Pathophysiology
Long amphibole (crocidolite) fibres reach terminal bronchioles/alveoli, trigger macrophage recruitment, chronic inflammation and progressive fibrosis with 'ferruginous bodies' (asbestos fibres coated with haemosiderin). Latency 20-40 y from first exposure.
Sources: ATS Diagnosis of Asbestos-Related Disease (Am J Respir Crit Care Med 2004;170:691); ERS/ATS IPF & Progressive Pulmonary Fibrosis (2022;205:e18); IARC Monograph Asbestos (Vol 100C)
Clinical presentation
Insidious exertional dyspnoea, dry cough, digital clubbing, bibasilar fine end-inspiratory 'velcro' crackles, and eventually cor pulmonale. Occupational history: shipbuilding, insulation, brake linings, plumbers, demolition.
Diagnosis
Chest HRCT: bilateral basilar reticular changes, honeycombing, and pleural plaques (pathognomonic marker of exposure). PFTs: restrictive pattern with reduced DLCO. Lung biopsy rarely needed.
Management
No disease-modifying therapy. Smoking cessation (synergistic lung-cancer risk), pulmonary rehabilitation, supplemental O2, pneumococcal/influenza vaccination, and surveillance for mesothelioma and lung cancer. Consider antifibrotics (nintedanib) if progressive fibrotic phenotype (INBUILD).
Prognosis & compensation
Progression variable; mesothelioma latency 30-40 y, driven even by low-level exposure. Legal notification and occupational compensation are essential.
