Plasma Metabolic Pro Ling of the Patients with Silicosis and Asbestosis
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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]). -
Hypersensitivity Pneumonitis: Challenges in Diagnosis and Management, Avoiding Surgical Lung Biopsy
395 Hypersensitivity Pneumonitis: Challenges in Diagnosis and Management, Avoiding Surgical Lung Biopsy Ferran Morell, MD1,2 Ana Villar, MD2,3 Iñigo Ojanguren, MD2,3 Xavier Muñoz, MD2,3 María-Jesús Cruz, PhD2,3 1 Vall d’Hebron Institut de Recerca (VHIR), Barcelona, Catalonia, Spain Address for correspondence Ferran Morell, MD, Vall d’Hebron Institut 2 Ciber de Enfermedades Respiratorias (CIBERES), Barcelona, Spain de Recerca (VHIR), PasseigValld’Hebron, 119-129, 08035 Barcelona, 3 Servei de Pneumologia, Hospital Universitari Vall d’Hebron, Catalonia, Spain (e-mail: [email protected]). Barcelona, Spain Semin Respir Crit Care Med 2016;37:395–405. Abstract This review presents an update of the currently available information related to Keywords hypersensitivity pneumonitis, with a particular focus on the contribution of several ► hypersensitivity techniques in the diagnosis of this condition. The methods discussed include proper pneumonitis elaboration of a complete medical history, targeted auscultation, detection of specific ► bronchoalveolar immunoglobulin G antibodies against the most common antigens causing this disease, lavage skin tests, antigen-specific lymphocyte activation assays, bronchoalveolar lavage, and ► fi speci c inhalation cryobiopsy. Special emphasis is placed on the relevant contribution of specificinhalation challenge challenge (bronchial challenge test). Surgical lung biopsy is presented as the ultimate ► bronchial challenge recourse, to be used when the diagnosis cannot be reached through the other methods test covered. -
Workers' Compensation for Occupational Respiratory Diseases
ORIGINAL ARTICLE http://dx.doi.org/10.3346/jkms.2014.29.S.S47 • J Korean Med Sci 2014; 29: S47-51 Workers’ Compensation for Occupational Respiratory Diseases So-young Park,1 Hyoung-Ryoul Kim,2 The respiratory system is one of the most important body systems particularly from the and Jaechul Song3 viewpoint of occupational medicine because it is the major route of occupational exposure. In 2013, there were significant changes in the specific criteria for the recognition of 1Occupational Lung Diseases Institute, Korea Workers’ Compensation & Welfare Service, Ansan; occupational diseases, which were established by the Enforcement Decree of the Industrial 2Department of Occupational and Environmental Accident Compensation Insurance Act (IACIA). In this article, the authors deal with the Medicine, College of Medicine, the Catholic former criteria, implications of the revision, and changes in the specific criteria in Korea by University of Korea, Seoul; 3Department of focusing on the 2013 amendment to the IACIA. Before the 2013 amendment to the IACIA, Occupational and Environmental Medicine, Hanyang University College of Medicine, Seoul, occupational respiratory disease was not a category because the previous criteria were Korea based on specific hazardous agents and their health effects. Workers as well as clinicians were not familiar with the agent-based criteria. To improve these criteria, a system-based Received: 20 December 2013 structure was added. Through these changes, in the current criteria, 33 types of agents Accepted: 6 April 2014 and 11 types of respiratory diseases are listed under diseases of the respiratory system. In Address for Correspondence: the current criteria, there are no concrete guidelines for evaluating work-relatedness, such Hyoung-Ryoul Kim, MD as estimating the exposure level, latent period, and detailed examination methods. -
Silicosis: Pathogenesis and Changklan Muang Chiang Mai 50100 Thailand; Tel: 66 53 276364; Fax: 66 53 273590; E-Mail
