Browsing by Subject "Arsenic"

Coal fired power plants generate approximately 45% of the electricity produced in the United States every year, and each year, over 100 million tons of coal ash are produced as a by-product of electricity generation. Coal ash is a solid waste made up principally of bottom ash, fly ash, and flue gas desulfurization materials. The chemical composition of coal ash varies depending on the feed coal source, combustion parameters, and the presence and type of air pollution control devices that remove contaminants from the flue gas into the solid waste stream. Although a significant portion of coal ash waste is recycled, the majority of coal ash is disposed in landfills and holding ponds. Coal ash impoundments have a long history of environmental degradation, which includes: contaminant leaching into groundwater, the discharge of contaminant-laden effluent into surface waters, and catastrophic impoundment failures and ash spills. Despite these known problems, coal ash is not considered a hazardous waste, and thus is not subject to stringent disposal requirements. The current coal ash management system is based on risk assessments of coal ash that do not include environmental parameters that have a profound impact on coal ash contaminant mobility, particularly for the toxic elements such as mercury, arsenic, and selenium. This dissertation research focused on the biogeochemical transformations of mercury, arsenic, and selenium associated with coal ash materials in an effort to: (1) define the key environmental parameters controlling mercury, arsenic, and selenium fate during disposal and ash spills; and (2) delineate the relationship between coal ash characteristics, environmental parameters, and leaching potential.

The impact of coal ash on mercury transformations in anaerobic systems was assessed using anaerobic sediment-ash microcosms to mimic an ash spill into a benthic aquatic system. Anaerobic sediments are the primary zones for the microbial conversion of inorganic mercury to methyl mercury (MeHg), a process that is mediated by anaerobic bacteria, particularly sulfate reducing bacteria (SRB). MeHg is a potent neurotoxin that biomagnifies up the aquatic food chain, presenting a human health risk-- especially to children and pregnant women. The results of the sediment-ash microcosm experiments indicated negligible net production of MeHg in microcosms with no ash and in microcosms amended with the low-sulfate/low-Hg ash. In contrast, microcosms amended with sulfate and mercury-rich ash showed increases in MeHg concentrations that were two to three times greater than control microcosms without ash. The enhancement MeHg production in the microcosms was likely due to large quantities of leachable sulfate that stimulated the activity of methylating bacteria. Overall, these results highlight the importance of considering both the geochemical conditions of the receiving environment and the chemical composition of the coal ash in assessing the MeHg potential of coal ash.

The hypothesis that sulfate-rich coal ash can change sediment microbial communities, enhancing MeHg production, was tested by analyzing coal ash impacts on the SRB community in the sediment-ash microcosms using Terminal Restriction Fragment Length Polymorphism (T-RFLP), Quantitative Polymerase Chain Reaction (q-PCR), and Reverse Transcription-qPCR (RT-qPCR). Coal ash did not appear to cause significant changes to the structure of the overall bacterial community, though results showed that it may have caused a decrease in the evenness for species distribution for both SRB and the overall microbial community. During the five-day incubation experiment, the coal ash had a temporary significant effect on SRB abundance during the first one to two days of the experiment and a more sustained effect on SRB activity. This stimulation of SRB population growth and activity also corresponded with increasing net MeHg production. Overall, results indicate that coal ash amendments do not cause large shifts in the overall microbial community or the SRB community, but results indicate that there are connections between SRB abundance/activity and MeHg production. More research is needed to determine how coal ash directly impacts Hg methylating microorganisms, which include diverse array of microorganisms outside of SRB.

