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Species | R L MelnickSummaryAffiliation: National Institutes of Health Country: USA Publications
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Publications
Summary of the National Toxicology Program's report of the endocrine disruptors low-dose peer reviewRonald Melnick
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Environ Health Perspect 110:427-31. 2002....
Suppression of crucial information in the IARC evaluation of DEHPRonald L Melnick
Int J Occup Environ Health 9:84-5; discussion 89. 2003- A Daubert motion: a legal strategy to exclude essential scientific evidence in toxic tort litigationRonald L Melnick
Environmental Toxicology Program, National Institute for Environmental Health Sciences, National Institutes of Health, Bethesda, MD, USA
Am J Public Health 95:S30-4. 2005..This could lead to the unfair exclusion of valid scientific evidence, particularly that which is essential to a plaintiff's case in toxic tort litigation... - Toxicity and carcinogenicity of the water disinfection byproduct, dibromoacetic acid, in rats and miceRonald L Melnick
Environmental Toxicology Program, National Institute of Environmental Health Sciences, P O Box 12233, Research Triangle Park, NC 27709, USA
Toxicology 230:126-36. 2007..These studies provide critical information for future re-evaluations of health-based drinking water standards for haloacetic acids... - Conflicting views on chemical carcinogenesis arising from the design and evaluation of rodent carcinogenicity studiesRonald L Melnick
National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC 27709, USA
Environ Health Perspect 116:130-5. 2008..Pharmacokinetic models and mechanistic hypotheses may provide insights into the biological behavior of the agent; however, they must be adequately tested before being used to evaluate human cancer risk... - A Darwinian perspective: right premises, questionable conclusion. A commentary on Niall Shanks and Rebecca Pyles' "evolution and medicine: the long reach of "Dr. Darwin""Paolo Vineis
Department of Epidemiology and Community Health, Imperial College London, St Mary s Campus, Norfolk Place, W2 1PG, London, UK
Philos Ethics Humanit Med 3:6. 2008..Epidemics of cancer could have been prevented if experimental data had been used to reduce human exposures or ban carcinogenic chemicals. We discuss examples... - Carcinogenicity and mechanistic insights on the behavior of epoxides and epoxide-forming chemicalsRonald L Melnick
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Ann N Y Acad Sci 982:177-89. 2002..Reducing occupational and environmental exposures to these chemicals will certainly reduce human cancer risks... - Is peroxisome proliferation an obligatory precursor step in the carcinogenicity of di(2-ethylhexyl)phthalate (DEHP)?R L Melnick
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Environ Health Perspect 109:437-42. 2001.... - Comparative carcinogenicity of 1,3-butadiene, isoprene, and chloroprene in rats and miceR L Melnick
National Institute of Environmental Health Sciences, National Institutes of Health, PO Box 12233, Research Triangle Park, NC 27709, USA
Chem Biol Interact 135:27-42. 2001..Epidemiology data for isoprene and chloroprene are not considered adequate to evaluate the potential carcinogenicity of these agents in humans... - Dose-response analyses of experimental cancer dataR L Melnick
Laboratory of Computational Biology and Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Drug Metab Rev 32:193-209. 2000.... - Regenerative hyperplasia is not required for liver tumor induction in female B6C3F1 mice exposed to trihalomethanesR L Melnick
Environmental Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Toxicol Appl Pharmacol 148:137-47. 1998..The possible contributions from other activation pathways, including GSH conjugation and reductive metabolism, need to be considered in assessments of the carcinogenicity of the trihalomethanes... - Multiple organ carcinogenicity of inhaled chloroprene (2-chloro-1,3-butadiene) in F344/N rats and B6C3F1 mice and comparison of dose-response with 1,3-butadiene in miceR L Melnick
National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Carcinogenesis 20:867-78. 1999..Cancer potency of chloroprene is greater in the mouse lung than in the rat lung, but greater in the rat kidney than in the mouse kidney and nearly equivalent in the mammary gland of each species... - High frequency of codon 61 K-ras A-->T transversions in lung and Harderian gland neoplasms of B6C3F1 mice exposed to chloroprene (2-chloro-1,3-butadiene) for 2 years, and comparisons with the structurally related chemicals isoprene and 1,3-butadieneR C Sills
Environmental Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Carcinogenesis 20:657-62. 1999..The major finding of K-ras A-->T transversions in lung and Harderian gland neoplasms suggests that this mutation may be important for tumor induction by this class of carcinogens... - Examination of low-incidence brain tumor responses in F344 rats following chemical exposures in National Toxicology Program carcinogenicity studiesR C Sills
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Toxicol Pathol 27:589-99. 1999.... - The privileged access model of 1,3-butadiene dispositionM C Kohn
Laboratory of Computational Biology and Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709 2233, USA
Environ Health Perspect 108:911-7. 2000.... - Toxicity of inhaled chloroprene (2-chloro-1,3-butadiene) in F344 rats and B6C3F(1) miceR L Melnick
National Institute of Environmental Health Services, Research Triangle Park, NC 27709, USA
Toxicology 108:79-91. 1996.... - Point mutations of K-ras and H-ras genes in forestomach neoplasms from control B6C3F1 mice and following exposure to 1,3-butadiene, isoprene or chloroprene for up to 2-yearsR C Sills
