Teratogen update: smoking and reproductive outcomes.

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The potential effects of cigarette smoke exposure on reproductive outcomes are a major scientific and public health concern, as evidenced by the myriad of published studies on outcomes ranging from germ cell morphology to morbidity among subsequent generations of offspring. Although the prevalence of maternal smoking has decreased over the past two decades, ,15% of women smoke throughout pregnancy (Kendrick and Merritt, ’96). Given that cigarette smoke contains hundreds of toxic components, it follows that maternal smoking may have adverse effects on certain reproductive outcomes. For the most part, specific components of cigarette smoke have not been studied in humans, but pieces of evidence point toward certain pathways. Some examples include: nicotine is known to be vasoactive and is thought to reduce placental and fetal circulation (Lehtovirta and Forss, ’78; Goodman, ’90; Mochizuki et al., ’94; Philipp et al., ’94); cotinine, a major metabolite of nicotine, has been measured in follicular fluid (Bureau et al., ’82; Weiss and Eckert, ’89); cyanide is a known toxin and has been studied as a marker for smoking because thiocyanate correlates well with smoking exposure (Sophian, ’68; Andrews and McGarry, ’72; Bottoms et al., ’82); carbon monoxide is known to deplete both maternal and fetal oxygen supplies (Bartlett, ’68; Meyer, ’78; Bureau et al., ’84); excess cadmium has been observed in the ovaries, follicular fluid, and placentas of smokers (Van der Velde et al., ’83; Kuhnert et al., ’88; Zenzes et al., ’93); lead is a known neurotoxin (Doull et al., ’80); and some polycyclic aromatic hydrocarbons are mutagenic (USDHHS, ’82). The more general exposure—cigarette smoking—is the focus of this review. Because of the abundance of published papers on smoking, the outcomes presented here were selected on the basis of public health relevance and the availability of published data from epidemiologic studies in humans. For each reproductive outcome covered, important epidemiologic issues are described and the findings are summarized in terms of an estimated relative effect of smoking (i.e., relative risk) (Rothman, ’86). For those outcomes that have been linked to smoking consistently across studies, the proportion of the outcome attributed to the exposure (i.e., attributable proportion) is estimated (Rothman, ’86). SUBFERTILITY