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Vaartnou, Manivalde. "EPR investigation of free radicals in excised and attached leaves subjected to ozone and sulphur dioxide air pollution." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29444.
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The X-band EPR spectrometry system was modified to allow for the in situ monitoring of free radical changes in attached, intact plant leaves, which were caused by stress factors such as exposure to excessive photon flux density, ozone or sulphur dioxide. This was done through use of the dewar insert of the variable temperature accessory as a guide, the construction of 'T' shaped cellulose acetate holders to which leaves could be attached with adhesive tape, and modification of the gas flow system used for controlled temperature studies.
Kinetic studies of free radical formation were possible with leaves which had minimal underlying Fe⁺⁺ and Mn⁺⁺ signals. In leaves with large underlying signals a Varian software program was used to subtract overlapping signals from each other, thereby revealing the free-radical signal changes which occurred under different light regimes and stress conditions. Preliminary investigation disclosed the formation of a new signal upon prolonged exposure to far-red light and the effect of oxygen depletion upon photosynthetic Signals I and II.
Leaves subject to high photon flux density reveal an unreported free-radical signal, which decays upon exposure to microwave radiation; and concomitant damage to Photosystems I and II. Upon elimination of this signal leaves return to the undamaged state or reveal permanent damage to either photo-system, depending upon the degree of damage.
Kentucky bluegrass and perennial ryegrass leaves subject to low levels of ozone (up to 80ppb) for periods of 8 hours show no changes in free-radical signal formation. At intermediate levels of ozone (80-250ppb) a new free-radical signal was formed within 3 hours of fumigation, Signal II was decreased and Signal I decayed. These changes were reversible if fumigation was terminated. At fumigation levels exceeding 250ppb a different new irreversible free-radical signal was formed in darkness within 1.5 hours of fumigation.
Radish, Kentucky bluegrass and perennial ryegrass leaves subject to high levels of sulphur dioxide (10-500ppm) reveal the formation of Signal I upon irradiation with broad-band white or 650nm light, thereby indicating an interruption of normal electron flow from PSII to PSI. Damage to the oxygen-evolving complex and reaction centre of PSII is also revealed through changes in Signal II and the Mn⁺⁺ signal. These changes in the normal EPR signals are dose-dependent. Leaves subject to low levels of sulphur dioxide (600-2000ppb) reveal the disappearance of Signal I after 3 hours of fumigation and the formation of a new free-radical signal with parameters similar to the sulphur trioxide free-radical signal. These latter changes are partially reversible upon termination of fumigation.
After prolonged exposure to either ozone or sulphur dioxid a free-radical signal with parameters similar to the superoxid anion free-radical signal is formed in plant leaves.Land and Food Systems, Faculty of
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Pérez, Grau Laura. "The urban health effects and impact of anthropogenic and natural air pollution." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7195.
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The differential role that airborne particulate matter (PM) size fractions, sources, and components play in producing adverse health effects is not fully understood. Specific gaps include the role of PM generated by traffic and the effects of PMs generated by natural sources. Source specific air pollution epidemiological research still lacks integration in the risk assessment process, a fundamental tool to inform policy makers and the public about the current situation or the impact of future or past air pollution policies. This thesis addresses both these gaps. To explore the effects of PM from different sources, we investigated the association between different PM size fractions and mortality in Barcelona, Spain and used PM chemical composition data to help determine the different sources and components linked to toxicity. To illustrate that local air pollution risk assessments are useful tools in evidence-based public health, we estimated the health and economic benefits that would result from different scenario of improved air quality in the Barcelona metropolitan area and in two communities of Southern California. These case studies include new methods to integrate into the risk assessment process the recent epidemiological evidence related to the effects of traffic exposure.This thesis contributes to a better understanding of the link between particulate matter size fraction, sources, and components and health effects, and to improve air pollution health impact assessment methods. Both contributions have important implications for public health and air pollution public policy.El papel diferencial en que las diferentes fracciones de partículas en suspensión en el aire (PMs), sus fuentes y componentes producen efectos adversos para la salud no está completamente entendido. Las lagunas actuales incluyen el papel de las PMs generadas por el tráfico y los efectos de las PMs generadas por fuentes naturales. La investigación epidemiológica relacionada con fuentes todavía falta ser integrada en el proceso de evaluación de impacto, una herramienta fundamental para informar a los tomadores de decisiones y el público sobre la situación actual o el impacto de futuras o pasadas políticas de contaminación atmosférica. Esta tesis trata estas áreas. Para explorar el papel de las PMs generadas por diferentes fuentes, se ha investigado la asociación entre diferentes fracciones de PMs y mortalidad en Barcelona (España) y se ha usado datos de composición química de PMs para identificar las fuentes y los componentes relacionados con la toxicidad. Para ilustrar que las evaluaciones de impacto a nivel local son herramientas útiles en salud pública, se ha estimado el beneficio en salud y económico que resultaría de diferentes escenarios de mejora de la calidad del aire en el área metropolitana de Barcelona y en dos comunidades de California del Sur. Estos estudios de casos incluyen nuevos métodos para integrar en las evaluaciones de impacto las nuevas evidencias epidemiológicas que relacionan la exposición al tráfico con los efectos en salud. Esta tesis contribuye a un mayor entendimiento del vínculo entre las fracciones de PM, sus fuentes y componentes y los efectos en salud así como a la mejora de los métodos de las evaluaciones de impacto. Estas contribuciones tienen importantes implicaciones para la salud pública y las políticas públicas de contaminación atmosférica.
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Hazin, Clovis Abrahao. "Release of radon from showers and its influence on the balance of radon indoors." Diss., Georgia Institute of Technology, 1990. http://hdl.handle.net/1853/16638.
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Ou, Chunquan, and 欧春泉. "Individual risk factors that modify the short-term effects of air pollution on mortality: a population-basedstudy of Chinese population." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40687399.
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Truluck, Timothy Francis. "Hospital admission patterns of childhood respiratory illness in Cape Town and their association with air pollution and meteorological factors." Master's thesis, University of Cape Town, 1993. http://hdl.handle.net/11427/17402.
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Bibliography: pages 103-119.The aims of this study were (a) to examine the profile of hospital admissions for selected respiratory illnesses for two major hospitals in Cape Town, and (b) to analyse the association of such admissions with air pollution indicators and meteorological variables. The first part of the study investigated the admission patterns of coloured and African children under twelve years of age who were diagnosed as suffering from asthma or acute respiratory infections at two major teaching hospitals in Cape Town. Computerized hospital admission records covering the years 1988-1990 from the overnight holding wards of the Red Cross War Memorial Children's Hospital and Tygerberg Hospital were used to determine patterns with respect to diagnosis, gender, race, age and date of admission. During the three year study period, respiratory admissions at both hospitals accounted for 15 078 (47.3%) out of a total of 31 887 admissions. Acute respiratory infections accounted for 63.6% and asthma 37.4 % of these respiratory admissions. Two factors of interest were noted: (1) Considerably more males than females were admitted with both asthma and acute respiratory infections. (2) Asthma admissions to Red Cross Hospital among African children were proportionally much less than those of coloured children when compared to the proportions of admissions for acute respiratory infections. After removal of the seasonal effect, a multiple linear regression model was fitted to the data to determine the individual associations between admissions and ambient environmental variables. Significant associations were found between: (1) acute respiratory infections and oxides of nitrogen, soiling index, and temperature; (2) asthma and oxides of nitrogen (3) total admissions and soiling index, average temperature and minimum temperature (negative). The study concluded that despite generally low levels of air pollution in Cape Town, childhood respiratory admissions to Red Cross War Memorial Children's Hospital and Tygerberg Hospital were statistically significantly associated with some ambient air pollutants as well as temperature. However, given the nature of both the exposure and admissions databases, these results should be treated with caution. More representative site selections for air pollution monitors, as well as searching and controlling for possible confounding factors (i.e. indoor air pollution, parental smoking, overcrowding), would allow a better understanding of the current air pollution problem and the possible effects on the respiratory health of children in metropolitan Cape Town.
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Fitch, Megan. "The Effects of Air Pollution on the Intestinal Microbiota: A Novel Approach to Assess How Gut Microbe Interactions with the Environment Affect Human Health." Thesis, University of North Texas, 2017. https://digital.library.unt.edu/ark:/67531/metadc984173/.
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This thesis investigates how air pollution, both natural and anthropogenic, affects changes in the proximal small intestine and ileum microbiota profile, as well as intestinal barrier integrity, histological changes, and inflammation. APO-E KO mice on a high fat diet were randomly selected to be exposed by whole body inhalation to either wood smoke (WS) or mixed vehicular exhaust (MVE), with filtered air (FA) acting as the control. Intestinal integrity and histology were assessed by observing expression of well- known structural components tight junction proteins (TJPs), matrix metallopeptidase-9 (MMP-9), and gel-forming mucin (MUC2), as well known inflammatory related factors: TNF-α, IL-1β, and toll-like receptor (TLR)-4. Bacterial profiling was done using DNA analysis of microbiota within the ileum, utilizing 16S metagenomics sequencing (Illumina miSeq) technique. Overall results of this experiment suggest that air pollution, both anthropogenic and natural, cause a breach in the intestinal barrier with an increase in inflammatory factors and a decrease in beneficial bacteria. This evidence suggests the possibility of air pollution being a potential causative agent of intestinal disease as well as a possible contributing mechanism for induction of systemic inflammation.
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Matyushenko, I. Yu. "Grave effects of air pollution." Thesis, Сумський державний університет, 2012. http://essuir.sumdu.edu.ua/handle/123456789/28649.
