Polystyrene nanoplastics increase migration in normal lung cells while inducing differential cytotoxicity in lung cancer cells.

Micro and nanoplastics, widely present in indoor and ambient air, are emerging inhalable contaminants that can accumulate in the respiratory tract. The potential health risks associated with their accumulation in the human body are increasingly recognized. Polystyrene nanoplastics (PS-NPs)-induced toxicity has been studied; however, the different responses between normal and cancerous lung cells remain poorly understood. In this study, we exposed normal (IMR90, BEAS-2B) and cancerous (A549, HCC1833, NCI-H727, NCI-H1755) human lung cell lines to various sizes of PS-NPs (50-1000 nm) and evaluated cellular uptake, viability, gene expression, and cell migration. Confocal imaging revealed an efficient internalization of PS-NPs across all cell types, indicating that differences in downstream responses are not caused by uptake efficiency. Cancer cells in the lungs showed increased sensitivity to PS-NPs-induced cytotoxicity, accompanied by significant downregulation of the antioxidant enzyme superoxide dismutase 1, implicating redox imbalance as a possible mechanism of toxicity. However, the cells in the normal lung exhibited no significant change in viability but displayed increased cell migration following exposure to PS-NPs. Collectively, our findings highlight the distinct and cell-type-specific effects of PS-NPs on lung cells, suggesting that inhaled nanoplastics may contribute to pulmonary dysfunction and malignancy through multiple mechanisms, including oxidative stress and altered cell migration.