help button home button
AJRCCM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH

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
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
200309-1238OCv1
169/3/367    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Maghni, K.
Right arrow Articles by Malo, J.-L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Maghni, K.
Right arrow Articles by Malo, J.-L.

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







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Proc. Am. Thorac. Soc. Am. J. Respir. Cell Mol. Biol.
Copyright © 2003 American Thoracic Society
  ATS State of the Art Course 2008