Division of Environmental Toxicology

Faculty and Research

Dr. Marshall Anderson, Professor
Director, Department of Environmental Health

Research in Progress:

Dr. Anderson’s research focus is on mechanisms of carcinogenesis, especially lung cancer and chemical carcinogenesis.

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Dr. Roy Albert, Professor

Research in Progress:

Contact sensitizing chemicals as environmental carcinogens. The current study is examining the structure – activity relationships for contact sensitization of several hundred chemicals that have had bioassays for carcinogenicity and genotoxicity by the national toxicology program at the national institute for environmental science. The object of the present study is to broaden and confirm the initial observation that contact sensitizers have a substantial likelihood of being carcinogenic in rodents.

Recent publications:

Albert, R. E., Miller, M., Cody, T., Talaska, G., Underwood, P., Andringa,A. (1996). Epidermal cytokinetics, DNA abducts and dermal inflammation in the mouse skin in response to repeated benzo(a)pyrene exposures, Toxicol Appl.Pharm. 136:67-74.

Albert, R. E., French, J. E., Maronpot, R., Spalding, J.,and Tennant, R. (1996). Mechanism of skin tumorigenesis by contact sensitizers: The effect of the corticosteroid Fluocinolone Acetonide on inflammation and tumor induction by 2,4 dinitro-1-fluorobenzene in the skin of the Tg.AC (v-Haras)mouse, Environmental Health Perspectives. 104:1062-1068.

Miller, M. L., Andringa, A., Albert R. E., and Cody, T. (1997). Colcemid alters S phase and other parameters in skin during chronic exposure to benzo(a)pyrene, Microscopy Research and Techniques. 135: 307-313.

Miller, M. L., Andringa, A. Cody, T., Dixon, K., and Albert, R. E. (1996). Cellproliferation and nuclear abnormalities are increased and apoptosis is decreased in the epidermis of the p53 null mouse after topical application of benzo(a)pyrene, Cell Proliferation. 29:561-576.

Albert, R. E. (1997). Allergic contact sensitizing chemicals as environmental carcinogens, Environmental Health Perspectives. 105:940-948.

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Dr. C. Stuart Baxter, Associate Professor
Ph.D., 1970, University of London, England

Research in Progress:

Development of new approaches and programs for gene and protein identification.

Creation of new databases for genes and pathways involved in cell response to environmental agents.

Creation of databases of knockout and transgenic animals with abnormal pulmonary and cardiac phenotypes.

Recent Publications:

Toxicology and Computational Biology Resource Site: http://www.med.uc.edu/baxtertox

Baxter, C. S., Doetschman, T., Boivin, G. P., and Leikauf, G. D. (1997). Adenoma and adenocarcinoma induction in mutant p53 transgenic mice treated with N,N-diethylnitrosamine, Proc. Amer.Assocn. Cancer Res. 38:486.

Baxter, C. S., Doetschman, T., Boivin, G. P., and Leikauf, G. D. (1996). Expression of a mutant p53 gene enhances N,N-diethylnitrosamine-induced lung adenocarcinoma incidence in transgenic mice, Proc. Amer.Assocn. Cancer Res. 37:573.

Other Areas of Interest:

Molecular and Genetic Mechanisms of Cancer, especially chemical carcinogenesis of the skin and lung.

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Dr. Eula Bingham, Professor

Research in Progress:

Dr. Bingham’s interests include the fields of risk assessment, regulatory toxicology, environmental carcinogenesis and occupational health surveillance.

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Dr. Michael Carvan, Assistant Professor

Research in Progress:

Dr. Carvan’s research interests are focused on the use and development of aquatic model systems to investigate the mechanisms by which environmental chemicals alter normal gene expression.

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Dr. Kathleen Dixon, Associate Professor
Deputy Director, Department of Environmental Health
Ph.D., 1970, University of Rochester, NY

Research Interests:

The Dixon Laboratory focuses on understanding the mechanisms by which environmental agents interact with cells leading to mutations.

