among pregnant and nonpregnant women, 25.2% and 14.4%, respectively in 1996 (Ebrahim et al., 2000). Even after learning that they are pregnant, 54% of women continue to smoke (Ebrahim et al., 2000). Additionally, maternal smokers who have experienced previous preterm delivery or small-for-gestational age infants do not show greater quit rates than smokers who have had uncomplicated deliveries (Cnattigius et al., 1999). According to the National Health Interview Survey (1992–1993), among female smokers in general, 72.5% reported that they wanted to quit smoking with 34% attempting to quit each year and 2.5% being successful.
The contribution of environmental tobacco smoke (ETS), including paternal smoking, to adverse reproductive health outcomes is uncertain, but ETS exposure is widespread among women of reproductive age. Data from the third National Health and Nutrition Examination Survey report a 32.9% prevalence of ETS exposure at home or at work among non-tobacco-using females age 17 and over.
Smoking has been associated with increased time to conception, decreased pregnancy rate in assisted reproduction, increased risk of ectopic pregnancy, and menstrual changes including early menopause. The risk of being unable to conceive within a year of trying is increased two- to threefold among smokers (Werler, 1997). Consistent with many previous studies, a recent cohort study of current and past smokers during assisted reproduction cycles suggested a dose-related decrease in ovarian function and a 50% reduction in pregnancy rates of current smokers (Van Voorhis et al., 1996). Also, a positive relationship (odds ratio, OR≅1.3–2.2) between cigarette smoke exposure at conception and during pregnancy and the risk of subsequent ectopic pregnancy has been documented, with mixed results regarding dose-response (Coste et al., 1991; Handler et al., 1989; Saraiya et al., 1998; Stergachis et al., 1991). Animal studies have suggested altered gonadotropin release, decrease in luteinizing hormone (LH) surge, inhibition of prolactin release, altered tubal motility, and impairment of blastocyst formation and implantation as possible mechanisms of fertility impairment among smokers (reviewed in Hughes and Brennan, 1996). Additional studies in rats have shown follicle destruction and oocyte depletion when exposed to benzo[a]pyrene (BaP), a tobacco smoke toxin (Cooper et al., 1999). Furthermore, an evaluation of the Women’s Health Study found that current and former smokers, after adjusting for age, race, education, marital status, number of sexual partners, frequency of intercourse, history of gonorrhea, and current method of contraception, had a significantly increased risk of pelvic inflammatory disease, possibly related to impairment of immunity and altered tubal