Fractionated exhaled breath condensate collection shows high hydrogen peroxide release in the airways

摘要

Background: Exhaled breath condensate (EBC) allows noninvasive monitoring of inflammation in the lung. Activation of inflammatory cells results in an increased production of reactive oxygen species, leading to the formation of hydrogen peroxide (H2O2). In addition, cigarette smoking causes an influx of inflammatory cells, and higher levels of H2O 2 have been found in EBC of smokers. However, there are still unresolved issues reflected by large variations in exhaled H2O 2 and uncertainties about the origin of H2O2 release in the lung. Methods: We collected EBC as fractionated samples from the airways and from the lung periphery in 10 nonsmokers, eight asymptomatic smokers, and in eight chronic obstructive pulmonary disease (COPD) patients, and H2O2 concentration and acidity (pH) were analyzed in the airway and the alveolar fraction. Results: In all subjects studied, H 2O2 was 2.6 times higher in the airway versus the alveolar fraction. Airway H2O2 was twofold higher in smokers and fivefold higher in COPD patients compared to nonsmokers. In all study groups, there was no significant difference in deaerated pH between the airway and the alveolar sample. Conclusions: Exhaled H2O2 is released at higher concentrations from the airways of all subjects studied, implying that the airways may be the dominant location of H2O2 production. Because many lung diseases cause inflammation at different sites of the lung, fractionated sampling of EBC can reduce variability and maintain an anatomical allocation of the exhaled biomarkers.