Li Mingyang, Gou Xiao, Zhang Chao, Zhang Xiaowei, Jiang Wei
Environment Research Institute, Shandong University, Qingdao 266237, China.
State Key Laboratory of Pollution Control & Resource Reuse, School of the Environment, Nanjing University, Nanjing 210023, China.
Environ Sci Technol. 2025 Jul 8;59(26):13131-13142. doi: 10.1021/acs.est.4c12932. Epub 2025 Jun 26.
The rapid advancement of perfluorooctanoic acid (PFOA) degradation techniques aims to eliminate PFOA molecules and meet stringent water quality standards. However, the environmental risks of PFOA degradation products have rarely been studied. In this study, PFOA (C8) was photocatalytically degraded with N-CQDs/TiO, producing C3-C7 perfluoroalkyl carboxylic acids (PFCAs) and fluoride ions. We investigated bioaccumulation and trophic transfer of PFCAs in a model food web of sp., , and (zebrafish). Degradation-induced acidification of the solution increased the bioaccumulation of both residual PFOA and the newly formed PFCAs, and the long-chain PFCAs (C6-C8) were able to undergo trophic transfer. Unexpectedly, the degradation products exhibited higher acute toxicity than PFOA in all three organisms, with zebrafish showing the highest sensitivity. Subsequently, concentration-dependent transcriptomics and adverse outcome pathway (AOPs) analysis indicated lipid metabolism disorders, oxidative stress, skeletal toxicity, and neurotoxicity in zebrafish, which were verified by biomarker tests. The toxic contributions of PFCAs, fluoride ions, and acidic pH in degradation products were further assessed by exposing zebrafish to them individually or in combination. The results indicated that lipid metabolism disorders stem from the abnormal activation of the peroxisome proliferator-activated receptor (PPAR) and liver X receptor (LXR) by PFCAs. Skeletal toxicity and oxidative stress are induced by the strong binding of fluoride ions to metallic elements. The solution acidification exacerbates toxic effects. The nervous system is particularly susceptible to exposure according to the lowest threshold concentration for neurotoxicity-related differentially expressed genes (DEGs). The degradation products impair neuronal development and disrupt neurotransmitter signaling. In conclusion, these findings indicate that the degradation of PFOA molecules does not equate to risk elimination; instead, incomplete degradation may heighten ecological toxicity and health risk.
全氟辛酸（PFOA）降解技术的快速发展旨在消除PFOA分子并满足严格的水质标准。然而，PFOA降解产物的环境风险鲜有研究。在本研究中，PFOA（C8）通过N-CQDs/TiO进行光催化降解，生成C3-C7全氟烷基羧酸（PFCA）和氟离子。我们研究了PFCA在斑马鱼、大型溞和斜生栅藻组成的模型食物网中的生物累积和营养转移。降解导致溶液酸化，增加了残留PFOA和新形成的PFCA的生物累积，并且长链PFCA（C6-C8）能够进行营养转移。出乎意料的是，在所有三种生物中，降解产物的急性毒性均高于PFOA，斑马鱼表现出最高的敏感性。随后，浓度依赖性转录组学和不良结局途径（AOP）分析表明斑马鱼存在脂质代谢紊乱、氧化应激、骨骼毒性和神经毒性，这些均通过生物标志物测试得到验证。通过将斑马鱼单独或组合暴露于PFCA、氟离子和降解产物中的酸性pH，进一步评估了它们的毒性贡献。结果表明，脂质代谢紊乱源于PFCA对过氧化物酶体增殖物激活受体（PPAR）和肝脏X受体（LXR）的异常激活。氟离子与金属元素的强烈结合诱导了骨骼毒性和氧化应激。溶液酸化加剧了毒性作用。根据神经毒性相关差异表达基因（DEG）的最低阈值浓度，神经系统对暴露尤为敏感。降解产物损害神经元发育并破坏神经递质信号传导。总之，这些发现表明PFOA分子的降解并不等同于风险消除；相反，不完全降解可能会增加生态毒性和健康风险。