Central Annals of Clinical Pathology Bringing Excellence in Open Access Review Article *Corresponding author Attapon Cheepsattayakorn, 10th Zonal Tuberculosis and Chest Disease Center, 143 Sridornchai Road Silicosis: Pathogenesis and Changklan Muang Chiang Mai 50100 Thailand; Tel: 66 53 276364; Fax: 66 53 273590; E-mail: Biomarkers Submitted: 04 October 2018 Accepted: 31 October 2018 1,2 3 Attapon Cheepsattayakorn * and Ruangrong Cheepsattayakorn Published: 31 October 2018 1 10 Zonal Tuberculosis and Chest Disease Center, Chiang Mai, Thailand ISSN: 2373-9282 2 Department of Disease Control, Ministry of Public Health, Thailand Copyright 3 Department of Pathology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand © 2018 Cheepsattayakorn et al. OPEN ACCESS Abstract Ramazzini first described this disease, namely “Pneumonoultramicroscopicsilicovolcanokoniosis” Keywords and then was changed according to the types of exposed dust. No reliable figures on the silica- • Silicosis inhalation exposed individuals are officially documented. How silica particles stimulate pulmonary • Biomarkers response and the exact path physiology of silicosis are still not known and urgently require further • Pathogenesis research. Nevertheless, many researchers hypothesized that pulmonary alveolar macrophages play a major role by secreting fibroblast-stimulating factor and re-ingesting these ingested silica particles by the pulmonary alveolar macrophage with progressive magnification. Finally, ending up of the death of the pulmonary alveolar macrophages and the development of pulmonary fibrosis appear. Various mediators, such as CTGF, FBRS, FGF2/bFGF, and TNFα play a major role in the development of silica-induced pulmonary fibrosis. A hypothesis of silicosis-associated abnormal immunoglobulins has been postulated. In conclusion, novel studies on pathogenesis and biomarkers of silicosis are urgently needed for precise prevention and control of this silently threaten disease of the world. -
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. -
Respiratory Function Changes After Asbestos Pleurisy
Thorax: first published as 10.1136/thx.35.1.31 on 1 January 1980. Downloaded from Thorax, 1980, 35, 31-36 Respiratory function changes after asbestos pleurisy P H WRIGHT, A HANSON, L KREEL, AND L H CAPEL From the Cardiothoracic Institute, London Chest Hospital, East Ham Chest Clinic, London, and the Division of Radiology, Clinical Research Centre, Northwick Park Hospital, Harrow ABSTRACT Six patients with radiographic evidence of diffuse pleural thickening after industrial asbestos exposure are described. Five had computed tomography of the thorax. All the scans showed marked circumferential pleural thickening often with calcification, and four showed no significant evidence of intrapulmonary fibrosis (asbestosis). Lung function testing showed reduc- tion of the inspiratory capacity and the single-breath carbon monoxide transfer factor (TLco). The transfer coefficient, calculated as the TLCO divided by the alveolar volume determined by helium dilution during the measurement of TLco, was increased. Pseudo-static compliance curves showed markedly more negative intrapleural pressures at all lung volumes than found in normal people. These results suggest that the circumferential pleural thickening was preventing normal lung expansion despite abnormally great distending pressures. The pattern of lung function tests is sufficiently distinctive for it to be recognised in clinical practice, and suggests that the lungs are held rigidly within an abnormal pleura. The pleural thickening in our patients may have been related to the condition described as "benign asbestos pleurisy" rather than the copyright. interstitial fibrosis of asbestosis. Malignant pleural effusion associated with meso- necessary in many of these early cases, and opera- thelioma or bronchial carcinoma is a recognised tion notes recorded the presence of marked http://thorax.bmj.com/ complication of asbestos exposure. -
Etiology and Aggravation in Thoracic Medicine
