A549 as an In Vitro Model to Evaluate the Impact of Microplastics in the Air

SIMPLE SUMMARY: This review article addresses the introduction and mechanism of action concerning the potential health effects of air-born microplastics on lung epithelial cell line A549. Micro- and nanoplastics are air-born pollutants, are inhaled, and cause lung toxicity by becoming internalized in cells, inducing genotoxicity, oxidative stress, immunomodulation, and morphological changes in A549 cells. These microplastics have the potential to accumulate in cells and trigger inflammation thereby contributing to the development of lung diseases. Numerous studies have investigated various aspects of micro- and nanoplastics on lung epithelial cells; however, the precise mechanism by which they initiate, or progress, lung toxicity is still subject to investigation. Nonetheless, the findings of previous studies strongly suggested that microplastics cannot be underestimated as insignificant air pollutants due to their potential to accumulate not only in the lungs but also in other organs such as the brain. This review article compiles studies on the effects of polystyrene microplastics on lung epithelial cells, highlighting existing research gaps, and providing suggestions for further research in this area. ABSTRACT: 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.