EXPIRED BREATH HYDROGEN-PEROXIDE IS A MARKER OF ACUTE AIRWAY INFLAMMATION IN PEDIATRIC-PATIENTS WITH ASTHMA

Citation
Aw. Dohlman et al., EXPIRED BREATH HYDROGEN-PEROXIDE IS A MARKER OF ACUTE AIRWAY INFLAMMATION IN PEDIATRIC-PATIENTS WITH ASTHMA, The American review of respiratory disease, 148(4), 1993, pp. 955-960
Citations number
18
Categorie Soggetti
Respiratory System
ISSN journal
00030805
Volume
148
Issue
4
Year of publication
1993
Pages
955 - 960
Database
ISI
SICI code
0003-0805(1993)148:4<955:EBHIAM>2.0.ZU;2-V
Abstract
Airway inflammation is important in the development and progression of many pulmonary disorders, including asthma. We hypothesized that the hydrogen peroxide (H2O2) concentration in expired breath may be a mark er of airway inflammation. Expired breath condensate was collected by cooling and the H2O2 concentration was measured fluorimetrically Thirt y-five samples were collected from 22 pediatric patients with asthma w ho were 7 to 18 yr of age and from 11 healthy, nonasthmatic controls. Asthmatic subjects were determined to be well or sick (acute disease o f the upper or lower respiratory tract) by clinical examination. Pulmo nary function tests were determined to be abnormal if there was a > 15 % reduction in FEV1 or > 20% reduction in FEF25-75 compared with basel ine values. Expired breath H2O2 was elevated in asthmatic subjects com pared with controls (0.81 +/- 0.70 versus 0.25 +/- 0.27 mumol/L). The difference was primarily due to elevation of H2O2 in sick asthmatic su bjects, whose expired breath H2O2 level of 1.5 +/- 0.5 (n = 10) was di fferent from that of well asthmatics (0.54 +/- 0.56, n = 25). There wa s a high correlation between expired breath H2O2 and clinical status. Elevation of expired H2O2 occurred with either acute upper or lower re spiratory tract disease. There was no statistically significant correl ation between expired breath H2O2 level and pulmonary function test re sults. We conclude that elevation of H2O2 in the expired breath conden sate is a simple, noninvasive method that can be used as a biochemical marker of airway inflammation.