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Dr. Ernest C. Foulkes, Professor
D.Phil., 1952, University of Oxford, England

Research Interests:

Dr. Foulkes' research has focused on the renal and intestinal toxicology of heavy metals,

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Dr. George D. Leikauf, Associate Professor
Director of Environmental Toxicology Division
Ph.D., 1981, NewYork University

Research Interests:

Dr. Leikauf's investigates the molecular and cellular mechanisms by which air pollutants exacerbate or cause airway diseases including asthma, bronchitis, and cystic fibrosis.

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Dr. John C. Loper, Adjunct Professor
Ph.D., 1960, Johns Hopkins University

Research Interests:

Dr. Loper’s research is in microbial pathogenesis and microbial eukaryotic genetics.

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Dr. Marian Miller, Associate Professor

Research in Progress:

The major focus of our research over the last five years has been to ascertain the fine structural expressions of molecular events. The primary paradigms for this endeavor have come from the transgenic mouse models for human diseases which are currently available. In collaboration with individuals from the Department of Molecular Genetics, and the Children’s Hospital Research Foundation, and our own Center for Environmental Genetics in the Department of Environmental Health, we have examined 8 different transgenic and knock-out mice. Using various experimental protocols and evaluating dozens of different tissues we have helped define these phenotypes. These embrace a wide range of changes, such as decreased apoptosis, increased cell mortality, failure to maintain cell organelles, production of irregular architecture, neurogenic deafness and inflammation.

Recent Publications:

Miller, M. L., Andringa, A., Elliott, J., Conwell, K. II, Dixon, K., Carty, M. P. (1998). The morphologic and spectral phenotype of apoptosis in HeLa cells varies following exposure to UV-C and the addition of inhibitors of ICE and CPP32, Cell Prolif. (In press).

Hastings, L., Miller, M. L. (1998). Developmental Neurotoxicity of Cadmium, in Handbook of Developmental Neurotoxicology, W. Slikker, and L. W. Chang, ed. Academic Press. (In press).

Schultheis, P. J., Clarke, L. L., Meneton, P., Harline, M., Boivin, G. P., Stemmermann, G., Duffy, J. J., Doetschman, T., Miller, M. L., Shull, G. E. (1998). Targeted disruption of the murine NHE2 Na⁺/H⁺ exchanger gene causes reduced viability of gastric parietal cells and loss of net acid secretion, J Biol Chem. (In press).

Liu, L. H., Paul, R. J., Sutliff, R. L., Miller, M. L., Lorenz, J. N., Pun, R. Y. K., Duffy, J. J., Doetschman T., Kimura, Y., MacLennan, D. H., Hoying, J. B., Shull, G. E. (1997). Defective endothelium-dependent relaxation of vascular smooth muscle and endothelial cell Ca²⁺ signaling in mice lacking Sacro(endo)plasmic reticulum Ca²⁺-ATPase isoform 3, J Biol Chem. 272:30538-30545.

Hastings, L., Miller, M. L. (1997). Olfactory loss secondary to toxic exposure, Taste and Smell Disorders , A. M. Seiden, ed. Thieme Publishers, 8:88-106.

Cheu, J., Talaska, G., Miller, M. L., Rice, C., Warshawsky, D. (1997). Benzo(a)pyrene coated ferric oxide and aluminum oxide particles: uptake, metabolism and DNA binding in hamster pulmonary alveolar macrophages and tracheal epithelial cells in vitro, Toxicol Appl Pharmacol, 136:67-74.

Miller, M. L., Andringa, A., Cody, T., Dixon, K., Albert, R. E. (1996). Cell proliferation and nuclear abnormalities are increased and apoptosis is decreased in the epidermis of the p53 null mouse after topical application of benzo(a)pyrene, Cell Prolif. 29:561-576.

Miller, M. L., Andringa, A., Albert, R. E., Cody, T. (1996). Colcemid alters S phase and other parameters in skin during chronic exposure to benzo(a)pyrene, Micros Res Tech. 35: 307-313.

