Int. J. Environ. Res. Public Health 2009, 6 211 guidelines [4]. This finding is of major clinical significance, in that it provides a scientific basis for the advice that can now be given to smokers that if they continue smoking lifelong, they have at least a one in two chances of developing COPD [12]. The costs of COPD to health services and society are substantial. Consultation rates in primary care are high and exacerbations of COPD are one of the most common causes of hospital admission. In developed countries, exacerbations of COPD account for the greatest burden on the health care system. In the European Union, the total direct costs of respiratory disease are estimated to be about 6% of the total health care budget, with COPD accounting for 56% (€38.6 billion) of this cost. In the United States in 2002, the direct costs of COPD were $18 billion and the indirect costs totaled $14.1 billion [4, 15]. 2. Pathogenesis and Pathophysiology of Tobacco Induced Lug Injury. Cigarette smoke contains an extremely high concentration of oxidants. The reactive oxidant substances generated by smoking induce inflammation in the lung and its airway [16]; cigarette smoking causes an inflammatory process in the central airways, peripheral airways, and lung parenchyma, which is present even in smokers with normal lung function [17]. Studies have shown that in bronchial biopsies obtained from central airways, smokers have chronic inflammatory changes, with increased numbers of specific inflammatory cell types in different parts of the lung, and structural remodeling resulting from repeated injury and repair [18]. The exact role of smoking cessation on the airway inflammation process in COPD is still unknown. Cross-sectional studies suggest that there is still ongoing inflammation in COPD even after smoking cessation [19]. In general, the inflammatory and structural changes in the airways increase with disease severity and persist despite smoking cessation. It is intriguing why airway inflammation is not resolved in COPD patients after 1 year of smoking abstinence, and even increases in some aspects. One explanation is that an inflammatory trigger persists after smoking cessation, keeping a local inflammatory response intact [20]. The persistent inflammation in chronic obstructive pulmonary disease may be, at least partly, related to repair of the smoke-induced tissue damage in the airways. It remains to be determined which parts of the observed inflammatory changes are beneficial and which harmful [20, 21]. A recently suggested hypothesis is that COPD may have an autoimmune component, which contributes to the airway inflammation even after smoking cessation [22]. These auto-antibodies may be directed against antigens present in tobacco or against endogenous auto-antigens that result from the smoking-induced inflammatory and oxidative lung injury [23]. 3. Smoking Cessation and COPD Smoking cessation is the single most effective—and cost-effective—treatment for COPD. Furthermore, smoking cessation is associated with a reduction in the risk of developing stroke, coronary heart disease, several types of cancer, and it is associated to an increased life expectancy [24].