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Os produtos derivados de asbesto são amplamente utilizados pelo setor industrial, sendo descritas diversas doenças relacionadas à sua exposição, entre elas, o tumor primário da pleura, ou mesotelioma. O mecanismo fisiopatológico da lesão pelas fibras de asbesto no espaço pleural ainda não está totalmente estabelecido. Entre os fatores possivelmente implicados estão os efeitos provocados por uma resposta inflamatória com migração celular e liberação de mediadores moleculares levando à necrose, apoptose e alterações na proliferação e fibrogênese. No entanto, existem dificuldades no estudo da resposta in vivo ao asbesto, principalmente em virtude da população multicelular da cavidade pleural. Neste sentido, tem sido preconizado na literatura o estudo envolvendo animais geneticamente modificados ou selecionados, a fim de melhor compreender o papel das diversas populações envolvidas neste processo. Neste trabalho, tivemos como objetivo estudar comparativamente a resposta inflamatória aguda no líquido pleural e em células mesoteliais em cultura expostas a diferentes fibras de asbesto. Para tanto, animais controle e geneticamente selecionados para alta (AIR max) e baixa (AIR min) resposta inflamatória, e células mesoteliais em cultura foram expostas às fibras de asbesto crocidolita ou crisotila. Após 4, 24 ou 48 horas foram avaliadas a produção das citocinas IL-1b, IL-6 e MIP-2. Adicionalmente, no modelo in vivo foi avaliado o perfil celular do líquido pleural e a expressão do Ra PDGF em RESUMO fragmentos de pleura, e no modelo in vitro a resposta celular de apoptose e necrose. Como resultados, as fibras de asbesto crocidolita e crisotila produziram, em animais AIR max, uma elevação significativa no líquido pleural de leucócitos, neutrófilos e da IL-1b em comparação aos controles e aos animais AIR min. Entretanto, não houve diferença no número de macrófagos, IL-6 e MIP-2. As células mesoteliais em cultura expostas tanto às fibras crocidolita quanto crisotila apresentaram elevados índices de apoptose e necrose e da produção das citocinas IL-1b, IL-6 e MIP-2 quando comparadas aos controles. Houve forte correlação das citocinas MIP-2 e IL-1b em cultura com os níveis no líquido pleural para ambas as fibras estudadas. Foi demonstrado, para ambas as fibras, uma forte expressão do Ra PDGF na superfície pleural tanto nos animais com alta quanto com baixa resposta inflamatória quando comparado aos controles. Como conclusão, caracterizamos o perfil da resposta inflamatória aguda a diferentes fibras de asbesto em modelos experimentais in vivo e in vitro, contribuindo para a melhor compreensão do mecanismo de agressão celular secundário a este material de uso comercial tão freqüente. / Asbestos-derived products are used thoroughly by industry. Several diseases related to asbestos exposition have been described, among them the primary tumor of the pleura mesothelioma. The mechanisms by which asbestos fibers produce injury to the pleural space are not clear. Among the factors possibly implicated are the effects secondary to an inflammatory response characterized by cellular migration and the release of molecular mediators leading to necrosis, apoptosis, cellular proliferation and fibrogenesis. However, it is difficulty to characterize the cellular response in vivo, mainly by virtue of the multi-cellular population present into the pleural cavity. Therefore, studies involving animals genetically modified or genetically selected have been proposed in the literature, in order to better understand the role of the several cellular populations involved in this complex process. In this study, our objective was to determine the inflammatory response of the pleural fluid and compare to the response of cultured mesothelial cells exposed to different asbestos fibers. Controls and mice genetically selected for high (AIR max) or low (AIR min) inflammatory response as well as mice cultured mesothelial cells were treated to crocidolite or chrysotile asbestos fibers. After 4, 24 or 48 hours the production of the cytokines IL-1b, IL-6 and MIP-2 were analyzed. In addition, the in vivo cellular profile of the pleural fluid and the Ra PDGF expression in the pleura fragments was documented. In parallel, the in vitro mesothelial cellular response of apoptosis and necrosis was quantified. Both asbestos fibers produced in AIR max mice a significant elevation in the pleural fluid total leukocytes, neutrophils and IL-1b levels in comparison to the controls and AIR min animals. However, no difference was found in the macrophage number, IL-6 and MIP-2 levels. Cultured mesothelial cells had a high apoptosis, necrosis, IL-1b, IL-6 and MIP-2 levels in comparison to the controls when exposed to either crocidolite or chrysotile. MIP-2 and IL-1b levels in cultured mesothelial cells strongly correlated with the levels of the pleural fluid for both fibers. In addition, a pronounced expression of Ra PDGF in the pleural surface was demonstrated in both high and low inflammatory selected mice when compared to the controls. In conclusion, we characterized the acute inflammatory response to the asbestos fibers crocidolite and chrysotile in an in vivo and in vitro experimental model, aiming to contribute to better understand the mechanism of cellular aggression secondary to this particulate material of such frequent commercial use.

