Medical Plants Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Environ Sci Pollut Res Int. 2021 Feb;28(6):6349-6373. doi: 10.1007/s11356-020-11620-3. Epub 2021 Jan 4.
Many reports have shown a strong association between exposure to neurotoxic air pollutants like heavy metal and particulate matter (PM) as an active participant and neurological disorders. While the effects of these toxic pollutants on cardiopulmonary morbidity have principally been studied, growing evidence has shown that exposure to polluted air is associated with memory impairment, communication deficits, and anxiety/depression among all ages. So, these toxic pollutants in the environment increase the risk of neurodegenerative disease, ischemia, and autism spectrum disorders (ASD). The precise mechanisms in which air pollutants lead to communicative inability, social inability, and declined cognition have remained unknown. Various animal model studies show that amyloid precursor protein (APP), processing, oxidant/antioxidant balance, and inflammation pathways change following the exposure to constituents of polluted air. In the present review study, we collect the probable molecular mechanisms of deleterious CNS effects in response to various air pollutants.
许多报告表明，重金属和颗粒物（PM）等神经毒性空气污染物作为活跃参与者与神经紊乱之间存在很强的关联。尽管这些有毒污染物对心肺发病率的影响主要已经被研究过，但越来越多的证据表明，暴露在污染的空气中与记忆力减退、沟通障碍以及所有年龄段的焦虑/抑郁有关。因此，环境中的这些有毒污染物会增加神经退行性疾病、缺血和自闭症谱系障碍（ASD）的风险。空气污染物导致沟通能力丧失、社交能力丧失和认知能力下降的确切机制仍不清楚。各种动物模型研究表明，暴露于污染空气中的成分会改变淀粉样前体蛋白（APP）、氧化/抗氧化平衡和炎症途径的处理。在本综述研究中，我们收集了针对各种空气污染物的有害中枢神经系统效应的可能分子机制。
