Our lab is currently exploring the role of oxidative stress in the pathophysiology and development of cardiopulmonary diseases (CPDs) induced by environmental toxicants. Exposure to environmental pollution increases the risk for many CPDs, including hypertension, diabetes, atherosclerosis, and chronic obstructive pulmonary disease. Together, these CPDs account for more than 4.2 million premature deaths per year globally. Increasing oxidative stress, caused by pollutant exposure, is primarily responsible for the pathogenesis of the CPDs. Our goal is to discover molecular mechanisms that explain how exposure to smoke/e-cig aerosols, heavy metals, organic compounds, and ultrafine particulate matter induces the oxidative stress that leads to CPD. A better understanding of the dynamic roles of pollutants and oxidative stress in the occurrence and exacerbation of CPD combined with a knowledge of the mechanisms that underlie this disease process will ultimately lead to improved prevention and treatment.

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Keywords: environmental toxicants, oxidative stress, cardiopulmonary diseases, molecular mechanisms