BPM Exposure Induces Pulmonary Dysfunction in Adult Mice and Adverse Intergenerational Pulmonary Effects in Offspring

High Resolution Image Download MS PowerPoint Slide Bisphenol M (BPM), a structural analogue of bisphenol A, has become increasingly prevalent in the environment, raising concerns about its potential health impacts. However, the pulmonary toxicity of BPM, particularly with regard to direct exposure in adults and potential intergenerational respiratory effects, is not well understood. This study systematically investigates the mechanisms of BPM-induced pulmonary dysfunction in adult mice using integrated transcriptomic and proteomic analyses while also evaluating intergenerational respiratory effects in the offspring of a pregnant mouse. In adult mice, BPM exposure impaired pulmonary function and induced histopathological alterations including inflammatory infiltration and early-stage fibrotic changes. At the molecular level, BPM disrupted pulmonary immune-inflammatory homeostasis by synergistically activating the NF-κB and MAPK pathways, while suppressing T-cell receptor─and Fc receptor─mediated immunoregulatory signals. Notably, maternal BPM exposure resulted in pulmonary impairment in female offspring, as evidenced by altered lung function parameters and the corresponding histopathological abnormalities. In summary, these findings demonstrate that BPM induces pulmonary dysfunction in adult mice by disrupting immune-inflammatory homeostasis while also conferring sex-specific intergenerational respiratory health risks.