Department of Public Health and Preventive Medicine, School of Medicine, Jinan University, Guangzhou, Guangdong, P.R. China.
Guangdong Provincial Engineering & Technology Research Center for Tobacco Breeding and Comprehensive Utilization, Key Laboratory of Crop Genetic Improvement of Guangdong Province, Crops Research Institute, Guangdong Academy of Agricultural Sciences, Guangzhou, Guangdong, P. R. China.
Ann Med. 2023 Dec;55(1):2216943. doi: 10.1080/07853890.2023.2216943.
Multiple animals and studies have demonstrated that perfluoroalkyl and polyfluoroalkyl substances (PFASs) exposure causes liver damage associated with fat metabolism. However, it is lack of population evidence for the correlation between PFAS exposure and nonalcoholic fatty liver disease (NAFLD). A cross-sectional analysis was performed of 1150 participants aged over 20 from the US. Liver ultrasound transient elastography was to identify the participants with NAFLD and multiple biomarkers were the indicators for hepatic steatosis and hepatic fibrosis. Logistics regression and restricted cubic splines models were used to estimate the association between PFASs and NAFLD. PFASs had not a significant association with NAFLD after adjustment. The hepatic steatosis indicators including fatty liver index, NAFLD liver fat score, and Framingham steatosis index were almost not significantly correlated with PFASs exposure respectively. But fibrosis indicators including fibrosis-4 index (FIB-4), NAFLD fibrosis score, and Hepamet fibrosis score were positively correlated with each type of PFASs exposure. After adjustment by gender, age, race, education, and poverty income rate, there was also a significant correlation between PFOS and FIB-4 with 0.07 (0.01, 0.13). The mixed PFASs were associated with FIB-4, with PFOS contributing the most (PIP = 1.000) by the Bayesian kernel machine regression model. The results suggested PFASs exposure appeared to be more closely associated with hepatic fibrosis than steatosis, and PFOS might be the main cause of PFASs associated with hepatic fibrosis.Key messagesCurrent exposure doses of PFAS did not significantly change the risk of developing NAFLD.PFASs exposure appeared to be more closely associated with hepatic fibrosis than steatosis.PFOS might be the main cause of PFASs associated with hepatic fibrosis.
多组动物实验和研究表明,全氟烷基和多氟烷基物质(PFAS)暴露会导致与脂肪代谢相关的肝损伤。然而,人群中 PFAS 暴露与非酒精性脂肪性肝病(NAFLD)之间的相关性证据不足。对来自美国的 1150 名年龄在 20 岁以上的参与者进行了横断面分析。使用肝脏超声瞬时弹性成像来识别 NAFLD 患者,并用多种生物标志物作为肝脂肪变性和肝纤维化的指标。使用逻辑回归和限制立方样条模型来估计 PFAS 与 NAFLD 之间的关联。调整后,PFAS 与 NAFLD 无显著相关性。肝脂肪变性指标,包括脂肪肝指数、NAFLD 肝脂肪评分和 Framingham 脂肪变性指数,与 PFAS 暴露均无显著相关性。但纤维化指标,包括纤维化-4 指数(FIB-4)、NAFLD 纤维化评分和 Hepamet 纤维化评分,与每种类型的 PFAS 暴露均呈正相关。在按性别、年龄、种族、教育程度和贫困收入比进行调整后,PFOS 与 FIB-4 之间也存在显著相关性,差异有统计学意义(PIP=0.07,0.01,0.13)。混合 PFASs 与 FIB-4 相关,贝叶斯核机器回归模型显示 PFOS 贡献最大(PIP=1.000)。结果表明,PFASs 暴露与肝纤维化的关系似乎比脂肪变性更密切,PFOS 可能是 PFASs 与肝纤维化相关的主要原因。