Cigarette smoking, the principal aetiology of chronic obstructive pulmonary disease (COPD) in the developed countries, delivers and generates oxidative stress within the lungs. This imbalance of oxidant burden and antioxidant capacity has been implicated as an important contributing factor in the pathogenesis of COPD. Oxidative processes and free radical generation orchestrate the inflammation, mucous gland hyperplasia, and apoptosis of the airway lining epithelium which characterises COPD. Pivotal oxidative stress/pro-inflammatory molecules include reactive oxygen species such as the superoxides and hydroxyl radicals, pro-inflammatory cytokines including leukotrienes, interleukins, tumour necrosis factor alpha, and activated transcriptional factors such as nuclear factor kappa-B and activator protein 1. The lung has a large reserve of antioxidant agents such as glutathione and superoxide dismutase to counter oxidants. However, smoking also causes the depletion of antioxidants, which further contributes to oxidative tissue damage. The downregulation of antioxidant pathways has also been associated with acute exacerbations of COPD. The delivery of redox-protective antioxidants may have preventative and therapeutic potential of COPD. Although these observations have yet to translate into common clinical practice, preliminary clinical trials and studies of animal models have shown that interventions to counter this oxidative imbalance may have potential to better manage COPD. There is, thus, a need for the ability to monitor such interventions and exhaled breath condensate is rapidly emerging as a novel and noninvasive approach in the sampling of airway epithelial lining fluid which could be used for repeated analysis of oxidative stress and inflammation in the lungs.