Diarrheal diseases are a global public health burden, killing 1.8 million people annually. Diarrhea disproportionately affects children and those in poverty. Most diarrheal cases can be prevented through safe drinking water, basic hygiene and/or sanitation measures, with drinking water interventions having the most impact on reducing diarrheal disease. There is no generally agreed-upon field method for determining biosand water filter effectiveness that is usable in low-resource communities. A pilot study was conducted of potential field use indicators, including the Colilert coliform presence/absence (P/A) test, hydrogen sulfide, alkalinity, hardness, pH, and fluorescently labeled latex microspheres. The study included both laboratory and field testing. The Colilert P/A test had the highest correlation to the United States Environmental Protection Agency standard method (IDEXX Quanti-trays), but more data are needed before making a recommendation. This study adds to understanding about evaluation of biosand water filters and provides preliminary data to address the need for a field use indicator for biosand water filters.

More than 270,000 km of rivers and streams are impaired due to fecal pathogens, creating an economic and public health burden. Fecal indicator organisms such as Escherichia coli are used to determine if surface waters are pathogen impaired, but they fail to identify human health risks, provide source information, or have unique fate and transport processes. Statistical and machine learning models can be used to overcome some of these weaknesses, including identifying ecological mechanisms influencing fecal pollution. In this study, canonical correlation analysis (CCorA) was performed to select parameters for the machine learning model, Maxent, to identify how chemical and microbial parameters can predict E. coli impairment and F+-somatic bacteriophage detections. Models were validated using a bootstrapping cross-validation. Three suites of models were developed; initial models using all parameters, models using parameters identified in CCorA, and optimized models after further sensitivity analysis. Canonical correlation analysis reduced the number of parameters needed to achieve the same degree of accuracy in the initial E. coli model (84.7%), and sensitivity analysis improved accuracy to 86.1%. Bacteriophage model accuracies were 79.2, 70.8, and 69.4% for the initial, CCorA, and optimized models, respectively; this suggests complex ecological interactions of bacteriophages are not captured by CCorA. Results indicate distinct ecological drivers of impairment depending on the fecal indicator organism used. Escherichia coli impairment is driven by increased hardness and microbial activity, whereas bacteriophage detection is inhibited by high levels of coliforms in sediment. Both indicators were influenced by organic pollution and phosphorus limitation.

Tumor-like proliferative vascular lesions manifest in several diseases such as peripheral arterial disease (PAD) and atherosclerosis (AS) after arterial injury. The cause of the vascular cell dysfunction in PAD patients is not known. Our recent novel discovery shows that inhibitor of differentiation 3 (ID3) is highly expressed in intimal lesions of clinical vascular disease samples. The central hypothesis of our study is: estrogenic chemical induced dysregulation of ID3 target genes is involved in the development of vascular disease. NHANES data analysis demonstrated higher geometric levels of all 6 PCB congeners in both PAD diagnosed participants and participants at risk of AS when compared to the rest of the population. Adjusted models showed association between higher exposure of PCBs, phthalates, BPA, and increased risk of PAD. Furthermore PCB153 was shown to have the highest geometric mean amongst all PCB congeners in both participants diagnosed with PAD and at risk of AS. Gene expression of ID3 & ID3 candidate targets in blood & tissue studies identified ID3 & ID3 candidate target genes as a driver of vascular disease. Overlapping ID3 & ID3 candidate target genes included: ABCB6, ACP1, BYSL, CAD, CDH15, DCBLD2, DHRS3, DNMT1, ID3, MCM4, and NDUFA7. The ID3 target genes involved in the: focal adhesion pathway were ACTN1, COL1A2, COL3A1, COL6A1, CTNNB1, IBSP, ID3, ITGA8, and MYL2; ECM-receptor interaction were COL1A2, COL3A1, COL6A1, IBSP, ID3, and ITGA8; oxidative phosphorylation pathway ATP5D, ATP5H, ATP6V0B, ATP6V0D1, ATP6V1B2, COX5A, COX7C, COX8A, CYC1, ID3, NDUFA1, NDUFA7, NDUFS4, NDUFV1, NDUFV2; and cell cycle pathway ANAPC10, ATM, CDKN2B, E2F5, MCM3, and MCM4. In summary our results showed an association between exposure to PCBs, phthalates, BPA, and increased risk of PAD and AS, and possible molecular mechanisms of interaction of ID3 target genes and estrogenic chemicals involved in PAD and AS.

