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

空气污染是最紧迫的问题之一，因为污染程度不断增加，特别是对居住在拥挤城市的人们来说。我们对颗粒空气污染物影响的机制的理解大多来自对空气中PM 2.5的研究，这些研究表明它们能够产生与炎症相关的氧化应激，从而形成与污染相关的呼吸道疾病的基础。这是一个及时的问题，因为我们走出封锁，交通水平再次回升，学校重新开放。PM2.5和PM0.1的毒性与细颗粒物的高比表面积有关。然而，很少有人注意到氧化成分的痕量氧化还原活性过渡金属，包括铜，铁，钼在颗粒燃烧源或刹车垫磨损。PM2.5和PM0.1中最具破坏性的氧化活性成分尚不清楚，尽管论文表明含有过渡金属特定混合物的超细PM可能起着关键作用。它们在肺细胞中的内化也仍然不清楚，尽管肺中的上皮细胞可以内化PM0.1量级的纳米级颗粒。超细胞损伤的机制，PM化学的作用，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。目的测量在伦敦区哈默史密斯和富勒姆周围不同地点收集的PM 2.5，PM 1和PM 0.1的尺寸，尺寸分布和化学物质（包括帝国西校区周围）和学校重新开放后的肯辛顿&切尔西，包括忙碌路边和学校附近。使用透射电子显微镜将细胞内PM2.5和PM0.1尺寸分布、化学和位置与鼻上皮细胞中细胞器的代谢改变相关联。它们被这些细胞内化了吗？哪些PM成分毒性最大？确定鼻上皮细胞（从受试者中获得，并通过测量氧化应激、线粒体功能/能量学置于培养物中）对雾化PM的生化反应。专题领域：气溶胶与健康

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