Black carbon modulates BDE-47-induced developmental toxicity in zebrafish larvae: Dual roles as pollutant carrier and toxic alleviator

Black carbon (BC), as a particulate pollutant prevalent in aquatic environments, exhibits strong adsorption affinity for polybrominated diphenyl ethers (PBDEs). Despite extensive studies on PBDEs' neurotoxicity, the role of BC in modulating these effects remains poorly understood. Exposure to BDE-47 (2, 20, 200 μg/L) induced concentration-dependent oxidative stress, neuroglial damage, locomotor/photoaxis behavioral abnormalities, and growth retardation. Co-exposure to BC (0.5 mg/L) mitigated these effects, reducing developmental retardation, heartbeat elevation, and malformations such as pericardial oedema and spinal curvature. BC also alleviated behavioral impairment and normalized the levels of thyroid hormones (triiodothyronine and thyroxine), neurodevelopment-related proteins (growth-associated protein 43, glial fibrillary acidic protein, and sonic hedgehog factor A), and neurotransmitters (serotonin, γ-aminobutyric acid, dopamine, and norepinephrine). BC alleviated the expression disorders of HPT axis and neural-related genes induced by BDE-47. Meanwhile, adsorption-desorption experiments revealed BC's carrier role in sequestering BDE-47, which demonstrated that BC acts as an effective adsorbent to sequester BDE-47, thereby reducing its bioavailability and alleviating its toxicity in zebrafish. These findings provide mechanistic evidence that BC mitigates PBDE-induced neurotoxicity through dual pathways: chemical adsorption and endocrine-axis modulation. This study highlights the necessity to reassess ecological risks of co-existing particulate pollutants and POPs, with critical implications for aquatic ecosystem protection and human health risk prediction.