Abstract

Introduction
One of us was asked to consider a diagnosis of occupational asthma for a man who had worked for 20 years as a metal turner in a large, modern factory producing specialised machine parts. He described a 2 year history of severe breathlessness that improved when he was not at work. His spirometry was restrictive with a FEV1 of 1.35 L (40% predicted) and FVC of 1.8 L (45% predicted), a ratio of 75%. Other lung function measurements indicated gas trapping; his TLC was 5.01 L (79% predicted) and RV/TLC 170% predicted. A high resolution CT scan of his lungs revealed a widespread ‘mosaic’ pattern of attenuation indicative of small airflow obstruction. We made a diagnosis of occupational extrinsic allergic bronchioloalveolitis and recommended that he change his work. After 12 months working elsewhere in the same company, away from the machine shop, his dyspnoea was greatly improved but had not disappeared; his FVC had increased to 2.41 L, his FEV1 to 1.45 L and his TLC to 5.36 L.

Four months later we were referred a man who was also a metal turner in the same factory. For 2 years he had been a patient in a specialist interstitial lung disease clinic with a diagnosis of chronic hypersensitivity pneumonitis. A marked lymphocytosis in his bronchoalveolar lavage suggested ongoing exposure to an external cause. The nature of this had not been established although the positive findings of an autoimmune screen had led to conjecture of an ‘autoimmune’ aetiology, and of a high level of serum-specific IgG antibodies to Aspergillus species, that exposure to ‘mould at home or work’ might be relevant; an occupational history noted only that he worked for a machine parts manufacturer.

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