Browsing by Subject "Urban air pollution"

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    Analysing Urban Air Pollution Using Low-Cost Methods and Community Science
    (2022-12) Heintzelman, Asrah; Filippelli, Gabriel; Moreno-Madriñan, Max J.; Wilson, Jeffrey S.; Wang, Lixin; Druschel, Gregory K.
    Rise in air pollution resulting in negative health externalities for humans has created an urgent need for cities and communities to monitor it regularly. At present we have insufficient ground passive and active monitoring networks in place which presents a huge challenge. Satellite imagery has been used extensively for such analysis, but its resolution and methodology present other challenges in estimating pollution burden. The objective of this study was to propose three low-cost methods to fill in the gaps that exist currently. First, EPA grade sensors were used in 11 cities across the U.S. to examine NO2. This is a simplistic way to assess the burden of air pollution in a region. However, this technique cannot be applied to fine scale analysis, which resulted in the next two components of this research study. Second, a citizen science network was established on the east side of Indianapolis, IN who hosted 32 Ogawa passive sensors to examine NO2 and O3 at a finer scale. These low-cost passive sensors, not requiring power, and very little maintenance, have historically tracked very closely with Federal Reference Monitors. Third, a low-cost PurpleAir PA-II-SD active sensors measuring PM2.5 were housed with the citizen scientists identified above. This data was uploaded via Wi-Fi and available via a crowd sourced site established by PurpleAir. These data sets were analyzed to examine the burden of air pollution. The second and third research studies enabled granular analyses utilizing citizen science, tree canopy data, and traffic data, thus accommodating some of the present limitations. Advancement in low-cost sensor technology, along with ease of use and maintenance, presents an opportunity for not just communities, but cities to take charge of some of these analyses to help them examine health equity impacts on their citizens because of air pollution.
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    The Role of the Lung-Brain Axis in the Ozone-Impaired Amyloid Associated Astrocytic and Vascular Phenotype
    (2024-06) Ahmed, Chandrama; Oblak, Adrian; Block, Michelle; Baucum, A. J.; Bissel, Stephanie J.; Nass, Richard M.
    Air pollution has been associated with an increased risk of Alzheimer’s Disease (AD). Studies show ozone (O3), a major component of urban air pollution, can exacerbate amyloid pathology. However, O3 reacts in its entirety with lung epithelial lining after inhalation, hence does not translocate to brain. Studies have implicated the lung−brain axis in O3 induced central nervous system (CNS) pathology. However, the mechanistic underpinnings of its role in amyloid pathology is obscure. Here, we explored the impact of O3 on the astrocytic and vascular response to amyloid plaque in 5xFAD mice and its link to the O3 lung response. O3 exposure increased GFAP positive astrocyte density correlating with increased plaque burden in the cortex. Focusing on the plaque microenvironment, we found O3 qualitatively altered plaque associated astrocytes, evidenced by both proteomic and transcriptomic changes. Along with loss of protein expression, proteomic changes reflected increased cell-cell interaction in plaque microenvironment. Specifically, we found increased astrocyte-microglia contact selectively in periplaque space from O3 exposure. Transcriptional analysis of periplaque astrocytes revealed an accelerated shift towards disease associated astrocyte (DAA) phenotype. Elevated circulating HMGB1 was previously found from O3 exposure. In this study we demonstrate deleting HMGB1 selectively in peripheral myeloid cells and not in CNS microglia ameliorates the lung immune response to O3 as well as downregulates DAA marker in the CNS, providing a potential link between peripheral HMGB1 and O3 induced astrocytic dysregulation. On examining vascular response to O3 we found increased vascular amyloid accumulation associated with an altered vascular proteomic profile. Our analysis indicates O3 potentially disrupts vascular function such as amyloid clearance. Taken together, our study demonstrates that astrocyte and neurovasculature are contributors to O3 lung-brain axis with important implications towards amyloid pathology progression and identifies peripheral myeloid HMGB1 as its potential modulator. Further studies are required to fully understand the consequences of this impact and its role in amyloid pathology.