[Air pollution and allergic airway diseases].
In the last decades, many studies have shown an increase in the prevalence of allergic rhinitis and asthma mainly in urban communities, especially in industrialized countries. Airborne pollutants such as diesel exhaust particles, ozone, nitrogen dioxide and sulphur dioxide have been implicated in the initiation and exacerbation of allergic airway diseases. Epidemiologic studies have shown clear associations between air pollution and allergic diseases, in vivo and in vitro studies have provided biologic link and potential molecular mechanisms. Particulate and gaseous pollutants can act both on the upper and lower airways to initiate and exacerbate cellular inflammation through interaction with the innate immune system. As a consequence, increased non-specific airway hyper-responsiveness and airway resistance have been observed in man. Diesel exhaust particles can both induce and exacerbate in vivo allergic responses. They can also modify the immune system's handling of the allergen. The effects of gaseous pollutants on immune responses to allergens are not fully understood. We review the different mechanisms involved in the enhancement of allergic inflammation by urban air pollutants, including effects on cytokine and chemokine production, as well as activation of different immune cells. We discuss the hypothesis that pollutants' effects on the immune system involve hierarchical oxidative stress. Susceptibility genes to air pollution inducing allergic diseases are also discussed.
Bonay
Marcel
M
Inserm U700 et Service de Physiologie-Explorations fonctionnelles, Université Paris 7 et Hôpital Bichat-Claude-Bernard, AP-HP, 46, rue Henri Huchard, 75018 Paris, France. marcel.bonay@bch.aphp.fr
Aubier
Michel
M
D000393:Air Pollutants / Q000009:adverse effects / Q000145:classification; D000397:Air Pollution / Q000009:adverse effects*; D000485:Allergens / Q000276:immunology; D000818:Animals; D001249:Asthma / Q000209:etiology / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000209:etiology / Q000503:physiopathology; D004847:Epithelial Cells / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis; D008264:Macrophages / Q000276:immunology; D008407:Mast Cells / Q000276:immunology; D018448:Models, Immunological; D009585:Nitrogen Dioxide / Q000009:adverse effects; D018384:Oxidative Stress; D010126:Ozone / Q000009:adverse effects; D012130:Respiratory Hypersensitivity / Q000453:epidemiology / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D013458:Sulfur Dioxide / Q000009:adverse effects; D001335:Vehicle Emissions
D000393:Air Pollutants; D000485:Allergens; D001335:Vehicle Emissions; D013458:Sulfur Dioxide; D007073:Immunoglobulin E; D010126:Ozone; D009585:Nitrogen Dioxide