Session date: May 21, 2023
This is part 2 of a 2-part symposium.
Part 1 is on Sunday, May 21, 9:00 a.m. -10:30 a.m. focuses on quantification of environmental exposures using state-of-the-art methods.
Part 2 focuses on the physiological and cellular impact of environmental exposures.
Occupational and environmental lung diseases are caused by the inhalation of chemical irritants, allergens or toxins in work or home environments. Most diseases are caused by repeated, long-term exposure, but even a one-time or indirect contact with a hazardous agent can result in lung diseases with lasting effects.
Environmental exposures related to fossil fuel and heavy metals and occupational exposures related to silica and coal mining generate oxidative stress and inflammation in the lungs. Sustained oxidative stress causes DNA damage, epigenetic instability, mitochondrial dysfunction, and cell cycle arrest in key progenitor cells in the lung.
Inhaled environmental exposures accelerate lung aging by injuring the lungs and damaging the cells responsible for wound healing. Novel exposure assessment methods, including functional imaging and –omics studies, together with mathematical models are needed to quantify environmental exposures. Interventions that minimize exposure to noxious antigens are critical to improve lung health, and novel research is required to expand our knowledge of therapies that may slow or prevent premature lung aging.
Each presentation will leave 5 minutes for questions and answers.
• understand the selection process for NEJM and JAMA articles
George Thurston, DSc
Jennifer Larson-Casey, PhD
Robert Tighe, MD, ATSF
Kymberly Gowdy, BS, MS, PhD
Air Pollution, Oxidative Stress, and Cardiopulmonary Diseases: A Life Course Epidemiologic Perspective
Environmental Toxins and Macrophages in Progression of Chronic Lung Disease
Role of Innate Immune System in Environmental Lung Diseases
Understanding the Molecular Mechanisms of How Air Pollution Increases Susceptibility to Pulmonary Infections