Introduction: Lung cancer is the leading cause of cancer death and oxidative stress secondary to carcinogens such as cigarette smoke has been implicated in its pathogenesis. Therefore, lung cancer patients were hypothesized to have higher levels of oxidative stress markers in their exhaled breath compared with controls.
Methods: Exhaled breath condensate (EBC) was collected from newly diagnosed subjects with non-small cell lung cancer (NSCLC) and control subjects in a cross-sectional observational study. The samples were then analyzed for hydrogen peroxide (H(2)O(2)), pH, 8-isoprostane, and antioxidant capacity.
Results: A total of 71 subjects (21 NSCLC patients, 21 nonsmokers, 13 exsmokers, and 16 smokers) were recruited. NSCLC patients had significantly higher EBC H(2)O(2) concentration (NSCLC subjects versus smokers, 10.28 microM, 95% confidence interval [CI]: 4.74-22.30 and 2.29 microM, 95% CI: 1.23-4.25, respectively, p = 0.003) and lower antioxidant capacity (NSCLC versus smokers, 0.051 mM, 95% CI: 0.042-0.063 and 0.110 mM, 95% CI: 0.059-0.206, p = 0.023; NSCLC versus all controls as a group, 0.051 mM, 95% CI: 0.042-0.063 and 0.087 mM, 95% CI: 0.067-0.112, p = 0.001). They also had significantly lower pH (5.9, 3.3-7.3) compared with exsmokers (6.7, 5.8-7, p = 0.009).
Conclusion: The significant increase of H(2)O(2) and reduction in antioxidant capacity in the EBC of lung cancer patients further support the concept of the disequilibrium between levels of oxidants and antioxidants in lung cancer, which leads to increased oxidative stress. These findings suggest oxidative stress is implicated in the development of lung cancer and may be an early marker of the disease.