COMMENTARY

Impact of Tobacco Smoke on Allergic Airway Disease

Mark T. O'Hollaren, MD

Disclosures

September 25, 2006

Challenge With Environmental Tobacco Smoke Exacerbates Allergic Airway Disease in Human Beings

Diaz-Sanchez D, Rumold R, Gong H
J Allergy Clin Immunol. 2006;118:441-446

These authors point out that there has been a troubling increase in the prevalence of allergic airway diseases over the last 200 years. There have been a number of possible explanations for this observation, none of which has emerged as the most likely culprit. The increase in the prevalence of allergic disease may also be the result of a combination of factors. Explanations proposed for this trend include exposure to indoor and outdoor pollution, dietary factors, childhood infections, allergen levels (such as dog, cat, and dust mite), and other factors.

This randomized, placebo-controlled, crossover study used 19 nonsmoking volunteers with ragweed allergy who underwent nasal lavage followed by controlled exposure to either environmental tobacco smoke (ETS) or clean air in a challenge chamber. The subjects randomly received immediate nasal challenge with either ragweed allergen or placebo. They then performed nasal lavage at 10 minutes, 24 hours, and 4 and 7 days after the exposure. Immunoglobulin E (IgE), cytokines, and histamine were then measured. Subsequent challenges were spaced at least 6 weeks after the first challenge.

The authors found that ETS promoted the production of IgE in nasal lavage fluid. Four days following the exposure to ETS and ragweed, IgE levels were on average 16.6-fold higher in those exposed to ETS/ragweed compared with those exposed to plain air and ragweed. The ETS/ragweed combination also promoted a TH2 cytokine milieu compared with the air/ragweed combination. The authors concluded that this study provides the first experimental evidence that secondhand smoke can exacerbate allergic responses in humans concomitantly exposed to allergens.

Secondhand cigarette smoke amplifies the response to inhaled allergen in this setting, and presumably in other settings as well. Of particular concern is the fact that the allergic antibody, IgE, is over 16-fold higher in nasal lavage fluid despite only 2 hours of exposure a full 4 days earlier. The implications of this findings on the risk of allergic response amplification are significant, particularly for those who work around secondhand smoke for 8 or more hours a day.

Abstract

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