Browsing by Subject "Air pollution"
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Item Open Access Air pollution, Fuel Usage and Health Outcomes in Madre de Dios, Peru: a Comparative Cross Sectional Study(2015) Chao, Christina AnnAir pollution is a common problem. Particulate matter generated from air pollution has been tied to adverse health outcomes associated with cardiovascular disease. Biomass fuels are a specific contributor to increased particulate matter and arise as a result of indoor heating, cook stoves and indoor food preparation. This is a two part cross sectional study looking at communities in the Madre de Dios region. Survey data was collected from 9 communities along the Madre de Dios River. Individual level household PM2.5 was also collected as a means to generate average PM data stratified by fuel use. Data collection was affected by a number of outside factors, which resulted in a loss of data. Results from the cross-sectional study indicate that hypertension is not a significant source of morbidity. Obesity is prevalent and significantly associated with kitchen venting method indicating a potential relationship.
Item Open Access Air Pollution, Water, and Sanitation: Household Response to Environmental Risk(2020) Pakhtigian, Emily LDespite the threats to morbidity, mortality, and human capital accumulation posed by environmental risks, investments in environmental health technologies remain low. This is especially evident in low- and middle-income countries, which disproportionately shoulder the burden of environmental risk exposure and consequence. Households face competing risks associated with poor air and water quality, necessitating choices about how to invest in technologies to reduce the consequences associated with their exposures. Yet, even in areas where access to environmental health technologies such as improved cookstoves, latrines, and insecticide-treated bednets has expanded and products are subsidized to make them more affordable, adoption and use of these technologies often lag. This dissertation examines some of the conditions that impact environmental health technology adoption and use decisions as well as the health implications of low investment.
In Chapter 1, I ask how air pollution exposure drives consumption behaviors and impacts health outcomes. I examine this question in the short term--asking how behavior and health respond to a large, yet transitory, spike in ambient air pollution--as well as over time--considering the responses to average ambient air pollution levels over a period of 19 years. I leverage variation in air pollution resulting from forest fire emissions in Indonesia between 1996 and 2015 to generate short-term exposure spikes and average exposures over time, and I combine these exposures with four waves household and individual-level survey data. I implement a cross-sectional, difference-in-difference analysis to estimate the immediate effects of an unexpectedly severe forest fire season in 2015, finding increased fuel demands among the most-exposed households as well as declines in lung capacity among emissions-affected children. I extend my analysis across the panel using an instrumental variables approach to estimate consequences of average exposure over time. I find that households facing higher average ambient air pollution exposures are more likely to utilize clean cooking fuels such as LPG. Even with these behavioral adjustments, more-exposed individuals face significant reductions in lung capacity. In line with existing literature, I find negative health implications resulting from short-term exposure shocks; however, my analysis demonstrates that these respiratory consequences are not fleeting, particularly in areas that experience elevated average ambient air pollution levels.
In Chapter 2, I turn to environmental risks posed by limited access to improved sanitation technologies to examine how social influences impact household sanitation decisions. Using three waves of data collected immediately before, a few months after, and a few years after a randomized latrine promotion campaign in rural Orissa, India, I evaluate the extent to which social influences impact sanitation choices. I find that a ten percentage point decrease in neighbors' open defecation reduces a household's likelihood of open defecation by 3-4 percentage points. The sanitation intervention decreased open defecation in the short term; however, this treatment was less effective in neighborhoods with higher rates of open defecation due to strong social effects. Disaggregating social effects by gender, I find that both women and men respond to sanitation behaviors among male neighbors in the short term and female neighbors in the longer term, perhaps because men have more control over initial latrine purchasing decisions while women are more influential in sustaining latrine use over time.
Finally, in Chapter 3, I expand on my analysis of social influences and sanitation practices and examine how households make decisions to contribute to collective action for sanitation. In this chapter, I analyze data from an experimental public goods game I designed and implemented among over 1500 households in rural Bihar and Orissa, India. I randomly assigned each of the 70 villages in the sample into groups that are either homogeneous or heterogeneous by gender for game play. In the context of rural India, individuals are more likely to frequently interact with and make decisions in front of others of the same gender. Thus, splitting the groups in this way provides a proxy for peer or social groups. Participants chose how much to contribute to improved sanitation by making decisions in the game that are associated with actual sanitation and hygiene choices they face every day. Payoffs were awarded after each round, and payoff amounts were dependent on both individual contributions and aggregated group contributions, generating a setting in which the benefits participants received were connected. Comparing the game behavior among participants in groups that were homogeneous and heterogeneous by gender, I find evidence that contributions to collective action for sanitation are higher in gender homogenous groups. Female participants drive this difference, and it is more distinct in the first round of game play. I also find evidence that preferences for improved sanitation as elicited during the experimental games are reflective of actual improved sanitation practices at the household level.
Item Open Access Biomonitoring of Amino-PAHs, Cotinine, and PAH-hemoglobin Adducts in Human Specimens(2018-04-27) Yan, PeijiaDiesel exhaust is a large source of outdoor air pollution in urban area, while smoking is an important contributor to indoor air pollution in our daily life. Exposure to these complex mixtures may lead to many adverse health effects such as cardiovascular diseases, respiratory diseases, and even several types of cancer. Especially, polycyclic aromatic hydrocarbons (PAHs) and nitrated polycyclic aromatic hydrocarbons (nitro-PAHs) are byproducts of incomplete combustion and are generated from diesel combustion process and from tobacco smoking. Amino-PAHs are metabolites of nitro-PAHs and have been suggested as traffic-related exposure biomarkers. The first and largest aim for this Master’s Project was to learn analytical chemistry methods to measure different biomarkers in human specimens. Firstly, cotinine and five types of amino-PAHs were measured as biomarkers of smoking and diesel exhaust exposure, respectively, in both types of samples. Then, as a proven mechanism for many air pollution associated health effects, oxidative stress was measured using urinary malondialdehyde (MDA), a well-established biomarker of lipid peroxidation by reactive oxygen species. The second aim for this project was to examine the relationship among different biomarkers. Especially, I focused on the relationship between nitro-PAHs exposure and oxidative stress, and the relationship between tobacco smoke exposure and oxidative stress.Item Open Access Co-effects of Transportation Means and Air Quality on Neurological, Pulmonary, and Cardiovascular Function(2021-04-15) Ong, Gui Xian; Zhang, Yang; Wang, HuapingThe guidelines on outdoor activities in the presence of air pollution vary. We aim to find out the effects of walking and air pollution among young adults. We conducted a randomized, 3-session cross-over trial, with 28 healthy Duke Kunshan University (DKU) students. Between October 2020 and February 2021 on days with varying air quality levels, students walked or took the bus from DKU to Scholars Hotel in Kunshan, China. Indicators of neurological function (reaction speed, visual memory, verbal memory, and numerical memory), pulmonary function (PEF, FEV1 , FVC, and FEV1 / FVC), and cardiovascular function (systolic pressure, diastolic pressure, and heart rate) were tested before and after the interventions. The paired t-test findings revealed that walking was beneficial for pulmonary function, with an average PEF increase of 40.29 ± 84.87 L/min (p<0.05). On the other hand, air pollution decreased diastolic pressure by an average of -3.85 ± 5.30 mmHg (p<0.05) and numerical memory by an average of -2.27 ± 2.37 points (p<0.01). The regressions results showed that air pollution was associated with statistically significant decreases in cognitive and pulmonary function. An increase in PM 2.5 (1 µg/m3 ) was associated with decreased numerical memory (-2.32 points; p<0.05) and a unit increase in AQI was correlated with decreased FEV 1 (-6.71 L; p<0.05). On the co-effects of walking and air pollution, our evidence was inconclusive. Walking outdoors during air polluted days may negatively affect pulmonary functions and neurological functions, while its effect on cardiovascular functions is not clear. Being cautious, individuals may refrain from exercising in air polluted environments to avoid potential negative health impacts. Nonetheless, we are unable to make strong inferences towards such behavioral recommendations due to the limited effect size.Item Open Access Developmental Programming of Brain and Behavior: A Role for the Innate Immune System of the Placenta and Brain?(2015) Bolton, Jessica LynnThe field of "perinatal programming" has increasingly implicated an adverse early-life environment in the etiology of many chronic health problems and mental disorders. The following dissertation research is based on the hypothesis that the programming of brain and behavior by an altered early-life environment is propagated by inflammatory mechanisms in the placenta and developing brain. Offspring outcomes of two different maternal environmental exposures--air pollution and a "Western diet" (both highly relevant for the modern world)--were assessed in a mouse model in order to identify mechanisms common to developmental programming more generally.
