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Environmental Health Sciences

The Biswal Laboratory

vaping study
There has been rapid increase in use of electronic cigarettes (ECs) among young adults, in part due to targeted advertising and the perception that ECs are safe.
Environmental Lung Diseases
Environmental lung diseases, such as COPD, asthma, and pulmonary fibrosis, are triggered by chronic exposure to a variety of environmental toxicants, including cigarette smoke, air pollution, and bacterial/viral infections.
Ambient Air Pollution
Ambient Air Pollution
Ambient air pollution, which is responsible for 3.2 million deaths per year, is most commonly associated with urban environments and includes combustion products from many sources, including vehicle exhaust, factories, power plants, incinerators, and furnaces.
Stress Response Genes
Upon exposure to environmental stressors, the transcription factor Nrf2 activates hundreds of cytoprotective genes, including antioxidants, xenobiotic detoxification enzymes, and proteins in the proteasomal pathway.
Bacterial and Viral Exacerbation
Exacerbations of COPD, which are defined as acute worsening of symptoms that are not fully reversible, are most commonly associated with bacterial and/or viral infections.
Indoor Air Pollution
Indoor Air Pollution
40% of the world uses biomass fuels for cooking and heating their homes, which is responsible for 3.7 million deaths per year.
Cigarette smoke is a potent source of oxidative stress. 20.5% of men and 15.8% of women in the US are smokers, and each puff of smoke produces 1x10^15 free radicals.
Electronic cigarettes have been introduced as a safe alternative to smoking. Their use has been rapidly increasing among smokers and non-smokers. We have been studying the biological and physiological effects in cells, animal models as well as users for generating the knowledge base that could guide public health policies.

Research Focus

Our laboratory is focused on discovering novel mechanisms of host defense against environmental toxicants that determine immunobiological and pathobiological susceptibility to lung diseases, in order to develop experimental therapeutics for their prevention and intervention among susceptible populations.

Exposure to environmental toxicants and stressors, such as cigarette smoke, indoor/outdoor air pollutants, respiratory bacteria/viruses and allergens, causes oxidative/nitrosative stress, inflammation, and cell injury and is associated with diverse pulmonary disease states. In response to environmental stressors, cells activate the transcription factor Nrf2 in lungs, which activates the host defense response via upregulation of a multitude of cytoprotective genes. A suboptimal or inappropriate host defense predisposes to inflammation, oxidative/nitrosative stress and cell injury and thus plays a critical role in determining susceptibility to various diseases.

We are developing a molecular understanding of the host defense factor Nrf2, which upregulates the stress response transcriptional program and protects against a range of pathological processes (oxidative stress, inflammation, and apoptosis) in environmental diseases, such as COPD. We have discovered that there is gain of Nrf2 function, via Keap1 mutation and other mechanisms, in cancers of the lung and other organs. In collaboration with NCATS, the first in class Nrf2 inhibitors are being developed as anti-cancer agents to ameliorate therapeutic resistance of lung and other incurable cancers.