Parental exposure to phenanthrene induces thyroid disruption in zebrafish offspring.

Polycyclic aromatic hydrocarbons (PAHs) constitute extensively studied pollutants present throughout environmental and food matrices. Phenanthrene (PHE), ranking among the most prevalent PAHs detected in food items and aquatic ecosystems, causes reproductive and developmental toxicity in zebrafish. However, the potential for PHE to transfer to zebrafish offspring and disrupt the thyroid endocrine system remains unclear. To investigate intergenerational thyroid disruption, adult zebrafish underwent PHE treatment (0, 0.85, 8.5, and 85 μg/L) for 60 days, with embryos (F1) subsequently cultured in clean water until 5 days postfertilization (dpf) and 14-dpf. Results demonstrated that PHE accumulated in zebrafish offspring through parental transmission. Parental PHE exposure induced developmental toxicity in zebrafish offspring, characterized by elevated deformation rates, diminished survival rates, and reduced body length. PHE exposure altered thyroid hormone levels and caused thyroid disruption in the F1 generation. Among F1 generation specimens (including 5 and 14-dpf larvae), L-thyroxine (T4) concentrations elevated, whereas 3,5,3'-L-triiodothyronine (T3) levels decreased. Additional investigation revealed that hypothalamic-pituitary-thyroid (HPT) axis gene transcription patterns underwent alteration following parental PHE treatment in F1 larvae. Collectively, this study established that PHE can transfer to the F1 generation from adult zebrafish, causing thyroid disruption and developmental toxicity.