• Ave Nagelmann, Äli Tonnov, Toivo Laks, Ruth Sepper, and Kaiu Prikk.
• Institute of Clinical Medicine, Tallinn University of Technology, Estonia.
• COPD. 2011 Jun 1;8(3):189-95.

AbstractCigarette smoking causes airflow limitation with lung hyperinflation being the primary causes of COPD. Fifty chronic smokers (CSs) with no signs of GOLD-adjusted COPD with smoking habit at least ≥10 pack-years (p/yrs) were divided into CS-mild (n = 24) with smoking history from ≥10 to ≤20 p/yrs and CS-heavy groups (n = 26) with smoking history ≥21 p/yrs. Spirometry, plethysmography and diffusing capacity were measured and lung computed tomography (CT) was performed. Residual volume (RV) (L) and RV/TLC (total lung capacity) ratio were significantly increased in CS-heavy when compared to CS-mild (p = 0.001, p = 0.03). A significant reduction of forced expiratory volume in 1 second/forced vital capacity (FEV(1)/FVC) ratio and airway specific conductance was shown in CS-heavy (p = 0.02, p = 0.03). Lung emphysema signs at CTs were revealed in 17 CSs and ten of them had declined diffusing capacity below 70% of predicted. The percentage of emphysematous lesions inversely and significantly correlated with measured diffusing capacity (p = 0.0009, r = --0.72). Study groups' smoking intensity inversely correlated the declined airway specific conductance (p = 0.004, r = --0.39) and increase of the RV (L) (p = 0.0004, r = 0.46). Multiple regression analysis determined that smoking intensity regardless of the subjects' age was significant factor for decline of airway specific conductance and increase of RV (L). Here we conclude that lung function deviation and lung structural changes are present in CSs before the clinical signs of airway obstruction reveal. Body plethysmography and diffusing capacity measurement with routine spirometry can provide valuable information for detection of changes reflecting to the early onset of COPD in CSs.

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