Albert, R. E., Miller, M. L., Talaska, G., Underwood, P., Cody, T. E., Andringa, A. (1996). Epidermal cytokinetics, DNA adducts, and dermal inflammation in the mouse skin in response to repeated benzo(a)pyrene exposures, Toxicol Appl Pharm. 136:67-74.

Sun, T.-J., Miller, M. L., Hastings, L. (1996). Effects of inhalation of cadmium on the rat olfactory system: Behavior and morphology, Neurotox Teratol. 18:89-98.

Outreach Activities:

Marian Miller and Anastasia Andringa have been instrumental in the publication of two newsletters, Kettering News, edited by CS Baxter, and the CEG Interface, edited by DW Nebert, which provide highlights from environmental genetics research and relevant social issues, updates on distinguished lecturers and the activities of colleagues, as well as a little humor.

Other Areas of Interest:

Tennis, tennis, tennis, art, and music.

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Dr. Daniel W. Nebert, Professor
MD., 1964, Oregon Health Sciences University, Portland

Research in Progress:

This laboratory has collaborated in development of the Ahr(-/-) knockout mouse line and has also completed the development of the Cyp1a2(-/-) knockout mouse line. CYP1A2 has been shown to enhance acetaminophen toxicity of the liver (this is very time- and dose-specific) but not the olfactory mucosa. The Cyp1a2(-/-) line has also been pivotal in showing that CYP1A2-mediated uroporphyrinogen oxidation is both necessary and sufficient for iron-induced experimental porphyria to occur. New directions with this mouse line include studies with human bladder carcinogens (4-aminobiphenyl) and N-heterocyclics, as well as the development of a human CYP1A2 allele-containing ("knock-in") mouse line. Work on oxidative stress and resistance to ethanol toxicity continues in the Ahr(-/-) knockout mouse line. To decrease "experimental noise," both of these lines have been bred five times into the C57BL/6J background--thereby producing >98% homogeneity of this genetic background. This laboratory has also localized the human AHR gene to chromosome 7p15 and, in a 3-generation family, has shown the "high CYP1A1 inducibility phenotype" segregates with this 7p15 region. The laboratories of Puga and Nebert have developed a combined oligonucleotide-hybridization and yeast two-hybrid system assay for being able to correlate the human AHR genotype with phenotype (Ah receptor ligand affinity) in large populations. The conventional and inducible Fah(-/-), Gcls(-/-), Gclr(-/-), Cyp1a1(-/-) and Nmo1(-/-) knockout mouse lines are under development, in order to understand the role of these genes and their gene products in oxidative stress-induced toxicity caused by numerous environmental agents.

Recent Publications:

Nebert, D. W. (1997). Polymorphisms in drug-metabolizing enzymes: what is their clinical significance and why do they exist?, Am J Hum Genet. 60:265-271.

Nebert, D. W., Carvan, M. J. III. (1997). Ecogenetics: from ecology to health, Toxicol Industr Health. 13:163-192.

Nebert, D. W., McKinnon, R. A. (1998). Genetic determinants of toxic response, in ILO Encyclopaedia of Occupational Health and Safety, J. M. Stellman, ed. International Labour Office, Geneva, Switzerland, pp 33.19-33.26.

Sinclair, P. R., Gorman, N., Dalton, T., Walton, H. S., Bement, W. J., Sinclair, J. F., Smith, A. G., Nebert, D. W. (1998). Uroporphyria produced in mice by iron and 5-aminolevulinic acid does not occur in Cyp1a2(-/-) null mutant mice, Biochem J. (In press).

Scientific Service:

1972- Service on 17 scientific journal editorial boards between 1972 and the present; six currently active

1992-97 Director, Center for Environmental Genetics, funded and approved by the National Institute of Environmental Health Sciences, includes 42 senior scientists with their own independent research programs from eight departments in the University of Cincinnati College of Medicine, College of Arts and Sciences, and The Children's Hospital Medical Center

1994- Member of the External Advisory Board, Center for Ecogenetics and Environmental Health, University of Washington School of Medicine, Seattle

1998- Member of the External Advisory Board, Howard University Cancer Center, Howard University Medical Center, Washington D.C.

