. Fourth National Report on Human Exposure to Environmental Chemicals 249 . and changes in thyroid hormone concentrations (Grasty et al..80) 640 1454 03-04 03-04 * * < LOD < LOD . Olsen et al. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400-. development in offspring was stunted and hypothyroxinemia was observed.500 (.. At high but non-toxic maternal doses of PFOS.10) . 2003.80) 485 538 962 Limit of detection (LOD. U.00) .S.. Olsen et al. 2003a). 2003. U. the potential to estimate risks to humans from animal doses is uncertain. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. reproductive. or increased cancer rates (Alexander et al. < LOD means less than the limit of detection..600-2.500) . population.400-1. 2003). Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. Kennedy et al. However. 2003a. 2007). At doses causing maternal toxicity.10) * 03-04 03-04 * * < LOD < LOD < LOD .00) .400-.500-1. 2004)..20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .. Fei et al. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.900 (.. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. developmental and teratogenic effects were demonstrated in offspring.400 (<LOD-.. 2007a. 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.600 (.500) .400 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0. 2005).. 1999. interval) Selected percentiles ( 95% confidence interval) Sample 95th .. 2005). possibly related to lung immaturity (Lau et al.50) .500 (.700 (. 2004).10) .400-1...500) 90th . 2007. PFOA.700) .40) .800 (.3.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. 2003). Thibodeaux et al. Harada et al.10 (. 2007a. elderly and children. In such studies.. population from the National Health and Nutrition Examination Survey.500-1.300-1.400) .500-3. Lau et al. 1992.

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

600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.S.300 (<LOD-. Survey Geometric mean (95% conf.300-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400 (.300 (<LOD-. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 251 .500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) 485 538 962 Limit of detection (LOD. see Data Analysis section) for Survey year 03-04 is 1.S. see Data Analysis section) for Survey year 03-04 is 0. < LOD means less than the limit of detection. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500-.0.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (<LOD-.600 (.900) < LOD .400 (<LOD-.400 (<LOD-.3.400) .600) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th . Survey Geometric mean (95% conf.

80) 90th 2.30) 03-04 03-04 .80-8.40 (1.40 (1.40 (1.17-1. 252 Fourth National Report on Human Exposure to Environmental Chemicals .00-1.50) 2.90) 8.826-1.60-4.20-1.05-2.70) 3.10) 8.6) 7.00 (2.30 (1.966 (. Survey Geometric mean (95% conf.60) 1.90 (1.0) 8.900-1.00 (1.60-7. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80-6.60 (6.809) 1.60 (1.80) 5.40) 2.70-5.60-2.20 (1.10-9.60-8.697-1.S.70) 2. interval) 1.50 (2.27) 1.30-6.16) .73-2.80-2.30 (3.92 (1.00-1.20) 1.70 (2.40) 1.60-2.72 (1.90-10.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.30 (2.10) 75th 1.00-6.30) 3.10) 75th 3.80) 4.86 (1.90) 1.50 (1.20 (6.10) 6.984 (.90-2.40-1.70-6.70-2.00 (.60-4.17 (1. see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey.40) 4.20 (1.861 (.51) 1.90) 3.5) 5.00) 3.60-3.03) 1.20) 03-04 03-04 2.5) 8.50-10.00 (1.20-2.10 (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 1.689 (.900 (.70) 13.900-1.77-2.30 (1.3 (9.10) 4.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.10) 1053 1041 03-04 03-04 03-04 .900-1.30 (1.80-7.20-3.10 (1.600-.60 (1.900-1.00-8.10 (4.70-7.700-1.30) 3.3.70-10.20 (1.00) 1.30-2.70-2.40) .835-1.70) 1.60-2.60) 9.900) 1.62-2.20-1.50) 2.90) 90th 5.50-6.586-.20-1.00-7.60 (1.80-4.00 (1.1) 485 538 962 Limit of detection (LOD.20-1.S.08) 2.90 (1.10 (.60-3.40) 1.80-12.20) 2.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (5.80-4.10) 4.42 (1.60) 3.80 (4.40 (1.50 (6.20 (6.80-8.93 (1.10) 1.40) 640 1454 03-04 03-04 1.50-3.50-6.10) 6.90 (2.50 (4.90 (1.12) .26) 2.30 (1.700 (.40) 640 1454 03-04 03-04 2.80-4.01 (1.20) 1.852 (.0) 1053 1041 03-04 03-04 03-04 1.00) 1.900-1.90-19.00 (.900 (.20 (1.20) 485 538 962 Limit of detection (LOD.800 (.80) 1.50 (6. see Data Analysis section) for Survey year 03-04 is 0.834-1.00) 2.30-12.30) 3.816-1.80-3.900-1.80 (1.10-5.30 (2.963 (.80 (1.80) 3.80-7.10) 5.800-1.50) 6.912-1.60) 2.30-9.56-1.40-3.50 (1.50 (1.721-1.80-3.04) .30) .10) 1.87-2.67-2. population from the National Health and Nutrition Examination Survey.50 (1.00 (1.14 (. interval) .72) 1.40-1.10-9.70) 2.30 (6.10 (.90 (4. Survey Geometric mean (95% conf.54) .50 (4.20) .91) 2.40 (2.09 (.90 (4.1.10 (.70 (1.90) 1.90) 1.90 (1.44 (2.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.30 (7.70) 1.

80-9.1) 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 4.6) 35.7-69.9 (19.1-24.0) 36.1-33.20) 4.6) 21.60-9.4) 56.60 (5.82) 4.3) 42.00) 3.0-70.6) 9.60) 8. Survey Geometric mean (95% conf.79) 4.9 (13.40) 75th 5.50-13.91) 3. Fourth National Report on Human Exposure to Environmental Chemicals 253 .4-25.7 (19.9) 22.8) 46.50 (4.5) 32.30) 6.00 (5.4 (23.30-11.20) 10.20) 5.60 (3.4) 20.5) 19.40-6.3 (17.53) 3.3) 28.50) 4. see Data Analysis section) for Survey year 03-04 is 0.1-52. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.6) 7.70 (3.2 (19.7-33.0) 23.5) 7. Survey Geometric mean (95% conf.20) 7.9-19.8) 32.70-7.9-38.70 (5.70-7.60-13.5-62.60 (6.70) 3.0-20.7 (35.0-16.4 (19.20-9.6-50.8-22.60 (7. see Data Analysis section) for Survey year 03-04 is 0.80 (6.6-45.7-49.3 (35.5) 9.5 (28.2 (16.20-4.8-22.6 (35.60 (4.10-3.40 (6.00 (5.90 (7.50) 7.2-57.8 (45.30) 7.3-61.4) 75th 30. interval) 3.70 (5.37 (2.2 (18.4) 640 1454 03-04 03-04 23.5-21.0) 485 538 962 Limit of detection (LOD.80 (7.8-78.27) 4.5) 18.2) 45.50 (3.30 (3.20 (4.4) 21.20) 7.30-3.35) 3.10 (3.9-23.47 (4.80 (5.8-81.20 (4.21-3.40) 5.90-4.S.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80 (6.80-4.1 (23.4-42.8) 27.0 (27.5) 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 21.30-6.5 (28.90 (7.9) 9.3 (28.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.96 (3.7 (13.8-35.40-6.30 (3.40 (4.0) 21.9) 22.7-53.1 (24.6 (42. population from the National Health and Nutrition Examination Survey.7) 39.5-23.2) 30.20-5.90-4.10) 5.40) 3.8 (37.8-30.0) 43.90-12.65-4.50-4.3) 41.2 (21.70) 4.20) 5.1-25.1) 57.0) 90th 41.40-17.10 (6.9 (22.30-5.7 (35.40-14.2 (28.6) 42.60 (6.3 (35.2) 640 1454 03-04 03-04 4.S.4 (19.1-35.70-5.2) 30.90) 6.9 (17.80) 8.3 (44. population from the National Health and Nutrition Examination Survey.70) 6.18 (3.4.89 (3.6) 18.00 (3.84-3.7-30.3-22.1.47-4.07-4.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.80-12.40) 90th 7. interval) 20.5) 8.5-33.60-6.3) 485 538 962 Limit of detection (LOD.0) 03-04 03-04 19.90 (5.99-3.6) 1053 1041 03-04 03-04 03-04 3.6-24.5) 1053 1041 03-04 03-04 03-04 14.11 (2.85-4.9) 27.0-66.50-6.70-10.90 (7.6 (19.60) 03-04 03-04 3.4 (28.70-9.7 (43.1-36.4 (17.60-14.0) 21.30-8.8-22.2-22.30 (5.7 (43.7-23.1) 15.8 (34.2 (27.67-4.0 (20.10 (3.1 (19.4-17.95 (3.6 (44.7 (7.5) 57.6) 62.40-10.

