An Environmental Justice Analysis: Superfund Sites and Surrounding Communities in Illinois

Is there an association between Superfund sites and the socioeconomic makeup of the surrounding communities? This research analyzes the current economic and racial demographics of Illinois counties that contain Superfund sites. Specifically, variables that are indicators of environmental injustice are analyzed; e.g. race, median household income, and home ownership. Since the inception of the environmental justice movement in the late 1980s, studies have been conducted nationally and at state levels in Michigan, California, Ohio, Florida, Texas, and South Carolina (i.e. Cutter 2006; Mohai & Saha 2006; Pastor et al. 2004; Anderton et al. 1997; Bevc et al. 2007; Bowen et al. 1995). However, environmental justice research specific to the state of Illinois is largely unexplored. This research will better identify environmental disparities in rural Illinois counties that have little or no minority population. Additionally, this research adopts a distance-based spatial analysis approach in an attempt to achieve results more precise than previous unit-hazard coincidence analysis methods (Mohai & Saha 2006). Areal apportionment methodology is used to analyze demographic data from the 2000 United States (U.S.) Census Summary Files (SF1 and SF3) for the impacted counties in Illinois. This research uses ArcView GIS™ (Version 9.2) to create buffer zones of one-, two-, and five-miles centered on X, Y coordinates obtained from the U.S. Environmental Protection Agency. These uniform neighborhoods are used to determine percentages of racial minority, median household income, and home ownership within these radii. The results are then compared to percentages calculated from the remainder of the county population to establish foremost, if specific environmental injustice criteria are met and subsequently, examine how social and racial demographics within the buffer zone vary with respect to the distance from the Superfund site. This research yields essential data for urban and community planners within Illinois. First, this research identifies areas of environmental inequality to be targeted for future amelioration. Secondly, this research better characterizes the relationship between environmental hazards and surrounding communities, both urban and rural. Thirdly, this research will enable city planners to site future environmental hazards judiciously. Lastly, this research is a stepping-stone toward a more detailed longitudinal study of environmental justice in Illinois.Ope

Genomic atlas of the human plasma proteome.

Although plasma proteins have important roles in biological processes and are the direct targets of many drugs, the genetic factors that control inter-individual variation in plasma protein levels are not well understood. Here we characterize the genetic architecture of the human plasma proteome in healthy blood donors from the INTERVAL study. We identify 1,927 genetic associations with 1,478 proteins, a fourfold increase on existing knowledge, including trans associations for 1,104 proteins. To understand the consequences of perturbations in plasma protein levels, we apply an integrated approach that links genetic variation with biological pathway, disease, and drug databases. We show that protein quantitative trait loci overlap with gene expression quantitative trait loci, as well as with disease-associated loci, and find evidence that protein biomarkers have causal roles in disease using Mendelian randomization analysis. By linking genetic factors to diseases via specific proteins, our analyses highlight potential therapeutic targets, opportunities for matching existing drugs with new disease indications, and potential safety concerns for drugs under development

Genome-wide meta-analysis identifies 127 open-angle glaucoma loci with consistent effect across ancestries

10.1038/s41467-020-20851-4Nature Communications121125

New insights into the genetic etiology of Alzheimer’s disease and related dementias

Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

New insights into the genetic etiology of Alzheimer’s disease and related dementias

Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele