Permanent URI for this collection
Browse
Recent Submissions
Publication Ambient Air Pollution During Spermatogenesis and Impact on Semen Quality and Infertility Treatment Outcomes(2025-02) Russo, LindseyWhile research suggests a detrimental association between criteria air pollutants and semen quality in countries with high levels of air pollution, a data gap exists in exploring this association in U.S. cities which tend to be characterized by low to moderate levels of air pollution. Additionally, few studies have characterized the impact of exposure to ambient air pollution during spermatogenesis with downstream couple-level infertility treatment outcomes. Both particulate and gaseous pollutants can cause an inflammatory response in the lungs, leading to an increase in inflammatory markers and an overproduction of reactive oxygen species which can damage the blood-testis barrier, leading to impaired spermatogenesis. Exposure to ambient air pollution may also result in DNA strand breaks and epigenetic changes which may lead to poor infertility treatment outcomes. Leveraging data from the Folic Acid and Zinc Supplementation Trial (FAZST) (2013-2018) for male partners of couples seeking infertility treatment in the Salt Lake City, Utah region, this dissertation aimed to answer critical questions surrounding the impact of ambient air pollution on semen quality (n=1,965) and couple-level infertility treatment outcomes in an IUI cohort (n=505 couples and 1,223 cycles) and an IVF cohort (n=221 couples and 280 cycles). This dissertation sheds new insight on the potential role of male preconception exposure to ambient air pollution during spermatogenesis on semen quality and infertility treatment outcomes in Salt Lake City, which may improve family planning.Item Salience of Trust in Discussions and Recommendations of the United States' COVID-19 Health Equity Task Force(2025) Kloft, Samantha; López-Cevallos, DanielObjective: The COVID-19 pandemic has further eroded trust in public health institutions across the United States. We examined the salience of trust in the federal government's discussions and recommendations of the US COVID-19 Health Equity Task Force (HETF). Methods: We conducted a thematic analysis of publicly available HETF documents, including the executive order, 8 meeting minutes, and 2 final deliverables. Given that trust operates at multiple levels of the socioecological continuum, we used an interpretive analytic approach to our inquiry. Results: We found that several barriers, facilitators, and influencers to trust were discussed during HETF meetings, but few were mentioned consistently across all documents. Trust was most frequently mentioned by individuals in the public comments section of HETF meetings, more so than HETF members or representatives of federal agencies. Public commenters comprised 52% of total mentions of trust. However, these mentions did not make their way into the final HETF deliverables, signaling a potential disconnect between insights from public commenters and HETF representatives. Conclusions: Our findings indicate that trust had limited prominence in HETF discussions and recommendations. To rebuild the public's trust, it is imperative that the federal government, in collaboration with state and local partners, further develop actionable mechanisms to foster trust as a pillar of public health practice. By ensuring ethical principles are applied in decision-making and implementation, gaps in (mis)trust may be bridged, ultimately boosting the efficacy of public health emergency response.Publication Role of NRF2 and GSH in Response to PFOS Exposure in the Pancreas(2024-09) Pereira Marin, Marjorie GuidaPerfluorooctanesulfonic acid (PFOS) is a widespread legacy contaminant frequently detected in environmental and human samples. Notably, PFOS can cross the placenta and has been found in both cord blood and breastmilk, highlighting the importance of understanding its impacts during early development. This dissertation investigates the role of Nrf2, a transcription factor that regulates antioxidant genes, in mediating PFOS toxicity, particularly during critical windows of susceptibility such as pre-conception and embryonic development. Maternal PFOS exposure resulted in dose-dependent transfer to offspring, affecting both wildtype embryos with functional Nrf2a and Nrf2a mutants with a loss-of-function mutation. In wildtype offspring, PFOS exposure decreased nutrient uptake, while in Nrf2a mutants, it surprisingly increased. Additionally, the insulin-producing cells in larvae exposed maternally to PFOS were identified as a target, with wildtype embryos showing aberrant β-cell morphology, whereas Nrf2a mutants appeared protected. Further studies in zebrafish exposed to PFOS during embryonic development revealed a truncated exocrine pancreas phenotype, more severe in Nrf2a mutants. Tissue-specific effects were observed: PFOS exposure decreased S-glutathionylation in the pancreas of wildtype larvae, but this decrease was absent in Nrf2a mutants. No significant changes were noted in liver tissue. Moreover, PFOS exposure decreased β-cell insulin fluorescence in wildtype larvae, a reduction not seen in Nrf2a mutants. In vitro experiments with pancreatic βTC-6 cells demonstrated that PFOS affected the expression of genes involved in lipid metabolism, hormone regulation, and endoplasmic reticulum stress. The glutathione redox potential shifted in response to PFOS, coinciding with decreased glucose-stimulated insulin secretion. PFOS also increased the amount of proinsulin disulfide-linked complexes, suggesting that PFOS disrupts insulin biosynthesis—a potential novel mechanism of PFOS toxicity. This dissertation advances our understanding of how the Nrf2 pathway mediates the adverse effects of PFOS during critical developmental windows and identifies the pancreas as a primary target organ. Furthermore, it demonstrates how PFOS induces lasting alterations in pancreatic β-cell redox homeostasis and function. Given the ubiquity of this pollutant, exploring the mechanisms underlying PFOS toxicity is crucial. Future research can build on these findings to deepen our understanding of PFOS toxicity and to identify populations vulnerable to the potential lifelong consequences of early-life exposure to PFOS.