Context Cigarette tobacco smoke is a potent environmental contaminant known to adversely affect health including fertility and pregnancy. Objective To examine the associations between second-hand cigarette tobacco-smoke exposure, or active smoking and serum concentrations of steroid hormones using tandem mass spectrometry. Design Healthy women (18–45 y) from the general community in the Metropolitan Washington, DC were recruited at the follicular stage of their menstrual cycle. Participants were assigned to one of three study groups: active smokers (N= 107), passive smokers (N= 86), or non-smokers (N= 100). Classifications were based on a combination of self-reporting and serum cotinine concentrations. Methods Serum androgens, estrogens, progestins, androstenedione, aldosterone, cortisol, corticosterone, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), 11-deoxycortisol and 25-hydroxy-vitamin D3 (25-OHVitD3) and cotinine were measured by isotope dilution tandem mass spectrometry (LC/MS/MS) (API-5000). Kruskal–Wallis tests were used to assess median differences among the three groups, with Dunn’s multiple comparison test for post hoc analysis. Results Serum estrone, estradiol, and estriol concentrations were lower in active and passive smokers than in non-smokers. The three study groups differed significantly in serum concentrations of 16-OHE1, aldosterone and 25-OHVitD3, as well as in the ratios of many of the steroids. Pair-wise comparison of the groups demonstrated significant differences in hormone concentrations between (i) smokers and nonsmokers for aldosterone: (ii) passive smokers and non-smokers for aldosterone, progesterone and estriol. Moreover, for smokers and passive smokers, there were no significant differences in these hormone concentrations. Conclusions Smoke exposure was associated with lower than normal median steroid hormone concentrations. These processes may be instrumental in explaining some adverse effects of tobacco smoke on female health and fertility.

The triptans are a class of tryptamine-based drugs indicated for in the treatment of migraine headaches. The triptans act as serotonin (5-hydroxytriptamine) (5-HT) agonists by binding to various serotonin receptors, causing vasoconstriction and neuronal inhibition to alleviate migraines. There are 7 types of triptans currently available on the U.S. market: almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, sumatriptan and zolmitriptan. The objective of this study was to examine the use and effects of triptans in pregnancy. Although three of the triptans have pregnancy registries maintained by the manufacturer, triptan use in pregnancy has not been extensively studied. Information on the use of sumatriptan during pregnancy is relatively more abundant, because it has been on the market longer than the other triptans and may also have a higher percentage of the market share. There are no data to suggest teratogenicity for any of the triptans, although preterm birth rates appear to be elevated.

Thyroid hormones are essential for cellular metabolism, growth, and development. In particular, an adequate supply of thyroid hormones is critical for fetal neurodevelopment. Thyroid hormone tissue activation and inactivation in brain, liver, and other tissues is controlled by the deiodinases through the removal of iodine atoms. Selenium, an essential element critical for deiodinase activity, is sensitive to mercury and, therefore, when its availability is reduced, brain development might be altered. This review addresses the possibility that high exposures to the organometal, methylmercury (MeHg), may perturb neurodevelopmental processes by selectively affecting thyroid hormone homeostasis and function.