Oxidative stress in COPD and its measurement through exhaled breath condensate

Oxidative stress and airway inflammation together form a vicious cycle, which is responsible for the disease progression in chronic pulmonary obstructive disease (COPD). The damaging effects of oxidative stress accumulate over the years, causing increased bronchial hyperresponsiveness and inflammation and destruction of airway epithelial cells and impairing the functions of antiproteases and surfactant. Although the lung expresses a number of antioxidants, cigarette smoking and recurrent infections associated with this disease overwhelm this protective mechanism. Studies of antioxidants in COPD have yielded conflicting results, probably due to the compartmentalization of these mediators, and because of the fact that the lung is a difficult organ to sample. Chronic exposure to oxidants upregulates the production of antioxidants, which become depleted during acute exacerbations. Future studies of the pathogenesis of COPD require a noninvasive yet accurate sampling procedure, of which exhaled breath condensate (EBC) is a good candidate. EBC samples the epithelial lining fluid, which contains the local oxidative stress markers in the lung. Oxidative stress markers such as hydrogen ions, hydrogen peroxide, 8-isoprostanes, thiobarbituric acid reactive products, nitrosothiols, and nitrite/nitrate have been identified in EBC of COPD patients, whereas many other markers of the oxidative-antioxidative balance have yet to be investigated.