Chronic respiratory symptoms are commonly reported by current and former cigarette smokers who lack spirometric evidence of COPD. These individuals are more likely to experience wheezing, breathlessness, limitation in exercise, chronic bronchitis, worse quality of life, exacerbations and more co-morbidities than healthy never-smokers [1][2][3][4] (Fig. 1). The natural history, pathophysiology and management of smokers without evidence of COPD is poorly understood. 3,4 Smoking-induced airway diseases include chronic bronchitis, emphysema, and small airway disease, occurring either alone or in combination. These diseases also occur in smokers with asthma.3 Previous studies of inflammation, physiology and computed tomography (CT) imaging provides indirect evidence that small airway disease (<2 mm in diameter) contributes to respiratory symptoms in smokers with normal spirometry. Cigarette smoking induces respiratory bronchiolitis of small airways before the development of emphysema.
5,6The function of peripheral airways is abnormal in some smokers without COPD assessed by physiological techniques, such as multiple breath nitrogen washout (MBNW) 7 and impulse oscillometry (IOS). 8,9 Analysis of expiratory and inspiratory computed tomography (CT) images detects increased nonemphysematous air trapping, a surrogate for functional small airways disease, in ever-smokers with normal spirometry.10-12 However, little is known about whether small airway dysfunction assessed by physiological tests, such as MBNW or IOS are worse in symptomatic smokers without COPD compared to asymptomatic smokers. In this issue of Respirology, Jetmalani et al.13 report the results of a prospective, observational study designed to determine the prevalence of respiratory symptoms (chronic bronchitis, dyspnoea, wheeze) and small airway dysfunction and their interrelationship in eighty young to middle-aged current and former smokers without spirometric COPD. Small airway dysfunction was assessed by measuring ventilation heterogeneity in diffusion-dependent (S acin ) and convection-dependent (S cond ) airways by MBNW and by measuring respiratory resistance at 5 (R5) and 20 (R20) Hz and reactance at 5 (X5) Hz by IOS.An important finding of the study was that abnormalities in either MBNW (predominantly S acin ) or IOS (predominantly R5) were found in three quarters of current and former smokers without spirometric COPD. Half the subjects had an abnormal MDNW or IOS measurement, and in one quarter there was an overlap in abnormal IOS and MBNW variables. The results of the study and those from previous studies using physiological tests 7-9 and CT imaging biomarkers 10-12 demonstrate that small airway dysfunction is commonly found in this group of current and former smokers. Interestingly, smokers without spirometric COPD following smoking cessation show sustained improvements of conductive airway dysfunction (S cond ), but not in acinar airway function (S acin ) suggesting that some abnormalities of small airway disease are reversible, possibly due t...