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Maternal Polystyrene Nanoplastic Exposure Impairs Cardiac Development in Mouse Offspring and Identifies Lactation as a Sensitive Window in Males
Summary
When pregnant mice were exposed to nanoplastics (tiny plastic particles), their babies developed weaker, damaged hearts — and surprisingly, exposure through breast milk caused even more harm than exposure in the womb. Male offspring also showed disrupted gut bacteria alongside the heart changes, suggesting the two problems may be linked. While this is animal research, it raises real concerns about how microplastic exposure during pregnancy and breastfeeding could affect infant heart development in humans.
Maternal exposure to nanoplastics is a growing concern, but its effects on offspring cardiac development and the relative importance of prenatal and lactational exposure remain unclear. Pregnant C57BL/6J mice were orally exposed to 50 nm polystyrene nanoplastics at 3, 15, or 75 μg/g body weight from gestational day 1 to postnatal day 21. A cross-fostering design was used to distinguish gestational exposure from lactational exposure. Maternal polystyrene nanoplastic exposure caused dose-dependent cardiac dysfunction in offspring, including reduced ejection fraction and fractional shortening, increased myocardial injury markers, cardiomyocyte hypertrophy, and fibrosis. Cross-fostering showed that lactationally exposed offspring exhibited more severe cardiac abnormalities than offspring exposed only during gestation, indicating that the nursing period may represent a more vulnerable window. In male offspring, polystyrene nanoplastic exposure was also associated with gut microbiota dysbiosis and cardiac transcriptomic changes. Enrichment analysis identified downregulation of genes related to AMP-activated protein kinase signalling, and integrated microbiome-transcriptome analysis suggested associations between altered gut taxa and cardiac differentially expressed genes. These findings indicate that maternal polystyrene nanoplastic exposure induces offspring cardiac developmental toxicity, with stronger effects during lactation, and suggest the involvement of gut microbial and cardiac molecular remodelling.