In vitro effects of aged low-density polyethylene micro(nano)plastic particles on human airway epithelial cells.

Airborne micro(nano)plastic (MNP) pollution has emerged as a major global concern due to its increasingly worrying adverse health effects. Environmental weathering and UV irradiation of plastic waste, together with tire wear, generate airborne MNPs with irregular shapes and varied sizes, with low-density polyethylene (LDPE) being the predominant plastic type. However, knowledge of MNPs' toxicological effects remains scarce, as current in vitro research mainly focuses on commercial polystyrene beads. In this study, we investigated for the first time the toxicological effects of environmentally relevant aged LDPE MNPs on human bronchial epithelial cells (BEAS-2B). UV-aged LDPE fragments of irregular sizes and shapes were used to mimic real atmospheric particles, and BEAS-2B cells were exposed to 10-1000 μg/cm of LDPE MNPs. Our results showed that MNPs were internalized by BEAS-2B cells and promoted epithelial-to-mesenchymal transition (EMT), characterized by reduced β-catenin and increased vimentin expression, enhanced motility, and disturbed cell cycle. Moreover, exposure to aged LDPE MNPs significantly increased intracellular ROS levels and reduced cell proliferation rate at the highest dose. LDPE MNPs triggered oxidative stress in BEAS-2B cells through activation of the NRF2 signaling pathway, with impaired autophagic flux indicated by increased expression of p62 and LC3A/B. Importantly, LDPE MNP exposure significantly increased the secretion of pro-inflammatory mediators (CD62E, CD62P, ICAM-1, IL-6, IL-8), accompanied by suppressive effects on mitochondrial respiration and glycolytic function at 1000 μg/cm. Taken together, our findings suggest that inhalation of LDPE MNPs could impact the morphology and function of the human airway epithelium and respiratory health in general.