Published ahead of print on October 24, 2003, doi:10.1164/rccm.200309-1238OC
Am. J. Respir. Crit. Care Med., Volume 169, Number 3, February 2004, 367-372
A more recent version of this article appeared on February 1, 2004
Submitted on September 8, 2003
Accepted on October 18, 2003
Airway inflammation after cessation of exposure to agents causing occupational asthma
Karim Maghni1, Catherine Lemiere1, Heberto Ghezzo1, Wu Yuquan1, and Jean-Luc Malo1*
1 Chest Medicine, Sacre-Coeur Hospital, Montreal, Quebec, Canada
* To whom correspondence should be addressed. 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 yrs (0.5-20.8 yrs) 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 PC20; 2) improved: increase in PC20 by 3.2-fold or more but PC20 still abnormal; 3) not improved: no significant change in PC20. Nine/28 subjects (32.1%) with no improvement vs 6/56 (10.7%) with partial and complete improvements had sputum eosinophils equal or greater than 2%, and 11/28 (39.3%) vs 11/56 (19.6%) showed sputum neutrophils equal or greater than 61%. Levels of interleukin-8 and of the neutrophil-derived myeloperoxidase (MPO) 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: Bronchial diseases, asthma, occupational diseases, sputum, interleukin-8, myeloperoxidase, eotaxin
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