Awards:

1978--Recipient of the U.S. Public Health Service Meritorious Service Medal, Washington, D.C.

1981--Listed among "The 1,000 Contemporary Scientists Most-Cited 1965-1978," from a compilation of more than 1 million names in all scientific fields. By Eugene Garfield, Institute for Scientific Information. [Current Contents, No. 41, 12 October 1981]

1984--Winner of the Frank Ayrey Fellow Award, among the most prestigious prizes in clinical pharmacology in the United Kingdom

1993--Recognized for the second time by the Institute for Scientific Information (ISI) as first author of a Citation Classic^(R): Nebert et al., DNA Cell Biology 6: 1-11 (1987). Citation Classic published in the 31 May 1993 issue of Current Contents.

1994--Elected to the rank of American Association for the Advancement of Science (AAAS) Fellow, to be awarded at the AAAS Fellows Forum, Annual Meeting of the AAAS, February, 1995, in Atlanta, Georgia.

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Dr. Ellen J. O'Flaherty, Associate Professor Emeritus
Ph.D., 1964, Yale University

Research Interests:

Toxicokinetics: physiology-based modeling of time-dependent kinetics; particularly the kinetics of elements, such as lead, uranium, and chromium, that are associated with bone.

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Dr. Alvaro Puga, Professor
Ph.D., 1972, Purdue University, West Lafayette, Indiana

Research in progress:

My laboratory investigates the impact of genetic diversity on the response of individuals or populations to toxic or carcinogenic environmental agents. The long-term objective of this work is to elucidate the molecular mechanisms that underlie this response. Many chemical compounds interfere with the control mechanisms that regulate gene expression, and some compounds may induce overexpression of target genes, while others may repress their normal expression levels. The ultimate effect of this process is an alteration of the steady-state levels of the proteins encoded by the genes affected. In recent years, however, it has become increasingly clear that this effect varies drastically as a result of genetic polymorphisms in the individuals affected. My interests are centered, on the one hand, on the molecular mechanisms of action of these toxic environmental agents, and on the other, on the analysis of genetic diversity in the response to these agents. The genes of interest are those that code for transcription factors with a regulatory role in the expression of detoxification enzymes. The experimental work in my laboratory is focused on three areas of gene regulation:

(1) Analyses of structure/function relationships of polymorphic forms of the gene coding for the aromatic hydrocarbon (Ah) receptor protein.

(2) Studies on molecular mechanisms of dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin; TCDD) action. TCDD, a ligand for the Ah receptor, causes a diversity of effects in many different tissues. We are analyzing the signal transduction pathways that affect the activation by TCDD of genes responsible for cell cycle regulation.

(3) A strong dose dependent relationship has recently been found between dioxin exposure and mortality from ischemic heart disease, suggesting that dioxin exposure is an important risk factor in the development of heart disease. We are currently developing suitable animal models to test the hypothesis that Ah receptor activation by dioxin exacerbates the development of atherosclerosis by disrupting the expression of genes critical to vascular function.

Recent publications:

Liang, H.-C. L., Li, H., McKinnon, R. A., Duffy, J. J., Potter, S. S., Puga, A., and Nebert, D. W. (1996). Cypla2(-/-) null mutant mice develop normally, but show deficient drug metabolism, Proc. Nat. Acad. Sci. USA. 93:1671-1676.

Nebert, D. W., McKinnon, R., and Puga, A. (1996). Human drug-metabolizing enzyme polymorphisms: effects on risk of toxicity and cancer, DNA and Cell Biol. 15:273-280.

Puga, A., Micka, J., Chang, C.-Y., Liang, H.-C., and Nebert, D. W. (1996). Role of molecular biology in toxicology, Adv. Exp. Med. Biol. 387:395-404.

