Maternal Electronic Cigarette Inhalation Exposure During Gestation: Impacts on Prolactin and Xanthine Oxidase.

Abstract

Pregnancy requires metabolic and endocrine changes that must occur to support fetal growth and development. Aberrations in these necessary modifications can impact maternal health and fetal growth. Exposure to toxicants during pregnancy can negatively affect fetal health and development, but studies on electronic cigarette (e-cig) exposure is limited. We hypothesized that maternal e-cig exposure during gestation leads to hormonal and redox imbalance and negatively impacts fetal development. Pregnant Sprague-Dawley rats were exposed to e-cig aerosols (1227 ± 131 mg/m³) or HEPA-filtered air for 90 min from gestational day (GD) 10-19 for a total of 6 days. Dams were euthanized on GD 20 and dam serum, liver, lung, ovaries, and placental tissue were collected for analysis. Fetal mass, placental mass, and sex ratios were assessed. Fetal and placental mass were significantly decreased in e-cig exposed compared to sham-control (2.61 ± 0.19 g vs. 3.37 ± 0.09 g and 0.62 ± 0.03 g vs. 0.70 ± 0.02 g, respectively). Placental xanthine oxidase (XO) activity was significantly increased in e-cig exposed compared to sham-control (5.29 ± 0.27 µU/mL vs. 4.28 ± 0.36 µU/mL). Circulating prolactin (PRL) levels of e-cig exposed dams were significantly decreased compared to sham-control (2.40 ± 0.06 ng/mL of plasma vs. 3.83 ± 0.64 ng/mL of plasma). Maternal e-cig inhalation exposure during gestation negatively impacted fetal growth, increased placental XO activity, and decreased circulating PRL levels. These data demonstrate two potential mechanisms that could lead to the observed reduction in fetal growth following maternal exposure: potential redox imbalance within the placenta and/or hormonal imbalance directly affects fetal growth and potentially influences growth later in life.