Exhaled ethane is elevated in cystic fibrosis and correlates with carbon monoxide levels and airway obstruction

Ethane is produced from lipid peroxidation and can be measured in the exhal ed air. Cystic fibrosis (CF) is characterized by recurrent respiratory infe ctions, release of reactive oxygen species by inflammatory cells, and incre ased oxidative stress. We measured exhaled ethane in 23 CF subjects (mean a ge +/- SEM, 21 +/- 4 yr; 10 male, FEV1 62 +/- 4%) and compared it with two other noninvasive markers of oxidative stress and inflammation, carbon mono xide (CO) and nitric oxide (NO). Exhaled ethane was collected during a flow and pressure-controlled exhalation into a reservoir discarding dead space air contaminated with ambient air. A sample (2 ml) of the expired air was a nalyzed by chromatography. Ethane levels were elevated in patients not on s teroids (n = 13, 1.99 +/- 0.20 ppb) compared with steroid-treated patients (n = 10, 0.67 +/- 0.09 ppb, p < 0.01) and with 14 nonsmoking control (8 men , age 33 +/- 2.8 yr) subjects (0.82 +/- 0.40 ppb, p < 0.05). In patients no t on steroid treatment ethane was correlated to airway obstruction as asses sed by the ratio of residual volume to total lung capacity (RV/ TLC) (r = 0 .66, p < 0.05) and exhaled CO (r = 0.65, p < 0.05). CO concentrations were also higher in patients not on steroid treatment (3.4 +/- 0.2 ppm) than in steroid-treated patients (2.6 +/- 0.1 ppm, p < 0.05), whereas NO concentrat ions were not influenced by steroid treatment (3.0 +/- 0.4 ppm and 2.9 +/- 0.2 ppm, p > 0.05) and were lower than in a control group (7.0 +/- 0.4 ppb, p < 0.05). Exhaled ethane is elevated in CF, reduced in steroid-treated pa tients and correlates with CO and RV/TLC; therefore, it may be a useful non invasive marker of oxidative stress.