AKT · Respiratory/ILD, sarcoid & occupationallow yield

Occupational & environmental lung disease

Lung disease from inhaled occupational dusts/antigens — asbestos, silica, coal, organic antigens

Overview

Lung diseases caused by inhaled occupational or environmental agents, where the EXPOSURE HISTORY is the diagnostic key. Asbestos causes pleural plaques, asbestosis (fibrosis) and mesothelioma (+ raises lung-cancer risk, multiplied by smoking). Silicosis and coal-worker's pneumoconiosis are nodular fibroses; hypersensitivity pneumonitis (extrinsic allergic alveolitis) is an immune reaction to organic antigens (e.g. farmer's/bird-fancier's lung). Many are compensable industrial diseases.

Recognise

Progressive breathlessness/cough with a relevant OCCUPATIONAL exposure (construction/shipyard — asbestos; mining/quarrying — silica/coal; farming/birds — organic antigens)
Asbestos: pleural plaques (benign marker of exposure), asbestosis (lower-zone fibrosis), MESOTHELIOMA (pleural malignancy — chest pain, effusion); asbestos + smoking multiplies lung-cancer risk
Hypersensitivity pneumonitis: acute (flu-like hours after exposure) or chronic (fibrosis); improves away from the antigen

Red flags

Mesothelioma (asbestos exposure + pleural effusion/chest pain/pleural thickening) → urgent investigation; it is compensable
Progressive fibrosis or massive silicosis → specialist management; report notifiable industrial diseases

Differentials & how to tell them apart

Idiopathic pulmonary fibrosisno exposure; UIP pattern — occupational fibrosis has the exposure history

Lung cancer / other ILDasbestos raises lung-cancer risk; distinguish mesothelioma from metastatic pleural disease

Sarcoidosisbilateral hilar lymphadenopathy, non-caseating granulomas

Investigations

Detailed occupational/exposure history; CXR/HRCT (pleural plaques, fibrosis pattern, nodules, pleural thickening/effusion); spirometry/DLCO (restrictive); pleural fluid/biopsy for suspected mesothelioma; serology/antigen avoidance response for hypersensitivity pneumonitis; report/compensation pathways.

Management

Remove the exposure; antigen avoidance ± steroids (HP); supportive care; mesothelioma → oncology + compensation

1Take the OCCUPATIONAL/exposure history — it is the diagnostic key. Image (CXR/HRCT) for plaques/fibrosis/nodules/pleural disease and assess lung function; remove the patient from the exposure.Gate: Asbestos exposure + pleural effusion/thickening/chest pain → suspect MESOTHELIOMA (investigate + compensation); asbestos + smoking multiplies lung-cancer risk — stop smoking.
2Hypersensitivity pneumonitis → antigen avoidance ± corticosteroids; supportive care for fibrosis; mesothelioma → oncology and compensation; report notifiable industrial diseases.

Remove from / avoid the exposure — the key intervention — especially in hypersensitivity pneumonitis (antigen avoidance) and ongoing dust exposure

Hypersensitivity pneumonitis: antigen avoidance ± corticosteroids — steroids for significant/acute disease; chronic fibrotic disease may persist

Supportive care for fibrosis (oxygen, rehab, vaccines) — as for ILD; smoking cessation (critical with asbestos)

Mesothelioma: specialist oncology + compensation; report industrial diseases — chemotherapy/palliative care; medicolegal/compensation referral

Key points

The EXPOSURE HISTORY makes the diagnosis. Asbestos → pleural plaques (benign), asbestosis (lower-zone fibrosis), MESOTHELIOMA, and (× smoking) lung cancer. Silica/coal → nodular fibrosis. Organic antigens (farmer's/bird-fancier's) → hypersensitivity pneumonitis (improves away from antigen). Mesothelioma is compensable — refer.

Monitor & prognosis

Lung function, disease progression, exposure cessation; compensation/reporting.

Variable; mesothelioma poor; hypersensitivity pneumonitis improves with antigen avoidance if caught early.

Source: BTS; industrial-disease reporting