Mixed-Dust Pneumoconiosis

Mixed dust pneumoconiosis is a fibrotic lung disease from inhaling mixed mineral dust containing a lower proportion of free silica than classical silicosis. By pathological convention, free silica in the lesions is under about 20%.

Exposure. Foundry work, welding, boiler scaling, mining, quarrying, brick and ceramic making, and shipbuilding.

Epidemiology. Common among exposed workers and often mislabelled. Latency is usually 10 years or more.

Classification. Pathology shows dust macules and mixed dust fibrosis with stellate nodules. Radiography shows small rounded or irregular opacities.

Complications. Progressive massive fibrosis, tuberculosis, lung cancer, chronic airflow obstruction, pneumothorax and rheumatoid pneumoconiosis (Caplan syndrome).

Pathophysiology.

Inhaled mixed particles deposit around respiratory bronchioles and are phagocytosed by macrophages. Cytokine release and reactive oxygen species stimulate fibroblast proliferation and collagen deposition.

Quartz content increases nodular fibrosis. Iron and other metals contribute to macule formation and oxidant injury.

• Usually asymptomatic early; abnormal imaging found at surveillance.
• Cough, sputum and exertional dyspnoea as fibrosis and airflow obstruction progress.
• Crackles and wheeze in advanced disease.

Red flags.

• Haemoptysis, fever, night sweats or weight loss (tuberculosis, cancer).
• Sudden pleuritic pain or dyspnoea (pneumothorax).
• Rapid radiographic change or cavitation within masses.

• Exposure history and work duration.
• Chest radiograph with classification of profusion and shape of small opacities and presence of large opacities.
• HRCT: centrilobular and subpleural nodules, fibrosis, masses, emphysema.
• Spirometry and gas transfer: mixed obstructive and restrictive defects.
• Sputum and molecular tests for tuberculosis when symptoms or new cavitation arise; interferon gamma release assay for latent infection.
• Biopsy only when atypical.

Differential diagnosis. Silicosis, coal workers' pneumoconiosis, asbestosis, hard metal lung disease, sarcoidosis, hypersensitivity pneumonitis, idiopathic pulmonary fibrosis, tuberculosis, metastases.

• No therapy reverses fibrosis. Remove from further exposure and control dust at source.
• Smoking cessation; influenza and pneumococcal vaccination; pulmonary rehabilitation.
• Airflow obstruction: inhaled bronchodilators and corticosteroids by usual practice for obstructive disease.
• Latent tuberculosis when tested positive and active disease excluded: rifampicin 10 mg/kg orally once daily (maximum 600 mg) for 4 months. Monitor liver enzymes at baseline and at 2 and 4 weeks, then as symptoms dictate. Check interactions (warfarin, direct oral anticoagulants, hormonal contraception, antiretrovirals, corticosteroids). No renal adjustment; avoid in severe liver disease.
• Long term oxygen when resting PaO2 is under 7.3 kPa, or 7.3 to 8 kPa with polycythaemia or cor pulmonale.

Monitoring. Spirometry and radiograph every 1 to 2 years.

Referral and escalation. Respiratory and occupational physician; transplant assessment in advanced progressive disease; notification and compensation where required.