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Structural changes and airway remodelling in occupational asthma at a mean interval of 14 years after cessation of exposure
Author(s) -
Sumi Y.,
Foley S.,
Daigle S.,
L'Archevêque J.,
Olivenstein R.,
Letuvé S.,
Malo J.L.,
Hamid Q.
Publication year - 2007
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2007.02828.x
Subject(s) - medicine , metaplasia , pathology , asthma , fibrosis , eosinophil , biopsy , inflammation , versican , squamous metaplasia , bronchoalveolar lavage , gastroenterology , epithelium , lung , cartilage , proteoglycan , anatomy
Summary Background Occupational asthma (OA) may cause alterations of airways with inflammation and remodelling after cessation of exposure. Although the long‐term clinical, functional and induced sputum sequelae have been examined in workers removed from exposure, the long‐term pathological outcomes are unknown. Objective We aimed to investigate whether airway inflammation and remodelling were present in bronchial biopsies of subjects with prior OA but without evidence of persisting asthma at a mean interval of 14 years after cessation of exposure. Methods Ten clinically and functionally asymptomatic subjects with a prior diagnosis of OA were recruited and underwent bronchoscopy, bronchoalveolar lavage and bronchial biopsy. Comparisons were made with biopsies from normal control subjects. Epithelial detachment, epithelial metaplasia, mucous gland and airway smooth muscle (ASM) areas as well as the distance between the epithelium and ASM were measured by image analysis. The amount of collagen present was assessed by van Gieson staining. The numbers of TGF‐β1‐ and eosinophil cationic protein (ECP)‐positive cells were evaluated by specific immunostaining. Results Statistically significant increases were found in the numbers of TGF‐β1‐ and ECP‐positive cells and in the amount of subepithelial fibrosis present in the biopsies of subjects with prior OA compared with control biopsies. The distance between the epithelium and ASM was significantly reduced in the OA group. Increases in epithelial metaplasia, ASM mass, mucous gland numbers, collagen deposition and eosinophilia in the OA group were not statistically significant. There was no evidence of ongoing inflammation in the group with prior OA as assessed by the number of T lymphocytes present. Conclusion Some aspects of airway inflammation and remodelling persist in subjects with prior OA long after cessation of exposure even in the absence of clinical, sputum and functional abnormalities. These findings are relevant to the assessment of long‐term sequelae in subjects with OA when reviewed after cessation of exposure.