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Liu, Liqun. "Health effects of air pollution and meteorology." Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-146119.
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Prinn, Ronald G., John M. Reilly, Marcus C. Sarofim, Chien Wang, and Benjamin Seth Felzer. "Effects of Air Pollution Control on Climate." MIT Joint Program on the Science and Policy of Global Change, 2005. http://hdl.handle.net/1721.1/7510.
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Urban air pollution and climate are closely connected due to shared generating processes (e.g., combustion) for emissions of the driving gases and aerosols. They are also connected because the atmospheric lifecycles of common air pollutants such as CO, NOx and VOCs, and of the climatically important methane gas (CH4) and sulfate aerosols, both involve the fast photochemistry of the hydroxyl free radical (OH). Thus policies designed to address air pollution may impact climate and vice versa. We present calculations using a model coupling economics, atmospheric chemistry, climate and ecosystems to illustrate some effects of air pollution policy alone on global warming. We consider caps on emissions of NOx, CO, volatile organic carbon, and SOx both individually and combined in two ways. These caps can lower ozone causing less warming, lower sulfate aerosols yielding more warming, lower OH and thus increase CH4 giving more warming, and finally, allow more carbon uptake by ecosystems leading to less warming. Overall, these effects significantly offset each other suggesting that air pollution policy has a relatively small net effect on the global mean surface temperature and sea level rise. However, our study does not account for the effects of air pollution policies on overall demand for fossil fuels and on the choice of fuels (coal, oil, gas), nor have we considered the effects of caps on black carbon or organic carbon aerosols on climate. These effects, if included, could lead to more substantial impacts of capping pollutant emissions on global temperature and sea level than concluded here. Caps on aerosols in general could also yield impacts on other important aspects of climate beyond those addressed here, such as the regional patterns of cloudiness and precipitation.Abstract in HTML and technical report in PDF available on the Massachusetts Institute of Technology Joint Program on the Science and Policy of Global Change website (http://mit.edu/globalchange/www/).
This research was supported by the U.S Department of Energy, U.S. National Science Foundation, and the Industry Sponsors of the MIT Joint Program on the Science and Policy of Global Change: Alstom Power (France), American Electric Power (USA), BP p.l.c. (UK/USA), ChevronTexaco Corporation (USA), DaimlerChrysler AG (Germany), Duke Energy (USA), J-Power (Electric Power Development Co., Ltd.) (Japan), Electric Power Research Institute (USA), Electricité de France, ExxonMobil Corporation (USA), Ford Motor Company (USA), General Motors (USA), Mirant (USA), Murphy Oil Corporation (USA), Oglethorpe Power Corporation (USA), RWE/Rheinbraun (Germany), Shell International Petroleum (Netherlands/UK), Statoil (Norway), Tennessee Valley Authority (USA), Tokyo Electric Power Company (Japan), TotalFinaElf (France), Vetlesen Foundation (USA).
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Tabor, Caroline Mary. "Effects of air pollution on vascular thrombosis." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5577.
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Increases in air pollution, especially the particulate component, are associated with increased cardiovascular mortality, possibly through increases in thrombogenic mechanisms. The research presented in this thesis addresses the hypothesis that diesel exhaust particulates (DEP) increase thrombogenicity by impairing the release of tissue plasminogen activator (t-PA) from vascular endothelial cells, thus inhibiting the endogenous fibrinolytic mechanisms that promote thrombus breakdown. The initial aims of this work were to develop an in vivo model of thrombosis, to determine whether exposure to DEP did alter clotting. Initial attempts to develop the Folts’ model (which stimulates thrombus formation via arterial stenosis and mechanical injury), first in male C57/Bl6 mice and later in male Wistar rats, were unsuccessful. An alternative approach, using ferric chloride (FeCl3) to induce chemical injury to the rat carotid artery was found to produce reliable and reproducible thrombotic occlusion: this model was used for all subsequent experiments. The effects of DEP on thrombus formation were assessed in vivo by applying the FeCl3 model. DEP were administered via intratracheal instillation or tail vein injection 2, 6 or 24 hours prior to induction of thrombosis. The effects of DEP were compared with vehicle and suitable controls: carbon black (a clean carbon nanoparticle); quartz (a large non-carbon particle that causes well-characterised pulmonary inflammation). The time to thrombotic occlusion was significantly reduced 6h after intra-pulmonary instillation of DEP (0.5ml of a 1mg/ml suspension). In contrast, instillation of carbon black or quartz had no significant effect on thrombosis, despite causing greater pulmonary (increased neutrophils and levels of interleukin-6, tumour necrosis factor-α and C-reactive protein in bronchoalveolar lavage fluid) and systemic (C-reactive protein in plasma) inflammation than DEP. Direct administration of DEP (0.5mg/kg) to the blood stream resulted in an acute (2 hours after injection) increase in time to thrombotic occlusion in the absence of pulmonary inflammation. A similar (but less pronounced) effect was observed following administration of carbon black (0.5mg/kg). These data suggest that the DEP-mediated increase in thrombosis is independent of pulmonary and systemic inflammation. The mechanisms involved were addressed by measuring platelet-monocyte interactions (flow cytometry) and markers of the endogenous fibrinolytic system (ELISA). Exposure (either instillation of injection) to DEP significantly increased platelet-monocyte aggregation. Carbon black and quartz produced no such effect (but did increase platelet-platelet aggregation). t-PA antigen and activity were reduced, whilst PAI-1 and fibrinogen were increased, following either instillation or injection of DEP. The final aim was to develop a suitable dispersant for use in cell culture to determine whether DEP alter the expression (real-time polymerase chain reaction; rtPCR) and generation (enzyme-linked immunosorbent assay; ELISA) of t-PA and plasminogen activator inhibitor (PAI-1). Cell culture medium containing bovine serum albumin (0.5mg/ml; BSA) provided the best combination for DEP dispersal and maintenance of small particle size (<200nM), without detrimental effects on human umbilical endothelial cells (HUVECs). Exposure (6 and 24 hours) of HUVECs to DEP resulted in reduced basal and thrombin stimulated t-PA and PAI-1 expression. This was mirrored by reduced detection of t-PA and PAI-1 in culture medium. In conclusion, these investigations confirm that exposure to DEP is capable of increasing the rate of thrombus formation and that this is, in part, mediated by an alteration in the endogenous fibrinolytic system. These changes did not appear to be secondary to pulmonary or systemic inflammation. Whilst cell culture experiments suggested DEP could directly alter endogenous fibrinolytic activity in endothelial cells, there was no evidence from these experiments of DEP translocation into the systemic circulation. Thus, this work suggests that DEP is capable of increasing thrombus formation in vivo via several mechanisms. Similar changes may account for the increased thrombus formation in humans exposed to diesel exhaust in air pollution.
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Yang, Trent, John M. Reilly, and Sergey Paltsev. "Air Pollution Health Effects: Toward an Integrated Assessment." MIT Joint Program on the Science and Policy of Global Change, 2004. http://hdl.handle.net/1721.1/5426.
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Scientists and policy makers have become increasingly aware of the need to jointly study climate change and air pollution because of the interactions among policy measures and in the atmospheric chemistry that creates the constituents of smog and affects the lifetimes of important greenhouse gases such as methane. Tropospheric ozone and aerosols, recognized constituents of air pollution, have important effects on the radiative balance of the atmosphere. Existing methods for estimating the economic implications of environmental damage do not provide an immediate approach to assess the economic and policy interactions. Towards that end, we develop a methodology for integrating the health effects from exposure to air pollution into the MIT Emissions Prediction and Policy Analysis (EPPA) model, a computable general equilibrium economic model of the economy that has been widely used to study climate change policy. The approach incorporates market and non-market effects of air pollution on human health, and is readily applicable to other environmental damages including those from climate change. The estimate of economic damages depends, of course, on the validity of the underlying epidemiological relationships and direct estimates of the consequences of health effects such as lost work and non-work time and increased medical expenses. We apply the model to the US for the historical period 1970 to 2000, and reevaluate estimates of the benefits of US air pollution regulations originally made by the US Environmental Protection Agency. We also estimate the economic burden of uncontrolled levels of air pollution over that period. Our estimated benefits of regulation are somewhat lower than the original EPA estimates, and we trace that result to our development of a stock model of pollutant exposure that predicts that the benefits from reduced chronic air pollution exposure will only be gradually realized. As modeled, only population cohorts born under lower air pollution levels fully realize the benefits. While other assumptions about the nature of health effects of chronic exposure are possible, some version of a stock model of this type is needed to accurately estimate the timing of benefits of reduced pollution.Abstract in HTML and technical report in PDF available on the Massachusetts Institute of Technology Joint Program on the Science and Policy of Global Change website (http://mit.edu/globalchange/www/).
Funding for the work was from the Joint Program on the Science and Policy of Global Change, through a consortium of industrial sponsors, and through grants from the US DOE, EPA, NOAA, NSF, and NASA.
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Hur, Jae-Seoun. "Effects of air pollution on Azolla-Anabaena symbiosis." Thesis, Lancaster University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359764.
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Gaarder, Marie Moland. "The distributional effects of illness and air pollution." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271115.
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Hussey, Shane J. K. "The effects of air pollution on respiratory bacteria." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/39149.
