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 (H(2)O(2)). In addition, cigarette smoking causes an influx of inflammatory cells, and higher levels of H(2)O(2) have been found in EBC of smokers. However, there are still unresolved issues reflected by large variations in exhaled H(2)O(2) and uncertainties about the origin of H(2)O(2) 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 H(2)O(2) concentration and acidity (pH) were analyzed in the airway and the alveolar fraction.
Results: In all subjects studied, H(2)O(2) was 2.6 times higher in the airway versus the alveolar fraction. Airway H(2)O(2) 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 H(2)O(2) is released at higher concentrations from the airways of all subjects studied, implying that the airways may be the dominant location of H(2)O(2) 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.