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Polyethylene Micro/Nanoplastics Exposure Induces Epithelial–Mesenchymal Transition in Human Bronchial and Alveolar Epithelial Cells
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When human lung cells were exposed to polyethylene micro- and nanoplastics (the most common type of plastic pollution), the cells underwent a transformation called epithelial-mesenchymal transition, where they changed shape, reorganized their internal structure, and gained increased ability to migrate. This cellular change is a known early step in both lung fibrosis and cancer development, suggesting that inhaling polyethylene plastics could contribute to serious lung diseases.
Micro/nanoplastics (MNPs), which are widely spread in the environment, have gained attention because of their ability to enter the human body mainly through ingestion, inhalation, and skin contact, thus representing a serious health threat. Several studies have reported the presence of MNPs in lung tissue and the potential role of MNP inhalation in triggering lung fibrosis and tumorigenesis. However, there is a paucity of knowledge regarding the cellular response to MNPs composed of polyethylene (PE), one of the most common plastic pollutants in the biosphere. In this study, we investigated the effects of low/high concentrations of PE MNPs on respiratory epithelial cell viability and migration/invasion abilities, using MTT, scratch, and transwell assays. Morphological and molecular changes were assessed via immunofluorescence, Western blot, and qRT-PCR. We demonstrated that acute exposure to PE MNPs does not induce cellular toxicity. Instead, cells displayed visible morphological changes also involving actin cytoskeleton reorganization. Our data underlined the role of epithelial-mesenchymal transition (EMT) in triggering this process. Moreover, a remarkable increase in migration potential was noticed, in absence of a significant alteration of the cell's invasive capacity. The present study highlights the potential impact of PE MNPs inhalation on the human respiratory epithelium, suggesting a possible role in carcinogenesis.
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