- Paper Report
- Open Access
Ethane as a marker of lipid peroxidation
- Michael Habib1
© Biomed Central Ltd 2001
- Received: 18 September 2000
- Accepted: 19 September 2001
- Published: 19 September 2001
Oxidative stress is believed to play a role in the pathogenesis of COPD due to the number of inflammatory cells found in the airways of these patients. Alkanes, pentane and ethane (hydrocarbon byproducts of lipid peroxidation) can be measured in exhaled breath. In this study, the authors not only measure ethane in the exhalate of patients with COPD but measure nitric oxide (NO) and carbon monoxide (CO) as well. They detail a simple single breath method for doing the ethane measurement that is portable and requires little equipment, thus making it acceptable for field tests.
Twenty-two stable, ex-smoking patients with COPD, who did not manifest response to bronchodilators on spirometric testing, were enrolled in the study. Ten of these subjects had received either inhaled steroids or oral steroids over the past 3 months. Fourteen healthy, but admittedly younger, subjects who had never smoked were used as controls. Smoking status of the participants was assessed using a urine test for nicotine.
Flow and pressure controlled exhalation was made into a reservoir, the anatomic dead space gas being discarded. The remaining sample was tested for ethane using gas chromatography. Intra- and extra-session reproducibility was 5.4% and 6.2%, respectively. Ethane concentration was flow dependent, with higher flows yielding lower results. All samples were collected between 10 and 11 LPM. Exhaled CO and NO were measured as usual with appropriate pressure and flow controls.
In the nonsteroid COPD group, there was a negative correlation between exhaled ethane and FEV1 (r = -0.67, P <0.05). Steroid naive subjects had more than twice the ethane in their exhalate as compared to controls (2.77 ± 0.25 vs 0.88 ± 0.009 ppb: P <0.05). The steroid treated patients had ethane levels of 0.48 ± 0.05 (P <0.01 vs steroid naive). CO levels between steroid (5.99 ± 0.50 ppm) and nonsteroid treated (5.96 ± 0.63 ppm) were similar, but the controls were lower (2.88 ± 0.2 ppm: P <-0.05). The NO values for nonsteroid patients and steroid patients were 11.86 ± 1.27 and 9.11 ± 0.53 ppb, respectively (not significant). These values were higher than for the controls (6.7 ± 0.5 ppb, P <0.05).
The elevated ethane levels in patients with COPD correlated negatively with degree of obstruction as measured by FEV1. In addition, steroid treatment reduced the ethane exhaled. These data suggest that ethane is a marker for airway inflammation and oxidative stress in patients with COPD. The failure of steroids to reduce NO and CO may relate to the lack of a steroid suppressive effect on neutrophils or the lack of eosinophilic inflammation. CO and NO may only be indirect measures of oxidative stress. Ethane on the other hand directly measures lipid peroxidative activity. Combined use of these three gases may be needed in order to better define the presence of ongoing inflammation in the airway which may have implications for the treatment and prevention of inflammation-induced structural damage to the airways.