The early developmental toxicity in zebrafish exposed by Phenanthrene (Phe) and Fluorene (Fl) was investigated by determining mortality and morphological malformation endpoints, such as no inflation of swimming bladder (no ISB), axial malformations (AM, crooked/clubbed), pericardial edema (PE) and yolk sac edema (YSE). The lethal concentration to cause 50% mortality (LC50) in embryos was 78.632 μmol L-1 for Phe and 236.930 μmol L -1 for Fl, respectively. Embryos exposed to 40 μmol L-1 Phe exhibited a reduction of blood stream speed and sharply increasing of axial malformation rate. When exposed to 80 μmol L-1 Phe, the significant (at p<0.05) increase of PE or YSE index was observed. Embryos exposed to Fl had significant axial malformations, but didn't cause significant PE, YSE and speed reduction of blood stream as those exposed to Phe. The joint effect of Phe and Fl was antagonistic. The 42-h and 114-h Phe-exposure results showed simi ar mortality and malformation rates. All of the toxic endpoints showed the significant differences (p<0.05) between 18-h and 114-h exposure, suggesting that 42-h exposure produced very serious and irreversible toxicological effects, but that 18-h Phe-exposure only generated slight, reversible toxic effects. At low concentrations (3.12-12.5 μmol L -1) of Phe producing no obviously morphological abnormality or mortality, the locomotion analysis on the larval zebrafish showed that Phe-exposed groups have significantly (p<0.05) higher speed movements (>15 mm/s) than control groups.