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Forty years ago, British investigators developed the hypothesis that recurrent bronchial infections were the reason that some smokers developed progressive airways obstruction and other did not 1. The classical studies of Fletcher et al. 2 were designed to test this proposition. They carried out a prospective study of working males, noting the frequency of respiratory infections, sputum quantity and quality, and rate of loss of lung function in the form of forced expiratory volume in one second (FEV1). They found that chronic cough and sputum production, and recurrent respiratory infections did not relate to lung function decline. They concluded that the chronic bronchitis syndrome (cough, sputum and episodes of acute bronchitis) was an epiphenomenon in so far as the development of chronic obstructive pulmonary disease (COPD) was concerned; both chronic bronchitis and COPD were caused by smoking, but the two were not related. This made sense, since chronic bronchitis symptoms largely reflected pathology in major conducting airways, and airways obstruction was related to lesions in small airways and the lung parenchyma. This view of the pathogenesis of COPD was essentially unchallenged for many years, in a large part because it was hard to do a better study that that of …
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N. R. Anthonisen (2004) studied this question.
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