Lung injury from occupational and environmental sources contributes to pulmonary fibrosis. Fibrotic and interstitial lung diseases are a significant cause of morbidity and mortality in affected people. In these diseases, injury occurs as a result of damage to the respiratory region of the lung resulting in scarring and remodeling of the alveolar region.

One area of specific interest in lung injury involves altered immune responsiveness to inhaled irritants like diesel exhaust particles. Dr. Ma at West Virginia University is seeking to continue promising research funding suggesting that diesel exhaust exposure reduces defensive mechanisms in the alveolar region enhancing lung injury and fibrosis.

Investigators at NIOSH are internationally recognized in the field of free radical damage mechanisms of lung injury. The Section of Pulmonary Medicine treats patients and has strong potential for collaborative and transitional research opportunities. Funding opportunities in this area have also been projected by DLD/NHLBI for SCCOR funding in 2007.

Welding Particles: Deposition of inhaled welding particles (red) among lung structures of lung airspaces after exposure.	Silica Dust Exposure: Three-dimensional image of lung nodule in an airspace that has develped after overexposure to silica dust in a workplace.	Coal Workers Pneumoconiosis: Dust deposits in macrophages. Macrophages get trapped in connective tissues. Sometimes continues to “Progressive Massive Fibrosis”.