From Current Opinion in Allergy and Clinical Immunology
Jump to full article: Medscape, 2009-06-22
Author: Carlos E. Baena-Cagnani; R. Maximiliano Gómez; Rodrigo Baena-Cagnani; G. Walter Canonica
Intro: Summary: Several deleterious effects have been described in asthma because of smoking: accelerated decline in lung function, more severe symptoms, impairment in quality of life and diminished therapeutic response to steroids. The harmful effect of tobacco smoking is not only on asthma but also on rhinitis playing a role in disease outcomes. Tobacco exposure can influence innate immunity diminishing innate production of antigen-presenting cells cytokines, as well as an impaired response to toll-like receptor ligands. Active smoking is associated with current symptoms of asthma and rhinitis and seems to be a risk factor for developing new asthma in patients with rhinitis. Tobacco smoking has been also found among the factors inducing nasal obstruction and decreased muco-ciliary clearance in nonallergic rhinitis. . . .
The early exposure to ETS, both prenatal and postnatal, increases the risk of IgE sensitization to indoor inhalant and, in particular, food allergens[13••,14] and subsequently may have effects on atopy and airway hyperresponsiveness, with the consequent presence of atopic diseases.[15,16]
More studies are needed to gain insight in the relationship between tobacco smoking, ETS and the immune response and inflammatory lower and upper respiratory illnesses. . . .
All these findings suggest tobacco exposure control should be a tool in the management of asthma.
Conclusion
1. Tobacco smoking provokes a strong immunological imbalance to those exposed. The innate immunity is impaired by tobacco exposure.
2. As a consequence, typical allergic diseases such as rhinitis and asthma could initiate or aggravate preexisting conditions or both. Active smoking is a factor for nasal obstruction in NAR.
3. Tobacco smoking (and probably ETS also) has a detrimental effect on the efficacy of inhaled corticosteroids, leukotriene receptor antagonists and on those patients in programs for controlling asthma in deprived populations.
4. Robust evidence is provided in order to empower both primary and secondary prevention by physicians.
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