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This Research-to-Practice full paper presents findings from the ASSETS program – a comprehensive support ecosystem developed to improve retention and reduce time to graduation for engineering transfer students. ASSETS builds on the momentum established by two statewide initiatives in Tennessee that place transfer students at the forefront: (1) Tennessee Promise – a nationally recognized scholarship program launched in 2015 that provides last-dollar scholarships for low-income students to attend any state community college, and (2) Tennessee Reconnect – a lastdollar grant established in 2018 that allows adults who do not have an associate degree to attend a community or technical college tuition-free. With over 100,000 students enrolled in these programs to date, the number of students transferring to four-year institutions is expected to increase exponentially in the coming years. Historically, transfer students have been at higher risk of attrition due to known academic and social barriers. This is especially true for the Engineering disciplines. In an effort to address these obstacles, we have developed the Academic Intervention, Social Supports, and Scholarships for Engineering Transfer Students (ASSETS) program. In its third year of operation, with 35 enrolled ASSETS scholars, the program is well underway. Among our findings, we have recognized the critical importance of nurturing a community of transfer students that emphasizes equity, diversity, and inclusion. Establishing such a community involves more than just adopting established best practices. It requires a shift in mindset on behalf of the student regarding what is required to succeed, as well as on the part of faculty on what is expected of incoming students. This paper presents the findings and outcomes of the ASSETS program towards providing support to and enhancing the success of engineering transfer students. 

Air pollutants such as ozone, particulate matter, and secondary organic aerosols (SOA) induce intracellular oxidative stress via the generation of reactive oxygen species (ROS). While ROS play important roles in regulating signaling pathways, supra-physiological levels disrupt redox homeostasis and potentiate inappropriate oxidation of regulatory thiols. We examined the effect of isoprene hydroxy hydroperoxide (ISOPOOH), an environmentally derived peroxide that contributes to SOA, on the interplay between bioenergetics and intracellular redox status. We used live cell imaging of human airway epithelial cells (HAECs) expressing the genetically encoded ratiometric biosensors roGFP, iNAP1, and HyPER, to monitor changes in the glutathione redox potential (EGSH), NADPH and H2O2, respectively. Non-cytotoxic exposure to ISOPOOH induced transient increases in EGSH in HAECs that were markedly potentiated by glucose deprivation. ISOPOOH-induced changes in EGSH were not driven by intracellular H2O2. Following ISOPOOH exposure, the addition of 1 mM glucose rapidly restored baseline EGSH and reversed ISOPOOH-induced reductions in NADPH levels, while lower concentrations of glucose (30 uM) induced a bi-modal EGSH recovery. Alternatively, the addition of the glycolytic inhibitor 2-deoxyglucose (2-DG) did not block recovery of NADPH levels nor EGSH restoration. To impair the recovery of EGSH and NADPH levels, we employed a lentiviral vector system to knockdown glucose-6-phosphate dehydrogenase (G6PD), a key enzyme involved in NADPH synthesis. The resulting G6PD knockdown (~50%) did not block glucose-mediated recovery of EGSH, implicating that a partial knockdown of G6PD may not be sufficient to manipulate NADPH levels and thereby EGSH. These findings underscore early mechanisms involved in the cellular response to ISOPOOH while providing a unique live view of the dynamic regulation of redox homeostasis in the human lung during exposure to environmental oxidants. THIS ABSTRACT OF A PROPOSED PRESENTATION DOES NOT NECESSARILY REFLECT EPA POLICY.