FitzGerald, C. T., Fernandez-Salguero, P., Gonzalez, F. J., Nebert, D. W., and Puga, A. (1996). Differential regulation of mouse Ah receptor gene expression in cell lines of different tissue origins, Arch. Biochem. Biophys. 333:170-178.

Hoffer, A., Chang, C.-Y. and Puga, A. (1996). Dioxin induces fos and jun gene expression by Ah receptor-dependent and -independent pathways, Toxicol. Appl. Pharmacol. 141:238-247.

Puga, A., Nebert, D. W., McKinnon, R. A., and Menon, A. G. (1997). Genetic polymorphisms in human drug-metabolizing enzymes: potential uses of reverse genetics to identify genes of toxicological relevance, Crit. Rev. Toxicol. 27:199-222.

Vasiliou, V., Reuter, S., Shia, T.-Y., Puga, A., and Nebert, D. W. (1997). Mouse dioxin-inducible Ahd4 gene: structure of the 5' flanking region and transcriptional regulation, Adv. Exp Med. Biol. 414:37-46.

Micka, J., Milatovich, A., Menon, A., Grabowski, G., Puga, A., and Nebert, D. W. (1997). Human Ah receptor (AHR) gene: localization to 7p15 and suggestive correlation of polymorphism with CYP1A1 inducibility, Pharmacogenetics. 7:95-105.

Puga, A., Hoffer, A., Zhou, S., Bohm, J. M., Leikauf, G. D., and Shertzer, H. G. (1997). Sustained increase in intracellular free calcium and activation of cyclooxygenase-2 expression in mouse hepatoma cells treated with dioxin, Biochem. Pharmacol. 54:1287-1296.

Chang, C.-Y., and Puga, A. (1998). Constitutive activation of the aromatic hydrocarbon receptor, Mol. Cell. Biol. 18:525-535.

FitzGerald, C. T., Nebert, D. W., and Puga, A. Regulation of mouse Ah receptor gene expression by members of the Sp family of transcription factors, Nucleic. Acids Res. (Submitted).

Maier, A., Micka, J., Miller, K., Denko, T., Chang, C.-Y., Nebert, D. W., and Puga, A. Aromatic hydrocarbon receptor (AHR) polymorphism: development of new methods to correlate genotype with phenotype, Environmental Health Persp. (Submitted).

Scientific service:

Associate Editor, Toxicology Methods
Editorial Board, Biochemical Pharmacology
Editorial Board, Chemico-Biological Interactions

Other areas of interest:

Science Fiction
SCUBA Diving
Cooking

More about Dr. A. Puga in his homepage

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Dr. Jon Reid, Research Assistant Professor

Research in Progress:

Dr. Reid’s research interests are risk assessment and analysis of sites contaminated with metals, especially lead and mercury.

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Dr. Howard G. Shertzer, Associate Professor
Assistant Director - Toxicology Training Program
Ph.D., 1973, University of California at Los Angeles

Research in Progress:

This underlying theme of my laboratory involves the regulation of redox homeostasis in cells and tissues. The focus of my current work regards the role of oxidative stress in mediating human disease conditions, and on developing strategies for reducing oxidative stress and resulting dysfunction. A part of this strategy is to understand the regulation of the expression of genes that are involved in oxidative stress signaling pathways. Several of these genes are members of the aromatic hydrocarbon and electrophile gene batteries. These genes affect the cellular redox balance, as well as the pathways for activation and detoxification of carcinogens and toxicants, especially electrophiles and free radicals including reactive oxygen. I am especially concerned with mitochondrial pathways for the production of reactive oxygen, and subsequent impact on cell cycle regulation, apoptosis and cell proliferation. The oxidative stress signaling pathways are involved in human disease conditions such as proliferative diseases (cancer and precancerous conditions), alcohol toxicity and alcoholism, and pulmonary inflammatory diseases. Besides studying the oxidative stress-related etiologies of human disease states, I am involved in the design and synthesis of novel compounds, or identification of natural dietary compounds, for the purpose of intervention in human diseases, especially involving free radicals or oxidative stress. Extensive use is made of inbred and derived mutant and transgenic mouse strains, and of cultured and engineered cells. Techniques in molecular genetics and enzymology, and cellular fluorescence imaging and computational chemistry are in regular use.

