Physiological mechanisms increasing risk of cardiovascular disease from smoking

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There are strong plausible hypotheses for the relation between exposure to tobacco and vascular disease. In animal and human studies, endothelial injury has been associated with carbon monoxide and nicotine. In contrast to healthy individuals, those with ischemic heart disease are affected by carbon monoxide during submaximal exercise, in part because carbon monoxide reduces the ability of hemoglobin to combine with oxygen and diminishes oxygen transport from the lungs to the tissues. Levels as low as 2.5 to 3% carboxyhemoglobin (COHb ) have been found to decrease exercise time before the onset of angina and prolong the duration of ischemia. For maximal exercise, the critical level is approximately 4.5% COHb. Above this level, both exercise and V02max are inversely related to CO concentration. Additionally, cigaret smokers may have baseline COHb in the 4 to 8% range (23).

Platelet and clotting factors predisposing to formation of thrombus, as well as vascular smooth muscle cell proliferation have also been observed with exposure to cigaret vapor components, including carbon monoxide and nicotine. Increased platelet aggregation has been found both in humans and in animals (24,25). Thrombolytic substances such as plasminogen have been found to be lower in smokers and to increase with cessation of smoking (26,27).

There is a growing body of evidence suggesting that oxidation of low density lipoprotein (LDL)-cholesterol particles may be a pivotal step in atherogenesis (28-30). Cigaret smoking, even for brief periods, can markedly enhance LDL-cholesterol oxidation as well as decrease high-density lipoprotein cholesterol (31). It also depletes body stores of vitamin C that may be an important antioxidant protection. Intake of the anti-oxidant beta carotene has been shown to be inversely related to the risk of coronary events among current smokers (relative risk 0.30) and former smokers (relative risk 0.60), but was not beneficial in persons who had never smoked (32,33).

Fibrinogen has also been implicated in atherogenesis and thrombus formation, and has been found to be elevated in smokers (34,35). The Framingham Study has shown that risk of cardiovascular disease (CVD) and stroke increased with increases in fibrinogen levels. In this study, as well as in other studies, smokers had a higher risk of developing claudication compared with nonsmokers with similar risk factor profiles (17,36-40).

Cigaret smoking can cause marked coronary vasoconstriction (41,42), and has been strongly associated with angiographically documented coronary spasm in men and women (43-45). Vascular endothelial damage from smoking can cause thromboxane A2 release, decreased prostacyclin production, a-adrenergic stimulation, and vasopressin generation in the process of provoking constriction of the coronary vessel. Cigarets elevate the circulating level of catecholamines and free fatty acids that can further alter vascular tone.

Smoking also:

• Decreases the useful blood levels of drugs like ^-blockers as a result of their increased metabolism (46).

• Increases both blood pressure and heart rate.

• Lowers the threshold for ventricular arrhythmias (13).

• Has a direct toxic effect on the ventricular myocardium (47,48) and may significantly increase myocardial oxygen demand.

Passive smoking is also associated with dose-related impairment of endothelium dependent dilatation, suggesting early arterial damage (49). Studies have concluded that the public health burden caused by environmental tobacco smoke (ETS) is likely to be much greater for heart disease than for lung cancer (50). Although environmental tobacco smoke is less dense, it is more toxic. Twice as much nicotine is emitted in sidestream as in mainstream smoke, and the ratio for benzene is 10:1. The concentration of carbon monoxide is 2.5 times higher in sidestream smoke than it is in mainstream smoke. Polycyclic aromatic hydrocarbons present on smoke as well as in environmental air pollution are capable of inducing and accelerating atherosclerosis. Tobacco smoke may also sensitize circulating neutrophils in humans, and may cause their subsequent activation and oxidant-mediated tissue damage, leading to atherosclerosis of the coronary and peripheral vessels (51).

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A Disquistion On The Evils Of Using Tobacco

A Disquistion On The Evils Of Using Tobacco

Among the evils which a vitiated appetite has fastened upon mankind, those that arise from the use of Tobacco hold a prominent place, and call loudly for reform. We pity the poor Chinese, who stupifies body and mind with opium, and the wretched Hindoo, who is under a similar slavery to his favorite plant, the Betel but we present the humiliating spectacle of an enlightened and christian nation, wasting annually more than twenty-five millions of dollars, and destroying the health and the lives of thousands, by a practice not at all less degrading than that of the Chinese or Hindoo.

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