Os produtos derivados de asbesto são amplamente utilizados pelo setor industrial, sendo descritas diversas doenças relacionadas à sua exposição, entre elas, o tumor primário da pleura, ou mesotelioma. O mecanismo fisiopatológico da lesão pelas fibras de asbesto no espaço pleural ainda não está totalmente estabelecido. Entre os fatores possivelmente implicados estão os efeitos provocados por uma resposta inflamatória com migração celular e liberação de mediadores moleculares levando à necrose, apoptose e alterações na proliferação e fibrogênese. No entanto, existem dificuldades no estudo da resposta in vivo ao asbesto, principalmente em virtude da população multicelular da cavidade pleural. Neste sentido, tem sido preconizado na literatura o estudo envolvendo animais geneticamente modificados ou selecionados, a fim de melhor compreender o papel das diversas populações envolvidas neste processo. Neste trabalho, tivemos como objetivo estudar comparativamente a resposta inflamatória aguda no líquido pleural e em células mesoteliais em cultura expostas a diferentes fibras de asbesto. Para tanto, animais controle e geneticamente selecionados para alta (AIR max) e baixa (AIR min) resposta inflamatória, e células mesoteliais em cultura foram expostas às fibras de asbesto crocidolita ou crisotila. Após 4, 24 ou 48 horas foram avaliadas a produção das citocinas IL-1b, IL-6 e MIP-2. Adicionalmente, no modelo in vivo foi avaliado o perfil celular do líquido pleural e a expressão do Ra PDGF em RESUMO fragmentos de pleura, e no modelo in vitro a resposta celular de apoptose e necrose. Como resultados, as fibras de asbesto crocidolita e crisotila produziram, em animais AIR max, uma elevação significativa no líquido pleural de leucócitos, neutrófilos e da IL-1b em comparação aos controles e aos animais AIR min. Entretanto, não houve diferença no número de macrófagos, IL-6 e MIP-2. As células mesoteliais em cultura expostas tanto às fibras crocidolita quanto crisotila apresentaram elevados índices de apoptose e necrose e da produção das citocinas IL-1b, IL-6 e MIP-2 quando comparadas aos controles. Houve forte correlação das citocinas MIP-2 e IL-1b em cultura com os níveis no líquido pleural para ambas as fibras estudadas. Foi demonstrado, para ambas as fibras, uma forte expressão do Ra PDGF na superfície pleural tanto nos animais com alta quanto com baixa resposta inflamatória quando comparado aos controles. Como conclusão, caracterizamos o perfil da resposta inflamatória aguda a diferentes fibras de asbesto em modelos experimentais in vivo e in vitro, contribuindo para a melhor compreensão do mecanismo de agressão celular secundário a este material de uso comercial tão freqüente. / Asbestos-derived products are used thoroughly by industry. Several diseases related to asbestos exposition have been described, among them the primary tumor of the pleura mesothelioma. The mechanisms by which asbestos fibers produce injury to the pleural space are not clear. Among the factors possibly implicated are the effects secondary to an inflammatory response characterized by cellular migration and the release of molecular mediators leading to necrosis, apoptosis, cellular proliferation and fibrogenesis. However, it is difficulty to characterize the cellular response in vivo, mainly by virtue of the multi-cellular population present into the pleural cavity. Therefore, studies involving animals genetically modified or genetically selected have been proposed in the literature, in order to better understand the role of the several cellular populations involved in this complex process. In this study, our objective was to determine the inflammatory response of the pleural fluid and compare to the response of cultured mesothelial cells exposed to different asbestos fibers. Controls and mice genetically selected for high (AIR max) or low (AIR min) inflammatory response as well as mice cultured