Study objectives: To quantify lung oxidative stress in asthmatic children by measuring concentrations of 8-isoprostane, a marker of oxidative stress, in exhaled breath condensate (EBC), which is a noninvasive method of sampling airway secretions. Secondary objectives were as follows: (1) to measure levels of exhaled prostaglandin (PG) E2, since impaired PGE2 production has been implicated in the pathogenesis of asthma in adults; and (2) to measure levels of fractional exhaled nitric oxide (FeNO), which is a marker of airway inflammation.
Design: Single-center, cross-sectional study.
Patients: Twelve healthy children, 12 steroid-naïve asthmatic children, and 30 children in stable condition with mild-to-moderate persistent asthma who were being treated with inhaled corticosteroids (ICSs) [average dose, 300 μg per day] were studied.
Interventions: Subjects attended the outpatient clinic on one occasion for the collection of EBC and FeNO measurements.
Measurements and results: 8-Isoprostane and PGE2 concentrations in EBC were measured with specific radioimmunoassays. FeNO was measured online by a chemiluminescence analyzer. 8-Isoprostane was detectable in the EBC of healthy children (mean [± SEM], 34.2 ± 4.5 pg/mL), and its concentrations were increased in both steroid-naïve asthmatic children (mean, 56.4 ± 7.7 pg/mL; p < 0.01) and steroid-treated asthmatic children (mean, 47.2 ± 2.3 pg/mL; p < 0.05). There was no difference in exhaled 8-isoprostane concentrations between the two groups of asthmatic children (p = 0.14). By contrast, exhaled PGE2 concentrations were similar among the three study groups (p = 0.56). FeNO levels were higher in steroid-naïve children with asthma (49.2 ± 9.6 parts per billion [ppb]; p < 0.05) and, to a lesser extent, in steroid-treated asthmatic children (37.8 ± 6.6 ppb; p < 0.05) compared with healthy children (15.2 ± 1.7 ppb).
Conclusions: Lung oxidative stress is increased in children who are in stable condition with asthma, as reflected by increased exhaled 8-isoprostane concentrations. This increase seems to be relatively resistant to treatment with ICSs. Decreased PGE2 lung production is unlikely to play a pathophysiologic role in childhood asthma.