Abstract：
Polycyclic aromatic hydrocarbons (PAHs), which are widely present in incompletely combusted air particulate matter <2.5 μm (PM2.5), tobacco and other organic materials, can enter the human body through various routes and are a class of environmental pollutants with neurotoxic effects. PAHs exposure can lead to abnormal development of the nervous system and neurobehavioral abnormalities in animals, including adverse effects on the nervous system of children and adults, such as a reduced learning ability, intellectual decline, and neural tube defects. After PAHs enter cells of the nervous system, they eventually lead to nervous system damage through mechanisms such as oxidative stress, DNA methylation and demethylation, and mitochondrial autophagy, potentially leading to a series of nervous system diseases, such as Alzheimer\'s disease. Therefore, preventing and treating neurological diseases caused by PAHs exposure are particularly important. From the perspective of the in vitro and in vivo effects of PAHs exposure, as well as its effects on human neurodevelopment, this paper reviews the toxic mechanisms of action of PAHs and the corresponding prevention and treatment methods to provide a relevant theoretical basis for preventing the neurotoxicity caused by PAHs, thereby reducing the incidence of diseases related to the nervous system and protecting human health.
摘要：
多环芳烃(PAHs),广泛存在于不完全燃烧的空气颗粒物<2.5μm（PM2.5）中，烟草和其他有机材料，可以通过各种途径进入人体，是一类具有神经毒性作用的环境污染物。PAH暴露可导致动物神经系统发育异常和神经行为异常，包括对儿童和成人神经系统的不良影响，比如学习能力下降，智力下降，和神经管缺陷。多环芳烃进入神经系统细胞后，它们最终通过氧化应激等机制导致神经系统损伤，DNA甲基化和去甲基化,线粒体自噬，可能导致一系列神经系统疾病，如老年痴呆症。因此,预防和治疗由PAH暴露引起的神经系统疾病尤为重要。从PAH暴露的体外和体内效应来看，以及它对人类神经发育的影响，本文综述了PAHs的毒性作用机制及相应的防治方法,为预防PAHs引起的神经毒性提供相关的理论依据,从而降低神经系统相关疾病的发病率，保护人类健康。
