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Gorr, Matthew W. "Air Pollution and Cardiovascular Dysfunction." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1428674045.
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Billah, Md Baki. "Chemical and toxicological characterization of chemical contaminants in air pollution particulate matter." HKBU Institutional Repository, 2015. https://repository.hkbu.edu.hk/etd_oa/155.
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In wintertime hazy episodes, the air pollution in northern China has always reached to an alarming level. In the winter of 2012-13, the trans-boundary air pollution from China has attracted national and global attention. An elevated public awareness to the unprecedented pollution levels has prompted much investigation on the health effects of fine particulate matter (PM), in particular PM2.5. Since PM-elicited harmful effects primarily depends on the composition of chemical contaminants adsorbed, in this study we characterized the chemical compositions of PM2.5 and determined its associated toxicity. Samples of PM2.5 were collected using high-volume samplers installed in five northern and southern cities in China. One typical (polycyclic aromatic hydrocarbons, PAHs) and one emerging (perfluorinated compounds, PFCs) family of organic pollutants were analyzed using gas chromatographymass spectrometry (GC-MS) or liquid chromatography-MS-MS (LC-MS-MS), followed by in-vitro or/and in vivo studies. In Chapters 2 and 3, sixteen PAH congeners in PM2.5 samples collected from five different cities (Hong Kong (HK), Guangzhou (GZ), Xiamen (XM), Xi’an (XA) and Beijing (BJ)) in the winter and summer time 2012-13 was analyzed. The biological effects of the sample extracts were determined using the human bronchial epithelial cells BEAS-2B. The total PAH concentrations ranged from 3.35 to 80.45 ng/m3 air, leading by BJ, followed by XA, XM, GZ and HK. In a comparison of the physical and chemical data of the samples obtained during the winter and summer sampling periods, the amount of PM collected per unit time and the concentrations of PAHs adsorbed were found to be remarkably greater in the winter time. In the cell culture study, the expression levels of the pro-inflammatory cytokine (interleukin-6, IL-6) and detoxifying enzymes (i.e. cytochrome p450 enzymes, CYP1A1 and CYP1B1) were found to be stimulated in the treatment. The cells exposed to sample extracts prepared from XA and BJ demonstrated significant migratory activities, indicating a sign of increase of tumorigenicity. These data highlighted the risk of getting lung cancer in local population. In chapters 4 and 5, we focused on the emerging pollutants PFCs, in particular PFOS. Chemical characterization was implemented using the winter samples. Biological effects of PFOS were conducted using omics approach in a maternal-fetal model. Therefore, in the first part of chapter 4, we measured the concentrations of nine PFC congeners in PM2.5 samples using LC-MS-MS. Generally, the eight PFCs, namely PFOS, PFDoA, PFUdA, PFDA, PFNA, PFOA, PFHxA and PFBA were detected in all the sampling cities, with the exception PFHxS which was below the limit of detection. The total PFC concentrations ranged from 121.2 to 192.2pg/m3, leading by GZ, followed by XA, BJ, XM and HK. The data denoted the risk of inhalation exposure to PFCs through PM2.5, which enter into blood circulations via lung alveoli, presumably penetrates through placenta in affecting fetal health. Therefore, in the latter part of chapter 4, the potential adverse effect of prenatal exposure to the prototypical PFC congener PFOS was used in the maternal-fetal mouse model to determine its effects on fetal liver and pancreas. Transcriptomic analysis demonstrated that the in-utero exposure to PFOS affect the expression of genes associated with fatty acid metabolism, lipid transport, and steroid synthesis in fetal livers. KEGG pathway analysis showed these changes were primarily associated with modulations of arachidonic, linoleic acid, retinol metabolism and PPAR signaling pathways in fetal liver. To identify additional target fetal tissue of PFOS, in chapter 5, we investigated the effects of PFOS on the protein expression in fetal pancreas using the technique of “Isobaric tags for relative and absolute quantitation (iTRAQ). We identified changes in the protein expressions involved in pancreatic secretion, protein digestion and absorption, protein processing in endoplasmic reticulum, fat digestion and absorption, glycerolipid metabolism and steroid biosynthesis. The perturbations to these targets may increase the risk of pancreatitis in mouse offspring. Collectively, this study provided a comprehensive chemical and biological analysis of PM2.5 collected in China and demonstrated the toxicities, in vitro and in vivo of the adsorbed chemical contaminants.
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Kim, Dasom. "PPAR-gamma Regulates T Cell Responses in Air Pollutant-associated Inflammation." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1522414820700163.
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Demer, Frank Robert 1961. "The impact of various cure parameters on the release of 4-phenylcyclohexene from carboxylated styrene-butadiene rubber latex." Thesis, The University of Arizona, 1989. http://hdl.handle.net/10150/277075.
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Research was initiated to examine the feasibility of removing the majority of 4-PCH from the XSBR latex employed in carpet manufacturing. The reduction of 4-PCH from such latices would lend insight into the control of certain carpet related illnesses.
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Bakand, Shahnaz Safety Science Faculty of Science UNSW. "Development of in vitro methods for toxicity assessment of workplace air contaminants." Awarded by:University of New South Wales. School of Safety Science, 2006. http://handle.unsw.edu.au/1959.4/24246.
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Exposure to air contaminants is significantly associated with both short-term and long-term health effects. However, the precise mechanisms that derive such effects are not always understood. While an extensive background database from in vivo toxicological studies have been developed, most toxicity data is from oral and dermal chemical exposures rather than inhalation exposure. There is a need to explore new alternative approaches to provide toxicity information particularly on this technically demanding area. This research explores the potential of in vitro methods for toxicity assessment of workplace air contaminants. A tiered approach for in vitro toxicity testing of workplace contaminants was designed in which appropriate air sampling and exposure techniques were developed. A diversified battery of in vitro assays including the MTS (tetrazolium salt, Promega), NRU (neutral red uptake, Sigma) and ATP (adenosine triphosphate, Promega) and a multiple human cell system including: A549- lung derived cells; HepG2-liver derived cells, and skin fibroblasts were used. Primarily the application and merits of in vitro methods for prediction of toxicity of selected workplace contaminants including Ammonium hydroxide, Cadmium chloride, Cobalt chloride, Formaldehyde, Glutaraldehyde, Manganese chloride, Mercuric chloride, Sodium dichromate, Sulphureous acid and Zinc chloride was confirmed. To study the toxicity of airborne contaminants an indirect exposure method was established using air sampling techniques followed by static and dynamic direct exposure methods by culturing cells on porous membranes to reveal representative data relating to human airborne exposures. The static method enabled the measurement of an airborne IC50 (50% inhibitory concentration) value for selected volatile organic compounds (VOCs) including: Xylene (IC50 = 5,350-8,200 ppm) and Toluene (IC50 = 10,500- 16,600 ppm) after 1 hr exposure. By implementing the dynamic method, airborne IC50 values were calculated for gaseous contaminants including: NO2 (IC50 = 11 ?? 3.54 ppm; NRU), SO2 (IC50 = 48 ?? 2.83 ppm; ATP) and NH3 (IC50 = 199 ?? 1.41 ppm; MTS). A higher sensitivity of in vitro methods was observed compared to in vivo published data. A range of in vitro bioassays in conjunction with exposure techniques developed in this thesis may provide an advanced technology for a comprehensive risk assessment of workplace air contaminants.
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Norris, Mary Jo. "A Study of Radon in Air and Water in Maine Schools." Fogler Library, University of Maine, 2002. http://www.library.umaine.edu/theses/pdf/NorrisMJ2002.pdf.
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Almeida, Daniela Sanches de. "Estudo da exposição pessoal ao material particulado atmosférico em Londrina." Universidade Tecnológica Federal do Paraná, 2016. http://repositorio.utfpr.edu.br/jspui/handle/1/1900.
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CNPq; CAPESA exposição humana a poluentes atmosféricos causam efeitos adversos à saúde. As áreas urbanas com alta densidade populacional e fluxos de veículos elevados são regiões críticas. Os poluentes do ar são onipresentes, e certo nível de exposição é inevitável, variável e dependente de uma série de fatores ambientais e individuais de cada um. O presente trabalho visou medir e avaliar a exposição pessoal ao material particulado atmosférico por indivíduos da cidade de Londrina em um estudo com 30 voluntários de 6 classes de ocupação. Utilizando monitores pessoais de concentração de material particulado atmosférico foram medidas as concentrações em massa e número de partículas no ar inalado. Células bucais dos voluntários foram coletadas antes e após a exposição para a determinação da genotoxicidade pelo teste do cometa. Foram realizadas campanhas de amostragem no inverno, em rotas georreferenciadas que variaram de acordo com a rotina de cada indivíduo. A partir das concentrações medidas, tempo de exposição e massa corporal foram calculadas as doses recebidas individualmente. As concentrações em massa (média de 8 h) encontradas para os voluntários variaram de 2,41 a 34,07 µg m-3 para MP1,0 e de 23,11 a 11060,54 µg m-3 para o MP10. As concentrações em número de partículas encontradas variaram de 14 a 183 partículas cm-3 para o MP0,3; para o MP2,5 elas variaram de 0,20 a 27 partículas cm-3. A categoria Construção e Indústria apresentou as doses recebidas mais elevadas, enquanto o setor Administrativo apresentou as menores. Através do teste de Kruskal-Wallis foi verificado que há diferença significativa de danos no DNA nas classes Comércio, Construção e Indústria e Transporte, quando comparadas ao controle (classe Administrativo). O modelo que melhor se adequou aos dados foi o Binomial Negativo, indicando associação positiva, principalmente das classes de ocupação e número de partículas com os danos ao DNA das células bucais. Os resultados da simulação de deposição pulmonar a partir das concentrações obtidas na amostragem indicaram que nos voluntários onde o diâmetro predominante das partículas era menor, a fração depositada no pulmão foi maior, embora a concentração em massa fosse maior. Os resultados obtidos evidenciam a relevância do tamanho das partículas e composição química nos efeitos à saúde, a importância de medidas de exposição pessoal para estudos epidemiológicos em saúde e a viabilidade deste tipo de amostragem pessoal, porém para resultados mais significativos é recomendável a ampliação deste estudo.
The exposure to air pollutants in humans causes damage effects on health. Urban areas with high population density and high vehicular flows are critical regions. Air pollutants are omnipresent, and some level of exposure is inevitable, variable and dependent on a number of environmental and individual factors of each. This work aimed to measure and assess personal exposure to airborne particulate matter by individuals in Londrina with 30 voluntaries from 6 occupation classes. Using personal monitors the concentration of airborne particulate matter concentrations were measured in mass and number of particles in the inhaled air. Buccal cells of the volunteers were collected before and after exposure to the determination of genotoxicity by Comet assay. Sampling campaigns were carried out in winter with georeferenced routes that varied according to the routine of each individual. From concentrations measured, time of exposure and body weight the received doses were calculated individually. The mass concentrations (average of 8 hours) found in the volunteers ranged from 2.41 to 34.07 µg m-3 for MP1,0 and 23.11 to 11060.54 µg m-3 for PM10. The concentrations in number of particles found varied from 14 to 183 particles cm-3 to MP0,3; for PM2.5 they varied from 0.20 to 27 particles cm-3. Construction and Industry category showed the highest doses, while the administrative sector had the lowest. Using the Kruskal Wallis test was found a significant difference of DNA damage in classes Trade, Construction and Industry and Transportation, when these were compared with the control group (Administrative class). The model best suited to the data was the Negative Binomial, indicating positive association, mainly of the occupation class, number of particles with damage to DNA from buccal cells. The results of the lung deposition simulation from the concentrations obtained in the sample show that in volunteers where the predominant particle diameter was smaller, the fraction deposited in the lungs was higher, although the bulk concentration was higher. The results show the importance of particle size and chemical composition on the health effects, the importance of personal exposure measurements for epidemiological studies on health and the feasibility of this type of personal sampling, but for more significant results it is recommended the magnification of this study.
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Ardiles, Leda Gabriela. "Risco à saúde atribuído à poluição do ar e variáveis meteorológicas na região metropolitana de Curitiba." Universidade Tecnológica Federal do Paraná, 2016. http://repositorio.utfpr.edu.br/jspui/handle/1/1907.