The first set of experiments characterized the long-term behavioral and metabolic consequences of prenatal air pollution exposure in adult offspring. The male offspring of diesel exhaust particle (DEP)-exposed dams were predisposed to obesity, insulin resistance, and increased anxiety following placement on a high-fat diet (HFD) in adulthood. Furthermore, DEP/HFD male offspring exhibited evidence of macrophage priming, both in microglia and peripheral macrophages. The next experiment examined whether prenatal air pollution exposure could also synergize with a simultaneous "second hit" (i.e., maternal stress) during gestation. The offspring of mothers exposed to both air pollution and stress during gestation were more anxious as adults, but only the male offspring of this group also exhibited impaired cognition, in conjunction with neuroinflammatory changes. A further experiment revealed that prenatal air pollution exposure altered microglial maturation in a TLR4- and sex-dependent manner, consistent with the previous results. However, we found limited evidence of a placental immune response to DEP, potentially due to analysis too late in gestation.
The second set of experiments characterized the enduring behavioral and metabolic consequences of maternal consumption of a "Western diet" (HFD in combination with BCAA supplementation) prior to and during gestation and lactation. The adult offspring of HFD-fed dams were more anxious in adulthood, despite being placed on a low-fat diet at weaning. Male HFD offspring were also hyperactive, whereas female HFD offspring exhibited more severe metabolic disturbances. Furthermore, there was evidence of microglial priming and peripheral macrophage priming in male HFD offspring, similar to the prenatal air pollution model. The next experiment also found evidence of altered microglial development due to maternal HFD, in conjunction with widespread, sex-specific immune gene regulation in the placenta in response to maternal diet. Moreover, maternal HFD decreased placental serotonin production, and also programmed long-term alterations in serotonergic function in the prefrontal cortex of adult HFD offspring. Taken together, these experiments define sexually dimorphic innate immune mechanisms in the placenta and developing brain that may underlie the long-term metabolic and behavioral consequences of maternal environmental exposures.
Item Open Access Essays in Environmental Economics and Policy(2020) Alshammasi, HussainThis dissertation is comprised of three research papers that entail implications for public policy. The first two papers are related to environmental policy, and specifically air pollution. The marginal willingness to pay to reduce air pollution is often estimated from the expenditures consumers undertake to avoid exposure to changes in air quality. Consumer awareness of air quality changes is commonly assumed even though limited attention causes decision-making in many settings to vary with the salience of features entering the utility function. The first paper (``Defensive Expenditures, Salience, and Limited Attention'') studies how defensive expenditures vary with the salience of air quality information while controlling for air quality, itself. It uses a 10-year panel data of defensive expenditures, comprised of masks and air-filter purchases from California. Salience is measured in three different ways. First, internet search intensity data from Google is used as a proxy for salience. Second, appearances of tweets about air pollution to Twitter users are used to measure salience. Finally, exogenous media shocks because of California fires are used as a proxy for pollution salience. Individuals are shown to exhibit inattention to air quality, causing estimates to understate willingness to pay for air quality improvements by 20\%.
The second paper (``Air Pollution and Averting Behavior Disparities: Evidence from NYC Transportation'') addresses the inequality in the burdens of air pollution. Exposure to air pollution is a function of averting behaviors that are likely to vary by income due to heterogeneous ability to pay and marginal utility of income. Consequently, poor and minorities may be relatively more exposed to pollution than other demographic groups even conditional on ambient concentrations. Using data on New York City taxi ridership and use of city bicycles, the paper identifies heterogeneous changes in transportation mode decisions across income groups in response to air pollution, exposure to which varies by mode. It shows that (1) high air pollution causes bike ridership to decrease and commute-related taxi trips to increase. (2) The increase in taxi trips is more pronounced in high income neighborhoods than in low income areas. These results suggest that transportation modes that involve higher exposure to air pollution are less desirable when air quality is low and that the utilization of alternative transportation modes to avert air pollution exposure is unequal across income groups.
The third paper (``Do Mask Mandates Work to Contain the Spread of COVID-19?'', with Qingran Li) is related to the recent COVID-19 pandemic disruptions, and studies the effects of mask mandates. With struggling economies and high unemployment rates, policy makers are seeking means to reopen the economy safely. In the absence of vaccines, discussions about mask mandates among non-pharmaceutical interventions emerged, and research is needed for informed, evidence based policy. The paper uses COVID-19 cases data, mobility data, and mask mandates data at the county level for all counties in the United States. It provides evidence that masks reduce cases, and cases conditional on the mobility of residents. The results show that while mobility marginally increases COVID cases, this marginal increase is reduced by 82\% when there is a public mask mandate. The paper also uses the synthetic control method for comparison, and finds causal evidence that mask mandates reduce COVID-19 cases. These findings have direct implications for disease control, and suggest that a mask mandate policy can reduce infection risks, when combined with economic reopening policies.
