Given the observed association between smoking, inflammation and airway hyperresponsiveness (AHR) one may predict that smoking cessation may improve AHR. However, only a few studies have investigated the effect of smoking on AHR and their results appear to be conflicting depending on the stimulus used in their bronchoprovocation protocol. The aim of the current study was to compare changes in AHR between direct (methacholine (Mch)) and indirect (adenosine 5′monophosphate (AMP)) stimuli before and at different time points after smoking cessation in smokers with allergic rhinitis (±asthma).

We have prospectively studied changes in AHR to inhaled Mch and AMP in smokers with allergic rhinitis (±asthma), before and at 6 and 12 months after smoking cessation.

It was found that 28% (16/57) of the participants had quit smoking by the end of the study. No significant change in AHR was observed in smoking cessation failures. A significant improvement in AHR to AMP but not Mch was observed 6 months after smoking cessation in quitters; a 1.2 doubling concentrations change in PC₂₀ AMP was measured whereas only a 0.4 doubling concentrations change was observed for PC₂₀ Mch. However, after 12 months smoking cessation the improvement in AHR became significant for both AMP and Mch, their dose–response curves being displaced to the right to a similar extent (1.4 and 1.1 doubling concentrations for AMP and Mch, respectively).

Smoking cessation can improve AHR in smokers who quit with a 6 months improvement being reported for the airways response to AMP but not Mch. AMP challenge may detect earlier changes in AHR in smokers during smoking cessation.