BACKGROUND: Hydrogen peroxide (H2O2) in exhaled air condensate is elevated in inflammatory disorders of the lower respiratory tract. It is unknown whether viral colds contribute to exhaled H2O2. AIM: To assess exhaled H2O2 during and after a common cold. METHODS: We examined H2O2 in the breath condensate of 20 normal subjects with acute symptoms of a common cold and after recovery 2 weeks later and, similarly, in 10 subjects without infection. H2O2 was measured with a fluorimetric assay. RESULTS: At the time of infection exhaled H2O2 (median, ranges) was 0.20 microM (0.03-1.2 microM), and this decreased to 0.09 microM (< 0.01-0.40 microM) after recovery (p = 0.006). There was no significant difference in lung function (forced vital capacity and forced expiratory volume in 1 sec) during and after colds. In the controls, exhaled H2O2 did not change over a 2-week period. CONCLUSIONS: H2O2 in exhaled air condensate is elevated during a common cold, and returns to normal within 2 weeks of recovery in healthy subjects. Hence, symptomatic upper respiratory tract infection may act as a confounder in studies of H2O2 as a marker of chronic lower airway inflammation.

Exhaled air is saturated with water at 37°C, and cooling causes condensation of this water vapor. Breath condensate can be analyzed for the presence of inflammatory mediators and other putative markers of inflammation, among which are hydrogen peroxide (H(2)O(2)), leukotrienes (LT), prostanoids, thiobarbituric acid reactive products (TBARs), and metabolites of nitric oxide (NO), including nitrites and nitrates. The methodology for these measurements has not been standardized. There is very little, if any, direct evidence that concentrations of substances detected in breath condensate actually reflect their concentration at the level of the intrapulmonary airways. However, studies that have correlated breath condensate findings to the presence and severity of lower airway disease suggest that this might be the case.