Item Open Access Filter sampling of particulate matter in exposure-relevant settings(2019) Vreeland, HeidiIt is well known that particulate matter (PM) has strong associations with various negative health endpoints. However, the precise mechanisms linking PM to these negative impacts are complex and not fully understood. The U.S. Environmental Protection Agency currently regulates PM on a mass concentration basis (μg of PM per m3 of air), which does not account for the differential toxicity of different particle species. More research is needed to improve understanding on how toxicity changes with different PM sources, and to answer: which environments have PM compositions that are particularly dangerous? The primary objective of this work is to characterize understudied aspects of particulate matter generated in environments that are relevant to human exposure (i.e., environments where people spend a large portion of their time). The exposure-relevant sites examined in this work investigate PM2.5 (particulate matter with diameters <2.5 microns) collected from inside cars during daily commutes in Atlanta, from urban India where roadside and residential trash burning is ubiquitously practiced, and from residential sites in rural and urban Guatemala. As mentioned, though the associations between negative health impacts and PM concentrations are striking, the toxicity pathways are not well understood. One proposed pathway of acute toxicity is related to an inhaled particle’s ability to generate reactive oxygen species (ROS) and exert oxidative stress on the lungs. In recent years, various assays have been developed to assess the ROS-generating capacity of particulate matter. Two of the most established assays used in air pollution research are the DTT (dithiotreitol) assay and the lung macrophage assay. These assays were used to make the first-ever measurements of oxidative potential of PM2.5 collected from in-vehicle commutes (in Atlanta) and from in-situ trash burning events (in Bangalore, India). In-vehicle results from ~2-hour morning commutes (n = 50) indicate that on-road DTT activity (median [IQR] = 0.68 [0.75] nmol min-1 m-3) is ~2 times higher than DTT activity measured from 23-hour roadside samples. Results highlight how gas-phase compounds make important contributions to DTT activity and that short-term exposures are associated with distinct changes in oxidative potential. This was echoed by results from trash-burning samples (n = 24), which suggest that ~1 minute of direct exposure to emissions from trash burning was equivalent in DTT activity to breathing in an entire day of ambient air in Bangalore. Though ambient samples (n = 6) show notable DTT activity (median [IQR] = 0.76 [0.03] nmol min-1 m-3), trash burning DTT activity was extremely high, averaging >1,000 nmol min-1 m-3. However, when considering DTT and macrophage results on a per-mass basis, ambient PM2.5 appears to be ~2 – 100 times more redox active than fresh trash-burning emissions, suggesting that many compounds found in fresh trash-burning emissions are not redox active; this may also indicate how atmospheric processing and aging can result in increased PM redox activity. Results highlight the importance of assessing PM with additional toxicity pathways since ROS activity alone is not sufficient to describe the many ways in which PM may impact health. Overall, results indicate that near trash-burning sources, exposure to redox-active PM can be extremely high. A follow-up project was launched in response to observing widely varying emissions from trash burning, which results from Bangalore show were vastly different even when comparing trash piles of similar size, composition, and burning conditions. This follow-up project was educational in nature as it was a collaborative effort between students at Duke University and the India Institute of Technology. To generate emissions in a more comparable way, we controlled for pile size, composition, and environmental variables (e.g., wind speed) that may affect burning conditions, and then we iteratively burned compiled mixtures of trash in a small-scale combustor. Burn piles (n = 28) were compiled to represent trash compositions observed and collected from six sites in Ahmedabad, India, where average pile composition was observed to be ~60% plastic by volume; plastic-only piles were also burned in the combustor. Plastic bottles were observed to generate the highest concentrations of PM2.5 and black carbon emissions, while plastic films emitted very low pollutant concentrations with PM2.5 close to background levels. Using low-cost sensors and thermocouples attached to the incinerator body proved to be an affordable way to make semi-quantitative assessments of controlled burns. We also demonstrate how low-cost sensors attached to a commercial UAV (unmanned aerial vehicle) could be useful for safely collecting pollutant data over a smoky municipal dumpsite. Trash burning is clearly a source of highly variable and spatially sporadic emissions. This follow-up project is valuable as it makes small but important steps toward finding affordable ways to measure and mitigate emissions. Lastly, a final project was pursued to assess air pollution and microbial concentrations from residential sites in Guatemala, including in a community where PM2.5 levels indoors were observed to be exceedingly high due to traditional cookstove use. Though many studies have measured PM in similar settings, existing research has not investigated microbial concentrations in the air at these settings (as the majority of existing research has focused on sites in high-income countries). Airborne viruses and bacteria were enumerated from filter samples using a staining microscopy technique. Air samples (n = 40) were collected at different times of day indoors and outdoors to provide insight on whether household or ambient sources dominate bioaerosol contributions. Results suggest that bioaerosols from indoor sources dominate in the mornings, while outdoor sources contribute more to bioaerosol concentrations in the afternoon. Links were observed between PM2.5 and microbial concentrations (Spearman’s rho, rs = 0.5; p < 0.001) but this correlation becomes insignificant when looking specifically at sites where cooking occurred; non-cooking sites continue to show significant correlation. Though the majority of viruses and bacteria are not pathogenic, recent research has indicated that even nonpathogenic and inactivated microbes may influence the oxidative potential of PM. Identifying important microbial sources in these high-PM environments is also necessary to create effect controls (for example, results show lowest microbial concentrations at two sampling environments that were well-sealed and where an air filter was present). In general, this work characterizes various aspects of PM2.5 in environments that many people encounter daily. Unless commutes can be shortened and traffic emissions reduced, or trash can be managed in ways other than burning, these will continue to be important factors in daily PM2.5 exposure.
Item Open Access Gene-Environment Interactions in Cardiovascular Disease(2014) WardCaviness, Cavin KeithIn this manuscript I seek to demonstrate the importance of gene-environment interactions in cardiovascular disease. This manuscript contains five studies each of which contributes to our understanding of the joint impact of genetic variation and environmental exposures to cardiovascular disease: a candidate gene study for gene-smoking interactions associated with early-onset coronary artery disease, an epidemiology study of the association between traffic-related air pollution and cardiovascular disease, a Genome-Wide Interaction Study for gene-by-traffic related air pollution interactions associated with peripheral arterial disease, a Genome-Wide Interaction Study for gene-by-traffic related air pollution interactions on coronary atherosclerosis burden, and a method for analyzing associations between high-dimensional genomics datasets.
Smoking is a strong risk factors for coronary artery disease, and may play a causative role in the incidence of coronary artery disease. Smoking had been implicated as a reason for heterogeneity observed in associations between genetic variants on chromosome three and coronary artery disease. I used a family-based early-onset coronary artery disease cohort (GENECARD) to study gene-smoking interactions. I also used data from the three independent cohorts to perform a meta-analysis of gene-smoking interactions focusing on the KALRN gene and Rho-GTPase pathway. I found significant evidence for gene-smoking interactions associations involving variants in KALRN and other Rho-GTPase pathway genes on chromosome 3.
