Production of Nitric Οxide (NO) is generally increased during inflammatory diseases, including asthma. The eventual fate of NO is oxidation to nitrite (NO2) and nitrate (NO3), end products of NO metabolism. H2O2 is increased in exhaled breath condensate of asthmatic subjects and may be used as a noninvasive marker of oxidative stress. NO has in some cases been shown to attenuate oxidant-induced lung injury. Total 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) SD yrs, FEV1 91 (10) % pred, PD20 to histamine 0.262 (0,16) pg, 20 on inhaled steroids, 20 smokers all steroid naive] and in 10 normal non atopic subjects [all males, age 23 (4) yrs, FEV1 101 (14)% pred, PD20 to histamine 1.3 (0.55) pg]. NO2/NO3 levels were significantly higher in patients with asthma compared to normal subjects (1.08, 95% Cl 0.86-1.3 μΜ vs 0.6, 95%Cl 0,46-0,8, p <0.001). Patients who were on inhaled steroids had significantly lower values compared to steroid naive (0.71, 95% Cl 0,55-0,87 μΜ vs 1.33, 95% Cl 1-1.65 μΜ, p <0.001). Similar results were observed between smokers and non smokers (1,11, 95% Cl 0.74-1.47 μΜ vs 1.77, 95% Cl 1,1-2,4 μΜ, p <0,0001). There was a significant positive correlation between NO2/NO3 levels and H2O2 concentration in expired breath condensate (r=0,48, p <0,0001). No correlation was observed between NO2/NO3 levels, airway obstruction and bronchial hyperreactivity as assessed by PD20 to histamine. Total NO2/NO3 levels in expired breath condensate are increased in patients with stable asthma and are significantly related to oxidative stress as assessed by H2O2 concentration. Measurement of expired breath NO2/NO3 and H2O2 levels may be clinically useful in the management of oxidation and inflammation mediated lung injury. Pneumon 2001, 14(3):224-231.