In chronic obstructive pulmonary disease (COPD), a chronic inflammatory airway disorder characterized by irreversible airflow obstruction induced mainly by tobacco smoking, studies have demonstrated that, in acute exacerbations of COPD and smoking, there is a marked imbalance of redox status. The increased oxidative stress results in the inactivation of alveolar antiproteases, airspace epithelial damage, increased influx of neutrophils into lung tissue and the expression of pro-inflammatory mediators. Similarly, patients with COPD also have increase neutrophils, lymphocytes and TNF-α in the peripheral blood. In fact, many studies have demonstrated the existence of low grade systemic inflammation and oxidative stress in patients with COPD. Important studies published in recent 5 years have also linked the elevation of these systemic biomarkers, in a dose-dependent manner, to COPD severity and increased prevalence of cardiovascular and cerebrovascular morbidity and mortality in patients with COPD.