Abstract
Abstract
As pervasive environmental contaminants, nanoplastics (NPs) have garnered increasing concern due to their potential health hazards. However, the impact of gestational and lactational exposure to NPs on offspring vascular structural injury remains unexplored. In this study, we used BALB/c mice to model gestational and lactational exposure to 100 nm polystyrene nanoplastics (PS-NPs) at doses of 0.1, 1, and 10 mg/L. Our findings revealed that PS-NPs exposure significantly reduced offspring body weight in both sexes. Histopathological analysis demonstrated that exposure induced multiorgan damage in offspring at postnatal day 21 (PND 21), with partial recovery by PND 90. Critically, PS-NPs exposure induced cardiovascular toxicity in offspring, which included acute vascular injuries (disordered elastic fibers and evident calcium salt deposition) at PND 21 that were largely resolved by PND 90, alongside more persistent issues of abnormal lipid deposition in the aortic root and dyslipidemia observed at both time points. Integrated biomarker response indices, principal component analysis, and hierarchical clustering confirmed dose-dependent toxicity in PS-NPs-exposed offspring. In vitro studies further showed that PS-NPs induced lipid accumulation in three major cardiovascular cell types: endothelial cells, smooth muscle cells, and macrophages. Our study firstly reveals that maternal PS-NPs exposure throughout gestation and lactation induces vascular injury and lipid deposition in mouse offspring, indicating that PS-NP pollution represents a critical environmental risk factor for offspring cardiovascular adverse outcomes later in life.