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Capes; Fundação AraucáriaEste trabalho visou determinar o risco atribuído à saúde da população pela exposição à poluição do ar e variáveis meteorológicas na Região Metropolitana de Curitiba (RMC) e com maior ênfase nas cidades de Araucária e Curitiba, no período de 2010 a 2014, nas faixas etárias de 0 a 9 anos, 10 a 19, 20 a 64, maiores de 64 anos e para todas as faixas etárias incluídas. Curitiba e Araucária são os maiores polos populacional e industrial do estado, respectivamente, com predominância de distintas fontes de emissão de poluentes. Neste estudo foi investigada as associações da qualidade do ar e variáveis meteorológicas com doenças circulatórias e respiratórias, calculado o Risco Relativo (RR) e o risco atribuído a saúde pelas concentrações de MP10 e O3. Os resultados indicaram que o modelo com distribuição Binomial Negativa foi o mais adequado aos dados e utilizado diferentemente da maioria dos estudos que usam Poisson. A partir dos coeficientes obtidos no modelo de regressão, foram calculados o risco relativo e o risco atribuído causados pelos poluentes do ar. O melhor ajuste de modelo (resíduo de Pearson mais próximo a um), se encontrou para o grupo de idosos com mais de 64 anos, em Araucária, para doenças circulatórias devido às concentrações de CO, e para internações respiratórias devido aos poluentes O3, SO2 e T-Tm, que é a temperatura diária menos a temperatura média de 2010 a 2014. Em Curitiba, o melhor ajuste ocorreu para o grupo com todas as faixas etárias para internações circulatórias devido ao MP10, e o grupo de 20 a 64 anos para internações respiratórias, para CO, O3 e T-Tm. As defasagens mais importantes ocorreram entre 3 a 7 dias após a exposição aos poluentes atmosféricos. Em Araucária, o RR mais significativo estatisticamente para internações circulatórias foi de 1,44635 em maiores de 64 anos para CO, e nas internações respiratórias foi de 2,4128 encontrado na faixa etária de 10 a 19 anos, também para o CO. Em Curitiba o RR mais significativo ocorreu para internações por doenças respiratórias com valor de 1,00315 na faixa de 0 a 9 anos para o MP10, de 1,14881 na faixa de 20 a 64 anos para CO, de 1,00329 entre 20 a 64 anos para O3, e de 1,13886 para maiores de 64 anos devido ao CO. Foram associadas 112 e 97 internações devido ao MP10, por doenças circulatórias e respiratórias na RMC no período de 2010 a 2014. Foram associadas 67 internações respiratórias, devido ao O3. Com a estimação destes valores, é possível avaliar o impacto que a poluição do ar na RMC representa para a saúde pública e que poderiam ser evitados e direcionados na prevenção dos efeitos adversos à saúde da população, na implantação de políticas e normas reguladoras para diminuição da emissão e concentração dos poluentes atmosféricos.
This study aimed to determine the risk attributed to human health by exposure to air pollution and meteorological variables in the Metropolitan Region of Curitiba (MRC). The greater emphasis is on the cities of Araucária and Curitiba, in the period from 2010 to 2014, for age groups of 0-9 years old, 10-19, 20-64, over 64 years, and another including all ages. Curitiba has the major populations and Araucaria has the major industrial centers of the state, with a predominance of different pollutant emission sources. This study investigated the associations of air quality and meteorological variables with circulatory and respiratory diseases, the relative risk (RR) and the risk assigned to health by concentrations of PM10 and O3. The results indicate that the model with Negative Binomial distribution is the most suitable, differently of most of the studies presented until now. The relative risk and attributable risk by air pollutants were calculated from the coefficients obtained in the regression model. The best adjustment was found for the group of people over 64 years in Araucaria, both for circulatory diseases due to CO, as for respiratory hospitalizations due to O3, SO2 and T-Tm. In Curitiba, the best adjustment of the model was for the group containing all ages for circulatory hospitalizations due to PM10, and the group of 20-64 years for respiratory hospitalizations for CO, O3 and T-Tm. The most significant lags were from 3 to 7 days after the exposure to air pollution. In Araucária the most statistically significant RR was 1.44635 for circulatory hospitalizations among people over 64 years due to CO. For respiratory hospitalizations, the RR was 2.4128, found in the age group 10 to 19 years, corresponding to the pollutant CO. The RR was also important in the group of 20-64 years for NO2, which was 1.00758. At Curitiba the most significant RR was by hospitalizations for respiratory diseases in the amount of 1.00315 to the group of 0-9 years due to PM10, of 1.14881 in the range of 20-64 years old for CO, of 1.00329 for 20-64 to O3, and 1.13886 for over 64 years old due to CO. 112 circulatory hospitalizations in the MRC were associated to PM10 and 97 respiratory hospitalization were associated with the PM10. 67 respiratory hospitalizations in the MRC were associated to O3. With the estimation of these values, it is possible to evaluate the impact in public health and how these costs could be avoided and focused on the prevention of adverse effects of public health, the implementation of regulatory policies and regulations to reduce the emission and concentration of air pollutants.
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Méausoone, Clémence. "Etude en Interface Air-Liquide de la toxicité des Composés Organiques Volatils lors d’expositions répétées : Cas du toluène, de ses homologues et des émissions issues de son traitement catalytique." Thesis, Littoral, 2019. https://documents.univ-littoral.fr/access/content/group/50b76a52-4e4b-4ade-a198-f84bc4e1bc3c/BULCO/Th%C3%A8ses/Toxicologie/these_Meausoone_Clemence.pdf.
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Le toluène est un solvant fréquemment utilisé par l’industrie manufacturière. Il appartient à la catégorie des composés organiques volatils (COV), dont nombre d’entre eux présentent des impacts néfastes sur la santé humaine et sont aujourd’hui classés cancérogènes, mutagènes et/ou reprotoxiques. Afin de diminuer la présence dans l’air de composés nocifs comme le toluène, il apparait essentiel d’envisager leur substitution dans les procédés industriels par des composés moins toxiques et/ou de réduire au maximum leurs émissions à la source. Dans ce contexte, le premier objectif du travail de recherche est d’étudier la toxicité aiguë et répétée du toluène, de ses homologues supérieurs, pouvant être utilisés comme composés de substitution, ainsi que de son homologue inférieur sur des cellules épithéliales bronchiques humaines à l’aide d’un dispositif d’exposition en interface air/liquide. Le deuxième objectif vise à évaluer le caractère toxique d’effluents gazeux issus de la dégradation du toluène par oxydation catalytique. Pour cela, les cellules BEAS-2B ont été exposées 1 heure par jour pendant 1, 3 et 5 jours au benzène, au toluène, au xylène ou au mésitylène, ainsi qu’aux effluents gazeux obtenus après traitement catalytique du toluène. Les effets toxiques ont été évalués au travers des paramètres de cytotoxicité, de réponse inflammatoire et d’expression génique des enzymes de métabolisation des xénobiotiques (EMX). L’exposition des cellules BEAS-2B au toluène et à ses homologues a révélé l’implication de voies métaboliques spécifiques à chaque composé. Une augmentation significative des marqueurs de l’inflammation a également été observée, avec une concentration plus importante pour le benzène et le xylène par rapport aux autres molécules. Concernant l’exposition aux effluents gazeux issus de l’oxydation catalytique du toluène, l’expression tardive de gènes impliqués dans le métabolisme des xénobiotiques organiques aromatiques, est compatible avec la présence de sous-produits, tels que le benzène ou les hydrocarbures aromatiques polycycliques. En conclusion, les résultats obtenus dans ce projet montrent l’intérêt de mener des expositions in vitro en condition répétée permettant de déceler de potentiels effets tardifs et la pertinence de la validation toxicologique des systèmes catalytiques avant leur formulation en pilote industrielToluene is a solvent widely used in manufacturing industries. It belongs to a family of volatile organic compounds (VOCs), many of which have adverse impacts on human health and are classified as carcinogenic, mutagenic or toxic for reproduction. Different measures have been implemented to reduce the emissions of toxic compounds, such as their replacement in the industry by less harmful compounds and/or reducing gas emissions at the source. In this context, the first objective of the research was to investigate the acute toxicity and the one after repeated exposure to toluene and its superior homologous solvents, which can be used as its substitution compounds, as well as its lower homologous on human bronchial epithelial cells using an air/liquid interface exposure device. The second objective was to assess the toxicity of gaseous effluents from the degradation of toluene by catalytic oxidation. For this purpose, BEAS-2B cells were exposed during 1 hour for 1, 3 or 5 days to benzene, toluene, xylene or mesitylene, and to the exhausts of catalytic oxidation of toluene. Toxic effects were evaluated through cytotoxicity, inflammatory response and gene expression of xenobiotic metabolism enzymes (XME). Exposure of BEAS-2B cells to toluene and its homologous compounds revealed the involvement of metabolic pathways specific to each compound. A significant increase in inflammatory marker response was also observed, with a higher concentration after cell exposure to benzene and to xylene compared to the other molecules. With regard to exposure to gaseous effluents from the catalytic oxidation of toluene, the late expression of genes involved in the metabolism of aromatic organic xenobiotics has made possible to highlight the presence of by-products, such as benzene or polycyclic aromatic hydrocarbons. In conclusion, the results obtained in this project show the interest of conducting repeated in vitro exposures to detect potential late effects, and the importance of toxicological validation of catalytic systems before scaling-up in industrial pilots
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André, Paulo Afonso de. "Câmara de Topo Aberto, CTA: construção e uso para observação de potencial tóxico da poluição atmosférica urbana com bioensaios em plantas." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-24102007-134900/.
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A Câmara de Topo Aberto, CTA, foi adaptada para gerar um gradiente da concentração da poluição atmosférica ambiente por material particulado fino, capaz de ser utilizado em experimentos toxicológicos. Uma vez que os aerossóis urbanos são composições quimicamente complexas, com comprovada toxicidade na saúde e mecanismos de ação sobre o homem ainda pouco conhecidos, a utilização conjunta da CTA com sistemas sentinela simples e de baixo custo, capazes de detectar efeitos tóxicos agudos, constituem alternativa para avaliação desse ambiente. A Câmara de Topo Aberto, CTA, foi documentada em termos de dimensões, especificações e características operacionais, e avaliada durante 60 dias. A concentração ambiental média diária de material particulado fino no período foi de 28,6 ug/m3 e a redução média dessa concentração obtida no interior da CTA foi de 75%. Tradescantia clone 4430, KU20 e pallida cv. Purpurea foram colocadas dentro e fora da CTA para avaliar a resposta de bioensaios nesse gradiente de exposição. O protocolo de mutação em inflorescência (Trad-MCN) foi aplicado nos três espécimes vegetais, e detectou uma menor quantidade de micronúcleos no interior da CTA (p=0,002). Nos clones foram aplicados os protocolos de mutação em pêlo estaminal (Trad-SHM) e aborto em grão de pólen, tendo sido detectada menor resposta para as plantas colocadas no interior da CTA (p=0,007 para pêlo estaminal e p= 0,041 para grão de pólen). Folhas dos três espécimes foram coletadas e submetidas à análise por fluorescência de raio-X. Foi detectada redução na concentração de titânio nas folhas coletadas dentro da CTA (p=0,049). A análise fatorial identificou a presença de fontes de solo e automotiva, com menor concentração observada nas folhas colhidas dentro da CTA. A utilização da CTA com bioensaios no ambiente urbano mostrou ser capaz de detectar efeitos agudos em plantas frente ao gradiente de exposição obtido.Open Top Chamber was modified to obtain a differential concentration on environmental pollution capable to be used on toxicological studies. Since urban aerosol constitutes a very complex chemical composition, with well known toxic action on health but requesting clarification about their biological mechanisms, the use of Open Top Chamber with low cost sentinel systems seems to be an alternative to detect acute toxic effects on such environment. Open Top Chamber was described on its dimensional and operational characteristics, and operated on a 60 days campaign. During this campaign the daily average concentration of fine particles was 28,6 ug/m3 and inside the Open Top Chamber it was obtained a reduction about 75% on such concentration. Tradescantia clone 4430, KU20 and pallida cv. Purpurea were placed inside and outside the chamber to evaluate bioassay response on each pollution concentration. The Trad-MCN bioassay detected a lower micronuclei count on plants inside the chamber (p=0,002). Clones were submitted to stamen hair mutation (Trad-SHM) and pollen mother cell abortion protocols, detecting also a lower effect on plants inside the chamber (p=0,007 for stamen hair mutation and p=0,041 for pollen mother cells abortion). Leaves of all spices were collected and submitted to X-ray fluorescence analysis. The titanium concentration was lower on samplers collected inside the chamber (p=0,049). The factorial analysis identified the presence of elements from soil and automotive sources with a lower concentration on samples collected inside the chamber. The combined use of Open Top Chamber with bioassay on urban environment is capable to detect acute effects on plants when submitted to the obtained particulate concentration reduction.
