Chapter 5 
BaP, have been found to accelerate the development of atherosclerosis in 
animal models; this suggests that cell injury and cell proliferation (or 
hyperplasia) may contribute to the development of the growing plaque 
(Glantz and Parmley, 1991). Hydrogen cyanide, nitrogen oxides, and 
chemical components of cigarette tar also have been implicated. Free 
radicals in cigarette smoke, which are highly reactive oxygen products, 
are damaging to the heart muscle cells (Church and Pryor, 1985). 
CIGARETTE SMOKING Cigarette smoking adversely affects sexual and reproductive 
AND HUMAN function in women in a number of different ways. Cigarette 
REPRODUCTION smoking appears to impair female fertility (Baird and Wilcox, 
1985; Daling et al., 1987; Mattison, 1982; U.S. Department of Health and 
Human Services, 1980). Among the possible mechanisms are direct toxicity 
to eggs, interference with motility in the female reproductive tract, and 
alterations in immunity that predispose female smokers to infections that 
block the Fallopian tubes (Chow et al., 1988). 
Maternal cigarette smoking has serious adverse effects on the outcome 
of pregnancy. These include retarded fetal growth; low birth weight; 
spontaneous abortion; certain complications of pregnancy, labor, and 
delivery, such as bleeding during pregnancy and prolonged premature 
rupture of membranes; and infant death (U.S. Department of Health and 
Human Services, 1980, 1989, and 1990; U.S. Department of Health, 
Education, and Welfare, 1979). Direct nicotine toxicity has been suggested 
as a mechanism for spontaneous abortion (U.S. Department of Health and 
Human Services, 1990). Although a smoking-induced reduction in maternal 
weight gain contributes to fetal growth retardation (U.S. Department of 
Health and Human Services, 1980; Werler et al., 1985), the evidence points 
to oxygen starvation of the fetus and placenta as important factors. Carbon 
monoxide in cigarette smoke can cross the placenta and bind to the 
hemoglobin in fetal blood. Smoking causes constriction of the umbilical 
arteries, impairing placental blood flow. Nicotine, which also crosses the 
placenta, can have a number of toxic effects on the fetus (U.S. Department 
of Health and Human Services, 1980). The carcinogen 4-aminobiphenyl 
crosses the placenta in a mother who smokes and adducts with the 
hemoglobin in the fetus' blood (Coghlin et al., 1991). Cyanide, another 
component of cigarette smoke, also has been implicated. 
Women currently smoking enter nonsurgical menopause about 1 to 
2 years earlier than nonsmokers (U.S. Department of Health and Human 
Services, 1990). Heavy smokers experience an even earlier menopause than 
light smokers. This effect has important consequences for women's health, 
because the rates of osteoporosis and atherosclerotic cardiovascular diseases 
increase after menopause. One proposed mechanism for early menopause is 
that PAHs in smoke are directly toxic to ovarian follicles (Mattison, 1980). 
Cigarette smoking also may affect male reproductive performance. In 
several studies, men who report impotence (i.e., the inability to maintain an 
erection sufficient for intercourse) were more likely to be cigarette smokers. 
This association between smoking and impotence is particularly common 
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