The evidence that asthma is increasing in prevalence is compelling. Th
is trend has been demonstrated not only in the US, but also in the UK,
New Zealand, Australia and several other Western countries. The cause
s of this increase are not known, but both indoor and outdoor air poll
ution are potential contributory factors. Although there is no convinc
ing evidence to implicate air pollutants in the increased prevalence o
f asthma, the pathophysiology of this disease provides a basis to iden
tify asthmatics as a subpopulation potentially sensitive to the effect
s of environmental pollutants. This contention is supported by both cl
inical and epidemiological studies. Epidemiologic studies of hospital
admissions for asthma have implicated O-3, the major component of phot
ochemcial smog as contributing to the exacerbation of asthma; however,
most study designs could not separate the O-3 effects from the concom
itant effects of acid aerosols and SO2. Controlled human clinical stud
ies have suggested that asthmatics have similar changes in spirometry
and airway reactivity in response to O-3 exposures compared to healthy
adults. However, a possible role of O-3 in worsening atopic asthma ha
s recently been suggested in studies combining allergen challenges fol
lowing exposure to O-3 Attempts at identification of factors that pred
ispose asthmatics to responsiveness to NO2 have produced inconsistent
results and thus further investigation is required. In summary, asthma
tics have been shown to be a sensitive population relative to O-3 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.