Research Capacity Training on Environmental Health and Noncommunicable Diseases in the Country of Georgia: Challenges and Lessons Learned during the COVID-19 Pandemic.

COVID-19 presented challenges for global health research training programs. The Clean Air Research and Education (CARE) program, which aims to enhance research capacity related to noncommunicable diseases and environmental health in the country of Georgia, was launched in 2020-as the COVID-19 pandemic began. At its foundation is mentorship and mentored research, alongside formal didactic training, informal training/meetings, and other supports. Current analyses examined CARE's initial 1.5 years (e.g., program benefits, mentorship relationships) using data from an evaluation survey among trainees and faculty in January 2022. Trainees (100% response rate: n = 12/12; 4 MPH, 8 PhD) and faculty (86.7% response rate: n = 13/15; 7 Georgia-based, 6 United States-based) rated factors related to mentor-mentee relationships highly, particularly mutual consideration of each other's thoughts, opinions, and perspectives; one major challenge was completing goals planned. Trainees and faculty identified several growth experiences and program benefits (e.g., skills development, expanding professional network) but also identified challenges (e.g., meeting program demands, communication gaps, unclear expectations)-exacerbated by the pandemic. Findings underscore the importance of strong mentorship relationships and that the pandemic negatively impacted communication and clarity of expectations. Given the likely ongoing impact of the pandemic on such programs, program leaders must identify ways to address these challenges.

The association between caffeine intake and testosterone: NHANES 2013-2014.

BACKGROUND: Caffeine is one of the most commonly used psychoactive drugs in the world, and provides many health benefits including alertness, improved memory, and reducing inflammation. Despite these benefits, caffeine has been implicated in a number of adverse health outcomes possibly due to effects within the endocrine system, effects that may contribute to impaired reproductive function and low testosterone in men. Previous studies have investigated associations between caffeine consumption and testosterone levels in men, although the quantity and generalizability of these studies is lacking, and the results between studies are conflicting and inconclusive. METHODS: Using data from a cross-sectional study of 372 adult men in the 2013-2014 NHANES survey cycle, the researchers set out to characterize the association between serum testosterone levels, caffeine, and 14 caffeine metabolites. RESULTS: Multivariable, weighted linear regression revealed a significant inverse association between caffeine and testosterone. Multivariable, linear regression revealed significant, inverse associations between 6 xanthine metabolic products of caffeine and testosterone. Inverse associations were observed between 5-methyluric acid products and testosterone, as well as between 5-acetlyamino-6-amino-3-methyluracil and testosterone. A significant, positive association was observed for 7-methyl xanthine, 3,7-dimethyluric acid, and 7-methyluric acid. Logistic regression models to characterize the association between 2 biologically active metabolites of caffeine (theobromine and theophylline) and odds of low testosterone (< 300 ng/dL) were non-significant. CONCLUSIONS: These findings suggest a potential role for caffeine's contribution to the etiology of low testosterone and biochemical androgen deficiency. Future studies are warranted to corroborate these findings and elucidate biological mechanisms underlying this association.

Long-term exposure to nitrogen dioxide and mortality: A systematic review and meta-analysis.

BACKGROUND: Ambient air pollution is among the greatest environmental risks to human health. However, little is known about the health effects of nitrogen dioxide (NO2), a traffic-related air pollutant. Herein, we aimed to conduct a meta-analysis to investigate the long-term effects of NO2 on mortality. METHODS: We conducted a systematic search for studies that were published up to February 2020 and performed a meta-analysis of all available epidemiologic studies evaluating the associations between long-term exposure to NO2 with all-cause, cardiovascular, and respiratory mortality. Overall pooled effect estimates as well as subgroup-specific pooled estimates (e.g. location, exposure assessment method, exposure metric, study population, age at recruitment, and key confounder adjustment) and 95% confidence intervals were calculated using random-effects models. Risk of bias assessment was accessed by following WHO global air quality guidelines. Publication bias was accessed by visually inspecting funnel plot and Egger's liner regression was used to test of asymmetry. RESULTS: Our search initially retrieved 1349 unique studies, of which 34 studies met the inclusion criteria. The pooled hazard ratio (HR) for all-cause mortality was 1.06 (95%CI: 1.04-1.08, n = 28 studies, I2 = 98.6%) per 10 ppb increase in annual NO2 concentrations. The pooled HRs for cardiovascular and respiratory mortality per 10 ppb increment were 1.11 (95%CI: 1.07-1.16, n = 20 studies, I2 = 99.2%) and 1.05 (95%CI: 1.02-1.08, n = 17 studies, I2 = 94.6%), respectively. The sensitivity analysis pooling estimates from multi-pollutant models suggest an independent effect of NO2 on mortality. Funnel plots indicate that there is no evidence for publication bias in our study. CONCLUSION: We provide robust epidemiological evidence that long-term exposure to NO2, a proxy for traffic-sourced air pollutants, is associated with a higher risk of all-cause, cardiovascular, and respiratory mortality that might be independent of other common air pollutants.

The Role of Nutrition and Inflammation on Cognition in a High-Risk Group for Alzheimer's Disease.

BACKGROUND: Alzheimer's disease (AD) is a prevalent neurodegenerative disease. Treatments are necessary to target people at high risk for AD. Inflammation, particularly tumor necrosis factor alpha (TNFα), appears to be an important marker associated with the development of AD pathophysiology. Consuming a high-fat diet induces tissue expression of TNFα. OBJECTIVE: This study investigates the relationship between nutrition, circulating inflammation, and cognition in African American women (age: M = 59.5 (±8.20) [42-73] years) at risk for developing AD. METHODS: Participants were split into high-fat and low-fat groups based on total dietary fat consumption self-reported on the Lower Mississippi Delta Nutrition Intervention Research Initiative Food Frequency Questionnaire (Delta NIRI FFQ). RESULTS: A high-fat diet was associated with increased blood serum TNFα (p = 0.02) compared to the low-fat diet. In addition, global cognition scores were 9.0% better in those who consumed a higher fat diet (p = 0.04). No significant differences across groups were noted for executive function, dual-tasking, and visuospatial performance. CONCLUSION: These results indicate that there may be multiple biological pathways involved in AD development, suggesting the need for more holistic approaches to mitigate AD-development risk.

Alteration to Dopaminergic Synapses Following Exposure to Perfluorooctane Sulfonate (PFOS), in Vitro and in Vivo.

Our understanding of the contribution exposure to environmental toxicants has on neurological disease continues to evolve. Of these, Parkinson's disease (PD) has been shown to have a strong environmental component to its etiopathogenesis. However, work is still needed to identify and characterize environmental chemicals that could alter the expression and function of the nigrostriatal dopamine system. Of particular interest is the neurotoxicological effect of perfluorinated compounds, such as perfluorooctane sulfonate (PFOS), which has been demonstrated to alter aspects of dopamine signaling. Using in vitro approaches, we have elaborated these initial findings to demonstrate the neurotoxicity of PFOS to the SH-SY5Y neuroblastoma cell line and dopaminergic primary cultured neurons. Using an in vivo model, we did not observe a deficit to dopaminergic terminals in the striatum of mice exposed to 10 mg/kg PFOS for 14 days. However, subsequent exposure to the selective dopaminergic neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) significantly reduced the expression of dopamine transporter (DAT) and tyrosine hydroxylase (TH), and resulted in an even greater reduction in DAT expression in animals previously exposed to PFOS. These findings suggest that PFOS is neurotoxic to the nigrostriatal dopamine circuit and this neurotoxicity could prime the dopamine terminal to more extensive damage following additional toxicological insults.