Abstract

Background Smoking asthmatics experience more severe symptoms, require more rescue medication and have more asthma-related hospitalizations than non-smoking asthmatics. However, studies in mice suggest that mainstream cigarette smoke may reduce airway inflammation and may attenuate airway hyperresponsiveness. A comparison of allergen-induced airway inflammatory responses of smoking and non-smoking atopic asthmatics has not been examined previously.

Objectives To determine whether allergen-induced airway responses and inflammatory profiles are attenuated in smoking when compared with non-smoking mild allergic asthmatic subjects.

Methods Allergen inhalation challenges were performed in 13 smoking and 19 non-smoking mild allergic asthmatic subjects. The forced expired volume in 1 s (FEV1) was measured up to 7 h after allergen inhalation. Methacholine airway responsiveness was measured before and at 24 h after allergen and sputum was induced before and at 7 and 24 h after allergen.

Results Both the smoking and non-smoking groups developed similar allergen-induced falls in FEV1 during the early and late asthmatic responses and similar increases in allergen-induced airway eosinophils. The mean maximum fall in FEV1 during the late response was 16.3±4.3% in non-smokers and 12.9±7.2% in smokers. The smoking asthmatics, however, did not develop allergen-induced methacholine airway hyperresponsiveness, whereas the non-smoking controls developed a 1.18 doubling dose shift in methacholine PC20 (P<0.05).

Conclusions and Clinical Relevance Mild allergic asthmatic subjects, who were current smokers with a mean 6-year pack history, develop allergen-induced eosinophilic airway inflammation and late responses, similar in magnitude to non-smoking asthmatics, but do not develop methacholine airway hyperresponsiveness associated with the allergen-induced airway eosinophilia.

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Comments

This study unexpectedly found that the increase in non-specific reactivity (nsbr) seen after a late asthmatic reaction was absent in mild asthmatics who smoked but present in the non-smokers as expected. A hypothesis presented was that increased CO in smokers may inhibit cGMP in bronchial muscles (as found in mice). However exhaled CO was not measured in this study. Although the challenges in this study were with environmental allergens (mainly ragweed and cat)the finding may account for the lack of nsbr found in about 30% of workers with occupational asthma

7/27/2011