Disturbances such as fire and grazing can degrade landscapes, but they can also rejuvenate them. I evaluated: 1) the practicality of strategically timed (fall), high intensity browsing of sagebrush (Artemisia tridentata ssp. tridentata, ssp. wyomingensis) by cattle; 2) the foraging behavior and body weights of cattle with varying levels of experience browsing sagebrush; and 3) the ensuing responses of grasses, forbs, and sagebrush to cattle grazing. In spatially and temporally replicated trials from 2007 to 2009, fall grazing by cattle reduced the abundance of sagebrush and promoted production of grasses and forbs. The cattle used in these trials were challenged to learn to eat sagebrush in the unfamiliar circumstance of confinement in small pastures. Throughout the trials from 2007 to 2009, pregnant cows with calves (2007), bred yearling heifers (2008), and first-calf heifer/calf pairs (2009) supplemented with protein and energy – to mitigate the effects of terpenes in big sagebrush – learned to select sagebrush as a significant portion of their diet. In virtually every case, experienced animals consistently used more sagebrush and lost less weight, or actually gained more weight, than naive animals in 2008 and 2009. My research suggests grazing by cattle during fall can be effective, biologically and economically, and can lead to habitat renovation and resilience. Moreover, grazing can create locally adapted systems in ways that landscape manipulations with chemical and mechanical treatments and prescribed fire cannot. These “technological fixes” are increasingly impractical due to environmental concerns, the high costs of fossil fuels, and the need to repeat outcome-based treatments rather than incorporating process-based approaches into managing landscapes. Rather than attempting to convert sagebrush steppe landscapes to grass at extravagant costs, as we have done historically, we must now consider ways to create locally adapted herds of livestock and complementary management practices to ensure long-term health of sagebrush steppe. As many ranchers already feed hay to cows during winter, using sagebrush steppe vegetation as an additional forage resource would allow ranchers to feed roughly half the hay, which would greatly reduce winter feed costs. In addition to financial savings in hay, the secondary benefits from improving sagebrush steppe condition and productivity would result in habitat improvements for both livestock and wildlife.

Food deserts are low-income areas lacking access to nutritious and affordable food. Such limited access has various implications for public health, particularly diet-related diseases such as diabetes. Among American Indian communities, diabetes is particularly rampant at nearly twice the rate of white populations in the U.S. On the Navajo Nation, diabetes incidence has been estimated to be as high as 1 in 3. According to the USDA, the majority of the Navajo Nation is considered a food desert. This paper utilizes food sovereignty as a lens for decolonization to identify the underlying causes of hunger and nutrition-related diseases within Diné communities. This paper will explore the histories of the change in the Diné diet and how colonial processes and the loss of traditional food systems affects current food and health patterns on the Navajo Nation. By expanding the scope of public health issues such as obesity and diabetes in Native American communities from food access and nutrition to power relations embedded in colonial structures that have resulted in the loss of indigenous sovereignty and power, I hope to pinpoint entry points for future indigenous researchers to develop and enact policies that will expand access to healthy and culturally significant foods on the Navajo Nation and contribute to efforts to restore food sovereignty of the Navajo Nation by rebuilding local food economies.

The overall objective of the research presented in this dissertation was to assess exposure to endocrine disrupting chemicals (EDCs), polychlorinated biphenyls (PCBs), phthalates, and bisphenol A (BPA) in the general population and evaluate their associations with adverse reproductive health effects, including cancers, in women. Given the proven contribution of unopposed estrogens to the risk for endometrial neoplasia or breast cancer, renewed health concerns have aroused about estrogen mimicking EDCs found in food, personal care products or as environmental contaminants. Our meta-analysis showed that exposure to estrogen mimicking PCBs increased summary risk of breast cancer and endometriosis. We further evaluated the relationship between endometriosis and breast cancer, and EDCs using a bioinformatics method. Our bioinformatics approach was able to identify genes with the potential to be involved in interaction with PCB, phthalates and BPA that may be important to the development of breast cancer and endometriosis. Therefore, we hypothesized that exposure to EDCs such as PCBs, phthalates, and BPA, results in adverse reproductive health effects in women. Using subject data and biomarkers available from the Center for Disease Controls National Health and Nutrition Examination Survey database we conducted a cross-sectional study of EDCs in relation to self-reported history of endometriosis, uterine leiomyomas, breast cancer, cervical cancer, ovarian cancer, and uterine cancer. Significantly higher body burdens of PCBs were found in women diagnosed with breast cancer, ovarian cancer, and uterine cancer compared to women without cancer. PCB 138 was significantly associated with breast cancer, cervical cancer, and uterine cancer, while PCBs 74 and 118 were significantly associated with ovarian cancer. The sum of dioxin-like PCBs were significantly associated with ovarian cancer (OR of 2.02, 95% CI: 1.06-3.85) and the sum of non-dioxin-like PCBs were significantly associated with uterine cancer (OR of 1.12, 95%CI: 1.03-1.23). Significantly higher body burdens of PCBs were also found in women diagnosed with endometriosis and uterine leiomyomas. Documenting the exposure to EDCs among the general U.S. population, and identifying agents associated with reproductive toxicity have the potential to fill research gaps and facilitate our understanding of the complex role environmental chemicals play in producing toxicity in reproductive organs.

