Embryonic exposure to phenanthrene caused developmental defects of craniofacial cartilage in F1 larvae.

As a representative polycyclic aromatic hydrocarbon with low ring numbers, phenanthrene (Phe) is ubiquitously present in the environment. In this study, zebrafish embryos were exposed to Phe at 0.05, 0.5, 5 and 50 nmol/L for 96 h, and then cultured to adulthood in clean water, the developmental defects of craniofacial cartilage were observed in F1 larvae produced by adult males and females mated with untreated fish. Delayed development of craniofacial cartilage, including a shorter and wider Meckel's cartilage and mandibular arch were observed in F1 larvae from adult fish of both sexes. Maternal F1 larvae showed a greater impact on the lower jaw than paternal F1 larvae, this may be connected with greater downregulation of the transcription of genes related to the development of craniofacial cartilage such as runt-related transcription factor 2 (runx2), fibroblast growth factor 8 (fgf8), sonic hedgehog (shh), Indian hedgehog (ihh). Further results indicated that the modification DNA methylation levels in the promotors of gene runx2 and shh in maternal and paternal F1 larvae were inherited from embryonic F0 larvae, and might be linked with the toxicity of craniofacial cartilage in F1 larvae. This study illustrated that embryonic exposure to Phe could induce adverse effects on craniofacial development in F1 offspring, emphasizing the importance of transgenerational toxicology studies in risk assessment.