mesothelial cells were treated to crocidolite or chrysotile asbestos fibers. After 4, 24 or 48 hours the production of the cytokines IL-1b, IL-6 and MIP-2 were analyzed. In addition, the in vivo cellular profile of the pleural fluid and the Ra PDGF expression in the pleura fragments was documented. In parallel, the in vitro mesothelial cellular response of apoptosis and necrosis was quantified. Both asbestos fibers produced in AIR max mice a significant elevation in the pleural fluid total leukocytes, neutrophils and IL-1b levels in comparison to the controls and AIR min animals. However, no difference was found in the macrophage number, IL-6 and MIP-2 levels. Cultured mesothelial cells had a high apoptosis, necrosis, IL-1b, IL-6 and MIP-2 levels in comparison to the controls when exposed to either crocidolite or chrysotile. MIP-2 and IL-1b levels in cultured mesothelial cells strongly correlated with the levels of the pleural fluid for both fibers. In addition, a pronounced expression of Ra PDGF in the pleural surface was demonstrated in both high and low inflammatory selected mice when compared to the controls. In conclusion, we characterized the acute inflammatory response to the asbestos fibers crocidolite and chrysotile in an in vivo and in vitro experimental model, aiming to contribute to better understand the mechanism of cellular aggression secondary to this particulate material of such frequent commercial use.

Functional and pathological responses of larval, juvenile, and adult Asiatic clams (Corbicula sp.), juvenile and adult fathead minnows (Pimephales promelas), and egg, larval and juvenile Japanese Medaka (Oryzias latipes) to chrysotile asbestos were investigated in 96-hour to 91-day tests. Chrysotile significantly reduced siphoning activity and shell growth of adult clams and siphoning, shell growth, and weight gain of juveniles at 10⁵ fibers/liter during 30-day tests. Larval Corbicula suffered significantly greater mortality and lower release by brooding adults at 10²-10⁸ fibers/liter. Adult and juvenile Corbicula exposed to 10⁸ fibers/liter for 30 days exhibited deteriorated gill tissue and significantly greater tissue water content. Corbicula accumulated up to 1000 fibers/mg in visceral tissue at 10⁸ fibers/liter. Clams collected from the California Aqueduct System exposed to 10⁹ fibers/liter accumulated up to 10⁵ fibers/mg in viscera. Corbicula can be used as a monitor for chrysotile contamination due to its ability to concentrate fibers. Adult and juvenile fathead minnows did not suffer acute toxicity at 10¹² fibers/liter and differential mortality relative to controls up to 10⁸ fibers/liter for 30 days. At the conclusion of the 30-day tests the length, weight, and swimming performance of adult minnows exposed to asbestos were not significantly affected relative to controls. Juvenile minnows exposed to 10⁶-10⁸ fibers/liter had significantly lower weight. Fish exposed to 10⁸ fibers/liter for 30 days accumulated up to 390 fibers/mg in kidney tissue. Egg and larval Medaka were exposed to 0-10¹⁰ fibers/liter of chrysotile until hatching and for thirteen weeks, respectively. Eggs responded erratically to asbestos exposure and no conclusive trends could be drawn. Larval Medaka exposed to 10⁶-10¹⁰ fibers/liter had reduced growth by 14 days. Fish exposed to 10¹⁰ fibers/liter suffered 100% mortality by 60 days. Fish exposed to asbestos developed epidermal tumors, thickened epidermal tissue, increased mucous cell density in the intestinal tract, constricted kidney tubules, and abnormal levels of lipid and endoplasmic reticulum in the liver. Maximum asbestos uptake occurred in fish exposed to 10⁸ fibers/liter for 91 days (400 fibers/mg). The extent of damage to fish and clams at levels greater than 10⁴ fibers/liter in the laboratory suggests that aquatically transmitted asbestos is a potential hazard to these species in the field. / Ph. D.