No description available.

No description available.

Silver nanoparticles (AgNPs) are expected to enter aquatic systems, but there are limited data on how they might affect microbial communities in pathogen impaired streams. We examined microbial community responses to citrate-AgNP (10.9 ± 0.7 nm) and polyvinylpyrrolidone (PVP)-AgNP (11.0 ± 0.7 nm) based on microbial concentration and enzyme activity in sediment from a pathogen impaired stream. Addition of each nanoparticle to sediment caused at least a 69% decrease in microbial concentration (1,264 ± 93.6 to 127 ± 29.5 CFU/g) and a 62% decrease in β-glucosidase activity (11.7 ± 2.1 to 1.3 ± 0.3 μg/g/h). Each AgNP reduced alkaline phosphatase activity but their effects were not statistically significant. Sediment exposed to 0.108 mg Ag/kg of AgNO3 resulted in a 92% decrease in microbial concentration and a reduced enzyme activity which was not statistically significant. Measured total silver in sediments treated with AgNPs which exhibited significant inhibition effects on the microbial community ranged from 0.19 ± 0.02 to 0.39 ± 0.13 mg Ag/kg. These concentrations tested in this study are much lower than the expected concentrations (2-14 mg Ag/kg) in freshwater sediments. The results of this study demonstrate that AgNPs can alter microbial community activity and population size, which may lead to false negative fecal indicator bacteria detection and enumeration using methods that rely on β-glucosidase activity. We conclude that the presence of AgNPs in impaired streams and recreational waters can influence pathogen detection methods, potentially affecting public health risk estimates.

Animal and human wastes introduce pathogens into rivers and streams, creating human health and economic burdens. While direct monitoring for pathogens is possible, it is impractical due to the sporadic distribution of pathogens, cost to identify, and health risks to laboratory workers. To overcome these issues, fecal indicator organisms are used to estimate the presence of pathogens. Although fecal indicators generally protect public health, they fall short in their utility because of difficulties in public health risk characterization, inconsistent correlations with pathogens, weak source identification, and their potential to persist in environments with no point sources of fecal pollution. This research focuses on characterizing the ecology of fecal indicators using both modeling and metabolic indicators to better understand the processes that drive fecal pollution. Fecal indicator impairment was modeled in Sinking Creek, a 303 (d) listed stream in Northeast Tennessee, using the ecological niche model, Maxent, for two different fecal indicators. While the use of Maxent has been well demonstrated at the macroscale, this study introduces its application to ecological niches at the microscale. Stream impairment seasonality was exhibited in two different indicators over multiple years and different resolutions (quarterly versus monthly sampling programs). This stresses the need for multiple year and month sampling to capture heterogeneity in fecal indicator concentrations. Although discharge is strongly associated with dissolved solutes, fecal indicator impairment was governed by other ecological factors such as populations of heterotrophic bacteria, enzyme activity, nutrient conditions, and other metabolic indicators. This research also incorporated metabolic indicators to characterize spatiotemporal variability in microbial community function, making connections to fecal and other pollution gradients. Communities differed in their ability to use a wide variety of substrates, and metabolic inhibition in sediments captured most of the interaction of aquatic and benthic communities. Sediment substrate activity was also indicative of degrees of pollution, suggesting that sediment is a potential reservoir for Escherichia coli in this stream, and there is possibility for resuspension, extended residence times, and increased duration for exposure. This research highlights the benefit of using models and other microbial indicators to better understand how environment shapes the niche of fecal indicators.