Lesson of the month: extrinsic allergic (bronchiolo) alveolitis and metal working fluids
Tuesday, July 22, 2014
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. While continuing to work he had been treated with pulsed methylprednisolone, cyclophosphamide, prednisolone, mycophenolate and N-acetyl cysteine with little evidence of success. His referral was occasioned by a (new) physician noting that his symptoms improved when he was not at work. On being informed that his illness was in all probability caused by his occupation, he chose not to return to work. Six months later, without any specific treatment, his lung function measurements had started to improve.
Following the first diagnosis, discussion with the factory's occupational health service led to a systematic survey of 250 employees who worked in the same area. Through this we established that another metal turner was a patient at a third hospital with a diagnosis of hypersensitivity pneumonitis made 2 years previously; to his bemusement, since he had never kept them, a probable attribution to ‘birds’ had been made. He had been treated, intermittently, with high doses of prednisolone with no evidence of lasting benefit. The survey of other employees and subsequent specialist investigation established a further two cases of occupational bronchioloalveolitis with probable onset in 2010–2011.
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