Though the estimated increase in incident cardiovascular disease or cardiovascular events due to air pollution exposure is modest at 3-5%, the ubiquitous nature of air pollution exposures means it has a substantial population-level impact on cardiovascular disease. Historically genome-wide interaction studies with air pollution have not yielded genome-wide significant interactions, however by implementing statistical tools novel to this field I have discovered significant interactions between genetic variants and traffic-related air pollution that are associated with cardiovascular diseases.
I studied interactions associated with peripheral arterial disease and the number of diseased coronary vessels (an indicator for coronary artery disease burden) using race-stratified cohort study designs. With peripheral arterial disease I observed that variants in both BMP8A and BMP2 showed evidence for interactions in both European-American and African-American cohorts. In BMP8A I uncovered the first genome-wide significant interaction with air pollution associated with cardiovascular disease. BMP2 gene expression is upregulated after exposure to black carbon, a major component of diesel exhaust, and coding variants within this gene showed evidence for interaction. With the number of diseased coronary vessels I observed that variants in PIGR showed significant evidence for involvement in gene-traffic related air pollution interactions. I observed that coding variation within PIGR was associated with coronary artery disease burden in a gene-by-traffic related air pollution interaction model. As PIGR is involved in the immune response it represents a strong candidate gene discovered via an unbiased genome-wide scan.
The use of high dimensional data to study chronic disease is becoming commonplace. In order to properly analyze high-dimensional data without suffering from high false-discovery rate penalties, the data is often summarized in a way that takes advantage of the correlation structure. Two common approaches for this are principal components analysis and canonical correlation analysis. However neither of these approaches are appropriate when one preferentially desires to preserve structure within the data. To address this shortcoming I developed constrained canonical correlation analysis (cCCA). With cCCA one can evaluate the correlation between two high dimensional datasets while preferentially preserving structure in one of the datasets. This has uses when studying multi-variate outcomes such as cardiovascular disease using multi-variate predictors such as air pollution. Additionally cCCA can be used to create endophenotype factors that specifically explain the variation within a high-dimensional set of predictors (such as gene expression or metabolomics data) with respect to potential endophenotypes for cardiovascular disease, such as cholesterol measures.
Item Open Access Plastic Dominates Developmental Toxicity Responses to Burn pit related Smoke in Zebrafish: Role for Polycyclic Aromatic Hydrocarbons(2023-04-27) Smoot, JacobCombustion of mixed materials during open air burning of refuse or housefires produces emissions that worsen air quality and may cause adverse health effects. Although previous studies have linked air pollution exposure from other sources to congenital defects, the potential developmental toxicity of mixed material combustion emissions remains uncertain. The purpose of this study was to compare the developmental toxicity of smoke derived from the combustion of 5 different material types (plywood, cardboard, plastic, mixture, and mixture plus diesel) in zebrafish larvae, a model often used to assess the behavioral and developmental effects of chemicals. Zebrafish have been shown to have similar physiological and biochemical responses to smoke exposure as other vertebrates and absorb chemicals (such as PAHs) through their epidermis from their surroundings. Larvae were exposed to organic extracts of each smoke at various concentrations and assessed for morphological and behavioral toxicity at 5 days post fertilization. All extracts caused concentration-dependent effects, including mortality, impaired swim bladder inflation, pericardial edema, spinal curvature tail kinks, or craniofacial deformities, although plastic and the mixture caused the most pronounced effects. Plastic also altered locomotor responsiveness to light changes to the greatest extent. Interestingly, some morphological and behavioral responses correlated strongly with total and specific polycyclic aromatic hydrocarbons concentrations in the smoke extracts. Overall, the findings suggest that material type and combustion chemistry impact the severity of developmental toxicity of mixed material smoke in zebrafish.Item Open Access Pollution, Health, and the Economy: Understanding and Modeling Their Interactions(2020) Ru, MuyeAir pollution, human health, and the economy are a connected system. Substantial efforts have been made in understanding and modeling these connections, so that we can predict the health and economic impacts of changes in air pollution to inform policymaking. However, simplifications and knowledge gaps are still present, and understanding of how these influence the entire system remain limited. This dissertation studies some of these simplifications and knowledge gaps, develops new tools to quantify them, and discusses their impacts to the system. These tools and impacts are used to facilitate more comprehensive evaluation of the impacts of air pollution, especially those that could have been underestimated, and to examine their sensitivity to certain assumptions. In general, air pollution has greater impacts than previously estimated, and future projections include assumptions that seem to be optimistic in the light of historical trajectories. The concluding chapter discusses implications for the sensitivities and uncertainties of the whole system, and how the system of economy-pollution-health should be integrated with the economy-climate system.
The relationships between economy and emissions of major air pollutants and greenhouse gases are basic inputs used to generate historical estimates and future emission scenarios. I show that these relationships vary over time across different widely-used global inventories, indicating the presence of large uncertainties within historical emission trajectories. More specifically, my examination of four major sectors (power, industry, residential, and transportation) and three pollutants (sulfur dioxide, carbon dioxide, and black carbon) demonstrates that long-term income-emission trajectories are both sector and pollutant specific. When assessing future projections of income-emission trajectories in reference scenarios, however, I show the persistence of faster rates of emission declines and estimates of earlier turnover incomes than estimated from historical data. This indicates some underlying uncertainties in such trajectories and that future projections of income-emission trajectories for integrated assessment should be used with appropriate caution.
In the next part of my analysis, I focus on the relationship between air pollution and health outcomes, which is based on epidemiological evidence. To date, epidemiologically-based quantitative relationships have been developed for many cardiovascular and respiratory diseases, as well as diabetes. A knowledge gap persists with respect to the exposure-response relationship between air pollution and incidence of dementia, due to relatively limited evidence. I assessed this exposure-response relationship by using a meta-analysis approach to collect data from existing epidemiological studies. I have developed an exploratory model of this relationship, and estimated that, globally, 1.1M [0.6M, 1.6M; 5-95% confidence] global incident cases and 0.34M [0.17M, 0.48M] premature deaths from dementia were attributable to ambient fine particulate matter (PM2.5) pollution in 2015. In addition, using model reconstructions of surface PM2.5 levels, I have shown that this burden of disease has grown 60~70% since 2000 as a consequence of globally increased exposures to ambient PM2.5. For the first time, our meta-analysis approach enables us to estimate that ambient PM2.5 pollution may be responsible for 15% of the premature deaths and 16% of the morbidity burdens associated with dementia across all risk factors.
