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The long-term in vitro co-exposure of polyethylene terephthalate (PET) nanoplastics and cigarette smoke condensate exacerbates the induction of carcinogenic traits
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Lab tests showed that when human lung cells were exposed to both nanoplastics from PET water bottles and cigarette smoke over a long period, the combination caused significantly more DNA damage and cancer-like changes than either substance alone. This suggests that the combined effect of inhaling nanoplastics and smoking may pose a greater cancer risk than previously understood.
This study examines the long-term impact of polyethylene terephthalate nanoplastics (PET-NPLs) and cigarette smoke condensate (CSC) on human lung BEAS-2B cells, focusing on key biological hallmarks of carcinogenesis. True-to-life PET-NPLs were generated from plastic water bottles and characterized to simulate environmental exposure conditions; and a comprehensive battery of assays was employed to assess genotoxicity, cellular transformation, and invasiveness. It was observed that, compared to passage control and individual exposures, co-exposure to PET-NPLs and CSC exacerbates oxidative stress, genotoxicity, and tumorigenic transformation, as evidenced by increased DNA damage, colony formation in soft agar, and enhanced cell migration and invasion. Transcriptomic analysis revealed a shift in cellular stress regulation including the upregulation of stress-response genes, including SLC7A11, NQO1, and HSPA1A, which are linked to oxidative stress adaptation and tumor survival. At the same time, key tumor-suppressor genes, such as LOX, and FN1, were significantly downregulated, promoting cellular transformation and invasiveness. These results provide compelling evidence that the combination of PET-NPLs and CSC enhances carcinogenic traits through oxidative stress, genomic instability, and disruption of tumor-suppressive pathways. This study underscores the importance of evaluating the synergistic effects of combined environmental exposures and their implications for human health.
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Long-Term Exposure to Real-Life Polyethylene Terephthalate Nanoplastics Induces Carcinogenesis In Vitro
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In a lab study, human lung cells exposed to PET nanoplastics (the same plastic used in water bottles) for 30 weeks developed signs of cancer, including DNA damage, the ability to grow without normal anchoring, and increased activity of cancer-related genes. These findings suggest that long-term, chronic exposure to nanoplastics through breathing could carry serious cancer risks that short-term safety tests would miss.
Long-TermExposure to Real-Life Polyethylene TerephthalateNanoplastics Induces Carcinogenesis In Vitro
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Long-term in vitro exposure of lung epithelial cells to real-life PET nanoplastics — particles collected from the environment rather than synthesized models — induced carcinogenic transformation including anchorage-independent growth and epithelial-to-mesenchymal transition, suggesting that chronic inhalation exposure to PET nanoplastics may contribute to lung cancer risk.
Toxicological assessment of benzo(a)pyrene - coated PET nanoplastics in vitro on a 3D model of the human bronchial epithelium
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Researchers assessed the toxicity of PET nanoplastics coated with benzo(a)pyrene, a polycyclic aromatic hydrocarbon, on airway cells in vitro to simulate inhalation exposure. The combined exposure to nanoplastics and PAH contamination showed greater toxicity than either pollutant alone.
Toxicological assessment of benzo(a)pyrene - coated PET nanoplastics in vitro on a 3D model of the human bronchial epithelium
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Researchers assessed the in vitro toxicity of PET nanoplastics coated with benzo(a)pyrene on airway epithelial cells, simulating inhalation of pollutant-loaded particles. The combination of nanoplastics and PAH contamination produced stronger toxic effects than either stressor tested alone.
Advancing the hazard assessment of nanoplastic exposure under environmentally realistic conditions using human in vitro models
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Scientists testing realistic nanoplastics (like those from plastic bottles, not just lab-grade plastic beads) on human cells found they can cause cell damage, inflammation, and DNA harm—and these effects get worse with long-term exposure and when combined with other pollutants like cigarette smoke. This matters because most safety studies use short, simplified tests with idealized plastic particles, meaning real-world nanoplastic exposure from our food, water, and air could pose bigger health risks than previously thought.
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