Please read the abstract in the section 00front of this document / Thesis (DSc)--University of Pretoria, 1966. / Geology / unrestricted

Carbon nanotubes (CNT) are a new form of industrially relevant nano-scale particle and are seen as the cutting edge of the burgeoning nanotechnology revolution which promises to impact on all our lives. Due to high length to diameter ratio, CNT are perhaps the most well known of a growing collection of high aspect ratio nanoparticles (HARN). However the production and use of carbon nanotubes has presented an interesting toxicological question based on its structure and raised the question ‘are carbon nanotubes like asbestos?’. Few people are unaware of the devastating global pandemic of diseases caused by asbestos and similarities in needle-like shape between asbestos and nanotubes have raised fears that nanotubes may mimic asbestos-type disease. The purpose of this study was to investigate this link, based on the wealth of information known about the toxic effects of certain forms of fibre on the respiratory system. From this we hope to identify those carbon nanotubes which are hazardous whilst not prejudicing the use of those industrially relevant materials which can be used safely. Within fibre toxicology there exists a central paradigm which outlines the main properties a fibrous particle must possess if it is to exert pathogenic effects in the body. This paradigm outlines the importance of length, thinness and biopersistence to a fibre and an absence of one or more of these attributes results in a loss of pathogenicity. We took this paradigm and, using suitable asbestos and non-asbestos controls, applied it various morphological forms of carbon nanotubes using an in vivo model. The resultant data demonstrates for the first time that asbestos-like pathogenic behaviour associated with carbon nanotubes is closely linked to the morphology of the nanotubes and their aggregates. Specifically our results showed that CNT which possessed a long, straight length were highly inflammogenic and fibrogenic within the peritoneal cavity of mice; a model sensitive to the pathogenic effects of fibres. As well as length, the importance of biopersistence in the pathogenesis of fibrous particles has been known for many years and is a central attribute affecting the pathogenicity of fibres. Amphibole asbestos is known to be durable, a commercially exploited attribute and as such is biopersistent in the lung which is a key feature of its pathogenicity. Glass fibre on the other hand is bio-soluble, and whilst long and inhalable, does not cause significant disease due to its lack of biopersistence. Based on the grapheme structure of CNT which impart exceptional strength and rigidity and the chemical inertness of carbon we would hypothesis that CNT would be biopersistent and therefore fulfil another of the criteria of the fibre pathogenicity paradigm (FPP). Our aim therefore has been to establish the durability of CNT against fibrous particles of known durability using a synthetic solution maintained at a pH to simulate the lung environment. Using a range of 4 CNT and using both durable and non-durable fibres such as amphibole asbestos and glass fibre to bench mark our result; we demonstrated that 3 of the 4 CNT tested displayed exceptional durability whilst the fourth lost approximately 30% of its mass during the experiment with concomitant reduction in pathogenicity. As well as length and biopersistence, the surface of a particle has been shown to contribute to the overall toxicity of a particle and in certain circumstances, such as that of quartz, the surface of the particle can be the biologically active component. In the case of carbon nanotubes, surface functionalisation is commonly used for various endpoints including the addition of various tags and labels for tracking. As such our further aim was to investigate the relationship between the length-dependent pathogenicity of a fibre sample and the surface of the fibre. By using different forms of functional groups attached to the surface of a pathogenic carbon nanotube we aim to critically test if the level of inflammation and fibrosis triggered in vivo can be altered by simple alteration of the surface. Our results showed that surface modification of CNT could alter the inflammogenic and fibrogenic effects of CNT which may have important implications when considering the hazard assessment of functionalised HARN. As CNT are not the only form of fibrous nanomaterial and within this project we also attempted to determine the applicability of the FPP to further high aspect ratio nanomaterials. In order to do this we set out to determine the generality of this hypothesis by asking whether nickel nanowires, a radically different form of HARN to CNT, show length-dependent pathogenicity. Nickel oxide nanowires synthesised to be predominantly long (>20 μm) act similarly to amphibole asbestos in showing the ability to elicit strong inflammation in the mouse peritoneal model in a dose dependent manner; inflammation was not seen with the short (<5 μm) nanowires. In summation, the results from this study are the first to show that long HARN can indeed behave like asbestos when in contact with the sensitive mesothelium. This study suggests a potential link between inhalation exposure to long nanotubes and asbestos-related disease, especially mesothelioma and as such this may have immediate implications across many disciplines if care is to be taken to avoid a long term legacy of harm.

