Developmental Multi‐Organ Toxicity in Zebrafish Exposed to 1, 2‐Dichloroethane

1,2-Dichloroethane (1,2-DCE), a common industrial organic solvent, enters humans primarily via inhalation, damaging the central nervous system and organs like the liver and kidneys. However, its cardiotoxicity and the multi-organ developmental toxicity in zebrafish remain unclear. This study investigated its cardiotoxicity, hepatotoxicity, and nephrotoxicity using a zebrafish model. Zebrafish embryos at 4 h after fertilization (hpf) were exposed to 0, 200, 400, or 800 μg/mL 1,2-DCE until 120 hpf, and morphological and genetic changes were assessed. As the dosage of 1,2-DCE increases, the mortality rates of zebrafish also increase (p < 0.05), and the LC₅₀ was determined as 867.5 μg/mL. Exposure to 1,2-DCE significantly increased pericardial area, heart rate, and sinus venosus-bulbus arteriosus (SV-BA) distance, upregulated nkx2.5 and gata4, and downregulated bmp4, cmlc1, vmhc, and spaw (p < 0.05). In the exposure groups, hepatic vacuolation and atrophy were observed, accompanied by downregulated cyp1a (p < 0.05). Renal tubule length decreased dose-dependently, with downregulation of pax2a, pax8, wt1a, wt1b, and nphsl (p < 0.05) in the exposure group. These data demonstrate that 1,2-DCE induces multi-organ toxicity in zebrafish, causing structural and functional impairments in the heart, liver, and kidney. This suggests that the harmful effects of 1,2-DCE on zebrafish should be taken into account when evaluating environmental risks in the future.