500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500) . 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 means less than the limit of detection.300-. < LOD means less than the limit of detection.200-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .400 (<LOD-.300 (. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 03-04 is 0.500) .300 (.300 (. 254 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.200-.300) .300 (.2.300-.200 (<LOD-.200-.200-. Survey Geometric mean (95% conf.500) 485 538 962 Limit of detection (LOD.300 (.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.500) < LOD 485 538 962 Limit of detection (LOD.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .300-.300 (.200-.300 (.300 (.300 (.200-. which may vary for some chemicals by year and by individual sample.300) .S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .300) .300-.500) .300) . Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (.300 (.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (.300 (.200-.200-.S.200-. see Data Analysis section) for Survey year 03-04 is 0.4.200-.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300) .300) .

population from the National Health and Nutrition Examination Survey.40) < LOD < LOD .10 (.900-1.700) .00 (. < LOD means less than the limit of detection.S.10) .300 (<LOD-.S.900-1.30) 1.90) .50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .10 (1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .10-1.600 (<LOD-1.00 (.900-1.3.10) * 03-04 03-04 * * < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30 (1. Survey Geometric mean (95% conf.10-1.700) 1.20) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60) 485 538 962 Limit of detection (LOD.30 (1. see Data Analysis section) for Survey year 03-04 is 0.10-1.900) 485 538 962 Limit of detection (LOD.00 (.600 (<LOD-.900 (<LOD-1.600 (<LOD-1.80) 1.80) 1.700 (<LOD-.30) .50 (1.900-1.00 (.400 (<LOD-1.30) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th . population from the National Health and Nutrition Examination Survey.300-2.60) 640 1454 03-04 03-04 * * < LOD < LOD . which may vary for some chemicals by year and by individual sample.900) 1.10 (.700) 1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .10-1.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample.50 (1.700 (<LOD-.700) 90th 1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .800) .700 (<LOD-.800) .10) 1.900) .20 (1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .900-1.800 (<LOD-.600) . < LOD means less than the limit of detection.10-1.700 (<LOD-.10) .500 (<LOD-.700 (<LOD-.30 (1.00) < LOD .10) 1.900 (.400 (<LOD-.70) 1.300 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 0.10 (.900-1.20-1.00-1.700 (<LOD-. Survey Geometric mean (95% conf.6.700 (<LOD-2.40) 1.900-1.600 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.

Moore RW. Environ Health Perspect 2007. Fei C. Caudill SP. Burris JM. Jarnberg U.99(2):253-261. Calafat AM.68(6):465-471. Calafat AM. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Environ Sci Technol 2005. Biegel LB. Seacat AM.63:490496.60(1):44-55. Needham LL. Kannan K. Kannan K. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Evans TJ. The influence of time. Kuklenyik Z. Characterization of risk for general population exposure to perfluorooctanoate. Day RD.115(11):1677-1682. Morikawa A. Birth Defects Res B Dev Reprod Toxicol 2003. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Calafat AM.39(23):9101-9108. Inoue K. Holmstrom KE. Kamiyama S.115(11):1596-1602. Herbstman JB. Koizumi A. Yamashita N. 2007b. Environ Res 2005. Laane RW. Androgenic deficiency in male rats treated with perfluorodecanoic acid.40:21282134. Wong LY. Falandysz J. Dinglasan MJ. Wijeratna S.S. Environ Health Perspect. Polyfluoroalkyl chemicals in the U. Kennedy GL Jr. Fluorotelomer alcohol biodegradation yields poly.Perfluorochemicals References Alexander BH. et al.60(10):722729. Tully JS. Mandel JH. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Tarone RE. Reidy JA. Needham LL. Toxicol Sci 2001. Needham LL. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Rodricks J. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Cook JC. Chemosphere 2006b. Rogers JM. Olsen J. Biegel LB. Yoshinaga T. 256 Fourth National Report on Human Exposure to Environmental Chemicals .S. Environ Sci Technol 2005. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. J Environ Monit 2005. Perfluorinated chemicals in selected residents of the American continent.7(4):371-377. Tully JS. Bandai N. Bignert A.38(10):2857-2864. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Liu RC. Murray SM. Kuklenyik Z. Loganathan BG. Butenhoff JL.46(2):141-147. et al. et al. Lau CS. Ingall GB. Cook JC. Chem Biol Interact 2000. Fillmann G. Environ Sci Technol 2004. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism.and perfluorinated acids. Grey BE.39(23):9057-9063. Hurtt ME. J Occup Health 2004.39(3):363-380. Hurtt ME. et al. Environ Sci Technol 2005. Kannan K. Mohotti KM. Saito N. Witter FR. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Hurtt ME. Toxicol Appl Pharmacol 1995. Yamashita N. Apelberg BJ. Peterson RE.104(2):322-333. Olsen GW. Environmental and toxicity effects of perfluoroalkylated substances. Aguilar-Villalobos M. in vivo. Yun SH. Environ Sci Technol 2007a. Reidy JA.179:99-121. Keller JM. Perkins RG. Taniyasu S. Guruge KS.113(2):209-217. and perfluorinated contaminants in livers of polar bears from Alaska. Corsolini S. Kawashima Y. et al. Serum concentrations of 11 polyfluoroalkyl compounds in the U.Koizumi A. Kuklenyik Z. Inoue K. Calafat AM. Calafat AM. Environ Sci Technol 2006a. McLaughlin JK. Edwards EA.38(17):4489-4495. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Chlorinated.134(1):18-25. Environ Sci Technol 2004. Ye Y.34(4):351-384. Halden RU. Toxicol Appl Pharmacol 1992. Toxicol Appl Pharmacol 1990. The toxicology of perfluorooctanoate.39(1):80-84. Frame SR. et al. Crit Rev Toxicol 2004. Kuklenyik Z. Watanabe T.115(11):1670-1676. Reidy JA. Saito N. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years.41:2237-2242. Gaylor DW. Reidy JA.124(2):119-132. et al. Bookstaff RC. Needham LL. Kumar KS. Arendt MD. Seneviratne HR. O’Connor JC. Moore JA. brominated. Occup Environ Med 2003. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Mabury SA. Suzuki E. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Frame SR. Grasty RC. Yoshinaga T. Kudo N. O’Connor JC. Mandel JH. Cook JC. Olsen GW. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Butenhoff JL. Sasaki S. Katakura M. Harada K. Olsen GW. and ex vivo studies. Caudill SP. Mandel JS. Regul Toxicol Pharmacol 2004. Environ Health Perspect 2007. Hekster FM.1968--2003. Rev Environ Contam Toxicol 2003. Taniyasu S. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. de Voogt P. Harada K.

