ERJ
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Permissions
Right arrowRequest Permissions
Right arrow Citation Map
Services
Right arrow Email this article to a friend
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Boulet, L.
Right arrow Articles by Malo, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Boulet, L.
Right arrow Articles by Malo, J.
Eur Respir J 1994; 7: 1567-1575
Copyright © ERS Journals Ltd 1994


Original Articles

Airway inflammation after removal from the causal agent in occupational asthma due to high and low molecular weight agents

LP Boulet, M Boutet, M Laviolette, M Dugas, J Milot, C Leblanc, L Paquette, J Cote, A Cartier, and JL Malo

In order to determine 1) the features of airway inflammation after removal from exposure to high (HMW) and low (LMW) molecular weight agents 2) if there are any differences in the pattern of inflammation induced by these two types of agents, we studied 18 subjects with a recently confirmed diagnosis of occupational asthma (OA) due to HMW (n = 11) and LMW (n = 7) agents. The duration of asthma symptoms varied from 2 to 108 months (mean 33 months), and withdrawal from exposure to the sensitizing agent from 3 to 24 weeks (mean 10 weeks). All subjects underwent measurements of expiratory flow rates, methacholine inhalation tests, and a flexible bronchoscopy with bronchoalveolar lavage (BAL) and bronchial biopsies. Endoscopic findings were compared with a group of 10 normal subjects. At the time of the bronchoscopy, asthma symptoms were minimal in most subjects. Although 15/18 subjects had normal forced expiratory volume in one second (FEV1 > 80% pred), all subjects had increased airway responsiveness to methacholine (provocation concentration producing a 20% fall in FEV1 = 0.2-10.0 mg.ml-1). BAL analysis showed similar median percentages of the total number of cells and differentials in control subjects and those exposed to HMW and LMW agents. Bronchial biopsies showed that mean inflammatory cell count, both epithelial and sub-epithelial, was similarly raised in OA subjects exposed to either HMW or LMW agents, compared to controls, except for epithelial lymphocyte count. In contrast to the controls, bronchial biopsy of both groups with OA also showed other changes such as extensive epithelial desquamation, ciliary abnormalities of the epithelial cells, smooth muscle hyperplasia and subepithelial fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
ChestHome page
D. L. Holness, S. Tabassum, S. M. Tarlo, G. M. Liss, F. Silverman, and M. Manno
Practice Patterns of Pulmonologists and Family Physicians for Occupational Asthma
Chest, November 1, 2007; 132(5): 1526 - 1531.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
C. E. Mapp, P. Boschetto, P. Maestrelli, and L. M. Fabbri
Occupational Asthma
Am. J. Respir. Crit. Care Med., August 1, 2005; 172(3): 280 - 305.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
P. Maestrelli
Natural History of Adult-Onset Asthma: Insights from Model of Occupational Asthma
Am. J. Respir. Crit. Care Med., February 1, 2004; 169(3): 331 - 332.
[Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
K. Maghni, C. Lemiere, H. Ghezzo, W. Yuquan, and J.-L. Malo
Airway Inflammation after Cessation of Exposure to Agents Causing Occupational Asthma
Am. J. Respir. Crit. Care Med., February 1, 2004; 169(3): 367 - 372.
[Abstract] [Full Text] [PDF]


Home page
Eur Respir JHome page
J. Sastre, O. Vandenplas, and H-S. Park
Pathogenesis of occupational asthma
Eur. Respir. J., August 1, 2003; 22(2): 364 - 373.
[Abstract] [Full Text] [PDF]


Home page
ChestHome page
L. Wang, B. E. McParland, and P. D. Pare
The Functional Consequences of Structural Changes in the Airways: Implications for Airway Hyperresponsiveness in Asthma
Chest, March 1, 2003; 123 (2009): 356S - 362S.
[Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
Proceedings of the First Jack Pepys Occupational Asthma Symposium
Am. J. Respir. Crit. Care Med., February 1, 2003; 167(3): 450 - 471.
[Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
L.-P. BOULET, H. TURCOTTE, M. LAVIOLETTE, F. NAUD, M.-C. BERNIER, S. MARTEL, and J. CHAKIR
Airway Hyperresponsiveness, Inflammation, and Subepithelial Collagen Deposition in Recently Diagnosed versus Long-standing Mild Asthma . Influence of Inhaled Corticosteroids
Am. J. Respir. Crit. Care Med., October 1, 2000; 162(4): 1308 - 1313.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
J. BOUSQUET, P. K. JEFFERY, W. W. BUSSE, M. JOHNSON, and A. M. VIGNOLA
Asthma . From Bronchoconstriction to Airways Inflammation and Remodeling
Am. J. Respir. Crit. Care Med., May 1, 2000; 161(5): 1720 - 1745.
[Full Text]


Home page
Am. J. Respir. Crit. Care Med.Home page
M. CHAN-YEUNG, H. OBATA, M. DITTRICK, H. CHAN, and R. ABBOUD
Airway Inflammation, Exhaled Nitric Oxide, and Severity of Asthma in Patients with Western Red Cedar Asthma
Am. J. Respir. Crit. Care Med., May 1, 1999; 159(5): 1434 - 1438.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Respir. Crit. Care Med.Home page
C. E. MAPP, A. BALBONI, R. BARICORDI, and L. M. FABBRI
Human Leukocyte Antigen Associations in Occupational Asthma Induced by Isocyanates
Am. J. Respir. Crit. Care Med., October 1, 1997; 156(4): S139 - S143.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1994 by the European Respiratory Society.