Malignant Mesothelioma (MM) is a fatal disease with a low median survival between 8 to 12 months after diagnosis. MM has a long latency period (10-60 years), is causally related to asbestos exposure, and is refractory to all available modes of therapy. Despite the causal association between asbestos exposure and MM however, the mechanisms by which asbestos induces this deadly disease remain unclear. Chronic inflammation due to the presence of asbestos fibers is believed to play an important role in all aspects of MM pathogenesis, from development to progression and resistance. Chronic inflammation has been shown to promote dysregulated wound repair, fibrosis and epithelial to mesenchymal transition (EMT). One of the inflammatory pathways that asbestos activates is the inflammasome (a multiprotein scaffold that assembles in response to various stimuli to facilitate the activation of caspase-1), which has been implicated in several chronic inflammatory diseases and disorders. The nucleotide binding oligomerization domain (NOD) - like receptor containing a pyrin domain 3 (NLRP3) inflammasome, both as a whole or via its components [NLRP3, apoptosis related speck-like protein containing a CARD (caspase activating and recruitment domain) (ASC) and caspase-1] as well as its products, IL-1β and IL-18, has been implicated in the development of EMT during chronic inflammation. Asbestos fibers, especially the amphiboles, are non-biodegradable and thus persist in tissues of the body for years after exposure. In mesothelial cells, the squamous epithelial-like cells that line the serosal cavities of the body, from which MM originates, asbestos chronically activates the NLRP3 inflammasome. Asbestos also activates the NLRP3 inflammasome in human macrophages that can lead to the establishment of a chronic inflammation environment. We therefore hypothesized that asbestos dependent regulation of the inflammasome played a role in mesothelial to fibroblastic transition to facilitate eventual neoplastic transformation of the mesothelial cells. Using in vitro models, siRNA knockdown approaches as well as in vivo models of asbestos exposure utilizing inflammasome component knockout mice, we demonstrate that asbestos-induced reactive oxygen species generation modulates the redox state of the endogenous antioxidant, thioredoxin, causing its dissociation from thioredoxin interacting protein to promote activation of the inflammasome. We also show that the inflammasome plays a role in asbestos-induced mesothelial to fibroblastic transition (MFT) (a form of EMT occurring in the mesothelial cells) both in vitro and in vivo with a requirement for caspase-1 in vivo to promote thickening of the submesothelium. Through our studies, we have identified tissue factor pathway inhibitor 2 (TFPI2) and fibroblast growth factor 2 (FGF2) as molecules that are upregulated in response to asbestos exposure with potential roles in the progression of asbestos-induced MFT. There is a dearth of diagnostic biomarkers that enable early detection of MM, thus with further studies these two molecules could be explored as biomarkers of asbestos exposure/disease progression. TFPI2 levels were downregulated in response to blockage of IL-1β signaling and thus could be harnessed as a potential marker for therapy efficiency with further studies.

