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Respiratory Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Ian Pavord, Nayia Petousi, Nick Talbot
This is a chronic fibrotic illness caused by inhalation of coal dust. As with asbestos, there is a dose–response relationship. There are two types: simple and complicated (known as progressive massive fibrosis).
The respiratory system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
A percentage of patients with simple CWP go on to develop complicated CWP. At an early stage this is asymptomatic, but a minority (<10%) develop extensive fibrosis with bullous emphysema, and complain of breathlessness, cough, and exertional dyspnoea, progressing to cor pulmonale. It is characterized by the development of progressive massive fibrosis. These are large areas of rubbery fibrosis containing coal dust which measure >1 cm and are more common in the upper lobe. These may reach several centimetres, show varying cavitation due to ischaemic necrosis, and can destroy a lobe or lobes. On histological examination dust is seen, free and within macrophages, and admixed with collagen.
Inorganic Particulates in Human Lung: Relationship to the Inflammatory Response
Published in William S. Lynn, Inflammatory Cells and Lung Disease, 2019
Victor L. Roggli, J. P. Mastin, John D. Shelburne, Michael Roe, Arnold R. Brody
In terms of fibrogenic capabilities, amorphous inorganic carbon appears to be biologically inert. Intratracheal instillation of inorganic carbon in mice results in a marked increase in alveolar macrophages, which are derived from the interstitial macrophage population as well as by recruitment of bone marrow monocytes.116 The nodular fibrotic lesions which may be found in the lungs of some coal workers are thought to be related to the silica content of the coal dust.113 A correlation can be demonstrated between the total quartz content of the lung and the development of progressive massive fibrosis in coal workers.117 On the other hand, no correlation could be found between lung “soot” (acid-insoluble dust) concentration and the presence of lung disease (e.g., chronic bronchitis or emphysema) in an autopsy population.118 Nevertheless, these findings do not exclude an association between emphysema or bronchitis and some component of the acid insoluble residue (see Section IV). The concept that inorganic particulate matter, such as amorphous carbon, might act as a concentrating surface for the accumulation of various organic carcinogens, permitting prolonged and proximate contact with cells of the lung119, 120 and hence enhancing carcinogensis in man, is an intriguing but as yet unproven hypothesis.
The interplay between TGF-β/SMAD and BMP/SMAD signaling pathways in the epithelial mesenchymal transition of A549 cells induced by silica
Published in Toxicology Mechanisms and Methods, 2018
Yanhua Yu, Yanming Lin, Gengxia Yang, Lin Tian
Silicosis, caused by the exposure to free crystalline silica (silicon dioxide), is one of the most common occupational diseases in China (Leung et al. 2012). The pulmonary progressive massive fibrosis is a significant feature of silicosis. Fibroblasts proliferation and collagen deposition are primarily responsible for silica-induced pulmonary fibrosis (Mossman and Churg 1998; Kolosova et al. 2011). The potential sources of pulmonary fibroblasts include directional differentiation of bone marrow stem cells, the proliferation of resident fibroblasts, and epithelial–mesenchymal transition (EMT). Prior study has shown EMT contributed to fibroblasts in bleomycin-induced lung fibrosis (Tanjore et al. 2009).
Disseminated blastomycosis in coalworkers’ pneumoconiosis
Published in Baylor University Medical Center Proceedings, 2019
Utsav Shrestha, Chetan Naik, Arthur Huen, Keely Marshall, Karunamurthy Arivarasan, John McDyer
Our patient had a known diagnosis of coalworkers’ pneumoconiosis with CT of the chest showing nodular consolidation and dense fibrosis extending to the periphery of the chest suggestive of progressive massive fibrosis. It also showed calcification indicative of silicosis.7 New pulmonary cavitation in progressive massive fibrosis with fever, hemoptysis, and weight loss was concerning for silico-tuberculosis.8
Is individual genetic susceptibility a link between silica exposure and development or severity of silicosis? A systematic review
Published in Inhalation Toxicology, 2020
Kaio Cezar Rodrigues Salum, Marcos Cesar Santos Castro, Ângela Santos Ferreira Nani, Fabiana Barzotto Kohlrausch
The exclusion criteria comprised the following items: (1) articles evaluating the effect of gene variants in coal workers’ pneumoconiosis (CWP), progressive massive fibrosis (PMF), and pneumoconiosis without sub-classification in silicosis, (2) incomplete data, (3) animal studies, (4) literature reviews.