Work

The long-term in vitro co-exposure of polyethylene terephthalate (PET) nanoplastics and cigarette smoke condensate exacerbates the induction of carcinogenic traits

Year: 2025

Type: article

Abstract: 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. • The coexposure effects of PET nanoplastics and tobacco condensates were evaluated. • Long-term and human lung cells was the defined exposure scenario. • Cancer hallmarks and transcriptomic analysys detect the induced effects. • Co-exposure exacerbates oxidative stress, genotoxicity, and cell transformation. • Transcriptomic analysis reveal shifts in cellular stress and key tumor-suppressor genes.

Source: Journal of Hazardous Materials

DOI: 10.1016/j.jhazmat.2025.138359