Hallmarks of aging including cellular senescence are increased in idiopathic pulmonary fibrosis (IPF) and other chronic lung diseases. To study aging-related mechanisms involved in IPF pathogenesis, we used human precision-cut lung slices (hPCLS) that preserve lung architecture and cellular composition, to induce aging ex vivo by exposing hPCLS to ionizing radiation (30Gy). Viability was evaluated by WST-1 and LDH release assays. Senescence and fibrosis-related markers were assessed by RT-qPCR, flow cytometry, and immunofluorescence (IF), and the senescence-associated secretory phenotype (SASP) was characterized using a cytokine array. Lung epithelial stem cell capacity was evaluated in an organoid assay. Irradiated (IR)-hPCLS remained viable 7 days post-irradiation (dpir) with no significant increase in LDH release. IF staining showed induction of DNA damage (?H2Ax), cell cycle arrest (p21), and SA-ß-Gal activity 7 dpir. IR-hPCLS-derived ATII cells exhibited reduced progenitor capacity, and flow cytometry analysis showed an enrichment of senescent SA-ß-Gal+ cells in the epithelial compartment. SASP profiling revealed an early acute inflammatory profile followed by induction of anti-apoptotic, developmental, and epithelial reprogramming-related pathways. Finally, pro-fibrotic markers such as COL1A1, ACTA2, PAI1, and TGFB1 and the release of Procollagen-3 N-Terminal Peptide (P3NP) were induced 7 dpir. In conclusion, we present a novel ex vivo model of epithelial cellular senescence and early fibrotic changes. Future work will focus on using senolytics and anti-fibrotic agents to understand the underlying mechanism and reverse the observed senescence-mediated fibrotic changes.