| pubmed-article:12619373 | pubmed:abstractText | 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 etiologic 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), oxides of nitrogen (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 disease which can be aggravated by inhaled compounds, health effects of air pollutants have received attention. In fact various studies have demonstrated that inhalation of air pollutants such as O3, nitrogen dioxide (NO2) and sulphur dioxide (SO2), either individually or in combination, can enhance the airway response to inhaled allergens in atopic subjects inducing asthma exacerbations. Moreover, experimental studies have shown that diesel exhaust particulate (DEP) causes respiratory symptoms and is able also to modulate the immune response by increasing immunoglobulin (Ig)E 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 so prime allergen-induced responses. However, air pollution and climatic changes may also have an indirect effect on the allergic response by influencing quantitatively and qualitatively the pollen production of allergenic plants. | lld:pubmed |
