Symptoms of bronchial asthma are a manifestation of airway inflammation. Circulatory leucocytes (predominantly eosinophils, mast cells and neutrophils), release inflammatory mediators, including reactive oxygen species, i.e. superoxide anion which is dismutated to hydrogen peroxide (H 2 O 2 ). Neutrophils from asthmatics generate greater amounts of these species than those of healthy subjects. Some of the H 2 O 2 and thiobarbituric acid-reactive products (TBARs) can evaporate from alveolar lining fluid, and could be expired from the airways of asthmatics. In this study, therefore, we determined whether asthmatic patients exhale more H 2 O 2 and TBARs than healthy subjects.We examined 10 healthy subjects as a control group and 21 asthmatic subjects. In asthmatic subjects, forced expiratory volume in one second (FEV1), was 68±9% of predicted value, peak expiratory flow rate (PEFR) was 65±8% pred, and bronchial reversibility was 34±5% of prebronchodilated FEV1. The mean H 2 O 2 level measured spectrofluorimetrically in the expired breath condensate of asthmatic subjects was 26 fold higher than that in healthy controls (0.26±0.29 vs 0.01±0.03 nM; p<0.05). The concentration of TBARs in breath condensate was also higher in asthmatic patients compared with nonasthmatics (0.073±0.071 vs 0.004±0.009 nM; p<0.05). There was a significant correlation between H 2 O 2 level and concentration of TBARs in asthmatic patients (r=0.74; p<0.01). There was also a strong inverse correlation between H 2 O 2 content of all asthmatics and FEV1% pred (r= -0.63; p<0.005) and PEFR% pred (r= -0.52; p<0.05).We conclude that there are elevated levels of hydrogen peroxide and thiobarbituric acid-reactive products in expired breath condensate of asthmatic patients, and that measurement of these substances in the expired breath condensate could be a simple, noninvasive method that could be used as a biochemical marker of airway inflammation. Eur Respir J 1997; 10: 1235-1241