Volume 118, Issue 2 , Pages 441-446, August 2006
Challenge with environmental tobacco smoke exacerbates allergic airway disease in human beings
Background
Despite widespread perceptions that environmental tobacco smoke (ETS) is a potent risk factor for allergic airway disease, epidemiologic studies studying this have been equivocal. There is a clear need for experimental studies to address these questions.
Objective
We directly tested the hypothesis that ETS could interact with allergen in human beings to alter immune responses and promote changes associated with allergic airway disease.
Methods
In a randomized, placebo-controlled crossover study, 19 nonsmoking volunteers with ragweed allergy underwent nasal lavage followed by controlled chamber exposures to 2 hours ETS or clean air followed by another nasal lavage. Subjects immediately randomly received nasal challenge with either ragweed allergen or placebo (300 μL saline). Lavages were also performed 10 minutes, 24 hours, and 4 and 7 days after challenge and IgE, cytokines, and histamine measured. The other arms of the study were spaced at least 6 weeks apart.
Results
Environmental tobacco smoke promoted the production of allergen-specific IgE, the hallmark of allergic disease in nasal lavage fluid. Four days after exposure to ETS/ragweed, levels were on average 16.6-fold higher than after clean air/ragweed challenge. In addition, ETS (vs air) promoted the induction of a TH2-cytokine nasal milieu (increased IL-4, IL-5, and IL-13 and decreased IFN-γ production), characteristic of an active allergic response. Moreover, nasal histamine levels were 3.3-fold greater after ETS/ragweed challenge than after clean air/ragweed challenge.
Conclusion
These studies provide the first experimental evidence that secondhand smoke can exacerbate allergic responses in human beings.
Clinical implications
The studies suggest that patients with allergies should avoid tobacco smoke.
Key words: Environmental tobacco smoke, IgE, pollution, histamine, allergic airway disease
Abbreviations used: DEP, Diesel exhaust particle, ETS, Environmental tobacco smoke, PM, Particulate matter
Supported by National Institute of Environmental Health Sciences 1PO1 ES09581-01 and US Environmental Protection Agency #R826708-01-0.Disclosure of potential conflict of interest: The authors have declared that they have no conflict of interest.
PII: S0091-6749(06)00942-0
doi:10.1016/j.jaci.2006.04.047
© 2006 American Academy of Allergy, Asthma and Immunology. Published by Elsevier Inc. All rights reserved.
Volume 118, Issue 2 , Pages 441-446, August 2006
