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Polyethylene Nanoplastic Exposure Causes Miscarriage by Impairing Trophoblast NAD + Metabolism via Mitochondrial Dysfunction
Summary
Scientists found tiny plastic particles (from everyday polyethylene, used in bags and packaging) in placental tissue from every pregnancy sample they studied, and higher levels were linked to increased miscarriage risk. In mice and lab-grown placental cells, these plastic particles damaged the cell's energy-producing mitochondria, which blocked processes needed for a healthy pregnancy to take hold, but treatments that protected mitochondria or restored key molecules reversed the damage. This research suggests everyday plastic exposure may pose a real risk to pregnancy, while also pointing to possible ways to protect against
ABSTRACT Micro‐ and nanoplastics (MNPs) are emerging environmental pollutants of global concern, yet their reproductive toxicity and underlying mechanisms remain poorly understood. Here, we identify villous accumulation of polyethylene (PE) as a potential risk factor associated with miscarriage and investigate the underlying mechanisms using well‐characterized PE nanoparticles. PE fragments were detected in all examined human villous tissues and higher levels of these fragments showed a positive association with miscarriage risk (OR = 1.13, 95% CI, 1.00–1.28). In mice, oral exposure to PE‐MNPs led to dose‐dependent embryo resorption. In trophoblasts, PE nanoplastics (PE‐NPs) were efficiently internalized and subsequently impaired cell migration and invasion. Mechanistically, PE‐NPs accumulated within mitochondria, causing structural damage, downregulation of nicotinamide phosphoribosyltransferase (NAMPT), and depletion of nicotinamide adenine dinucleotide (NAD + ), which in turn suppressed fibroblast growth factor 2 (FGF2) expression, resulting in impaired trophoblast migration and invasion. Supplementation with mitochondria‐protective peptide, NAD + or FGF2 attenuated trophoblast dysfunction and reduced embryo resorption. These findings provide mechanistic insight into PE‐NPs‐induced reproductive toxicity and suggest a potential therapeutic target to mitigate the impact of NPs exposure on maternal‐fetal health.