Wu Lu-Yin, Liang Li-Xia, Zhou Yang, Mohammed Zeeshan, Qian Zhengmin Min, McMillin Stephen Edward, Tabet Maya, Chu Chu, Fan Yuan-Yuan, Zhou Jia-Xin, Huang Jing-Wen, Tan Wei-Hong, Dong Guang-Hui, Lin Li-Zi
Joint International Research Laboratory of Environment and Health, Ministry of Education, Guangdong Provincial Engineering Technology Research Center of Environmental Pollution and Health Risk Assessment, Department of Occupational and Environmental Health, School of Public Health, Sun Yat-sen University, Guangzhou 510080, China.
State Environmental Protection Key Laboratory of Environmental Pollution Health Risk Assessment, South China Institute of Environmental Sciences, Ministry of Environmental Protection, Guangzhou 510655, China.
Environ Health (Wash). 2024 Mar 28;2(6):390-400. doi: 10.1021/envhealth.3c00148. eCollection 2024 Jun 21.
Evidence from animal experiments has shown that chlorinated polyfluoroalkyl ether sulfonic acids (Cl-PFESAs) can induce vision dysfunction in zebrafish. However, environmental epidemiological evidence supporting this hypothesis remains limited. In our case-control study, samples collected from 270 individuals (135 controls and 135 cases) from the Isomers of C8 Health Project data were analyzed for Cl-PFESAs. We also repeated our analysis on zebrafish to support our findings in humans and to decipher the mechanism underlying Cl-PFESA eye toxicity. The serum levels of per- and polyfluoroalkyl substances (PFASs) and alternatives were significantly higher in the cases than in the controls. Higher serum Cl-PFESA levels were associated with greater odds of eye diseases, and the trend showed a statistically significant dose-dependent relationship. The Shapley additive explanations (SHAP) value indicated that 8:2 Cl-PFESA was the dominant eye disease risk factor among the 13 studied PFASs. In zebrafish experiments, Cl-PFESAs induced eye toxicity in adult zebrafish by oxidative damage and cell apoptosis. Compared to the control group, there was significantly reduced thicknesses of the inner plexiform layer (IPL), outer plexiform layer (OPL), and retinal tissue in the zebrafish exposed to Cl-PFESAs. Our study provides human clinical and animal experimental data, showing that exposure to PFASs increases the odds of the development of eye toxicity.
动物实验证据表明，氯化多氟烷基醚磺酸（Cl-PFESAs）可导致斑马鱼视力功能障碍。然而，支持这一假设的环境流行病学证据仍然有限。在我们的病例对照研究中，对从C8健康项目数据的270名个体（135名对照和135名病例）采集的样本进行了Cl-PFESAs分析。我们还在斑马鱼身上重复了分析，以支持我们在人类中的发现，并解读Cl-PFESA眼部毒性的潜在机制。病例组中全氟和多氟烷基物质（PFASs）及其替代物的血清水平显著高于对照组。血清Cl-PFESA水平越高，患眼病的几率越大，且该趋势显示出具有统计学意义的剂量依赖性关系。夏普利加性解释（SHAP）值表明，在研究的13种PFASs中，8:2 Cl-PFESA是主要的眼病危险因素。在斑马鱼实验中，Cl-PFESAs通过氧化损伤和细胞凋亡诱导成年斑马鱼眼部毒性。与对照组相比，暴露于Cl-PFESAs的斑马鱼的内网状层（IPL）、外网状层（OPL）和视网膜组织厚度显著降低。我们的研究提供了人类临床和动物实验数据，表明接触PFASs会增加眼部毒性发生的几率。
