Nanoscale Analysis of London Pollutant Particles and their Interaction with Airway Epithelial Cells

伦敦污染物颗粒及其与气道上皮细胞相互作用的纳米级分析

• 批准号: 2593441
• 金额: --
• 依托单位: Imperial College London
• 依托单位国家: 英国
• 项目类别: Studentship
• 财政年份: 2021
• 资助国家: 英国
• 起止时间: 2021 至 无数据
• 项目状态: 未结题
• 来源: https://gtr.ukri.org/projects?ref=studentship-2593441
• 关键词: Nanoscale; Analysis; London; Pollutant; Particles

Air pollution is one of the most pressing issues because of the increasing levels of pollution, particularly for people living in congested cities. Most of our understanding of the mechanisms underlying the effects of particulate air pollutants arise from studies of airborne PM 2.5 that have demonstrated their ability to generate oxidative stress linked to inflammation that form the basis for respiratory diseases associated with pollution. This is a timely issue as we come out of lockdown, traffic levels pick up again and schools reopen. The toxicity of PM2.5 and PM0.1 has been related to the high specific surface area of fine particles. However, there has been less attention given to the oxidising constituents of trace quantities of redox-active transition metals, including Cu, Fe, and Mo in particles from combustion sources or break-pad wear. The most damaging, oxidatively-active components of PM2.5 and PM0.1 are unknown, although papers indicate that ultrafine PM containing specific mixtures of transition metals may play a key role. Their internalisation in lung cells also remains unclear, although epithelial cells in the lung can internalise nm-sized particles of the order of PM0.1. The mechanisms of ultracellular damage, role of PM chemistry i.e. which PM sizes/chemistries are internalised by cells and effects on cell function remain to be determined.AimsTo measure the sizes, size distributions and chemistries of PM2.5, PM1 and PM0.1 collected at different sites around London boroughs of Hammersmith and Fulham (including around the Imperial West campus) and Kensington & Chelsea after schools reopened, including busy roadsides and near schools. To relate intracellular PM2.5 and PM0.1 size distribution, chemistry and location to altered metabolism of cell organelles in nasal epithelial cells using transmission electron microscopy. Are they internalised by these cells? Which PM components are most toxic? To determine the biochemical response of nasal epithelial cells (obtained from subjects and placed in culture to aerosolised PM by measuring oxidative stress, mitochondrial function/energetics). Thematic Area: Aerosols and Health

由于污染程度不断增加，空气污染是最紧迫的问题之一，特别是对于生活在拥挤城市的人们来说。我们对空气颗粒污染物影响机制的大部分了解都来自于对空气中 PM 2.5 的研究，这些研究表明，PM 2.5 能够产生与炎症相关的氧化应激，而炎症是与污染相关的呼吸道疾病的基础。随着我们解除封锁、交通水平再次回升、学校重新开放，这是一个及时的问题。 PM2.5和PM0.1的毒性与细颗粒的高比表面积有关。然而，人们对痕量氧化还原活性过渡金属的氧化成分关注较少，这些过渡金属包括来自燃烧源或刹车片磨损的颗粒中的铜、铁和钼。 PM2.5 和 PM0.1 中最具破坏性的氧化活性成分尚不清楚，尽管论文表明含有特定过渡金属混合物的超细 PM 可能发挥关键作用。尽管肺中的上皮细胞可以内化 PM0.1 数量级的纳米级颗粒，但它们在肺细胞中的内化仍不清楚。超细胞损伤的机制、PM 化学物质的作用（即哪些 PM 尺寸/化学物质被细胞内化以及对细胞功能的影响）仍有待确定。目的测量伦敦哈默史密斯和富勒姆区（包括帝国西校区周围）以及肯辛顿和切尔西学校重新开放后（包括繁忙的学校）不同地点收集的 PM2.5、PM1 和 PM0.1 的尺寸、尺寸分布和化学物质。 路边和学校附近。使用透射电子显微镜将细胞内 PM2.5 和 PM0.1 大小分布、化学和位置与鼻上皮细胞中细胞器代谢的改变联系起来。它们被这些细胞内化了吗？哪些 PM 成分毒性最强？确定鼻上皮细胞（从受试者获得并置于培养物中，通过测量氧化应激、线粒体功能/能量）对雾化 PM 的生化反应。主题领域：气溶胶与健康