Background Use of electronic cigarettes (e-cigarettes) and other nicotine containing products is increasing among women of reproductive age. The short- and long-term effects of these products on both mother and fetus are unknown. Methods Because e-cigarettes are nicotine delivery systems, we sought to conduct a comprehensive review of the effects of nicotine on the fetus. Results In utero nicotine exposure in animal models is associated with adverse effects for the offspring lung, cardiovascular system and brain. In the lung, this included reduced surface area, weight, and volume, as well as emphysema-like lesions. In adulthood, exposed offspring demonstrate elevated blood pressure and increased perivascular adipose tissue. In the brain, exposure alters offspring serotonergic, dopaminergic, and norepinephrine networks, which in turn are associated with behavioral and cognitive impairments. We also review current data on the lack of efficacy of nicotine replacement therapy in pregnant women, and highlight different nicotine containing products such as snuff, snus, and hookah. Conclusion We conclude that no amount of nicotine is known to be safe during pregnancy, and studies specifically addressing this risk are crucial and an imminent public health issue.

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OBJECTIVE: The prevalent use of e-cigarettes and other nicotine products are increasing among women of reproductive age, making their effect on pregnancy an important public health concern. Nicotine is associated with adverse effects on the fetus including reduced placental blood perfusion and decreased fetal pulmonary function. Utilizing a rat model of in utero nicotine exposure, we have recently demonstrated epigenetic alterations in the lung and brain of offspring at postnatal day 1. Moreover, previous studies in nonhuman primates show effects of nicotine on fetal pulmonary function and oxidant radical production, and these effects are mitigated by treatment with the anti-oxidant Vitamin C (VC). Studies have also shown that nicotine is a potent histone deacetylase inhibitor. Based on these observations, we sought to determine the underlying molecular mechanisms. We hypothesized that differential histone post translational modifications (PTMs) would be detected in these tissues in response to nicotine, which may be further modulated upon Vit C treatment. STUDY DESIGN: In this preclinical study, PTMs were investigated in histones isolated from fetal lung and placenta from near term Rhesus macaques. Mothers received Vit C (VC) or placebo, and nicotine or saline to yield six different treatment groups (n¼7-9); control (placebo + saline), saline + 50mg/kg VC or 250mg/kg VC, nicotine + placebo, and nicotine + 50mg/kg or 250 mg/kg VC daily. Western blots were performed for the following histone PTMs: H3K4me3, H3K9me3, H3K27me3, H3K9ac, H3K14ac, H3PanAc and H4PanAc. Total histone H3 was used for normalization. RESULTS: As shown (Figure), analysis of specific histone PTMs demonstrate a significant difference between control and nicotine + 250mg/kg Vit C (NVC) groups in the placenta (H3K9me3, H3K9Ac, H3K27me3; p¼0.016, 0.027, 0.027 respectively) and in the lung (H3K4me3; p¼0.039). CONCLUSION: Nicotine and Vit C demonstrated a significant synergistic effect on the fetal placental and lung epigenome, with notable site-specific histone PTMs. Further study is warranted to investigate the effects of these epigenomic modifications on fetal lung and placental transcriptional networks following nicotine and Vit C exposure. These findings suggest that while Vit C may abrogate clinical impacts of nicotine exposure, the mechanisms are distinct.126 To inhale or not to inhale: a descriptive study of marijuana use and its effects in pregnancy from a contemporary large, population based cohort

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