Chronic obstructive pulmonary disease (COPD) is a chronic inflammation of the airways, including the parenchyma and the pulmonary vasculature. The burden of COPD is increasing around the world in terms of morbidity and mortality in adult population. Active smoking is a major risk factor for COPD, although there is individual susceptibility to the effects of tobacco smoke. This variability could result from host as well as environmental factors. Even passive smoking in early childhood as well as intrauterine exposure could pave the way for COPD. Tobacco smoke induces a specific, persistent inflammation, different from that of asthma. Three other processes accompany and interact with inflammation: imbalance of both the proteases- antiproteases, the oxidants-antioxidants, and improper repair mechanisms. These processes respectively lead to mucus hypersecretion and alveol wall destruction, dysfunction and death of biological molecules, damage to the extracellular matrix and pulmonary fibrosis with adventitial, submucosal and smooth muscle thickening. The earlier the smoke exposure, the greater the level of decline in lung function. Combined mucus hypersecretion, reduced clearance, and impairment of the lung defence mechanisms explain why COPD patients even with stable condition, carry potential respiratory pathogens in significant concentration, paving the way for infection and acute exacerbations of COPD. Every additional exacerbation in a smoker deteriorate more the lung function. Fortunately, smoking cessation, which is a part of the respiratory rehabilitation could reduce the number of hospitalisations and the decline of lung function, and thus reduce the management cost of the disease and improve the quality of life. The earlier the quitting, the better the improvement of FEV1. “Smoking cessation is the single effective and cost effective way to reduce exposure to COPD risk factors” (GOLD, evidence A).