The role of air pollution in asthma

: Laboratory studies have clearly shown that inhalation of SO2 by asthmatics can cause a significant degree of wheezing at concentrations considerably lower than those which affect non-asthmatics. Concentrations as low as 0.2 p.p.m. have a significant effect, especially in subjects who are mouth breathing or undergoing heavy exercise. The effects of SO2 appear to be short-lived and not increased by more prolonged exposure (10 min versus 1 hr). WHO air quality guidelines on levels of SO2 have been based to a large extent on these studies and are set at or just below the reported threshold for effects on at risk groups. Thus the 1 hr recommended maximum is 0.16 p.p.m. (350 micrograms/m3). These guidelines have been exceeded in the U.K. on many occasions in the recent past [2] suggesting that asthmatics are at risk in high pollution areas from SO2 induced exacerbations of their asthma. This is particularly true considering that virtually all the laboratory studies have been performed on mild asthmatics. The effects on moderate and severe asthmatics, or those with marked lability of their asthma, could conceivably be seen at much lower concentrations of SO2. Similarly O3 can cause impairment in lung function at concentrations frequently detected in ambient air in the U.K. in both asthmatics and non-asthmatics with no evidence of an increased effect on asthmatics. This appears to be a restrictive rather than an obstructive defect. Ozone can also cause an increase in airways responsiveness to both non-specific bronchoconstrictors such as histamine and specific allergen. Both these effects are likely to be due to the pro-inflammatory effects of ozone and as such could be implicated both in exacerbating asthma through increased airway responsiveness and causing asthma through triggering an inflammatory reaction in the airways. No study has addressed the important question as to whether the incidence of bronchial hyperresponsiveness is increased in areas of high ozone pollution. The results with NO2 in the laboratory are equivocal. On balance the evidence suggests that any effect on asthmatics is likely to be small. Similarly while inhalation studies with acid aerosols have demonstrated some impairment in lung function in asthmatics the changes have been small and of brief duration. Laboratory studies while raising the level of suspicion and allowing dose response curves to be calculated cannot accurately mimic the effects of real air pollution with its combination of interacting circumstances and effects of prolonged exposure.(ABSTRACT TRUNCATED AT 400 WORDS)