In this retrospective cohort from 2002 through 2007, 104,003 singleton live births in Hillsborough County, Florida were analyzed to elucidate the relationship between feto-infant morbidity outcomes and prenatal exposure to six criteria air pollutants. This study is based on three linked databases: The Florida Hospital Discharge database; The vital statistics records of singleton live births; Air Pollution meteorological data from the Environmental Protection Agency. There are six common air pollutants, particulate matter 2.5 (PM2.5), particulate matter 10 (PM10), ground-level ozone (O3), carbon monoxide (CO), nitrogen (NOx), and lead (Pb). These pollutants are harmful to human health and the environment. The primary outcomes of interest were low birth weight (LBW), preterm births, and small for gestational age (SGA). The intent of this project is to address these issues of air pollution effects and the methodology surrounding the study of air pollution. Using modeling, exposure values of the six criteria air pollutants were assigned to mothers over their period of pregnancy. To address these methodological concerns, this study utilizes the structural equation modeling, quartile groupings with dose response, and trimester groupings to evaluate the relationship between air pollution and birth outcomes of pregnant residents. Using structural equation modeling a significant B value of 0.35 indicated that exposure to the six criteria pollutant in pregnancy may have a significant relationship to all five birth outcomes if they are broken down into latent variables. Quartile data demonstrated that NOx seemed to have most significant associations with all outcomes with a dose response for SGA. PM10 and PM2.5 had some association to LBW and VLBW at high levels. PM10 demonstrated significance in the higher doses for SGA. However, the only dose response relationship that was demonstrated for PM10 and PM2.5 was in VLBW. PM10 also demonstrated a dose response with very preterm. If sub-divided into trimester data, PM10 demonstrated a significant relationship between exposures in all trimesters and LBW, VLBW, and SGA. PM2.5 demonstrated a significant relationship between exposures in all trimesters and VLBW. CO demonstrated a significant relationship in the 2nd trimester for LBW as well as for SGA. Mothers and their babies are a vulnerable population who are more susceptible to lower levels of pollution. These air pollutants can possibly have long-term effect on their children. Implantation of laws and regulations, warning system, or more strict EPA standards may be needed to adequately control the cost to our society.

A base case modelling investigation was conducted to explore the chemical and physical behaviour of ground-level ozone (O3) and its precursor nitrogen dioxide (NO2) in Ontario using the U.S. Environmental Protection Agency (EPA) Community Multiscale Air Quality (CMAQ) model. Two related studies were completed to evaluate the performance of CMAQ in reproducing the behaviour of these species in both rural and urban environments by comparing to surface measurements collected by the Ontario Ministry of the Environment (MOE) network of air quality stations. The first study was a winter examination and the second study was conducted for a period during the summer of the same year. The municipality of North Bay was used to represent a rural setting given its smaller population relative to the city of Ottawa which was the base of the urban site. Statistical and graphical analyses were used to validate the model output. CMAQ was found to replicate the spatial variation of O3 and NO2 over the domain in both the winter and summer, but showed some difficulty in simulating the temporal allocation of the species. Validation statistics for North Bay and Ottawa showed overall O3 mean biases (MB) of 3.35 ppb and 2.25 ppb, respectively, and overall NO2 MB of -8.75 ppb and -4.37 ppb, respectively for the winter. Summer statistics generated O3 MB of 4.66 ppb (North Bay) and 10.05 ppb (Ottawa) while both MB for NO2 were between -2.20 ppb to -2.55 ppb. Graphical analysis showed that the model was not able to reproduce the lower levels of O3, especially at night, or the higher levels of NO2 during the day at the North Bay site for either season. This was expected since the comparisons were made between point measurements and 36 km grid-averaged model results. The presence of high amounts of NO2 emissions local to the monitoring sites compared to the levels represented in the emissions inventory may also be a contributing factor. The simulations for Ottawa demonstrated better agreement between model results and measurements as CMAQ provided a more accurate reproduction of both the higher and lower mixing ratios of O3 and NO2 during the winter and summer seasons. Results indicate that CMAQ is able to simulate urban environments better than rural ones.