Mandel JH. II: postnatal evaluation. et al. et al. Rogers JM. Lundberg JK. Olsen GW. Olsen GW. Richards JH. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Yamashita N. and food items prepared in their packaging. Stanton ME. Toxicol Sci 2003. Seacat AM.1177(2):183-190. (Erratum in: Toxicol Sci 2004. Rogers JM.40(1):32-44. Lau C. Zobel LR.51(8-12):658-668. Korzeniowski SH. Biol Pharm Bull 2003. Lundberg JK. Burris JM. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Burris JM. Environ Health Perspect 2003a. Bronson R. Ellefson ME.S. fish. et al.68(1):249-264. 2003. Available from URL: http://www. Coordinate induction of acyl-CoA binding protein. Buck RC. 2003a. Taniyasu S.55:3203-3210. Mandel JH. Thibodeaux JR. Gamo T. A global survey of perfluorinated acids in oceans. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. 1/15/06 Vanden Heuvel JP. Ehresman DJ.37(12):2634-2639. Rogers JM. Toxicol Appl Pharmacol 2004. and humans from Japan. Chemosphere 2007b. Butenhoff JL. The developmental toxicity of perfluoroalkyl acids and their derivatives.Perfluorochemicals Kudo N. Sources. Olsen GW. Environ Sci Technol 2006. J Ag Food Chem 2007. J Occup Environ Med 2003b. Grey BE. Mandel JH. Horii Y. Church TR. Sterchele PF. 2007a. Seacat AM. J Occup Environ Med 1999. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Seymour C. Ehresman DJ.68:105–111. Cousins IT. Church TR. Toxicol Sci 2003. Nesbit DJ.45(3):260-270. Pepper K.82(1):359.2(1):53-76. Butenhoff JL. Barbee BD. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Olsen GW. van Belle G.113(5):539-545. Hansen KJ. Olsen GW.26(1):47-51. Miller JP. Hanari N. et al.54(11):1599-1611. Mar Pollut Bull 2005. Olsen GW.. htm.epa. fast foods.perfluorohexanesulfonate. Mandel JH. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. I: maternal and prenatal evaluations. Grey BE. Larson EB.198(2):231-241. Olsen GW.gov/opptintr/pfoa/pfoara. Thomford PJ. Petrick G. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. and perfluorooctanoate in retired fluorochemical production workers. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Peterson RE. Hanson RG.111(16):1892-1901. birds. Burris JM. Toxicol Sci 2002. Butenhoff JL. Historical comparison of perfluorooctanesulfonate.41(9):799-806. Chemosphere 2004a. Church TR. Helzlsouer KJ. et al. Horii Y. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Environ Health Perspect. EPA). Lau C. Cao XL et al. Case MT. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Butenhoff JL. Olsen GW. Washington. J Children’s Health 2004b.74(2):369-381. Thibodeaux JR. perfluorooctanoate andother fluorochemicals in human blood. Burris JM. Butenhoff JL. Froehlich JW. fish. Hansen KJ. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Reagen WK. Environmental Protection Agency (U. Butenhoff JL. Taniyasu S.) Tittlemier SA. et al. Moisey J. Prevedouros K. Hanson RG. Mair DC. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Kawashima Y. U. Hansen KJ. Biochim Biophys Acta 1993. Half-life of serum elimination of perfluoroo ctanesulfonate.115(9):1298-1305. Yamashita N. Environ Health Perspect 2005.74(2):382-392. (Erratum in: Environ Health Perspect. Huang HY.S. Kannan K. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Hansen KJ. Kannan K. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. fate and transport of perfluorocarboxylates. Burlew MM. Burris JM. Hansen KJ.111(16):1900) Olsen GW. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Environ Sci Technol 2003.

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

Drug Metab Rev 1989. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Kessler et al. Jongeneelen FJ. Cousins IT.cdc. Peck and Albro.e.cdc. 2001. van der Broek PH. Also. reducing estrogen production. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. 2004). Mackay D.. Population estimates of concentrations of specific phthalate metabolites may differ by age. McKee et al. 1985. 2002).. Silvapathasundaram S.html).. 2004.html. dibutyl phthalate (DBP). Metabolism of di(2-ethylhexyl) phthalate.. Toxicological profile for di-n-butyl phthalate update [online]. phthalates have been shown to induce peroxisomal proliferation in rodents. 1982. 1986). Anderson WA. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. 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.. 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... but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. and race/ethnicity (Silva et al. Corbett JT. McDonnell DP. 2005. but there are known species-related differences in the hydrolysis of diester phthalates. In animals. High doses of di2-ethylhexyl phthalate (DEHP). variation also occurs in the same person during repetitive monitoring (Fromme et al. Available at URL: http://www. References Agency for Toxic Substances and Disease Registry (ATSDR). Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites.. Clark K.3. Jordan S. pp. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. gender. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. Available at URL: http://www. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester.. 2004. Castle L..gov/toxpro2.atsdr. Slakman AR. Food Addit Contam 2001.45:19-25. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. Evaluation of a recombinant yeast cell estrogen screening assay. 2007). Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . 2003. These differences may contribute to species-specific differences in toxicity (ATSDR. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. Dave M. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al..nih.. efficiency of intestinal absorption. Calafat AM. 2001. Silva MJ. Environ Health Perspect 1997. 2005).gov/ reports/index. 2000c. interactions with macromolecules and species differences in metabolism of DEHP.. 2004. ovarian abnormalities in the female animals (Jarfelt et al.805:49-56. Herbert AR. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. 2004. Connor C. Scotter MJ. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). Information about external exposure (i. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. NTP-CERHR.21:13-34. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. The Handbook of Environmental Chemistry. 4/20/09 Albro PW. which may be a pathway to the development of liver toxicity and cancers in these animals. However. Schroeder JL. at higher doses. Sauer MJ.html. Hauser et al.gov/ toxprofiles/tp9. Springer. Assessment of critical exposure pathways. 2003.cdc. 2006).18(12):10681074. Pharmacokinetics.. Springall C.atsdr. at very high levels.gov/toxprofiles/ tp135. Lovekamp-Swan and Davis. 2006). Biomonitoring studies on levels of phthalate metabolites provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of phthalates than are found in the general population. Coldham NG. and extent of metabolite conjugation to glucuronide (Albro et al. Hauser et al. Dirven HA. 2007.. and Sertoli cell abnormalities in the male animals and. 2002).Phthalates and metabolites have been tested. testicular atrophy. 105:734-742. Rhodes et al. J Chromatogr B 2004. 2000a.. 2000b. Part Q: Phthalate Esters. phthalates produced anti-androgenic effects by reducing testosterone production and. Matthews HB.html.New York. 2002. Needham LL. Albro PW and Lavenhar SR. Environ Health Perspect 1982. 227-262. Hoppin et al. Massey RC.niehs. Vol. atsdr. 2001). In Staples CA (ed). 1982).

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Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro.112(17):1740]. Mortensen GK. Gans G. Meeker JD. Biol Pharm Bull 2003. Duty S. Zhang S. Wang P.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Environ Health Perspect 2003. Ryan L. Koch HM. Hauser R. and infant formula by tandem mass spectrometry (LC-MS-MS). Giwercman A. Boehmer S. Filser J.105:802-811. Lovekamp-Swan T.html.106(1):23-26. Numtip W.64(8):555-560. Epidemiol 2005. Stringer WT. Silva MJ.gov/chemicals/dehp/dehp-eval. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Anal Bioanal Chem 2005. Borch J. Kano I. et al. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP).niehs. 2000c [online].niehs. Harris CA. Jonsson BAG. Leffers H. Reproducibility of urinary phthalate metabolites in first morning urine samples.niehs. 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Peters JM. Pratt IA. Clemons JH. et al. Malek NA. Urinary levels of seven phthalate metabolites in the U. Zacharewski TR. Albro PW. Caudill SP. Cunningham ML. Peck CC. et al. Environ Health Perspect 1982.Phthalates phthalate (DEHP): a cross-sectional study in China. Toxicol Sci 1998. Abbott BD.65:299-308. Bratt H.S. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Wu ZF. Hodge CC. Matthews JB. Batten PL. Environ Health Perspect 2006. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man.36:459-479. Fielden MR. Environ Health Perspect 2004. Rusyn I. Barr DB. Orton TC. et al.112(3):331-338. Jackson SJ. 112(5):A270]. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Parks LG. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Reidy JA. Toxicol Sci 2000.58:339349. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters.46:282-293. Crit Rev Toxicol 2006. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Silva MJ. Klinefelter GR. Ostby JS. Meek MD.45:11-17. Environ Health Perspect 1986. Lambright CR.114(11):1643-1648. Barlow NJ. Rhodes C.

