A wealth of evidence suggests that allergic diseases such as rhinitis, bronchial asthma and atopic dermatitis 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 nitric oxides (NOx), ozone (03), and respirale particulate (PMI0), may be linked to the increased prevalence of allergic diseases. 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. Despite all these evidences, there is still much to be learned about the causal relationship between allergic diseases and air pollution. The future challenge is to tackle the complex interplay between environmental factors and genetic determinants that will eventually contribute to a better understanding and to better prevention strategies for such multifactorial conditions as asthma and allergies.