Epidemiological evidence suggests that an increase in liquid petroleum
derived pollutants is associated with exacerbation of allergic airway
disease, and that the effects of pollution may occur 1-2 days later.
Laboratory based studies have demonstrated that the pollutants respons
ible for the adverse effects on respiratory health include nitrogen di
oxide (NO2), sulphur dioxide (SO2), ozone (O-3) and respirable particu
lates (PM(10)). More recently, studies of asthmatic individuals expose
d to O-3, NO2 and a combination of NO2 and SO2 have indicated that the
se agents increase the airway responsiveness of these individuals to i
nhaled allergen, and that this effect may be maximal 24 h after exposu
re to the pollutants. Studies investigating the putative mechanisms un
derlying the effects of these pollutants suggest that exposure to thes
e agents may lead to perturbation of the airway epithelium and release
of pro-inflammatory mediators from the epithelial cells, which then i
nfluence the activity of inflammatory cells, such as eosinophils.