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Lehmann, Catherine. "Le radon dans les habitations." Bordeaux 2, 1995. http://www.theses.fr/1995BOR2P072.
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Sentissi, Maya. "Impact sanitaire de la pollution atmosphérique urbaine particulaire." Paris 5, 1999. http://www.theses.fr/1999PA05P032.
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Pariselli, Fabrizio. "Evaluation in vitro de la nocivité des composés organiques volatils de l'air intérieur : développement d'une technique d'exposition dynamique." Paris 5, 2008. http://www.theses.fr/2008PA05P643.
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Des centaines de composés chimiques volatils (COV et aldéhydes) sont présents dans l'air que nous respirons dans les environnements d'intérieur (maisons, bureaux, lieux publics…) à des concentrations souvent supérieures à celles mesurées à l’extérieur. De plus, l’homme passant la majeure partie de son temps en intérieur, la durée d’exposition et les conséquences sur la santé sont loin d’être négligeables. L’objectif de cette thèse de doctorat était d’évaluer, par des techniques in vitro, les effets biologiques potentiels des mélanges de faibles concentrations de polluants chimiques caractéristiques de l’air intérieur. Pour cela, une méthode d’exposition in vitro dynamique, utilisant un module appelé CULTEX® et permettant l’exposition directe de cellules en interface air/liquide, a été mise au point. Nous avons étudié les effets de l’exposition au toluène, benzène et formaldéhyde sur différentes lignées cellulaires humaines représentant les organes cibles des polluants. L’application de faibles concentrations (proche des valeurs détectées dans les espaces intérieurs) des polluants, seuls puis en mélanges, sur les lignées cellulaires a permit de révéler la sensibilité et la spécificité du système d’étude aux polluants par la détection d’effets cytotoxiques, inflammatoires, oxydatifs et dénaturant sur l’ADN propres à chaque produit et à leurs mélanges. D’autres études ont été menées pour étudier l’étendue des possibilités du système d’exposition utilisé: l’étude de la combinaison de l’exposition à différents types d’agents environnementaux (physiques et chimiques) et des tests d’exposition in situ où des atmosphères recrées dans une chambre climatique à partir de matériels communs de construction ont été testéesHundreds of chemicals like volatile organic compounds (VOCs) are present in the indoor environment and are suspected to cause acute and chronic adverse health effects. At present, there is a lack of substantial information on toxicological effects caused by VOC mixtures at low concentrations; therefore, new experimental approaches should be designed to detect biological effects at typical indoor air concentrations. The aim of this PhD thesis was the in vitro evaluation of biological effects of low concentrations of indoor air pollutants. Toluene, benzene and formaldehyde were selected as representing key contaminants in indoor non-occupational environments. Human derived cell cultures, representing VOCs target organs were exposed to low concentrations of these air pollutants by means of an original exposure device, named CULTEX®, which permits the application of the volatile compounds directly on cell surface at the air/liquid interface. The exposition of cell cultures to low concentrations of selected volatile compounds, alone and in mixture, were able to initiate different biological effects in terms of toxicity, inflammatory response, oxidative stress and DNA damage. Further studies were performed in order to exploit the peculiarities of the exposure device: i. E. The combination of physical (UV) and chemical agents and the use of atmospheres generated in a climatic room by common construction materials
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Dendene, Marie-Aude. "Exposition au monoxyde de carbone et aux hydrocarbures aromatiques monocycliques : étude comparative des divers modes de déplacement urbain et recherche de biomarqueurs de l'air expiré." Paris 5, 1995. http://www.theses.fr/1995PA05P016.
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Carteret, Marion. "Evaluation de l’exposition des personnes aux polluants issus des chauffages d’appoint au pétrole." Thesis, Lille 1, 2012. http://www.theses.fr/2012LIL10005/document.
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Les poêles à pétrole sont des appareils de chauffage dépourvus d’évacuation des gaz brûlés vers l’extérieur de la pièce. Ils ont été à l’origine de 49 cas d’intoxication aiguë au monoxyde de carbone en France en 2007. Ce type de chauffage est aussi probablement responsable d’intoxications chroniques, mais celles-ci ne sont pas documentées. Cette thèse a pour objet la quantification en laboratoire des émissions gazeuses de poêles à pétrole récents et l’élaboration de protocoles de mesure pour l’étude de la qualité de l’air à l’intérieur de logements du Nord-Pas-de-Calais. Deux types de poêles à pétrole (à mèche et électronique) ont été étudiés dans une enceinte de 8 m3. Ils émettent principalement NO, NO2, CO, CO2 et des particules. Trois COV préoccupants (formaldéhyde, benzène et 1,3-butadiène) ont également été quantifiés. Les facteurs d’émission dépendent du type de poêle et de la composition du carburant utilisé, en particulier sa teneur en soufre, et en esters méthyliques d’acides gras dans le cas d’un carburant « bio ». L’accumulation de suies sur le poêle à mèche au cours de son utilisation s’accompagne d’une forte augmentation des émissions de CO, qui peut conduire à des intoxications chroniques et aiguës. Des mesures de terrain chez six volontaires ont permis de tester nos protocoles dans un milieu plus complexe que celui du laboratoire. Le rôle prépondérant des poêles à pétrole sur les niveaux de pollution dans les logements a été mis en évidence. Ce travail servira de base à une future étude épidémiologique portant sur la santé respiratoire des utilisateurs de tels appareils de chauffageUnvented kerosene space heaters were responsible for 49 cases of acute carbon monoxide poisoning in France in 2007. This kind of heater may also induce chronic intoxications, but no information on these is available. The aim of this work is the laboratory quantification of the gaseous emissions from recent models of kerosene space heaters and the preparation of an indoor air quality study in the Nord-Pas-de-Calais region. Two types of kerosene heaters (wick and injector) were tested in an 8 m3 instrumented environmental chamber. They emit mainly CO2, CO, NO, NO2, particles and some VOCs (especially formaldehyde, benzene, 1,3-butadiene). Emission factors depend upon the kind of heater and upon the type of fuel, and particularly on the fatty acid methyl esters and sulfur content. The accumulation of soot on the wick heater during use leads to a high increase of the CO emissions, and could be responsible for chronic and acute CO intoxications. Field measurements were undertaken to assess the effective exposure of users to pollutants emitted by kerosene space heaters in a complex environment. Kerosene space heater emissions were found to be the main source of pollution. This work will be applied to an epidemiological study on respiratory diseases caused by these heaters
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Ndong, Awa. "Pollution de l'air extérieur et intérieur à Dakar (Sénégal) : caractérisation de la pollution, impact toxicologique et évaluation épidémiologique des effets sanitaires." Thesis, Littoral, 2019. http://www.theses.fr/2019DUNK0510/document.
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La pollution atmosphérique constitue de nos jours un enjeu sociétal majeur, tant pour ses conséquences néfastes sur la santé humaine que sur l'environnement. L'objectif général de ce présent travail était de déterminer le niveau de la pollution atmosphérique dakaroise, extérieure et intérieure, et d'évaluer son impact sanitaire au sein de la population urbaine. Les particules fines (PM₂.₅) et une fraction plus grossière (PM>₂.₅) échantillonnées sur un site urbain de Dakar (HLM), caractérisées par de fortes émissions du trafic routier, ont été comparées aux particules échantillonnées dans une zone rurale, Toubab Dialaw, située à environ 40 kms de Dakar. Les caractéristiques physicochimiques des échantillons ont révélé que les particules différaient par leurs propriétés physiques (surface) et chimiques (en termes de CHN, métaux, ions, paraffines, COV et HAP) de 65 à 75 % plus élevées dans les échantillons urbains. Selon les différentes sources et les différentes propriétés physiques et chimiques, la réponse inflammatoire (TNF-α, IL-1β, IL-6, IL-8) et les dommages oxydatifs (protéines carbonylées totales et 8-OHdG) se sont révélés plus importants dans les cellules bronchiques BEAS-2B exposées aux particules urbaines. La campagne de mesure de la qualité de l'air a montré que l'intérieur du bus était plus pollué en PM₁₀, CO, CO₂ et NO que le marché et les sites intérieurs urbains et ruraux. La comparaison de la qualité de l'air entre les sites intérieurs et extérieurs a révélé que, particulièrement dans les zones urbaines, la qualité de l'air intérieur pouvait être moins bonne que celle des sites extérieurs correspondants. Le suivi de l'exposition individuelle aux polluants a montré que les ménagères de la zone urbaine et rurale étaient plus exposées que les professionnels à la pollution de l'air, confirmant les observations précédentes d'un niveau d'exposition potentiellement plus élevé des polluants dans l'environnement intérieur. Cependant, il convient de tenir compte du niveau d'exposition des commerçants et des conducteurs d'autobus résultant de l'échappement du trafic avec des véhicules souvent anciens, mal entretenus et non contrôlés, en raison des niveaux élevés de polluants gazeux rapportés iciAir pollution is nowadays a major societal challenge, as much for its harmful consequences on human health as on the environment. The general objective of this work was to determine the level of Dakar air pollution, outdoor and indoor, and to assess its health impact in the urban population. Fine particles (PM₂.₅) and a coarser fraction (PM>₂.₅) sampled at an urban site in Dakar (HLM), characterized by high road traffic emissions, were compared with particles sampled at a rural area, Toubab Dialaw located about 40 km from Dakar. The physicochemical characteristics of samples revealed that PMs differ for their physical (surface area) and chemical properties (in terms of CHN, metals, ions, paraffins, VOCs and PAHs) that were 65 to 75 % higher in urban samples. In accordance with the different sources and different physical and chemical properties, the inflammatory response (TNF-α, IL-1β, IL-6, IL-8) and the oxidative damage (total carbonylated proteins and 8-OHdG) were found higher in bronchial BEAS-2B cells exposed to urban PMs. The air quality measurement campaign showed that the bus interior was more polluted with PM₁₀, CO, CO₂ and NO than the market and the urban and rural indoor sites. The comparison of air quality between indoor and outdoor sites revealed that, particularly in urban areas, indoor air quality may be worse than the corresponding outdoor one. Monitoring individual exposure to pollutants showed that housewives in urban and rural sites were more exposed than professionals to air pollution, confirming previous observations of potential higher individual exposure level to pollutants in indoor environment. However, exposure level of traders and bus drivers that would result from the exhaust of traffic with often old, poorly maintained and uncontrolled vehicles has to be taken into consideration due the higher levels of gaseous pollutants here reported
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Badran, Ghidaa. "Pollution atmosphérique particulaire : caractérisation physico-chimique et comparaison des effets toxiques des fractions extractible et non-extractible des PM₂.₅ In-vitro evaluation of organic extractable matter from ambient PM₂.₅ using human bronchial epithelial BEAS-2B cells : Cytotoxicity, oxidative stress, pro-inflammatory response, genotoxicity, and cell cycle deregulation. Toxicity of fine and quasi-ultrafine particles : focus on the effects of organic extractable and non-extractable matter fractions. Toxicological appraisal of the chemical fractions of ambient fine (PM₂.₅-₀.₃) and quasi-ultrafine (PM₀.₃) particles in human bronchial epithelial BEAS-2B cells." Thesis, Littoral, 2019. http://www.theses.fr/2019DUNK0547.