1 (10.9) 15.4-15.7 (53.8 (21.1) 31.4-127) 80.6 (21.8 (50.3) 63.5) 27.8-76.0) 23.2) 33.4) 49.2-17.7-16. car care products.0) 16.6) 13.8 (71.7) 23. and 03-04 are 0.2-33.3-161) 99.8) 63.6-132) 103 (84.3-34.0-85.8-48.9 (21.2-16.8) 14.2-116) 122 (102-143) 101 (84.1) Selected percentiles ( 95% confidence interval) 50th 17.1 (14.0-130) 101 (86.4-62.4) 98.4) 80.1-16.8 (28.2-16.6 (66.3-74.6 (13.8 (71.3-75.6) 15.5-97.6-92.9) 12.0) 90th 67.5 (13.1) 13.9-27.8-72.8-14. 2001-2002.8 (10.3 (12.9 (11.4) 51. because it is not bound to products in which it is incorporated. 2000).3-18. some personal care products.1 (13.2) 78.6 (32.0 (55..8-14.2) 32.4) 33. and diet is the major source for general population exposure.6-72.2 (19.1) 32.5 (55.8-133) 89. NTPCERHR.4 (31.1 (19.3) 23. BzBP can be released into the environment during its production and.7 (12..4 (10.1) 12.4) 71.5-33.0) 20.5-84.5) 55.0-106) 58.4 (32. and to a lesser extent.1 (58. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.9) 43.2) 17.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.9) 18.3 (29.S. 2004.7-172) 103 (74.6 (53.2-19.8-17.9) 14.7-16.6) 67.1-35.5 (66.6) 14. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4 (10. and 0.6) 95th 103 (94.9-16.7-16. High dose BzBP and its monoester metabolites.8-64.3) 13.3-125) Total 15.3 (22.1-90.9-47.1-18.5-14.9-87.5 (76. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2) 14.6-116) 122 (102-142) 101 (85.5 (57.5) 15.3 (30.0-55.0 (20.4) 12.7-17.1 (55.2) 12.6) 50.5 (67.9-62.8) 33.1-43. can produce developmental and reproductive toxicity in rodents.7 (11.0) 33.7 (13.7-15.6-29.9 (12.3) 54.8 (53.0) 70.3 (54.4-92.5) 23.4) 14.6-92.0 (34.9-28.7-119) 99.8 (14.4 (13.3) 15. and 2003-2004 were generally similar those reported in U.3) 94.9-14.6 (12.9 (70.7 (51.4 (63.0 (14.8 (80.0 (26.9 (39.3-91. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.3-21.9) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 39.1) 68.6) 35. particularly male animals (McKee et al.6) 29.1 (13.1-16. Food crops take up BzBP.2 (10.3-27.6 (13.4) 75th 35.0-26.9 (13.8-41.5) 65.8-121) 79.2) 22.0 (15.6) 16.6-38.0 (30.5 (61.1 (20.5) 15.2) 15.5 (47. interval) 15.8) 28.2) 13.1-61.5-94.2-115) 113 (91.7-25.5-40.2-39.6-17. residents (Blount et al.4) 35.5-41.3) 37.7-35.1-15.3-88.1-15.4 (32.2-40. 262 Fourth National Report on Human Exposure to Environmental Chemicals .8 (12.7) 40.3-130) 122 (88.6) 25.7) 38.3 (29.4) 129 (98.5-35.Phthalates Benzylbutyl Phthalate CAS No.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) 37.4 (68.9) 49. it can be released into the ambient air during use or disposal of the products.6) 24.6) 14.4) 65.5-62. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.6 (13.6 (13. 0.1) 14.3 (33.8 (30.7 (80.8-98.1 (14.8-35. respectively.3 (13.1-116) 122 (93.8-18.4) 38. see Data Analysis section) for Survey years 99-00. 2000).1) 29.2 (43.7-14.8-16.7-170) 169 (134-198) 152 (99.4-16.4 (53.3 (12.2 (25.9-30.8-13.4 (59.0 (12.6) 13.3-12.5-25.9-190) 86.1) 76.5-18.4) 81.9) 14.1) 67.8 (38.7 (82.2) 66. including MBzP.3-18.9-49.1-214) 166 (116-191) 145 (110-213) 88.7 (70.4 (27.6-43.1-39.8.6 (41.2-183) 101 (78.3 (12.3) 13.7-58.1-38.3-82.0) 32.4-25.3.4) 108 (96.9 (22.8-16. population from the National Health and Nutrition Examination Survey.4 (48. 01-02.6-18.0 (43.5-36.5-145) 138 (106-241) 143 (127-179) 120 (99.4) 35.6) 35.2 (14.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16.7 (15.6) 63. vinyl tile.9 (16.9) 11.2) 69.9) 13.9 (12.3-43.2 (19. sealants.5 (26.0 (30.2-31.5) 82.5-36.0 (11.6-150) 94.1.6-39.2 (47.2-38.1 (32.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4 (53.5) 16.6-79.1-120) 52.8-17.9 (28.0 (33. IARC considers BzBP not classifiable with respect to human carcinogenicity.7-13.4 (29.0) 34.5) 30.0 (15.5 (27.3 (44.8 (86.2 (11.2-20.2-155) 91.S.0) 24.8) 24.7-82.4-24.2) 14.0 (23.0 (27.

7 (54.1-29.4-60. Survey years 99-00 01-02 03-04 Geometric mean (95% conf..9) 42.8-13.7 (14.4-90.4) 50. Limited studies in children younger than 2 years old have found median and geometric mean urine MBzP that were similar to children aged 6-11 years in the NHANES subsamples (Brock et al.1 (53.5) 41.9-14.5 (9.5-13.0 (33.9 (24.3-34.5) 95th 77.8) 13.2) 26.4-23.4-19.9 (12.9 (12.6 (34.8-64.8 (69.2-51. in men attending a Boston infertility clinic (Duty et al.9-16.6 (11. population from the National Health and Nutrition Examination Survey.8-48.8-14.7) 46.0-26.8) 53.7-14.3) 16.4) 14.9) 64.6-20.5) 20.4 (11. In an annual sample of German university students.9 (10.4-15.6-15.8 (64.7-20.7 (11. 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.7 (21.8-14.9 (15.4) 13.5 (56.0-90.6 (15.9-13.7-123) 77.4) 104 (89.8) 108 (75. 2005).6-81.1) 35.1 (21.1 (25..6) 12.S.5-29. 2004.7) 11.0 (62.0 (13.5 (10.4-79.5) 14.1 (9.0) 60.8) 53.9-83.3) 21.8 (11.1 (14..4 (12.5) 16.1 (21.9) 100 (80.6 (11.8-34. in young Swedish men (Jonsson et al.8 (50.3 (24.6) 25.6 (24.6 (30.3) 37.2-49.7) 56.1-120) 77.5-23.2) 11.8 (57.5 (48.2) 11.6-47.7-15.1) 12.6-116) 74.6 (14.4-18.6) 30.3) 89.7-397) 70.5 (11.1 (46.5) 17.95-14.4) 90th 50.4 (74.7-56.5-16.2-78.2) 11.7 (38.8) 80.5-26.3 (35.8-80.1-14.3) 12. 2002.4-102) 70.1 (18.9) 12.7-19.7 (12.8) 54. adolescents compared with adults. Weuve et al.5-57.4 (34.5 (35.9 (39.7-20.8-15.5-61.5-79.1) 80.2-12.4 (11.6) 73.9) 11.9-115) 57.1) 27.4) 44.4) 25.3-16.7-15.9 (54..3-73.0 (67.2-15.6) 58.2) 67.Phthalates York City (Adibi et al.4 (33.2 (41.5) 46. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4) 60.7) 38.4-14.9 (51.1) 17.9-69.4) 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 12.0-53.1 (23.5) 13.5) 78.0) 12.1 (21.73-12.7 (13.3 (39. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.6) 75th 25.1-125) 86.1) 39.9) 52.0) Selected percentiles ( 95% confidence interval) 50th 13.2) 12.7-12.4-93.3-11.0 (12.9-40.7-31.8) 71..5-58.8-16. A small study of African-American women in Washington.4) 13.1 (13.3) 67.2-13.7-90.8) 68.9 (29.7 (13.0) 24.2) 32. 2006).4) 28.6 (57. 2003).4) 21.2) 15.5-31.7) 25.4 (63.5) 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 . 2004).0-15.4 (25.69-11.1 (21.0 (10.8 (30.1) 142 (99.3) 29.7 (11.0 (11.7-19.5-38.6-12.1 (19.5 (12.9-13.7 (59.7 (11.3-38.2-57.9-62.7-29.3 (38.4-27.7-14.8) 16..0) 24.8-39.8) 11.6 (51.2-13.7-61.8-27.2 (40.8) 33.0-27.5) 10.9) 11.7 (18.0-51.9) 12.8 (49.9 (43.8-85.8) 34. 2003).1-35.9 (24.4) 17. 2007).0 (38. Hauser et al.5-42.5-99.3 (13.0) 49.3) 90.1 (11.8-42.6-40.1 (34.8-13.3) 55.3) 13.7 (19.0-48. 2005.4-42.1) 24.5-58.3) 14.6) 13.8) 33.6-13.1-79.8) 46.6-99.7) 19.1 (13.8 (46.3) 13.7-69.9-28.3) 73.2 (69.4 (11. Urinary Mono-benzyl phthalate (MBzP) (creatinine corrected) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4 (69.0 (12.7 (23.2-26.4-116) 73.6) 53. and females compared to males (Silva et al..1-12.4) 12.0) 11.8) 24.9 (15.1-27..8 (10.1-58.9-23.6) 12.5 (10.8-60.6 (19.8 (13. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.6 (30.5-76.1-12.6 (36.4-99.8-15.8 (12.6 (22.2-15. interval) 14.8-69.2-21.6-26.5) 23. 2007).1) 23.9 (10.0 (49..5-26.9 (55.6-86.4-14.9 (22.0) 13. and in a small sample of German residents (Koch et al.2-17.0-109) 65.4 (21.3 (12.8) 56. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.1 (41.2 (56. 2002).3) 13.5-213) 49.9) 12.7 (55.4-142) 134 (116-176) 136 (85.4 (60.4) 51.9) 24.2-117) 95.9) Total 14.3) 36.3) 18. In NHANES 1999-2000.3 (60.5 (49.8) 15.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.4) 15.2 (27.0) 15.5 (42.4 (13.9 (9.8) 26.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.3 (15.1 (43.8-173) 195 (121-305) 229 (99.1 (15.6) 38.4 (26..4 (10.6 (11. Hoppin et al.4 (46.3 (23.0 (41.8-13.3) 14.0 (41.4-17.3-64. 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.1) 24.9-104) 62.

