Embryonic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin impairs prey capture by zebrafish larvae.

As a ubiquitous, persistent environmental contaminant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has the potential to cause lethal deformities in larval fishes. Few studies have examined its impacts on larval growth and craniofacial development in conjunction with feeding capability. The authors used morphological and behavioral assessments to demonstrate that feeding capability of larvae is impaired even when craniofacial structures are not grossly malformed. Zebrafish embryos were exposed to 25 pg TCDD/mL, 50 pg TCDD/mL, or 100 pg TCDD/mL or <0.1% dimethyl sulfoxide for 1 h at 4 h postfertilization and then raised in clean water for 21 d or 90 d to assess craniofacial morphology, feeding capability, and long-term survival. The lower jaw was 5% smaller in 21-d larvae exposed to ≥ 50 pg TCDD/mL, and those larvae caught 10% fewer prey items; survival was reduced by 13% to 23%. The direct cause of TCDD's impacts on feeding capability is not known, but feeding success was correlated with growth, length of lower jaw, and survival. Since low larval mortality rates are key for recruitment, this suggests that exposure to concentrations of TCDD during embryonic development that do not initially cause mortality still has the potential to impact the recruitment success of feral fish. Furthermore, the present work provides additional evidence that behavioral end points are often more sensitive than morphological ones and should be included when assessing the sublethal toxicity of environmental contaminants.