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Editor - Urmila P Kodavanti | United States Environmental Protec | 5271
ISSN: 2161-0525

Journal of Environmental & Analytical Toxicology
Open Access

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Urmila P Kodavanti

Urmila P Kodavanti
Urmila P. Kodavanti
National Health and Environmental Effects Research Laboratory
United States Environmental Protection Agency
Research Triangle Park
United States Environmental Protection Agency


Dr. Kodavanti is a Senior Research Biologist at the US EPA and a diplomat of the American Board of Toxicology. She is also an adjunct Associate Professor at the University of North Carolina, Curriculum in Toxicology Program, Chapel Hill, North Carolina, USA. Her research focus is environmental pollutants, cardiopulmonary interactions and host susceptibility variations. Her research includes the use of healthy and cardiopulmonary compromised animal models. OMICS is an integral part of her research approach. Her expertise is in the inhalational hazards associated with air pollutants, including metals, ozone, asbestos, and nano materials. She is an Associate Editor of two toxicology journals, and is on the editorial board of several other major environmental and toxicology journals. She has won numerous awards for her research publications including the Best paper Award from the SOT in 2004 and Level 1 Scientific and Technological Achievement award from the EPA in 2006.

Research Interest

Cell and molecular mechanisms of acute and chronic cardiopulmonary pathobiology with special emphasis on the role of host susceptibility factors. The research approach involves the use of susceptible animal models of human cardiovascular and pulmonary diseases. The role of genetic and environmental factors is considered in identification of mechanisms of variations in susceptibility. A variety of high throughput and molecular technologies are used with special emphasis on underlying oxidative stress and the role of host pathologies and genetic differences associated with disease susceptibility. The research also focuses on identifying source/components of air pollution, asbestos and nano particles that are associated with enhanced susceptibility and cardiopulmonary disease progression. Molecular mechanisms of cardiopulmonary interactions.



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