Airway responsiveness to inhaled mannitol was measured in smokers (n=42), and non-smokers (n=45). In smokers, the mannitol test was repeated 3 months after smoking cessation.
Demographics including age, lung function and atopy status were similar for smokers and non-smokers (p=ns). Compared with non-smokers (2.2 % ), AHR to mannitol expressed by 15 % fall in FEV1 was significantly more common in smokers (26.2 % ) (p=0.001). The provoking dose to induce a 15 % fall in FEV1 (PD15), a measure of sensitivity, was median [IQR] 291 mg [207–377] in the 11 positive smokers. The response–dose ratio (RDR) ( % fall in FEV1/cumulative dose), a measure of reactivity, was significantly higher in smokers (0.013 [0.006–0.029]) compared with non-smokers (0.004 [0.002–0.007]), (p<0.0001). After successful smoking cessation, the RDR decreased in most cases (p=0.01) and only one patient still recorded a
15 % fall in FEV1. None of the patients with a negative mannitol test turned positive, irrespective of the outcome of smoking cessation.
AHR to mannitol is quite common in smokers compared to non-smokers and decreases significantly after smoking cessation. Thus, the mannitol test may be sensitive to non-asthmatic inflammation of the airways.