Laboratory of Experimental Pathology, Environmental Toxicology Program, National Institute of Environmental Health Sciences, PO Box 12233, Research Triangle Park, NC 27709, USA
Chem Biol Interact 135:373-86. 2001.... - Alleged misconceptions' distort perceptions of environmental cancer risksL Tomatis
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
FASEB J 15:195-203. 2001..Dismissing animal carcinogenicity findings would lead to human cancer cases as the only means of demonstrating carcinogenicity of environmental agents. This is unacceptable public health policy... - Induction of peroxisomal acyl CoA oxidase activity and lipid peroxidation in primary rat hepatocyte culturesK E Tomaszewski
National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709
Toxicology 65:49-60. 1990.... - A physiologically based pharmacokinetic model for inhalation and intravenous administration of naphthalene in rats and miceB A Willems
Laboratory of Computational Biology and Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Toxicol Appl Pharmacol 176:81-91. 2001..However, conclusions regarding which metabolite(s) may be responsible for the lung toxicity could not be reached... - Physiological modeling of butadiene disposition in mice and ratsM C Kohn
Laboratory of Computational Biology and Risk Analysis, National Institute of Environmental Health Sciences, National Institutes of Health, PO Box 12233, Mail Drop A3 06, Research Triangle Park, NC 27709, USA
Chem Biol Interact 135:285-301. 2001..The model also predicts considerable accumulation of epoxybutanediol, in agreement with the observation that most of the DNA adducts in animals exposed to butadiene arise from this metabolite... - A physiological model for ligand-induced accumulation of alpha 2u globulin in male rat kidney: roles of protein synthesis and lysosomal degradation in the renal dosimetry of 2,4,4-trimethyl-2-pentanolM C Kohn
Laboratory of Computational Biology and Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Toxicology 136:89-105. 1999..Induced lysosomal activity and increased production of toxic metabolites may both contribute to the nephrotoxicity observed in male rats exposed to an alpha2u ligand or its precursor... - Pharmacokinetics of sodium nitrite-induced methemoglobinemia in the ratMichael C Kohn
Laboratory of Computational Biology and Risk Analysis, National Institute of Environmental Sciences, Research Triangle Park, North Carolina 27709, USA
Drug Metab Dispos 30:676-83. 2002..Replacement of the V(max) of methemoglobin reductase with a value representative of humans predicted a 10% methemoglobinemia following an intravenous dose of 5.8 mg/kg, in close agreement with an observed value of 5.7 mg/kg for humans... - Evaluation of genetic alterations in cancer-related genes in lung and brain tumors from B6C3F1 mice exposed to 1,3-butadiene or chloropreneThai Vu Ton
Environmental Toxicology Program and Environmental Carcinogenesis Program, National Institute of Environmental Health Sciences, MD B3 08, 111 Alexander Drive, Research Triangle Park, NC 27709, USA
Chem Biol Interact 166:112-20. 2007.... - Hexavalent chromium is carcinogenic to F344/N rats and B6C3F1 mice after chronic oral exposureMatthew D Stout
National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709, USA
Environ Health Perspect 117:716-22. 2009..Hexavalent chromium [Cr(VI)] is a human carcinogen after inhalation exposure. Humans also ingest Cr(VI) from contaminated drinking water and soil; however, limited data exist on the oral toxicity and carcinogenicity of Cr(VI)... - Genetic alterations in brain tumors following 1,3-butadiene exposure in B6C3F1 miceYongbaek Kim
Laboratory of Experimental Pathology National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Toxicol Pathol 33:307-12. 2005..The observed findings are similar in part to the genetic alterations reported in human brain tumors... - Mutations of ras protooncogenes and p53 tumor suppressor gene in cardiac hemangiosarcomas from B6C3F1 mice exposed to 1,3-butadiene for 2 yearsH H Hong
Environmental Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA
Toxicol Pathol 28:529-34. 2000.... - Biochemical origins of the non-monotonic receptor-mediated dose-responseM C Kohn
Environmental Toxicology Program, National Institute of Environmental Health Sciences, PO Box 12233, MD A3 06, Research Triangle Park, North Carolina 27709, USA
J Mol Endocrinol 29:113-23. 2002..This model indicates that a non-monotonic dose-response is a plausible outcome for xenobiotic agents that activate nuclear receptors in the same manner as natural ligands... - In vitro evidence for involvement of CoA thioesters in peroxisome proliferation and hypolipidaemiaK E Tomaszewski
National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709
Biochim Biophys Acta 1220:118-24. 1994..Hypolipidaemia caused by treatment with peroxisome proliferators may, therefore, be related to inhibition of fatty-acid synthesis by the corresponding CoA thioester derivative... - The IARC evaluation of di(2-ethylhexyl)phthalate (DEHP): a flawed decision based on an untested hypothesisRonald L Melnick
National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Int J Occup Environ Health 8:284-6. 2002 - The IARC evaluation of DEHP excludes key papers demonstrating carcinogenic effectsRonald L Melnick
National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
Int J Occup Environ Health 9:400-2. 2003 - Declaring chemicals "not carcinogenic to humans" requires validation, not speculationRonald L Melnick
Environ Health Perspect 111:A203-4. 2003 - Testing toxic pesticides in humans: health risks with no health benefitsRonald L Melnick
Environ Health Perspect 112:A459-61. 2004