Meeker JD. Eckard R. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.nih.110(5):515-518. Ryan L. Gans G. Malek NA. Poland. Hoppin JA.16(4):487-493. NTP-CERHR.S. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Jacek R. Environ Health Perspect 2002. et al. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Research Triangle Park (NC). Environ Health Perspect 2003. Schettler T. Weuve J.22(3):688-695. Angerer J. Environ Health Perspect 2000. J Androl 2004. Reproducibility of urinary phthalate metabolites in first morning urine samples. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Wittassek M. Helm D. Sampson EJ. Prenatal exposures to phthalates among women in New York City and Krakow. Hodge CC. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. et al. Silva MJ.114(9):1424-1431. Hu H. Giwercman A. Available at URL: http://cerhr. Environ Health Perspect 2004. Perera FP. Barr D. Centers for Disease Control and Prevention (CDC). Bull Environ Contam Toxicol 2002. et al. Barr DB. Phthalate monoesters levels in the urine of young children. Koch HM.18(1):122. Chen Z. Richthoff J.111(14):1719-1722. Caudill SP. 2000 [online].25(2):293-302.108(10):979-982. Sanchez GN. Blount BC.112(3):331-338.210(3-4):319-333. et al. Silva MJ. Hum Reprod 2007. Hauser R.Phthalates References Adibi JJ. Hilborn ED. Rossbach B. Environ Res 2003.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. McKee RH. 264 Fourth National Report on Human Exposure to Environmental Chemicals . 4/20/09 Silva MJ. Camann DE. Singh NP. Calafat AM. et al.93:177-185. David RM. Urinary levels of seven phthalate metabolites in the U. Pirkle JL. Rylander L. Jonsson BAG. Reprod Toxicol 2004. Needham LL. Brock JW. Ryan L. Hagmar L.68:309-314. et al. Reidy JA. Duty SM. Silva MJ. Dobler L. 112(5):A270]. Caudill SP. Butala JH. Needham LL. Levels of seven urinary phthalate metabolites in a human reference population. Silva MJ. Epidemiol 2005. Koch HM. Caudill SP. Brock JW. Calafat AM. Atlanta (GA). Jedrychowski W. Davis BJ.html. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. 2005. Third National Report on Human Exposure to Environmental Chemicals. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Brock JW. Int J Hyg Environ Health 2007. Baird DD. Drexler H. Wiesmuller GA. Green RA. Duty S.niehs. Environ Health Perspect 2006. et al.

0-14.02) 4.7 (18.97) 2.4 (20.5 (11.7 (7.20-6.80 (3.68 (2.90-4.00 (7.30 (3.10) 3.6-34.6 (13.1-25..4-27.30-7. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.0-38.97) 4.5-16.40-17.80 (5. 2000). population from the National Health and Nutrition Examination Survey.9-14.8 (9.30-11.0 and 0. 84-74-2 Di-isobutyl Phthalate CAS No.46 (2. Hauser et al.8) 677 652 703 699 1216 1088 Limit of detection (LOD. and insecticides.6) 16. and also in some printing inks.26 (2.S.2-14.30-3.70 (2.5) 18.5-16.60 (4.50) 7.10) 8.40-3.00-11.. 2005.S.66) 2.40 (2.00 (5.73 (2.9-23.11-3.3 (11.30) 10.0 (11.3-20.7-20.0) 24.80 (5.00) 4.1) 22.1 (8.3.49-2.3) 18.20-9.80 (2. DBP can produce reproductive toxicity in male rodents (McKee et al.5 (17. CDC.3-24.70) 5.7 (9.50) 8.50-10.4 (14.7) 18.3-18.91) 4.5) 18.00) 7.71 (2.6 (10.84) 4..10) 2.9) 10..96) 3. Following oral administration of DBP to humans.1-12.40-4.3 (13.5 (27.8) 21..67 (5. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.50 (3.10-2. mostly as MnBP (Anderson et al.50 (6.. pharmaceutical coatings.90-4.22) 3. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.10 (3.2) 5.30 (4. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 265 . 2000.81 (3.46 (3.00) 4. 2004.3-48.9 (16.90 (4. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine..9 (16.6-20.0-18.46) 2.8) 40.00-6.7-31.30-6.10-9. 2001).33 (2.40-12.5) 25.1-17.60-6.60 (8. Koch et al.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.20-2.56 (5.5) 12.3-43.6) 17.80-5.7 (16.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.7 (17.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.6) 16.2 (8.3 (16.56-4.00-6.00) 6.3 (13.50) 5.6 (10.3 (16.46-5.5) 14. 2003).30-13.30) 2.40-4.6) 26.44-2.6 (13.30) 5.90-2.82-3.80-5.2-22.20 (6.2 (11.40) 5.56 (3.10) 11.0-25.73-5.3) 33.6) 17.70) 3.0) 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 (20.1) 16.7-18.30-6. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.0) 20. NTP-CERHR. OSHA has established a workplace air standard for external exposure to DBP. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.72-3.50) 18.5) 22.85-6.2-33.40-5.43) 6.5-24.7) 14.5-29.70-4.10-9.80) 75th 5.7) 4.56) 3.50-6.70 (5. residents (Blount et al.30) 6. Studies of children found age-related differences in urine MBP levels.0 (13.3) 3. 2005).1-20.3-19.7) 15.40 (3.6-18. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate. they have been referred to as monobutyl phthalate (MBP).10) 9.0 (19. and in a small sample of Japanese adults (Itoh et al.0) 9. 2004.7) 7. 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.30) 10.17 (2.. 2005).6 (29.5 (10.24-8. about 65% to 80% of a dose is eliminated in urine within 24 hours.00-9.90-7.48 (2.40-9.20 (3.50-2.30-2.1 (13.0 (13.70-8.50) 2.17) 4.55) 2. in men attending a Boston infertility clinic (Duty et al.55 (3. in a small sample of pregnant women in New York City (Adibi et al.40-3.7-31.59) 3.0) 12.20 (7.80 (2. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.4) 12.5) 19.20) 7.3 (18.3-30.00) 10..30 (1.40 (7.90 (4. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.2 (12.20-12.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.19-3.40 (2.28-5.3 (19.60 (2.6) 12.37) 6.60 (5. Biomonitoring Information Median concentrations reported in the NHANES 19992000.10 (4.6 (14.22 (3.00-4.4) 5.6-14. 2003).0) 13.63) 3.97-7.90 (6.70-4.60) 3. When total DBP metabolites have been measured.20-12. 2005).5) 23. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.9) 15.6) 10.50-4.6-26.40 (6.Phthalates Di-n-butyl Phthalate CAS No.6 (9.90) 12. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.20) 4.4-12.4) 22. 2007).10 (4.7 (17.1) 25. interval) 2. In addition.90 (3.6 (11.07 (3.6 (14.50) 90th 12.

