Faculty Bibliography

The use of E-cigarettes, often considered a safer alternative to traditional smoking, has been associated with high rates of cellular toxicity, genetic alterations, and inflammation. Neuroinflammatory impacts of cigarette smoking during pregnancy have been associated with increased risks of adverse childhood health outcomes; however, it is still relatively unknown if the same propensity is conferred on offspring by maternal vaping during gestation. Results from our previous mouse inhalation studies suggest such a connection. In this earlier study, pregnant C57BL/6 mice were exposed daily to inhaled E-cig aerosols (i.e., propylene glycol and vegetable glycerin, [PG/VG]), with or without nicotine (16 mg/mL) by whole-body inhalation throughout gestation (3 h/d; 5 d/week; total ~3-week) and continuing postnatally from post-natal day (PND) 4-21. As neuroinflammation is involved in the dysregulation of glucose homeostasis and weight gain, this study aimed to explore genes associated with these pathways in 1-mo.-old offspring (equivalent in humans to 12-18 years of age). Results in the offspring demonstrated a significant increase in glucose metabolism protein levels in both treatment groups compared to filtered air controls. Gene expression analysis in the hypothalamus of 1 mo. old offspring exposed perinatally to E-cig aerosols, with and without nicotine, revealed significantly increased gene expression changes in multiple genes associated with neuroinflammation. In a second proof-of-principal parallel study employing the same experimental design, we shifted our focus to the hippocampus of the postpartum mothers. We targeted the mRNA levels of several neurotrophic factors (NTFs) indicative of neuroinflammation. While there were suggestive changes in mRNA expression in this study, levels failed to reach statistical significance. These studies highlight the need for ongoing research on E-cig-induced alterations in neuroinflammatory pathways.

Human health effects can arise from unregulated manual disassembly of electronic waste (e-waste) and/or hydraulic fracturing fluid spills. There is limited literature on the effects of e-waste and hydraulic fracturing wastewater exposure on the male reproductive system. Thus, this proof-of-concept study begins to address the question of how wastewater from two potentially hazardous environmental processes could affect sperm quality. Therefore, three groups of eight-week-old adult mice were exposed (5 d/wk for 6 wks) via a mealworm (Tenebrio molitor and Zophabas morio) feeding route to either: (1) e-waste leachate (50% dilution) from the Alaba Market (Lagos, Nigeria); (2) West Virginia hydraulic fracturing flowback (HFF) fluid (50% dilution); or, (3) deionized water (control). At 24-hours (hr), 3 weeks (wk), or 9-wk following the 6-wk exposure period, cohorts of mice were necropsied and adverse effects/persistence on the male reproductive system were examined. Ingestion of e-waste leachate or HFF fluid decreased number and concentration of sperm and increased both chromatin damage and numbers of morphological abnormalities in the sperm when compared to control mice. Levels of serum testosterone were reduced post-exposure (3- and 9-wk) in mice exposed to e-waste leachate and HFF when compared to time-matched controls, indicating the long-term persistence of adverse effects, well after the end of exposure. These data suggest that men living around or working in vicinity of either e-waste or hydraulic fracturing could face harmful effects to their reproductive health. From both a human health and economic standpoint, development of prevention and intervention strategies that are culturally relevant and economically sensitive are critically needed to reduce exposure to e-waste and HFF-associated toxic contaminants.