Occurrence of triethylamine in water bodies of a chemical industrial park and its toxicological mechanisms on zebrafish embryo-larvae.

Triethylamine (TEA) is extensively used in industry, and its aquatic ecological risks have attracted regulatory attention. This study assessed TEA occurrence in groundwater and surface water within a chemical industrial park, and evaluated its toxicity and mechanisms in zebrafish embryo-larvae. The results revealed elevated TEA concentrations, reaching 41.2 mg/L in groundwater and 0.377 mg/L in surface water, both of which substantially exceeded the groundwater drinking water risk screening reference value of the U.S. EPA Regional Screening Levels (0.015 mg/L). Toxicity assessments showed reduced heart rate, abnormal behavior, and increased malformations in zebrafish exposed to 0.015-10.00 mg/L TEA. Mechanistically, TEA induced significant oxidative stress, evidenced by elevated catalase (CAT) activity and glutathione (GSH) content, with non-linear changes in malondialdehyde (MDA) content and superoxide dismutase (SOD) activity, and a marked increase in hepatic aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) activities. Additionally, TEA exposure significantly reduced the levels of thyroid hormone T3 and T4, and altered the gene expression of hypothalamus-pituitary-thyroid (HPT) axis including TTR, UGT1ab, and TSHβ. Correlations revealed significant associations among T3, T4, and HPT axis gene expression with oxidative stress markers and hepatic enzymes, whereas molecular docking revealed no strong binding between TEA and HPT axis proteins. Collectively, this study reveals the high-risk occurrence of TEA in a chemical industrial park and its multifaceted toxicity in zebrafish embryos, and elucidates the key mechanism of TEA-induced thyroid disruption mediated by oxidative stress and liver injury. These findings provide a key scientific basis for the ecological and environmental risk management of TEA.