Research indicates that ethnic minority groups experience disproportionate exposure to air pollution caused by vehicular transportation. It is well known that differential exposure to air pollution causes increased health risks in vulnerable communities. Disparities in air pollution exposure are significant since they exacerbate comorbidities, increasing the risk of diseases like COVID-19. This study examined the relationship between exposure to Transportation-Related Air Pollution (TRAP) and census tract racial demographics in Seattle, WA. We hypothesized that communities with greater percentages of non-white residents are more likely than white-dominated communities to experience greater exposures to TRAP, because of historical factors such as “redlining”, segregation, and discrimination. This is because they are forced to live in less desirable areas and are unable to resist polluting infrastructure in their neighborhoods. We used the Environmental Protection Agency’s Environmental Justice Database to relate diesel particulate matter (PM), a proxy for TRAP, to census tract demographics, from the 2020 U.S. census. We measured diesel PM concentrations at systematic distances along three North/South transects through Seattle, roughly corresponding with the location of Interstate 5 (I-5). Measurement locations were taken sufficiently far from I-5 so as to not be affected by I-5. We found no correlation between the percent non-white population and diesel PM concentration, thus rejecting our hypothesis. There are several reasons for our unsupported hypothesis: first, our transect did not adequately sample majority non-white neighborhoods. Second, diesel PM is only one proxy for air pollution, and may be distributed relatively evenly throughout our study area irrespective of racial demographics. An analysis of other pollutants may support our hypothesis. While it is optimistic that we failed to find disproportionate exposures to diesel PM in our study area, continued analysis of differential exposure to various forms of pollution is critical to identifying and addressing environmental injustice.

The quality and accessibility of greenspaces are positively correlated with urban quality of life. The presence of greenspaces increases mental and physical health, economic activity, air quality, and other critical facets of well-being. In this study, we tested the hypothesis that household income is an indicator of the quality and accessibility of greenspaces in Seattle. Specifically, individuals living in higher average household income areas experience higher quality and accessibility of greenspaces than individuals living in lower income areas. We utilized data from the American Community Survey on King County’s annual average household income, along with geographic information on public parks from the City of Seattle GIS database to relate park accessibility and quality to household income by census tracts. We defined accessibility as the number of parks present in a given tract. A Park Quality Index was used to assign a quality score to each park, allowing us to calculate an average park quality rating for each census tract. Park quality was determined by acreage and the presence of natural and man-made elements. We found a weak positive correlation between average household income and park quality but no correlation between income and the number of parks available in a census tract. While our findings showed only weak support for one part of our hypothesis, we believe the lack of support is in part due to the fact that census tracts are too large a scale for analysis. With growing evidence for micro-segregation by race (and by extension, income) within census tracts in Seattle, it is likely that lower income neighborhoods within larger census tracts do in fact experience reduced access to high quality greenspaces. Future research should investigate this question at the scale of neighborhood or city block in order to further investigate what is likely to be an environmental justice issue in Seattle.

Air pollution is not evenly distributed geographically or demographically. For historical reasons related to race and class, ethnically diverse neighborhoods often have a higher rate of negative health effects related to air pollution, as compared to predominantly white communities. In this study, we explore the relationship between the demographic indicator, "percent people of color," to exposure to air pollution and subsequent cancer risk in the Seattle/Tacoma area. Our analysis utilizes data from the Environmental Protection Agency’s Environmental Justice Screening and Mapping Tool, with the independent variable being the air toxics cancer risk, based on the National Air Toxics Association (NATA) calculated Cancer Risk from inhalation of air toxics and measured in percentiles of risk per million people. Our dependent variable, the percent people of color population, was collected from the 2015-2019 American Community Survey, a subset of the US Census, and is defined as everyone who does not identify as non-hispanic white. We performed our analysis using a disproportionate stratified random sample of census tracts from the King-Snohomish County dividing line in the north to the intersection of I5 and Highway 512 in the south, bounded by 122.05’ W on the east margin and the eastern shoreline of Puget Sound on the west margin. For each selected tract, we recorded percent people of color and NATA Air Toxics Cancer Risk National Percentiles. Our data reveals a positive linear relationship between cancer risk percentile and percentage people of color in the population. These findings highlight the importance of recognizing and addressing the lasting effects of racism on health, and the need for continued work towards securing environmental justice.
 

Several factors influence students’ ability to access the disability accommodations necessary to complete coursework; one of the main factors, however, is the degree to which instructors are willing or able to accommodate their students’ needs. Crucially, students often need to discern if instructors will accommodate their needs before they can register for class. Students must navigate differences in communication styles and perspectives on what constitutes reasonable accommodation. Further, instructors’ knowledge of their own responsibilities, rights, and the process by which accommodations are accessed, is limited. Instructors are not made aware of their role in providing accommodations or the timeline for their involvement. They are often reluctant to provide assistance for fear of overstepping boundaries set by their institutions. The ambiguity of the instructor’s role in accessibility is actively causing harm. Multiply-marginalized students face a number of additional barriers: students who have less wealth have impaired access to healthcare, and are more likely to face poor healthcare outcomes. Further, the effects of marginalization ensure that students with intersectional identities are less likely to be wealthy. While these facts are rarely officially disputed, it is often difficult to determine what supports are missing, why they are missing, and how support can be provided to the benefit of all stakeholders. In order to establish how students and instructor perceptions differ from each other and from the recommended process, more data is sorely needed; this study utilized a basic survey to identify the areas in which instructors and students need further support. Most queries were designed to have quantifiable responses; freeform responses were evaluated to identify the most common topics and positionality respondents presented. Responses which directly oposed the most common positionalities were then quantified. Expected results largely aligned with known areas of need, specifically the need for more transparency and training surrounding accessibility. 

