CHUN-WEN CHENGYU-FAN LIUCHANE-YU LAI2026-10-162026-10-162026-08-01Pure ID: 15390416Pure UUID: 223e2438-931f-4d88-8acb-f8cf1415c47110.1016/j.hazadv.2026.101276https://www.scopus.com/pages/publications/105041255339https://scholars.csmu.edu.tw/handle/123456789/26740Particulate matter ≤ 2.5 µm (PM2.5) is increasingly recognized as a hazardous airborne contaminant capable of promoting cancer progression. This study investigated the biological effects of construction-derived, water-extractable PM2.5 (W-PM2.5) collected continuously over 24 months from a residential earthwork and demolition site. Chemical characterization revealed elevated levels of water-soluble transition metals, particularly copper, nickel, and lead, during the mud work phase. MDA-MB-231 human breast cancer cells were exposed to graded concentrations of W-PM2.5, and cell viability, migration, and invasion were assessed using CCK-8, wound healing, and Boyden chamber assays. The potential molecular mechanisms were examined via Western blot analysis. Exposure to metal-enriched PM2.5 significantly enhanced breast cancer cell proliferation, motility, and invasion in a dose-dependent manner. Western blot findings further confirmed activation of autophagy signaling, characterized by increased Beclin-1 expression and LC3-II conversion, suggesting an autophagy-dependent promotion of breast cancer malignancy. These results demonstrate that construction-generated metal-rich PM2.5 may exacerbate cancer progression through inhalable metal-induced cellular signaling pathways. In conclusion, this study underscores the need for strengthened occupational exposure control measures at construction sites, including engineering dust suppression, real-time air quality monitoring, and the use of filtering facepiece respirators (FFRs) to mitigate health risks among workers. Future investigations should incorporate size-fractionated sampling and explore the role of ultrafine metal-bound particles to further elucidate toxicity mechanisms.enjournal article