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La pollution de l'air et les particules fines (PM₂.₅) ont été classées cancérigènes (groupe 1) par le Centre International de la Recherche sur le Cancer en 2013. Cette fraction particulaire représente un mélange complexe dont la composition, très variable, influe sur la toxicité. Cependant, peu d'études ont déterminé l'implication respective des différentes fractions chimiques constitutives des PM dans leurs effets toxiques. Dans ce travail de thèse, des particules fines (PM₂.₅₋₀.₃) et quasi-ultrafines (PM₀.₃) ont été échantillonnées au niveau d'un site urbain à Beyrouth (Liban). Après avoir réalisé la caractérisation physico-chimique de ces deux types de particules, leurs effets toxiques (cytotoxicité globale, activation métabolique, génotoxicité, inflammation, stress oxydant, autophagie et apoptose) ont été étudiés sur une lignée de cellules épithéliales bronchiques humaines (BEAS-2B). L'analyse des fractions organiques a révélé des différences entre les teneurs en hydrocarbures aromatiques polycycliques (HAP), de même qu'en congénères oxygénés (O-HAP) et nitrés (N-HAP), respectivement 43, 17 et 4 fois plus élevées dans les PM₀.₃ que dans les PM₂.₅₋₀.₃. L'étude toxicologique a porté sur les particules fines considérées dans leur entièreté (PM₂.₅₋₀.₃), la fraction organique extractible (EOM₂.₅₋₀.₃) et la fraction non-extractible par le dichlorométhane (NEM₂.₅₋₀.₃). De plus, les effets spécifiques de la fraction organique extraite des particules quasi-ultrafines (EOM₀.₃) ont été comparés à ceux de la fraction organique extraite des particules fines (EOM₂.₅₋₀.₃). Nos résultats montrent que chacune des fractions considérées a été capable d'activer au moins un des mécanismes étudiés. Les PM₂.₅₋₀.₃ ont induit des effets toxiques généralement plus marqués que les EOM₂.₅₋₀.₃ et NEM₂.₅₋₀.₃. La fraction organique des particules quasi-ultrafines (EOM₀.₃), plus riche en composés organiques et notamment en HAP et autres congénères, est apparue responsable d'effets délétères globalement plus importants que celle extraite des particules fines (EOM₂.₅₋₀.₃). Les résultats de ce travail ont apporté des éléments nouveaux sur la toxicité relative des différentes fractions extractibles et non extractibles des particules fines et soulignent le rôle crucial joué par les particules ultrafines, encore trop peu étudiéesAir pollution and particulate matter (PM₂.₅) were classified as carcinigens (group 1) by the International Agency for Research on Cancer in 2013. This particulate fraction represents a complex mixture with a highly variable composition influencing the toxicity. However, few studies have determined the respective involvement of the different chemical fractions of PM in their toxic effects. In this work, fine particles (PM₂.₅₋₀.₃) and quasi-ultrafine particles (PM₀.₃) were sampled in an urban site located in Beirut (Lebanon). After performing the physicochemical characterization of these two types of particles, their toxic effects (global cytotoxicity, metabolic activation, genotoxicity, inflammation, oxidative stress, autophagy and apoptosis) were investigated on a human bronchial epithelial cell line (BEAS-2B). The analysis of the organic content revealed differences between the concentrations of polycyclic aromatic hydrocarbons (PAHs), as welle as oxygenated (O-PAH) and nitrated (N-PAH) congeners, respectively 43, 17 and 4 times higher in PM₀.₃ than in PM₂.₅₋₀.₃.The toxicological study was based on the comparison of the toxicity of the fine particles considered in their entirety (PM₂.₅₋₀.₃), the extracted organic fraction (OEM₂.₅₋₀.₃) and the fraction not extracted by the dichloromethane (NEM₂.₅₋₀.₃). In addition, the specific effects of the organic fraction extrated from the quasi-ultrafine particles (OEM₀.₃) were compared with those of the organic fraction extracted from the fine particles (OEM₂.₅₋₀.₃). Our results showed that all the studied fractions were able to induce at least one of the studied mechanisms. PM₂.₅₋₀.₃ was able to induce toxic effects greater than those induced by OEM₂.₅₋₀.₃ and NEM₂.₅₋₀.₃. The organic fraction extracted from the quasi-ultrafine particles (OEM₀.₃), richer in organic compounds and in particular in PAHs and other congeners, appeared to be responsible for deleterious effects globally greater than that extracted from the fine particles (OEM₂.₅₋₀.₃). The results of this work have brought new elements on the relative toxicity of the different fractions of the fine particles and underline the crucial role played by ultrafine particles, still too little studied
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Gaimoz, Cécile. "Caractérisation expérimentale des sources de composés organiques volatils dans deux mégapoles contrastées : Paris et Pékin." Versailles-St Quentin en Yvelines, 2009. http://www.theses.fr/2009VERS0040.
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Ce travail de thèse a eu pour objectif la caractérisation des Composés Organiques Volatils (COV) affectant l’atmosphère de deux mégapoles - Paris et Pékin - sélectionnées pour le contraste de leur situation. Cette étude s’appuie sur un important travail expérimental qui comprend des optimisations instrumentales et la participation à deux campagnes de terrain réalisées en mai-juin 2007 à Paris et en août 2007 à Pékin. Suite à l’analyse descriptive des bases de données constituées, ainsi qu’à l’application du modèle sources-récepteur PMF - sept et dix sources respectivement ont été identifiées à Paris et Pékin. Les émissions liées au trafic automobile ont été révélées comme principales sources locales/régionales de COV pour les périodes considérées contribuant à 54% et 35% des émissions. Cependant l’impact des émissions continentales ou régionales sur les teneurs en COV et sur les sources affectant les sites a également été mis en évidence, ces émissions se trouvant être dépendantes de l’origine des masses d’air. Ainsi Paris, en condition anticyclonique, est fortement influencée par l’importation des émissions d’Europe du Nord-Est, et Pékin par les émissions régionales du bassin de la province de Hebei située au Sud-Est. Enfin, les sources identifiées et leurs contributions ont été comparées aux données d’inventaire d’émissions. Dans le cas de Paris, il a été mis en évidence une importante incohérence entre nos résultats et les données issues du dernier inventaire d’émissions locales, et en particulier la contribution des émissions liées à l’utilisation de solvant serait fortement surestimée dans l’inventaireThis work aims at characterizing Volatile Organic Compounds VOC sources and variability in two contrasted megacities (Paris and Beijing). This study based on an important experimental work, which includes instrumental optimization and participation in two intensive fields campaigns performed in May-June 2007 in Paris and in August 2007 in Beijing. Following qualitative analysis of the data sets and using a receptor model based on the PMF method, seven and ten sources of VOC were extracted for Paris and Beijing respectively. Traffic emissions are major VOC local/regional sources contributing to 54% and 35% of emissions in Paris and Beijing respectively. However, continental or regional emissions are also playing a significant role in the measured concentrations and so in the strength of VOC sources at sites receptors. Thus Paris is highly influenced by emissions from north-eastern Europe under anticyclonic condition, and Beijing by regional emissions from the Hebei province, in the south-east sector. Finally, identified sources and their contributions are compared to emission inventory data. For Paris, these results show significant differences with the local emission inventory, and suggest an overestimation of solvent emissions in the inventory
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Borgie, Mireille. "Étude des particules fines et ultrafines en suspension dans l'air au Liban : caractérisation physicochimique et évaluation des effets toxicologiques sur des cellules pulmonaires humaines BEAS-2B." Thesis, Littoral, 2014. http://www.theses.fr/2014DUNK0366/document.
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Les principaux objectifs de cette étude, une des premières menée au Liban, étaient d’acquérir une meilleure connaissance des caractéristiques physico-chimiques des particules atmosphériques fines (PF ou PM₂.₅₋₀.₃) et ultrafines (PUF ou PM₀.₃), et d’évaluer in vitro, leur potentiel toxique sur des cellules épithéliales bronchiques humaines (BEAS-2B). L’échantillonnage de PF et de PUF a été mené au Liban à la fois sur un site urbain (Sin El-Fil, du 18 mai au 2 sept. 2011) et un site rural (Beije, du 5 sept. au 28 oct. 2011). Les PF et les PUF ont fait l’objet d’une caractérisation physico-chimique par la détermination de leur composition en éléments et ions inorganiques, carbone total et composés organiques. Ensuite, des échantillons composites de PF et de PUF ont été préparés afin d’exposer les cellules BEAS-2B et évaluer les mécanismes toxiques sous-jacents. Nos résultats ont montré une influence des sources de combustion plus notable pour les particules collectées sur le site urbain, et cela par la présence de carbone total, de composés organiques, de métaux et d’ions inorganiques secondaires à des niveaux de concentration supérieurs à ceux rencontrés sur le site rural. D’autre part, une cytotoxicité plus prononcée a été provoquée par les PUF par comparaison aux PF. Les mécanismes de génotoxicité et de modifications épigénétiques que nous avons étudiés, à savoir l’activation métabolique des composés organiques, la modification de l’expression de trois microARNs, l’activation de la télomérase et l’induction de cassures au niveau de l’ADN, ont été induits par les deux échantillons de PF, avec un effet plus prononcé pour les particules d’origine urbaine. L’exposition des cellules BEAS-2B aux PF collectées, notamment celles d’origine urbaine, pourraient donc favoriser la transformation des cellules pulmonaires en cellules immortelles, et par conséquent, l’initiation ou la promotion de la cancérogenèse broncho-pulmonaireThe objectives of this study, one of the first conducted in Lebanon, were to acquire a better knowledge on the physico-chemical characteristics of atmospheric fine particles (FP or PM₂.₅₋₀.₃) and ultrafine ones (UFP or PM₀.₃), and to assess their potential toxicity. Particles were collected at two coastal sites between may and sept. 2011 at Sin El-Fil (urban site in Greater Beirut), and between sept. and oct. 2011 at Bejje (rural site). After sampling, FP and UFP were subjected to a physico-chemical characterization by quantifying their inorganic ions and elements, total carbon and organic compounds contents. Then, composite samples of FP and UFP were prepared in order to expose bronchial epithelial cells (BEAS-2B) in culture, and therefore to assess the underlying toxic mechanisms. Our results showed an influence of combustion sources especially for urban particles that are richer in total carbon, organic compounds, metals and secondary inorganic ions than rural ones. On the other hand, a more pronounced cytotoxicity was caused by UFP when compared to FP. In addition, epigenetic modifications and genotoxicity mechanisms, such as metabolic activation of organic compounds, changes in three microRNAs expression, telomerase activation and DNA breaks induction, which are potentially involved in the initiation and promotion of carcinogenesis, were induced by the two samples of FP, with a more pronounced effect of urban particles. Exposure of BEAS-2B cells to collected FP, especially urban ones, may therefore induce the transformation of lung cells to immortal cells, and consequently the initiation or the promotion of broncho-pulmonary carcinogenesis
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Fougère, Bertrand. "Influence de l'âge et du tabac sur les mécanismes génotoxiques et épigénétiques précoces de cancérogénèse broncho-pulmonaire en réponse à la pollution particulaire urbaine." Thesis, Littoral, 2014. http://www.theses.fr/2014DUNK0377/document.
