Tetrabromobisphenol A bis (2-hydroxyethyl) ether (TBBPA-DHEE), a derivative of TBBPA, has been frequently detected in the environment. In this study, the median lethal concentration (LC₅₀) of TBBPA-DHEE at 96 h post-fertilization (hpf) was 1.573 mg/L. Based on the reported environmental concentrations, we investigated the effects of TBBPA-DHEE on the nervous system of zebrafish embryos following exposure to varying concentrations (0, 20, 100, and 500 μg/L) for 4 to 144 hpf. Our results indicated that exposure to 100 μg/L at 144 hpf led to behavioral abnormalities in zebrafish. Furthermore, exposure to TBBPA-DHEE inhibited the development of the central nervous system and motor neurons in zebrafish. Real-time polymerase chain reaction (PCR) analysis revealed that exposure to TBBPA-DHEE significantly downregulated the expression levels of neurodevelopmental genes (shha, syn2a, elavl3, gfap, and gap43). Additionally, TBBPA-DHEE increased oxidative stress in zebrafish. Transcriptomic analysis demonstrated that exposure to TBBPA-DHEE affected the signaling pathways involved in neurodevelopment. Overall, this study demonstrated that TBBPA-DHEE may disrupt the early development of the nervous system, leading to abnormal motor behavior in zebrafish larvae, and provided novel insights into the potential mechanisms of TBBPA-DHEE neurotoxicity.

2-(Methylthio) benzothiazole (MTBT) is widely used in the industrial and pharmaceutical fields, but limited research has been conducted on its aquatic toxicity. In this study, we established a zebrafish model to systematically evaluate its developmental and functional toxicity, focusing on the cardiovascular systems of larvae. The results showed that MTBT significantly reduced heart rate, caused pericardial edema and deformity, delayed cardiac maturation, decreased stroke volume and cardiac output, and led to vascular structural defects. Mechanistically, MTBT upregulated the expression of the core target PTGS2, activated the apoptotic pathway, and mediated cardiovascular toxicity. This study is the first to systematically confirm the cardiovascular toxicity of MTBT, supplementing its toxicological database and providing a scientific basis for the establishment of environmental safety thresholds and risk management.

Degradation is a key natural attenuation mechanism governing the fate of PPCPs during anaerobic digestion (AD) and subsequent soil exposure. Nevertheless, the combined impact of this sequential treatment (AD followed by land application) remains poorly understood. This study evaluated the degradation characteristics of nine PPCPs during mesophilic AD in three distinct soil types. The concentration changes in the nine PPCPs were monitored after 0, 5, 10, 15, 20, 25, and 30 days of anaerobic incubation at 38 °C, as well as after 0, 2, 5, 8, 10, 12, 15, 20, and 30 days of dark incubation at 25 °C with humidity at 75% in three soils. AD effectively removed sulfamethoxydiazine, ciprofloxacin, and oxytetracycline (>80%). The removal efficiencies for carbamazepine, progesterone, triclosan, naproxen, and megestrol acetate were relatively poor, with the removal rates ranging from 50% to 80%, while gemfibrozil exhibited minimal degradation (<50%). The degradation behavior of nine PPCPs fits well with first-order kinetic equations. Calculated half-lives (days) in the three soils were as follows: sulfamethoxydiazine (20.39 to 23.10), carbamazepine (36.48 to 77.02), megestrol acetate (11.18 to 20.39), progesterone (6.08 to 23.90), ciprofloxacin (11.75 to 63.01), oxytetracycline (13.08 to 30.14), naproxen (7.79 to 40.77), gemfibrozil (8.45 to 30.14), and triclosan (14.75 to 46.21). The corresponding R² values ranged from 0.8882 to 0.9320 for sulfamethoxydiazine, 0.8579 to 0.9248 for carbamazepine, 0.8745 to 0.9658 for megestrol acetate, 0.9026 to 0.9560 for progesterone, 0.8147 to 0.9571 for ciprofloxacin, 0.8136 to 0.9063 for oxytetracycline, 0.8961 to 0.9156 for naproxen, 0.8802 to 0.9497 for gemfibrozil, and 0.9099 to 0.9457 for triclosan. Soil physicochemical properties significantly influenced PPCP degradation rates. Gemfibrozil warrants immediate attention due to its poor degradation; the five PPCPs presenting moderate concern—namely carbamazepine, ciprofloxacin, oxytetracycline, naproxen, and triclosan—require further risk assessment, while sulfamethoxydiazine, megestrol acetate, and progesterone pose low persistence risk according to current evidence.

Polyhalogenated carbazoles (PHCZs) are emerging persistent organic pollutants that have attracted widespread attention due to their environmental occurrence and potential ecological risks. 1-Bromo-3,6-dichlorocarbazole (1-B-36-CCZ), which is a typical homolog of PHCZs produced as a byproduct in the dye industry, has been widely detected in various environmental media. In this study, we employed an integrated approach using an in vivo zebrafish model and network toxicology methods to systematically evaluate the vascular developmental toxicity of 1-B-36-CCZ and elucidate its underlying mechanisms. The experimental results revealed that the 96 h-LC₅₀ of 1-B-36-CCZ in zebrafish larvae was 4.52 mg/L. Sublethal exposures (0.045–45 μg/L) significantly induced an increase in heart rate (p < 0.05) and an enlargement of the pericardial edema area (p < 0.01). Using Tg(flk:eGFP) transgenic zebrafish embryos to assess vascular toxicity at concentrations of 0, 0.045, 0.45, 4.5, and 45 μg/L, we observed that 1-B-36-CCZ exposure significantly reduced the length and anastomosis rate of intersegmental vessels (ISVs) at 30 hpf, and inhibited the development of the common cardinal vein (CCV) at 48 and 72 hpf as well as the subintestinal vessel (SIV) at 72 hpf. Quantitative PCR (qPCR) analysis further revealed that the expression of key angiogenic genes (flk, kdr, and vegfa) was significantly downregulated, thus corroborating the phenotypic observations. Moreover, a “compound–target–pathway” network model predicted that SRC kinase is a key molecular target for 1-B-36-CCZ action. Enrichment analysis of target protein-coding genes and verapamil replication experiments indicated that 1-B-36-CCZ may cause damage to early vascular development in zebrafish larvae by altering intracellular calcium ion content through the activation of the SRC-mediated calcium ion signaling pathway. This study provides new experimental evidence for elucidating the toxic mechanisms of PHCZ-type pollutants and offers a theoretical basis for environmental health risk assessments.