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Depts of 1 Pathology, and 2 Pulmonology, University Hospital Groningen
CORRESPONDENCE: B.W.M. Willemse, Dept of Pathology, University Hospital Groningen, Hanzeplein 1, 9713 GZ, Groningen, The Netherlands. Fax: 31 503632510. E-mail: b.w.m.willemse@path.azg.nl
Keywords: chronic obstructive pulmonary disease, inflammation, review, smoking cessation
Received: February 5, 2003
Accepted October 29, 2003
Abstract
Smoking is the main risk factor in the development of chronic obstructive pulmonary disease (COPD), and smoking cessation is the only effective treatment for avoiding or reducing the progression of this disease.
Despite the fact that smoking cessation is a very important health issue, information about the underlying mechanisms of the effects of smoking cessation on the lungs is surprisingly scarce. It is likely that the reversibility of smoke-induced changes differs between smokers without chronic symptoms, smokers with nonobstructive chronic bronchitis and smokers with COPD. This review describes how these three groups differ regarding the effects of smoking cessation on respiratory symptoms, lung function (forced expiratory volume in one second), airway hyperresponsiveness, and pathological and inflammatory changes in the lung.
Smoking cessation clearly improves respiratory symptoms and bronchial hyperresponsiveness, and prevents excessive decline in lung function in all three groups.
Data from well-designed studies are lacking regarding the effects on inflammation and remodelling, and the few available studies show contradictory results. In chronic obstructive pulmonary disease, a few histopathological studies suggest that airway inflammation persists in exsmokers. Nevertheless, many studies have shown that smoking cessation improves the accelerated decline in forced expiratory volume in one second, which strongly indicates that important inflammatory and/or remodelling processes are positively affected.
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