The third linkage closes the loop of the air pollution, health, and the economy system, by estimating the direct economic costs associated with morbidity burdens (hospital admissions, emergency room visits, restricted activity days, etc.). Unlike mortality burdens, costs associated with morbidity burdens directly affect market activities. These costs include medical expenditures shared by households and the public health sector, productivity loss due to lost work hours, and the costs of private and public care for the ill. Identifying and estimating these costs is important for decision-making. For this analysis, I developed statistical models of seven exposure-response relationships for five acute morbidity endpoints, using data collected from meta-analysis. I quantified uncertainties associated with these exposure-response functions by randomization and simulation. I showed that these morbidity effects per unit increase in exposure generally reduce as exposures increase, unlike previous approaches that assume they are fixed over the entire range of exposures. Therefore, these functions are particularly useful to analyze impacts of air pollution in high-exposure regions or on a global scale.
I concluded that this dissertation demonstrated the importance of further understanding of uncertainties in this economy-pollution-health system. In particular, we should study interactions and propagations of uncertainty throughout this non-linear system. Moreover, research on the economy-pollution-health and the economy-climate systems should be more integrated, because the two systems overlap and the research methodology to analyze each also has many similarities. Insights from one system can inform challenges from the other system.
Item Open Access Spatial and Statistical Analysis of High Risk Chloroprene Emissions in Laplace, Louisiana(2019-04-21) Li, JiaqiObjective: High concentrations of chloroprene, which is a monomer used to produce synthetic rubber and is classified as likely to be carcinogenic to humans, have been measured in the vicinity of the Denka Performance Elastomer facility in LaPlace, LA. New emission reduction projects were implemented by the company to reduce chloroprene emissions in 2018. This project explores the relationships between chloroprene concentrations and multiple geospatial and meteorological factors through spatial and statistical analyses. Methods: Multiple geospatial factors, including distance from the facility to monitoring sites and main roads and land use types around the monitoring sites and the facility, were determined by ArcGIS Pro. A chloroprene mapping tool was created to interpolate chloroprene levels based on ambient air monitoring data. Correlation tests and linear regression models were conducted to investigate correlations between chloroprene concentrations and meteorological factors, including wind speed and wind direction. Results: There is an inverse correlation between mean chloroprene concentration and distance from the facility to the monitoring sites. The land cover types around each monitoring site differ from each other and may influence the chloroprene concentrations. Wind speed was inversely correlated with chloroprene concentrations in five out of six monitoring sites, while temperature was also inversely correlated with chloroprene concentrations in two out of six sites. Wind direction also shows an effect on chloroprene concentration. The dominant wind directions are from the south and the east in LaPlace. Chloroprene concentrations tend to be higher at the monitoring sites to the west of the facility when the wind is blowing from the east, i.e., from the facility and toward a residential area. Chloroprene concentrations were statistically significantly decreased after the emission reduction projects were implemented. Conclusions: Even though there is a substantial decrease in chloroprene concentrations in the vicinity of the facility as a result of the emission reduction projects, mean chloroprene concentrations at the six monitoring sites still far exceed concentrations estimated to produce a 1 in 10,000 cancer risk by inhalation. It is recommended that Denka Performance Elastomer improve the effectiveness of their emission reduction projects and also consider limiting chloroprene emitting operations when meteorological factors such as low wind speed and winds from the east present a higher level of chloroprene concentrations in residential areas near the facility.Item Open Access The Effects of Negative Ion Indoor Air Filtration on Selected Biomarkers in Healthy Adults: A Randomized Double-Blind Crossover Trial(2020-04-24) Sun, YanAir pollution is a significant challenge in environmental health. According to the World Health Organization (WHO), about 91% of world’s population live in areas where WHO’s air quality guidelines were not met. Ambient air pollution causes approximately 4.2 million premature deaths worldwide. While outdoor ambient air quality is associated with global mortality, indoor air pollution also possesses a significant challenge to people’s health and well-being. In countries with less desirable air quality, the use of air filtration devices is common. Despite the rise of negative ion air filtration device usage, the purification efficiency and health effects of these devices remain unclear. The goal of this project is to evaluate health impacts of indoor negative ion air filtration intervention in healthy young adults. The intervention is hypothesized to reduce indoor fine particulate matter exposure and reduce adverse health effects associated with indoor PM2.5 pollution. We conducted a randomized, double-blind, cross-over study with two specific aims: first, to evaluate the effectiveness of PM2.5 removal by negative ion air filtration device; second, to evaluate differences in health endpoints associated with PM2.5 exposure between the two interventions. Fifty-five healthy adults participated in this study. Each participant received a random sequence of true and sham filtration intervention, with two weeks of washout period in between. Before and after each intervention period, these participants provided biological samples so we could measure specific biomarkers of interest to assess health impacts of each intervention. My project only assessed urinary biomarkers. Overall, only one out of the five biomarkers selected has statistically significant result. No significant difference between true and sham intervention is observed for urinary fMDA and (biomarkers of lipid peroxidation, reflecting cell membrane damage), 8-OHdG (a biomarker of oxidative damage to DNA), and 11-OHTXB1 (a biomarker of platelet activation, reflecting thrombosis risk). The findings indicate that the negative ion filtration did not lead to significant changes in biomarkers expected to be associated with fine particle exposure reduction. More research is needed to investigate other health endpoints and long-term changes associated with the use of negative ion air filtration device.Item Open Access The Effects of Residential Greenness and Air Pollution on Oxidative Stress Levels in Urban and Peri-urban Residents of Beijing(2021) Qi, WenhaoBackground and Aims Exposure to air pollution has been associated with increased risks of cardiopulmonary diseases, cancer, and mortality. Simultaneously, greenspace has also documented to be protective of mortality. Oxidative stress may be an intermediate biomarker in these processes. There has been little investigation on the effects of residential greenness and air pollution on oxidative stress. There are two aims of this study: 1) To explore the association of personal and ambient air pollution exposure with urinary oxidative stress levels; 2) To investigate the association of quantified-contemporary greenness with urinary oxidative stress levels and the interaction between greenness and air pollution exposure in affecting oxidative stress levels, respectively.