Birth asphyxia is the inability of a newborn to begin and maintain breathing. Twenty-three percent of neonatal deaths globally are caused by birth asphyxia [1]. Birth asphyxia results in a neurological injury called hypoxic ischemic encephalopathy (HIE). Rapid HIE screening within six hours after birth is crucial to identify neonates at risk. Unfortunately, the diagnostic equipment is impractical for low resource settings because it is costly ($20/test and $5,000 for equipment) and requires technical staff, that are in short supply, to operate. We hypothesize that a cost-effective device can be developed for HIE analysis. pHast Cam quickly screens for birth asphyxia and HIE in infants via a paper-based blood pH sensor. The device combines an inexpensive pH sensitive dye, a smartphone camera, and a fixture that controls the imaging environment to quickly identify acidosis that results from HIE. A low-cost paper-based strip is made with a water-soluble resin doped with a pH-sensitive dye, bromothymol blue (BTB), and a membrane to filter out red blood cells. The fixture removes lighting variation. The smartphone camera records the pH indicator image, and an algorithm captures, reduces noise, and accesses color change. pHast Cam incorporates four features: 1) accurate assessment of acidity within 0.05 pH units, 2) require only a few microliters of blood, 3) use electrical hardware and software only from the smartphone, and 4) affordability. At this stage, we have achieved a regressive linear model that predicts buffered solution acidity. In the future, we will transition from measuring buffered solutions to blood-plasma. Ultimately, we expect pHast Cam to screen for HIE by quantifying plasma pH in neonates so that timely therapeutic interventions and plans to address long-term complications may occur. [1] Diaz-Rosello JGP, Niermeyer S, et al. WHO Basic guidelines on new born resuscitation. 2012.

Inherited retinal diseases (IRDs) are a diverse family of disorders which cause vision loss and retinal degeneration. With only 1-2% of the genome being protein-encoding, genetic variation within the expansive noncoding genome is critical to the development of disease phenotypes in the retina. Macular Telangiectasia Type II (MacTel) is an IRD resulting in disruption of central vision and greatly impacting vision-related quality of life. MacTel has an estimated prevalence of 1 in 1000 individuals, affecting approximately two million people globally. Though MacTel etiology largely remains unknown, accumulation of improperly degraded lipids within the retina is a leading hypothesis in its pathogenesis. Additionally, genome-wide association studies have implicated numerous loci in the development of MacTel, including the novel gene locus ceramide synthase 4 (CERS4). As CERS4 plays a critical role in the synthesis of lipid precursors and is highly expressed in the retina, it stands as a promising candidate for influencing MacTel development. We hypothesize that cis-regulatory element (CRE) mutations are central to the genetic frameworks underlying MacTel. We aim to characterize the sufficiency of putative enhancer regions to drive gene expression. We have identified potential CERS4 enhancer regions through a machine learning approach using adult human retina ATAC sequencing datasets. Sufficiency of candidate enhancer regions will be evaluated by insertion to a barcoded reporter library and electroporation into mouse retinas. Following proof of sufficiency, we will perform saturation mutagenesis on identified enhancers to investigate the impact of all possible single nucleotide variants (SNVs) within these regions. The results of our investigation will aid in identifying SNVs of interest within the CERS4 locus, potentially implicating specific mutations towards the development of MacTel. Greater understanding of CRE mutations will improve early clinical diagnosis and inform future therapies for patients with MacTel.

Many age-related diseases in humans such as Parkinson's and Alzheimer's involve intracellular protein aggregation, but much is still unknown about the molecular mechanisms behind how this occurs. Characterizing these mechanisms is therefore important for developing effective treatments for age-related illnesses. Our work investigates the relationship between cell life span and aggregation of processing bodies (P-bodies), which are cytoplasmic ribonucleoprotein (RNP) granules that form inside cells experiencing stress and perform several molecular functions that appear to benefit cells experiencing stress. Using GFP-tagged Dcp2 as a P-body marker in S. cerevisiae and microfluidics to study single-cell lifespans, I demonstrated that P-bodies aggregated in aging cells that were not experiencing other forms of stress. P-body aggregation also correlated to the remaining lifespan of any given cell. To investigate this link further, I adjusted cytosol pH and observed a relationship between cytosolic pH and P-body aggregation rate. Slowing of P-body aggregation correlated to extension of cell lifespan. This suggests the need for additional research to determine whether there is a causal link between P-body aggregation and fatal single-cell pathogenesis and if so, whether these pathogenesis mechanisms are conserved in human cells and therefore a possible target for treatment for age-related illnesses.

Macular telangiectasia type II is a late-onset retinal degeneration disease which causes loss of central vision and a disruption in cell class proportions in the retina. Genome-wide association studies have identified a point mutation in the 5q14.3 enhancer as associated with MacTel. This enhancer has been shown to regulate the activity of microRNA 9-2. To elucidate the function of this particular enhancer on retinal health and cell class composition, both enhancer knockout and miR9-2 mice models were generated. In adult enhancer knockout mice, there were no significant changes in cell class composition compared with wild-type mice. In the miR9-2 knockout mouse model, it was found that at the 5 week time point, there was a significant increase in müller glial cells. Müller glial cell loss has been observed in Mactel patients, and these cells have been shown to play a crucial role in maintaining proper vascular networks. Future experiments to determine the effects of enhancer and miR9-2 loss on vasculature in the retina would help further identify the role of the 5q14.3 enhancer and its targets on retinal health.