Background <p>Paraquat (PQ), a widely used herbicide, poses significant ecological and health risks due to its potent oxidative toxicity, particularly affecting the lungs. While fibrotic outcomes of PQ exposure are well documented in mammals, the short-term pulmonary responses of pre-metamorphic amphibians remain poorly characterized. Amphibian tadpoles, which inhabit agricultural environments and undergo rapid respiratory development, provide a tractable model to study environmentally induced lung remodeling during early developmental stages.</p> Results <p>Here, we investigated the acute pulmonary response to environmentally relevant PQ exposure in <i>Microhyla fissipes</i> tadpoles using histological analysis, behavioral assays, and single-cell RNA sequencing (scRNA-seq). PQ exposure over a 15-day period induced non-fibrotic lung remodeling, characterized by alterations in epithelial-mesenchymal coordination, oxidative stress responses, and extracellular matrix organization, without activation of canonical fibrotic gene programs. Immune-mediated adaptation was observed, involving alveolar epithelial cells, fibroblasts, and macrophages, each displaying distinct redox-sensitive transcriptional states. Several cell types reactivated developmental signaling pathways, including Wnt/β-catenin, suggesting that conserved developmental modules are repurposed during environmentally triggered remodeling.</p> Conclusions <p>These findings reveal a non-fibrotic, immune-driven remodeling program in amphibian tadpole lungs under acute chemical stress, highlighting the plasticity of the respiratory system at early developmental stages. We emphasize that these conclusions are specific to tadpole stages and short-term exposures, and further studies are needed to assess long-term or post-metamorphic outcomes. This work provides a framework for using amphibians as tractable models to study acute injury responses, resilience, and developmental plasticity in vertebrate lungs.</p> Graphical Abstract <p></p>