Croisant théorie néo-institutionnaliste et théorie des mouvements sociaux, cette thèse en stratégie explore la dialectique entre travail institutionnel disruptif et travail institutionnel défensif mettant ainsi en évidence les stratégies et contre stratégies qui peuvent être déployées au sein d’un champ organisationnel. Grâce à une étude de cas longitudinale, nous étudions l’histoire de l’amiante en France, entre 1970 et 1997. Entre contestation et collaboration, le cas est marqué par des luttes institutionnelles longues et complexes. Notre analyse s’appuie sur des données d’archives variées dont des archives audiovisuelles. Notre étude souligne l’évolution des répertoires tactiques mobilisés contre l’institution. Les tactiques persuasives conduiront à un changement de la pratique institutionnalisée pourtant maintenue par un travail de défense marqué par la mise en place d’une organisation frontière, le Comité Permanent Amiante, appelé aujourd’hui le « lobby de l’or blanc ». Seules des tactiques destructrices, portant sur les dimensions les plus ouvertes de l’institution, conduiront à sa délégitimation. Nous soulignons alors le rôle du pilier régulatif dans cette stratégie / Within the field of strategy, the thesis deals with the role of social movements inthe process of deinstitutionalization through the concept of repertoire of tactics. This research studies how social movement actions lead to the delegitimization of a taken for granted practice. We focus on the dialectic between defensive and disruptive institutional work. Our method is based on a processual case study. Drawing from the asbestos industry in France from 1970’ to 1990’, we study dialectical struggles between social movement and institution. Our study emphasizes the evolution of repertoire of tactics. Persuasive tactics lead to an institutional change and yet the practice is maintained due to the creation of a boundary organization. Only destructives tactics, directed against more opened institutional pillars, can lead to the ban of the practice. We emphasize the role of the regulative dimension in this strategy

Les expositions professionnelles représentent la 2nde étiologie de cancer du poumon. Parmi elles, les laines minérales (LM) utilisées comme substitut à l’amiante sont suspectées d’augmenter le risque de cancer du poumon en raison de leur structure proche de celle de l’amiante. Dans ce contexte, ce travail a pour objectif d'évaluer le rôle de l'histoire professionnelle et en particulier celui de l'exposition professionnelle aux LM dans la survenue de cancer du poumon en tenant compte des expositions à l'amiante, à la silice, autres substances très prévalentes dans le secteur de la construction. Une dernière partie a consisté à étudier le risque de cancer du poumon associé à l'exposition professionnelle aux poussières de ciment.Nous avons analysés les histoires professionnelles complètes des cas et témoins inclus dans l'étude cas-témoins en population générale ICARE, identifiés dans 10 départements français abritant un registre général de cancer. Au total, 2 276 cas de cancer du poumon chez les hommes et 2 780 témoins ont été inclus ainsi que 650 cas de cancers du poumon féminins et 775 témoins. Deux stratégies d'évaluation des expositions aux LM et à l'amiante ont été utilisées: une matrice emplois-expositions (MEE) et une matrice tâche-exposition élaborée par des hygiénistes industriels et tenant compte des données individuelles. Les expositions à la silice et au ciment ont toujours été évaluées par MEE. Nos résultats confirment le rôle important des expositions professionnelles comme déterminant du risque de cancer du poumon en mettant en évidence des associations avec de nombreuses professions et secteurs d'activité. L'hypothèse d'une association entre le risque de cancer du poumon et l'exposition professionnelle aux LM est suggérée sans toutefois pouvoir exclure une confusion résiduelle par l'amiante car ces deux expositions sont très corrélées. Par ailleurs, nos résultats confirment le rôle cancérogène de l'amiante et de la silice et suggèrent une association entre l'exposition aux poussières de ciment et le risque de cancer du poumon. / Occupational exposures are the second main risk factor of lung cancer. Asbestos has progressively been substituted by mineral wools (MW). Because of their similarity in shape with asbestos, they have been suspected of causing cancer of the respiratory system. In this context, the objectives of this work were to assess the role of occupational history in lung cancer risk; to investigate in details lung cancer risk associated with exposure to MW, carefully taking into account occupational exposures to asbestos and crystalline silica, two common potential carcinogenic exposure among construction workers; and to study the risk of lung cancer associated with occupational exposure to cement dusts.We analysed lifetime occupational history of cases and controls included in the ICARE study, a large multi-centre, population-based, case-control study. They were recruited in 10 French départements with a general cancer registry. The study included 6481 subjects (men: 2 276 lung cancer cases and 2 780 controls, women: 650 lung cancer cases and 775 controls). Two strategies of assessment of occupational exposure to MW and asbestos were used: a job-exposure matrix (JEM) and a task-exposure matrix constructed by trained hygienist and taking into account individual information. Occupational exposures to crystalline silica and cement dusts were both assessed using specific JEMs.Our results confirm the important role of occupational exposure as a determinant of lung cancer risk by showing associations between lung cancer risk and several occupations or industries. An association between MW exposure and lung cancer risk is suggested without being able to exclude a potential residual confounding by asbestos since these two exposures are deeply correlated. Our results also confirm asbestos and silica carcinogenicity and suggest an association between cement dusts and lung cancer risk.

