Smoking and inflammation: Their synergistic roles in chronic disease
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Corresponding author Bente Halvorsen, MSc, PhD Research Institute for Internal Medicine, Rikshospitalet Medical Center, University of Oslo, N-0027 Oslo, Norway. E-mail: [email protected] Current Cardiovascular Risk Reports 2008, 2:446–451 Current Medicine Group LLC ISSN 1932-9520 Copyright © 2008 by Current Medicine Group LLC
Cigarette smoking is a major risk factor for the development and progression of cardiovascular and other chronic diseases. Cigarette smoke increases inflammatory mediators in the circulation and generates high amounts of reactive oxygen species, which are potent triggers of the inflammatory response and thought to play a central role in the development of atherosclerosis. Low-grade inflammation, atherogenic lipoprotein profile, and hypercoagulability are characteristic of smokers, and smoking cessation has been associated with a rapid improvement in the inflammatory balance. In individuals with high risk of coronary disease, 1 year of smoking cessation significantly counteracts impaired endothelial function, as assessed by a decreased plasma level of intercellular adhesion molecule. This review focuses on the connection between smoking and inflammation and their role in chronic disease.
Introduction Epidemiologic studies have established that cigarette smoking is an important cause of cardiovascular morbidity and mortality worldwide [1], and cigarette smoking causes more deaths due to cardiovascular disease (CVD) than other diseases [2]. A large Chinese population study (n = 14,578) recently showed a dose-dependent association between smoking and stroke [3••], and numerous studies have demonstrated that smoking is associated with almost all forms of CVD [4]. Other diseases, such as various cancers, are also closely associated with cigarette smoking [5], and smoking is responsible for almost 90% of all cases of lung cancer. Several reports have shown that continued smoking causes progression and adverse treatment outcomes across a range of common chronic diseases, such as chronic obstructive
pulmonary disease, diabetes, asthma, and HIV-related disorders (reviewed by Gritz et al. [6]). Environmental tobacco exposure, also called passive smoking and secondhand smoking, is associated with a 30% increased risk of coronary artery disease (CAD), whereas active smokers have an 80% increased risk of CAD [7,8]. Close to 25% of adults in the United States are current smokers [9], and there are many more secondhand smokers. It is estimated that more than 50,000 annual deaths are caused by environmental tobacco smoke in the United States. [10].
Constituents of Tobacco Smoke Cigarette and tobacco smoke can be divided in two phases: tar and gas-phase smoke. Mainstream cigarette smoke comprises 8% tar and 92% gaseous components [11]. Both phases contain high concentrations of reactive oxygen species (ROS), nitric oxide (NO) peroxynitrite, and free radicals produced from organic compounds; in total, more than 5000 chemicals have been identified [12]. Nicotine has been the component thought to cause ad
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