Air pollution is ranked by the World Health Organisation as one of the top ten contributors to the global burden of disease and injury. Epidemiological studies have shown that exposure to air pollution is associated with cardiorespiratory diseases. However, most of the previous studies have looked at this issue using air pollution data from a single monitoring site or average values from a few monitoring sites in a city. There is increasing concern that the relationships between air pollution and mortality may vary with geographical area, particularly for a big city. This thesis consisted of three interlinked studies that aimed to examine the spatial variation in the relationship between long-term exposure to air pollution and cardiorespiratory mortality in Brisbane, Australia. The first study evaluated the long-term air pollution trends in Brisbane, Australia. Air pollution data used in this study were provided by the Queensland Environmental Protection Agency (QEPA). The data comprised the daily average concentrations of particulate matter less then 10 µm in aerodynamic diameter (PM10), nitrogen dioxide (NO2), ozone (O3) and sulphur dioxide (SO2) between 1 January 1980 and 31 December 2004 in two monitoring sites (i.e. Eagle farm and Rocklea), and in other available monitoring sites between 1 January 1996 and 31 December 2004. Computerised data files of daily mortality between 1 January 1996 and 31 December 2004 in Brisbane city were provided by the Office of Economic and Statistical Research of the Queensland Treasury. Population data and the Socio-Economic Indexes for Areas (SEIFA) data in 2001 were obtained from the Australian Bureau of Statistics (ABS) for each statistical local area (SLA) of the Brisbane city. The long-term air pollution (the daily maximum 1-hour average or daily 24-hour average concentrations of NO2, O3 and PM10) trends were evaluated using a polynomial regression model in two monitoring sites (Eagle Farm and Rocklea) in Brisbane, Australia, between 1980 and 2003. The study found that there were significant up-and-down features for air pollution concentrations in both monitoring sites in Brisbane. Rocklea recorded a substantially higher number of days with concentrations above the relevant daily maximum 1-hour or 24-hour standards than that in Eagle Farm. Additionally, there was a significant spatial variation in air pollution concentrations between these areas. Therefore, the results indicated a need to examine the spatial variation in the relationship between long-term exposure to air pollution and cardiorespiratory mortality in Brisbane. The second study examined the spatial variation of SO2 concentrations and cardiorespiratory mortality in Brisbane between 1999 and 2001. Air pollutant concentrations were estimated using geographical information systems (GIS) techniques at a SLA level. Spatial distribution analysis and a multivariable logistic regression model were employed to investigate the impact of gaseous air pollution on cardiorespiratory mortality after adjusting for potential confounding effects of age, sex, calendar year and SEIFA. The results of this study indicate that for every 1 ppb increase in annual average SO2 concentration, there was an estimated increase of 4.4 % (95 % confidence interval (CI): 1.4 - 7.6 %) and 4.8 % (95 % CI: 2.0 - 7.7 %) in cardiovascular and cardiorespiratory mortality, respectively. We estimated that the excess number of cardiorespiratory deaths attributable to SO2 was 312 (3.4% of total cardiorespiratory deaths) in Brisbane during the study period. Our results suggest that long-term exposure to SO2, even at low levels, is a significant hazard to population health. The final study examined the association of long-term exposure to gaseous air pollution (including NO2, O3 and SO2) with cardiorespiratory mortality in Brisbane, Australia, 1996 - 2004. The pollutant concentrations were estimated using GIS techniques at a SLA level. Logistic regression was used to investigate the impact of NO2, O3 and SO2 on cardiorespiratory mortality after adjusting for potential confounding effects of age, sex, calendar year and SEIFA. The study found that there was an estimated 3.1% (95% CI: 0.4 - 5.8%) and 0.5% (95% CI: -0.03 - 1.3 %) increase in cardiorespiratory mortality for 1 ppb increment in annual average concentration of SO2 and O3, respectively. However there was no significant relationship between NO2 and cardiorespiratory mortality observed in the multiple gaseous pollutants model. The results also indicated that long-term exposure to gaseous air pollutants in Brisbane, even at the levels lower than most cities in the world (especially SO2), were associated with cardiorespiratory mortality. Therefore, spatial patterns of gaseous air pollutants and their impact on health outcomes need to be assessed for an evaluation of long-term effects of air pollution on population health in metropolitan areas. This study examined the relationship between air pollution and health outcomes. GIS and relevant mapping technologies were used to display the spatial patterns of air pollution and cardiorespiratory mortality at a SLA level. The results of this study show that long-term exposure to gaseous air pollution was associated with cardiorespiratory mortality in Brisbane and this association appeared to vary with geographic area. These findings may have important public health implications in the control and prevention of air pollution-related health effects, since now many countries and governments have paid more attention to control wide spread air pollution and to protect our environment and human health.

