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首页> 外文期刊>Journal of Toxicology and Environmental Health, Part B: Critical Reviews >Pulmonary Endpoints (Lung Carcinomas and Asbestosis) Following Inhalation Exposure to Asbestos
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Pulmonary Endpoints (Lung Carcinomas and Asbestosis) Following Inhalation Exposure to Asbestos

机译:吸入石棉后的肺端点(肺癌和石棉沉着症)

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Lung carcinomas and pulmonary fibrosis (asbestosis) occur in asbestos workers. Understanding the pathogenesis of these diseases is complicated because of potential confounding factors, such as smoking, which is not a risk factor in mesothelioma. The modes of action (MOA) of various types of asbestos in the development of lung cancers, asbestosis, and mesotheliomas appear to be different. Moreover, asbestos fibers may act differentially at various stages of these diseases, and have different potencies as compared to other naturally occurring and synthetic fibers. This literature review describes patterns of deposition and retention of various types of asbestos and other fibers after inhalation, methods of translocation within the lung, and dissolution of various fiber types in lung compartments and cells in vitro. Comprehensive dose-response studies at fiber concentrations inhaled by humans as well as bivariate size distributions (lengths and widths), types, and sources of fibers are rarely defined in published studies and are needed. Species-specific responses may occur. Mechanistic studies have some of these limitations, but have suggested that changes in gene expression (either fiber-catalyzed directly or by cell elaboration of oxidants), epigenetic changes, and receptor-mediated or other intracellular signaling cascades may play roles in various stages of the development of lung cancers or asbestosis.View full textDownload full textRelated var addthis_config = { ui_cobrand: "Taylor & Francis Online", services_compact: "citeulike,netvibes,twitter,technorati,delicious,linkedin,facebook,stumbleupon,digg,google,more", pubid: "ra-4dff56cd6bb1830b" }; Add to shortlist Link Permalink http://dx.doi.org/10.1080/10937404.2011.556047
机译:在石棉工人中发生肺癌和肺纤维化(石棉沉着症)。由于潜在的混杂因素(例如吸烟)不是间皮瘤的危险因素,因此了解这些疾病的发病机理非常复杂。各种类型的石棉在肺癌,石棉和间皮瘤发展过程中的作用方式(MOA)似乎不同。此外,石棉纤维在这些疾病的各个阶段可能起不同的作用,并且与其他天然和合成纤维相比,具有不同的功效。这篇文献综述描述了吸入后各种类型的石棉和其他纤维的沉积和保留方式,在肺内的移位方法以及各种类型的纤维在体外肺隔室和细胞中的溶解。在人类吸入的纤维浓度以及双变量尺寸分布(长度和宽度),纤维类型和来源方面,全面的剂量反应研究很少在已发表的研究中进行定义,因此是必需的。特定物种的反应可能会发生。机理研究具有这些局限性,但已表明基因表达的变化(直接由纤维催化或通过细胞的氧化剂氧化作用),表观遗传学变化以及受体介导的或其他细胞内信号级联反应可能在基因表达的各个阶段发挥作用。查看全文下载相关全文var addthis_config = {ui_cobrand:“ Taylor&Francis Online”,services_compact:“ citeulike,netvibes,twitter,technorati,delicious,linkedin,facebook,stumbleupon,digg,google,more” ,pubid:“ ra-4dff56cd6bb1830b”};添加到候选列表链接永久链接http://dx.doi.org/10.1080/10937404.2011.556047

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