Abstract Production of nitric oxide (NO) is generally increased during inflammatory diseases including asthma. The eventual fate of NO is oxidation to nitrite (NO 2) and nitrate (NO 3), both of which are end-products of NO metabolism. Hydrogen Peroxide (H 2O 2) 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 NO 2/NO 3concentration and H 2O 2levels 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 (FEV 1) 91(10)% predicted, PD 20to 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, FEV 1101 (14)% predicted, PD 20to histamine 1·3 (0·55) mg]. NO 2/NO 3levels were significantly higher in patients with asthma than in normal subjects (1·08, 95% CI 0·86–1·3 μ M vs. 0·6; 95% CI 0·46–0·8, P <0·001). Patients who were on inhaled steroids had significantly lower values compared to steroid-naive (0·71, 95% CI 0·55–0·87 μ M vs. 133, 95% CI 1–1·65 μ M , P<0·001). Similar results were observed between smokers and non-smokers (1·11, 95% CI 0·74–1·47 μ M vs. 1·77, 95% CI 1·1–2·4 μ M , P <0·0001). There was a significant positive correlation between NO 2/NO 3levels and H 2O 2concentration in expired breath condensate ( r=0·48, P<0·0001). No correlation was observed between NO 2/NO 3levels, airway obstruction and bronchial hyper-reactivity as assessed by PD 20to histamine. Total NO 2/NO 3levels in expired breath condensate are raised in patients with stable asthma and are significantly related to oxidative stress as assessed by H 2O 2concentration. Measurement of expired breath NO 2/NO 3and H 2O 2levels may be clinically useful in the management of oxidation and inflammation mediated lung injury.