Afin de répondre aux problématiques écologique et économique du traitement des Matériaux Contenant de l’Amiante (MCA), un procédé complet permettant de traiter de manière optimale ces déchets a été proposé. Pour cela, trois types de déchets ont d’abord été analysés par plusieurs techniques de caractérisation complémentaires (diffraction des rayons X, microscopie électronique à balayage, infrarouge et RMN du solide). Ces analyses ont permis l’identification des différentes phases présentes au sein des déchets. Cette identification est nécessaire, car elle permet d’adapter de manière optimale le procédé de destruction au déchet. La première étape de ce procédé est le traitement en température des MCA dans une solution d’acide nitrique. Elle permet la dissolution de la matrice du déchet et la dénaturation des fibres de chrysotile qui sont présentes dans 95 % des déchets amiantés. Deux phases sont alors récupérées à l’issue de ce traitement : une phase solide composée de silice pure et une phase liquide contenant, notamment, du calcium, du magnésium et du fer. Si les déchets contiennent des fibres de type amphibole (5 % des MCA) ils sont ensuite traités par voie hydrothermale dans un autoclave contenant une solution de soude. Cette étape mène à la dissolution complète du déchet. Une solution basique contenant du silicium est ainsi récupérée. Différentes voies de valorisations ont été développées. Les ions présents dans la solution acide sont récupérés par précipitation sélective des hydroxydes. Une autre voie consiste à synthétiser une zéolithe à partir de la silice pure et de la solution basique. Les isothermes d’adsorption de cette dernière ont été tracés afin de déterminer sa capacité d’adsorption de certains cations métalliques polluants. Pour terminer, une étude fondamentale a été menée sur les nanotubes de silice obtenus avec le traitement de fibres d’amiante pures et différentes applications de ces nanotubes de silice ont été évoquées. / To answer the ecological and economic problems of the treatment of Materials Containing Asbestos (MCA), a complete process allowing to handle in an optimal way these waste was proposed. For that purpose, three types of waste were analyzed by several complementary techniques of characterization (X-rays diffraction, Scanning Electron Microscopy, infrared and NMR spectroscopy). These analyses allowed the identification of the present various phases within waste. This identification is necessary, because it allows to adapt in the optimal way for the destruction of the waste. The first stage of the process is a treatment in temperature of the MCA in a solution of nitric acid leading to the dissolution of the matrix of the waste and the denaturation of the fibers of chrysotile which are present in 95 % of MCA. Two phases are then got back at the end of this treatment: a solid phase of pure silica and a liquid phase containing, in particular, calcium, magnesium and iron ions. If previous waste contains fibers of amphibole type (5 % of the MCA) they are then treated through a hydrothermal process in an autoclave containing a solution of soda. This stage leads to the complete dissolution of the waste. The basic solution containing some silicon is so got back. Various ways of valuations were then developed. The present ions in the acid solution are chemically sorted out by a selective precipitation of hydroxides. Another way consists in synthesizing a zeolite from the pure silica coming from the acid treatment and from the basic solution after hydrothermal treatment. The isotherms of adsorption of this synthesized zeolite were established to determine its capacity of adsorption of certain polluting metallic cations. To finish, a fundamental study was led on the nanotubes of silica obtained after the acid treatment of pure asbestos fibers and diverse applications of these nanotubes of silica were evoked.