Tibaldi Eva, Gnudi Federica, Mandrioli Daniele, Bruno Caterina, Zona Amerigo, Fazzo Lucia, Comba Pietro
Ramazzini Institute, Cesare Maltoni Cancer Research Center, Via Saliceto 3, Bologna, Bentivoglio, 40010, Italy.
Enviroment and Health Department, Istituto Superiore Sanità (ISS), Roma, Italy.
J Occup Med Toxicol. 2024 Dec 13;19(1):45. doi: 10.1186/s12995-024-00434-5.
An increased incidence of pleural mesotheliomas in Biancavilla (Italy) was attributed to the environmental exposure to fluoro-edenite (FE). Results from the Ramazzini Institute (RI) in vivo long-term study confirmed the evidence that exposure to FE fibres is correlated with an increase of malignant pleural mesotheliomas in Sprague-Dawley rats. Recently asbestosis-like features were substantiated in Biancavilla residents without known occupational exposures. Aim of this work was to establish whether FE induce lung fibrosis with a pathogenetic mechanism similar to other asbestiform fibres.
Original slides from the RI study were systematically re-examined to characterize the FE-induced lesions. Quantitative analysis of lung fibrosis was assessed following the Ashcroft method. Immunohistochemical analysis of protein involved in fibrotic responses and histochemical staining for FE-fibres identification were performed.
Like asbestos, FE caused fibrotic lesions, pleural plaques or nodules and mesotheliomas. A significant increase of lung fibrosis (p < 0.001) was observed in the FE-treated groups compared to untreated controls. In the fibrotic responses to FE, vimentin was the most expressed protein, followed by collagen-I and alpha-SMA. Finally, ferruginous bodies, characterized by iron deposits and ferritin expression, were observed in FE-induced lesions.
This study confirmed that FE exposure promotes the onset of fibrotic lesions at pleural level, as fibrous plaques or nodules and fibrosis, through a mechanism similar to other form of asbestos. These results combined with epidemiological study reported in Biancavilla residents, corroborate the need to promote health and epidemiological surveillance plans of respiratory diseases in population living in FE contaminated sites.
意大利比安卡维拉胸膜间皮瘤发病率的增加归因于环境中氟透辉石（FE）的暴露。拉马齐尼研究所（RI）的体内长期研究结果证实了FE纤维暴露与斯普拉格-道利大鼠恶性胸膜间皮瘤增加之间的关联。最近，在没有已知职业暴露的比安卡维拉居民中证实了类似石棉沉着病的特征。这项工作的目的是确定FE是否通过与其他石棉状纤维相似的致病机制诱导肺纤维化。
对RI研究的原始切片进行系统重新检查，以表征FE诱导的病变。按照阿什克罗夫特方法评估肺纤维化的定量分析。进行参与纤维化反应的蛋白质的免疫组织化学分析和用于FE纤维鉴定的组织化学染色。
与石棉一样，FE引起纤维化病变、胸膜斑或结节以及间皮瘤。与未处理的对照组相比，在FE处理组中观察到肺纤维化显著增加（p < 0.001）。在对FE的纤维化反应中，波形蛋白是表达最多的蛋白质，其次是I型胶原蛋白和α-平滑肌肌动蛋白。最后，在FE诱导的病变中观察到以铁沉积和铁蛋白表达为特征的含铁小体。
本研究证实，FE暴露通过与其他形式石棉相似的机制，促进胸膜水平纤维化病变的发生，如纤维斑块或结节以及纤维化。这些结果与比安卡维拉居民的流行病学研究相结合，证实了有必要在居住在FE污染地区的人群中促进呼吸系统疾病的健康和流行病学监测计划。
