Exhaled hydrogen peroxide correlates with the release of reactive oxygen species by blood phagocytes in healthy subjects.

Various cells including polymorphonuclear leukocytes, alveolar macrophages and type-II pneumocytes may be a source of exhaled hydrogen peroxide (H2O2) in airways of humans. H2O2 can convert into hydroxyl radicals leading to peroxidative damage of airways structures and formation of volatile thiobarbituric acid-reactive substances (TBARs). We tested whether exhalation of H2O2 and TBARs by healthy subjects depends on reactive oxygen species generation from blood phagocytes. The expired breath condensate (EBC) and blood specimens were collected from 41 healthy, never smoked subjects (mean age 20.7 +/- 0.8 years, 18 men, 23 women) and then the EBC concentration of H2O2 and TBARs and 2 x 10(-5) M fMLP-provoked whole blood chemiluminescence response was measured. The mean concentration of H2O2 and TBARs in EBC was 0.28 +/- 0.17 and 0.04 +/- 0.13 microM with ratio of positive readings reaching 36/41 and 4/41, respectively. The chemiluminescence response to n-formyl-methionyl-leveyl-phenylalanine stimulation was obtained in all cases and the following parameters were estimated: basal chemiluminescence (bCl); peak chemiluminescence (pCl); absolute light emission (aCl); and peaktime. H2O2 levels in EBC positively correlated (Spearmann test) with bCl (r=0.41, P<0.01), pCl (r=0.47, P<0.01), aCl (r=0.49, P<0.001), peaktime (r=0.52, P<0.001) in the whole group and with bCl (r=0.56, P<0.01), pCl (r=0.67, P<0.01), aCl (r=0.66, P<0.01) in men and with aCl (r=0.41, P<0.05) and peaktime (r=0.48, P<0.05) in women. No association between exhaled TBARs and blood phagocytes activity was found. These results indicate that H2O2 exhalation in healthy never smoked subjects depends on ability of blood phagocytes to generate reactive oxygen species.