Environmental risk factors in atopic asthma

Abstract

The evidence that asthma is increasing in prevalence is compelling. This trend has been demonstrated not only in the US, but also in the UK, New Zealand, Australia and several other Western countries. The causes of this increase are not known, but both indoor and outdoor air pollution are potential contributory factors. Although there is no convincing evidence to implicate air pollutants in the increased prevalence of asthma, the pathophysiology of this disease provides a basis to identify asthmatics as a subpopulation potentially sensitive to the effects of environmental pollutants. This contention is supported by both clinical and epidemiological studies. Epidemiologic studies of hospital admissions for asthma have implicated O3, the major component of photochemcial smog 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 exposures compared to healthy adults. However, a possible role of O3 in worsening atopic asthma has recently been suggested in studies combining allergen challenges following exposure to O3. Attempts at identification of factors that predispose asthmatics to responsiveness to NO2 have produced inconsistent results and thus further investigation is required. In summary, asthmatics have been shown to be a sensitive population relative to O3 and possibly other air pollutants. Further research linking epidemiologic, clinical, and toxicologic approaches is required to better understand and characterize the risk of exposing asthmatics to these pollutants.