Aluminosis

Aluminosis is a rare occupational lung disease caused by inhaling fine aluminium dust or fume. It presents as interstitial fibrosis, a sarcoid like granulomatous reaction, or, in bauxite and corundum workers, fibrosis with emphysema and frequent pneumothorax (Shaver's disease). Evidence rests mainly on case reports and small series.

Exposure. Risk arises in fine aluminium powder and flake production (paints, pyrotechnics, stamping), abrasive manufacture from bauxite, smelting, and aluminium grinding or welding. Disease usually follows years of heavy exposure to respirable particles.

Epidemiology. Few cases are documented and incidence is unknown. Most reported patients are men in manufacturing, and the disease is probably under recognised.

Course and complications. Progressive restriction, spontaneous pneumothorax and respiratory failure occur, and fatal cases are reported. Progression can continue after exposure ends in advanced disease.

Pathophysiology.

Respirable aluminium particles deposit in respiratory bronchioles and alveoli and are engulfed by macrophages. Persistent particle burden drives chronic inflammation, fibroblast activation and interstitial fibrosis.

The granulomatous form is thought to be an immune mediated reaction with non-caseating granulomas. In Shaver's disease, co-exposure to silica and other fume constituents may contribute. Mechanisms remain incompletely defined.

• Insidious exertional dyspnoea, dry cough and chest tightness over years of exposure.
• Fine end inspiratory basal crackles in established fibrosis; the examination may be normal early.
• Fever, weight loss or arthralgia are uncommon and suggest the granulomatous form or a complication.

Red flags.

• Sudden pleuritic chest pain with dyspnoea (pneumothorax).
• Haemoptysis, fever, night sweats or weight loss (tuberculosis, malignancy).
• Rapidly progressive dyspnoea or resting hypoxaemia.

• Task-by-task exposure history: product, process, duration, dust control, respiratory protection.
• Chest radiograph: diffuse reticulonodular opacities; upper zone bullae and pneumothorax in the Shaver pattern.
• HRCT: fibrosis, nodules, traction bronchiectasis; hilar nodes in the granulomatous form.
• Spirometry and gas transfer: restriction with reduced TLC and DLCO, sometimes mixed with obstruction.
• Bronchoalveolar lavage or biopsy: particle analysis by electron microscopy with X-ray spectroscopy showing aluminium; non-caseating granulomas; mycobacterial and fungal cultures.
• Urinary or serum aluminium shows exposure only and does not confirm lung disease.

Differential diagnosis. Sarcoidosis, chronic beryllium disease (lymphocyte proliferation test), hypersensitivity pneumonitis, idiopathic pulmonary fibrosis, silicosis, other pneumoconioses, tuberculosis, drug induced lung disease.

• Remove from further exposure and control dust at source.
• Smoking cessation; influenza and pneumococcal vaccination.
• Evidence for drug therapy is weak. For the granulomatous or inflammatory form: prednisolone 0.5 mg/kg orally once daily in the morning, maximum 40 mg daily, for 4 weeks as a test course. If symptoms, spirometry or imaging improve, taper to the lowest effective dose over 8 to 12 weeks; otherwise stop or taper over 2 weeks. Monitor glucose, blood pressure, weight, mood and infection, with bone protection if therapy exceeds 3 months. Exclude active tuberculosis first. Caution in diabetes and peptic ulcer; no renal adjustment.
• Pneumothorax: aspiration or intercostal drainage by size and symptoms; surgical pleurodesis for recurrence or persistent air leak.
• Long term oxygen when resting PaO2 is under 7.3 kPa, or 7.3 to 8 kPa with polycythaemia or cor pulmonale.

Monitoring. Spirometry, gas transfer and imaging every 6 to 12 months initially.

Referral and escalation. Respiratory and occupational physician at diagnosis; transplant assessment in advanced progressive disease; urgent review for pneumothorax.