Rojas Catherine M, Wiersielis Kimberly R, Roepke Troy A
Joint Graduate Program in Toxicology, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA.
Department of Pharmacology and Toxicology, School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA.
Endocrinology. 2025 Apr 22;166(6). doi: 10.1210/endocr/bqaf074.
Flame retardants have been used extensively to reduce flammability in household and industrial materials raising significant concerns due to their toxicological effects, particularly on neurodevelopment and cognition. These chemicals, including legacy compounds such as polybrominated diphenyl ethers and newer organophosphate flame retardant, exhibit endocrine-disrupting properties that interfere with hormonal pathways, neurotransmission, and synaptic plasticity. Epidemiological studies have linked flame retardant exposure to adverse developmental outcomes, including anxiety and cognitive deficits. Mechanistic research reveals that flame retardants disrupt neurogenesis, synaptogenesis, and neurotransmitter pathways, often mediated through oxidative stress, mitochondrial dysfunction, and nuclear receptor modulation. Animal studies corroborate these findings, showing impaired spatial memory, altered anxiety-like behaviors, and disrupted neurochemical homeostasis following perinatal and postnatal exposure to flame retardants. Emerging organophosphate flame retardants, such as bis(2-ethylhexyl) phenyl phosphate, demonstrate comparable or increased toxicity, further emphasizing the need for regulatory scrutiny and safer alternatives. This review synthesizes current knowledge on the neurotoxic mechanisms of flame retardants, highlighting their impact on anxiety and cognition across developmental stages. Understanding these pathways is essential to mitigating the long-term environmental and human health effects of flame retardant exposure.
阻燃剂已被广泛用于降低家用和工业材料的可燃性,但由于其毒理学效应,尤其是对神经发育和认知的影响,引发了人们的重大担忧。这些化学物质,包括多溴二苯醚等传统化合物和新型有机磷酸酯阻燃剂,具有内分泌干扰特性,会干扰激素途径、神经传递和突触可塑性。流行病学研究已将阻燃剂暴露与不良发育结果联系起来,包括焦虑和认知缺陷。机制研究表明,阻燃剂会破坏神经发生、突触形成和神经递质途径,通常是通过氧化应激、线粒体功能障碍和核受体调节介导的。动物研究证实了这些发现,表明围产期和产后接触阻燃剂后会出现空间记忆受损、焦虑样行为改变以及神经化学稳态破坏。新型有机磷酸酯阻燃剂,如双(2-乙基己基)苯基磷酸酯,表现出相当或更高的毒性,进一步强调了进行监管审查和寻找更安全替代品的必要性。这篇综述综合了关于阻燃剂神经毒性机制的当前知识,突出了它们在不同发育阶段对焦虑和认知的影响。了解这些途径对于减轻阻燃剂暴露对环境和人类健康的长期影响至关重要。