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Particulate Matter (PM), a major component of air pollution, is associated with a variety of cardiorespiratory diseases including acute lower respiratory tract infections. It is well established that PM has detrimental effects on the host, causing tissue damage, oxidative stress, and modulating the immune system. However there has been extremely limited research into the effects of PM on bacteria, the organisms responsible for the respiratory infections associated with PM exposure. This project investigated whether Black Carbon (BC), a major component of PM produced as a by-product of fossil fuel combustion, directly affects respiratory tract bacteria. Two model opportunistic pathogens of the respiratory tract were chosen for this investigation, Streptococcus pneumoniae and Staphylococcus aureus. BC was found to alter biofilm formation, structure, matrix composition, and functioning, of both S. pneumoniae and S. aureus, as well as inhibiting planktonic growth. Interestingly, these effects were strain-dependent. Furthermore, BC promoted dissemination of S. pneumoniae from the nasopharynx to the lower respiratory tract in an in vivo murine colonisation model. BC was not observed to alter the respiratory tract microbiota in this project, however a variety of limitations which may have prevented a definitive conclusion being reached are presented. This study provides the first evidence to show that bacteria are directly affected by PM, and thereby suggests that the adverse health effects of PM may not only be due to effects on host tissues, but that modulation of bacterial behaviour may also have a role. The findings of this study therefore show the potential importance of this overlooked field.
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Penney, Kathy Coreen. "The effects of ozone air pollution on plant competition." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/26025.
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Low levels of ozone air pollution have been shown to cause reductions in plant growth. It has been proposed that these reductions could translate into effects on a plant's competitive ability, and hence, on the inter-relationships of plants in a community.
Experiments were carried out to determine if there was an effect of low levels of ozone on intra- and inter-specific competition of barnyardgrass (BYG), redroot pigweed (RPW) and green foxtail (GFT). Three ozone treatments (a filtered air control, and 75 ppb/7 hr and 150 ppb/3.5 hr daily) were applied to monocultures and binary mixtures in replacement and additive series. The two ozone treatments represent the same ambient dose. The effects of each on the plants studied were compared and contrasted.
The order of competitive ability of the three species was found to be BYG > RPW > GFT. There were significant differences in the interaction of the species between the three ozone treatments. BYG experienced significant intra-specific competition only in the two ozone-added treatments; GFT was significantly affected by its own density only in the control. In contrast, RPW experienced significant intra-specific competition effects in all treatments.
BYG benefitted significantly from the presence of GFT in the control. A similar positive effect of GFT density on BYG yield is seen in the 150 ppb/3.5 hr treatment. It is suggested that this localized positive allelopathic effect may be due to the upward transport of a volatile compound released by GFT, or disseminated through the soil. All inter-specific competitive relations of GFT and RPW were significant in all ozone treatments.
RPW appeared to experience the most ozone effects of the three species studied. RPW and GFT in replacement series mixtures showed over-yielding in the control treatment, equal replacement in the 75 ppb/7 hr treatment and under-yielding in the 150 ppb/3.5 hr treatment. This interaction of ozone and competition treatments between RPW and GFT was significant for root dry weight per pot. BYG yield was significantly enhanced in the 75 ppb/7 hr ozone treatment over the control and 150 ppb/3.5 hr treatments. This may reflect an acclimation of BYG plants to the low (0.01-0.04 ppm) ambient background levels of ozone. The concept of an appropriate control treatment is discussed.
Although the 75 ppb/7 hr and 150 ppb/3.5 hr treatments represent the same ambient dose, the species used in this study reacted quite differently to the two treatments. Overall, the more acute 150 ppb/3.5 hr dose had a more detrimental effect on the yield variables measured for RPW and GFT, and the 75 ppb/7 hr treatment had a significant enhancing effect on BYG yield over that of the control and the 150 ppb/3.5 hr dose.
An examination of the size frequency distributions of the three species confirms that BYG is competitively dominant, whereas the GFT size distributions do not appear to be sensitive to competitive suppression. RPW displays a very skewed size frequency distribution under all treatments. It is suggested that RPW has inherent genetic variability for a wide size distribution in the populations studied. There were no ozone effects on the size frequency distributions of any species studied.Land and Food Systems, Faculty of
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Hajat, Shakoor. "Effects of air pollution on daily general practitioner consultations." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252350.
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Beghelli, Silvia. "Health effects of noise and air pollution : empirical investigations." Thesis, King's College London (University of London), 2018. https://kclpure.kcl.ac.uk/portal/en/theses/health-effects-of-noise-and-air-pollution(edfd9ba5-4378-49b3-8cd1-3d8b190c5faa).html.
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The assessment of the relationship between pollution emissions and health has direct economic implications. Health status is an important factor influencing worker productivity, and hence economic growth, as well as impacting on individual well- being. We implement various strategies to disentangle the relationship between short-term noise and air pollution exposure and health. In two studies we look at airports, which are sources of both environmental stressors. In the first study we use an administrative dataset on all hospitalisations in England, the Hospital Episode Statistics (HES). We compare hospital visits between people living within certain noise levels near airports to people living further away. In the second study we focus on prescription drugs in regions around London Heathrow airport. This study exploits a trial performed over five months at Heathrow airport that redirected approaching aircraft to reduce early morning noise in designated areas. A third study implements an instrumental variable approach, where the endogenous variable of daily levels of air pollution is instrumented with daily indicators of wind direction. In this case, the health outcomes investigated are again HES visits. Informed by the medical literature, this thesis focuses on three different health cat- egories: nervous, circulatory and respiratory. The results of the first study show statically significant increases in visits for nervous and respiratory outcomes for people living near airports. Furthermore, we observe a substitution of admissions from elective to emergency hospitalisations. The study that exploits the Heathrow airport trial shows that prescribed medication usage is significantly correlated with air traffic around that airport. Compared to the control regions, we observe a significant decrease in prescribed drugs for respiratory and nervous system conditions in the areas affected by a reduction in air traffic. The third study on daily variation of air pollution, finds a statistically significant increase in nervous emergency hospital visits. Across the three different approaches, nervous conditions are the mostly affected. These conditions include sleep disturbance, attention deficits and other stress-related diseases.
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Lee, Mark. "Air pollution and climate change effects on grassland ecosystems." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9697.
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Grassland ecosystems extend across a substantial area of the world’s surface, providing many valuable ecosystem services including carbon sequestration, biodiversity preservation and food provision. Global and local environmental changes are anticipated in the future, including shifts in climatic conditions and changes to the composition of the atmosphere. This thesis adds to our understanding of how grassland communities respond to air pollution and climate change using two key methodologies. Firstly, a suite of environmental variables were measured in calcareous grassland ecosystems along transects adjacent to roads. This allowed quantification of plant compositional changes and identification of the likely drivers of plant compositional changes nearer roadsides. Evidence of road-derived changes to air quality, soil biogeochemistry and hydrology at roadsides are presented. The key messages being that road proximity was associated with increased abundances of nitrophilic species and also of species not typical of calcareous habitats. Secondly, a mesotrophic grassland ecosystem was exposed to a factorial combination of end-of-century rainfall regimes (+ 15 % winter rainfall and – 30 % summer rainfall) based on IPCC 4th Assessment projections and nitrogen enrichment. Plant productivity and species composition were resistant to nitrogen enrichment throughout the three year study. Above-ground plant biomass declined in rainfall manipulated plots by the third year, with evidence of increasing forb abundance and declining grass abundance. These data can assist projections of grassland responses to environmental change in the future and inform management decisions aimed at preventing decline in natural grasslands and declines in the ecosystem services that grasslands currently provide.
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Kurmi, Om Prakash. "Health effects of indoor air pollution in both rural and urban Nepal." Thesis, University of Aberdeen, 2010. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=103117.
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The research reported in this thesis describes: the prevalence of respiratory symptoms, COPD and cardiovascular problems in rural and urban adults taking account of all major confounding factors; and estimates of exposures, both indoor and outdoor, and assessment of the relationships between measured exposure and health outcomes. A cross-sectional study was conducted in an adult population (16+ years) in Nepal to compare the respiratory and cardiovascular risk of indoor air pollution in a rural population exposed to biomass smoke compared to an urban population using liquefied petroleum gas using an investigator-delivered questionnaire, lung function and blood pressure measurements. Direct measures of indoor particular exposure (PM2.5 and CO) and outdoor PM2.5 were made with other relevant factors obtained by questionnaire. Direct measures of 24-hour indoor PM2.5 were carried out in 245 rural and equal numbers of urban homes. Health outcomes were assessed in 846 rural and 802 urban dwellers. The main risk factors studied were socio-economic status, smoking, fuel types, stove types, ventilation, BMI, income, ETS and cooking. The result suggests that cooking with biomass is associated with reduced lung function and thus a higher prevalence of COPD in the rural dwellers compared to the non-exposed urban dwellers. No clear relationship between biomass smoke exposure and cardiovascular endpoints was found although reported cooking with biomass fuel was associated with higher blood pressure and chest pain. Methodological issues including more invasive assessment of cardiovascular disease will in future studies be important in interpretation of this relationship.
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Jacquemin, Leonard Bénédicte. "Traffic-related air pollution: exposure assesment and respiratory health effects." Doctoral thesis, Universitat Pompeu Fabra, 2007. http://hdl.handle.net/10803/7175.
