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Allergen inhalation challenge in smoking compared with non-smoking asthmatic subjects

Authors

  • Z. Meghji,

    1. Firestone Institute for Respiratory Health, St. Joseph's Hospital and Department of Medicine, McMaster University, Hamilton, Ontario, Canada
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  • B. Dua,

    1. Firestone Institute for Respiratory Health, St. Joseph's Hospital and Department of Medicine, McMaster University, Hamilton, Ontario, Canada
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  • R. M. Watson,

    1. Firestone Institute for Respiratory Health, St. Joseph's Hospital and Department of Medicine, McMaster University, Hamilton, Ontario, Canada
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  • G. M. Gauvreau,

    1. Firestone Institute for Respiratory Health, St. Joseph's Hospital and Department of Medicine, McMaster University, Hamilton, Ontario, Canada
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  • P. M. O'Byrne

    1. Firestone Institute for Respiratory Health, St. Joseph's Hospital and Department of Medicine, McMaster University, Hamilton, Ontario, Canada
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Correspondence:
Dr. Paul O'Byrne, MB, HSC 3W10, McMaster University, 1200 Main St West, Hamilton, Ontario, Canada L8N 3Z5. E-mail: obyrnep@mcmaster.ca

Summary

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.

Cite this as: Z. Meghji, B. Dua, R. M. Watson, G. M. Gauvreau and P. M. O'Byrne, Clinical & Experimental Allergy, 2011 (41) 1084–1090.

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