Asbestosis

Chronic fibrosing pneumoconiosis of the lungs caused by prolonged inhalation of asbestos fibers.

• Often manifests decades after exposure, so occupational history is critical. It carries a high risk of malignancy – asbestos workers have greatly increased incidence of lung cancer (especially with smoking) and mesothelioma. No cure exists once fibrosis develops, making prevention and early recognition vital.

• Typically an older adult (50s–70s) with a history of heavy asbestos exposure (e.g., construction, shipyard, insulation) 20–30 years prior. Presents with gradually progressive dyspnea on exertion and a dry cough.
• Physical exam often reveals fine "Velcro" crackles at the lung bases, reduced chest expansion (restrictive pattern), and clubbing of the fingers in ~1/3 of cases.
• Chest imaging shows diffuse reticular interstitial fibrosis most prominent in the bilateral lower lobes, along with pleural plaques (calcified thickened pleura, especially over the diaphragms) which are a hallmark of asbestos exposure.

1. Always take a detailed occupational history for patients with ILD. Ask about past asbestos exposure in high-risk jobs (shipyard, construction, pipefitting, brake repair).
2. Chest X-ray is the first step: look for basilar reticulonodular infiltrates and pleural plaques. If findings are equivocal or more detail is needed, get a high-resolution CT scan to confirm extent of fibrosis and plaques.
3. Pulmonary function tests (PFTs) will show a restrictive pattern (↓TLC, ↓FVC) with reduced diffusion capacity (↓DLCO) consistent with interstitial fibrosis.
4. Exclude other causes of pulmonary fibrosis: Asbestosis typically lacks hilar adenopathy or upper lobe nodules (those suggest silicosis, sarcoidosis, etc.). If diagnosis remains uncertain, consider lung biopsy or bronchoalveolar lavage to identify asbestos bodies (ferruginous bodies) and definitively attribute fibrosis to asbestos.
5. Monitor for complications: Patients with asbestos exposure require vigilance for lung cancer (new cough, hemoptysis, weight loss) and mesothelioma (chest pain, pleural effusion) as potential late sequelae.

1. No specific cure for asbestosis exists – supportive care and risk reduction are key. Eliminate further asbestos exposure and enforce smoking cessation to reduce synergistic lung cancer risk; provide influenza & pneumococcal vaccinations.
2. For symptomatic patients: provide supplemental oxygen for significant resting or exertional hypoxemia, and bronchodilators if there is concurrent obstructive lung disease (many asbestos patients have a smoking history). Pulmonary rehabilitation can improve exercise capacity.
3. No proven medications halt the fibrotic process – corticosteroids and immunosuppressants have shown little benefit. Advanced cases (progressive respiratory failure) may warrant evaluation for lung transplantation if the patient is a candidate.

• Asbestos in the ceiling (insulation) leads to fibrosis at the lung bases, whereas silica in the soil causes disease in the lung apices. (Remember: asbestos → base, silica → summit.)
• Among pneumoconioses, only asbestos exposure predisposes to mesothelioma (pleural cancer). In fact, asbestos exposure more often leads to bronchogenic carcinoma (especially with smoking) than mesothelioma.
• Ferruginous bodies (asbestos fibers coated with iron-protein) may be seen on biopsy or sputum; they appear as beaded, Prussian blue–positive rods and are pathognomonic of asbestos exposure.

• New hemoptysis, unintentional weight loss, or a change in cough in an asbestosis patient → evaluate for lung cancer (e.g., obtain imaging).
• Development of a unilateral pleural effusion or chest wall pain → suspect mesothelioma (often presents with exudative, hemorrhagic effusions); prompt imaging and referral for biopsy is indicated.

1. History of significant asbestos exposure (e.g., ≥10 years in insulation/construction) ≥15–20 years ago + insidious respiratory symptoms → suspect asbestosis.
2. Chest X-ray: look for lower lobe reticular markings and pleural plaques. If CXR is abnormal or unclear, get HRCT to better characterize interstitial changes and plaques.
3. PFTs: confirm a restrictive pattern (↓FVC, ↓TLC) with reduced DLCO correlating with fibrosis severity.
4. If atypical features (e.g., hilar adenopathy or nodules) are present, reconsider other diagnoses – asbestosis rarely causes those. In uncertain cases, perform lung biopsy or BAL to detect asbestos fibers and exclude alternate etiologies.
5. Management: remove patient from asbestos exposure, treat symptomatically (O₂, rehab, etc.), and schedule regular follow-ups. Educate about smoking cessation and be vigilant for any signs of malignancy (early cancer detection).

• Retired construction worker with a 20-year asbestos exposure (lagged by 20+ years) now has progressive SOB, dry cough, bibasilar inspiratory crackles, clubbing, and calcified pleural plaques on CXR → asbestosis.
• Older shipyard veteran with weight loss, unilateral pleural effusion, and chest pain decades after asbestos exposure → mesothelioma (malignant pleural tumor due to asbestos).