Thirty-nine electronics workers were investigated by bronchial provocation testing to soldering fluxes containing colophony and were followed up one to four years later. At presentation and on follow-up each worker had nonspecific bronchial reactivity measured with inhaled histamine, and also had detailed measurements of lung function and estimation of total immunoglobulin levels. They completed a questionnaire designed to detect residual disability. The workers were divided into three groups. Twenty had left work after their initial diagnosis, eight had been moved to alternative work within their original factories, and 11 were thought to have asthma unrelated to colophony exposure as they failed to react to colophony at presentation. Histamine reactivity had returned to normal in half the workers who had left their original factories, but in only one worker who had moved within her original factory. This suggested that the nonspecific bronchial reactivity to histamine was the result rather than the cause of the occupational asthma, and that indirect exposure at work was sufficient to delay recovery of histamine reactivity. However, only two of the 20 affected workers who had left their original factories were symptom free on follow-up, and most had a considerable reduction in their quality of life by continuing asthma, which was particularly provoked by exercise, respiratory infections, and nonspecific irritants. Continuing symptoms may have been caused by domestic sources of colophony, or possibly the failure to eliminate colophony from the lungs.
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