COPD-Like Phenotypes\nin TBC-Treated Mice Can be Effectively\nAlleviated via Estrogen Supplement

Tris(2,3-dibromopropyl) isocyanurate (TBC), recognized\nas an endocrine\ndisruptor, can cause inflammatory injury to the lung tissue of mice.\nTo investigate the specific respiratory effects of TBC, male C57BL/6J\nmice were administered a daily dose of 20 mg/kg of TBC over 14 days.\nPostexposure, these mice developed chronic obstructive pulmonary disease\n(COPD)-like symptoms characterized by inflammatory lung damage and\nfunctional impairment. In light of the antiestrogenic properties of\nTBC, we administrated estradiol (E2) to investigate its potential\nprotective role against TBC-induced damage and found that the coexposure\nof E2 notably mitigated the COPD-like phenotypes. Immunohistochemical\nanalysis revealed that TBC exposure reduced estrogen receptor alpha\n(ERα) expression and increased nuclear factor kappa-light-chain-enhancer\nof activated B cells (NF-κB) expression, while E2 treatment\nrebalanced the expression levels of ERα and NF-κB to their\nnormative states. Our findings indicate that TBC, as an antiestrogenic\nagent, may contribute to the pathogenesis of COPD through an ERα-mediated\ninflammatory pathway, but that E2 treatment could reverse the impairment,\nproviding a potentially promising remedial treatment. Given the lung\nstatus as a primary target of air pollution, the presence of antiestrogenic\ncompounds like TBC in atmospheric particulates presents a significant\nconcern, with the potential to exacerbate respiratory conditions such\nas COPD and pneumonia.