Mechanisms of pollution-induced allergy and asthma

Evidence from a number of epidemiological and exposure chamber studies suggests that an increase in air pollutants, such as ozone (O3), oxides of nitrogen (NOx), respirable particulates (PM10) and volatile organic chemicals (VOCs), resulting from increased use of liquid petroleum gas or kerosene, may be linked to an increase in the prevalence of allergic disease, particularly in the developed countries. Several studies have indicated that there is an association between hospital emergency room visits due to asthma and increased air pollution. Studies from Japan and Germany have demonstrated that there is a significant association between increased vehicle exhaust pollution and increased incidence of rhino-conjunctivitis and hay-fever. Exposure chamber studies have shown that acute inhalation of air pollutants such as O3, nitrogen dioxide (NO2) and sulphur dioxide (SO2), either individually or in combination, may increase the airway response to inhaled allergen in atopic asthma. Studies investigating the mechanisms underlying pollution-induced pathogenesis of allergic airways disease have demonstrated that there is an association between air pollutants and an increase in mean total/specific serum IgE level and increased positive skin reactions. Bronchial and nasal lavage studies have shown that O3 and NO2 can induce significant increase in epithelial damage and permeability, an influx of inflammatory cells and release of pro-inflammatory cytokines into the respiratory tract. We have shown that exposure of human bronchial epithelial cells to NO2, O3, diesel exhaust particles (DEP) and cigarette smoke (CS), in vitro, leads to significant epithelial cell dysfunction and significant release of proinflammatory cytokines such as interleukin-8 (IL-8), tumour necrosis factor-α (TNF-α), granulocytemacrophage colony stimulating factor (GM-CSF) and regulated on activation, normal T-cell expressed and secreted (RANTES). We have also shown that epithelial cells of atopic individuals release significantly greater amounts of these cytokines. The epidemiological and direct in vivo and in vitro exposure studies presented in this paper provide evidence that exposure to pollutants precipitate attacks of asthma and may also be one of several causes of the increase in the prevalence of this disorder. The mechanisms by which pollutants exert their effect are likely to be direct and dose-dependent actions on epithelial cells leading to changes in permeability and generation of pro-inflammatory mediators including cytokines.