Acute toxicity of dichloroacetonitrile (DCAN), a typical nitrogenous disinfection by-product (N-DBP), on zebrafish (Danio rerio)

• Toxicity of DCAN was the first time investigated on zebrafish.
• DCAN caused significant developmental toxicity to zebrafish embryos.
• DCAN was easily accumulated in zebrafish liver, followed by the gill and muscle.
• DCAN induced acute metabolism damage to adult zebrafish.
• DCAN could cause acute genomic DNA damage to adult zebrafish.

Dichloroacetonitrile (DCAN) is a typical nitrogenous disinfection by-product (N-DBP) and its toxicity on aquatic animals is investigated for the first time. The present study was designed to investigate the potential adverse effects of DCAN on zebrafish. DCAN could induce developmental toxicity to zebrafish embryos. A significant decrease in hatchability and an increase in malformation and mortality occurred when DCAN concentration was above 100 µg/L. Heart function alteration and neuronal function disturbance occurred at concentration higher than 500 and 100 µg/L, respectively. Further, DCAN was easily accumulated in adult zebrafish. The rank order of declining bioconcentration factor (BCF) was liver (1240–1670)> gill (1210–1430)> muscle (644–877). DCAN caused acute metabolism damage to adult zebrafish especially at 8 days exposure, at which time the “Integrated Biomarker Response” (IBR) index value reached 798 at 1 mg/L DCAN dose. Acute DNA damage was induced to adult zebrafish by DCAN even at 10 µg/L dose.