University of Montana, Missoula, Montana 59812, United States.
Universidad del Valle de México, 14370 Mexico City, México.
Environ Sci Technol. 2022 Jun 7;56(11):6847-6856. doi: 10.1021/acs.est.1c04706. Epub 2022 Feb 22.
Exposure to particulate matter (PM) pollution damages the human brain. Fossil fuel burning for transportation energy accounts for a significant fraction of urban air and climate pollution. While current United States (US) standards limit PM ambient concentrations and emissions, they do not regulate explicitly ultrafine particles (UFP ≤ 100 nm in diameter). There is a growing body of evidence suggesting UFP may play a bigger role inflicting adverse health impacts than has been recognized, and in this perspective, we highlight effects on the brain, particularly of young individuals. UFP penetrate the body through nasal/olfactory, respiratory, gastrointestinal, placenta, and brain-blood barriers, translocating in the bloodstream and reaching the glymphatic and central nervous systems. We discuss one case study. The 21.8 million residents in the Metropolitan Mexico City (MMC) are regularly exposed to fine PM (PM) above the US 12 μg/m annual average standards. Alzheimer's disease (AD), Parkinson's disease (PD), and TAR DNA-binding protein (TDP-43) pathologies and nanoparticles (NP ≤ 50 nm in diameter) in critical brain organelles have been documented in MMC children and young adult autopsies. MMC young residents have cognitive and olfaction deficits, altered gait and equilibrium, brainstem auditory evoked potentials, and sleep disorders. Higher risk of AD and vascular dementia associated with residency close to high traffic roadways have been documented. The US is not ready or prepared to adopt ambient air quality or emission standards for UFP and will continue to focus regulations only on the total mass of PM and PM. Thus, this approach raises the question: As research continues to answer the remaining questions about UFP sources, exposures, impacts, and controls, the precautionary principle should call us to accelerate and expand policy interventions to abate or eliminate UFP emissions and to mitigate UFP exposures. For residents of highly polluted cities, particularly in the developing world where there is likely older and dirtier vehicles, equipment, and fuels in use and less regulatory oversight, we should embark in a strong campaign to raise public awareness of the associations between high PM pollution, heavy traffic, UFP, NP, and neuropsychiatric outcomes, including dementia. Neurodegenerative diseases evolving from childhood in polluted, anthropogenic, and industrial environments ought to be preventable.
颗粒物(PM)污染会损害人类大脑。化石燃料燃烧用于交通能源,占城市空气和气候污染的很大一部分。虽然目前美国(US)标准限制了 PM 环境浓度和排放量,但它们并没有明确规定超细颗粒(直径≤100nm 的 UFP)。越来越多的证据表明,UFP 可能比人们认识到的更能造成不良健康影响,在这种观点下,我们强调了对大脑的影响,特别是对年轻人的影响。UFP 通过鼻腔/嗅觉、呼吸、胃肠道、胎盘和血脑屏障穿透身体,在血液中迁移,并到达神经胶质和中枢神经系统。我们讨论了一个案例研究。居住在大都市区墨西哥城(MMC)的 2180 万居民经常受到高于美国 12μg/m 年平均标准的细颗粒物(PM)的暴露。在 MMC 儿童和年轻成年人的尸检中已经发现了阿尔茨海默病(AD)、帕金森病(PD)和 TAR DNA 结合蛋白(TDP-43)病理学以及关键脑器官中的纳米颗粒(直径≤50nm 的 NP)。MMC 年轻居民有认知和嗅觉缺陷、步态和平衡改变、脑干听觉诱发电位和睡眠障碍。居住在靠近交通繁忙道路附近的人患 AD 和血管性痴呆的风险更高。美国还没有准备好或准备好采用超细颗粒的环境空气质量或排放标准,并且将继续只关注 PM 和 PM 总质量的法规。因此,这种方法提出了一个问题:随着研究继续回答有关超细颗粒的来源、暴露、影响和控制的剩余问题,预防原则应该呼吁我们加快和扩大政策干预措施,以减轻或消除超细颗粒的排放,并减轻超细颗粒的暴露。对于污染严重的城市居民,特别是在发展中国家,那里可能使用的车辆、设备和燃料更旧、更脏,监管也更少,我们应该发起一场强大的运动,提高公众对高 PM 污染、交通繁忙、超细颗粒、纳米颗粒和神经精神结果(包括痴呆症)之间关联的认识。在污染、人为和工业环境中从童年开始发展的神经退行性疾病应该是可以预防的。