277 resultados para Asbestos.


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The government of the State of Victoria has been slow to acknowledge the social costs of asbestos-related diseases (ARD) in the Latrobe Valley. Despite the emphasis on ‘community’ in the discipline of public health and in public health services since the 1970s, ARD was only recognised as a community-wide health problem because of the advocacy of people directly affected by it. An historical view of responses to ARD in a community established as an appendage to the publicly owned power industry and infused with an ethic of public service, shows that contests over the definition of ‘community’ lay at the heart of these responses. It also shows that such disputes did not arise only from the reluctance of authorities to acknowledge the problems resulting from the extensive use of asbestos in power stations. The paper highlights the political nature of the notion of ‘community’ and in doing so raises questions that have implications beyond its narrow regional focus.

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The Latrobe Valley region of Victoria, Australia, has the highest rate of asbestos disease in the state due to extensive past use of asbestos in the power industry. Current responses to asbestos disease epidemics in Australia and internationally are dominated by medical, scientific, legal and government perspectives. The voices and perspectives of those most directly affected – exposed and diseased workers, their families and communities – are relatively rarely heard.A qualitative interview study was conducted to determine what people in the Latrobe Valley community think could or should be done following their own asbestos disease epidemic. Analysis identified several themes. Notably, these represent a sophisticated community understanding of issues that is largely consistent with state-of-the-art occupational health and public health knowledge.Some themes are well known already, eg the need for fair and timely compensation, adequate healthcare facilities and services, and more education. Others point to neglected possibilities, such as the need for reconciliation and social healing to complement the dominant individual medico-legal focus. Employer suppression of hazard information and denial of asbestos-related disease in past decades continues to have a profound effect on people's views in the present. Reconciliation in some form, eg acknowledgement of or apology for past wrongs, was identified as a necessary first step in developing new and better policy and practice responses; action in this regard has important implications for the implementation and effectiveness of other policy and practice interventions. Further, a need for substantive community participation in the development of policy and practice responses – currently lacking – was identified. Findings suggest that community is an under-recognised and under-utilised resource in responding to a local asbestos disease epidemic.The Latrobe Valley situation is a microcosm of the broader Australian and international story. It offers insights on the perspectives of those most affected by asbestos issues, how such people and their views can be used to strengthen current policy and practice responses, and how their participation is essential to building comprehensive public and social health responses to this global problem.

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Asbestos-contaminated vermiculite attic insulation (VAI) produced from a mine near Libby, Montana, may be present in millions of homes along with other commercial asbestos-containing materials (ACM). The primary goal of the research described here was to develop and test procedures that would allow for the safe and effective weatherization of low-income homes with asbestos. The presence of asbestos insulation was confirmed by bulk sampling of the suspect asbestos material. The homes were then tested for the presence of asbestos fibers in the living spaces. All 40 homes containing VAI revealed the presence of amphibole asbestos in bulk samples. Asbestos (primarily chrysotile) was confirmed in bulk samples of ACM collected from 18 homes. Amphibole asbestos was detected in the living space of 12 (26%) homes, while chrysotile asbestos was detected in the living space of 45 (98%) homes. These results suggest that asbestos sources in homes can contribute to living space contamination

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Karst Kamp, a southwestern Montana recreation re­sort, is 32 road miles south of Bozeman on the east bank of the Gallatin River in a narrow V-shaped valley flanked on the west by the rugged Madison mountain range and on the east by the equally rough Gallatin range. The asbestos deposit itself lies approximate­ly one-half mile northwest of the ranch on a heavily timbered "Al­pine-like" slope nearly 1200 feet above the floor of the valley.

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A cohort study was conducted in Texas and Louisiana Gulf Coast area on individual workers who have been exposed to asbestos for 15 years or more. Most of these workers were employed in petrochemical industries. Of the 15,742 subjects initially selected for the cohort study, 3,258 had positive chest X-ray findings believed to be related to prolonged asbestos exposure. These subjects were further investigated. Their work out included detailed medical and occupational history, laboratory tests and spirometry. One thousand eight-hundred and three cases with positive chest X-ray findings whose data files were considered complete at the end of May 1986 were analyzed and their findings included in this report.^ The prevalence of lung cancer and cancer of the following sights: skin, stomach, oropharyngeal, pancreas and kidneys were significantly increased when compared to data from Connecticut Tumor Registry. The prevalence of other chronic conditions such as hypertension, emphysema, heart disease and peptic ulcer was also significantly high when compared to data for the U.S. and general population furnished by the National Center for Health Statistics (NCHS). In most instances the occurrence of cancer and the chronic ailment previously mentioned appeared to follow 15-25 years of exposure to asbestos. ^

