Enhanced Ecological Risk of PFOA Degradation Products: Insights from Concentration-Dependent Transcriptomics, Adverse Outcome Pathways, and Biomarker Verification

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/TiO₂, producing C3-C7 perfluoroalkyl carboxylic acids (PFCAs) and fluoride ions. We investigated bioaccumulation and trophic transfer of PFCAs in a model food web of Chlorella sp., Daphnia magna, and Danio rerio (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.