The effect of aerobic and anaerobic conditions on arsenic and selenium leaching from coal ash in an ash spill scenario was also assessed using sediment-ash microcosms. The fate of arsenic and selenium associated with coal ash is of particular concern due to the leachability of these elements at neutral pH and their tendency to bioaccumulate in aquatic organisms. Both the redox speciation of arsenic and selenium, and the pH of the aquatic system, are known to influence leaching into the environment, yet current environmental risk assessments of coal ash focus on pH alone as the primary driving force for arsenic and selenium leaching from coal ash and do not take into account the effects of anaerobic conditions and microbial activity. In this research, total dissolved concentrations of arsenic and selenium, dissolved speciation of arsenic, and solid phase speciation of selenium were monitored to determine the biogeochemical transformations and leaching of arsenic and selenium under differing redox conditions. The results from the sediment-ash microcosm studies showed that redox potential was the major determinant of arsenic and selenium mobility in the microcosm systems with greater arsenic leaching occurring in anaerobic microcosms and greater selenium leaching occurring in aerobic microcosms. Furthermore, the experiments provided clues to how coal ash influences the geochemistry of the benthic environment and how these influences affect the speciation and longer term solubility of arsenic and selenium.

Finally, experiments were conducted to determine how differing CaO, SO3, and Fe2O3 concentrations in coal ash affect the release of arsenic and selenium from sediment-ash mixtures in a simulated ash spill environment. Aerobic and anaerobic sediment-ash microcosms were constructed to mimic an ash spill into a benthic aquatic system, and a variety of coal ash materials were tested as amendments, including seven fly ashes, one lime-treated fly ash sample, and two FGD samples. Results showed that, in most cases, the sediment in the microcosm buffered the system at neutral, which counteracted leaching impacts of differing CaO and SO3 concentrations in the microcosms. Regardless of ash material, leaching of selenium was greater under aerobic conditions and was correlated with the total selenium content of the microcosm. Maximum leaching of arsenic occurred in anaerobic microcosms for some ash materials and in aerobic microcosms for other materials, suggesting that ash material chemistry played a significant role in controlling arsenic mobility. In both aerobic and anaerobic microcosms, dissolved arsenic concentration was correlated with total arsenic content of the ash material and in anaerobic microcosms, dissolved arsenic concentrations also correlated with the total iron content of the ash material. Overall, the results of these experiments showed that arsenic and selenium release under environmentally relevant conditions cannot be predicted by the CaO and SO3 content of the ash material. Rather, the total arsenic, total selenium content, and total iron content of the ash material are good predictors of the worst case environmental leaching scenario.

These investigations illuminated two major conclusions: (1) microbial activity and differing redox conditions are key in determining the impact of coal ash on the environment and in determining the mobility of coal ash contaminants, and (2) coal ash characteristics, such as sulfate and iron content, can change the redox chemistry and microbial activity of the surrounding environment, further influencing the fate of ash contaminants. This work will be useful in designing a framework that accurately predicts the leaching potential of ash contaminants under environmentally relevant conditions. The results will also be helpful in developing treatment technologies for ash impoundment effluent, guiding decisions on ash pond closure and remediation, and in designing long-term monitoring plans and remediation strategies for ash-impacted sites.

Arsenic (As) exposure via groundwater consumption is a global health problem affecting millions. Monitoring exposure is a key step in understanding and predicating future health outcomes. This thesis explores the relationships between arsenic concentrations in toenails and arsenic in water. Three case studies were investigated, with residents from: North Carolina, USA (n=103); the Rift Valley, Ethiopia (n=60); and the Mekong Delta, Vietnam (n=65). Arsenic concentrations above the WHO's recommended 10ppb limit were found in groundwater from the three research sites.

Arsenic in toenails was analyzed by inductively coupled plasma mass spectrometry (ICP-MS).

In the Rift Valley of Ethiopia, 53% of the tested drinking wells (n=34) had As above the WHO's limit. Arsenic concentrations in toenails (n=60) were significantly correlated to As concentrations in groundwater (r=0.72; p<0.001), reflecting the direct exposure of rural communities to As in well water, which is their principle water source. Male minors (<18 years old) were found to have greater nail-As concentrations compared with adults consuming equal amounts of As (p<0.05). Estimated As dose specifically from drinking water sources was also associated with nail concentrations (p<0.01).