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Asbestos and silica are important industrial hazards. Exposure to these dusts can result in pulmonary fibrosis and, in the case of asbestos, cancer. Although the hazards of asbestos and silica exposure have long been known, the pathogenesis of dust-related disease is not well understood. Both silica and asbestos are thought to alter the function of the alveolar macrophage, but the nature of the biochemical alteration is unknown. Therefore, this study examined the effect of asbestos and silica on the activation pathway of the guinea pig alveolar macrophage. Activation of macrophages by physiological agents results in stimulation of phospholipase C causing phosphatidyl inositol turnover and intracellular calcium mobilization. Phosphatidyl inositol turnover produces diacylglycerol which activates protein kinase C causing superoxide anion production.^ Chrysotile stimulated alveolar macrophages to produce superoxide anion. This stimulation proceeded via phospholipase C, since chrysotile stimulated phosphatidyl inositol turnover and intracellular calcium mobilization. The possible involvement of a coupling protein was evaluated by pretreating cells with pertussis toxin. Pertussis toxin pretreatment partially inhibited chrysotile stimulation, suggesting that chrysotile activates a coupling protein in an non-classical manner. Potential binding sites for chrysotile stimulation were examined using a series of nine lectins. Chrysotile-stimulated superoxide anion production was blocked by pretreatment with lectins which bound to N-acetylglucosamine, but not by lectins which bound to mannose, fucose, or N-acetylgalactosamine. In addition, incubation with the N-acetylglucosamine polymer, chitin, inhibited chrysotile-stimulated superoxide anion production, suggesting that chrysotile stimulated superoxide anion production by binding to N-acetylglucosamine residues.^ On the other hand, silica did not stimulate superoxide anion production. The effect of silica on agonist stimulation of this pathway was examined using two stimulants of superoxide anion production, N-formyl-nle-leu-phe (FNLP, which stimulates through phospholipase C) and phorbol-12,13-dibutyrate (which directly activates protein kinase C). Sublethal doses of silica inhibited FNLP-stimulated superoxide anion production, but did not affect phorbol-12,13-dibutyrate-stimulated superoxide anion production, suggesting that the site of inhibition precedes protein kinase C. This inhibition was not due to cell membrane damage, since cell permeability to calcium-45 and rubidium-86 was not increased. It is concluded that chrysotile binds to N-acetylglucosamine residues on macrophage surface glycoproteins to stimulate the physiological pathway resulting in superoxide anion production. In contrast, silica does not stimulate superoxide anion production, but it did inhibit FNLP-stimulated superoxide anion production. ^

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In this study, an attempt is made to evaluate certain parameters that might indicate the beginning of a certain fibrogenic activity in the lung parenchyma, even before such changes become visible on the chest x-ray. The hypothesis is that studies such as certain bronchoalveolar immunological characteristics and Gallium-67 lung scans may be more sensitive indicators of parenchymal lung damage in response to asbestos inhalation than conventional radiographic criteria. If so, then in those cases where the criteria for the diagnosis of asbestosis lack the presence of parenchymal changes, it would be unwise to deny the diagnosis unless further investigations, such as the bronchoalveolar lavage fluid analysis and the Gallium-67 lung scan techniques, are made available.^ Four groups of individuals have been included in this study. The volunteer group showing no history of asbestos exposure with normal chest x-rays has been used as a normal healthy comparison group. The other three groups are all asbestos-exposed but differ as to their findings in the chest radiographs. One has parenchymal changes (0/1 or more, ILO Classification), the second has no parenchymal but pleural changes, and the third has neither.^ The most significant laboratory parameter for bronchoalveolar lavage, in this study, is that of Neutrophils (PMNs). All three asbestos-exposed groups showed no differences when compared with each other, while such differences were statistically significant when such groups were separately compared with the normal comparison group. A similar finding existed also when the Helper: Suppressor T-Cell ratios were compared, and found to be higher in all the asbestos-exposed groups.^ Another sensitive test is that of Gallium-67 lung scan. This was found to be positive in some patients where parenchymal changes were absent. Even in some of those who showed neither parenchymal nor pleural changes in their chest x-ray showed positive test results. Such changes indicate a state of an underlying pathogenic process that is still undetectable by conventional radiography. This highly recommends the future application of such tests for the early detection of active pulmonary disease, especially in those who show no parenchymal changes in their chest x-rays. (Abstract shortened with permission of author.) ^

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Recent sediments with distinct signs of hydrothermal alteration sampled in the Hess Deep(Galapagos Ridge, East Pacific Rise) contained a piece of ash-gray rock, which differed from other rock fragments by degree of consolidation, conchoidal fracture, and had properties of asbestos. Our studies found that the sample represented mixture of asbestos-like pyroxene of diopside-hedenbergite composition, amphibole of tremolite composition and a new mineral, which basic structure consisted of bands of triple pyroxene chains with the radical [Si6O16]. The latter can be regarded as intermediate between amphiboles and layered silicates. Also in some parts of the sample presence of trioctahedral vermiculite-chlorite was indicated. Genesis of the studied asbestos rock is considered from the standpoint of high-temperature hydrothermal-metasomatic alteration of sediment by post-magmatic mineralized halide solutions.

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Mesothelioma, a malignancy associated with asbestos, has been recently linked to simian virus 40 (SV40). We found that infection of human mesothelial cells by SV40 is very different from the semipermissive infection thought to be characteristic of human cells. Mesothelial cells are uniformly infected but not lysed by SV40, a mechanism related to p53, and undergo cell transformation at an extremely high rate. Exposure of mesothelial cells to asbestos complemented SV40 mutants in transformation. Our data provide a mechanistic explanation for the ability of SV40 to transform mesothelial cells preferentially and indicate that asbestos and SV40 may be cocarcinogens.