Recent Publications:

Westerlund, C., Ostlund-Lindqvist, A.-M., Sainsbury, M., Shertzer, H. G., Sjoquist, P.-O. (1996). Characterization of novel indenoindoles. Part I. Structure-activity relationships in different model systems of lipid peroxidation, Biochem. Pharmacol. 51:1397-1402.

Zhu, H., He, M., Bannenberg, G. L., Moldeus, P., Shertzer, H. G. (1996). Effects of glutathione and pH on the oxidation of biomarkers of cellular oxidative stress, Archives of Toxicology. 70:628-634.

Shertzer, H. G., Tabor, M. W., Hogan, I. T. D., Brown, S. J., Sainsbury, M. (1996). Molecular modeling parameters predict antioxidant efficacy of 3-indolyl compounds, Archives of Toxicology. 70:830-834.

Shertzer, H. G., Dietrich, K. N. (1996). Environmental Neurobehavioral Toxicology, in: Disability Analysis Handbook: Tools for Independent Practice, K. N. Anchor, ed. Kendall Hunt Publishers, pp. 205-220.

Puga, A., Hoffer, A., Zhou, S., Bohm, J. M., Leikauf, G. D., Shertzer, H. G. (1997). Sustained increase in intracellular free calcium and activation of cyclooxygenase-2 expression in mouse hepatoma cells treated with dioxin, Biochem. Pharmacol. 54:1287-1296.

He, X.-X., Nebert, D. W., Vasiliou, V., Zhu, H., Shertzer, H. G. (1997). Genetic Differences in alcohol drinking preference between inbred strains of mice, Pharmacogenetics. 7:223-233.

Leikauf, G. D., Prows, D. R., Shertzer, H. G., Carrigan, P. E., Zhao, Q., Borchers, M. T., Ormerod, E., Simpson, L. G., Weaver, T. E., Clark, J. C., Lee, N. A., Whitsett, J. A., Lee, J. J., Driscoll, K. F. Asthma and acute lung injury: Transgenic models and genetic determinants, Exp. Toxicol. Path. (In Press).

Prows, D. R., Shertzer, H. G., Daly, M. J., Sidman, C. L., Leikauf, G. D. Genetic analysis of ozone-induced acute lung injury, Nature Genetics.(In Press).

Outreach Activities:

Teaching and Development of Programs in Environmental Genetics and Toxicology in Public Schools.

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Dr. Raymond Suskind, Professor

Research in Progress:

Dr. Suskind’s research interests have addressed problems concerning the adverse effects of toxic agents on the skin and accompanying systemic effects.

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Dr. David Warshawsky, Professor
Ph.D., 1972, University of Cincinnati

Research in Progress:

Dr. Warshawsky's research is focused on the mechanisms of chemical carcinogenesis in liver, skin and lung. He is examining the early events in the carcinogenic process for polycyclic and N-heterocyclic aromatic hyrocarbons, to ascertain the metabolic differences and to develop biomarkers of exposure and effect and methods for the microbial biodegradation of these recalcitrant compounds. This research involves the investigation of the metabolism, binding of reactive metabolites to DNA and protein, mutagenicity, gene expression and growth factor regulation. Research is underway to assess the relationship of DNA adducts with specific mutations in the activated ras oncogene and p53 tumor suppressor gene in target tissues. Biomarkers of exposure related to biological eventsin the carcinogenic process are being developed to assess the risk of exposure to carcinogens. Selection of biomarkers will be based on optimal sensitivity and specificity. Microbial degradation of recalcitrant polycyclic aromatics found at coal gasification sites is also being investigated. Microorganisms have been isolated and characterized that enhance degradation of 3-to 5- ring polycyclic aromatics. Research is also underway on determining whether inhibitors of angiogenesis can serve as chemoprophylactics for breast cancer in high risk women.

