Hard Metal Lung Disease

Hard metal lung disease is an interstitial lung disease caused by inhaling dust or fume from cemented tungsten carbide, an alloy of tungsten carbide particles bound with cobalt (6 to 25 percent), sometimes with titanium, tantalum, nickel or chromium carbides. Cobalt is the causative agent.

Exposure occurs in tool grinding and sharpening, diamond polishing with cobalt containing wheels, drill bit and saw manufacture, and powder metallurgy.

Fewer than 5 percent of exposed workers are affected, which points to individual susceptibility, probably an immune mechanism with a genetic component.

Three patterns occur: occupational asthma (the commonest, with onset within months), hypersensitivity type alveolitis, and giant cell interstitial pneumonia, the pathognomonic histological form with bizarre multinucleated macrophages and epithelial cells filling the alveoli. Latency ranges from months to more than 10 years. Early disease reverses after removal from exposure. Persistent exposure leads to fibrosis, respiratory failure and death. Lung cancer risk is increased.

• Work related cough, wheeze and dyspnoea that improve at weekends and holidays (early or asthmatic form).
• Progressive exertional dyspnoea, dry cough, fatigue, weight loss and chest tightness in the interstitial form.
• Bibasal fine end inspiratory crackles; clubbing in advanced disease.
• Rhinitis, conjunctivitis and contact dermatitis (cobalt allergy) often coexist.
• Acute or subacute presentations can mimic pneumonia with fever and bilateral infiltrates.
• Red flags: rapid progression over weeks, hypoxaemia at rest, pneumothorax, haemoptysis, traction bronchiectasis.
• Complications: pulmonary fibrosis, pulmonary hypertension, cor pulmonale, lung cancer.

• Start with a detailed occupational history, including the exact process (wet or dry grinding, ventilation, respirator use) and the temporal relation of symptoms to work.
• Chest radiograph: normal early; later diffuse small nodular or reticular opacities.
• High resolution CT: ground glass opacities, centrilobular nodules, consolidation, then traction bronchiectasis and honeycombing in advanced disease.
• Spirometry and gas transfer: restrictive pattern with reduced DLCO (below 80 percent predicted); serial peak flow charting at and away from work for the asthmatic form (diurnal variation above 20 percent, fall on working days).
• Urine cobalt (above 15 micrograms per litre at end of shift end of week indicates recent exposure; exposure marker only, not diagnostic).
• Bronchoalveolar lavage: lymphocytosis and multinucleated giant macrophages (above 5 percent supports diagnosis). Tungsten and cobalt may be identified in tissue by electron microscopy with energy dispersive analysis.
• Surgical or cryobiopsy: giant cell interstitial pneumonia pattern.
• Exclude sarcoidosis, hypersensitivity pneumonitis from organic antigens, idiopathic pulmonary fibrosis, desquamative interstitial pneumonia, and infection.

• Permanent removal from cobalt exposure is the essential step. Redeployment is advised even in mild disease; a respirator alone is not sufficient.
• Mild or asthmatic disease: remove from exposure, then inhaled budesonide 400 micrograms twice daily with salbutamol 200 micrograms inhaled as needed, reviewed at 3 months.
• Symptomatic interstitial disease: prednisolone 0.5 to 1 mg/kg orally once daily (usual adult dose 40 mg) for 4 to 6 weeks, tapered by 5 mg every 2 weeks to 10 mg, then continued for 6 months in total depending on response. Add co-trimoxazole 480 mg orally once daily for pneumocystis prophylaxis while prednisolone exceeds 20 mg daily for more than 4 weeks, calcium 1000 mg and vitamin D 800 IU daily, and omeprazole 20 mg daily.
• Severe or progressive disease despite steroids: add azathioprine 1 to 2 mg/kg orally once daily (check thiopurine methyltransferase first, monitor full blood count and liver enzymes every 2 weeks for 3 months). Long term oxygen when resting PaO2 is below 7.3 kPa; transplant assessment for end stage fibrosis.
• Follow up: spirometry and DLCO every 3 months for the first year, then every 6 months; CT at 6 months. Annual CT surveillance in those with ongoing fibrosis.
• Prevention: wet grinding, local exhaust ventilation, enclosure, urine cobalt monitoring, and preplacement and periodic spirometry for exposed workers.
• Counselling: stop smoking, report as an occupational disease, compensation assessment.