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Maternal exposure to polystyrene nanoplastics induces sex-specific cardiotoxicity in offspring mice
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When pregnant mice were exposed to polystyrene nanoplastics, their offspring developed heart damage that differed between males and females. Female offspring lost more body and heart weight, while males showed signs of atherosclerosis and females showed viral heart inflammation markers. This study suggests that prenatal nanoplastic exposure could program sex-specific cardiovascular problems in children, raising concerns about plastic exposure during pregnancy.
Globally, plastic pollution threatens human health, particularly affecting the hearts of offspring exposed to maternal environmental factors early in development. Few studies have specifically addressed sex-specific cardiac injury in offspring resulting from maternal exposure to polystyrene nanoplastics (PS-NPs). This study investigates the potential cardiac injury in offspring following maternal exposure to 1 mg/L PS-NPs. Pregnant C57BL/6J mice were exposed to PS-NPs until 3 weeks postpartum to establish a maternal exposure model. Heart tissues were collected and weighed, and the transcriptomes of the offspring hearts were sequenced and analyzed using high-throughput RNA sequencing. Immunohistochemical staining was performed to assess the effects of PS-NPs on cardiac immune infiltration, fibrosis, and apoptosis in the offspring. PS-NPs caused a significant reduction in heart and body weight in female offspring compared to males. Additionally, PS-NPs induced sex-specific transcriptional reprogramming and metabolic disruptions in the offspring. PS-NPs also induced significant fibrosis, apoptosis, and increased CD68+ macrophage infiltration in offspring hearts. Notably, PS-NPs induced distinct cardiovascular diseases in the offspring. Fluid shear stress and atherosclerosis were significantly enriched in PS-NP-treated male offspring, while viral myocarditis was predominantly enriched in PS-NP-treated females. Our findings suggest that PS-NPs induce cardiotoxicity in offspring by disrupting metabolism, impairing immunity, and triggering fibrosis and apoptosis, with sex-specific differences. This study provides novel insights and a foundation for understanding sex-specific pharmacological differences and interventions in PS-NP-induced cardiovascular disease in offspring.
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Sex differences in cardiac fibrosis induced by gestational exposure to polystyrene nanoplastics in mice offspring
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Researchers exposed pregnant mice to polystyrene nanoplastics and examined the hearts of their adult offspring, finding dose-dependent cardiac fibrosis and cell death that differed between males and females. Male offspring showed greater changes in estrogen receptor gene expression compared to females, which may explain the observed sex differences in heart damage. The study suggests that prenatal nanoplastic exposure could have lasting effects on heart health, with males potentially more vulnerable.
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Researchers exposed pregnant rats to airborne micro- and nanoplastics and tracked heart development and function in their offspring from before birth through three months of age. They found that the exposure caused sex-specific cardiac changes, including altered heart wall thickness and chamber dimensions that persisted into adulthood. The study suggests that prenatal microplastic exposure may program lasting cardiovascular differences, with male and female offspring affected in distinct ways.
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Researchers found that when pregnant mice were exposed to polystyrene nanoplastics (nano-sized plastic particles), their male offspring suffered more severe kidney damage than females — including reduced kidney cell numbers, increased scarring, and altered immune responses. The sex-specific nature of these effects suggests that nanoplastic exposure during pregnancy may carry different long-term health risks depending on the sex of the child.
Effects of polystyrene nanoplastic gestational exposure on mice
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Researchers exposed pregnant mice to airborne polystyrene nanoplastics and studied the effects on both mothers and offspring. High-dose exposure caused fatty liver disease in the mothers and in adult female offspring, but not in male offspring, with each group showing different underlying molecular mechanisms. The study suggests that prenatal exposure to airborne nanoplastics may have sex-specific effects on metabolic health that persist into adulthood.
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