In the Mekong Delta of Vietnam (Dong Thap Province), 36 out of the 68 tested wells had As content above the WHO's recommended limit of 10ppb, with levels as high as 981 ppb. Arsenic contents in nails collected from local residents (n=62) were significantly correlated to As in drinking water (r=0.49, p<0.001). Demographic and survey data show that the ratio of As in nail to As in water varies among residents that reflects differential As accumulation in the exposed population. The data show that water filtration and diet, particularly increased consumption of animal protein and dairy and reduced consumption of seafood, were associated with lower ratios of As in nail to As in water and thus could play important roles in mitigating As exposure.

Sixty-one wells were tested from Union County, North Carolina, with 15 out of 61 wells exceeded the WHO's 10 ppb limit. Arsenic values ranged from below the limit of detection (0.07) to 130ppb, with a mean of 11ppb (median=1.5ppb). Nails were collected from county residents (n=103) and were statistically correlated with As-water concentrations (r=0.48, p<0.001).

Integration of the data from the three cases studies across different populations and ethnicities show high correlation between As concentrations in groundwater and As in nails in all the three locations (r(Union County)= 0.48, p<0.001; r(Ethiopia)=0.72 p<0.001; r(Vietnam)=0.49, p<0.001). For As-nail to As-water pairs in which As in water was above 1ppb, these three locations are statistically indistinguishable from one another (r=0.62, p<0.001, n=176). These results support the hypothesis that nails can be used as a biomarker of exposure regardless of geographic or ethnic differences in populations considered. Nutrition (meat, seafood, and milk consumption) rather than gender, ethnicity, or dose is suggested to be the major confounding issue affecting the magnitude of As exposure in the human body.

Mitochondria are the main cellular producers of ATP, and play key roles in cellular signaling and apoptosis. Mitochondria also contain their own genomes (mtDNA), which encode 13 subunits of the electron transport chain (ETC), 22 tRNAs, and 2 rRNAs, making mtDNA integrity critical to both mitochondrial and organismal health. Mitochondria are dynamic organelles that fuse and divide to maintain mitochondrial shape, number, and size. However, mitochondrial fission and fusion also play a major role in the mitochondrial stress response. For example, mildly damaged mitochondria can fuse with healthy mitochondria allowing contents to mix, resulting in the generation of healthy mitochondria, which is known as functional complementation. Alternatively, when mitochondria become damaged beyond repair, they are targeted for autophagosomal degradation, or mitophagy. The overall importance of fission, fusion, mitophagy, and mtDNA is demonstrated by the fact that deficiencies in these processes and mtDNA content cause human disease. Interestingly, the age of onset, and severity of clinical manifestations of mitochondrial disease vary from patient to patient, even in individuals harboring identical mutations. These observations suggest a role for the environment in the development and progression of certain mitochondrial diseases; however, the relationship remains poorly understood.

To investigate the role of environmental toxicants in the development, progression, and exacerbation of mitochondrial disease I have taken two approaches using the in vivo model organism Caenorhabditis elegans. First, ten known and suspected mitochondrial toxicants (2,4-dinitrophenol (DNP), acetaldehyde, acrolein, aflatoxin B1 (AfB1), arsenite, cadmium, cisplatin, doxycycline, paraquat, rotenone) were screened for exacerbation of larval growth delay in wild-type, fission-, fusion-, and mitophagy-deficient nematodes using the COPAS Biosort. Second, a C. elegans model of mtDNA depletion was developed using chronic low-dose ethidium bromide exposure. Five toxicants (AfB1, arsenite, paraquat, rotenone, ultraviolet C radiation (UVC)) were tested for exacerbation of mitochondrial function (assessed via changes in steady-state ATP levels) in nematodes with reduced mtDNA content. Mitochondrial health was then further assessed for some of the identified gene-environment interactions. Mitochondrial respiration was measured using the Seahorse XFe24 Extracellular Flux Analyzer, while steady-state ATP levels were assessed using transgenic luciferase expression nematodes and traditional extraction protocols. Gene expression, mtDNA, and nuclear DNA copy number were assessed using real-time PCR, while enzyme activity was assessed using microplate reader-based assays.

