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Published ahead of print on October 24, 2003, doi:10.1164/rccm.200309-1238OC
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American Journal of Respiratory and Critical Care Medicine Vol 169. pp. 367-372, (2004)
© 2004 American Thoracic Society

Airway Inflammation after Cessation of Exposure to Agents Causing Occupational Asthma

Karim Maghni, Catherine Lemière, Heberto Ghezzo, Wu Yuquan and Jean-Luc Malo

Department of Chest Medicine, Sacré-Coeur Hospital, Montreal, Quebec, Canada

Correspondence and requests for reprints should be addressed to Jean-Luc Malo, M.D., Department of Chest Medicine, Sacré-Coeur Hospital, 5400 W. Gouin Blvd., Montreal, PQ, H4J 1C5, Canada. E-mail: malojl{at}meddir.umontreal.ca

Subjects with occupational asthma (OA) generally present asthma symptoms and airway hyperresponsiveness after cessation of exposure. We hypothesized that they are also left with airway inflammation. We assessed 133 subjects with OA at a mean interval of 8.7 years (0.5–20.8 years) after cessation of exposure by questionnaire, airway caliber, and responsiveness to methacholine. Satisfactory samples of induced sputum were obtained from 98 subjects. We defined three groups of subjects: (1) cured: normalization of the concentration of methacholine provoking a 20% decrease in FEV1 (PC20), (2) improved: increase in PC20 by 3.2-fold or more but PC20 still abnormal, and (3) not improved: no significant change in PC20. In all, 9/28 subjects (32.1%) with no improvement versus 6/56 (10.7%) subjects with partial and complete improvements had sputum eosinophils equal to or greater than 2% and 11/28 (39.3%) subjects versus 11/56 (19.6%) subjects showed sputum neutrophils equal to or greater than 61%. Levels of interleukin-8 and of the neutrophil-derived myeloperoxidase were significantly more elevated in sputum of subjects with no improvement. Those in the cured or improved groups had a significantly longer time lapse since diagnosis and a higher PC20 at the time of diagnosis. We conclude that failure to improve after cessation of exposure to an agent causing OA is associated with airway inflammation at follow-up.

Key Words: asthma • occupational diseases • sputum • interleukin-8 • myeloperoxidase




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