Occupational and Environmental Lung Disease: Exposure, Latency, and Pattern
Take an exposure history
The occupational history must include specific job tasks, duration, protective equipment, symptom timing (better on weekends and holidays suggests work-related asthma), and coexposures such as smoking. Latency matters: pneumoconioses typically require 15–20 years or more, and hypersensitivity pneumonitis can present acutely, subacutely, or chronically.
Pattern recognition
Silicosis causes upper-lobe nodules, eggshell hilar calcification, and an increased risk of tuberculosis and autoimmune disease; it appears in sandblasters, miners, and countertop fabricators. Asbestosis is lower-lobe, peripheral-predominant fibrosis with reduced DLCO, usually accompanied by pleural plaques; plaques themselves are asymptomatic and do not impair lung function but mark exposure and latent cancer risk. Coal worker's pneumoconiosis produces small opacities that may progress to massive fibrosis, sometimes with rheumatoid arthritis (Caplan syndrome). Chronic beryllium disease mimics sarcoidosis with granulomas and is diagnosed by the beryllium lymphocyte proliferation test. Byssinosis causes Monday-morning chest tightness in textile workers.
Work-related asthma
Sensitizer-induced asthma has a latency period after exposure (isocyanates, flour, latex) and persists after removal; irritant-induced asthma follows a high-level exposure without latency. Serial peak expiratory flow at and away from work supports the diagnosis, and removal from exposure is the key intervention.
Worked rule
Upper lobes with eggshell calcification = silica; lower lobes with pleural plaques = asbestos. In either case, counsel about smoking synergy for lung cancer.