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Récemment reconnus comme cancérogènes certains pour l'homme par l’IARC, la pollution atmosphérique et les particules fines (PM₂.₅) peuvent être inhalées et pourraient être retenues au niveau pulmonaire ou passer dans la circulation systémique. Ceci peut causer ou renforcer de nombreuses pathologies auxquelles les personnes âgées sont souvent plus sensibles. Cette thèse s’inscrit dans une démarche d’identification des processus impliqués dans la modulation du potentiel cancérogène des PM₂.₅, en lien avec l’âge ou le statut tabagique. Les particules ont été collectées à Dunkerque, agglomération présentant des influences maritimes mais également caractérisée par des activités industrielles et un trafic automobile importants. Pour évaluer l'influence de l'âge, des lymphocytes sanguins prélevés chez 90 patients issus de trois classes d'âge (25-30, 50-55 et 75-80 ans) ont été exposés ex vivo à des PM₂.₅ d’origine urbaine. Les lymphocytes isolés ont été exposés aux PM₂.₅ pendant 72 heures, avant de mesurer l'activité télomérase et la modulation d'expression de gènes tels que P16INK4A et MGMT. Les PM₂.₅ entraînent des variations de l'activité télomérase et de la longueur des télomères dans toutes les tranches d'âge indifféremment. L’expression du gène P16INK4A est significativement augmentée avec l'âge après exposition aux PM₂.₅. L'âge augmenterait l'expression du gène MGMT après exposition aux particules, en diminuant le niveau de méthylation de son promoteur uniquement dans le groupe des patients les plus âgés. Concernant le rôle du statut tabagique, 26 lavages broncho-alvéolaires ont été réalisés chez des patients fumeurs et non-fumeurs. Les macrophages issus de ces prélèvements ont été mis en culture avec des cellules épithéliales bronchiques BEAS-2B, avant exposition aux PM₂.₅ (3 et 15 µg/cm², 72 h). L’activité télomérase et la longueur des télomères varient après exposition aux PM2.5 et le statut tabagique modifie ces paramètres dans les cellules BEAS-2B et les macrophages alvéolaires. La méthylation des promoteurs et l’expression des gènes P16INK4A et MGMT ne sont pas modifiées dans les cellules BEAS-2B, alors que dans les macrophages alvéolaires les particules induisent l’expression de ces gènes par une diminution de la méthylation de leurs promoteurs. Le statut tabagique fumeur semble au contraire accroître la méthylation et limite l’expression de ces deux gènes. En conclusion, il apparaît que l’échantillon de PM₂.₅ étudié peut induire ex vivo plusieurs lésions décrites dans les étapes d’initiation et de promotion de la cancérogenèse broncho-pulmonaire. L’âge et le tabagisme sont susceptibles de moduler les effets toxiques des particules. Alors que les symptômes du cancer du poumon apparaissent seulement à une étape avancée de la maladie, nos résultats pourraient aider à la découverte de nouveaux marqueurs de diagnostic précoce permettant ainsi d’améliorer la survieRecently recognized as carcinogenic to human by IARC, air pollution and fine particulate matter (PM₂.₅) can be inhaled and could be retained into the lung or reach the systemic circulation. This can cause or worsen many diseases for which the elderly are often more sensitive. The PhD objective corresponds to the identification of the mechanisms of action involved in the modulation of carcinogenic potential of PM₂.₅, in connection with age or smoking status. PM₂.₅ were collected in Dunkerque, a French seaside city characterized by important industrial activities and heavy motor vehicle traffic. In order to estimate the influence of age, blood lymphocytes sampled from 90 patients from age classes (25-30, 50-55 and 75-80 years old) were ex vivo exposed to PM₂.₅ during 72 hours, before evaluation of telomerase activity and gene expression modulation of P16INK4A and MGMT. PM₂.₅ modulated telomerase activity and telomeres length in all age groups without any influence of age. P16INK4A gene expression increased significantly with age after exposure to PM₂.₅. Age could enhance MGMT gene expression after exposure to particles by decreasing the level of promoter methylation in the oldest group. Regarding the role of smoking status, 26 broncho-alveolar lavage were performed in smoker and non-smoker people. Macrophages were cultured with bronchial epithelial BEAS-2B cells before PM₂.₅ exposure (3 or 15µg/cm²; 72h). The telomerase activity and telomere length vary after exposure and the tobacco modify these parameters in BEAS-2B cells and alveolar macrophages. Methylation of P16INK4A and MGMT genes promoters and their expression are not modified in BEAS-2B cells. In alveolar macrophages, particles lead to a decrease of methylation of P16INK4A gene promoter. The smoking status seems also to increase methylation and to down-regulate expression of these two genes. In conclusion, it seems that the studied PM₂.₅ sample can induce ex vivo modifications described in the initiation and promotion of lung carcinogenesis. The age and smoking status may modulate the toxic effects of particles. Since lung cancer symptoms appear only at an advanced stage, our results could help in proposing new biomarkers of carcinogenesis allowing an early diagnosis to improve survival
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Lepers, Capucine. "Pollution atmosphérique de proximité et toxicité respiratoire : recherche in vitro des mécanismes d'action toxique induits par des aérosols atmosphériques particulaires (PM₂.₅) industriels, urbains et ruraux." Thesis, Littoral, 2013. http://www.theses.fr/2013DUNK0352/document.
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Les particules fines (PM₂.₅) présentes dans l'air extérieur peuvent être inhalées puis retenues au niveau pulmonaire, conduisant à l'apparition ou à l'aggravation de différentes pathologies cardio-respiratoires. La composition complexe des PM₂.₅ rend d'autant plus difficile l'étude de leurs mécanismes d'action. Cette thèse s'inscrit donc dans une démarche d'identification des processus impliqués dans un éventuel potentiel cancérigène des PM₂.₅, en lien avec leur composition chimique. Nous avons étudié la toxicité de six échantillons de PM₂.₅, collectés sous influence industrielle, urbaine ou rurale au cours des saisons printemps-été 2008 et automne-hiver 2008-2009. L'étude de la fraction biologique a révélé la diversité et la richesse des particules en contaminants fongiques et bactériens. Le test d'Ames nous a permis de mettre en évidence une forte mutagénicité des PM₂.₅, vraisemblablement liée aux composés nitro-aromatiques. Sur la base de tests de cytotoxicité préalables, nous avons étudié l'effet de 3,75 et 15 µg/cm² de particules sur la lignée de cellules épithéliales bronchiques humaines BEAS-2B. Nous avons mis en évidence une induction génique de différents enzymes impliquées dans l'activation métabolique des hydrocarbures aromatiques polycycliques, associée à une augmentation d'activité catalytique. Cette induction semble conduire à la formation d'adduits encombrants à l'ADN. De plus, les PM₂.₅ induisent des cassures simple- et double-brin de l'ADN, la formation de micronoyaux, ainsi que des perturbations de l'activité télomérase. Ces effets génotoxiques sont associés à des altérations épigénétiques que sont une hyperméthylation du promoteur de P16ᴵᴺᴷ⁴ᴬ, des modifications post-traductionnelles de l'histone 3 et des changements dans l'expression des miRNA étudiés. Considérant l'influence de la composition des PM₂.₅, les composés organiques semblent être responsables des effets génotoxiques les plus importants, alors que les métaux paraissent avoir des effets épigénétiques supérieurs. En conclusion, il apparaît que les échantillons de PM₂.₅ étudiés, de par l'action conjointe de leurs fractions organique et inorganique, sont susceptibles d'induire in vitro de multiples lésions décrites dans les étapesd'initiation et de promotion de la cancérogénèse broncho-pulmonaireFine airborne particulate matter (PM₂.₅) can be inhaled and retained in deep lung for long periods, leading to onset or exacerbation of cardio-respiratory diseases. However, the complex composition of PM₂.₅ makes difficult the study of their mechanisms of action. This work fits into a global approach aiming to identify the toxicity mechanisms involved in a putative PM₂.₅ carcinogenicity, in association with PM composition. We study six PM samples collected either under industrial, urban or rural area, in spring-summer 2008 or autumn-winter 2008-2009 seasons. Biological fraction analysis revealed numerous and diverse bacterial and fungal components. We carried out Ames tests revealing a high mutagenic potency for PM samples, presumably linked to their nitro-aromatic content. Based on previous cytotoxicity assays, we studied PM effect on bronchial epithelial cell line BEAS-2B, at two concentrations (3.75 and 15µg/cm²). We demonstrated gene induction of several xenobiotic metabolizing enzymes involved in polycyclic aromatic hydrocarbons metabolic activation. This was associated with an increase in their catalytic activity, leading to bulky DNA-adducts formation in exposed cells. Furthermore, PM₂.₅ lead to DNA single- and double-strand breaks, micronuclei formation, and disturbed telomerase activity. In addition to these genotoxic effects, our study revealed epigenetic alterations such as P16ᴵᴺᴷ⁴ᴬ promoter hypermehylation, histone 3 post-translational modifications, and miRNAs expression changes. Considering the impact of chemical composition on PM toxicity, organic compounds lead to the highest genotoxicity, whereas metals seem to induce more pronounced epigenetic modifications. Altogether, our results indicate that the studied PM₂.₅ samples, through cooperative action of organic and inorganic fractions, may lead in vitro to multiple alterations involved in initiation and promotion steps toward pulmonary carcinogenesis
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Ly, Hamidou. "De New York à Dakar : pour une approche critique et méthodologique de la justice environnementale." Thesis, Paris 8, 2016. http://www.theses.fr/2016PA080089.
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Le thème des inégalités et ses corollaires, telles la pauvreté, la précarité, l’exclusion ou encore la ségrégation, se posent de plus en plus d’un point de vue de la justice et concerne à la fois les enjeux spatiaux et environnementaux. Comme pour marquer le paroxysme des inégalités, la question de la justice environnementale vient relancer le débat autour de l’accès aux ressources au sein des catégories sociales et spatiales, ainsi que le débat autour de l’inégale répartition et répercussion des externalités, causées entre autres par l’usage de ces dernières d’un point de vue environnemental.De New York à Dakar, malgré les différences de contextes socio-culturels et économiques, les mêmes phénomènes d’inégalités face aux conditions environnementales s’observent avec cependant des nuances dans les formes de manifestations et d’interprétations.Ce travail vise à réfléchir sur les déclinaisons que peuvent avoir les injustices environnementales dans la ville de Dakar à partir d’une approche élaborée dans les villes américaines, berceau des mouvements de revendications. Deux localités situées dans la baie de Hann sont choisies en raison des pollutions industrielles dont elles souffrent. Il s’agit de Hann-Bel-Air et de Thiaroye-Sur-mer.Partant de l’analyse des nuisances environnementales liées à la pollution industrielle, il s’agit de montrer l’importance de la « contextualisation » dans l’étude des injustices environnementales au regard des dynamiques socio-spatiales, mais aussi des perceptions face aux situations dites d’injusticeThe theme of inequality and its corollaries, such as poverty, insecurity, exclusion or segregation, comes more and more from a perspective of justice and concern at the same time the spatial and environmental issues. As to mark the paroxysm of inequalities, the issue of environmental justice comes revive the debate over access to resources within the social and spatial categories, as well as the debate about the unequal distribution and impact of externalities caused by the use of these resources from an environmental point of view.From New York to Dakar, despite the differences in socio-cultural and economic contexts, the same phenomena of inequality to environmental conditions are observed with some differences in the forms of manifestations and interpretations. This work aims to reflect on the variations that can have these phenomena of environmental injustice in the city of Dakar from an approach developed in American cities, the cradle of the protest movements. This work aims to reflect on the variations that can have these phenomena of environmental injustice in the city of Dakar from an approach developed in American cities, the cradle of the protest movements.Thus, based on the analysis of environmental pollution linked to industrial pollution, it is to show the importance of "contextualization" in the study of environmental injustice in terms of socio-spatial dynamics but also perceptions of the said situations of injustice
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Al, Zallouha Margueritta. "Étude prospective pilote des effets d'une exposition ex vivo de lymphocytes T humains à la pollution atmosphérique particulaire : recherche de biomarqueurs et influence de l'âge." Thesis, Littoral, 2017. http://www.theses.fr/2017DUNK0472/document.
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Les particules fines atmosphériques (PF) sont capables de pénétrer dans les poumons où certains composés transportés peuvent interagir avec les cellules pulmonaires et atteindre la circulation sanguine. L'exposition aux PF affecte particulièrement les populations sensibles telles que les personnes agées. Cette thèse s'inscrit dans une démarche d'identification des effets des PF sur les lymphocytes T humains (LT) tout en visant à déterminer des biomarqueurs liés à l'exposition et à évaluer la variation de la réponse cellulaire en fonction de l'âge. Des LT ont été isolés de prélèvements sanguins de 91 volontaires appartenant à trois classes d'age (20-30, 45-55, 70-85 ans) puis exposés ex vivo pendant 72h à 45 µg/µl de PF collectées à Dunkerque. Les étapes d'isolement, purification et activation des LT ont d'abord été optimisées. Suite à la caractérisation de la population échantillonnée, une population d'étude homogène a été sélectionnée ( 10 sujets / classe d'âge). Nous avons mis en évidence une induction génique d'enzymes impliquées dans l'activation métabolique des HAP identifiés dans l'échantillon de PF. La caractérisation du profil des Lt a permis de proposer un profil mixte Th1/Th2 causé par l'exposition. L'étude transcriptomique des miARN a mis en évidence une surexpression de miR-124-3p impliqué dans la régulation de plusieurs fonctions au niveau du système immunitaire et de miR-1290 impliqué dans plusieurs types de cancer. Quant à l'influence de l'âge, une surexpression des gènes codant pour les enzymes antioxydantes (NQO1 et HMOX1), une augmentation de la concentration des cytokines (IL-4 et IL-13) ainsi qu'une modification du profil d'expression de certains miARN ont été notées chez les sujets les plus âgésAtmospheric fine particulate matter (FP) are able to enter the lungs where some compounds can interact with lung cells and reach the bloodstream . Exposure to FP affects in particular susceptible populations such as the elderly. This thesis is part of a project aiming to identify the effects of FP on human T lymphocytes (LT) while attempting to determine biomarkers related to exposure and to evaluate the variation of the cellular response as a function of age. LT were isolated from blood samples of 91 volunteers belonging to three age groups (20-30, 45-55, 70-85 years) then exposed ex vivo for 72h to 45 µg/µl of FP collected in Dunkirk. The steps of isolation, purification and activation of LT were first optimized. Following the characterization of the sampled population, a homogeneous study population was selected (10 subjects/age class). We have demonstrated an induction of the genes coding for the enzymes involved in the metabolic activation of PAH identified in the PF sample. Characterization of the LT profile made it possible to propose a mixed th1/th2 profile cause by the exposure. Teh transcriptomic study of miRNAs revealed an overexpression of miR-124-3p involved in the regulation of several functions in the immune system and miR-1290 involved in several types of cancer. As for the influence of age, overexpression of the genes coding for the antioxidant enzymes (NQO1 and HMOX1), an increase in the concentration of cytokines (IL-4 and IL-13) as well as a modification of the expression profile of some miRNAs were noted on the elderly
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Barnhisel, Taylor. "Carbaryl Exposure to Danio rerio Leads to Activation of the Aryl Hydrocarbon Receptor Pathway." Wittenberg University Honors Theses / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=wuhonors1617979942441695.
