Does Smoking Reduce the Late-Phase Allergic Asthma Response?
Volume 18, Number 1Inhaled corticosteroid (ICS) therapy may be less effective in asthma patients who smoke. Little is known about how smoking affects the ICS-induced attenuation of the early and late asthmatic responses. Allergen-induced airway responses were compared for ICS-treated allergic asthma patients who did and did not smoke.
The randomized, double-blind crossover study included 17 smoking and 18 nonsmoking patients with atopic asthma. All received 7 days of treatment twice-daily fluticasone propionate (FP) 100 μg, FP 500 μg, and placebo. On day 6 of each treatment period, airway responses were assessed by measuring FEV1 for up to 10 hours after allergen challenge. This was followed on day 7 by assessment of exhaled nitric oxide, induced sputum cell counts, and methacholine responsiveness.
In both smokers and nonsmokers, FP significantly suppressed the late asthmatic response (LAR). In addition, the LAR was significantly attenuated during the placebo periods in smokers compared to nonsmokers. Fluticasone suppressed the early allergic response in smokers, but not nonsmokers.
Nonsmokers had a greater reduction in methacholine responsiveness while on FP, compared to smokers. Smokers had lower allergen-induced increases in exhaled NO and sputum eosinophils compared to nonsmokers; in both groups, these responses were suppressed by FP.
In allergic asthma, smokers and nonsmokers have similar allergen-induced LARs at the end of a week of ICS therapy, compared to placebo. However, attenuation of the LAR in smokers is only partly explained by the effects of ICS. Further study is needed to clarify the significance of the observed reduction of the LAR in smokers during placebo treatment.
Comment: This study is the first to evaluate the effects of smoking status on the efficacy of ICS in the allergen-induced asthmatic response. The allergen-induced LAR was similar in amplitude between smokers and nonsmokers. However, smokers also had marked attenuation of the LAR compared to nonsmokers when on placebo. Why this reduction in LAR occurred in the smoking subset is an interesting question. The authors examined several other parameters and found that the smoking group also had lower baseline exhaled NO and sputum eosinophil count. Thus immunologic changes associated with smoking in allergic asthma patients might explain the reduction in LAR. More work is needed in this arena; however, I am not prepared to recommend that asthmatic patients begin smoking.
Keywords: asthma (adult), inhaled corticosteroids, smoking