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La contaminació atmosfèrica és un problema de salut pública, causa més de 380 000 morts a la Unió Europea. La present tesis té per objectius avaluar l'exposició i efectes sobre el tracte respiratori de la contaminació provinent del tràfic. Les concentracions exteriors y personals de sulfurs i de carbó són bons indicadors de exposició personal en una ciutat mediterrània; per a PM2.5 hi ha altres fonts a considerar. La molèstia deguda a la contaminació no és un bon indicador d'exposició, però reflecteix la percepció del subjecte. La contaminació que prové del tràfic augmenta els símptomes d'asma y probablement també causa asma en adults. El PM2.5 provinent de la combustió augmenta la permeabilitat de la barrera epitelial pulmonar. El tràfic és una font important de contaminació. Es requereixen eines adequades per a mesurar la seva exposició. La contaminació del tràfic es un factor de risc important per a la salut respiratòria.La contaminación atmosférica es un problema de salud pública, causa 380 000 muertes anuales en la Unión Europea. Esta tesis tiene como objetivo evaluar la exposición a la contaminación debida al tráfico y sus efectos en la salud respiratoria. Los niveles diarios de carbón y sulfuro medidos centralmente son buenos indicadores de exposición personal en una ciudad mediterránea, para PM2.5 fuentes de emisión alternas se tienen que considerar. La molestia debida a la contaminación no es un marcador de exposición, pero es importante porque refleja las percepciones individuales. La contaminación proveniente del tráfico aumento los síntomas del asma, y probablemente también causa asma en adultos. El PM2.5 proveniente de la combustión aumenta la permeabilidad de la barrera epitelial pulmonar. El tráfico es una fuente importante de la contaminación. Herramientas adecuadas para medir su exposición son requeridas. La contaminación del tráfico es un factor de riesgo importante para la salud respiratoria.
Air pollution is a major public health concern causing annually 380 000 deaths in the European Union. This thesis aims to study traffic-related air pollution exposure assessment and its association with respiratory effects. Daily levels of carbon and sulphur of outdoor central measurements are good surrogates for personal exposure in a Mediterranean setting; for PM2.5 other sources have to be taken into account. Annoyance due to air pollution is not a valid maker of air pollution exposure but is valuable in its own right as it integrates individual perceptions. Traffic-related air pollution increases asthma symptoms in adults and an association with new asthma onset is suggested. Furthermore, PM2.5 from combustion might lead to an increase in the lung's epithelial barrier permeability. Traffic-related air pollution is a major source of pollution. Adequate tools to assess its exposure are still needed. Traffic-related air pollution is an important risk factor for respiratory morbidity.
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Huang, Kai Katie, and 黄恺. "The effects of walkability on air pollution and public health." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46937213.
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Pearson, Mark. "Physiological responses of some broadleaved trees to ozone and water stress." Thesis, Lancaster University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385645.
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Rivera, Marcela 1982. "Atherosclerosis and air pollution: understanding traffic-related exposure and its effects." Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/81931.
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This thesis contributes to the characterization of the spatial distribution of NO2, heavy metals and UFP in Girona, to the methodology in air pollution exposure assessment studying different markers of traffic-related air pollution, measurement instruments and protocols, as well as to the development of the LUR technique identifying potential bias in the resulting coefficients of the health model and practical solutions to avoid them. Finally, this thesis added to the evidence that long-term exposure to traffic-related air pollution is associated with atherosclerosis and identified potential susceptibility factors for the Mediterranean population.Esta tesis contribuye a la caracterización de la distribución espacial del NO2, los metales pesados y las UFP en Girona, a la metodología de la evaluación de la exposición a contaminación atmosférica habiendo estudiado diferentes marcadores de contaminación por tráfico, instrumentos de medida y protocolos, así como al desarrollo de la técnica de modelos LUR para los que se identificaron sesgos potenciales sobre la estimación del efecto sobre la salud de dicha exposición y aporta soluciones prácticas para evitarlos. Finalmente, esta tesis añade a la evidencia de que la exposición a largo plazo a la contaminación procedente del tráfico se asocia a la aterosclerosis e identifica factores de susceptibilidad potenciales para la población mediterránea.
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Salt, David Thomas. "Effects of gaseous air pollution on root-feeding aphids of spruce." Thesis, Lancaster University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333442.
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Honour, Sarah Louise. "The effects of urban air pollution on native herbaceous plant species." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411646.
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McGowan, James Andrew. "Effects of particulate air pollution on cardiorespiratory admissions in Christchurch, NZ." Thesis, University of Canterbury. Mathematics and Statistics, 2000. http://hdl.handle.net/10092/1265.
Full textAbstract:
Abstract Objective: In Christchurch there is concern that winter air pollution, dominated by particulate matter (PM₁₀) from domestic heating, causes a local increase in cases of cardiorespiratory disease. Our aim was to investigate whether the particulate levels did influence emergency hospital admissions, and if so to what extent. Method: Air pollution and meteorological data was obtained from a Canterbury Regional Council monitoring station. Two local hospitals provided data on emergency admissions for both adults and children with cardiac and respiratory disorders. All data was obtained for the period from June 1988 to December 1998. Missing PM₁₀ data was interpolated from other known pollution values when necessary. The PM₁₀ data was compared to the admissions data using a time series analysis approach, with weather variables controlled for using a generalised additive model. Results: There was a significant association between PM₁₀ levels and cardiorespiratory admissions. For children and adults combined there was a 3.4% increase in respiratory admissions for every interquartile (14.8 µg/m³) increase in PM₁₀. In adults there was a 1.3 % increase in cardiac admissions for each interquartile increase in PM₁₀. There was no relationship between PM₁₀ levels and appendicitis, the condition that we selected to be our control. Conclusion: In Christchurch there is a significant relationship between particulate levels and the admissions for cardiac and respiratory illnesses. The size of the effect is comparable to other international studies, and the greatest impact is seen on the respiratory system.
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Loxham, Matthew. "The potential health effects of transition metals in particulate air pollution." Thesis, University of Southampton, 2013. https://eprints.soton.ac.uk/387176/.
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Pullen, Jon. "The effects of acidic air pollutants on concrete." Thesis, Open University, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357226.
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Bansal, Gaurav. "Modeling the Effects of Local Air Pollution Control Measures on Air Quality in the Shenandoah Valley." Thesis, Virginia Tech, 2008. http://hdl.handle.net/10919/34297.
Full textAbstract:
Air quality in the Shenandoah Valley has deteriorated in recent years. The valley exceeds the National Ambient Air Quality Standards for ozone (O3) a few days each year, and with stricter fine particulate matter (PM2.5) standards coming into effect, the valley risks exceeding those as well. Visibility is poor in the valley region, and the haze obscures the spectacular vistas from the Shenandoah National Park. To solve the growing problem local governments in the valley joined forces to find economically and politically feasible ways to reduce air pollution. In this study we aim to provide the scientific basis for air quality management strategies through modeling the sensitivity of various pollutants to changes in emissions. We distinguish between locally generated versus regionally transported air pollution as well as assess the impacts of proposed local air pollution control measures on ambient air quality in the valley. The first part of this thesis assesses air pollutant emissions in the Shenandoah Valley. Emissions were assigned to one of 14 source categories and allocated by county or city. Biogenic sources were responsible for 56% of the volatile organic compounds (VOCs) emitted in the valley. VOCs are important because they, together with nitrogen oxides (NOx) react to form O3 in the presence of sunlight. On-road and off-road mobile sources were the largest anthropogenic sources of VOCs as well as 63% of the NOx. PM2.5 emissions were not dominated by any single source, but fuel combustion, dust, and agriculture were important contributors. The second part of this thesis focuses on modeling ambient air pollution concentrations in the Shenandoah Valley based on the emissions generated in the first portion. We developed a set of three alternative emissions scenarios for comparison to the base case. We first zeroed anthropogenic emissions in the valley, allowing us to determine how much pollution was produced by local sources versus transported into the valley from upwind areas. We then developed a scenario that contained nine different pollution reduction strategies being considered by local governments. Finally we modeled a similar scenario in which we predicted the impact of ten proposed greenhouse gas reduction strategies on concentrations of O3 and PM2.5. We found that PM2.5 concentrations fell when emissions in the valley were reduced, but O3 did not. PM2.5 concentrations fell by 26-57% for the Zero Case and by 10-27% for the other two cases, depending on the time of year and location. Conversely for O3 there was either no change in most seasons or a small increase in concentrations in the fall. These results suggest that PM2.5 in the valley can be controlled with local measures but O3 is a more geographically wide problem.Master of Science
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Shaltanis, Jennifer Lynn Hehl. "Source apportionment of Spokane fine fraction air pollution using the Spokane health effects database and positive matrix factorization." Online access for everyone, 2006. http://www.dissertations.wsu.edu/Dissertations/Fall2006/j_shaltanis_112606.pdf.
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Yau, Tik-shan Yoki, and 游迪珊. "A geographic comparison of air quality station data to assess possiblecross-boundary effects." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31255693.
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Hannam, Kimberly. "The effects of air pollution on perinatal outcomes in North West England." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/the-effects-of-air-pollution-on-perinatal-outcomes-in-north-west-england(34e537c5-66aa-4928-a6cf-aad26a9b0dd6).html.
