Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032273 (pneumoconiosis)
 1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The respiratory health of 3,027 carbon black workers employed in 19 plants (18 Western Europe, 1 U.S.A.) was assessed by questionnaire and spirometry; chest radiographs were used to assess 935 workers in the group. The results showed that the group of workers who were exposed to carbon black dust had an increased prevalence of chronic cough, sputum production and wheezing and the mean forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1.0) and flow between 25% and 75% of the FVC (MMEF 25-75%) were significantly less than those of the nonexposed group. Multiple regression analysis showed that the decline in respiratory health was related to the influence of smoking and age, with only a small part being associated with the combined effects of dust exposure and age. A simple type of pneumoconiosis was found in 6 of the workers, all of whom had more than 10 yr of dust exposure. Carbon black should be regarded as a nuisance dust without specific effect on the lungs.
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PMID:The respiratory health of carbon black workers. 361 91

Korea has a short history in research on occupational health like as short history of industrialization. During last four decades, however, Korea has experienced what developed countries have experienced for more than a hundred year. Research on occupational health in Korea has also drastically developed. Since industrialization in 1970s, many workers were exposed to hazardous working environment and suffered from occupational accidents and diseases. The main research topics were pneumoconiosis, noise-induced hearing loss and some chemical poisoning. However, improving working condition was not the top priority until the late 1980s. Carbon disulfide poisoning gave a big impact to the society. It made the government take many actions to improve working condition through regulation, enforcement, supporting academia, raising research fund, and establishing a research institute. Recently, classical occupational diseases have decreased and the interest from researchers has also reduced. Many claims for stress-related cardio-cerebrovascular diseases brought much concern and research on job stress. Work-related musculoskeletal disease became a major issue. Many workers are interested in quality of life, such as health promotion. Therefore, research on health promotion, job stress, and psychological problem from work organization would be the main research topics in the future, although research on occupational diseases, such as asthma, cancer and various diseases caused by chemicals are still attractive to researchers.
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PMID:Recent advances in occupational health research in Korea. 1512 57

Carbon nanotubes (CNTs) are newly developed materials with unique properties and a range of industrial and commercial applications. A rapid expansion in the production of CNT materials may increase the risk of human exposure to CNTs. Studies in rodents have shown that certain forms of CNTs are potent fibrogenic inducers in the lungs to cause interstitial, bronchial, and pleural fibrosis characterized by the excessive deposition of collagen fibers and the scarring of involved tissues. The cellular and molecular basis underlying the fibrotic response to CNT exposure remains poorly understood. Myofibroblasts are a major type of effector cells in organ fibrosis that secrete copious amounts of extracellular matrix proteins and signaling molecules to drive fibrosis. Myofibroblasts also mediate the mechano-regulation of fibrotic matrix remodeling via contraction of their stress fibers. Recent studies reveal that exposure to CNTs induces the differentiation of myofibroblasts from fibroblasts in vitro and stimulates pulmonary accumulation and activation of myofibroblasts in vivo. Moreover, mechanistic analyses provide insights into the molecular underpinnings of myofibroblast differentiation and function induced by CNTs in the lungs.In view of the apparent fibrogenic activity of CNTs and the emerging role of myofibroblasts in the development of organ fibrosis, we discuss recent findings on CNT-induced lung fibrosis with emphasis on the role of myofibroblasts in the pathologic development of lung fibrosis. Particular attention is given to the formation and activation of myofibroblasts upon CNT exposure and the possible mechanisms by which CNTs regulate the function and dynamics of myofibroblasts in the lungs. It is evident that a fundamental understanding of the myofibroblast and its function and regulation in lung fibrosis will have a major influence on the future research on the pulmonary response to nano exposure, particle and fiber-induced pneumoconiosis, and other human lung fibrosing diseases.
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PMID:Myofibroblasts and lung fibrosis induced by carbon nanotube exposure. 2781 27

