E-cigarette vapor exposure in utero causes long-term pulmonary effects in offspring.

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 suggest that e-cigarette use 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: 1) e-cigarette vapor with nicotine (PV + Nic; 2% Nic in 50:50 propylene glycol: vegetable glycerin), 2) e-cigarette vapor without nicotine [PV; (50:50 propylene glycol:vegetable glycerin)], or 3) HEPA filtered air (FA). Dams were removed from exposure upon giving birth. At 5 mo of age, 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 with the FA group. Furthermore, 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 with the FA group. Lung histology revealed increased collagen deposition around the vessels/airways and in alveolar tissue in PV and PV + Nic groups. Furthermore, 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 lung dysfunction and structural impairments that persist in the offspring to adulthood.

Short-term PM exposure and social stress cause pulmonary and cardiac dysfunction.

Ambient particulate matter (PM) exposure increases risk for cardiopulmonary health problems which may be exacerbated in a stressful environment. Co-exposure to PM and stress characterizes the experience of many deployed military personnel and first responders but has not been thoroughly investigated. This is especially relevant to military personnel who have been exposed to high PM levels in conjunction with stressful military conflict situations. To understand the mechanisms and time-course of the health consequences following burn pit exposure, we exposed mice to moderate levels of ambient PM less than 2.5 µM in diameter (PM2.5) alone or in combination with psychological stress. We found male mice exposed to PM2.5 alone or in combination with stress had significantly reduced pulmonary function when subjected to methacholine, indicating increased airway hyperreactivity. These mice experienced increased goblet cell hyperplasia in their lungs, with no change in alveolar density. Mice exposed to PM2.5 and/or stress also exhibited reduced cardiac contractility, right ventricular (RV) output, and changes in RV capillary density and cardiac inflammatory markers. Taken together, these data indicate that short-term exposure to PM2.5 with or without stress causes a clear reduction in pulmonary and cardiac function. We believe that this model is well-suited for the study of military and other occupational exposures, and future work will identify potential mechanisms, including the inflammatory progression of these co-exposures.