Recent Publications:

Warshawsky, D., Mitchell, K., Xue, W., Jager, M., Schneider, J., and Talaska, G. (1998). Comparative oncogenic activation of 7H-dibenzo[c,g]carbazole and dibenz[a,j]acridine, Polycyclic Aromatic Compounds. (Submitted).

Schneider, J., Grosser, R. J., Jayasimhulu, K., Xue, W., and Warshawsky, D. (1997). Biodegradation products of carbazole formed by a microorganism isolated from hydrocarbon contaminated soil. (Submitted).

Underwood, P. M., Zhou, Q., Jaeger, M., Reilman, R., Warshawsky, D., and Talaska, G. (1997). Chronic, topical administration of 4-aminobiphenyl induces tissue specific DNA adducts in mice, Toxicol. Appl. Pharmacol. 144:325-31.

O'Connor, P., Fremont, S., Schneider, J., Dowty, H., Jaeger, M., Talaska, G., and Warshawsky, D. (1997). Combination of high performance liquid chromatography anti thin layer chromatography separation of five adducted nucleotides isolated from liver resulting from I.P. administration with 7H-dibenzo(c, g)carbazole to mice, J. Chromatogr., J. of Chromatog. B. 700:49-57.

Xue, K., LaDow, K., and Warshawsky, D. (1997). Synthesis, characterization and mutagenicity of nitrated 7Hdibenzo(c, g)carbazole and its phenolic derivatives, Chem. Res. Toxicol. 10:432-38.

Cheu, J., Talaska, G., Miller, M., Rice, C., and Warshawsky, D. (1997). Benzo(a)pyrene coated ferric oxide and aluminum oxide particles: uptake, metabolism and DNA binding in hamster pulmonary alveolar macrophages and tracheal epithelial cells in vitro, Carcinogenesis. 13:167-75.

Sutton, S., Shann, J., Warshawsky, D., and Vestal, R. (1996). Aerobic degradation of 4-methylquinoline by a soil bacterium, Appl. Environ. Microbiol. 62:2910-14.

Talaska, G., Jaeger, M., Reilman, R., Collins, T., and Warshawsky, D. (1996). Chronic, topical exposure to benzo(a)pyrene induces relatively high steady-state levels of DNA adducts in target tissues and alters kinetics of adduct loss, Proc. Natl. Acad. Sci. 93:7789-93.

Warshawsky, D., Talaska, G., Xue, W., and Schneider, J. (1996). Comparative carcinogenicity, metabolism, mutagenicity and DNA binding of 7H-dibenzo(c, g)carbazole and dibenz(a, j)acridine, CRC Crit. Rev. Toxicol. 26:21349.

Warshawsky, D., Talaska, G., Schamer, M., Collins, T., Galati, A., You, L., and Stoner, G. (1996). Carcinogenicity, DNA adduct formation and K-ras activation by 7H-dibenzo(c, g)carbazole in strain A/J mouse lung, Carcinogenesis. 17:865-71.

Schneider, A, Grosser, R., Jayasimhu, K., Xue, W., and Warshawsy, D. (1996). Biodegradation of pyrene, benz(a)anthracene and benzo(a)pyrene by Mycobacterium sp. strain RJGII. 135, isolated from a former coal gasification site, Appl. Environ. Microbiol. 62:13-19.

Other Areas of Interest:

Board member of International Society of Polycyclic Aromatic Compounds.

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Dr. Jonathan Wiest, Assistant Professor

Research in Progress:

Dr. Wiest's research focuses on genetic alterations that occur in lung cancer. His major goal is to identify novel tumor oppressor genes that may be inactivated on chromosome 9p in lung tumorigenesis.

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