Background There are a few epidemiological studies that (1) link increased ambient air pollution (AP) with an increase in lung cancer incidence rates and (2) investigate whether residing in green spaces could be protective against cancer. However, it is completely unclear whether other forms of cancer are also affected by AP and if residential green spaces could lower cancer incidence rates in general. Therefore, the objective was to estimate whether AP and green space are associated with several cancer types. Methods The analysis was based on routine health care data from around 1.9 million people from Saxony who were free of cancer in 2008 and 2009. Incident cancer cases (2010–2014) of mouth and throat, skin (non-melanoma skin cancer - NMSC), prostate, breast, and colorectum were defined as: (1) one inpatient diagnosis, or (2) two outpatient diagnoses in two different quarters within one year and a specific treatment or death within two quarters after the diagnosis. Exposures, derived from freely available 3rd party data, included particulate matter with aerodynamic diameter of less than 10 μm (PM10) and nitrogen dioxide (N02) as well as green space (Normalized Difference Vegetation Index - NDVI). Associations between air pollutants, green space, and cancer incidence were assessed by multilevel Poisson models. Age, sex, physician contacts, short- and long-term unemployment, population density, and having an alcohol-related disorder were considered as potential confounders. Results Three thousand one hundred seven people developed mouth and throat cancer, 33,178 NMSC, 9611 prostate cancer, 9577 breast cancer, and 11,975 colorectal cancer during the follow-up period (2010–2014). An increase in PM10 of 10 μg/m3 was associated with a 53% increase in relative risk (RR) of mouth and throat cancer and a 52% increase in RR of NMSC. Prostate and breast cancer were modestly associated with PM10 with an increase in RR of 23 and 19%, respectively. The associations with N02 were in the same direction as PM10 but the effect estimates were much lower (7–24%). A 10% increase in NDVI was most protective of mouth and throat cancer (− 11% RR) and of NMSC (− 16% RR). Colorectal cancer was not affected by any of the exposures. Conclusions In addition to the studies carried out so far, this study was able to provide evidence that higher ambient AP levels increase the risk of mouth and throat cancer as well as of NMSC and that a higher residential green space level might have a protective effect for NMSC in areas with low to moderate UV intensity. Nevertheless, we cannot rule out residual confounding by socioeconomic or smoking status.

