Production of nitric oxide (NO) is generally increased during inflammatory
diseases including asthma. The eventual fate of NO is oxidation to nitrite
(NO2) and nitrate (NO3), both of which are end-products of NO metabolism. H
ydrogen Peroxide (H2O2) is increased in exhaled breath condensate of asthma
tic subjects and may be used as a noninvasive marker of oxidative stress. N
O has in some cases been shown to attenuate oxidant-induced lung injury. To
tal NO2/ NO3 concentration and H2O2 levels were measured in expired breath
condensate in 50 clinically stable asthmatics [all males, all atopics, mean
age 22 (3) SID yrs, forced expiratory volume in I sec (FEVI) 91 (10)% pred
icted, PD20 to histamine 0.262 (0.16) mg 20 on inhaled steroids, 20 smokers
, all Steroid-naive] and in 10 normal, non-atopic subjects [all males, age
23 (4) yrs, FEVI 101 (14)% predicted, PD20 to histamine 1.3 (0-55) mg]. NO2
/NO3 levels were significantly higher in patients with asthma than in norma
l subjects (1.08,95% Cl 0.86-1.3 mum vs. 0.6; 95% Cl 0.46-0.8, P < 0.001).
Patients who were on inhaled steroids had significantly lower values compar
ed to steroid-naive (0.71, 95% Cl 0.55-0.87 mum vs. 133, 95% Cl 1-1.65 pm,
P < 0.001). Similar results were observed between smokers and non-smokers (
1.11. 95% Cl 0.74-1.47 <mu>m vs. 1.77, 95% Cl 1.1 -2.4 mum, P < 0.0001). Th
ere was a significant positive correlation between NO2/NO3 levels and H2O2
concentration in expired breath condensate (r = 0.48, P < 0.0001). No corre
lation was observed between NO2/NO3 levels, airway obstruction and bronchia
l hyper-reactivity as assesed by PD20 to histamine. Total NO2/NO3 levels in
expired breath condensate are raised in patients with stable asthma and ar
e significantly related to oxidative stress as assessed by H2O2 concentrati
on. Measurement of expired breath NO2/NO3 and H2O2 levels maybe clinically
useful in the management of oxidation and inflammation mediated lung injury
. (C) 2001 Harcourt Publishers Ltd.