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Peiffer, Julie. "Étude de la neurotoxicité d’un Polluant Organique Persistant chez le rat : effets à court et à long terme de l’inhalation répétée de fluorène sur le développement sensori-moteur du jeune et le comportement à l’âge adulte." Thesis, Vandoeuvre-les-Nancy, INPL, 2011. http://www.theses.fr/2011INPL103N/document.
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La pollution atmosphérique est omniprésente du fait de nombreuses sources émettrices de composés chimiques. Dans ce contexte, les Hydrocarbures Aromatiques Polycycliques (HAP) sont largement diffusés dans l’air et ont déjà montré des effets délétères sur la santé.Ce travail a consisté en l’évaluation de la neurotoxicité du fluorène, composé choisi comme molécule représentative de la pollution liée aux HAP, chez le rat adulte exposé par voie i.p., par voie orale ou par inhalation. Le modèle d’exposition par inhalation a ensuite été appliqué à l’étude des effets du polluant sur le développement sensori-moteur et l’activité comportementale de l’animal exposé in utero ou au cours de la lactation.Ces études ont montré que le fluorène était susceptible d’affecter le niveau d’anxiété et l’activité locomotrice du rat adulte exposé directement et indirectement au polluant, et n’avait aucun effet sur les capacités d’apprentissage. En revanche, aucune atteinte majeure de la maturation des fonctions sensori-motrices n’a été mise en évidence. L’analyse de la présence du composé et de trois de ses métabolites a par ailleurs montré que le polluant était capable de traverser la barrière hémato-encéphalique et d’être métabolisé au niveau du cerveau. Les réponses physiologiques et comportementales étant variables entre les études, les effets induits par le fluorène dépendent donc de la voie d’entrée, du niveau de contamination et du moment d’exposition.Ces résultats ont ainsi révélé chez l’animal la toxicité comportementale du fluorène à des niveaux de contamination réalistes, confirmant ainsi le risque sanitaire de l’exposition aux HAP tout au long de la vie des individusActually air pollution is ubiquitous due to the emission of chemical compound from many sources. In this context, Polycyclic Aromaric Hydrocarbons (PAH)related compounds are widely distributed in the air and have shown deleterious health effects.Fluorene was chosen as a representative compound of PAHs pollution. This work consisted in the evaluation of its neurotoxic effects in adult animals, exposed i.p., orally or by exposure nose-only. The inhalation model of exposure was then applied to the study of its effects on sensorimotor development and on behavioral activity of animals exposed in utero or during lactation.The results showed that fluorene is able to induce behavioral changes in adult animals exposed directly or indirectly on the level of anxiety and the locomotor activity, whereas no effect on learning and memory abilities has been observed. However, no defect on the development of motor and sensory functions was demonstrated. Furthermore, the analysis of the presence of the compound and three of its metabolites showed that the pollutant was able to cross the blood brain barrier and can be metabolized in the brain. Moreover, variations have been observed concerning behavioral and physiological responses between studies, showing that effects induced by fluorene are dependent on the way of administration, the level of contamination and the time of exposure.In conclusion, these results demonstrate in animals the behavioral toxicity of fluorene at levels of contamination corresponding to human cases of exposure, confirming so the risk of PAH exposure throughout life
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Bandaly, Victor. "Etude de la persistance de virus sur les filtres des centrales de traitement d'air : influence des paramètres de procédé et impact sur la santé." Thesis, Rennes 1, 2017. http://www.theses.fr/2017REN1B038/document.
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La pollution de l'air est l'un des principaux problèmes de santé publique de notre siècle et surtout de l'air intérieur alors que nous passons environ 90% de notre temps dans des environnements fermés. Parmi les polluants les bioaérosols ont été peu étudiés. Cependant des études épidémiologiques ont déjà montré une relation entre les bioaérosols et la santé. Le but de cette thèse est d’étudier les virus respiratoires dans les milieux clos via les systèmes de ventilation. A l’issue d’un état de l’art des polluants de l’air, il est important de définir ceux nécessitant d’être traités, les systèmes de ventilation, les procédés de filtration par médias fibreux et les procédés de traitement pouvant être mis en oeuvre. Les effets des bioaérosols viraux dans les environnements intérieurs sur la santé publique ont été discutés dans une revue bibliographique. Une méthodologie a été mise en oeuvre pour étudier le comportement des virus dans une centrale de traitement de l’air (CTA). Les virus respiratoires, mengovirus (virus nu à ARN de la même famille que les rhinovirus responsables du rhume) et adénovirus (virus respiratoire nu à ADN), ont été choisis et étudiés dans un système expérimental miniature représentatif des systèmes de traitement d’air. La performance de filtration d’un filtre de CTA vis-à-vis des aérosols viraux a été évaluée avec une validation du système expérimental utilisé. Cette étude a montré la capacité des virus de passer à travers le filtre tout en restant infectieux. Peu de littérature existant sur le sujet, ce projet a permis d’ajouter de nouvelles données pertinentes quant à la persistance des virus respiratoires dans l’air intérieur et plus précisément au niveau des filtres dans les centrales de traitement d’airAir pollution is one of the major public health problems of our century and especially of indoor air as we spend about 90% of our time in closed environments. Among pollutants bioaerosols have been poorly studied. However, epidemiological studies have already shown a relationship between bioaerosols and human health. The aim of this PhD work is to learn about respiratory viruses in closed environments via ventilation systems in order to study indoor air quality. At the end of state of the art of air pollutants, it is important to define those present in the air that need to be treated, ventilation systems, filtration processes by fibrous media and the processing methods being able to be implemented. The effects of viral bioaerosols on public health in indoor environments were discussed and drafted in a bibliographic review. The methodology of the study was to assess the fate of respiratory viruses, mengoviruses and adenoviruses, in a miniature experimental system similar to air treatment systems used in closed environments. The experimental system used was validated and the filter performance against viral aerosols was investigated. This study presented originality for the characterization and the fate of two non-enveloped respiratory viruses, mengovirus (RNA) and adenovirus (DNA), in indoor environments and their fate on fiber glass filter. This study showed the ability of viruses to pass through the filter and to remain infectious upstream and downstream the filter. There is scarce literature on this subject, and this project allowed us to add new relevant data on the persistence of respiratory viruses in indoor air and more precisely at the level of filters in air handling units
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Cassien, Mathieu. "Etudes in vitro/in vivo de la toxicité de polluants atmosphériques. Implication du stress oxydant dans les mécanismes génotoxiques et sur la variation des paramètres biochimiques." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM4703.
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La pollution atmosphérique particulaire représente un facteur de risque potentiel même à de faibles concentrations. Quelle que soit leur composition, les nanoparticules (NP) sont parmi les plus nocives en raison de leur capacité à atteindre profondément les tissus pulmonaires, la circulation sanguine et les organes. Notre travail constitue une base solide dans la compréhension des effets induits par une sélection de polluants atmosphériques représentatifs, utilisés dans un contexte environnemental réaliste. Nos résultats in vitro fournissent l'évidence d'un effet génotoxique à dominance clastogène lors de l’exposition de cellules à des NP contenant du CeO2, qui d’une part exercent une action mécanique sur le noyau, et d’autre part stimulent la production de O2•- / H2O2 via la NADPH oxydase et la mitochondrie, favorisant la production d’HO•. En présence de 1-Nitropyrène, on observe selon la dose utilisée deux mécanismes génotoxiques successifs, passant d'une dominance aneugène à clastogène, cet effet étant relié à une surproduction de HO• détectable par RPE. L'étude in vivo chez le rat a mis en œuvre un système de génération d'aérosols de NP contenant des pesticides, réalisant une exposition quotidienne et chronique à de faibles doses. Un effet direct sur la fonction hémodynamique myocardique reflétant l'apparition de dommages cellulaires irréversibles a été observée, ainsi que des lésions rénales, hépatiques, et l'installation d'un stress oxydant et d’une inflammation systémiques. Sur le long terme, l'effet des NP modifie les profils lipidiques et favorise la survenue d’une intolérance au glucose. Des modes d'action spécifiques à chaque pesticide employé ont été proposésEpidemiological studies have consistently reported that particulate matter in ambient air pollution is associated with increases in cardiopulmonary diseases and mortality. Because they can deeply penetrate lung tissue, reaching blood stream and organs, nanoparticles (NPs) are considered particularly harmful. Here, our foray into the specific mutagenicity and cytotoxicity of NPs focused on manufactured nano-CeO2 (a fuel additive) and NPs known to form in air from a variety of atmospheric toxicants (eg, combustion residues, pesticides). We first revealed a genotoxic effect of nanoCeO2 on human fibroblasts by a clastogenic mechanism following stimulation of the release of O2•-/H2O2 by NADPH oxidase and mitochondria. However, upon exposure of these cells to nM doses of 1-nitropyrene (a combustion byproduct) promotion of DNA damage involving an aneugenic mechanism occurred before a clastogenic effect was seen at µM doses. Second, using a home-made chamber equipped with an aerosol generator, we determined indices of oxidative stress and tissue damage in rats chronically inhaling toxicant NPs for 1-5 months at environmentally relevant doses. Long term exposure, even at low NPs doses, provoked systemic oxidative stress, lipid peroxidation, kidney damage, liver dysfunction, changes in lipid profile and occurrence of disorders of glucose tolerance. Moreover, a strong impairment of hemodynamic performance was evidenced in hearts from NP-exposed rats. By extending literature data of the in vitro toxicity of NPs to the in vivo situation, our study incriminates the nano-sized components of atmospheric particulate matter as a privileged vector of genotoxicity and cardiotoxicity
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Melki, Pamela. "Health impact of airborne particulate matter in Northern Lebanon : from a pilot epidemiological study to physico-chemical characterization and toxicological effects assessment." Thesis, Littoral, 2017. http://www.theses.fr/2017DUNK0444/document.
