Asbestos-Related Pleural Disease

Asbestos related pleural disease is the group of benign pleural conditions caused by asbestos fibre exposure: pleural plaques, benign pleural effusion, diffuse pleural thickening and rounded atelectasis. It is separate from malignant mesothelioma, though the two share an exposure cause.

Epidemiology. Pleural plaques are the commonest manifestation. Reported prevalence varies widely with exposure intensity and with the imaging used, being higher on CT than on radiograph.

Latency. Plaques usually appear 20 to 40 years or more after first exposure. Benign effusion tends to appear earlier, often within 10 to 20 years.

Significance. Plaques mark exposure but are not themselves premalignant. Lung cancer and mesothelioma risk follows cumulative dose.

Types of lesion. Parietal plaques, effusion, visceral pleural fibrosis with diffuse thickening, and folded lung (rounded atelectasis).

Pathophysiology.

Fibres reach the pleura through lymphatic drainage and accumulate at parietal pleural stomata. Persistent fibres provoke macrophage activation, oxidant injury and profibrotic cytokines such as TGF-beta.

Parietal pleural plaques form from hyalinised collagen on the diaphragm and lower chest wall, sparing the apices and costophrenic angles. Visceral involvement after effusion leads to diffuse thickening and fibrous encasement.

• Plaques are usually asymptomatic and found on imaging.
• Diffuse thickening causes exertional dyspnoea and sometimes chest wall pain.
• Benign effusion may be asymptomatic or cause pleuritic pain and breathlessness.
• Rounded atelectasis is usually found incidentally and may mimic a mass.

Red flags.

• New or persistent chest pain, weight loss or sweats.
• Rapid increase in thickening, nodularity, circumferential or mediastinal pleural involvement, or parietal thickening over 1 cm.
• Blood stained or enlarging effusion (mesothelioma, other malignancy).

• Detailed occupational and environmental exposure history with latency.
• Chest radiograph and CT: calcified or non-calcified parietal plaques; diffuse thickening; folded lung with the comet tail sign and pleural contact.
• Ultrasound for effusion and pleural thickness.
• Spirometry and gas transfer: a mild or moderate restrictive defect when diffuse thickening is present.
• Pleural fluid: protein, LDH, glucose, pH, cell count, cytology, culture, adenosine deaminase. Image directed or thoracoscopic pleural biopsy for undiagnosed or persistent effusion.

Differential diagnosis. Mesothelioma, metastatic pleural disease, tuberculous pleurisy, post-infectious fibrothorax, rheumatoid pleurisy, drug induced pleural disease, old haemothorax, rib fracture callus, subpleural fat.

• No treatment is needed for plaques. Counsel on exposure related cancer risks and smoking cessation.
• Influenza and pneumococcal vaccination.
• Symptomatic effusion: therapeutic aspiration. Recurrent symptomatic effusion: pleurodesis or indwelling pleural catheter after malignancy is excluded.
• Diffuse thickening: symptom control, pulmonary rehabilitation, and surgical decortication only in carefully selected patients with severe disability.
• Lung cancer screening by low dose CT where programmes exist and eligibility is met.

Monitoring. Clinical review and radiograph or CT at 6 to 12 months if new or changing disease.

Referral and escalation. Respiratory physician; urgent referral when any malignancy feature appears; occupational notification and compensation where required.