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Exposure to polyethylene terephthalate micro(nano)plastics exacerbates inflammation and fibrosis after myocardial infarction by reprogramming the gut and lung microbiota and metabolome
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Researchers found that PET microplastics and nanoplastics, one of the most common plastic types found in human coronary blood, worsen heart damage after a heart attack. The plastic particles activated an inflammatory pathway (NLRP3) and disrupted the balance of gut and lung bacteria, leading to chronic inflammation and increased scarring of heart tissue. These findings suggest that plastic pollution exposure may make recovery from heart attacks more difficult.
Micro(nano)plastics (MNPs), a ubiquitous environmental pollutant, have received increasing attention for their impacts on human health. We conducted an in-depth study on the role of polyethylene terephthalate (PET) MNPs in myocardial infarction (MI). Blood from the coronary circulation of MI patients was collected to detect microplastics (MPs). Peripheral monocytes (PBMCs) and AC16 cells were used to assess inflammation, cell proliferation and apoptosis after PET nanoplastics (NPs) stimulation. The mouse MI model was established after PET NPs respiratory or oral exposure. The results showed that various types of MPs, including high levels of PET MPs, were detected in the coronary circulation. PET NPs promoted inflammatory factors secretion by PBMCs, inhibited AC16 cell proliferation and promoted hypoxia-induced AC16 cell apoptosis. PET NPs exacerbated post-MI inflammation and fibrosis through activating the NLRP3 inflammasome pathway. Through macrogenetic sequencing and metabolomics analyses, we observed that PET NPs reprogrammed the intestinal and lung microbiota and metabolome in MI mice, leading to chronic inflammation. In conclusion, PET MPs were widely present in the coronary circulation of MI patients. PET MNPs can activate the NLRP3 inflammasome pathway to exacerbate post-MI ventricular remodelling, which may be related to the reprogramming of the gut and lung microbiota and metabolome.
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In a study of 142 heart attack patients, researchers found microplastics and nanoplastics in the coronary blood of nearly all participants, with polyvinyl chloride (PVC) detected in over 95% of samples. Higher PVC levels were linked to increased inflammatory markers and a significantly greater risk of major heart complications over the 31.5-month follow-up period. For every 10-unit increase in PVC concentration, the risk of a major cardiac event more than doubled.
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Doctors found tiny plastic particles (microplastics) in the blood vessels of heart attack patients far more often than in people with milder heart disease or healthy hearts — and these particles showed up alongside higher inflammation levels, more air pollution exposure, and smoking. While this doesn't prove plastics *cause* heart attacks, it adds to growing evidence that the plastic and pollution we're exposed to daily may be building up in our bodies and could be linked to heart disease risk, making a case for reducing plastic and air pollution exposure where possible.
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