Maternal exposure to microplastics and nanoplastics: Placental lipid metabolic dysregulation as a potential link to fetal growth restriction

Microplastics and nanoplastics (MNPs) are pervasive environmental contaminants linked to reproductive and developmental health. Plastic particles or polymeric residues have been detected in human blood, placenta, meconium, breast milk, fetal appendages, and umbilical venous blood, indicating maternal-fetal interface exposure during pregnancy. Fetal growth restriction (FGR) is a placental syndrome in which the fetus fails to achieve its growth potential, and impaired placental vascular, transport, endocrine, immune, and metabolic functions contribute to its pathogenesis. Experiments with polystyrene or polyethylene particles report fetal growth impairment, altered placental hemodynamics, defective trophoblast differentiation, mitochondrial and endoplasmic-reticulum stress, disrupted cholesterol and nicotinamide metabolism, lipid remodeling, and ferroptosis-associated injury. This targeted narrative review synthesizes human biomonitoring, animal, ex vivo, and omics evidence, with emphasis on placental fatty-acid uptake and oxidation, cholesterol trafficking, glycerophospholipid remodeling, nicotinamide/NAD⁺ homeostasis, oxidative lipid injury, and ferroptosis. Current evidence supports a plausible framework in which MNP exposure contributes to placental lipid metabolic dysregulation and thereby increases vulnerability to fetal growth impairment. However, human causal evidence remains insufficient, and the term MNPs should not obscure important differences between microplastics and nanoplastics in particle size, tissue penetration, detectability, and biological activity. Major uncertainties include contamination control, polymer and particle heterogeneity, environmental dose translation, gestational timing, co-exposure to additives and pollutants, and inconsistent FGR phenotyping. Prospective pregnancy cohorts and human-relevant placental models integrating validated particle detection, fetal growth trajectories, spatial and single-cell omics, metabolic-flux analysis, and rescue experiments are required to determine whether placental lipid dysregulation is a causal mediator of MNP-associated fetal growth restriction.