The Budinger laboratory is interested in determining the mechanisms by which environmental stress contributes to the development of acute lung injury and fibrosis. His group has focused on the mechanisms by which resident lung cells, particularly alveolar macrophages and alveolar epithelial cells, “sense” environmental triggers of injury. His laboratory is particularly interested in the observation that many different environmental factors associated with the development of acute lung injury and fibrosis, including particulate matter air pollution, bleomycin, and a number of infectious pathogens, activate signaling pathways that converge on the generation of reactive oxygen species in the mitochondria. His laboratory has explored the upstream signaling pathways that trigger mitochondrial ROS generation in response to environmental stress and the mechanisms by which these ROS function as signaling molecules to orchestrate the inflammatory response in the lung and other organs. Dr. Budinger’s work is important for our understanding of many diseases important in pulmonary and critical care medicine, including pneumonia, pulmonary fibrosis, and the increased risk of ischemic cardiovascular events in patients with inflammatory lung disorders.