Abstract
A 26-year-old white male, lifelong non-smoker presented with a history of increased shortness of breath, for approximately 1 year. He had a history of welding aluminum parts. He had evidence of partially reversible reactive airways disease with a non obstructive component as well. VATS biopsy revealed evidence of airway and parenchymal inflammation consistent with aluminum pneumoconiosis. Approximately 5–10% of COPD is attributable to non-smoking causes including occupational exposures. There are studies to suggest that the persistence of aluminum particulate may cause ongoing inflammation despite removal from exposure. It is possible that the persistence of particulate matter from tobacco smoke remaining in the lung may contribute to the persistent inflammatory response found in former smokers. Further study is required to examine the importance of this potential inflammatory mechanism both in occupationally exposed and in cigarette smokers. Reduction of certain particulate components of cigarette smoke may have implications for prevention of disease or at least disease progression in some COPD patients.