Chest
Special FeatureSystemic Effects of Smoking
Section snippets
Systemic Oxidative Stress in Smokers
Cigarette smoke contains approximately 1017 oxidant molecules per puff.7 This oxidative stress can be registered in several different ways, either by direct measurements of the oxidative burden (reactive oxygen species [ROS] production by peripheral blood cells) or by the effects of oxidative stress on target molecules (lipid peroxidation products and oxidized proteins), or as the responses to the oxidative stress (antioxidant capacity of plasma)8 [Table 1].
Only a few studies9, 1011 have used
Systemic Inflammation in Smokers
Activation and release of inflammatory cells into the circulation, and an increase in circulating inflammatory mediators such as acute phase proteins and proinflammatory cytokines, characterize the systemic inflammation.
Circulating Inflammatory Cells
The systemic inflammatory response is characterized by the stimulation of the hematopoietic system, specifically the bone marrow resulting in the release of leukocytes and platelets into the circulation. Numerous studies32, 3334 have shown that long-term cigarette smoking increases total WBC counts, mainly due to an increase in polymorphonuclear neutrophil (PMN) counts in the circulation of smokers. A large population-based study35 of 6,902 men and 8,405 women performed in Great Britain
Inflammatory Mediators in Peripheral Blood of Smokers
Activated inflammatory cells produce a great variety of inflammatory mediators in response to cigarette smoke, first of all, acute-phase proteins (APPs) and cytokines. Conditions that commonly lead to substantial changes in the plasma concentrations of APPs and cytokines include infection, trauma, surgery, burns, tissue infarction, various immunologically mediated inflammatory conditions, and cancer. In recent years, these inflammatory mediators have been studied as potential markers of subtle
Smoking and Markers of Endothelial Dysfunction, Coagulation, and Hemostasis
The biological mechanism linking smoking and atherogenesis, the process leading to cardiovascular diseases, is complex and not fully understood. Besides inflammation, proposed potential mechanisms by which smoking increases the risk of cardiovascular pathology include several other pathways: vascular endothelial dysfunction, systemic hemostatic and coagulation disturbances, and lipid abnormalities. Many of these indexes including fibrinogen (marker of coagulation), fibrin d-dimer (a marker of
Vascular Endothelial Dysfunction
Endothelial dysfunction is mainly caused by diminished production or availability of NO.61 It has been demonstrated that the serum concentration of nitrate and nitrite, metabolic end-products of NO, is significantly decreased in smokers relative to that in nonsmokers.74 In cigarette smokers, low-density lipoprotein (LDL) is more prone to oxidation due to higher level of ROS and reactive nitrogen species.75 Oxidatively modified LDL limits the bioactivity of endothelium-derived NO; and, in turn,
Hemostatic and Coagulation Markers
There is increasing evidence that blood levels of rheologic variables are associated with subsequent cardiovascular events.70 These indexes include whole-blood viscosity and its main determinants: hematocrit and plasma viscosity, principally composed by plasma fibrinogen and lipoproteins.67 Several studies33, 67 revealed that current smokers have increased blood viscosity, associated with increased hematocrit or/and plasma viscosity resulting in a procoagulant condition. Increased plasma
Conclusion
The possible biological mechanisms responsible for the observed association of smoking with various diseases and global mortality are numerous and, in spite of a many attempts to find causative relationships, are still unclear. It is a great scientific task to unravel exact pathways through which smoking affects human health. Although the effects of smoking on inflammatory markers may persist for many years, a majority of the adverse health effects of smoking are reversible. Therefore, quitting
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Funding was provided by the European Respiratory Society (fellowship No. 161).
The authors have no conflicts of interest to disclose.
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