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pubmed:abstractText |
The evidence that asthma is increasing in prevalence is becoming increasingly compelling. This trend has been demonstrated not only in the United States, but also in the United Kingdom, New Zealand, Australia, and several other Western countries. In the United States, the increase is largest in the group under 18 years of age. There is mounting evidence that certain environmental air pollutants are involved in exacerbating asthma. This is based primarily on epidemiologic studies and more recent clinical studies. The U.S. Clean Air Act of 1970 provides special consideration to the class of outdoor air pollutants referred to as criteria pollutants, including O3, sulfur dioxide (SO2), particulate matter (PM), NOx, CO, and Pb. Standards for these pollutants are set by the U.S. Environmental Protection Agency with particular concern for populations at risk. Current evidence suggests that asthmatics are more sensitive to the effects of O3, SO2, PM, and NO2, and are therefore at risk. High SO2 and particulate concentrations have been associated with short-term increases in morbidity and mortality in the general population during dramatic air pollution episodes in the past. Controlled exposure studies have clearly shown that asthmatics are sensitive to low levels of SO2. Exercising asthmatics exposed to SO2 develop bronchoconstriction within minutes, even at levels of 0.25 ppm. Responses are modified by air temperature, humidity, and exercise level. Recent epidemiologic studies have suggested that exposure to PM is strongly associated with morbidity and mortality in the general population and that hospital admissions for bronchitis and asthma were associated with PM10 levels. In controlled clinical studies, asthmatics appear to be no more reactive to aerosols than healthy subjects. Consequently, it is difficult to attribute the increased mortality observed in epidemiologic studies to specific effects demonstrated in controlled human studies. Epidemiologic studies of hospital admissions for asthma have implicated O3 as contributing to the exacerbation of asthma; however, most study designs could not separate the O3 effects from the concomitant effects of acid aerosols and SO2. Controlled human clinical studies have suggested that asthmatics have similar changes in spirometry and airway reactivity in response to O3 exposure compared to healthy adults. However, a possible role of O3 in worsening atopic asthma has recently been suggested in studies combining allergen challenge following exposure to O3. Attempts at identification of factors that predispose asthmatics to responsiveness to NO2 has produced inconsistent results and requires further investigation. In summary, asthmatics have been shown to be a sensitive subpopulation relative to several of the criteria pollutants. Further research linking epidemiologic, clinical, and toxicologic approaches is required to better understand and characterize the risk of exposing asthmatics to these pollutants.
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