Full textAbstract:
Over the past decade there has been a substantial increase in evidence suggesting an increased risk of adverse pregnancy outcomes from ambient air pollution exposure. However, there is yet to be enough convincing evidence to confirm a causal link between specific air pollutants and adverse pregnancy outcomes. The objective of this project was to address the paucity of evidence from the UK on the risk from air pollution in pregnancy. The research aim was to investigate the effects of ambient air pollution on adverse pregnancy outcomes using retrospective birth outcome data from the ‘North West Perinatal Survey Unit’ (NWPSU) during the period 2004 to 2008.In addition, primarily to determine the most appropriate exposure estimation method, a prospective comparison study (n=85) was performed to compare personal measurements of nitrogen oxides (NOx) and specifically nitrogen dioxide (NO₂) with commonly used exposure estimation techniques. This study informed two further studies which quantified the effects from air pollution in pregnancy using a large retrospective cohort from the NWPSU. The first, investigated the effects of maternal residential proximity to major roads on low birthweight (LBW), small for gestational age (SGA) and preterm birth (PTB). The second, investigated the effects of NOx, NO₂, carbon monoxide (CO) and particulate matter (PM₂.₅ and PM₁₀) based on estimates from a novel spatio-temporal air pollution model and stationary monitor sites on SGA, PTB and mean birth weight change. Linear and logistic regression models were used to quantify the risk of adverse pregnancy outcomes from living in close proximity to a major road and to specific ambient pollutants. Odds ratio (OR) associations and mean birth weight change were calculated for each of the pollutants with exposure averaged over the entire pregnancy and for specific pregnancy periods to establish critical windows of exposure. Models were adjusted for maternal age, ethnicity, parity, socio-economic status, birth season, body mass index and smoking. No statistically significant associations were found between living <200m from a major road and adverse pregnancy outcomes. Based on the spatio-temporal modelled air pollution estimates, an increased risk of SGA was found in later pregnancy with NO₂ (OR=1.14, 95%CI= 1.00-1.30), CO (OR=1.21, 1.02-1.42), PM₂.₅ (OR=1.10, 1.00-1.21) and PM₁₀ (OR=1.12, 1.00-1.25). This study provides additional evidence that women exposed to high air pollution concentrations in pregnancy are at an increased risk of an SGA birth, but not for PTB. However, there was no evidence of an effect on SGA for exposures below the current legal air quality limits.
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Hampel, Regina. "Environmental effects and gene-environment interactions: air pollution and temperature effects on cardiovascular risk factors." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-138583.
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Barlow, Peter George. "The effects of air pollution particles on clearance mechanisms within the lung." Thesis, Edinburgh Napier University, 2004. http://researchrepository.napier.ac.uk/Output/1052591.
Full textAbstract:
The effects of inhaled air pollution particles on lung clearance mechanisms is an important factor in understanding how the mammalian lung deals with such pollutants and, as such, how exposure to these pollutants can be regulated. The nanoparticle(diameter S lOOnm) and transition metal components of PMIO (particulate matter with a diameter less than lO~m) have been implicated as playing major roles in the impairment of alveolar macrophage function and the subsequent retention of particles in the respiratory system. The aim of this study was to investigate the effects of components of PMIO on macrophage functions both directly, by examining macrophage phagocytosis and migration, and indirectly, by studying peripheral factors affecting macrophagefunction such as recruitment by type II cells and complement based mechanisms. We hypothesised that the alveolar epithelial type II cell line would release leukocyte chemoattractants in response to particle exposure and that this could be measured by use of a macrophage migration assay. A sub-toxic dose (125 ~g/ml)of surrogate air pollutionparticles (fine and nanoparticle carbon black and titanium dioxide) was established by measuring LOH release from a murine alveolar macrophage cell line (1774.2) and an alveolar epithelial type II cell line (L-2) in response to particle exposure. Optimisation ofa chemotaxis assay and measurement of macrophage migration towards conditioned medium obtained from the particle-exposed type II cells was conducted and it was determined that carbon black nanoparticles induced type II cells to secrete a chemoattractant that resulted in significant increases in macrophage migration compared to the negative control. This was in contrast to other particle types tested in this study which did not induce any increases in macrophage migration. It was also hypothesised that complement proteins could be involved in macrophage recruitment to sites of particle deposition and, as such, the migration of macrophages towards particle exposed blood serum was examined in vitro. Foetal bovine serum (FBS) was exposed to fine and nanoparticle caroon black and titanium dioxide (l-Smg/ml) for 2 hours. It was found, in accord with the previous study involving type II cells, that carbon black nanoparticles could activate the generation of chemotactic factors in serum that could subsequently induce significant increases (p < 0.001) in macrophage migration when serum was diluted to 10% using serum-free RPMI 1640 culture medium. This effect could be ameliorated by co-incubating the particle-treated serum in the presence of the antioxidant Trolox suggesting that oxidative stress played a role in the generation of the chemoattractant molecules. However, incubation of the serum with a pure oxidant at a range of doses did not result in the generation of chemotactic molecules suggesting that another factor could be involved in the chemoattractant generation. Further investigation to determine the exact molecular mechanism behind the chemoattractant generation is warranted. In contrast to the previous studies, we have also found evidence that components of PM₁₀ can cause decreased efficacy of macrophage clearance mechanisms in vivo and in vitro. It was hypothesised that PM₁₀ instillation would result in a decrease in macrophage phagocytic potential and an increase in chemotactic potential ex vivo. Rats were instilled with 125 and 250μg of PM₁₀ collected from North Kensington, London or sterile saline (negative control). Post-instillation (18 hours), significantly elevated concentrations of TNFa were detected in the BAL fluid together with a significant increase in the number of BAL neutrophils. Phagocytosis and chemotaxis assays conducted with BAL macrophages ex vivo showed that macrophage migration towards a positive chemoattractant, Zymosan Activated Serum (ZAS), was significantly lower than the macrophages obtained from the negative control rats. Macrophage phagocytosis of latex beads ex vivo was also found to be significantly decreased when PM₁₀ was visible inside the cell. An in vitro study where a macrophage cell line (J774.Al) was exposed to a low dose of nanoparticle carbon black (31.25μg) together with varying concentrations (100μM - 100nM) of zinc chloride (ZnCl₂) was also conducted. Exposure of macrophages to nanoparticle carbon black and zinc chloride alone induced a decrease in macrophage phagocytosis. It was found that when macrophages were co-exposed to nanoparticle carbon black and ZnCl₂, there was an additive decrease in macrophage phagocytic potential. The results contained within this manuscript demonstrate that the components of PM₁₀ can induce adverse effects on specific aspects of macrophage clearance mechanisms, but that nanoparticles can also stimulate the production of chemoattractants to aid in the recruitment of phagocytes and subsequent particle clearance. Although a contrary relationship appears to exist between these findings, the recruitment of leukocytes in response to particulate exposure is a mechanism that supports particle clearance. However, the retardation of phagocytic and chemotactic mechanisms in particle exposed macrophages may help to explain the increased toxicity, inflammation and retention time observed with nanoparticle inhalation.
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Ren, Cizao. "Evaluation of interactive effects between temperature and air pollution on health outcomes." Thesis, Queensland University of Technology, 2007. https://eprints.qut.edu.au/16384/1/Cizao_Ren_Thesis.pdf.
Full textAbstract:
A large number of studies have shown that both temperature and air pollution (eg, particulate
matter and ozone) are associated with health outcomes. So far, it has received limited
attention whether air pollution and temperature interact to affect health outcomes. A few
studies have examined interactive effects between temperature and air pollution, but produced
conflicting results. This thesis aimed to examine whether air pollution (including ozone and
particulate matter) and temperature interacted to affect health outcomes in Brisbane, Australia
and 95 large US communities.
In order to examine the consistency across different cities and different countries, we used
two datasets to examine interactive effects of temperature and air pollution. One dataset was
collected in Brisbane City, Australia, during 1996-2000. The dataset included air pollution
(PM10, ozone and nitrogen dioxide), weather conditions (minimum temperature, maximum
temperature, relative humidity and rainfall) and different health outcomes. Another dataset
was collected from the 95 large US communities, which included air pollution (ozone was
used in the thesis), weather conditions (maximum temperature and dew point temperature)
and mortality (all non-external cause mortality and cardiorespiratory mortality).
Firstly, we used three parallel time-series models to examine whether maximum temperature
modified PM10 effects on cardiovascular hospital admissions (CHA), respiratory hospital
admissions (RHA), cardiovascular emergency visits (CEV), respiratory emergency visits
(REV), cardiovascular mortality (CM) and non-external cause mortality (NECM), at lags of
0-2 days in Brisbane. We used a Poisson generalized additive model (GAM) to fit a bivariate
model to explore joint response surfaces of both maximum temperature and particulate matter
less than 10 μm in diameter (PM10) on individual health outcomes at each lag. Results show
that temperature and PM10 interacted to affect different health outcomes at various lags. Then,
we separately fitted non-stratification and stratification GAM models to quantify the
interactive effects. In the non-stratification model, we examined the interactive effects by
including a pointwise product for both temperature and the pollutant. In the stratification
model, we categorized temperature into two levels using different cut-offs and then included
an interactive term for both pollutant and temperature. Results show that maximum
temperature significantly and positively modified the associations of PM10 with RHA, CEV,
REV, CM and NECM at various lags, but not for CHA.
Then, we used the above Poisson regression models to examine whether PM10 modified the
associations of minimum temperature with CHA, RHA, CEV, REV, CM and NECM at lags
of 0-2 days. In this part, we categorized PM10 into two levels using the mean as cut-off to fit
the stratification model. The results show that PM10 significantly modified the effects of
temperature on CHA, RHA, CM and NECM at various lags. The enhanced adverse
temperature effects were found at higher levels of PM10, but there was no clear evidence for
synergistic effects on CEV and REV at various lags. Three parallel models produced similar
results, which strengthened the validity of these findings.