T helper (Th) 2-dependent type 2 immune pathways have been recognized as an important driver for the development of fibrosis. Upon stimulation, activated Th2 immune cells and type 2 cytokines interact with inflammatory and tissue repair functions to stimulate an overzealous reparative response to tissue damage, leading to organ fibrosis and destruction. In this connection, type 2 pathways are activated by a variety of insults and pathological conditions to modulate the response. Carbon nanotubes (CNTs) are nanomaterials with a wide range of applications. However, pulmonary exposure to CNTs causes a number of pathologic outcomes in animal lungs, dominated by inflammation and fibrosis. These findings, alongside the rapidly expanding production and commercialization of CNTs and CNT-containing materials in recent years, have raised concerns on the health risk of CNT exposure in humans. The CNT-induced pulmonary fibrotic lesions resemble those of human fibrotic lung diseases, such as idiopathic pulmonary fibrosis and pneumoconiosis, to a certain extent with regard to disease development and pathological features. In fibrotic scenarios, immune cells are activated including varying immune pathways, ranging from innate immune cell activation to autoimmune disease. These events often precede and/or accompany the occurrence of fibrosis. Upon CNT exposure, significant induction and activation of Th2 cells and type 2 cytokines in the lungs are observed. Moreover, type 2 pathways are shown to play important roles in promoting CNT-induced lung fibrosis by producing type 2 pro-fibrotic factors and inducing the reparative phenotypes of macrophages in response to CNTs. In light of the vastly increased demand for nanosafety and the apparent induction and multiple roles of type 2 immune pathways in lung fibrosis, we review the current literature on CNT-induced lung fibrosis, with a focus on the induction and activation of type 2 responses by CNTs and the stimulating function of type 2 signaling on pulmonary fibrosis development. These analyses provide new insights into the mechanistic understanding of CNT-induced lung fibrosis, as well as the potential of using type 2 responses as a monitoring target and therapeutic strategy for human fibrotic lung disease.
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PMID:Type 2 Immune Mechanisms in Carbon Nanotube-Induced Lung Fibrosis. 2987 41

Carbon nanotubes (CNTs) are nanomaterials with unique physicochemical properties that are targets of great interest for industrial and commercial applications. Notwithstanding, some characteristics of CNTs are associated with adverse outcomes from exposure to pathogenic particulates, raising concerns over health risks in exposed workers and consumers. Indeed, certain forms of CNTs induce a range of harmful effects in laboratory animals, among which inflammation, fibrosis, and cancer are consistently observed for some CNTs. Inflammation, fibrosis, and malignancy are complex pathological processes that, in summation, underlie a major portion of human disease. Moreover, the functional interrelationship among them in disease pathogenesis has been increasingly recognized. The CNT-induced adverse effects resemble certain human disease conditions, such as pneumoconiosis, idiopathic pulmonary fibrosis (IPF), and mesothelioma, to some extent. Progress has been made in understanding CNT-induced pathologic conditions in recent years, demonstrating a close interconnection among inflammation, fibrosis, and cancer. Mechanistically, a number of mediators, signaling pathways, and cellular processes are identified as major mechanisms that underlie the interplay among inflammation, fibrosis, and malignancy, and serve as pathogenic bases for these disease conditions in CNT-exposed animals. These studies indicate that CNT-induced pathological effects, in particular, inflammation, fibrosis, and cancer, are mechanistically, and in some cases, causatively, interrelated. These findings generate new insights into CNT adverse effects and pathogenesis and provide new targets for exposure monitoring and drug development against inflammation, fibrosis, and cancer caused by inhaled nanomaterials.
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PMID:Integration of inflammation, fibrosis, and cancer induced by carbon nanotubes. 3153 43

Carbon nanotube (CNT)-induced pulmonary inflammation and fibrosis have been intensively observed and characterized in numerous animal studies in the past decade. Remarkably, CNT-induced fibrotic lesions highly resemble some human fibrotic lung diseases, such as IPF and pneumoconiosis, regarding disease development and pathological features. This notion leads to a serious concern over the health impact of CNTs in exposed human populations, considering the rapidly expanding production of CNT materials for diverse industrial and commercial applications, and meanwhile provides the rationale for exploring CNT-induced pathologic effects in the lung. Accumulating mechanistic understanding of CNT lung pathology at the systemic, cellular, and molecular levels has demonstrated the potential of using CNT-exposed animals as a new disease model for the studies on inflammation, fibrosis, and the interactions between these two disease states. Tissue microenvironment plays critical roles in maintaining homeostasis and physiological functions of organ systems. When aberrant microenvironment forms under intrinsic or extrinsic stimulation, tissue abnormality, organ dysfunction, and pathological outcomes are induced, resulting in disease development. In this article, the cellular and molecular alterations that are induced in tissue microenvironment and implicated in the initiation and progression of inflammation and fibrosis in CNT-exposed lungs, including effector cells, soluble mediators, and functional events exemplified by cell differentiation and extracellular matrix (ECM) modification, are summarized and discussed. This analysis would provide new insights into the mechanistic understanding of lung inflammation and fibrosis induced by CNTs, as well as the development of CNT-exposed animals as a new model for human lung diseases.
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PMID:Microenvironmental Alterations in Carbon Nanotube-Induced Lung Inflammation and Fibrosis. 3218 74