Abstract

Background: Cigarette smoking is the cardinal cause of chronic obstructive pulmonary disease (COPD), but only a relatively small percentage of smokers are developing clinically overt disease, suggesting, therefore, that other risk factors than smoking are involved. Several studies have shown that the bronchodilator response (BR) is related to the progress of COPD, as assessed by the fall in forced expiratory volume in 1 s (FEV<sub>1</sub>). However, the relationship between BR and fall in FEV<sub>1</sub>, is a disputed one. Objective: To assess the relationship between BR and fall in FEV<sub>1</sub> in a group of long-term smokers and ex-smokers who were 60 years old on the average. Methods: Questionnaire, spirographic tests and BR were assessed in 56 smokers and ex-smokers of mean age 62.5 ± (SD) 2.7 years at the end of a 13-year follow-up period. BR was expressed as a percentage change of the prebronchodilator value (‘% initial’) and as a percentage change of predicted value (‘% predicted’). Results: The FEV<sub>1</sub>/VC vital capacity was 68.9 ± 7.6% at the start and 64.5 ± 11.3% at the end of the study. The average fall in FEV<sub>1</sub> over 13 years was 26 ± 25 ml/year. The FEV<sub>1</sub> increased after albuterol on the average with 5.9 ± 6.6%, 4.5 ± 3.9% of predicted, and the vital capacity with 2.5 ± 6.5%, 2.3 ± 6.4% of predicted. BR and fall in FEV<sub>1</sub> were correlated: the greater the BR, the more rapid the fall in FEV<sub>1</sub> (r = 0.4 and p < 0.01 for FEV<sub>1</sub>% and r = 0.3 and p < 0.05 for FEV<sub>1</sub> predicted). However, when adjusting for prebronchodilator FEV<sub>1</sub>, the BR was no more related to the fall in FEV<sub>1</sub> (r = 0.15, p > 0.05). Conclusions: In long-term smokers and ex-smokers, the BR measured at the end of the follow-up period was correlated with the fall in FEV<sub>1</sub>. However, after adjusting for prebronchodilator FEV<sub>1</sub> values, BR was no more related to the decline in FEV<sub>1</sub>. The BR appears not to be associated with the development of COPD.

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