Methods In an existing panel study named AIRLESS (Effects of AIR pollution on cardiopuLmonary disEaSe in urban and peri-urban reSidents in Beijing), 123 residents living in an urban district (Haidian district) and 128 residents in a peri-urban district (Pinggu) of Beijing participated in the study. All participants were non-smokers, ≥ 49 years of age, and included 110 men and 140 women. Personal and ambient exposures to air pollutants were assessed for each participant during winter 2016 and summer 2017, respectively. Each participant was instructed to carry a validated personal air monitor (PAM) to measure particulate matters (PM1, PM2.5, and PM10), nitrogen dioxide, carbon monoxide, and ozone concentrations at a high spatiotemporal resolution seven consecutive days in each sampling season. We calculated contemporaneous green space coverage level by the average daily satellite-derived Normalized Difference Vegetation Index (NDVI) in the zone with 500m*500m grids by Google Earth Engine (GEE) using the Moderate-resolution Imaging Spectroradiometer (MODIS) dataset from NASA (National Aeronautics and Space Administration). We used the coordinates of the ambient air pollution monitoring stations and monitoring dates to match the NDVI data. Multiple oxidative stress biomarkers were measured, including urinary free malondialdehyde (MDA), urinary total MDA, and urinary 8-hydroxydeoxyguanosine (8-OHdG). All biomarkers were normalized by urinary creatinine in statistical analyses. Due to the right skewness, all biomarkers data were ln-transformed in the aim-specific analyses. (1) The association of personal and ambient air pollution exposure with the percent change of urinary oxidative stress biomarkers was estimated using linear mixed-effects models and the distributed lag linear model was used to investigate daily air pollutants’ hysteresis effects on the percent change of urinary oxidative stress biomarkers. (2) The association between tertiary NDVI with urinary oxidative stress biomarkers was estimated using linear mixed-effects regression and subgroup analysis was used to test the robustness of the association between quantified NDVI with the mean percent change of oxidative stress biomarkers using the linear mixed-effects model in different groups. (3) To explore the interaction between greenness and air pollution in affecting oxidative stress by each of these exposure variables, stratified analyses were conducted to examine whether air pollution exposure modifies the effect of greenness and whether greenness modifies the effect of air pollution. Tertiles of NDVI, personal PM2.5 exposure, and personal ozone exposure were used in these analyses.
Results We found positive associations of CO and ozone personal exposure, respectively, with percent change of the three oxidative stress biomarkers. The association tended to be significant only in the ozone model with the percent change of 8-OHdG [8.69% 95%CI: (2.98,14.39), p-value=0.004]. However, in the models of ambient air pollution, some non-significantly negative associations were observed. Consistent positive associations of ambient lag 1- and 2- day CO exposure with the percent change in levels of each of the three oxidative stress biomarkers were weakly persisted. However, the positive associations remained significant between CO exposure and total MDA (p value=0.033) only in lag2-day. In the analyses of greenness as the exposure variable, we observed that individuals who lived in greener areas tended to have lower levels of oxidative stress. Participants in the highest NDVI tertile (0.36-0.83) had significantly lower free and total MDA levels, mean and (95%CI) by -20.21% (-37.84%, -1.30%) and -17.77% (-32.89%, -2.16%), respectively, compared to the lowest NDVI tertile (0.11-0.25) (p-value =0.028). In the urban area, we found significant negative associations of NDVI with free MDA (p-=0.003), total MDA (p =0.005), and 8-OHdG (p=0.022), but not in the peri-urban area. In the modification (interaction) analyses, we observed negative estimates of quantified NDVI associated with each of the three biomarkers in the low personal ozone exposure group (Ozone≤18.7 ppb). We also observed negative estimates of quantified NDVI associated with free and total MDA in the low PM2.5 exposure group (PM2.5≤32μg/m3). In addition, we observed significant effects of personal ozone exposure on 8-OHdG [17.77 95%CI: (8.04, 27.56), p value=0.010]; personal CO exposure on free MDA [12.48 95%CI: (3.15, 21.85), p value=0.012 and total MDA [9.06 95%CI: (1.28, 16.64), p value=0.021] only in participants falling in the lowest NDVI tertile; and the positive associations were no longer significant in participants with higher tertiary NDVI.
Conclusion The protective effects of greenness on oxidative stress, especially in urban residents, elucidates the importance of green space in the urban built environment. Additionally, the adverse effects of air pollution exposure on oxidative stress indicates the noteworthiness of personal protection against air pollution exposure in urban residents.
Item Open Access The Health Impact of Indoor Air Filtration in Healthy Adults and Asthmatic Children(2018) Cui, XiaoxingThe World Health Organization (WHO) estimated that 92% of the world’s population lived in areas with outdoor air pollution levels exceeding the WHO guidelines in 2014. Although the ultimate solution is to control emission sources, exposure reduction strategies at the individual level can address more immediate needs. As people typically spend approximately 80% of their time indoors, improvement of indoor air quality, such as using air filtration technologies, may lead to reduced total exposure. However, evidence is limited to support the effectiveness of air filtration in bringing beneficial health effects to the users. The goal of this dissertation research is to evaluate the health impact of indoor air filtration in healthy adults and asthmatic children using two randomized, double-blind, crossover trials (Aim 1 and Aim 2). Utilizing data from these two trials and other data, this dissertation also addresses two methodological questions. Aim 3 examines the relationship between free and total malondialdehyde, a biomarker of oxidative stress commonly used in air pollution research, in various types of human specimens. Aim 4 evaluates the relationship between the subjective evaluation of asthma control by childhood asthma control test (C-ACT) and objective indicators of lung pathophysiology using longitudinal measurements.
In Aim 1 of this dissertation, a double-blinded, randomized, crossover study was conducted to examine the cardiorespiratory health effect of a sporadic, overnight use of indoor air filtration. Seventy healthy non-smoking adults were recruited from the medical and nursing students who were living in the same dormitory building in a suburb of Shanghai, China. The participants were aged 19 to 26 years old and included 41 (59%) females. Each participant received a true and a sham indoor air filtration session in a randomized sequence. Participants and research staff that performed health assessments were blinded to this sequence until the end of the study. Each filtration session was approximately 13 hours long. True and sham filtration sessions were separated by a two-week “washout” interval. During the study period, outdoor PM2.5 concentrations ranged from 18.6 to 106.9 µg/m3, which overlapped with levels measured in Western Europe and North America. Compared to sham filtration, true filtration on average decreased indoor PM2.5 concentration by 72.4% to 10.0 µg/m3 and particle number concentration by 59.2% to 2316/cm3. For lung function measured immediately after the end of filtration, true filtration significantly lowered airway impedance at 5 Hz (Z5) by 7.1% [95% CI: 2.4%, 11.9%], airway resistance at 5 Hz (R5) by 7.4% [95% CI: 2.4%, 12.5%], and small airway resistance (R5-R20) by 20.3% [95% CI: 0.1%, 40.5%], reflecting improved airway mechanics especially for the small airways. However, no significant improvements for spirometric indicators of lung function (FEV1, FVC) were observed. True filtration also significantly lowered von Willebrand factor (VWF) by 26.9% [95% CI: 7.3%, 46.4%] 24 hours after the end of filtration, indicating reduced risk for thrombosis. Stratified analysis in male and female participants showed that true filtration significantly decreased pulse pressure by 3.3% [95% CI: 0.8%, 7.4%] in females, and significantly reduced VWF by 42.4% [95% CI: 17.4%, 67.4%] and interleukin-6 by 22.6% [95% CI: 0.4%, 44.9%] in males. Effect modification analyses indicated that filtration effects in male and female participants were not significantly different. These findings suggest that a single overnight residential air filtration, capable of reducing indoor particle concentrations substantially, can lead to improved airway mechanics and reduced thrombosis risk.
