Asbestos Safety Manual

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Asbestos Safety Manual D. Potential Health Effects Related to Asbestos Routes of Entry While asbestos fibers may gain entry into the body through ingestion, the major route of exposure is inhalation. Asbestos fibers have no odor, and those that you may inhale are invisible to the naked eye. The Respiratory System The respiratory system includes the mouth, nose, wind pipe (trachea), bronchi, and lungs. The lungs are located within the pleural cavity. Lying within the cavity and covering the lungs is a lining called the pleural mesothelium. The lungs contain air sacks called alveoli. The alveoli are the sites where oxygen is absorbed into the blood and carbon dioxide is removed from the blood. The body’s respiratory system has defense mechanisms to keep foreign particles from causing damage. Amazingly, estimates indicate that these mechanisms are 95 to 98 percent effective. Examples of some defense mechanisms and their functions are: • The mouth and nose filter out very large particles. • Coated bronchi filter out smaller particles. • Cilia, which are hair-like protrusions on cells lining the airways (bronchial tree), move particles up to the back of the mouth where they are swallowed or expelled. • Alveoli in the lower respiratory system trap the smallest particles. The particles may be attacked by large cells, known as macrophages, which try to digest them. Because asbestos is a mineral fiber, the macrophages are often not successful. Asbestos Health Risks Most of the information about asbestos disease comes from studying workers in the various asbestos industries. The bulk of data comes from World War II shipbuilding activities and the asbestos industries in the United States and England. Exposure to very high levels of airborne asbestos typical of asbestos trades prior to 1972 has been linked with the following diseases: Asbestosis is a chronic disease in which the lungs become scarred (fibrosis) as a result of a biological reaction to the inhalation of asbestos fibers. Scarring causes thickening of the walls of the lungs 14 15.

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Occupational Airborne Particulates
Environmental Burden of Disease Series, No. 7 Occupational airborne particulates Assessing the environmental burden of disease at national and local levels Tim Driscoll Kyle Steenland Deborah Imel Nelson James Leigh Series Editors Annette Prüss-Üstün, Diarmid Campbell-Lendrum, Carlos Corvalán, Alistair Woodward World Health Organization Protection of the Human Environment Geneva 2004 WHO Library Cataloguing-in-Publication Data Occupational airborne particulates : assessing the environmental burden of disease at national and local levels / Tim Driscoll … [et al.]. (Environmental burden of disease series / series editors: Annette Prüss-Ustun ... [et al.] ; no. 7) 1.Dust - adverse effects 2.Occupational exposure 3.Asthma - chemically induced 4.Pulmonary disease, Chronic obstructive - chemically induced 5.Pneumoconiosis - etiology 6.Cost of illness 7.Epidemiologic studies 8.Risk assessment - methods 9.Manuals I.Driscoll, Tim. II.Prüss-Üstün, Annette. III.Series. ISBN 92 4 159186 2 (NLM classification: WA 450) ISSN 1728-1652 Suggested Citation Tim Driscoll, et al. Occupational airborne particulates: assessing the environmental burden of disease at national and local levels. Geneva, World Health Organization, 2004. (Environmental Burden of Disease Series, No. 7). © World Health Organization 2004 All rights reserved. Publications of the World Health Organization can be obtained from Marketing and Dissemination, World Health Organization, 20 Avenue Appia, 1211 Geneva 27, Switzerland (tel: +41 22 791 2476; fax: +41 22 791 4857; email: [email protected]).
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Pneumoconiosis
Prim Care Respir J 2013; 22(2): 249-252 PERSPECTIVE Pneumoconiosis *Paul Cullinan1, Peter Reid2 1 Consultant Physician, Royal Brompton and Harefield NHS Foundation Trust, London, UK 2 Consultant Physician, Western General Hospital, Edinburgh, UK Introduction Figure 1. Asbestosis; the HRCT scan shows the typical The pneumoconioses are parenchymal lung diseases that arise from picture of subpleural fibrosis (solid arrow); in addition inhalation of (usually) inorganic dusts at work. Some such dusts are there is diffuse, left-sided pleural thickening (broken biologically inert but visible on a chest X-ray or CT scan; thus, while arrow), characteristic too of heavy asbestos exposure they are radiologically alarming they do not give rise to either clinical disease or deficits in pulmonary function. Others – notably asbestos and crystalline silica – are fibrogenic so that the damage they cause is through the fibrosis induced by the inhaled dust rather than the dust itself. Classically these give rise to characteristic radiological patterns and restrictive deficits in lung function with reductions in diffusion capacity; importantly, they may progress long after exposure to the causative mineral has finished. In the UK and similar countries asbestosis is the commonest form of pneumoconiosis but in less developed parts of the world asbestosis is less frequent than silicosis; these two types are discussed in detail below. Other, rarer types of pneumoconiosis include stannosis (from tin fume), siderosis (iron), berylliosis (beryllium), hard metal disease (cobalt) and coal worker’s pneumoconiosis. Asbestosis Clinical scenario How is the diagnosis made? Asbestosis is the ‘pneumoconiosis’ that arises from exposure to A man of 78 reports gradually worsening breathlessness; he has asbestos in the workplace.1 The diagnosis is made when, on the no relevant medical history of note and has never been a regular background of heavy occupational exposure to any type of asbestos, smoker.
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Pathological Aspects of Asbestosis
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medRxiv preprint doi: https://doi.org/10.1101/2021.03.09.21253224; this version posted March 12, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-ND 4.0 International license . What role for asbestos in idiopathic pulmonary fibrosis? Findings from the IPF job exposures study Carl J Reynolds1, Rupa Sisodia1, Chris Barber2, Cosetta Minelli1, Sara De Matteis3, Miriam Moffatt1, John Cherrie4, Anthony Newman Taylor1, Paul Cullinan1 on behalf of the IPFJES collaborators (Sophie Fletcher, Gareth Walters, Lisa Spenser, Helen Parfrey, Gauri Saini, Nazia Chaudhuri, Alex West, Huzaifa Adamali, Paul Beirne, Ian Forrest, Michael Gibbons, Justin Pepperell, Nik Hirani, Kim Harrison, Owen Dempsey, Steve O’Hickey, David Thickett, Dhruv Parekh, Suresh Babu, Andrew Wilson, George Chalmers, Melissa Wickremasinghe, and Robina Coker) 1 National Heart and Lung Institute, Imperial College London, United Kingdom 2 Centre for Workplace Health, University of Sheffield, United Kingdom 3 Department of Medical Sciences and Public Health, University of Cagliari, Italy 4 Institute of Occupational Medicine, Edinburgh, United Kingdom Corresponding author Dr Carl J Reynolds National Heart and Lung Institute, 1b Manresa Road, London, United Kingdom, SW3 6LR email: [email protected] Authors’ Contributions: CJR, CB, CM, MM, ANT, JC, PC made substantial NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. medRxiv preprint doi: https://doi.org/10.1101/2021.03.09.21253224; this version posted March 12, 2021.
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