Stannosis

Stannosis is the benign pneumoconiosis produced by inhalation of tin dust or fume, almost always tin oxide (SnO2). Exposure occurs in tin smelting, tin ore processing, tin plating, solder manufacture and the handling of tin compounds. Tin oxide is chemically inert, so retained particles evoke only a minimal macrophage reaction with no fibrosis and no impairment of function.

The disease is notable for the contrast between the dramatic radiograph, with dense punctate opacities, and the near absence of symptoms or lung function loss. Exposure to organotin compounds, which are toxic, is a separate hazard and does not cause stannosis. Cases usually appear after 5 or more years of exposure, and radiographic change slowly clears after exposure stops. There is no recognised increase in lung cancer or tuberculosis from tin alone.

• No symptoms in most patients.
• Occasional mild cough or mucoid sputum.
• Normal examination, normal oxygen saturation.
• No clubbing, no crackles. Any such finding indicates another disease or a mixed dust exposure.
• Skin and eye irritation after contact with tin chlorides.
• Red flags: dyspnoea, weight loss, haemoptysis, which suggest silica, lead, cadmium or a different disease.

• Occupational history of tin oxide exposure of several years.
• Chest radiograph: numerous small, discrete, dense, sharply outlined opacities (1 to 4 mm), symmetrical, throughout both lungs, more radio opaque than those of silicosis, with normal hilar nodes and normal heart size.
• High resolution CT: dense centrilobular and perilymphatic nodules, no fibrosis, no architectural distortion.
• Spirometry and DLCO: normal.
• Tissue or lavage demonstration of tin by electron microscopy with energy dispersive analysis or inductively coupled plasma analysis when needed. Biopsy is seldom justified.
• Exclude silicosis, sarcoidosis, miliary tuberculosis, metastatic calcification, pulmonary alveolar microlithiasis, and baritosis or siderosis in mixed metal workers.

• No specific drug therapy is needed because no pathological reaction occurs.
• Remove from continued heavy exposure when radiographic density is marked, although function is intact.
• Control exposure: local exhaust ventilation, wet processes, enclosed furnaces, and half face respirators with P2 filters.
• Screening: exposed workers have a chest radiograph and spirometry at employment, then every 3 years. Tuberculosis testing when radiographic change is unusual or the worker has symptoms.
• Smoking cessation: nicotine replacement with patch 21 mg per 24 hours for 6 weeks, then 14 mg for 2 weeks, then 7 mg for 2 weeks, plus nicotine gum 2 mg as needed.
• If obstruction develops from smoking, treat as COPD: salbutamol 200 micrograms inhaled as needed, tiotropium 18 micrograms inhaled once daily.
• Follow up: radiographic regression over 2 to 10 years after leaving exposure confirms the diagnosis. Persisting or progressive change prompts reassessment for another diagnosis.
• Counselling: the condition is benign and not a risk to life; reassurance reduces unnecessary investigation.