1. Placental crossing — Nicotine crosses the placenta and reaches the fetus at concentrations detectable in fetal blood and amniotic fluid. The fetus cannot metabolize nicotine as efficiently as an adult.
2. Vascular constriction — Nicotine constricts blood vessels in the placenta, reducing the flow of oxygen and nutrients to the fetus. This is the primary mechanism behind low birth weight and SGA.
3. Neurodevelopmental interference — Nicotine binds to nicotinic acetylcholine receptors in the fetal brain, disrupting normal neural development. Animal studies show persistent memory, attention, and behavioral deficits.
4. Lung development impairment — Oxidative stress and inflammation from e-cigarette vapor impair the development of fetal lung tissue, potentially increasing the risk of respiratory problems after birth.
5. Endocrine disruption — Altered gene expression (clock genes, antioxidant pathways, sirtuin-1) suggests that prenatal nicotine exposure may have epigenetic effects that persist beyond the immediate fetal period.