related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.1) 4. 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.51) 5.36-7.3 (13.20 (2.1) 7.31 (2.03 (5.6) 11. the students’ median values for MiBP levels remained relatively unchanged.66) 2. In an analysis of NHANES 1999-2000.53-4.02 (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. population from the National Health and Nutrition Examination Survey..86-4.2-13.5 (11.18-10.51) 2.26 (2.S.58-3.02-10.3) 18.6 (12.62-12.42) 2.58-4.30) 2.0) 3.6) 13.53-3.56-4. 2004). than adults in NHANES subsamples during the same time period.0 (10.69) 6.33 (3.98 (2.66) 10.11) 5.89-5.20-4.57-4.20-3.54) 2.18) 3.17 (2.52-20.56-15.82 (4.64-7.18 (4.75 (6.65 (4. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.3) 16.68) 3.38 (6.1 (11.95) 10.2) 8.93-6.32) 7.68) 5.2) 24.4 (12.0 (12.69-7.01-2.76-15.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.52) 3. ranging from more than one-tenth the NHANES median (Itoh et al.95) 2..28-13.46 (2.38-10.37) 3.43) 3.08) 75th 4. 2007). while MnBP declined (Wittassek et al.20 (2.64-7.11-2.4) 7.44 (3.56) 5.81 (3.76-3.36-2.65-4.85 (2.1-25.72) 5..79-6.8 (8.6 (10.43) 3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. respectively.3) 13. 2007).25) 5.47 (3.22 (2. Between 1998 and 2003.6 (8.9 (11. 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.31 (7.4) 23.3) 28.8) 10. 2006).82) 4.7 (21.78) 9.1-15.64-10.55-6. 2004).1) 10.27-12. up to four and 13 fold.7-28.84 (4.32 (7.00-3.0) 11.03-7.8-13.57 (3.2 (11.00-7.11 (5.8-18.10-5.19 (2..74 (4.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals . 2005).1-12.7) 3.72-7.. 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.and gender.35) 3.86) 6.1) 13.04) 7.94) 6.78) 8.17) 90th 8.99) 7.8 (10.0 (8.47-12. 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.31) 2.7) 11.5 (9.7 (11.21) 10.91-6.32 (3.00-3.04-5. samples from German university students had consistently higher median urine levels of MnBP and MiBP.59 (4.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.4) 15.18) 4.7) 10.8-36.14 (4.94-12.52-3.05) 2.80) 7.9 (9.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.41 (2.69) 4.62 (6.9-16.03-11.57 (3.29-8.92 (7. Over this time.33-9.2) 9.6 (15.18-4.66) 4.78-8.7 (9.00 (3.1) 15.84 (8. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.75 (4.39) 5.96 (3. to about two to fourfold higher (Fromme et al.3) 13.47-5.15-4.81) 4.7) 19.9-26.69 (2.56) 2.9) 12.08-2.3 (17.20-2.6-19.8 (9.83 (2.29-3. 2005).04) 3.89) 6.76-3.0) 7.43) 3.88 (2.20 (7.6 (8.53-5.45) 3..4-16.31) 2.94 (5.52 (2.6 (9.17-12.39-3.09-2.46) 3.2-15.5) 15.80-3.5) 13.66 (8.74-3.81) 9.0) 15.79 (4.1 (10.68 (2.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.15) 3.1-24.34 (3. Survey Geometric mean (95% conf.21 (5.81 (6.33) 3.73 (5.99-4.54 (2.18 (1.5-19.67-5.33 (2.65-11. 2002.54 (4.9 (15.1) 11.13-6.13 (2.46-11.97-2.9-40.0-18.2 (10.61-3.95-3.6-19.80 (3.30 (6.79-8.76 (3. An analysis of NHANES 2001-2002 showed similar age.7 (13. Weuve et al.26-2.8-18.24) 3.89 (3.51) 15.07 (2.07-5. interval) 2.28 (4.

2) 42.2) 90th 98.1) 47.3 (30. see Data Analysis section) for survey years 99-00.6) 17.4 (71.4-159) 107 (84.6 (55.1 (62.1) 20.0-26.2-56.5) 26.0) 84.9-33.7-53.7-26. 01-02.5) 17. Fourth National Report on Human Exposure to Environmental Chemicals 267 .2-32.5) 24.6) 71.3 (36.7 (43.9-92.9 (17.0 (25.1 (19.3 (60.1) 36.1) 23.1 (41.2 (58. *In the 1999-2000 survey period.6-36.1) 30.3-136) 137 (107-162) 119 (90.1-24.2 (21.8-22.5) 78.6 (22.1 (17.6-113) 108 (90.1-51.7 (16.7) 92.3-76.8) 23.5-43.5-47.1-82.2) 20.7-92.5-60.4 (38.6-20.9 (20.7-20.8) 48.6-49.3 (23.0 (31.3-21.9-22.2) 68.7-116) 95.8-132) 95.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.3 (30.5) 31.1.9) 71.7-91.2-87.1 (58.7-34.7 (38.6) 80.5 (59.0 (72.1 (31.5-47.2 (79.8) 62.3-96.9 (17.0 (30.5) 36.1-20.7-127) 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 22.9) 26.3 (51.0 (45.2-63. population from the National Health and Nutrition Examination Survey.6 (90.0) 20.0 (15.3) 36.1 (36.9.7 (28.4) 20.8-29.6-44.6) 38.0-19.3 (23.3) 40.7) 124 (98.1-29.5-53.1) 46.9) 75.0-24.0-32.2 (25.3-79.4-25.2-93.9) 46.3) 23. and 03-04 are 0.2-114) 73.4 (35.0-24.3-60.4-26.4 (23.5 (74.5-27.5) 20.4-31.6-69.0) 120 (98.2 (18.7-24.3) 19.4 (25.4 (35.6) 21.7 (19.2) 38.9-87.7-111) 64.6) 20.5) 19.7-117) 118 (108-143) 93.7-42.6 (32.0) 30.0 (36.2-49.6 (65.7 (18.7) 28.5) 65.5) 34.7 (18.1 (21.3-67. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.4-20.1 (19.6-29.3 (42.4-18.3) 26.7 (22.8) 43.4 (84.2 (78.9) 29.5 (29.0) 27.5) 37.8-123) 101 (90.0 (17. referred to as monobutyl phthalate (MBP).0 (23.5) 47.0-58.4-60.3 (56.5) 95.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.2 (19.0 (78.6-143) 127 (99.7-124) 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.6-29.1 (51.6 (48.2) 62.0-51.1 (19.1 (18.1) 23.4) 22.2-33. interval) 24.5-42.7 (64.2 (17.4 (35.9-28.6-24.3) 21.9) 21.9-53.6-33.3) 24.2 (74.9-42.5) 36.2 (21.4 (72.9 (79.2 (59.0 (20.0 (18.8 (19.9) 36.1-27.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.6 (61.6-40.2-22.6) 46.7-34.8 (57.7) 42. respectively.3 (17.5 (28.1) 19.1-75.0-21.6 (26.1) 23.7 (51.7) 74.1-22.4) 59.4 (21.S.6-37.1 (19.3-145) 85.6 (19.3-85.8) 19.2-21. Survey Geometric mean (95% conf.0) 21.0) 31.4-42.9) 18.7 (24.9-79.6) 39.4.6-31.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.7-121) 97.5) 21.0-19.5 (59.4-44.8) 58.5-44.9-22.1-80.5-121) 106 (94.8) 75th 51.0) 117 (104-131) 112 (84.1-92.6-48.0-73.1 (16.1) 17.3 (37.1 (28.1 (34.5 (30.2-24.1) 31.7-42.6) 35.8-119) 90.2 (75.2-159) 92.9-101) 77. 1. and 0.1) 25.1 (54.2) 26.8-25.7 (70.4) 64.0) 38.8-42.4 (19.2) 32.5) 40.3-24.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.7 (33.5) 85.2 (20.9 (79.2-23.1 (26.6 (16.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.4 (35.6 (44.7) 52.5-117) 95.4) 52.3) 18.9-114) 116 (97.3-40.7-106) 69.4 (36.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.