Thirdly, we examined whether there were the interactive effects between maximum
temperature and ozone on NECM in individual communities between April and October,
1987-2000, using the data of 60 eastern US communities from the National Morbidity,
Mortality, and Air Pollution Study (NMMAPS). We divided these communities into two
regions (northeast and southeast) according to the NMMAPS study. We first used the
bivariate model to examine the joint effects between temperature and ozone on NECM in
each community, and then fit a stratification model in each community by categorizing
temperature into three levels. After that, we used Bayesian meta-analysis to estimate overall
effects across regions and temperature levels from the stratification model. The bivariate
model shows that temperature obviously modified ozone effects in most of the northeast
communities, but the trend was not obviously in the southeast region. Bayesian meta-analysis
shows that in the northeast region, a 10-ppb increment in ozone was associated with 2.2%
(95% posterior interval [PI]: 1.2%, 3.1 %), 3.1% (95% PI: 2.2%, 3.8 %) and 6.2 % (95% PI:
4.8%, 7.6 %) increase in mortality for low, moderate and high temperature levels, respectively,
while in the southeast region, a 10-ppb increment in ozone was associated with 1.1% (95% PI:
-1.1%, 3.2 %), 1.5% (95% PI: 0.2%, 2.8%) and 1.3% (95% PI: -0.3%, 3.0 %) increase in
mortality.
In addition, we examined whether temperature modified ozone effects on cardiovascular
mortality in 95 large US communities between May and October, 1987-2000 using the same
models as the above. We divided the communities into 7 regions according to the NMMAPS
study (Northeast, Industrial Midwest, Upper Midwest, Northwest, Southeast, Southwest and
Southern California). The bivariate model shows that temperature modified ozone effects in
most of the communities in the northern regions (Northeast, Industrial Midwest, Upper
Midwest, Northwest), but such modification was not obvious in the southern regions
(Southeast, Southwest and Southern California). Bayesian meta-analysis shows that
temperature significantly modified ozone effects in the Northeast, Industrial Midwest and
Northwest regions, but not significant in Upper Midwest, Southeast, Southwest and Southern
California. Nationally, temperature marginally positively modified ozone effects on
cardiovascular mortality. A 10-ppb increment in ozone was associated with 0.4% (95%
posterior interval [PI]: -0.2, 0.9 %), 0.3% (95% PI: -0.3%, 1.0%) and 1.6% (95% PI: 4.8%,
7.6%) increase in mortality for low, moderate and high temperature levels, respectively. The
difference of overall effects between high and low temperature levels was 1.3% (95% PI: -
0.4%, 2.9%) in the 95 communities.
Finally, we examined whether ozone modified the association between maximum temperature
and cardiovascular mortality in 60 large eastern US communities during the warmer days,
1987-2000. The communities were divided into the northeast and southeast regions. We
restricted the analyses to the warmer days when temperature was equal to or higher than the
median in each community throughout the study period. We fitted a bivariate model to
explore the joint effects between temperature and ozone on cardiovascular mortality in
individual communities and results show that in general, ozone positively modified the
association between temperature and mortality in the northeast region, but such modification
was not obvious in the southeast region. Because temperature effects on mortality might
partly intermediate by ozone, we divided the dataset into four equal subsets using quartiles as
cut-offs. Then, we fitted a parametric model to examine the associations between temperature
and mortality across different levels of ozone using the subsets. Results show that the higher
the ozone concentrations, the stronger the temperature-mortality associations in the northeast
region. However, such a trend was not obvious in the southeast region.
Overall, this study found strong evidence that temperature and air pollution interacted to
affect health outcomes. PM10 and temperature interacted to affect different health outcomes at
various lags in Brisbane, Australia. Temperature and ozone also interacted to affect NECM
and CM in US communities and such modification varied considerably across different
regions. The symmetric modification between temperature and air pollution was observed in
the study. This implies that it is considerably important to evaluate the interactive effect while
estimating temperature or air pollution effects and further investigate reasons behind the
regional variability.
36
Ren, Cizao. "Evaluation of interactive effects between temperature and air pollution on health outcomes." Queensland University of Technology, 2007. http://eprints.qut.edu.au/16384/.
Full textAbstract:
A large number of studies have shown that both temperature and air pollution (eg, particulate matter and ozone) are associated with health outcomes. So far, it has received limited attention whether air pollution and temperature interact to affect health outcomes. A few studies have examined interactive effects between temperature and air pollution, but produced conflicting results. This thesis aimed to examine whether air pollution (including ozone and particulate matter) and temperature interacted to affect health outcomes in Brisbane, Australia and 95 large US communities. In order to examine the consistency across different cities and different countries, we used two datasets to examine interactive effects of temperature and air pollution. One dataset was collected in Brisbane City, Australia, during 1996-2000. The dataset included air pollution (PM10, ozone and nitrogen dioxide), weather conditions (minimum temperature, maximum temperature, relative humidity and rainfall) and different health outcomes. Another dataset was collected from the 95 large US communities, which included air pollution (ozone was used in the thesis), weather conditions (maximum temperature and dew point temperature) and mortality (all non-external cause mortality and cardiorespiratory mortality). Firstly, we used three parallel time-series models to examine whether maximum temperature modified PM10 effects on cardiovascular hospital admissions (CHA), respiratory hospital admissions (RHA), cardiovascular emergency visits (CEV), respiratory emergency visits (REV), cardiovascular mortality (CM) and non-external cause mortality (NECM), at lags of 0-2 days in Brisbane. We used a Poisson generalized additive model (GAM) to fit a bivariate model to explore joint response surfaces of both maximum temperature and particulate matter less than 10 μm in diameter (PM10) on individual health outcomes at each lag. Results show that temperature and PM10 interacted to affect different health outcomes at various lags. Then, we separately fitted non-stratification and stratification GAM models to quantify the interactive effects. In the non-stratification model, we examined the interactive effects by including a pointwise product for both temperature and the pollutant. In the stratification model, we categorized temperature into two levels using different cut-offs and then included an interactive term for both pollutant and temperature. Results show that maximum temperature significantly and positively modified the associations of PM10 with RHA, CEV, REV, CM and NECM at various lags, but not for CHA. Then, we used the above Poisson regression models to examine whether PM10 modified the associations of minimum temperature with CHA, RHA, CEV, REV, CM and NECM at lags of 0-2 days. In this part, we categorized PM10 into two levels using the mean as cut-off to fit the stratification model. The results show that PM10 significantly modified the effects of temperature on CHA, RHA, CM and NECM at various lags. The enhanced adverse temperature effects were found at higher levels of PM10, but there was no clear evidence for synergistic effects on CEV and REV at various lags. Three parallel models produced similar results, which strengthened the validity of these findings. Thirdly, we examined whether there were the interactive effects between maximum temperature and ozone on NECM in individual communities between April and October, 1987-2000, using the data of 60 eastern US communities from the National Morbidity, Mortality, and Air Pollution Study (NMMAPS). We divided these communities into two regions (northeast and southeast) according to the NMMAPS study. We first used the bivariate model to examine the joint effects between temperature and ozone on NECM in each community, and then fit a stratification model in each community by categorizing temperature into three levels. After that, we used Bayesian meta-analysis to estimate overall effects across regions and temperature levels from the stratification model. The bivariate model shows that temperature obviously modified ozone effects in most of the northeast communities, but the trend was not obviously in the southeast region. Bayesian meta-analysis shows that in the northeast region, a 10-ppb increment in ozone was associated with 2.2% (95% posterior interval [PI]: 1.2%, 3.1 %), 3.1% (95% PI: 2.2%, 3.8 %) and 6.2 % (95% PI: 4.8%, 7.6 %) increase in mortality for low, moderate and high temperature levels, respectively, while in the southeast region, a 10-ppb increment in ozone was associated with 1.1% (95% PI: -1.1%, 3.2 %), 1.5% (95% PI: 0.2%, 2.8%) and 1.3% (95% PI: -0.3%, 3.0 %) increase in mortality. In addition, we examined whether temperature modified ozone effects on cardiovascular mortality in 95 large US communities between May and October, 1987-2000 using the same models as the above. We divided the communities into 7 regions according to the NMMAPS study (Northeast, Industrial Midwest, Upper Midwest, Northwest, Southeast, Southwest and Southern California). The bivariate model shows that temperature modified ozone effects in most of the communities in the northern regions (Northeast, Industrial Midwest, Upper Midwest, Northwest), but such modification was not obvious in the southern regions (Southeast, Southwest and Southern California). Bayesian meta-analysis shows that temperature significantly modified ozone effects in the Northeast, Industrial Midwest and Northwest regions, but not significant in Upper Midwest, Southeast, Southwest and Southern California. Nationally, temperature marginally positively modified ozone effects on cardiovascular mortality. A 10-ppb increment in ozone was associated with 0.4% (95% posterior interval [PI]: -0.2, 0.9 %), 0.3% (95% PI: -0.3%, 1.0%) and 1.6% (95% PI: 4.8%, 7.6%) increase in mortality for low, moderate and high temperature levels, respectively. The difference of overall effects between high and low temperature levels was 1.3% (95% PI: - 0.4%, 2.9%) in the 95 communities. Finally, we examined whether ozone modified the association between maximum temperature and cardiovascular mortality in 60 large eastern US communities during the warmer days, 1987-2000. The communities were divided into the northeast and southeast regions. We restricted the analyses to the warmer days when temperature was equal to or higher than the median in each community throughout the study period. We fitted a bivariate model to explore the joint effects between temperature and ozone on cardiovascular mortality in individual communities and results show that in general, ozone positively modified the association between temperature and mortality in the northeast region, but such modification was not obvious in the southeast region. Because temperature effects on mortality might partly intermediate by ozone, we divided the dataset into four equal subsets using quartiles as cut-offs. Then, we fitted a parametric model to examine the associations between temperature and mortality across different levels of ozone using the subsets. Results show that the higher the ozone concentrations, the stronger the temperature-mortality associations in the northeast region. However, such a trend was not obvious in the southeast region. Overall, this study found strong evidence that temperature and air pollution interacted to affect health outcomes. PM10 and temperature interacted to affect different health outcomes at various lags in Brisbane, Australia. Temperature and ozone also interacted to affect NECM and CM in US communities and such modification varied considerably across different regions. The symmetric modification between temperature and air pollution was observed in the study. This implies that it is considerably important to evaluate the interactive effect while estimating temperature or air pollution effects and further investigate reasons behind the regional variability.