La pollution de l’air liée au trafic automobile constitue un problème de santé majeure et est reconnue comme un facteur de risque important pour les maladies cardiovasculaires. La contribution de la phase particulaire des émissions de moteur Diesel dans ces effets sanitaires a été bien établie. Cependant, les études portant sur la phase gazeuse sont peu nombreuses alors que l’évolution des systèmes de dépollution permettant un abattement des particules Diesel, ont conduit à un accroissement des polluants de la phase gazeuse tels que le Dioxyde d’azote (NO2),un polluant majeur et toxique. Par conséquent, l’objectif général de ce travail a été d’évaluer la part imputable de la phase gazeuse, et plus spécifiquement du NO2, dans les effets cardiovasculaires induits par des émissions Diesel représentatives du parc automobile actuel. Dans un premier temps, une étude comparative a été réalisée chez le rat Wistar exposé par inhalation au NO2 seul ou à des émissions Diesel, produisant du NO2, et prélevées en amont et en aval d’un filtre à particules(Fap). Afin de comprendre les mécanismes d’action mis en jeu, la fonction mitochondriale et le stress oxydant ont été évalués, parallèlement aux mesures de fonction cardiaque après une exposition unique (une seule exposition de 3h) et après une exposition répétée (3h/jour, 5jr/semaine pendant 3 semaines). Dans un deuxième temps, une étude portant plus spécifiquement sur les effets du NO2sur la fonction vasculaire et ses conséquences éventuelles dans un modèle d’hypertension artérielle a été réalisée en utilisant deux modèles expérimentaux : un modèle physiologique (rat Wistar) et un modèle d’hypertension artérielle (rat SHR). L’évaluation de la fonction vasculaire a été réalisée par une approche ex vivo à partir d’artères coronaires isolées après des expositions uniques et répétées chez le rat Wistar et uniquement après une exposition unique chez le rat SHR. Pour ce dernier, des expositions répétées ont également été réalisées pour explorer la fonction mitochondriale. Nos résultats montrent que l’exposition unique aux émissions, en amont et en aval du Fap induisent une légère altération de la fonction cardiaque, qui est cependant plus importante lors des expositions à 5 ppm de NO2 mais réversible. Après trois semaines d’expositions répétées, la dysfonction cardiaque persiste puisque le lendemain de la dernière exposition, les diamètres ventriculaires restent élevés, que ce soit après les expositions aux émissions Diesel, amont et aval, et au NO2. La dysfonction cardiaque est accompagnée d’une altération de la vasorelaxation des artères exposées au NO2. En parallèle à ces altérations, nous avons observé une dysfonction mitochondriale, plus particulièrement lors des expositions au NO2 indépendamment d’un stress oxydant myocardique ou systémique. L’exposition au NO2 aggrave la dysfonction mitochondriale préexistante au cours de l’hypertension artérielle, ce qui suggère l’aggravation de la fonction cardiovasculaire. L’ensemble de ces résultats démontre l’effet de la phase gazeuse, notamment du NO2 sur la fonction mitochondriale dans les deux modèles expérimentaux témoignant de l’importance de la prise en considération de l’action de la phase gazeuse dans les systèmes de dépollution à venir. / Air pollution from car traffic is a major health issue and is recognized as an importantrisk factor for cardiovascular disease. The contribution of the particulate phase of Diesel engine emissions to these health effects has been well established. However, studies on the gas phase are few in number, while the evolution of the depollution systems allowing a reduction of the Diesel particles, led to an increase in pollutants of the gas phases such as nitrogen dioxide (NO2) a major and toxic pollutant. consequently, the general objective of this work was to evaluate the attributable part of the gaseous phase, and more specifically NO2, in the cardiovascular effects induced by Diesel emissions representative of the current fleet. In a first step, a comparative study was conducted in the Wistar rat exposed by inhalation to NO2 alone or to Diesel emissions, producing NO2, and taken upstream and downstream of a particulate filter (PF). In order to understand the mechanisms of action involved, mitochondrial function and oxidative stress were evaluated, in parallel with cardiacfunction measurements after a single exposure (a single exposure of 3 h) and after repeated exposure (3 h / day, 5 days / week for 3 weeks). Second, a more specific study on the effects of NO2 on vascular function and its possible consequences in a hypertension model was carried out using two experimental models: a physiological model (Wistar rat) and a model of hypertension (SHR). Evaluation of the vascular function was performed by an ex vivo approach from isolated coronary arteries following single and repeated exposures in the Wistar rat and only after a single exposure in the SHR. For the latter, repeated exposures were also performed to explore mitochondrial function. Our results show that single exposure to emissions upstream and downstream of PF induces a slight alteration of cardiac function, which is more important at 5 ppm NO2 but reversible. After three weeks of repeated exposure, cardiac dysfunction persists as ventricular diameters remain high the day after the last exposure, both after exposures to upstream and downstream Diesel emissions and to NO2. Cardiac dysfunction is accompanied by an alteration in the vasorelaxation of the arteries exposed to NO2. In parallel with these alterations, weobserved mitochondrial dysfunction, particularly during NO2 exposures independently of myocardial or systemic oxidative stress. Exposure to NO2 aggravates pre-existingmitochondrial dysfunction during hypertension, suggesting worsening of cardiovascular function. All these results demonstrate the effect of the gaseous phase, in particular NO2, on the mitochondrial function in the two experimental models, indicating the importance of taking into account the action of the gas phase in the depollution systems to come up.

Poor air quality has been projected to be the world’s top cause of environmental premature mortality by 2050 surpassing poor sanitation and dirty water (IGBP / IGAC press release, 2012 ). One of the major challenges of air quality management is how to adequately quantify both the spatial and temporal variations of pollutants for the purpose of implementing necessary mitigation measures. The work described in this thesis aims to address this problem using novel electrochemical based air quality (AQ) sensors. These instruments are shown to provide cost effective, portable, reliable, indicative measurements for urban air quality assessment as well as for personal exposure studies. Three principal pollutants CO, NO and NO2 are simultaneously measured in each unit of the AQ instrument including temperature / RH measurements as well as GPS (for time and position) and GPRS for data transmission. Laboratory studies showed that the electrochemical sensor nodes can be highly sensitive, showing linear response during calibration tests at ppb level (0-160 ppb). The instrumental detection limits were found to be < 4 ppb (CO and NO) and < 1 ppb for NO2 with fast response time equivalent to t90 < 20 s. Several field studies were carried out involving deployment of both the mobile and static electrochemical sensor nodes. Results from some short-term studies in four different cities including Cambridge (UK), London (UK), Valencia (Spain) and Lagos (Nigeria) are presented. The measurements in these cities represent snapshot of the pollution levels, the stark contrast between the pollution level especially CO (mean mixing ratio of 16 ppm over 3 hrs) in Lagos and the other three cities is a reflection of the poor air quality in that part of the world. Results from long-term AQ monitoring using network of 46 static AQ sensors were used to characterise pollution in different environments ranging from urban to semi-urban and rural locations. By coupling meteorological information (wind measurements) with pollution data, pollution sources, and phenomena like the street canyon effect can be studied. Results from the long-term study also revealed that siting of the current fixed monitoring stations can fail to represent the actual air quality distribution and may therefore be unrepresentative. This work has shown the capability of electrochemical based AQ sensors in complementing the existing fixed site monitors thus demonstrating an emerging measurement paradigm for air quality monitoring and regulation, source attribution and human exposure studies.