6-22.5) 39.4-76.1 (46.4-61.3-78.3-49.4 (17.3-39.2 (83.9-100) 86.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3 (17.1-32.3 (19.1) 20.5-76.3-21.6 (29.6-155) 91.1-83.9 (30.6) 25.8 (18.7-78.5-64.5) 21.1-21.5-23.0) 53.8 (33.0 (27.6-74.9-36.8 (18.6) 14.6-16.1) 22.1 (32.7 (60.3 (48.7 (57.0) 19.9-68.1) 21.2-22.8-24.2-106) 64.2) 74.9-14.9 (35.4 (37.2) 21.9-34.4-164) 96.9-70.1-18.4) 15.7-51.6) 65.9) 49.3) 20.4-135) 71.5-142) 81.6-24.8) 17.5-37.6-44.0 (18.4 (47.5) 90th 68.4 (68.9 (37.8 (17.3-17.9-56.S.5 (64.3 (69.6) 18.4 (31.1) 50.1) 42.7 (43.3) 33.3 (21.2 (38.1) 61.3 (46.6) 23.2) 59.4) 53.4 (33.9 (16.9-68.7-19.2-61.0 (70.8 (18.2-21.8) 22.7-23.0) 26.6 (41.3) 18. 268 Fourth National Report on Human Exposure to Environmental Chemicals .3 (42.0) 108 (71.7 (81.8) 75th 38.5) 84.9 (56.8) 23.6) 38.9 (35.4) 20.3 (16.1-128) 97.4-103) 117 (83.0) 94.5-30.1) 44.8-43.0 (20.6 (25.5 (81.6 (19.5) 134 (93.2-73.6 (17.3 (24.0) 25.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.1) 20.3) 19.7 (14.3-18. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.3 (28.6-53.4) 15.5-18.4) 62.3-32.2-28.9 (30.8) 30.2) 159 (102-263) 147 (93.7 (73.7-26.3 (52.8 (16.0) 28.7 (12.6) 64.6 (25.3-81.0) 75.4 (31.8-235) 137 (108-198) 88.2-85.3 (17.7-80.9 (39.1) 53.5) 91.9) 30.0) 70.9) 28.8 (65.2-179) 84.4 (50.6 (31.9 (30.1 (61.0-19.7 (54.9 (21.0-41.6 (27.9 (73.4) 51.8) 20.4-47.9) 20.6 (72.7 (60.5) 82.0 (50.0-60.3 (60.4 (50.3-26.1 (29.2-16.2) 65.0-75.0) 59.8) 63.4-72.1 (15.8 (50.1) 37.3-20.0) 55.9) 19.9-26.3-23.6-24.1 (21.4 (53.6-23.8) 17.4 (45.2 (19.0-92.3 (52.2) 16.6) 31.0 (61.3) 52.6-43.6 (61.0-113) 104 (83.8) 19.3-40.0-17.3-106) 74.6-28.4-34.7-37. population from the National Health and Nutrition Examination Survey.5 (15.6-27.7 (16. interval) 22.8 (22.5 (18.4 (16.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.0 (18.4 (20.0 (71.1) 35.9 (19.2 (19.8) 34.2-22.3) 21.4 (17.3-38.0 (52.3) 17.0) 35.9-49.6 (57.7-20.8) 17.9) 91.4) 16.0 (16.8) 40.6-92.5) 60.3-21.6) 37.0) 81.6-119) 63.7 (27.0 (26.5-22. Survey Geometric mean (95% conf.7 (19.5 (30.7-21.0) 41.3 (17.0 (19.6-50.9) 39.6-19.3) 19.9 (20.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.3) 33.0 (34.9 (58.4-24.7) 20.8-24.8 (13.7-19.3) 59.8) 13.8) 28.0-47.4 (18.3 (55.6) 39.4-131) 81.8 (25.6-32.9-38.2-18.4 (16.4) 19.4) 21.1 (56.7-28.9) 62.5-41.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.5-70.5-21.8-32.6-42.5-15.6 (74.1-23.9 (64.0-90.0) 29.0 (69.5-16.2 (35.2-86.9) 52.6-128) 96.7) 36.1-99.5) 17.7-42.2 (16.3-71.3) 35.3 (76.6-44.4 (19.6) 24.7) 42.5 (18.2-27.2-48.3) 67.5 (14.4 (13.6-23.1 (34.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9) 24.9) 14.6) 83.1-62.2-22.1-99.8) 34.0 (15.0 (43.8) 20.3 (71.7-39.7 (28.8-23.7) 19.4 (23.3-114) 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) 17.9-105) 85.4 (31.2) 31.4-65.9-84.6) 24.6-26.6) 34.4 (56.5-142) 89.7 (20.8) 35.0-38.

Massey RC. Fromme H. Bolte G. et al. et al. Centers for Disease Control and Prevention (CDC). Urinary phthalate metabolites and biomarkers of reproductive function in young men. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Wiesmuller GA. Fourth National Report on Human Exposure to Environmental Chemicals 269 . A biomarker approach to measuring human dietary exposure to certain phthalate diesters. et al. Brock JW. NTP-CERHR. Prenatal exposures to phthalates among women in New York City and Krakow. Brock JW.210:21-33. Yoshida K.111(14):1719-1722. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Environ Health Perspect 2006. Calafat AM.html. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. 112(5):A270]. Research Triangle Park (NC). Itoh H.gov/chemicals/ phthalates/dbp/dbp-eval. Chen Z. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.108(10)979-982. Sampson EJ. Richthoff J. Drexler H. Rossbach B. Epidemiol 2005. Third National Report on Human Exposure to Environmental Chemicals. Springall C. Barr DB. Boehmer S. Reidy JA. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Needham LL. Hu H. Silva MJ.16(4):487-493. Drexler H. Helm D. Environ Res 2003. Malek NA. Dobler L. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Camann DE. Pirkle JL. et al. Jedrychowski W. Blount BC. Schettler T. 2000 [online].18(12):10681074. Singh NP.25(2):293-302. Duty SM.niehs. Giwercman A. Hodge CC. Environ Health Perspect 2004. Koch HM. Caudill SP. Weuve J. Int J Hyg Environ Health 2005.S. Angerer J. Hum Reprod 2007. Masunaga S.112(3):331-338. Wittassek M. Environ Health Perspect 2003. Jacek R. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.93:177-185. et al. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Caudill SP. 4/20/09 Silva MJ.Phthalates References Adibi JJ. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Needham LL. Meeker JD. McKee RH. Environ Health Perspect 2000. Koch HM. Silva MJ. Ryan L.nih. Hauser R. Bull Environ Contam Toxicol 2002. Butala JH. Perera FP. Int J Hyg Environ Health 2007. Eckard R. Gans G.208:237-245. 2005. Phthalate monoesters levels in the urine of young children.68:309-314.18(1):122. Available at URL: http://cerhr. Silva MJ. Urinary levels of seven phthalate metabolites in the U. Barr D. Scotter MJ. Jonsson BAG. Silva MJ. Hilborn ED. Rylander L.210(3-4):319-33. Int J Hyg Environ Health 2007. Calafat AM.22(3):688-695. Sanchez GN. Hagmar L. Koch HM. Caudill SP. Reprod Toxicol 2004. Atlanta (GA).114(9):1424-1431. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Duty S. Green RA. et al. David RM. Angerer J. Poland. Anderson WA. Food Addit Contam 2001. J Androl 2004. Castle L. et al. Levels of seven urinary phthalate metabolites in a human reference population. Ryan L. et al.

270 Fourth National Report on Human Exposure to Environmental Chemicals .500) 1.300 (.200-.00-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.700) . In this Report.20) .500) < LOD < LOD .500 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (<LOD-.600) < LOD .200-.900-1.10) .500) .200-.300-.500) < LOD 1.10 (<LOD-1.500) . Survey Geometric mean (95% conf.70) . 0.300-.70) . 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.400-.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 . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. see Data Analysis section) for Survey years 99-00.70 (1. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.500 (.400-. polyvinyl acetate.10 (.2.400 (.400-.600 (.200-.300-.200 (<LOD-.600) .400-.400-.300-.400-.400) 1.400 (.500 (.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.400 (.50) .500-. and 0.400) < LOD < LOD .400 (<LOD-. including nitrocellulose. 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. respectively.50) .200-.600) .400-.500) < LOD < LOD .00-2. only levels at or above the 90th percentile could be characterized.80) .400 (<LOD-.500) .300 (.500 (.3. 01-02.400 (<LOD-.300) < LOD .600) .400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . resins.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. < LOD means less than the limit of detection.500 (.400 (.600) .500 (.700) .300-.10 (<LOD-2. and 03-04 are 0.300-.300-.400 (.300-.400 (.300-.00 (<LOD-1.300 (.700) .500 (.Phthalates Dicyclohexyl Phthalate CAS No. 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. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70 (1. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.00 (<LOD-1.9. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.300 (.10 (<LOD-1.500) 1.300 (<LOD-.300) < LOD .600) .300 (.300) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200-.500) .S. and polyvinyl chloride.500) 1.300-.400) < LOD 1.00) .400 (.500 (. and polymers.500 (.90) .300 (.400) 1.00 (<LOD-1.300 (.

