Maternal lung inflammation and apoptosis following gestational exposure to secondhand smoke and E-cigarette vapor: Implications for maternal-fetal health.

Pregnancy is a vulnerable period where maternal exposure to environmental toxicants like secondhand smoke (SHS) and electronic cigarette (eCig) aerosols can harm maternal and fetal health. This study examines the differential impacts of SHS and eCig exposure on maternal lung tissue during late gestation, focusing on inflammation, apoptosis, and oxidative stress. Pregnant C57BL/6 mice were exposed to SHS or eCig aerosols for four or six days from embryonic day 12.5 or 14.5, with lung tissues collected on day 18.5 for analysis. Bronchoalveolar lavage fluid and lung tissue were assessed for inflammation, apoptosis, and oxidative stress. SHS exposure caused pronounced immune activation and mitochondrial-mediated apoptosis, while eCig exposure induced a milder inflammatory response with evidence of epithelial remodeling and oxidative imbalance. Collectively, both exposures disrupted maternal pulmonary homeostasis, with SHS producing stronger inflammatory effects. Unlike SHS, eCig exposure caused transient apoptosis with partial preservation of anti-apoptotic pathways (Bcl-2, IGF-1), while SHS exhibited stronger pro-inflammatory effects, eCig exposure still contributed to oxidative stress and immune dysregulation. These findings underscore the risks of both exposures during pregnancy, emphasizing the need for stringent public health policies regulating eCig use to protect maternal and fetal health.