Ja. Nightingale et al., Effect of inhaled ozone on exhaled nitric oxide, pulmonary function, and induced sputum in normal and asthmatic subjects, THORAX, 54(12), 1999, pp. 1061-1069
Background-Nitric oxide (NO) may have a role in the pathophysiology of tiss
ue injury in response to inhaled ozone in animals.
Methods-A double blind, randomised, placebo controlled, crossover study was
undertaken to investigate the effects of inhaled ozone in 10 normal and 10
atopic asthmatic volunteers. Subjects were exposed to 200 ppb ozone or cle
an air for four hours with intermittent exercise, followed by hourly measur
ement of spirometric parameters and exhaled NO for four hours. Nasal NO and
methacholine reactivity were measured and exhaled breath condensate and in
duced sputum samples were collected four and 24 hours after exposure.
Results-Exposure to ozone caused a fall in forced expiratory volume in one
second (FEV,) of 7% in normal subjects (p<0.05) and 9% in asthmatic subject
s (p<0.005). There was a 39% increase in sputum neutrophils at four hours i
n normal subjects (p<0.05) and a 35% increase at four hours in asthmatic su
bjects, remaining high at 24 hours (p<0.005 and p<0.05, respectively). Ther
e were no differences between normal and asthmatic subjects. There were no
changes in methacholine reactivity, exhaled or nasal NO, nitrite levels in
exhaled breath condensate, or sputum supernatant concentrations of interleu
kin 8, tumour necrosis factor a, or granulocyte-macrophage colony stimulati
ng factor in either group.
Conclusions-Exposure to 200 ppb ozone leads to a neutrophil inflammatory re
sponse in normal and asthmatic subjects but no changes in exhaled NO or nit
rite levels.