Airborne PM10 Decreases Ku80 Expression and Ku70–Ku80 Heterodimer Levels of the Non-Homologous End Joining Repair Pathway in Lung Epithelial Cells

The global population constantly breathes particulate matter with an aerodynamic diameter of ≤10 µm (PM10)—a human carcinogen linked to lung cancer. Previous studies have indicated that PM10 causes DNA damage, including double-strand breaks (DSBs). In particular, DSBs are primarily repaired by the non-homologous end joining (NHEJ) pathway, which is essential for maintaining genomic stability; however, the effects of PM10 exposure on this pathway are unknown. To address this, A549 lung epithelial cells were exposed to 10 µg/cm2 of PM10 for 6, 12, and 24 h. We determined that DSBs increased with prolonged exposure, and an increase in the frequency of micronuclei was found. Despite the accumulated DNA damage, no changes in the cell cycle were observed. Reductions in the levels of the Ku80 gene and protein, as well as the Ku70–Ku80 heterodimer—which is essential for initiating NHEJ-mediated repair—were observed. Levels of Artemis (which is responsible for processing DNA damage) remained stable, while levels of the XRCC4 gene and protein (responsible for completing repair) decreased. We conclude that PM10 disrupts two key proteins in the NHEJ pathway, impairing the capacity for DSB repair. This could promote the accumulation of DNA damage and induce genomic instability, contributing to the development of cancer.