Smoking and Tobacco Control Monograph No. 7 
cerebrovascular disease. Atherosclerosis involving the arteries to the limbs is 
called peripheral vascular disease (PVD). 
In numerous epidemiologic studies of millions of people, cigarette 
smokers have been found to have higher rates of heart attack, sudden death, 
and other manifestations of CHD. They also have higher rates of stroke, PVD, 
and other atherosclerotic lesions (U.S. Department of Health and Human 
Services, 1984b and 1989; U.S. Department of Health, Education, and Welfare, 
1979). In the Cancer Prevention Study II (CPS-II) of more than 1 million 
people followed from 1982 through 1986, men currently smoking had a 
94-percent greater risk of CHD than lifelong nonsmokers, whereas women 
currently smoking had a 78-percent greater risk. In smokers younger than 
age 65, men had a 181-percent greater risk and women a 200-percent greater 
risk (U.S. Department of Health and Human Services, 1989). 
Cigarette smoking is sometimes called an independent risk factor for 
CHD because smokers' CHD rates are found to be higher even when other 
risk factors such as gender, blood pressure, and cholesterol level are taken into 
account. It is sometimes called a modifiable risk factor because one can 
reduce or stop smoking. Although smoking obviously cannot be a cause of 
CHD in someone who never smoked, it can be an important contributor to 
CHD in a smoker. Among 548,000 deaths from CHD in the United States in 
1985, an estimated 115,000 would not have occurred but for the presence of 
cigarette smoking (U.S. Department of Health and Human Services, 1989). 
Cigarette smoke appears to enhance the atherosclerotic process by several 
different mechanisms (U.S. Department of Health and Human Services, 1990; 
Glantz and Parmley, 1995). Cigarette smoking affects cholesterol metabolism. 
Smokers repeatedly have been observed to have lower levels of the protective 
high-density lipoprotein (HDL) cholesterol (Willett et al., 1983), and smoking 
cessation raises HDL cholesterol (Rabkin, 1984). In animal models, cigarette 
smoke can damage the inner lining of blood vessels, thus enhancing the 
transfer of low-density lipoprotein (LDL) cholesterol particles across the 
arterial wall and into the developing cholesterol-laden plaque (Krupski et al., 
1987; Zimmerman and McGeachie, 1987; Penn et al., 1994). Cigarette 
smoking also can affect the blood clotting system, including the adherence 
of blood platelets to the lining of arterial blood vessels (Pittilo et al., 1984; 
U.S. Department of Health and Human Services, 1984b; Burghuber et al., 
1986) and the formation of blood clots that block a narrowed artery. Acrolein 
in cigarette smoke may be partly responsible for its platelet-adhering effects 
(Selley et al., 1990). Cigarette smoke also can cause spasm of the coronary 
arteries. 
Many chemical components of cigarette smoke have been implicated in 
the development of atherosclerotic disease. Nicotine, the major psychoactive 
component of smoke, causes powerful changes in heart rate and blood 
circulation. Nicotine appears to cause injury to the arterial lining (Krupski et 
al., 1987). Carbon monoxide in cigarette smoke binds to the hemoglobin in 
red blood cells, thereby reducing the oxygen-carrying capacity of the blood 
(Sheps et al., 1990). PAHs, such as 7,12-dimethylbenz(«,/;)anthracene and 
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