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Toxicological Review of Dichloroacetic Acid (CAS No. 79-43

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Toxicological Review of Dichloroacetic Acid (CAS No. 79-43 EPA 635/R-03/007 www.epa.gov/iris TOXICOLOGICAL REVIEW OF DICHLOROACETIC ACID (CAS No. 79-43-6) In Support of Summary Information on the Integrated Risk Information System (IRIS) August 2003 U.S. Environmental Protection Agency Washington, DC DISCLAIMER This document has been reviewed in accordance with U.S. Environmental Protection Agency policy and approved for publication. Mention of trade names or commercial products does not constitute endorsement or recommendation for use. Note: This document may undergo revisions in the future. The most up-to-date version will be made available electronically via the IRIS Home Page at http://www.epa.gov/iris. ii TABLE OF CONTENTS LIST OF TABLES .............................................................v LIST OF FIGURES ........................................................... vi FOREWORD ............................................................... vii AUTHORS, CONTRIBUTORS, AND REVIEWERS ............................... viii 1. INTRODUCTION ..........................................................1 2. CHEMICAL AND PHYSICAL INFORMATION RELEVANT TO ASSESSMENTS .....3 3. TOXICOKINETICS .........................................................4 3.1. ABSORPTION .....................................................4 3.2. DISTRIBUTION ....................................................4 3.3. METABOLISM .....................................................4 3.3.1. Mechanistic Metabolic Considerations ...........................11 3.4. ELIMINATION ....................................................14 3.5. PHYSIOLOGICALLY-BASED TOXICOKINETIC MODELS ..............15 4. HAZARD IDENTIFICATION ............................................17 4.1. STUDIES IN HUMANS .............................................17 4.2. STUDIES IN ANIMALS .............................................21 4.2.1. Acute and Subchronic Studies .................................21 4.2.2. Chronic Studies and Cancer Bioassays ...........................30 4.3. REPRODUCTIVE/DEVELOPMENTAL STUDIES .......................37 4.4. OTHER STUDIES ..................................................42 4.4.1. Mechanistic Studies .........................................42 4.4.2. Genotoxicity Studies .........................................51 4.5. SYNTHESIS AND EVALUATION OF MAJOR NONCANCER EFFECTS .... 58 4.5.1. Metabolic Alterations ........................................58 4.5.2. Hepatic Toxicity ............................................59 4.5.3. Reproductive/Developmental Toxicity ...........................61 4.5.4. Neurotoxicity ..............................................61 4.6. SYNTHESIS AND EVALUATION OF CANCER EFFECTS AND MODE OF ACTION .......................................................62 4.6.1. Data Summary .............................................62 4.6.2. Potential Mode of Carcinogenicity ..............................65 4.6.3. Cancer Characterization ......................................71 4.7. SUSCEPTIBLE POPULATIONS AND LIFE STAGES ....................72 5. DOSE-RESPONSE ASSESSMENTS ..........................................74 5.1. ORAL REFERENCE DOSE (RfD) .....................................74 5.1.1. Methods of Analysis .........................................74 5.1.2. NOAEL/LOAEL Approach ...................................74 iii 5.1.3. Benchmark Dose Approach ...................................80 5.1.4. Summary of Oral RfD Derivation ...............................88 5.2. INHALATION REFERENCE CONCENTRATION (RFC) ..................88 5.3. CANCER ASSESSMENT ............................................89 5.3.1. Choice of Principal Studies and Cancer Endpoints .................89 5.3.2. Dose-Response Data .........................................89 5.3.3. Dose Conversion ............................................90 5.3.4. Dose-Response Characterization in the Range of Observation ........ 90 5.3.5. Selection of a Dose-Response Model ............................91 5.3.6. Extrapolation to Doses Below the Range of Observation ............ 