A wealth of evidence suggests that allergic respiratory diseases such as rhinosinusitis and bronchial asthma have become more common worldwide in recent years and a great deal of etiological and pathogenic research has been carried out to evaluate the possible causes of this increasing trend. There is also some evidence that increased atmospheric concentrations of pollutants such as ozone (O3), nitric oxides (NOx), respirable particulate (PM10) and volatile organic chemicals (VOC5), which result from increased use of liquid petroleum gas or kerosene, may be linked to the increased prevalence of allergic diseases which develop more frequently in urban areas of developed countries. Since bronchial asthma is a syndrome which can be aggravated by inhaled compounds, the effects of air pollutants on health have been the focus of attention. In fact, various studies have demonstrated that inhalation of air pollutants such as O3, nitrogen dioxide (NO2) and sulfur dioxide (SO2), either individually or in combination, can enhance the airway response to inhaled allergens in atopic subjects, thus inducing asthma exacerbations. Moreover, experimental studies have shown that diesel exhaust particulate causes respiratory symptoms and is able also to modulate the immune response by increasing IgE synthesis in predisposed animals and humans. There is also some evidence that air pollutants can interact with aeroallergens in the atmosphere and/or on human airways, potentiating their effects. In fact, by inducing airway inflammation which increases epithelial permeability, some pollutants overcome the mucosal barrier and lead to allergen-induced responses. However, air pollution and climatic changes should also have an indirect effect on allergic response by influencing quantitatively and qualitatively the pollen production by allergenic plants.