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L'exposition à la pollution atmosphérique, notamment aux particules fines (PM₂.₅), représente un risque majeur pour la santé dans le monde entier, et d'autant plus dans les pays en développement.Le Nord du Liban est ainsi affecté par plusieurs sources de pollution d'origine anthropique, urbaine et industrielle. Pourtant, dans cette région, aucune étude ne s'est intéressée à l'impact des PM₂.₅ sur la santé publique. Il faut également souligner que les mécanismes de toxicité des PM₂.₅ ne sont pas totalement identifiés. Le but de ce travail est d'étudier la nature et l'impact sanitaire de la pollution atmosphérique particulaire dans le Nord du Liban. Nous avons procédé à une enquête épidémiologique, et prélevé des particules fines que nous avons caractérisées sur les plans physico-chimiques et toxicologiques. Deux régions ont été considérées dont une est située à proximité d'activités industrielles. L'étude épidémiologique et de perception menée dans les deux zones du Nord du Liban (310 questionnaires/zone traitée), a montré une relation entre gêne, maladies respiratoires et proximité des industries. Cette enquête a ainsi confirmé l'intérêt de mener une étude toxicologique dans cette région. Afin de renforcer les connaissances sur la toxicité pulmonaire des aérosols atmosphériques particulaires avec une attention toute particulière portée à l'étude de certains des mécanismes d'action suspectés d'être impliqués dans la cancérogénécité, les caractéristiques physico-chimiques et toxicologiques des particules fines (PM₂.₅₋₀.₃) prélevées sur les deux sites ont été étudiées. Les particules collectées ont montré une composition similaire sur les deux sites concernant les espèces majeures. La contribution des activités industrielles a été mise en évidence par des teneurs légèrement plus élevées de certains éléments traces, d'HAP et surtout par une teneur jusqu'à 100 fois plus élevée en dioxines. Nos résultats ont mis en évidence l'influence de nombreuses sources de combustion (diesel, essence, charbon et biomasse) ; la combustion de déchets et d'autres procédés industriels sont également suspectées. Un potentiel génotoxique et mutagène plus prononcé a été mis en évidence pour les particules collectées sur le site sous influence industrielle par rapport aux particules provenant du site sous influence rurale, à l'aide du test d'Ames en milieur liquide et le SOS chromotest. Les effets observés sont très probablement influencés par la fraction organique des particules. Afin d'approfondir la recherche des mécanismes génotoxiques des PM, des cellules bronchiques humaines (BEAS-2B) ont été exposées à différentes concentrations de particules. Les mécanismes de toxicité, tels que l'activation métabolique des HAP(CYP1A1) et les cassures double-brins (quantification de yH2AX par cytométrie de flux et in-cell western), ont été induits par les deux échantillons de PM₂.₅₋₀.₃ avec un effet plus prononcé pour les particules industrielles. Par ailleurs, les PM ont montré une tendance à perturber le fonctionnement du système de réparation de l'ADN (par l'expression des gènes OGG1, NTH1, APE1, NUDT1, DNMT1, MGMT, XPA et XRRC1, et l'expression des protéines PARP1, DNMT1 et OGG1). Les mécanismes de réparation des dommages de l'ADN ont ainsi été réprimés jusqu'à 48h d'exposition aux PM, notamment aux PM₂.₅₋₀.₃ collectées sous influence industrielle, et réactivés après 72h d'exposition. Ces dommages concernent les adduits encombrants à l'ADN, et ceux causés par le stress oxydant, des cassures des brins d'ADN et la méthylation. Nos résultats suggèrent des mécanismes d'action mutagènes, génotoxiques et épigénétiques impliqués dans la cancérogénécité des particules fines, en partie liés à la composition de la fraction organiqueExposure to air pollution, especially fine particulate matter (PM₂.₅), remains a major health risk, mainly in the developing countries. Northern Lebanon is affected by several sources of anthropogenic, urban and industrial pollution. However, no studies have examined the impact of PM₂.₅ on public health in this region. In addition, it should be noted that the toxicity mechanisms of PM₂.₅ are not fully identified. The aim of this work is to study the composition and the health impact of the atmospheric particulates in Northern Lebanon. An epidemiological survey was performed and fine particles were extracted and characterized physico-chemically and toxicologically. This study was conducted in two sites, one of which is influenced by industrial activities. Perception and epidemiological survet, conducted in two areas in Northern Lebanon, rural and industrial (310 treatable questionnaires/area), showed a relationship between annoyance, respiratory diseases and living in proximity to industrial activities. Moreover, results confirmed the interest in conducting a toxicological study in this region. Hence, to contribute to fulfill the gap of knowledge about the pulmonary toxicity of particulate matter and the mechanisms of action involved in the carcinogenicity, the study of physicochemical characteristics and toxicological endpoints of PM₂.₅₋₀.₃ from both sites were performed. Physicochemical analyses of the collected particles evidenced similar characteristics in major species. In particular, we have shown slightly higher levels of PAHs and trace metals and up to 100 times higher dioxins concentrations at the vicinity of industries. Our results evidenced the influence of numerous combustion sources (diesel, gasoline, coal and biomass burning) ; waste combustion and other industrial processes are also suspected. A more pronounced genotoxic and mutagenic potential was evidenced after exposure to particles collected at the vicinity of industries when compared to the rural ones, using the Ames fluctuation test and SOS chromotest. The effects of the collected particles are probably related to their organic composition. In order to assess the underlying toxic mechanisms, human bronchial epithelial cells (BEAS-2B) were then exposed to different concentrations of the sampled PM₂.₅₋₀.₃. Genotoxicity mechanisms such as metabolic activation of organic compounds (CYP1A1) and consecutive DNA damages such as DNA strands breaks (yH2AX quantification by flow cytometry analysis and in-cell western assay) were induced by the two samples of PM₂.₅₋₀.₃ , with a more pronounced effect of industrial particles. Moreover, PM showed tendency to alter the DNA repair process (OGGI, NTH1, APE1, NUDT1, DNMT1, MGMT, XPA, XRRC1 gene expression and PARP1, DNMT1, OGG1 proteins expression). DNA repair mechanisms were repressed up to 48h of exposure to PM especially to the industrial influenced PM₂.₅₋₀.₃ and reactivated after 72h of exposure. The DNA damages involve bulky DNA adducts, oxidative stress damages, DNA strand breaks and methylation. These results suggest mutagenic, genotoxic and epigenetic mechanisms of action involved in the carcinogenicity of fine particles, partly related to their organic composition
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Gaudreau, Jennifer A. "Traffic Related Air Pollution and Lung Function in Bilateral Lung Transplant Patients." 2018. https://scholarworks.umass.edu/masters_theses_2/643.
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Scharber, Helen. "Three essays on racial disparities in infant health and air pollution exposure." 2011. https://scholarworks.umass.edu/dissertations/AAI3482725.
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This three-essay dissertation examines racial disparities in infant health outcomes and exposure to air pollution in Texas. It also asks whether the EPA's Risk-Screening Environmental Indicators Geographic Microdata (RSEI-GM) might be used to assess the effects of little-studied toxic air pollutants on infant health outcomes. Chapter 1 contributes to the “weathering” literature, which has shown that disparities in infant health outcomes between non-Hispanic black and non-Hispanic white women tend to widen with age. In this study, we ask whether the same patterns are observed in Texas and among Hispanic women, since other studies have focused on black and white women from other regions. We find that black and Hispanic women in Texas do “weather” earlier than white mothers with respect to rates of low birthweight and preterm birth. This differential weathering appears to be mediated by racial disparities in the distribution and response to socioeconomic risk factors, though a large gap between black and white mothers across all ages remains unexplained. Chapter 2 extends the statistical environmental justice literature by examining the distribution of toxic air pollution across infants in Texas. We find that, within Texas cities, being black or Hispanic is a significant predictor of how much pollution one is exposed to at birth. We further find that, among mothers who move between births, white mothers tend to move to significantly cleaner areas than black or Hispanic mothers. In Chapter 3, we use geocoded birth records matched to square-kilometer pollution concentration estimates from the RSEI-GM to ask whether the pollution-outcome relationships that emerge through regression analysis are similar to the effects found in previous research. If so, the RSEI-GM might be used to study the health effects of nearly 600 chemicals tracked in that dataset. We conclude, based on instability of results across various specifications and lack of correspondence to previous results, that the merged birth record-RSEI data are not appropriate for statistical epidemiology research.
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"A comparison of particulate matter (PM101) in industrially exposed and non exposed communities." Thesis, 2008. http://hdl.handle.net/10413/556.
Full textAbstract:
BACKGROUND For many years, the Durban south community has raised concerns about ambient air pollution including particulate matter. The Durban South Industrial Basin (DSIB) may be high risk for exposure to significant levels ofPMI0 due to its geographic relationship with two major petroleum refineries, together with a pulp and paper manufacturing facility. While potential sources of elevated levels of PMlOin the south are industrial, the north is likely to be exposed to controlled burning of vacant fields and use ofbiomass fuels, particularly in informal settlements. Adverse health effects from particulate matter (PM) were well documented by extensive epidemiological observations by animal and human studies, following laboratory exposures. Studies across a variety of environmental settings have demonstrated a strong association between ambient air particulate matter (PMlO) and cardiopulmonary morbidity and mortality. Studies have reported that particulate matter is associated with adverse health effects resulting from inflammatory responses in the lower respiratory tract. Exposure to particulate matter may increase the risk of lung cancer. Some studies suggested that small temporal increases in ambient particulate matter are sufficient to cause health impacts. Other studies attributed strong seasonality to temperature inversions associated with temperature changes. Studies also illustrated the impact of temporal variation on PMl 0 levels across regions. OBJECTIVES The main objectives of this study were to determine and compare the levels of ambient PMIO in industry exposed and non-industry exposed communities, to determine temporal variation and to make recommendations. METHODS This study focused on determining the 24-hour ambient PMI0 levels in the Durban south community. The PMIO levels in Durban south (industry exposed) were compared with the PM10 levels in an area north of Durban (non-industry exposed). Relevant data obtained from the monitoring program of the South Durban Health Study (SDHS) was reviewed for the purposes of this study. The different techniques used to measure PMI0 are gravimetric sampling and tapered elemental oscillating microbalance (TEaM). Both methods were used to collect PMI0 data. The data comprised of quantitative and categorical variables. The dependent variable was the PM10 values and the independent variable was the sampling sites. Non-parametric tests were used to analyse the data. RESULTS PMI0 was recorded in all sites in north and south areas. The levels varied across all sites. Both the north and south areas recorded high PMI0 values at regular intervals. No particular trend was observed when the 24 hour PM10 concentration was compared against the standard. All sites recorded medians that were generally in the region of 40-S0,ug/m3. The site with the highest median (SIA,ug/m3 ) was Assegai. Briardale recorded the lowest median (34.9,ug/m3 ). Exceedances of the South African National Standard code 1929 maximum 24-hour concentrations of7S,ug/m3 were observed across all sites. Overall there were 163 (16.7 % of all samples) exceedances, and these ranged widely between the various sites, with no particular regional trend. Overall .June experienced the highest PMl 0 values. No differences in seasonal trends were observed in north and south. CONCLUSION On average the levels ofPMI0 do not exceed national or international standards. The findings did not reveal any statistical difference in exposure levels between the industry exposed and non-industry exposed areas.Thesis (MMed.)-University of KwaZulu-Natal, Durban, 2008.
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"Measurement and health risk assessment of volatile organic air pollution in fenceline and control communities in south Louisiana." Tulane University, 2004.
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Smith, Nadia. "Air quality monitoring with polar-orbiting hyperspectral infrared sounders : a fast retrieval scheme for carbon monoxide." Thesis, 2014. http://hdl.handle.net/10210/12282.
Full textAbstract:
D.Phil. (Geography)The Infrared Atmospheric Sounding Interferometer (lASI), operational in polar-orbit since 2006 on the European MetOp-A satellite, is the most advanced of its kind in space. It has been designed to provide soundings of the troposphere and lower stratosphere at nadir in a spectral interval of 0.25 em" across the range 645-2 760 em". Fine spectral sampling such as this is imperative in the sounding of trace gases. Since its launch, the routine retrievals of greenhouse, species from IASI measurements have made a valuable contribution to atmospheric chemistry studies at a global scale. The main contribution of this thesis is the development of a new trace gas retrieval scheme for IASI measurements. The goal was to improve on the global operational scheme in terms of the algorithm complexity, speed of calculation and spatial resolution achieved in the final solution. This schemedirectly retrieves column integrated trace gas densities at single field-of-view (FOV) from IASI measurements within a 10% accuracy limit. The scheme is built on the Bayesian framework of probability and based on the assumption that the inversion of total column values, as apposed to gas profiles, is a near-linear problem. Performance of the retrieval scheme is demonstrated on simulated noisy measurements for carbon monoxide (CO). Being a linear solution, the scheme is'highly dependent on the accuracy of the a priori. A statistical estimate of the a priori was computed using a principal component regression analysis with 50 eigenvectors. The corresponding root-mean-square (RMS) error of the a priori was calculated to be 9.3%. In general terms, the physical retrieval improved on the a priori, and sensitivity studies were performed to demonstrate the accuracy and stability of the retrieval scheme under a numberof perturbations. A full system characterization and error analysis is additionally preformed to elicidate the nature of this complex problem. The hyperspectral IASI measurements introduce a significant correlation error in the retrieval. The Absorption Line Cluster (ALC) channel selection method was developed in this thesis, to address the correlation error explicitly. When a first neighbour correlation factor of 0.71 is assumed in the measurement error covariance for the clusters of ALC channels, then most of the correlation error is removed in the retrieval. In conclusion, the total column trace gas retrieval scheme developed here is fast, simple, intuitive, transparent and robust. These characteristics together make it highly suitable for implementation in an operational environment intended for air quality monitoring on a regional scale.
