Occupational lung diseases result from inhalation of workplace dusts, fumes, gases, and biologic agents. Advanced forms include: silicosis (silica dust — mining, sandblasting, stone work) progressing from simple to progressive massive fibrosis (PMF), with increased TB and lung cancer risk; coal worker's pneumoconiosis (CWP) similarly progressing to PMF and rheumatoid Caplan syndrome; asbestosis (asbestos exposure — shipbuilding, insulation, construction) causing pleural plaques, diffuse pleural thickening, asbestosis (interstitial fibrosis), benign asbestos pleural effusion, mesothelioma, and lung cancer.
Hypersensitivity pneumonitis (HP) results from immune-mediated inflammation to inhaled antigens (farmer's lung from thermophilic actinomycetes, bird fancier's lung from avian proteins, hot tub lung from M. avium complex, isocyanate exposure, machine operator's lung). Acute, subacute, and chronic forms exist; chronic HP can progress to fibrotic disease resembling IPF with poor prognosis. Berylliosis from beryllium exposure (electronics, aerospace) causes granulomatous disease similar to sarcoidosis.
Diagnosis requires detailed occupational history, chest imaging (HRCT essential for staging), pulmonary function tests, bronchoalveolar lavage, and sometimes lung biopsy. Specific antibodies (precipitins for HP), beryllium lymphocyte proliferation test (BeLPT), and asbestos body counts aid in identification. Management focuses on exposure cessation, surveillance for complications (TB in silicosis, malignancy in asbestos exposure), corticosteroids for HP and acute silicosis, and antifibrotics (pirfenidone, nintedanib) for fibrotic HP. Lung transplantation may be considered for advanced disease.