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Cardiotoxicity of polystyrene nanoplastics and associated mechanism of myocardial cell injury in mice
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Mice exposed to polystyrene nanoplastics for 42 days developed enlarged hearts, thinner heart walls, and weaker heart contractions in a dose-dependent manner. The nanoplastics triggered inflammation and oxidative stress in heart muscle cells through specific signaling pathways. These findings suggest that nanoplastic exposure could contribute to heart disease, including a condition called dilated cardiomyopathy.
AIMS: Nanoplastics (NPs) are emerging organic pollutants generated by plastic degradation and are ubiquitous in the environment. They can be accumulated through the food webs and enter the human body through dietary intake, posing health risks. The main target organs of NP accumulation are the lungs, liver, heart, and kidneys. However, compared with that for other target organs, research on the adverse effects of NPs on the heart is limited. We aimed to investigate the toxic effects of polystyrene NPs on the heart and the associated mechanisms. METHODS AND RESULTS: Forty-eight male C57BL/6 mice were randomly divided into control and experimental groups. Three experimental groups were exposed to NP doses of 30, 60, and 100 mg/L for 42 days. The mice exhibited enlarged ventricular chambers, thinned ventricular walls, decreased ejection fraction, reduced heart rate, and lowered blood pressure with increasing PS-NP concentration. In vitro experiments using H9C2 myocardial cells demonstrated that PS-NPs activate the TNF-α/NF-κB and P38/MAPK signaling pathways and thereby induce inflammatory infiltration and oxidative stress. This can lead to myocardial fibrosis and apoptosis and thus eccentric cardiac hypertrophy and impaired contractile function. CONCLUSIONS: This study provides new evidence regarding the potential mechanisms of PS-NP cardiovascular toxicity as well as insights into the diagnosis and treatment of unexplained dilated cardiomyopathy in clinical settings.
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Researchers exposed mice to polystyrene nanoplastics through inhalation and found that even short-term breathing exposure caused heart damage, including inflammation and weakened heart function. The damage got worse with higher doses and longer exposure times, with energy production in heart cells being disrupted through mitochondrial damage. This is one of the first studies to show that breathing in nanoplastics can directly harm the heart, raising concerns about airborne plastic particle exposure in humans.
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Mice exposed to airborne polystyrene nanoplastics for just two weeks showed significant heart damage, including reduced heart mass, slowed heart rate, and signs of heart failure. The study suggests that inhaled nanoplastics harm cardiac tissue through specific molecular pathways, raising concerns about the cardiovascular risks of breathing in plastic-contaminated air.
Micro(nano)plastics in the Development of Myocardial Fibrosis: From Clinical Detection to Molecular Mechanism
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Researchers found that micro- and nanoplastic burden in human cardiac tissue—particularly nanoplastics—was positively associated with myocardial fibrosis severity, and confirmed in mice that polystyrene nanoplastic exposure worsens stress-induced cardiac remodeling by activating inflammatory, extracellular matrix, and metabolic pathways.
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Researchers demonstrated that oral exposure to polystyrene nanoplastics in mice causes cardiac fibrosis, cardiomyocyte death, and impaired heart function by upregulating the protein HIPK2 and activating P53 and TGF-β1/Smad3 signaling pathways, with effects worsened in animals with pre-existing heart disease — implicating nanoplastics as a cardiovascular risk factor.
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