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"In vitro cytotoxicity of metal ions and roadside dust collected in Hong Kong." 2002. http://library.cuhk.edu.hk/record=b5895982.
Full textAbstract:
Lau Wing-Ngar Vivian.Thesis (M.Phil.)--Chinese University of Hong Kong, 2002.
Includes bibliographical references (leaves 135-144).
Abstracts in English and Chinese.
Acknowledgements --- p.i
Abstract --- p.ii
Abbreviations --- p.vi
List of figures --- p.viii
List of tables --- p.xi
Contents --- p.xiii
Chapter 1 --- Introduction --- p.1
Chapter 1.1 --- General introduction --- p.1
Chapter 1.2 --- Roadside air pollution worldwide and in Hong Kong --- p.2
Chapter 1.2.1 --- Air quality in Hong Kong --- p.3
Chapter 1.3 --- Characteristics of particulate matter --- p.9
Chapter 1.4 --- Composition and sources of particulate matter --- p.11
Chapter 1.5 --- Toxic effects of particulate matter --- p.12
Chapter 1.5.1 --- Lung injury --- p.12
Chapter 1.5.2 --- Cardiovascular injury --- p.15
Chapter 1.5.3 --- Mutagenesis and carcinogenesis --- p.16
Chapter 1.6 --- Aims of my study --- p.16
Chapter 2 --- Toxic Effects of Heavy Metals Ions on Selected Cultured Cell-lines --- p.18
Chapter 2.1 --- Introduction --- p.18
Chapter 2.1.1 --- Metals --- p.18
Chapter 2.1.1.1 --- Cadmium --- p.22
Chapter 2.1.1.2 --- Chromium --- p.23
Chapter 2.1.1.3 --- Lead --- p.25
Chapter 2.1.1.4 --- Zinc --- p.26
Chapter 2.1.2 --- Metallothioneins --- p.28
Chapter 2.1.3 --- p53 --- p.31
Chapter 2.1.4 --- Tumor Necrosis Factor-alpha (TNF-α) --- p.32
Chapter 2.1.5 --- Aims of this chapter --- p.32
Chapter 2.2 --- Materials and methods --- p.35
Chapter 2.2.1 --- Reagents --- p.35
Chapter 2.2.2 --- Cultured Cell lines --- p.35
Chapter 2.2.2.1 --- PU5-18 --- p.36
Chapter 2.2.2.2 --- LL24 --- p.36
Chapter 2.2.2.3 --- HBE4-E6/E7 --- p.37
Chapter 2.2.3 --- Cytotoxicity assays --- p.37
Chapter 2.2.4 --- ELISA assays --- p.40
Chapter 2.2.4.1 --- ELISA assay ofp53 levels --- p.41
Chapter 2.2.4.2 --- ELISA assay of TNF-α levels --- p.43
Chapter 2.2.5 --- MT gene expression studies by Luciferase assay --- p.44
Chapter 2.2.5.1 --- PCR amplification --- p.44
Chapter 2.2.5.2 --- 5´ة End modification of PCR amplified DNA --- p.44
Chapter 2.2.5.3 --- Ligation of DNA fragment to linearized vector --- p.46
Chapter 2.2.5.4 --- E. coli. transformation by heat shock --- p.46
Chapter 2.2.5.5 --- PCR sequencing --- p.47
Chapter 2.2.5.6 --- Transfection of plasmid into HBE4-E6/E7 cells --- p.49
Chapter 2.2.5.7 --- Data analysis --- p.50
Chapter 2.3 --- Results and discussion --- p.51
Chapter 2.3.1 --- Cytotoxicity assays --- p.51
Chapter 2.3.2 --- Combination effects of metals on cytotoxicity --- p.61
Chapter 2.3.3 --- p53 --- p.65
Chapter 2.3.4 --- TNF-α --- p.68
Chapter 2.3.5 --- MT gene expression studies by Luciferase assay --- p.69
Chapter 2.4 --- Conclusion --- p.74
Chapter 3 --- Effects of Polycyclic Aromatic Hydrocarbons (PAHs) on Cultured Cell-lines --- p.75
Chapter 3.1 --- Introduction --- p.75
Chapter 3.2 --- Materials and methods --- p.79
Chapter 3.2.1 --- Reagents --- p.79
Chapter 3.2.2 --- Cell culture --- p.79
Chapter 3.2.3 --- AlamarBlue assay --- p.80
Chapter 3.2.4 --- EROD assay --- p.80
Chapter 3.3 --- Results and discussion --- p.84
Chapter 3.4 --- Conclusion --- p.88
Chapter 4 --- Chemical and Biological Assays on Roadside Dust --- p.89
Chapter 4.1 --- Introduction --- p.89
Chapter 4.1.1 --- Composition of particulate matter in Hong Kong --- p.89
Chapter 4.1.2 --- Metal contents of particulate matter in Hong Kong --- p.91
Chapter 4.1.3 --- Possible adverse health impacts of particulate matter --- p.94
Chapter 4.1.3.1 --- In vitro studies using different cell models --- p.94
Chapter 4.1.3.2 --- In vivo studies using rodents --- p.97
Chapter 4.1.3.3 --- Epidemiological studies --- p.98
Chapter 4.1.4 --- Aims of this chapter --- p.100
Chapter 4.2 --- Materials and methods --- p.101
Chapter 4.2.1 --- Sampling of roadside dust --- p.101
Chapter 4.2.2 --- Chemical analysis of roadside dust --- p.104
Chapter 4.2.2.1 --- Reagents --- p.104
Chapter 4.2.2.2 --- Total metal contents --- p.105
Chapter 4.2.2.3 --- Extractable metal contents --- p.105
Chapter 4.2.3 --- Biological assays --- p.105
Chapter 4.2.3.1 --- Cell models --- p.106
Chapter 4.2.3.2 --- Pretreatment of roadside dust --- p.106
Chapter 4.2.3.3 --- AlamarBlue assay --- p.106
Chapter 4.2.3.4 --- ELISA assays --- p.108
Chapter 4.2.3.5 --- Luciferase assay --- p.108
Chapter 4.3 --- Results and discussion --- p.110
Chapter 4.3.1 --- Total metal contents --- p.110
Chapter 4.3.2 --- Extractable metal contents --- p.113
Chapter 4.3.3 --- AlamarBlue assay --- p.116
Chapter 4.3.4 --- p53 --- p.122
Chapter 4.3.5 --- TNF-α --- p.122
Chapter 4.3.6 --- Luciferase assay --- p.126
Chapter 4.4 --- Conclusion --- p.129
Chapter 5 --- General discussion and conclusion --- p.130
Chapter 6 --- References --- p.135
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Nunez, Yanelli. "The effect of air pollution on aggravation of neurodegenerative diseases: an analysis of long-term exposure to fine particulate matter and its components." Thesis, 2020. https://doi.org/10.7916/d8-cj8x-7534.
Full textAbstract:
Background: Air pollution is one of the leading environmental issues in the world today. In 2015, pollution-related diseases accounted for 16% of all deaths worldwide — that is an estimated 9 million premature deaths were linked to air pollution. In addition to the substantial effects on human health, air pollution-related diseases result in productivity losses that reduce countries’ gross domestic product. Although air pollution disproportionately affects middle- and low-income countries, it is still a major issue in high-income countries, such as the United States, where 25% of Americans breath air with pollutant levels above the national regulatory standards. Fine particle matter (particles with diameter ≤ 2.5 μm, PM₂.₅ ) is the most extensively studied air pollutant and it has been causally linked with a wide range of adverse health outcomes, including cardiovascular and pulmonary disease, myocardial infarction, hypertension, congestive heart failure, arrhythmias, chronic obstructive pulmonary disease, and lung cancer. Moreover, recent scientific evidence suggests that PM₂.₅ affects the nervous system and possibly contributes to the development and exacerbation of neurodegenerative diseases. This is increasingly relevant as populations are aging and the number of adults living with neurodegenerative diseases increases, negatively affecting families, communities, and health-care systems around the world. Although millions of people suffer from neurodegenerative diseases, there is currently no treatment that slows the progression of these conditions and no known cure or cause. Thus, determining whether a link exists between air pollution and neurodegenerative diseases is a goal of increasing importance.
Objective: The research presented in this dissertation has two main objectives: (1) to characterize the relationship between long-term exposure to PM₂.₅ and disease aggravation in two of the most prevalent neurodegenerative diseases worldwide: Alzheimer’s (AD) and Parkinson’s disease (PD), as well as in the rare and devastating neurodegenerative motor disorder amyotrophic lateral sclerosis (ALS); (2) to identify the specific PM₂.₅ chemical components that are associated with disease aggravation in PD.
Methods: We used data from the New York Department of Health Statewide Planning and Research Cooperative System from 2000–2014 to identify patients’ first hospitalization with a primary or secondary diagnosis of AD, PD, or ALS. With these data, we constructed annual AD, PD, and ALS first hospitalization county counts (total and sex- and age-stratified) for all of New York State (NYS). A patient’s first hospital admission was used as a surrogate for disease aggravation, indicating the crossing point into a more severe stage of the disease. We used prediction estimates from well-validated models that incorporate satellite information and ground-based monitoring data to estimate annual PM₂.₅ and PM₂.₅ chemical component (nitrate, sulfate, organic matter, sea salt, black carbon, and soil) concentrations across NYS at a high spatial resolution. In Chapter 2, we used outcome-specific (AD, PD, or ALS) mixed quasi-Poisson models with county-specific random intercepts to assess the relationship between long-term exposure to PM₂.₅ and disease aggravation. In Chapter 3, we used a multi-pollutant mixed quasi-Poisson model with county-specific random intercepts to identify specific PM₂.₅ components associated with disease aggravation in PD. In all analyses, we evaluated potential nonlinear exposure–outcome relationships using penalized splines and accounted for potential confounders.
Results: We observed a total of 264,075 AD, 114,514 PD, and 5,569 ALS first admissions between 2000 and 2014. The hospitalization annual average counts per county were 284, 131, and 6 for AD, PD, and ALS, respectively. In Chapter 2, we found a nonlinear association between total PM₂.₅ exposure and PD hospitalizations, which plateaued at higher concentrations of PM₂.₅ (> 13 μg/m³, RR=1.08, 95% CI: 1.04–1.13 for a PM₂.₅ increase from 8 to 10 μg/m³, Figure 2.3). We also found that patients with a first PD hospitalization at age 70 or younger are at slightly higher risk for disease aggravation at lower PM₂.₅ concentrations relative to those age >70. In the case of AD, we observed evidence of a potential association between annual increases in PM₂.₅ exposure and disease aggravation, but only in a sensitivity analysis aiming to decrease outcome misclassification. We found no association for ALS in the main analysis, but we observed an unexpected negative association in those <70 years in the stratified analysis. We found no evidence of effect modification by sex for any of the outcomes. In Chapter 3, we observed a linear association between disease aggravation in PD and long-term exposure to the PM₂.₅ components nitrate (RR = 1.05, 95%CI: 1.02–1.09 per one standard deviation (SD) increase) and organic matter (RR = 1.05, 95%CI: 1.02– 1.07 per one SD increase), and a nonlinear association for black carbon with a negative association above the 96th percentile of the BC concentration distribution (Figure 3.4). We found no evidence of an association with sulfate, sea salt or soil.
Conclusion: Overall, our studies provide an analysis of the potential association between long-term exposure to PM₂.₅ , both as an overall pollution mixture and by chem- ical composition, and disease aggravation in AD, PD, and ALS. Our findings suggest that annual increases in county-level PM₂.₅ concentrations are associated with disease aggravation in PD and possibly AD. We found that the PM₂.₅ components organic matter and nitrate are particularly harmful in the association between PM₂.₅ and dis- ease aggravation in PD. Additionally, our results indicate that current national PM₂.₅ standards may not be strict enough to safeguard the population’s neurological health. Specifically, in Chapter 2, we observed that the PM₂.₅ –PD association has a steeper slope at lower concentrations that are well below the current annual National Ambient Air Quality Standards for PM₂.₅ . Thus, our findings warrant further investigation into the potential link between long-term PM₂.₅ exposure and disease aggravation, particularly in the context of PD. Our results also indicate that the chemical composition of PM2.5 affects its neurotoxicity. Further research into how PM₂.₅ composition influences the overall PM₂.₅ adverse effects is needed to fully understand the mechanisms that underlie the association between exposure to PM₂.₅ and aggravation of neurodegenerative diseases.