Progressive pulmonary fibrosis (PPF) is an incurable disease with a higher incidence in the elderly. The Bleomycin (BLM)-induced lung fibrosis model is widely used but lacks chronicity and age-related factors essential for studying PPF. We hypothesized that ERCC1?/- mice, with accelerated aging due to impaired DNA repair, would show a prolonged fibrotic response to low-dose of BLM, modelling progressive fibrosis. A single intratracheal dose of 0.09 IU of BLM or saline was administered to mice. Micro-CT imaging quantified fibrotic tissue and lung aeration longitudinally at key time points?day 7 (inflammatory phase), day 21 (fibrotic phase), and day 56 (endpoint). Inflammatory cell populations were assessed in the bronchoalveolar lavage fluid (BALF)  and lung tissues were examined histologically. Longitudinal micro-CT analysis revealed persistent and non-resolving fibrosis in BLM-treated ERCC1?/- mice, with significant reductions in aerated lung volume and non-aerated tissue, representative of scar tissue, that persisted for at least 8 weeks post-administration, consistent with histological findings. Flow cytometry confirmed elevated levels of inflammation, with a marked increase in the recruitment and activation of macrophages in the lungs of BLM-treated ERCC1?/- mice compared to saline controls. We conclude that ERCC1?/- mice, treated with BLM, exhibit a prolonged fibrotic response characterized by sustained macrophage activation. This model more accurately reflects the chronic nature of human lung fibrosis and might serve as a valuable tool for the development and testing of antifibrotic therapies.