Abstract
Recent epidemiological evidence suggests that air pollution, resulting from vehicle exhaust emissions and burning of liquid petroleum gas or kerosene, may play an important role in the development of allergic airways disease. Further, agents such as O3 and NO2 are thought to be major proponents of disease and act by damaging the airway epithelium. It is hypothesised that this pollution-induced damage results in the generation of mediators which lead to inflammation and possibly airway hyperreactivity.
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