92 5.3.7. Confidence in the Cancer Assessment ...........................93 6. MAJOR CONCLUSIONS IN THE CHARACTERIZATION OF HAZARD AND DOSE-RESPONSE ....................................95 6.1. HUMAN HAZARD POTENTIAL .....................................95 6.2. DOSE-RESPONSE ................................................100 7. REFERENCES .......................................................102 APPENDIX A: RESPONSE TO PEER REVIEW SUMMARY DOCUMENT APPENDIX B: SUMMARY OF STUDIES ON DCA TOXICITY AND APPLICABILITY FOR BMD ANALYSIS APPENDIX C: BENCHMARK DOSE-RESPONSE FOR NONCANCER ENDPOINTS APPENDIX D: BENCHMARK DOSE-RESPONSE FOR CANCER ENDPOINTS DEANGELO ET AL., 1999 (5 DOSES) APPENDIX E: BENCHMARK DOSE-RESPONSE FOR CANCER ENDPOINTS DEANGELO ET AL., 1999 (4 AND 6 DOSES) iv LIST OF TABLES -1 -1 Table 3-1. Enzyme kinetics for GSTZ: kcat/Km ratios (M sec ) ............................13 Table 4-1. Biomarkers of tissue DCA exposure: incidence (%) of altered hepatic history ........................................44 Table 4-2. Frequency of spontaneous and DCA-induced mutations of codon 61 in exon 2 of the H-ras oncogene mutations in B6C3F1 mice ........................48 Table 4-3. Summary of in vitro genotoxicity tests .....................................53 Table 4-4. Summary of in vivo genotoxicity tests .....................................55 Table 4-5. Drinking water exposures, cancer response and simulated internal dose metrics .......64 Table 5-1. Summary of noncancer studies considered for benchmark modeling ................76 Table 5-2. Criteria for selecting studies appropriate for BMD modeling .....................82 Table 5-3. Cardiovascular defects induced by DCA ...................................83 Table 5-4. Effects of DCA on fetal body weight .......................................84 Table 5-5. Liver weight data set ...................................................85 Table 5-6. Male reproductive data sets used for BMD modeling ...........................85 Table 5-7. Summary of noncancer BMD modeling results ................................87 Table 5-8. Cancer dose-response data evaluated using BMD modeling: male mice .............89 Table 5-9. Summary of cancer BMD modeling results ...................................92 v LIST OF FIGURES Figure 3-1. Metabolism of DCA ...................................................7 Figure 5-1. Summary of noncancer effects of DCA .....................................77 Figure 5-2. Multistage dose-response model fit for combined hepatocarcinoma and adenoma incidence in male mice ..........................................93 vi FOREWORD The purpose of this Toxicological Review is to provide scientific support and rationale for the hazard and dose-response assessment in IRIS pertaining to chronic exposure to dichloroacetic acid (DCA). It is not intended to be a comprehensive treatise on the chemical or toxicological nature of DCA. In Section 6, EPA has characterized its overall confidence in the quantitative and qualitative aspects of hazard and dose response. Matters considered in this characterization include knowledge gaps, uncertainties, quality of data, and scientific controversies. This characterization is presented in an effort to make apparent the limitations of the assessment and to aid and guide the risk assessor in the ensuing steps of the risk assessment process. For other general information about this assessment or other questions relating to IRIS, the reader is referred to EPA’s IRIS Hotline at 202-566-1676. vii AUTHORS, CONTRIBUTORS, AND REVIEWERS CHEMICAL MANAGER Joyce Morrissey Donohue, Ph.D. Health and Ecological Criteria Division Office of Science and Technology Office of Water U.S. Environmental Protection Agency Washington, DC AUTHORS Joyce Morrissey Donohue, Ph.D. Health and Ecological Criteria Division Office of Science and Technology Office of Water U.S. Environmental Protection Agency Washington, DC Hend Galal-Gorchev, Ph.D. Health and Ecological Criteria Division Office of Science and Technology Office of Water U.S. Environmental Protection Agency Washington, DC William Brattin, Ph.D. ISSI Consulting Denver, Colorado John J. Liccione, Ph.D. Sciences International, Inc. Alexandria, VA Kara B. Altshuler, Ph.D. ICF Consulting Fairfax, VA REVIEWERS This document and summary information on IRIS have received peer review both by EPA scientists and by independent scientists external to EPA. Subsequent to external review and incorporation of comments, this assessment has undergone an Agency-wide review process viii whereby the IRIS Program Director has achieved a consensus approval among the Office of Research and Development; Office of Air and Radiation; Office of Prevention, Pesticides, and Toxic Substances; Office of Solid Waste and Emergency Response; Office of Water; Office of Policy, Economics, and Innovation; Office of Children’s Health Protection; Office of Environmental Information; and the Regional Offices. INTERNAL EPA REVIEWERS Jeff Gift National Center for Environmental Assessment U.S. Environmental Protection Agency Karen Hogan National Center for Environmental Assessment U.S. Environmental Protection Agency John Lipscomb, Ph.D. National Center for Environmental Assessment U.S. Environmental Protection Agency Carolyn Smallwood, Ph.D. National Center for Environmental Assessment U.S. Environmental Protection Agency EXTERNAL PEER REVIEWERS Richard Bull, Ph.D. Department of Pharmacology/Toxicology Washington State University Tricities Denise Robinson, Ph.D. International Life Sciences
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