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

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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