Non-invasive methods to assess biomarkers of exposure and early stage of pulmonary disease in smoking subjects

Cigarette smoking is the major factor implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD), despite the fact that only susceptible smoking subjects develop this respiratory disease. In the last few years non–invasive techniques such as induced sputum (IS), exhaled nitric oxide (eNO) measurement and exhaled breath condensate (EBC) collection have been successfully established revealing an inflammatory status and oxidative stress indicators in the airways involved in the pathogenesis of several pulmonary diseases. Using these new non-invasive experimental tools recently, several efforts have been made to find new biomarkers in order to assess and monitor early lung damage induced by smoking. Tobacco smoke can acutely reduce eNO levels in healthy smokers and non-smoker subjects so it can play a role in anti-smoking programmes; its increase can be a positive parameter for subjects who are going to stop cigarette smoking and at the same time be used as an anti-smoking indicator. It can be useful to investigate the mechanism of cigarette-induced lung damage in an experimental setting and may potentially be useful for assessing of Environmental Tobacco Smoke (ETS) effects. Markers of oxidative stress have been detected in induced sputum of COPD subjects even though only few studies investigated the use of induced sputum to study smoke effects on the lungs of healthy subjects. Exhaled breath condensate (EBC) obtained by cooling exhaled air under conditions of spontaneous breathing is a promising biological fluid that could provide a real-time assessment of pulmonary pathobiology. The analysis of induced sputum and of exhaled air is feasible and non-invasive, can be useful to identify new biomarkers of exposure or susceptibility in COPD patients to enhance the understanding of airways changes due to current smoking and may be useful to find new biomarkers in order to assess and monitor early lung damage induced by smoke in order to prevent the progression of obstructive disease.