“…Activation of AhR occurred upon ligand binding. Studies indicated that AhR knockout rats, mice, and fish exhibited a range of developmental abnormalities and long-term health effects. − Hyperactivation of the AhR led to embryonic lethality or severed developmental defects in multiple tissues, including the kidney, palate, teeth, prostate, lung, heart, and vasculature. − AhR served as a crucial environmental sensor and transcription factor, activated by a wide range of environmental chemicals, including polycyclic aromatic hydrocarbons, the primary toxic component of PM 2.5 . , Some data illustrated the activation of AhR induced by PM 2.5 in vitro and in vivo models (Table S2). It was reported that EOM enhanced the activation of AhR in zebrafish embryos and murine P19 embryonal carcinoma cells. ,− ,− Some strong AhR agonists like 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) and 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) were shown to induce cardiac malformations in zebrafish embryos. − Additionally, folic acid and resveratrol were found to protect against EOM-induced heart defects by inhibiting AhR activity and reducing ROS production .…”