More deaths are attributed to coronary heart disease and stroke as a result of smoking than deaths due to cancer caused by smoking[1]. Although smoking rates for women in the United States are lower than those for men, smoking has declined more slowly among women than men. For example, male smoking rates decreased 46% from 1965 to 1990 (from 52% to 28%), the rate among women decreased by 32% during this time (from 34% to 23%).
Case-control and cohort studies illustrate that smoking more than doubles the incidence of CHD and increases mortality due to CHD by approximately 70%. Several studies have confirmed the correlation between smoking and CHD:
In the Nurses' Health Study, a prospective cohort study among more than 121,000 middle aged female nurses in the United States, the heaviest smokers were six times more likely to develop coronary heart disease than non-smokers[2].
Hansen et al., [3] reported that cigarette smoking triples the risk for MI among pre-menopausal women and is also a significant contributor to sudden cardiac deaths in younger women.
There is a relationship between the dose intake by smoking and CHD. Evidence shows that the risk of CHD is two to four times higher in women who are heavy smokers (individuals who smoke 20 or more cigarettes/day) than women who do not smoke[4].
Women that are classified as "light" smokers (smoking one to four cigarettes per day) will more than double their risk for CHD[2].
Furthermore, smoking is responsible for lowering the average age of menopause by 1-1/2 to 2 years, with a longer period of menopausal status possibly increasing coronary risk[3].
Also, a study by Stadel[5], illustrated the potential increase of risk for CHD due to a combination use of oral contraceptives (with more than 50 µg of estrogen) and smoking. Since this initial study other studies have confirmed the potential risk as a result of this synergistic effect of oral contraceptives and smoking[6].
New information
S-cholesterol, s-triglycerides, fasting blood glucose, body weight and body mass index were all radically elevated among the heavy smokers, as reported by Lundqvist et al[7]. Social and lifestyle factors differed significantly between heavy smokers and never smokers, but without genderdifferences. They concluded that heavy smokers carry a risk factor pattern corresponding to a greater risk of developing cardiovasculardisease. Unfavorable changes in serum lipids and in glucose metabolism can exacerbate other deleterious effects of tobacco smoke on the cardiovascular system. Clearly, heavy smokers and never smokers differ not only in regard to biomedical variables but also to lifestyle and social health determinants. These are essential factors to consider in public health efforts aimed at reducing the increased risk for cardiovasculardiseases among smokers[7].
Smoking remains a major health problem especially among women. It influences estrogen metabolism and the risk for multiple estrogen sensitive outcomes. Many indirect effects of smoking exist through the ability of the by-products to change a variety of drugs, enzymes, and hormones.
The results of several in vitro studies have shown that constituents of cigarette smoke have significant effects on production and metabolism of estrogens. In some cases, such as osteoporosis and endometrial cancer, smoking appears to attenuate the effects of estrogen. However, for other outcomes such as breast cancer, venous thromboembolic events (VTE), and coronary heart disease (CHD), the relationship between smoking and estrogen exposure is less defined.
Based on the preponderance of evidence, smokers are likely to require higher doses of hormone replacement therapy (HRT) to achieve comparable clinical effect to that observed in nonsmokers. However, uptitrating the dose of HRT in smokers to achieve a desired systemic level or clinical response may simultaneously increase risk for adverse effects that are primarily driven by hepatic rather than systemic exposure[8].
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1. Lonn, E., (2000) Canadian Cardiovascular Society Consensus Conference: Women and Ischemic Heart Disease, October 2000: 3/1-3/40.
2. Willett WC, Green, A., Stampfer, MJ., et al. (1987) Relative and absolute Excess Risks of Coronary Heart Disease Among Women who Smoke Cigarettes. N Engl J Med. 317: 1303-1309.
3. Hansen, E.F., Andersen, L.T., Von Eyben F.E., (1993) Cigarette Smoking and Age at First Myocardial Infarction and Influence of Gender and Extent of smoking. Am J Cardiol, 171: 1439-1442.
4. Bartecchi,C., Mackenzie,T., Schrier, R., (1994) The Human Costs of Tobacco Use. N Engl J Med. 330: 907-912.
5. Stadel, B. (1981) Oral Contraceptives and Cardiovascular Disease. N Eng J Med, 305: 672-677.
6. Thorgood, M., Mann, J., Murphy, M., Vessey, M., (1991) Is Oral Contraceptive Use Still Associated with an Increased Risk of Fatal Myocardial Infraction? Report of a Case Control Study. Br J Obstet Gynecol, 98: 1245-1253.
7. Lundqvist G, Weinehall L., Smokers in Vasterbotten County, Sweden. What contributes to increased cardiovascular risk among heavy smokers?, Scandinavian Journal of Primary Health Care. 21(4):237-41, 2003
8. Tansavatdi K, McClain B, Herrington DM.,The effects of smoking on estradiol metabolism, Minerva Ginecol. 2004 Feb;56(1):105-14
