Abstract

Various metals have been described as causing occupational asthma (OA), mostly chromium, nickel, and cobalt. The mechanism of action by which these metals can produce OA is generally immunological, either IgE-mediated or not.1,2To date, only 2 cases of OA caused by zinc have been described, and in both cases, an IgE-dependent mechanism was involved in the pathogenesis of the disorder.We describe, for the first time, a worker exposed to zinc who developed OA via a non-IgE-mediated immunological mechanism. Our patient was a 30-year-old man, former smoker of 5 pack-years, whose only clinical history consisted of a diagnosis of bronchial asthma in childhood, which had remitted, and for which he had not required treatment for 15 years. He had been working for 4 years as an industrial mechanic, making metal parts, and was in regular contact with copper, cadmium, zinc, and manganese dust. The patient consulted due to a 5-month history of cough, expectoration, wheezing, and dyspnoea. Symptoms appeared some time after start of exposure and improved during the weekends and periods of sick leave. He had had to attend the emergency department on 5 occa-sions since the onset of symptoms. Chest radiograph was normal. Clinical laboratory tests showed a total IgE of 140 kU/l. Skin tests for airborne allergens were positive for house dust mites, while contact skin tests for metal, including nickel sulfate, potassium dichromate, cadmium, cobalt chloride, and zinc 2.5%, were negative. Forced spirometry showed FVC 6360 ml (112%), FEV14390 ml (98%), andFEV1/FVC 69%. A methacholine challenge was positive with a PC20of4 mg/ml. A provocation test was performed, according to standard methodology for testing metals,1,5for which concentrations of 0.1 mg/ml, 1 mg/ml, and 10 mg/ml of zinc sulfate were prepared. The 0.1 mg/ml solution was nebulized for a total of 5 min, split into periods of 1, 2, and 2 min. Four hours after exposure, a 23% reduction in FEV1from baseline was observed (Fig. 1), along with cough, wheezing, and dyspnoea. These symptoms abated after administration of a ß2 agonist. Ten hours after exposure, the patient presented the same symptoms, with a 29% reduction in FEV1, requiring administration of intravenous corticosteroids in addition to ß2 agonist, and a 12-h stay in the emergency department

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