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 microL 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.