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Article Tier 2 Human Health Effects Nanoplastics Reproductive & Development Sign in to save

Embryonic exposure of polystyrene nanoplastics affects cardiac development

The Science of The Total Environment 2023 43 citations

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Researchers found that polystyrene nanoplastics disrupted the development of heart cells grown from human embryonic stem cells, producing smaller and weaker heart tissue in the lab. The nanoplastics caused oxidative stress in mitochondria and blocked important cellular cleanup processes, reducing the stem cells' ability to properly form heart cells. In zebrafish embryos, nanoplastic exposure also reduced heart contractions and blood flow, suggesting that nanoplastic exposure during pregnancy could pose risks to fetal heart development.

Polymers
Study Type In vivo

Micro- and nanoplastics have recently been detected in human blood and placentas, indicating inevitable embryonic exposure to these particles. However, their influence on human embryogenesis and the underlying mechanisms are still unknown. In this study, the effects of polystyrene nanoplastics (PS-NPs) exposure on cardiac differentiation of human embryonic stem cells (hESCs) were evaluated. Uptake of PS-NPs not only caused cellular injury, but also regulated cardiac-related pathways as revealed by RNA-sequencing. Consequently, the efficiency of cardiomyocyte differentiation from hESCs was compromised, leading to immature of cardiomyocytes and smaller cardiac organoids with impaired contractility. Mechanistically, PS-NPs promoted mitochondrial oxidative stress, activated P38/Erk MAPK signaling pathway, blocked autophagy flux, and eventually reduced the pluripotency of hESCs. Consistently, in vivo exposure of PS-NPs from cleavage to gastrula period of zebrafish embryo led to reduced cardiac contraction and blood flow. Collectively, this study suggests that PS-NPs is a risk factor for fetal health, especially for heart development.

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Researchers exposed zebrafish embryos to polystyrene nanoplastics and found dose-dependent cardiac developmental defects linked to disruption of the Notch and Wnt signaling pathways — key regulators of heart development — alongside oxidative stress, endoplasmic reticulum stress, and reduced mitochondrial activity.

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Researchers found that even low doses of polystyrene microplastics can damage heart tissue in both mice and lab-grown human heart organoids. The microplastics triggered oxidative stress and disrupted energy production in heart cells, leading to inflammation and cell death. This is one of the first studies to show heart-specific toxicity from microplastics at doses meant to reflect realistic human exposure levels.

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Zebrafish embryos exposed to plastic nanoparticles (polystyrene) that had been artificially aged by UV light showed more heart defects, faster heart rates, and disrupted heart development than those exposed to unaged particles. Aged particles also caused greater damage to mitochondria, the cell structures that produce energy, which may help explain the stronger effects.

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Polystyrene nanoplastics trigger mitochondrial and metabolic reprogramming in cardiomyocytes: Evidence from integrated transcriptomic and metabolomic analysis

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Scientists found that tiny plastic particles called nanoplastics can damage heart cells by disrupting their powerhouses (mitochondria) and reducing their ability to produce energy. When researchers exposed human heart cells and mice to these nanoplastics, they observed weakened heart function and signs of early heart damage. This research suggests that the growing amount of microscopic plastic pollution in our environment could pose previously unknown risks to heart health.

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