RespiratoryTier 2Topic

Effects of environmental toxins, such as cigarettes and asbestos on the respiratory system

Overview

Inhaled occupational/environmental agents cause a spectrum of lung disease depending on particle size, composition, and exposure duration/intensity
Latency is often decades for fibrotic pneumoconioses (asbestos, silica) - a detailed occupational history, including remote/past jobs, is essential and easily missed

Agents and diseases

Agent	Disease	Key feature
Asbestos	Asbestosis (fibrosis), pleural plaques, mesothelioma, lung cancer	Latency often >20-30 years; mesothelioma risk not clearly dose-dependent
Silica	Silicosis	Upper zone nodular fibrosis; increased TB risk
Coal dust	Coal workers' pneumoconiosis	Progressive massive fibrosis in advanced disease
Organic dusts (mouldy hay, bird droppings)	Hypersensitivity pneumonitis	Immune-mediated, not dose-toxic; improves with antigen avoidance
Beryllium	Chronic beryllium disease	Granulomatous, mimics sarcoidosis

Occupational history

Occupational history is central (job, duration, protective equipment used); imaging pattern (upper vs lower zone, pleural plaques) narrows the differential
Some exposures (asbestos, silica) have specific compensation/notification pathways

Management

Exposure cessation/avoidance is the primary intervention for most, especially hypersensitivity pneumonitis, which can be reversible if caught early
No specific treatment reverses established asbestosis/silicosis fibrosis - supportive care as for other ILD

Cancer risk

Mesothelioma, lung cancer (asbestos and silica both increase risk), TB (silicosis), hypersensitivity pneumonitis

Compensation

Compensation schemes exist for occupational lung disease in Australia - diagnosis has both clinical and medicolegal/compensation significance

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