INCREASED HYDROGEN-PEROXIDE AND THIOBARBITURIC ACID-REACTIVE PRODUCTSIN EXPIRED BREATH CONDENSATE OF ASTHMATIC-PATIENTS

Symptoms of bronchial asthma are a manifestation of airway inflammatio n, Circulatory leucocytes (predominantly eosinophils, mast cells and n eutrophils), release inflammatory mediators, including reactive oxygen species, i.e. superoxide anion which is dismutated to hydrogen peroxi de (H2O2) Neutrophils from asthmatics generate greater amounts of thes e species than those of healthy subjects, Some of the H2O2 and thiobar bituric acid-reactive products (TBARs) can evaporate from alveolar lin ing fluid, and could be expired from the airways of asthmatics, In thi s study, therefore, we determined whether asthmatic patients exhale mo re H2O2 and TBARs than healthy subjects. We examined 10 healthy subjec ts as a control group and 21 asthmatic subjects, In asthmatic subjects , forced expiratory volume in one second (FEV1), was 68+/-9% of predic ted value, peak expiratory flow rate (PEFR) was 65+/-8% pred, and bron chial reversibility was 34+/-5% of prebronchodilated FEV1, The mean H2 O2 level measured spectrofluorimetrically in the expired breath conden sate of asthmatic subjects was 26 fold higher than that in healthy con trols (0.26+/-0.29 vs 0.01+/-0.03 nM; p<0.05), The concentration of TB ARs in breath condensate was also higher in asthmatic patients compare d with nonasthmatics (0.073+/-0.071 vs 0.004+/-0.009 nM; p<0.05), Ther e was a significant correlation between H2O2 level and concentration o f TBARs in asthmatic patients (r=0.74; p<0.01), There was also a stron g inverse correlation between H2O2 content of all asthmatics and FEV1% pred (r= -0.63; p<0.005) and PEFR% pred (r= -0.52; p<0.05). We conclu de that there are elevated levels of hydrogen peroxide and thiobarbitu ric acid-reactive products in expired breath condensate of asthmatic p atients, and that measurement of these substances in the expired breat h condensate could be a simple, noninvasive method that could be used as a biochemical marker of airway inflammation.