Relative to traditional methods, air-liquid interface (ALI) exposures constitute a superior in vitro model for assessing the toxicological activity of complex aerosols. By removing the medium barrier, aerosols can be delivered to the cells at their apical surface. This project investigated the utility of the commercially available VITROCELL® exposure system for comparative toxicological assessment of complex aerosols (freshly-generated diluted diesel exhaust and simulated urban smog). The system setup was modified to improve control of aerosol properties (temperature and humidity) and cellular responses (dynamic range). Following optimization, cytotoxicity (WST-1 and LDH assays) and expression of selected genes involved in proinflammatory signalling and oxidative stress responses (via quantitative RT-PCR) were quantified following 1 hour aerosol exposures. The results showed only limited, variable responses following exposures to high concentrations of diesel exhaust. Lack of consistent and robust responses are likely due to poor deposition of particulate matter from the test aerosols.

Du fait de l’omniprésence de l’homme au sein du compartiment intérieur, y passant jusqu’à 90% de son temps au cours d’une journée, il est devenu essentiel de caractérisé correctement l’atmosphère et donc les polluants présent dans ce milieu. Ce travail de thèse prend la suite d’une étude menée au sein de notre laboratoire montrant une importante présence de radicaux hydroxyles dans cette atmosphère. Le polluant précurseur des radicaux supposé au cours de cette étude est l’acide nitreux (HONO), présent dans des quantités de l’ordre du ppb pour l’intérieur. Ce travail de thèse a donc eu pour but, dans un premier temps de caractériser la photolyse de l’acide nitreux conduisant à la formation de radicaux hydroxyles, et dans un second temps d’établir ses différentes voies de formation, directes et indirectes, afin de quantifier ses sources dans les atmosphères intérieures. / People in Western societies spend about 90% of their time indoors, predominantly within indoor places. The residence time of the airborne indoor pollutants is much longer due to the smaller volumes compared to the outdoor atmosphere and low air exchange rates. Therefore, a comprehensive understanding of indoor air quality is essential.Nitrous acid (HONO) is an emerging indoor pollutant because 1) it can lead to human respiratory tract irritation and formation of carcinogenic nitrosamines, and 2) it can be effectively photolyzed leading to a pulse of hydroxyl radicals (OH).The PhD work here presented is focused on understanding of the formation processes of oxidizing species such as HONO and, hence, OH radicals in the built environment.

The thesis deals with an analyses of emission and harmful particles of exhaust fumes of automobiles with an environmental impact. More precisely, it describes the basic characteristics of current fuel types and emission produced by internal combustion engines. Next, it deals with the measures and possibilities of decreasing car traffic emission with respect to environmental impact. It also describes the current European standards for emission and the systems of the cars that are able to decrease emission. The work also deals with the measuring of emission and the methods that are used. According to the measuring methods, the analysis of exhalation is done and it is based on the data of the real car fleet. Values of the emission analyses are compared. The financial aspect is a part of the analyses.

This master‘s thesis deals with denitrification of brown coal-fired boiler of electric power plant. First chapters describe technical characteristics of the boiler and possible measurements which would lead to lowering NOx emissions. In order for boiler to meet emission standards valid from 1.1.2016 flue gas treatment by selective catalytic reduction is proposed. Main part of the thesis is thermal calculation of the boiler with modifications necessary in order to apply SCR. The aim of calculation is to determine flue gas exit temperature and temperature at catalyst area in order to assess the suitability of proposed modifications.