Ethane is a product of lipid peroxidation as a result of oxidative stress a
nd can be detected in the exhaled air. Oxidative stress plays a role in the
pathogenesis of asthma. We measured exhaled ethane in 26 asthmatic subject
s (mean age +/- SEM, 38 +/- 8 yr; 15 male, FEV1 60 +/- 4%) and compared it
with exhaled nitric oxide (NO) measured by chemiluminescence, a noninvasive
marker of oxidative stress and inflammation. Exhaled ethane was collected
during a flow- and pressure-controlled exhalation into a reservoir discardi
ng dead space air contaminated with ambient air. A sample of the expired ai
r was analyzed by chromatography. Exhaled ethane levels were elevated in as
thma patients not receiving steroid (n = 12, 2.06 +/- 0.30 ppb) compared wi
th steroid-treated patients (n = 14, 0.79 +/- 0.70 ppb, p < 0.01) and to 14
nonsmoking control subjects (0.88 +/- 0.09 ppb, p < 0.05). In patients not
receiving steroid treatment there was a positive correlation between exhal
ed ethane and NO (r = 0.55, p < 0.05) and air trapping assessed by the rati
o of residual volume to total lung capacity (RV/TLC) (r = 0.60, p < 0.05).
In addition, untreated patients with FEV1 < 60% predicted value had higher
concentrations of ethane (2.86 +/- 0.37 ppb) compared with less obstructed
patients (FEV1 > 60%, 1.26 +/- 0.12 ppb, p < 0.05). NO concentrations were
higher in patients not on steroid treatment (14.7 +/- 1.7 ppb) than in ster
oid-treated patients (8.6 +/- 0.5 ppb, p < 0.05). Exhaled ethane is elevate
d in asthma, reduced in steroid-treated patients, and correlates with NO an
d airway obstruction. It may be a useful noninvasive marker of oxidative st
ress.