Results from the fission, fusion, and mitophagy toxicant screen revealed that fusion-deficient nematodes were sensitive to a variety of toxicants (DNP, AfB1, arsenite, cisplatin, paraquat, rotenone), while pink-1 mitophagy-deficient nematodes were sensitive to rotenone, and fission- and pdr-1 mitophagy-deficient nematodes were only mildly sensitive to paraquat, and rotenone, respectively. As mitochondrial disease is rare, but chronic arsenite exposure is widespread, we further investigated the mechanisms underlying arsenite sensitivity in fission- and fusion-deficient nematodes. Although not sensitive in the larval growth assay, fission-deficient nematodes were sensitive to arsenite later in life in both reproduction and lethality assays. Seahorse and ATP analysis revealed that arsenite disrupts mitochondrial function in fusion-deficient nematodes at multiple life stages (L4, 8- and 12-days of age), while enhancing mitochondrial function in 8-day old wild-type nematodes, and has minimal effect on mitochondrial function in fission-deficient nematodes. Lastly, arsenite inhibited both pyruvate and isocitrate dehydrogenase activity in fusion-deficient nematodes, suggesting a disruption of pyruvate metabolism and Krebs cycle activity underlie the observed mitochondrial dysfunction. These results suggest that deficiencies in mitochondrial fusion may sensitive individuals to arsenite toxicity.

Lastly, I have found that reducing mtDNA content 35-55% only mildly sensitized nematodes to certain secondary toxicant exposures, including UVC and arsenite. Alternatively, reduced mtDNA content did not sensitize nematodes to acute or chronic paraquat or AfB1 exposure, and provided resistance to rotenone. However, we also found that EtBr can induce cytochrome P450s (CYPs), which play a major role in rotenone metabolism; thus, it is likely that induction of CYPs and not reduced mtDNA content is responsible for rotenone resistance. These results suggest that individuals with reduced mtDNA content may be sensitive to certain toxicant exposures, but also highlight the robust mechanism that exist to maintain the integrity of mitochondria and mtDNA.

Collectively, these results suggest individuals suffering from mitochondrial disease caused by mutations in mitochondrial fission, fusion, or mitophagy genes, or by depletion of mtDNA, may be especially sensitive to certain environmental toxicant exposures, including arsenic. Arsenic’s pervasive contamination of drinking water results in chronic exposure for over 100 million people worldwide; thus, dramatically increasing the probability of exposure for individuals suffering from mitochondrial disease, and warrants further investigation in the human populous.

This dissertation examines the potential of information-provision in motivating behavior that reduces human exposure to arsenic in drinking-water in Bangladesh. In chapter 2, the longer-term effects of the countrywide arsenic-testing and information-program are examined by tracking tube-well switching behavior of households over a five-year period. Chapter 3 focuses on the effects of arsenic information communication formats on tube-well switching behavior, by employing a randomized field experiment. In chapter 4, an instrumental variables approach is used to understand whether a household's decision to switch sources is affected by its proximate neighbors' decisions to switch sources. To answer these questions, primary data was collected by the researchers through field-work in Bangladesh. The results suggest that arsenic-testing and information-provision programs produce persistent behavioral changes that reduce exposure to arsenic, with their impact increasing over time. Comparing the impacts of risk-communication formats, we find that quantitative formats do not significantly increase source-switching behavior, in comparison to that generated by qualitative formats. Lastly, despite econometric identification issues, our data suggest that households gather information about source-switching by observing the actions of their neighbors. In sum, the results presented in this dissertation suggest that the provision of information to rural households can motivate health-improving behavior that reduces households' exposure to arsenic in Bangladesh. This dissertation contributes to the use of information disclosure as a policy instrument to reduce exposure to environmental contaminants.