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, epiderniologic 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 mu L 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 T(H)2-cytokine nasal milieu (increased IL-4, IL-5, and IL-13 and decreased IFN-gamma 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.