Ethane is a product of lipid peroxidation as a result of oxidative stress and can be detected in the exhaled air. Oxidative stress plays a role in the pathogenesis of asthma. We measured exhaled ethane in 26 asthmatic subjects (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 discarding dead space air contaminated with ambient air. A sample of the expired air was analyzed by chromatography. Exhaled ethane levels were elevated in asthma patients not receiving steroid (n = 12, 2.06 ± 0.30 ppb) compared with steroid-treated patients (n = 14, 0.79 ± 0.10 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 exhaled ethane and NO (r = 0.55, p < 0.05) and air trapping assessed by the ratio 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 steroid-treated patients (8.6 ± 0.5 ppb, p < 0.05). Exhaled ethane is elevated in asthma, reduced in steroid-treated patients, and correlates with NO and airway obstruction. It may be a useful noninvasive marker of oxidative stress.
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