44) .34) .770-1.11) .670 (<LOD-.450 (.670-1.400-.740) .940 (.220 (<LOD-.880 (.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.620) < LOD .450 (.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 .420-.910 (.530 (.36-1.250 (. Survey Geometric mean (95% conf.770-1.00) .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 1.500) 3.420-.240-.410 (.330 (.500-.630 (<LOD-.82 (1.910 (.290-.53) .770) < LOD 2.590 (.690 (.33) .420-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.270) < LOD .74) .54-6.54 (<LOD-2.54) .16 (<LOD-3. Fourth National Report on Human Exposure to Environmental Chemicals 271 .800-1.370 (<LOD-.53) .500 (.510-.170-.43 (1.06) .14 (<LOD-3.560) 1.710) .740) < LOD < LOD .470) 3.470 (.630 (<LOD-.310-.00 (<LOD-3.950 (.660) < LOD < LOD .22 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) .S.310) < LOD .770 (.660) .380-.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.330 (.400-.530-.33 (<LOD-3.530-1.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .17) .690-1.67 (1.390 (.18) .590 (<LOD-.12-1.260-.350-.690) < LOD < LOD .490) .82) .610 (.830) 1.480 (.510 (.16) .380 (.790-1.05) .690) < LOD 2.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .910 (. population from the National Health and Nutrition Examination Survey.530) 1.06) .770-1.360-.910 (.

5) 81. 272 Fourth National Report on Human Exposure to Environmental Chemicals . 0. 2002).4. and hand lotions.9 (61. 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.. 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. and also in men attending a Boston infertility clinic (Hauser et al..S. 2007). see Data Analysis section) for Survey years 99-00.4 (62. shampoos.7 (70. 2003) and African-American women in Washington. 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. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. DC (Hoppin et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7) 71.3 (82.1-93. and 0. 01-02. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.8-111) 85. In contrast.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. and 03-04 are 1. colognes..Phthalates Diethyl Phthalate CAS No. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 2001-2002.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75.9-92.1 (71.3 (74.2. respectively. deodorants. particularly those containing fragrances.2-102) 95. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. soaps. Products that may contain DEP include perfumes. Biomonitoring Information MEP levels in the NHANES 1999-2000. population from the National Health and Nutrition Examination Survey.

6 (77. In an analysis of NHANES 1999-2000..9 (82.S.. 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. Analysis of NHANES 2001-2002 showed similar findings.6 (65. 2004)..0 (66.5-114) 101 (87. interval) 163 (149-178) Selected percentiles ( 95% confidence interval) 50th 141 (129-157) 148 (133-162) 153 (137-177) 75th 360 (307-422) 388 (330-435) 452 (386-504) 90th 905 (753-1180) 969 (805-1180) 1110 (889-1290) Total 167 (150-185) 181 (163-202) Sample size 1950 (1670-2310) 2536 1840 (1450-2200) 2782 2040 (1640-2540) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 92.0-156) 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 .7-110) 81.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.3-105) 87.9-110) 96. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Phthalates 2002 (Brock et al.5-113) 122 (93. 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. with adjusted geometric mean levels of urinary MEP that increased with age (CDC. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Other population estimates also differed by sex and race ethnicity (Silva et al.2 (66. 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. 2005). 2002). This age-related trend is opposite the direction seen for other phthalates. population from the National Health and Nutrition Examination Survey. 2003) were slightly lower than levels found in NHANES 2001-2002. Median MEP levels found in a small sample of German residents (Koch et al. 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.

et al. et al.111(14):1719-1722. Silva MJ. Environ Res 2003. Caudill SP. Hilborn ED. Hum Reprod 2007.Phthalates References Adibi JJ. Meeker JD. Environ Health Perspect 2004. Needham LL.22(3):688-695. Davis BJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. 2005. Duty S. 112(5):A270]. Atlanta (GA). 274 Fourth National Report on Human Exposure to Environmental Chemicals . Caudill SP. Rossbach B. Prenatal exposures to phthalates among women in New York City and Krakow. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. et al. Ryan L. Environ Health Perspect 2002. Hoppin JA. Silva MJ. Hodge CC. Silva MJ.68:309-314. Urinary levels of seven phthalate metabolites in the U. Koch HM. Camann DE. Bull Environ Contam Toxicol 2002. Barr D. Hauser R.110(5):515-518. Reproducibility of urinary phthalate metabolites in first morning urine samples. Third National Report on Human Exposure to Environmental Chemicals. Reidy JA.S. Baird DD. Brock JW. Jacek R. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Brock JW. Poland. Angerer J. Drexler H.93:177-185. Phthalate monoesters levels in the urine of young children. Barr DB. Centers for Disease Control and Prevention (CDC). Singh NP. Jedrychowski W. Perera FP.112(3):331-338. Malek NA. Environ Health Perspect 2003.

50-5.10-4.70-5.60) 3. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.25-3.9 (7.1-48.90-3.70) 2.6 (41.40 (4.1-17..40) 4.5 (12.80-8.2-28. as glucuronide conjugates (Albro et al.2-39.50 (7.0 (18.40-8.3-64.70-6.6 (9.50-11.92) 4.6) 9.90) 1.50 (2.10-11.7-58.60) 9.00-4.3 (19.6) 39.6 (12. 1989.6) 14.2) 29.92-5.4-42. 1982.8-36.1) 19.69) Selected percentiles ( 95% confidence interval) 50th 3.3-57.0) 31.00) 11.20 (3.3 (10.91-3.70-3.5) 37.0) 23.80 (2.30 (6.5-41.8 (19.75 (3.5 (12.20 (3.90) 4.96-5.98) 2.9) 15.89-3.80-5.42-5.40) 2.1-29.12 (4.70-2.4) 33.10 (6.5-28.90 (3.50-6.10) 2.4-27.16-3.5) 21.94-3.23) 3.0 (9.50-16.50-2.0 (19. and 03-04 are 1.0-29.41 (3.90) 4.50 (3.80 (8.70 (7.8 (17.9-29.80 (8.84-4.50) 4.96) 4.84) 3.31 (3.00 (2.10) 3. and in humans.4) 7.7) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.4) 6.5) 40.9) 13.40) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50 (7. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.70 (5.7) 37.2 (10.23 (2.5) 32.8) 17.5) 43.7-18.31-4.9) 13.86) 2.23 (3.70 (3.00-3.70-4.60) 7.00) 1.3) 28.8 (19.7) 6. ATSDR.50 (8.03-2.30) 2.6-60.85 (3.40-9.50-6.14 (1.3) 52.4) 23.40 (6.5 (11.40 (2.40) 8.90-5.90-11.50 (3.9 (26.0) 23.27) 2.30 (7.5 (20.00) 19.70) 7.9-48.85) 4.40) 75th 7.41) 3.60) 4.90-4.60-11.79) 2.90-8.61 (3.00) 9.70 (1.10 (2.4-40.60) 10.93) 6.5-27.S.4) 22.9 (29.9-19.4-53.50-20.8-50.80-9.1-27.2.90 (4.5 (18.0 (17.30 (4.46) 3.9 (17.2) 42.2) 4.68 (3.00) 2.70 (2. mainly polyvinyl chloride. Fourth National Report on Human Exposure to Environmental Chemicals 275 .10-5.7) 27.30-8.2 (7.39) 3.5) 23.3 (15.5-36.50-14. Following ingestion.4-20.90) 4. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).80 (1.4) 22.30 (3. which is used for many consumer products.27 (3.70 (3.75-4.7) 35.3) 13.0 (14.0 (19.2-35.7 (17.00-5.80) 6.10 (5. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood. and 0.50-5.6-38.10 (4.1 (8.10) 8.00) 3.15 (1.80) 9.5-28.0 (13.80-3.10 (3.5 (25.6 (16.92-2.0) Total 4.6) 15.49 (3.2) 6.60 (6.70-2.6-25.00) 5.5 (24.19-3.00 (4.7-32.40) 9.44) 4.9) 27.60) 8. Albro and Lavenhar. Concentrations in plastic materials may reach 40% by weight.7 (14.67-4.0-18.4 (16.2 (11.9 (13.0.9 (29.0) 35.51) 4.9 (16.8) 15. DEHP has been removed from or replaced in most toys and food packaging in the United States.63-4.40-12. interval) 3.90) 7. toys.00) 1.10-5.6 (10.90 (1. see Data Analysis section) for Survey years 99-00.21 (2.50-3.84 (2.37-4.3-26.86) 2. 1.4) 20.62) 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 5.5-40.9) 18.60 (5.6-23. respectively.5