Environmental Tobacco Smoke and Cardiovascular Disease
This chapter reviews evidence demonstrating that environmental tobacco smoke (ETS) is a risk factor for heart disease in both adults and children. ETS is a mixture of sidestream (SS) and mainstream smoke (MS), and SS is richer in certain carcinogens than MS. Various animal studies on passive smoking have duplicated disease conditions, particularly the effects of SS on heart disease. ETS causes heart damage through hematological, neurohormonal, metabolic, hemodynamic, molecular genetic, and biochemical pathways. Many components in tobacco smoke have a role in the process of heart function damage, including carbon monoxide, free radicals, nicotine, and carcinogens such as polycyclic aromatic hydrocarbons, 7,12-dimethyl-benzanthracene, and benzo(a)pyrene. ETS may increase the risk of cardiovascular disease (CVD) by promoting platelet aggregation and oxidation damage to arterial endothelium and by inducing myocardial apoptosis. In addition, ETS exerts significant adverse effects on heart disease by reducing the body’s ability to deliver and utilize oxygen via depressing cellular respiration at the level of mitochondria. The carcinogens in ETS may begin and accelerate the development of atherosclerotic plaque. Evidence also suggests that direct and indirect exposure to ETS increases the heart rate, blood pressure, rate-pressure product, and cardiac output and maximal first derivative of left ventricular pressure. The most effective way to prevent CVD is to eliminate exposure; however, this goal is difficult to achieve. Nutritional treatment of people exposed to ETS is theoretically useful because ETS is highly associated with oxidative stress. Increased consumption of fruits, vegetables, and fish oils should decrease CVD risk in people exposed to SS. Treatment with agents such as aspirin and pycnogenol can reduce platelet aggregation