37
Wilson, Martin Robert. "Pulmonary inflammatory effects of environmental and surrogate environmental particulates and their components." Thesis, Edinburgh Napier University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270524.
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Kwan, Stephanie Hoiyee. "An analysis of the local and regional effects on air quality in Shanghai, China from August 2003 to July 2004." Thesis, Available online, Georgia Institute of Technology, 2006, 2006. http://etd.gatech.edu/theses/available/etd-11192006-184027/.
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Thesis (M. S.)--Civil and Environmental Engineering, Georgia Institute of Technology, 2007.Bergin, Michael H., Committee Chair ; Russell, Armistead G., Committee Co-Chair ; Mulholland, James A., Committee Member.
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Maggs, Richard. "The effects of ozone and nitrogen dioxide on Pakistan wheat ('Triticum aestivum' L.) and rice ('Oryza sativa' L.) cultivars." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244057.
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Murtadha, H. A. A. "Monitoring hydrocarbon pollution of coastal waters using Mytilus edulis L. : analysis and physiological effects." Thesis, Swansea University, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.638282.
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Jarraud, Nicolas Stephane. "The effects of ambient air pollution on leaf pathogens of rose and sycamore." Thesis, Imperial College London, 2000. http://hdl.handle.net/10044/1/11424.
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Brown, Michael James. "The health effects of PM₁₀ air pollution in Reefton, South Island New Zealand." Thesis, University of Canterbury. Geography, 2009. http://hdl.handle.net/10092/2607.
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The aim of this thesis is to assess the health effects of PM₁₀ air pollution in Reefton which is located on the West Coast of the South Island, New Zealand. Two principle objectives were investigated to achieve the overall aim. Firstly, whether there is a link between PM₁₀ exposure and increased respiratory and cardiovascular hospital admissions in Reefton. Secondly, the evaluation of whether PM₁₀ pollution exacerbates selected health symptoms associated with PM₁₀ exposure among study participants during a short term cohort study within Reefton. To address the first research objective, data for respiratory and cardiovascular hospital admissions were collected and comparisons were made with past-till-present PM₁₀ levels monitored in Reefton. The second research objective was carried out during a four week period in July 2008 in Reefton. A total of 78 people from the general population participated whereby they recorded their daily health status in a symptoms diary. Symptoms monitored included phlegm build-up, coughing, breathing problems, wheezing, throat discomfort, and eye irritation. Associations between PM₁₀ exposure and exacerbation of health symptoms among participants were examined through statistical analysis. Results showed no clear link between PM₁₀ exposure and increased respiratory and cardiovascular hospital admissions. The lack of association could be attributed to the limited amount of PM₁₀ data available for comparison, along with the low number of hospital admissions in Reefton due to the towns’ small population. Conversely, several associations were observed between PM₁₀ exposure and specific health symptoms among study participants. Associations were frequently small and positive while several reached statistical significance. In conclusion, PM₁₀ air pollution in Reefton could not be linked with an increase in respiratory and cardiovascular hospital admissions, however it was associated with the exacerbation of several health symptoms known to be aggravated by exposure to PM₁₀.
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Sow, Mamadou Laity. "The Effects of Air Pollution on Infant Health: An Empirical Evaluation of Georgia." unrestricted, 2006. http://etd.gsu.edu/theses/available/etd-07242006-120455/.
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Thesis (Ph. D.)--Georgia State University, 2006.Title from title screen. Mary Beth Walker, committee chair; Laura O. Taylor, M. Melinda Pitts, Sally Wallace, committee members. Electronic text (89 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed May 21, 2007. Includes bibliographical references (p. 84-88).
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Mills, Nicholas Linton. "Effects of combustion derived air pollution on vascular and fibrinolytic function in man." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4282.
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Observational studies have consistently demonstrated associations between exposure to air pollution and increased cardiovascular morbidity and mortality. These associations are strongest for fine particulate matter (PM), of which particulates from the combustion of fossil fuels are an important component. In Europe, the contribution to urban PM from diesel emissions is increasing with the popularity of diesel engines for road transport. Despite the strength of the epidemiological evidence and the emergence of promising hypotheses, the important constituents and biological mechanisms responsible for the cardiovascular effects of air pollution are largely unknown. It is possible that nanoparticulates or soluble components of PM may translocate into the bloodstream, resulting in direct effects on the vascular endothelium and thrombotic pathways. I investigated the potential for inhaled radiolabelled nanoparticulates to translocate into the circulation in man. Using two unique human exposure facilities I assessed the effects of exposure to combustion-derived particulates in dilute diesel exhaust and concentrated ambient fine and ultrafine particles on vascular endothelial, endogenous fibrinolytic and myocardial function in healthy volunteers and patients with stable coronary artery disease. In total, forty-two healthy men and thirty-two patients with stable coronary artery disease were exposed to particulates or filtered air for 1-2 hours in a series of double blind randomised crossover studies. At levels encountered in an urban environment, inhalation of dilute diesel exhaust impaired two important and complementary aspects of vascular function in man: the regulation of vascular tone and endogenous fibrinolysis. Vascular dysfunction persisted for up to 24-hours following exposure and was associated with an increase in systemic inflammatory cytokines. In patients with coronary heart disease exposure to diesel exhaust did not aggravate pre-existing vasomotor dysfunction, but did exacerbate exercise-induced myocardial ischemia and reduce acute endothelial tissue plasminogen activator release. In contrast, exposure to concentrated ambient particulates, low in combustion component, did not affect vascular function in either healthy volunteers or patients. I found little evidence that inhaled radiolabelled nanoparticles translocate into the circulation and suggest the adverse vascular effects of combustion derived air pollution are mediated primarily by their soluble components rather than by a direct interaction between nanoparticles and the vasculature. My findings have identified ischemic, vascular and thrombotic mechanisms that may explain in part the observations that exposure to combustion-derived air pollution is associated with adverse cardiovascular events including acute myocardial infarction. Ongoing research in this area will provide further insight into the adverse effects of PM, with the possibility of targeted interventions, such as the use of retrofit particle traps on diesel powered vehicles, to reduce the impact of environmental air pollution on cardiovascular disease a realistic goal.
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Gouveia, Nelson Da Cruz. "Air pollution and health effects in Sao Paulo, Brazil : a time series analysis." Thesis, London School of Hygiene and Tropical Medicine (University of London), 1998. http://researchonline.lshtm.ac.uk/1620625/.
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A time series study was conducted to investigate the association between variations in daily levels of air pollution and health effects in the city of sao Paulo, Brazil. This study was prompted by positive associations reported in other time series studies, principally in North AmeriE:a and Europe, and preliminary results from some limited analyses reported for sao Paulo. Its aims were to examine specific causes of mortality and hospital admissions, to identify more vulnerable subgroups defined in terms of age, to assess the role of socio-economic conditions in modifying the association and to detail the impact of other potential risk factors, especially meteorological. Daily measurements of air pollutants (PM10, S02, N02, 0 3 and CO) for 12 monitoring stations across the city and several meteorological variables, along with daily counts of mortality for all ages during 3 years and hospitalisations for children during 23 months were available. The time series models used Poisson regression analysis and were adjusted for effects of trend, cyclical patterns (including season), weekday, holidays, meteorological factors, and autocorrelation. Increases in PM10 and S02 were associated with a 3-4% increase in daily deaths for all causes in the elderly (results are presented for an increase from the 10th to the 90th centile of pollution measurements). Cardiovascular deaths were additionally associated with CO (4% increase). Respiratory deaths in the elderly showed higher increases (6%) associated with PM10• No significant effects for children's mortality were observed. Nevertheless, respiratory or pneumonia hospital admissions for children showed significant increases associated with 0 3 (5-8%), N02 (9%), and to a lesser extent with PM10 (9%). There was a significant trend of increasing risk of death according to age with effects only evident for older subjects. However, this age effect was more evident for all cause mortality. There was a weak suggestion of larger effects on mortality for areas economically more affluent. Some indication was found of a harvesting effect occurring in the mortality and hospital admission series in sao Paulo. Results are broadly consistent with those previously reported but somewhat smaller in magnitude. In contrast with an earlier preliminary analysis in Sao Paulo, there were no effects on mortality for children. However, new analyses for hospital admissions indicated that children are at an increased risk of non-fatal illness in relation to air pollution.
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Kaminskaya, J. O. "Risk assessment of non-carcinogenic effects of ambient air pollution in Donetsk region." Thesis, Sumy State University, 2014. http://essuir.sumdu.edu.ua/handle/123456789/45259.
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The methodology of risk is actively developing in Ukraine nowadays. The risk of contaminant exposure of species is defined as the probability of a person to have any adverse effect as a result of the impact. The concept of environmental risk can provide a quantitative description of the environmental hazards of a wide class of phenomena and processes. This quality of risk assessment is interesting for environmental monitoring. A comparative analysis of risk assessment was made in selected settlements in Donetsk region, in Donetsk, Yenakievo, GorlivkaMakiyivka, Mariupol, Thorez, Slaviansk and Artemovsk. This risk assessment is connected with the health of population and non-carcinogenic effects of air pollution.