Air pollution exposure is a well-established risk factor for asthma exacerbation. In individuals with asthma, indoor air filtration has only been evaluated for allergen removal in areas with low outdoor levels of PM2.5. As asthmatic individuals may be responsive to short-term changes in air pollution levels, it is not clear whether the exposures occurring outside the home environment can override the potential health benefits of residential indoor air filtration. In Aim 2 of this dissertation, I investigated the respiratory impact of residential indoor air filtration in asthmatic children living with moderate levels of outdoor PM2.5. This double-blind, randomized crossover trial recruited 43 participants (40% females) aged 5 to 13 with mild or moderate asthma. From February to April 2017, each participant used a true filtration device and a sham filtration device, respectively in their bedrooms for two weeks. A two-week washout period separated the two sessions. During the study, the average PM2.5 concentrations for outdoor, indoor with sham filtration, and indoor with true filtration were 56.5 µg/m3, 34.1µg/m3, and 14.8 µg/m3, respectively. Compared to sham filtration, on average, true filtration reduced indoor PM2.5 concentrations by 53.3%. Concomitantly, true filtration significantly decreased fractional exhaled oxide (FeNO) by 5.1 [95% CI: 0.5, 9.6] ppb, airway impedance at 5Hz (Z5) by 14.7% [3.7%, 25.8%], respiratory resistance at 5Hz (R5) by 22.4% [9.6%, 35.2%], and small airway resistance (R5-R20) by 40.6% [10.2,% 70.9%]. Peak expiratory flow (PEF) measurements were made twice daily throughout each two-week intervention session. PEF values during true filtration were 1.5% [0.7%, 2.4%] higher than the measurements during sham filtration. True filtration also introduced a non-significant increase on FEF25-75 by 5.80% [-4.09%, 15.68%]. Stratified analyses show that the participants with blood eosinophil count ≤ 500/mm3, compared to those with blood eosinophil count > 500/mm3, had a 24.3% greater increase of FEF25-75 by true filtration; and that the participants allergic to dust mite had smaller improvements in small airway resistance (R5 and R5-R20). These findings suggest that a two-week long intervention of indoor air filtration, capable of significantly reducing indoor PM2.5 concentrations, can lead to reduced respiratory inflammation, improved lung function (PEF) and airway mechanics in asthmatic children.
Oxidative stress is a core mechanism involved in the cardiorespiratory effects of air pollution. Malondialdehyde (MDA) is a well-established marker of oxidative stress. However, most of its use in existing studies were conducted by researchers in clinical medicine and epidemiology, who were unaware that MDA is present in both unconjugated and conjugated forms. Aim 3 of this dissertation examined the relationship between free MDA (unconjugated MDA) and total MDA (the sum of both unconjugated and conjugated MDA) in various types of human biospecimens. Using bio-banked samples from multiple studies, free MDA and total MDA were measured simultaneously in nasal fluid (N=158), saliva (N=158), exhaled breath condensate (N=40), serum (N=232), and urine samples (N=429). MDA quantification was performed using an HPLC-fluorescence method with high sensitivity and specificity. Due to the right-skewed distribution of free MDA and total MDA, natural-log transformation was performed before subsequent statistical analyses. The relationship between the natural log of free and total MDA was evaluated by R2 of simple linear regression. T-test was used for comparisons of means between two groups. One-way analysis of variance was used in combination with Tukey’s test to compare the natural log of the ratio of free MDA to total MDA across various types of biospecimens. For exhaled breath condensate, serum, urine, nasal fluid and saliva samples, the R2 between free and total MDA were 0.61, 0.22, 0.59, 0.47 and 0.06, respectively; the medians of the free MDA to total MDA ratio were 48.1%, 17.4%, 9.8%, 5.1% and 3.0%, respectively. The free MDA to total MDA ratio in EBC > serum > urine > nasal fluid > saliva (P<0.001 for pairwise comparisons). These findings indicate that, for exhaled breath condensate and urine samples, using either free or total MDA can provide information regarding the level of oxidative stress; however, that is not the case for serum, nasal fluid, and saliva, given the low correlations between free and total MDA. For these types of biospecimens, future research is needed to examine which form of MDA better reflects oxidative stress, in a mechanistic fashion. Given these findings, free MDA in urine samples was measured in the Aim 1 study.
The Childhood Asthma Control Test (C-ACT) is a validated questionnaire that provides a subjective evaluation of asthma control using collective inputs from children and their caregivers. Cross-sectional studies have identified cut-points for discerning different degrees of asthma control. However, few studies have examined whether changes in the C-ACT score are reflective of changes in airway pathophysiology in longitudinal measurements from the same individuals. In Aim 4 of this dissertation, I utilized data from four clinical visits originally conducted for Aim 2. The clinical visits were scheduled bi-weekly over a period of six weeks. Thirty-seven children aged 5 to 10 with mild or moderate asthma (43% female) took the C-ACT. The scores were 24.4 ± 2.4 (mean ± standard deviation) and ranged from 16 to 27. Linear mixed-effects models were used to examine the association between C-ACT and clinical measurements from the same participants. As a change of two points in the C-ACT score is considered as the minimal clinically important difference, I reported the change in biomarkers associated with a two-point decrease in C-ACT score. Results showed that a two-point decrease was significantly associated with a 1.7% [95% CI: 0.1%, 3.3%] decrease in FEV1, a 1.6% [0.5%, 2.8%] decrease in FVC, and a 3.8% [0.0%, 7.6%] increase in airway resistance at 5 Hz (R5). For PEF measurements conducted within two weeks before the C-ACT, a two-point decrease in C-ACT score was significantly associated with a 17.3% [95%CI: 6.8%, 27.8%] increase in the coefficient of variation, while no significant association was observed with the average PEF value (P=0.12). In contrast, within-participant measurements showed no significant associations of C-ACT with respiratory inflammation (FeNO) or any of the small airway function and mechanics parameters (FEF25-75, FEF25-75, R5-R20, X5, and Fres). When examining individual questions of the C-ACT, none of the questions answered by the caregiver were significantly associated with indicators of lung function and respiratory inflammation. In contrast, three out of the four questions answered by the child demonstrated significant or marginally significant associations with FEV1, FVC, FEF25-75, R5, and R20. This suggests that in spite of the relatively young age of the participants, their perception of disease control provides important information for asthma control assessment. Overall, the findings in Aim 4 indicate that subjective evaluation of asthma control using the C-ACT was associated with objective measurements of airway obstruction, airway restriction, respiratory resistance and the variation of airflow limitations in longitudinal measurements. However, the C-ACT is not reflective of changes in respiratory inflammation and small airway mechanics, indicating that its use should be complementary to but not a substitute for these measurements.
