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. Hydrogen Peroxide (H2O2) is increased in exhaled breath condensate of asthmatic subjects and may be used as a non-invasive 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, forced expiratory volume in 1 sec (FEV1) 91 (10)% predicted, 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, FEV1 101 (14)% predicted, PD20 to histamine 1.3 (0.55) mg]. NO2/NO3 levels were significantly higher in patients with asthma than in normal subjects (1.08, 95% CI 0.86-1.3 microM vs. 0.6; 95% CI 0.46-0.8, P < 0.001). Patients who were on inhaled steroids had significantly ower values compared to steroid-naive (0.71, 95% CI 0.55-0.87 microM vs. 133, 95% CI 1-1.65 microM, P < 0.001). Similar results were observed between smokers and non-smokers (1.11, 95% CI 0.74-1.47 microM vs. 1.77, 95% CI 1.1-24 microM, 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 hyper-reactivity as assessed by PD20 to histamine. Total NO2/NO3 levels in expired breath condensate are raised 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.