Particle Uptake, Migration, and Cytotoxicity in Lung Cancer Cells and Monocytes Exposed to Urban PM₁₀ and PM_2.5

Particulate matter (PM) in the air, classified as PM_2.5 and PM₁₀, enters the body through the nose and mouth during breathing and reaches the lungs. PM is linked to respiratory damage, lung cancer, and the activation of immune system cells, including inflammation and metastasis. Previously, our work group showed that PM upregulates the expression of adhesion molecules and their ligands in lung cancer cells (A549), favoring their adhesion to monocytes; however, its role in cancer progression remains unclear. Therefore, this study examined whether PM exposure promotes a pro-migratory behavior and cell death in A549 cells and monocytes (U937). PM uptake was detected in cells by transmission electron microscopy (TEM) and flow cytometry; cell migration was measured by wound-healing and transwell assays in cocultures of U937 and A549 cells; and cell death was measured by Annexin-V-FLUOS/propidium iodide-mediated flow cytometry. In A549 cells, both PM exposures led to cellular uptake, morphological changes, and increased cell migration. In cocultures of U937 and A549 cells, treatment of both cells with 10 μg/cm² of PM_2.5 and PM₁₀ resulted in the most significant increase in monocyte migration, and PM₁₀ had the maximum effect compared to PM_2.5. High PM concentrations (30 μg/cm²) induced necrosis in A549 cells, with rates of 17.7% for PM_2.5 and 63.3% for PM₁₀. Therefore, these results suggest that PM exposure in lung cancer cells and monocytes could promote an inflammatory environment and tumor cell progression.