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Гладченко, Оксана Робертівна, Оксана Робертовна Гладченко, Oksana Robertivna Hladchenko, Любов Павлівна Ярмак, Любовь Павловна Ярмак, Liubov Pavlivna Yarmak, and J. O. Kaminskaya. "Risk assessment of non-carcinogenic effects of ambient air pollution in Donetsk region." Thesis, Sumy State University, 2014. http://essuir.sumdu.edu.ua/handle/123456789/42705.
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Zabrocki, Léo. "Improving the Design of Studies on the Acute Health Effects of Air Pollution." Thesis, Paris, EHESS, 2022. http://www.theses.fr/2022EHES0041.
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L’objectif de cette thèse est d’améliorer la conception des études observationnelles sur les effets à court terme de la pollution de l’air sur la santé. Dans le premier chapitre écrit avec Anna Alari et Tarik Benmarhnia, nous préconisons d’utiliser des méthodes d’appariement pour améliorer la phase de conception des études qui exploitent les changements de direction du vent comme variables instrumentales. Nous montrons que les directions du vent sont fortement reliées à des facteurs de confusion et qu’il y a souvent peu d’observations contrefactuelles pour comparer l’effet propre à chaque direction. A l’aide d’une analyse de sensibilité, nous montrons aussi, de manière quantitative, que les effets des directions du vent sur les concentrations des polluants aériens ne sont pas biaisés par l’existence d’un facteur inobservé. Notre approche pourrait être pertinente pour des stratégies similaires fondées sur des instruments binaires comme les inversions thermiques ou les grèves de transports publics. Dans le deuxième chapitre rédigé avec Marion Leroutier et Marie-Abèle Bind, nous étudions l’impact du trafic de croisière sur la pollution de l’air à Marseille. Avec une méthode d’appariement conçue pour les séries temporelles, nous créons des expériences hypothétiques et estimons l’effet à court terme d’une augmentation du trafic maritime sur la pollution de l’air. Nous utilisons aussi l’inférence par randomisation, ce qui permet d’éviter de faire des approximations asymptotiques et des hypothèses sur la forme de la distribution de la statistique test. Nous trouvons que l’arrivée de navires de croisière augmente au niveau de la ville les concentrations de dioxyde d’azote ainsi que des particules fines. Nos résultats suggèrent que des expériences hypothétiques permettent de mieux comprendre les externalités négatives du trafic maritime. Dans le troisième chapitre, nous expliquons avec Vincent Bagilet que la combinaison d’un biais de publication en faveur des résultats statistiquement significatifs et d’un manque de puissance statistique pourrait produire des effets surestimés de la pollution de l’air sur la santé. Nous rassemblons d’abord l’ensemble des effets estimés et leur erreur type publiés en épidémiologie et en économie. En utilisant des calculs de puissance statistique, nous montrons que cette puissance est inférieure à 80% pour la moitié des articles et qu’ils pourraient donc produire des effets deux fois trop grands. Nous menons ensuite des simulations sur des vraies données pour identifier les paramètres qui affectent la puissance statistique. Nous trouvons que le nombre de chocs exogènes ainsi que le nombre de cas journaliers de décès ou d’admissions en urgence influencent fortement la puissance. Ces résultats sont importants car de nombreuses études exploitent de rares chocs exogènes et se concentrent sur des sous-groupes comme les enfants ou les personnes âgées. A la fin du chapitre, nous proposons plusieurs recommandations pour prendre en compte ce problème négligé de puissance statistique. Le quatrième et dernier chapitre est une généralisation du troisième chapitre. Pour surmonter le biais de confusion, les études quasi-expérimentales se concentrent sur des sources spécifiques de variation du traitement. Cela peut alors entraîner une perte de puissance statistique. Les effets publiés peuvent cependant surestimer la taille des vrais effets quand la puissance est faible. A l’aide de simulations sur des fausses données, nous montrons avec Vincent Bagilet que toutes les méthodes d’inférence causale font face à un compromis entre le biais de confusion et l’exagération du vrai effet à cause d’un manque de puissance. Nous expliquons à la fin du chapitre que les calculs de puissance et les analyses de sensibilité pourraient permettre de mieux prendre en compte cette tensionThe goal of this thesis is to improve the design of observational studies on the acute health effects of air pollution.In the first chapter jointly written with Anna Alari and Tarik Benmarhnia, we advocate using matching procedures to enhance the design stage of studies exploiting changes in wind directions as instrumental variables. We show that observed confounders are imbalanced across wind directions and that the common support of the data is small. An outcome regression analysis might therefore suffer from interpolation and extrapolation biases. Using a sensitivity analysis, we also provide quantitative evidence that the estimated effects of wind directions on air pollutant concentrations seem robust to the presence of hidden bias. Our approach could be relevant for similar strategies based on binary instruments such as thermal inversions or public transport strikes.In the second chapter co-authored with Marion Leroutier and Marie-Abèle Bind, we study the impact of cruise traffic on air pollution in Marseille. With a pair-matching algorithm designed for time series data, we create hypothetical randomized experiments and estimate the change in air pollution caused by a short-term increase in cruise traffic. We also rely on randomization-inference—a mode of inference which is not based on large-sample approximation and is distribution-free—to compute confidence intervals. We find that cruise vessels’ arrivals increase city-level concentrations of nitrogen dioxide and particulate matter. Our results suggest that well-designed hypothetical randomized experiments provide a principled approach to better understand the negative externalities of maritime traffic.In the third chapter, Vincent Bagilet and I explain that the combination of publication bias for statistically significant results and low statistical power could lead to inflated estimates on the short-term health effects of air pollution. We first gather a unique corpus of estimates and standard errors of all available articles found in the standard epidemiology and economics literatures. Using statistical power calculations, we show that at least half of the literature could have a power below 80% and produce estimates that are two times too large. We then run simulations based on real data to identify which parameters of research designs affect statistical power. We find that the number of exogenous shocks and cases of a health outcome are key drivers of power. These results matter since many studies exploit rare exogenous shocks and focus on subgroups such as children and the elderly. At the end of the paper, we provide several recommendations to take into account this highly important but overlooked issue.The fourth chapter is an extension and generalization of the third chapter. To avoid confounding, quasi-experimental studies focus on specific sources of treatment variation. This could lead to a reduction in statistical power. Yet, published estimates can overestimate true effects sizes when power is low. Using fake data simulations, Vincent Bagilet and I show that for all causal inference methods, there could be a trade-off between confounding and exaggerating true effect sizes due to a loss in power. We discuss how power calculations and sensitivity analysis could help take this trade-off into account
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Gerson, R. "The environmental effects of air pollution from the energy sector in South Africa." Master's thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/18220.
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The literature and data describing the environmental effects of air pollution in South Africa were examined, with a focus on the effects that are produced by the use of energy. This examination consisted of three parts: The emissions resulting from the use of the different fuels were calculated, with a complete sectorial and regional breakdown for pollution sources. A review of the data obtained from pollution monitoring programmes conducted in South Africa was completed. It was found that while monitoring is conducted in various regions and urban districts, there are areas with recognised pollution problems, such as townships, where little or no monitoring has been conducted. Often the resulfs of monitoring programmes were not published, or only available in unprocessed form. The literature describing environmental effects related to air pollution was reviewed. The number of studies pertaining to South African environments was found to be limited and tended to focus on certain areas, while neglecting others. Areas requiring further study and research were identified.
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Bigazzi, Alexander Y. "Bicyclists' Uptake of Traffic-Related Air Pollution: Effects of the Urban Transportation System." PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/2064.
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While bicyclists and other active travelers obtain health benefits from increased physical activity, they also risk uptake of traffic-related air pollution. But pollution uptake by urban bicyclists is not well understood due to a lack of direct measurements and insufficient analysis of the determinants of exposure and ventilation (breathing). This knowledge gap impedes pollution-conscious transportation planning, design, and health impact assessment.
The research presented in this dissertation generates new connections between transportation system characteristics and pollution uptake by bicyclists. The primary research questions are: 1) how do urban bicyclists' intake and uptake of air pollution vary with roadway and travel characteristics and 2) to what extent can transportation-related strategies reduce uptake.
Breath biomarkers are used to measure absorbed doses of volatile organic compounds (VOCs). This research is the first application of breath biomarkers to travelers and the first uptake measurements of any pollutant to include roadway-level covariates. Novel methods to collect and integrate bicycle, rider, traffic, and environmental data are also introduced.
Bicyclist exposure concentrations, exhaled breath concentrations, respiratory physiology, and travel characteristics were collected on a wide range of facilities in Portland, Oregon. High-resolution trajectory and pollution data were then integrated with roadway and traffic data. Models of exposure, ventilation, and uptake of VOCs were estimated from the on-road data. Important new quantifications in the models include the effects of average daily traffic (ADT) on multi-pollutant exposure, the lagged effect of on-road workload on ventilation, and the effects of exposure and ventilation on absorbed VOCs.
Estimated models are applied to situations of interest to travelers and transportation professionals. Sample applications include the inhalation dose effects of road grade, cruising speed choice, stops, and detouring to parallel low-traffic facilities. In addition, dose-minimizing routing behavior is compared with revealed routing preferences in the literature. Finally, findings from this research and the literature are distilled so that they can be incorporated into bicycle network design guidelines.