Nicotine Exposure During Gestation: From Placental Dysfunction to Long‐Term Neurobehavioral Outcomes
Abstract
BACKGROUND: Prenatal nicotine exposure (PNE) remains a significant public health concern due to persistent tobacco use, electronic nicotine delivery systems, and second-hand exposure during pregnancy. Epidemiological and experimental evidence has demonstrated that nicotine can readily cross the placenta, disrupt placental development, and interfere with tightly regulated processes of fetal organogenesis. These early perturbations are increasingly recognized as initiating a cascade of structural, functional, and molecular alterations that extend beyond gestation and influence health trajectories across the lifespan. However, existing studies are often compartmentalized by developmental stage, limiting mechanistic integration across prenatal, natal, postnatal, and later-life outcomes. METHODS: This review aims to (i) synthesize evidence from placental biology, developmental toxicology, neurobiology, and epigenetics to propose an integrated, life-course cascade model of PNE; (ii) delineate how nicotine-induced placental dysfunction and fetal hypoxia during prenatal development transition into structural, physiological, perinatal autonomic, and cardiorespiratory vulnerability, contributing to adverse birth outcomes and increased risk of sudden infant death syndrome; and (iii) examine how early disruption of nicotinic acetylcholine receptor mediated signaling alters neuronal differentiation, synaptic maturation, neuroimmune interactions, and stress-response pathways, leading to…
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