Airway responsiveness to a beta-adrenergic agonist in smokers

Airway hyperresponsiveness (AHR) is the most characteristic feature of asthma, which is reported in chronic obstructive pulmonary disease (COPD) patients and smoker subjects. However, there are controversies regarding airway responsiveness to β-adrenergic agonists in asthma, as well as COPD and smoker subjects. Our previous studies have shown AHR to β-agonists in asthmatic patients. Therefore, in the present study, airway sensitivity to a β-agonist was examined in smoker subjects. The threshold concentration of inhaled salbutamol required for a 20% increase in forced expiratory volume in 1 sec (FEV1), as PC20, or a 35% increase in specific airway conductance (sGaw), as PC35, was measured in 12 nonsmoker and 12 smoker subjects. Airway responsiveness to salbutamol was greater in smokers (PC20 = 65.83 ± 14.77 mg/L and PC35 = 27.75 ± 18.41 mg/L) than nonsmokers (PC20 = 244.17 ± 44.2 mg/L and PC35 = 90.50 ± 28.67 mg/L, P < 0.001 for both cases). There was a significant correlation between FEV1 with PC20 salbutamol (r = 0.547, P < 0.005). The relationship between the amount of smoking and PC 35 salbutamol was also statistically significant (r = –0.654, P < 0.001). The slope of concentration-response curve for salbutamol was significantly greater in smokers than nonsmoker subjects, by measuring both FEV1 and sGaw (P < 0.001 for both cases). The increased sensitivity of smokers to inhaled salbutamol suggests that they could also be more sensitive to their endogenous adrenaline, which may thus dilate and stabilize their airways.