The effect of smoking cessation on airway inflammation in young asthma patients
Smoking has been shown to have several detrimental effects on asthma, including poor symptom control, attenuated treatment response and accelerated decline in lung function. In spite of this, smoking is at least as common among asthma patients as in the rest of the population. The aggravations of smoking on asthma may be caused by effects on airway inflammation, which has been found to be changed in asthmatic smokers. It is not known whether these smoking-induced airway inflammation changes are reversible after smoking cessation.
The aim of this study was to assess airway changes in asthmatic smokers before and during smoking cessation.
Forty-six smokers with asthma, all steroid-free (age range: 19–40), were recruited. All participants attempted smoking cessation over a period of 3 months. Visits were performed at weeks 0, 6 and 12 and included induced sputum, FeNO, methacholine challenge, lung function, Asthma Control Questionnaire (ACQ6) and exhaled CO.
Twenty-six of 46 patients succeeded in quitting smoking. In the quitters, improvements in methacholine AHR (77% before and 52% after smoking cessation, respectively, P = 0.016) and ACQ6 score (1.7–0.7, P = 0.034) and FeNO (8.7–14.8 p.p.b., P = 0.002) were observed, whereas no significant changes were found regarding eosinophils or lung function. A small but significant decrease in neutrophils (54.1–52%, P = 0.003) was present in quitters compared with the non-quitters. Non-quitters experienced no changes in any parameters.
Smoking cessation improved asthma control, but the changes were not related to change in eosinophilic inflammation, and the reduction in neutrophils was small. Thus, airway inflammation with eosinophils and neutrophils may be less important drivers of asthma control in smokers than other factors.
Smoking cessation may improve clinically important disease parameters such as AHR and symptom score, but likely unrelated to changes in airway inflammation.