Airborne microplastics raise significant concerns due to their potential health impacts. Having a small size, larger surface area, and penetrative ability into the biological system, makes them hazardous to health. This review article compiles various studies investigating the mechanism of action of polystyrene micro- and nanoplastics affecting lung epithelial cells A549. These inhalable microplastics damage the respiratory system, by triggering a proinflammatory environment, genotoxicity, oxidative stress, morphological changes, and cytotoxic accumulation in A549 cells. PS-NP lung toxicity depends on various factors such as size, surface modifications, concentration, charge, and zeta potential. However, cellular uptake and cytotoxicity mechanisms depend on the cell type. For A549 cells, PS-NPs are responsible for energy imbalance by mitochondrial dysfunction, oxidative stress-mediated cytotoxicity, immunomodulation, and apoptosis. Additionally, PS-NPs have the ability to traverse the placental barrier, posing a risk to offspring. Despite the advancements, the precise mechanisms underlying how prolonged exposure to PS-NPs leads to the development and progression of lung diseases have unclear points, necessitating further investigations to unravel the root cause. This review also sheds light on data gaps, inconsistencies in PS-Nos research, and provides recommendations for further research in this field.
Keywords: A549; air pollutants; alveolar epithelial cells; nanoplastics; polystyrene.