In the U.S., morbidity associated with human rhinovirus (RV) infection represents a major
health problem. In asthmatics, up to 80% of asthma exacerbations are associated with upper
respiratory infections. Despite evidence that environmental oxidant pollutants, such as
ozone, may increase the severity of viral disease, the mechanisms underlying such an effect
have not been identified. This study will test the hypothesis that exposure of allergic
asthmatic subjects to ambient levels of ozone directly enhances viral disease by increasing
infectivity and intensifying virus-induced inflammation.
In mild asthmatics, the study will investigate: (1) if exposure to ozone will enhance the
viral infective process in the nasal epithelium, (2) the effect of ozone exposure on
RV-induced inflammatory gene expression, mediator release and inflammatory cell influx into
the upper and lower airways, and (3) the interactive effects of ozone and RV on airway
reactivity. This information will improve our understanding of the risk associated with
oxidant pollutant exposure in this population of individuals in whom RV infection may
represent a significant health concern.
Subjects recruited will be non-asthmatic controls or mild allergic asthmatics using
beta-agonists, mostly on an "as needed" basis. Selection criteria will include good
general health by medical history and physical examination, no history of smoking, and the
absence of respiratory infection in the preceding 6 week period. Subjects will undergo
serologic testing and must have a negative test for neutralizing antibodies to RV16 to
participate in all but one study of the project.