Item Open Access The Role of Melatonin in Pathophysiologic Responses to Air Pollution Exposure(2020) He, LinchenAbstractIt is widely accepted that the pathophysiologic pathways linking air pollution exposure and adverse health effects are via the augmentation of oxidative stress and inflammation in the respiratory tract and the circulatory system. Melatonin is a potent antioxidant and anti-inflammatory molecule and may thereby affect individuals’ biological responses to air pollution exposure. This dissertation aims to investigate the role of melatonin in pathophysiological responses to air pollution exposure. In Aim 1 of this dissertation research, a method was developed to simultaneously measure urinary concentrations of 6-sulfatoxymelatonin (aMT6s) and 8-hydroxy-2'-deoxyguanosine (8-OHdG). As a major metabolite of melatonin excreted in the urine, aMT6s has been widely used as a surrogate of circulating melatonin. Urinary 8-OHdG, a stable product of DNA oxidative damage, has been used as an oxidative stress biomarker. This new method is expected to have important applications in biomedical and environmental health studies involving the oxidative stress pathophysiological pathway. In Aim 2 of this dissertation research, the role of melatonin in oxidative stress responses to air pollution exposure was examined. Stored urine samples collected from 159 healthy adults, and their personal air pollution exposure data were used. These urine samples were analyzed for aMT6s and 8-OHdG; and statistical analyses were conducted to examine the relationships among aMT6s, 8-OHdG and another previously measured urinary oxidative stress biomarker, malondialdehyde (MDA), and pollutant exposures. The results of this analysis suggest the need for controlling for aMT6s as a confounder in using urinary 8-OHdG and MDA as biomarkers of oxidative stress related to short-term air pollution exposure. In Aim 3 of this dissertation research, the role of melatonin in inflammatory responses to air pollution exposure was examined. Blood inflammatory cytokines and urinary aMT6s were measured in 53 healthy adults three times within 2 consecutive months. Personal air pollution exposure was calculated prior to biospecimen collections. The study found that concentrations of proinflammatory cytokines were significantly and negatively associated with O3 exposures averaged over the preceding 12 hours while significantly but positively associated with O3 exposures averaged over the preceding 2 weeks. These findings suggest that exposure to O3 for different time durations may affect systemic inflammatory responses in different ways. In addition, the study found that pro-inflammatory responses to O3 exposure in the preceding 2 weeks may partly result from the depletion of endogenous melatonin by O3. In Aim 4 of this dissertation research, the role of melatonin in pathophysiologic and oxidative stress responses to air pollution exposure in asthmatic children was examined. Urine, nasal fluid, and pulmonary physiology data were obtained from 43 asthmatic children four times with a 2-week interval between the consecutive clinic visits. At each visit, pulmonary physiology indicators, comprised of airway mechanics, lung function, airway inflammation, and asthma symptom scores were measured. Stored urine samples were analyzed for aMT6s, 8-OHdG, and MDA; stored nasal fluid samples were analyzed for MDA. Personal exposures to PM2.5 and O3 prior to a health outcome measurement were calculated. Three major analyses were conducted in the Aim 4 study. First, the associations of personal air pollutant exposures with the indicators of pulmonary physiology were examined. The results show that daily changes in personal exposure to PM2.5 were associated with significantly increased small airway resistance, total airway resistance, and airway inflammation (fractional exhaled nitric oxide, FeNO). The findings suggest the importance of reducing personal exposure to PM2.5 as part of the asthma management plan to improve airflow limitation. Second, statistical analyses were conducted to examine the relationships among personal pollutant exposures, nasal fluid MDA, urinary 8-OHdG, urinary MDA, FeNO, and asthma symptom scores. The results showed that increased personal exposures to PM2.5 and O3 exposure were both associated with increased nasal MDA concentrations and worsened asthma symptom scores. Increased nasal MDA concentration was associated with decreased asthma symptom scores indicating worsening of asthma symptoms. These findings support that MDA in the nasal fluid may serve as a useful biomarker for monitoring asthma status, especially in relation to PM2.5 and O3 exposure, two known risk factors of asthma exacerbation. Third, statistical analyses were conducted to investigate the relationship of urinary aMT6s with personal air pollutant exposures, biomarkers of oxidative stress, and indicators of pulmonary physiology. The results showed that increasing urinary MDA or 8-OHdG concentration and personal exposures to PM2.5 and O3 were associated with increased urinary aMT6s concentrations in asthmatic children. We also found that increased concentration of urinary aMT6s was associated with improved pulmonary inflammation and airway resilience. The results suggest a potential biological mechanism that increased systemic oxidative stress may stimulate the excretion of melatonin as a defense mechanism to alleviate the adverse effects of air pollution exposure. In summary, the findings from this dissertation research support that endogenously generated melatonin can modulate oxidative, inflammatory, and physiological responses to air pollution exposure in a beneficial way. This dissertation research supports the need for future trials to assess the efficacy or effectiveness of using melatonin supplementation to mitigate the adverse health effects of air pollution exposure at the individual level. This is particularly important for susceptible populations living in highly polluted areas (e.g., developing countries and regions subject to frequent wildfires), people with melatonin deficiency, and those using dirty household fuels.
Item Open Access Treatment of Low Concentrations of Volatile Organic Compounds by Non-thermal Plasma(2012) Karatum, OsmanNon-thermal plasma (NTP) technology is an emerging method to degrade otherwise recalcitrant volatile organic compounds (VOCs) in air. Here, a dielectric barrier discharge (DBD) NTP was used to evaluate the degradation efficiency of several VOCs (toluene, benzene, ethylbenzene, MEK (methyl ethyl ketone), MTBE (methyl-tert-butyl ether) 3-pentanone and n-hexane) under constant experimental conditions (6.6 L/min, 95 and 100 ppm average inlet concentrations). The efficiency with which toluene, ethylbenzene, benzene, MEK, MTBE, 3-pentanone, and n-hexane were removed was 74.03 ± 0.30%, 80.94 ± 0.07%, 57.82 ± 0.06%, 50.00 ± 0.20%, 80.00 ± 1.40%, 76.00 ± 1.4%, and 90.00 ± 0.30 %, respectively, at an inlet concentration 95 ppm, gas flow rate 6.6 L/min, and a specific input energy (SIE) of 350 J/L. The effects of various operating conditions on pollutant removal were investigated. Interestingly, the highest removal efficiencies were observed for compounds that have the highest percentage of hydrogen in the molecular structure.
During treatment of toluene and ethylbenzene, a deposit was formed inside the plasma reactor. This deposit was dark brown in color and gave off an oil-like odor, suggesting the formation of higher-order hydrocarbon compounds. The deposit mass was quantified and the impact of the deposit on the DBD reactor performance was discussed. It was noted that the time required for the deposit to clog the reactor depended on the experimental conditions. The clogging time when treating toluene in dry air conditions was more than 1.5 times greater than under humidified conditions (30% RH), suggesting that attention to the treated air relative humidity is critical. The quantity and structure of the deposits depended on both input VOC molecular structure as well as the experimental conditions. Thus, this study provides recommendations for the current applications of this technology.