The in utero environment is sensitive to toxicant exposure, altering the health and growth of the fetus, and thus sensitive to contaminant exposure. Though recent clinical data have the use of e-cigarettes does no further harm to birth outcomes than a nicotine patch, this does not account for the effects of vaping during pregnancy on the long-term health of offspring. Pregnant mice were exposed to: (a) e-cigarette vapor with nicotine (PV + Nic; 2% Nic in 50:50 propylene glycol: vegetable glycerin), (b) e-cigarette vapor without nicotine (PV; (50:50 propylene glycol: vegetable glycerin)), or (c) HEPA filtered air (FA). Dams were removed from exposure upon giving birth. At adulthood, pulmonary function tests on the offspring revealed female and male mice from the PV group had greater lung stiffness (Ers) and alveolar stiffness (H) compared to the FA group. Further, baseline compliance (Crs) was reduced in female mice from the PV group and in male mice from the PV and PV + Nic groups. Lastly, female mice had decreased forced expiratory volume (FEV0.1) in the PV group, but not in the male groups, compared to the FA group. Lung histology revealed increased collagen deposition around the vessels/airways and in alveolar tissue in PV and PV + Nic groups. Further, goblet hyperplasia was observed in PV male and PV/PV + Nic female mice. Our work shows that in utero exposure to e-cigarette vapor, regardless of nicotine presence, causes consequences in lung function and structure that persists in the offspring to adulthood.
Introduction
The in‐utero environment is delicate, as it fosters the proper health and growth of the fetus. Negative environmental effects during gestation increase the chances of long‐term developmental consequences. As e‐cigarettes gain popularity in pregnant mothers, the aim of this study is to observe the chronic pulmonary function of adult mice exposed to e‐cigarette vapor during gestation.
Methods
Pregnant mice underwent exposure for 4 hours a day, 5 days a week beginning from the first day of pairing for breeding and ending at birth. Mice were separated into three exposure groups each receiving one 70 mL e‐cig vapor puff per minute of (1) E‐cig vapor with nicotine Nic(+) (2% Nic 50:50 propylene glycol:vegetable glycerin), (2) E‐cig exposure without nicotine Nic(‐) (propylene glycol: vegetable glycerin), or (3) continuous filtered air exposure (FA)HEPA filter. Resulting pups from each group were examined at adulthood (4‐5 months). Data including baseline lung mechanic scan and a dose response to different concentrations of methacholine, a drug used to induce airway hyperreactivity, were obtained via the FlexiVent FX2 (SCIREQ Inc.)
Results
Male and female offspring of mice exposed to Nic(‐) and Nic(+) witnessed a significant decrease in overall lung function as compared to the FA group. Baseline compliance (Crs) was significantly decreased in the Nic(‐) female group and Nic(‐) and Nic(+) male groups (P < 0.05 via ANOVA). Female and male mice in the Nic(‐) had greater stiffness (Ers) than the corresponding FA group (P < 0.05). Upon addition of methacholine, female mice in the Nic(‐) and male mice in the Nic(+) had an increased amount of lung resistance (Rrs)upon inhalation (P < 0.05). Female mice in the Nic(‐) had decreased forced expiratory volume (FEV0.1) in comparison with the FA group (P < 0.05).
Conclusion
Preliminary data supports that in‐utero exposed mice to e‐cigarette vapor with or without nicotine causes long term alterations in lung function. Future directions aim to understand the mechanisms of change through observing changes in histology, altered gene expression, protein analysis, and epigenetic changes through DNA methylation. Results of this work demonstrate that vaping may not be a safe alternative to smoking during pregnancy as the health of the offspring have detrimental pulmonary effects in adulthood.
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