Respiratory allergic diseases (rhinitis, rhinosinusitis, bronchial asthma and its equivalents) appear to be increasing in most countries and subjects living in urban and industrialized areas are more likely to experience respiratory allergic symptoms than those living in rural areas. This increase has been linked, among various factors, to air pollution, which is now an important public health hazard. Laboratory studies confirm the epidemiologic evidence that inhalation of some pollutants, either individually or in combination, adversely affect lung function in asthmatics. The most abundant air pollutants in urban areas with high levels of vehicle traffic are respirable particulate matter, nitrogen dioxide and ozone. In particular ozone, respirable particulate matter and allergens impair lung function and lead to increased airway, responsiveness and bronchial obstruction in predisposed subjects. However, besides acting as irritants, airborne pollutants can modulate the allergenicity of antigens carried by airborne particles. By attaching to the surface of pollen grains and of plant-derived paucimicronic particles, pollutants can modify the morphology of these antigen-carrying agents and alter their allergenic potential. In addition, by inducing airway inflammation, which increases airway epithelial permeability, pollutans overcome the mucosal barrier and so facilitate the allergen-induced inflammatory responses. Experimental studies have shown that diesel exhaust particulate (DEP) can modify the immune response in predisposed animals and humans. Indeed, DEP increases in vivo IgE and cytokine production at the human respiratory mucosa thereby inducing allergic inflammation of the respiratory airway and the subsequent development of clinical respiratory symptoms. All these results implicate DEP in the enhanced allergic inflammatory response Pollen allergy is a useful model with which to study of the relationship between air pollution and respiratory allergic diseases. It has been suggested that air pollutants promote airway sensitisation by modulating the allergenicity of airborne allergens. Furthermore, airway mucosal damage induced by air pollution may facilitate the access of inhaled allergens to the cells of the immune system. Several factors can influence this interaction: type of air pollutant, plant species, climatic factors, degree of airway sensitisation and hyperresponsiveness of exposed subjects. However, the role of climatic factors such as barometric pressure, temperature and humidity in triggering and/or exacerbating respiratory allergic symptoms is still poorly understood.