Particulate Air Pollution and Risk of Neuropsychiatric Outcomes. What We Breathe, Swallow, and Put on Our Skin Matters.
Particulate Air Pollution and Risk of Neuropsychiatric Outcomes. What We Breathe, Swallow, and Put on Our Skin Matters.
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DOI：
10.3390/ijerph182111568
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发表时间：
2021-11-03
影响因子：
--
通讯作者：
Ayala A
中科院分区：
文献类型：
--
作者：
Calderón-Garcidueñas L;Stommel EW;Rajkumar RP;Mukherjee PS;Ayala A
我们评估了新积累的颗粒物污染对大脑影响的证据、进入的门户、神经损伤机制，以及最终与暴露统计相关的神经学和精神病学结果。PM污染来自自然和人为来源，如化石燃料燃烧、工程纳米颗粒(NP≤100 nm)、野火和木材燃烧。在正常的日常活动中，我们都经常接触到不同大小的颗粒物污染-PM2.5(≤2.5um)、超细PM(UFP≤100 nm)或NPs。吸入、摄取和皮肤吸收是进入的关键途径。精选的文献提供了美国环境保护局(US EPA)环境空气质量标准、独立颗粒物审查小组的结论、内燃排放的重要性以及表明UFP/NPs跨越生物屏障并到达大脑的证据。NPS产生氧化应激和神经炎症、神经血管单位、线粒体、内质网和DNA损伤、蛋白质聚集和错误折叠等作用。暴露在环境PM2.5浓度等于或低于当前美国标准的环境中，可能会增加TIA、缺血性和出血性中风、认知缺陷、痴呆症以及阿尔茨海默氏症和帕金森氏症的风险。居住在污染严重的特大城市中，99.5%的11个月至≤40岁的居民患有阿尔茨海默病的神经病理特征。帕金森病的风险和加重与空气污染有关，暴露在柴油尾气中会增加肌萎缩侧索硬化的风险。总体而言，这些文献支持颗粒物污染对有针对性的神经和精神结果的影响，并强调了导致神经损伤的病理生理机制的复杂性和污染特征的显著差异。排放源强度、遗传、营养、合并症等因素也起到了作用。PM2.5是神经和精神疾病的威胁。因此，未来的研究应该特别关注UFP/NPs在诱导神经损伤中的潜在作用。
We appraise newly accumulated evidence of the impact of particle pollution on the brain, the portals of entry, the neural damage mechanisms, and ultimately the neurological and psychiatric outcomes statistically associated with exposures. PM pollution comes from natural and anthropogenic sources such as fossil fuel combustion, engineered nanoparticles (NP ≤ 100 nm), wildfires, and wood burning. We are all constantly exposed during normal daily activities to some level of particle pollution of various sizes—PM2.5 (≤2.5 µm), ultrafine PM (UFP ≤ 100 nm), or NPs. Inhalation, ingestion, and dermal absorption are key portals of entry. Selected literature provides context for the US Environmental Protection Agency (US EPA) ambient air quality standards, the conclusions of an Independent Particulate Matter Review Panel, the importance of internal combustion emissions, and evidence suggesting UFPs/NPs cross biological barriers and reach the brain. NPs produce oxidative stress and neuroinflammation, neurovascular unit, mitochondrial, endoplasmic reticulum and DNA damage, protein aggregation and misfolding, and other effects. Exposure to ambient PM2.5 concentrations at or below current US standards can increase the risk for TIAs, ischemic and hemorrhagic stroke, cognitive deficits, dementia, and Alzheimer’s and Parkinson’s diseases. Residing in a highly polluted megacity is associated with Alzheimer neuropathology hallmarks in 99.5% of residents between 11 months and ≤40 y. PD risk and aggravation are linked to air pollution and exposure to diesel exhaust increases ALS risk. Overall, the literature supports that particle pollution contributes to targeted neurological and psychiatric outcomes and highlights the complexity of the pathophysiologic mechanisms and the marked differences in pollution profiles inducing neural damage. Factors such as emission source intensity, genetics, nutrition, comorbidities, and others also play a role. PM2.5 is a threat for neurological and psychiatric diseases. Thus, future research should address specifically the potential role of UFPs/NPs in inducing neural damage.
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DOI：
10.1080/10962247.2020.1826366
发表时间：
2021-03
期刊：
Journal of the Air & Waste Management Association (1995)
影响因子：
--
作者：
Habre R;Girguis M;Urman R;Fruin S;Lurmann F;Shafer M;Gorski P;Franklin M;McConnell R;Avol E;Gilliland F
通讯作者：
Gilliland F
影响因子：
2.6
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Annor, Francis B.;Bayakly, Rana A.;Simon, Thomas R.
通讯作者：
Simon, Thomas R.
与低水平锰暴露有关的神经结局，在无症状焊接学员中。
DOI：
10.5271/sjweh.3466
发表时间：
2015-01
期刊：
Scandinavian journal of work, environment & health
影响因子：
--
作者：
Baker MG;Criswell SR;Racette BA;Simpson CD;Sheppard L;Checkoway H;Seixas NS
通讯作者：
Seixas NS
DOI：
10.1080/21678421.2021.1887262
发表时间：
2021-08
影响因子：
2.8
作者：
Bear, Todd M.;Malek, Angela M.;Foulds, Abigail;Rager, Judith;Deperrior, Sarah E.;Vena, John E.;Larson, Theodore C.;Mehta, Paul;Horton, D. Kevin;Talbott, Evelyn O.
通讯作者：
Talbott, Evelyn O.
影响因子：
2.9
作者：
Byrne, Colm Patrick;Bennett, Kathleen E.;Williams, David J.
通讯作者：
Williams, David J.