We hypothesized that ozone, a common air pollutant, potent in producing air
way inflammation, would increase the production of exhaled nitric oxide (NO
). If so, measurement of exhaled NO;could potentially be a valuable tool in
population studies of air pollution effects.
Eleven healthy non-smoking volunteers were exposed to 0.2ppm ozone (O-3) an
d filtered air for 2h on two separate occasions. Exhaled NO and nasal NO we
re measured before and on five occasions following the exposures. Changes i
n exhaled and nasal NO after ozone exposure were adjusted for changes after
air exposure.
There was a slight decrease in exhaled NO (-0.6; - 3.1-1.2 ppb) (median and
95% confidence interval) and of nasal NO (- 57; - 173-75 ppb) directly aft
er the ozone exposure. No significant changes in exhaled or nasal NO were h
owever found 6 or 24 h after the exposure.
Within the examined group, an O-3 exposure level proven to induce an airway
inflammation caused no significant changes in exhaled or nasal NO levels.
Hence, the current study did not yield support for exhaled NO as a useful m
arker of ozone-induced oxidative stress and airway inflammation after a sin
gle exposure. This contrasts with data for workers exposed to repeated high
peaks of ozone. The potential for exhaled NO as a marker of oxidative stre
ss therefore deserves to be further elucidated.