EDITORIAL Collaboration between smokers and tobacco in endothelial dysfunction

This editorial refers to ‘Cytokines present in smokers ’ serum interact with smoke components to enhance endothelial dysfunction ’ by S.S. Barbieri et al., pp. 475–483, this issue. Cigarette smoking is the most addictive but modifiable habit and a major health hazard. Smoking primarily affects the respiratory tract and causes chronic obstructive lung diseases and cancers of the lung and pharynx. Smoking is also a major independent risk factor for atherosclerotic vascular diseases, including coronary artery disease and cerebrovascular attack. Smoking-related respiratory diseases can be explained by the direct exposure to cigarette smoke. In contrast, the mechanisms responsible for the acceleration of atherosclerosis by smoking are still elusive, although deleterious effects of smoking on the cardiovascular system are well established.1 The exact toxic components of cigarette smoke are largely unknown and the mechanisms of vascular damage induced by ciga