DePaul Law Review Volume 21 Issue 1 Fall 1971: Medico-Legal Symposium II Article 6 Etiology and Aggravation in Thoracic Medicine W. B. Buckingham Follow this and additional works at: https://via.library.depaul.edu/law-review Recommended Citation W. B. Buckingham, Etiology and Aggravation in Thoracic Medicine, 21 DePaul L. Rev. 103 (1971) Available at: https://via.library.depaul.edu/law-review/vol21/iss1/6 This Article is brought to you for free and open access by the College of Law at Via Sapientiae. It has been accepted for inclusion in DePaul Law Review by an authorized editor of Via Sapientiae. For more information, please contact [email protected]. ETIOLOGY AND AGGRAVATION IN THORACIC MEDICINE W. B. BUCKINGHAM* INTRODUCTION N THE practice of thoracic medicine, misconceptions about the etiology and/or the aggravation of thoracic diseases are common- place. These errors are frequently perpetuated by patients and occasionally by well-meaning lawyers and well-trained physicians. Superficial analysis indicates that most of these misconceptions arise from the concept of post hoc ergo propter hoc. In diseases affecting the thorax, multiple etiological factors commonly operate over pro- longed periods of time. Under such circumstances it is extremely difficult to sort out cause and effect. Thus, in light of the imperfec- tions in diagnosis, misconceptions about etiology and aggravation of disease can be appreciated. There are substantial limitations and uncertainties to any medical diagnosis. The semantic derivation of the word "diagnosis" comes through the Greek words whose meaning is "to know through" or "to understand by means of the manifestations of." A complete diagnosis in the modem sense of the term is a disease entity in which the causative mechanisms are clearly understood, and the man- ifestations readily appreciated both in clinical signs and symptoms and in laboratory findings. -
Pathological Aspects of Asbestosis
POSTGRAD. MED. J. (1966), 42, 613. Postgrad Med J: first published as 10.1136/pgmj.42.492.613 on 1 October 1966. Downloaded from PATHOLOGICAL ASPECTS OF ASBESTOSIS D. O'B. HOURIHANE, M.D., M.C.Path., D.C.P.(Lond.), M.R.C.P.I. W. T. E. MCCAUGHEY, M.D., M.C.Path. School ofPathology, Trinity College, Dublin WIDESPREAD recognition of asbestosis dates from the work of Merewether and Price in 1930. They investigated 363 asbestos workers and concluded that there was a pneumoconiosis resulting from asbestos inhalation, that this condition shortened life, and that measures to diminish the atmospheric concentration of asbestos dust would reduce the incidence of the disease. In 1931 asbestosis was accepted as a compensatable disease in Great Britain and steps were taken to reduce the risk in the asbestos industry. 18 years later Wyers (1949) found that the age at death in this disorder had Protected by copyright. increased and that finger-clubbing had become more common. He suggested that these changes were due to a more chronic form of the disease resulting from improved dust control in the industry following the legislation of 1931. Currently however, the number of new cases of asbestosis in Great Britain is increasing, their frequency suggesting an incidence rate of at least five per thousand of those occupation- ally exposed (McVittie, 1965). Though earlier reports indicated that tuberculosis was common in asbestosis (Wyers, 1949; Gloyne, 1951; Bonser, Foulds and Stewart, 1955) it appears to be a rare I 0 n < ,. ' complication at the present time (Buchanan, 1965). -
Screening of Pulmonary Hypertension in Chronic Obstructive Pulmonary Disease and Silicosis by Discriminant Functions
Eur Resplr J 1992, 5, 444-451 Screening of pulmonary hypertension in chronic obstructive pulmonary disease and silicosis by discriminant functions H. Evers, F. Liehs, K. Harzbecker, D. Wenzel, A. Wilke, W. Pielesch, J. Schauer, W. Nahrendorf, J. Preisler, A. Luther, D. Scheuler, W. Reimer, W. Schilling Screening of pulmonary hypertension in chronic obstructive pulmonary disease and Research Project Lung Diseases of the silicosis by discriminant functions. H. Evers, F. Liehs, K. Harzbecker, D. Wenzel, A. Ministry of Health, Berlin. Wilke, W. Pielesch, J. Schauer, W. Nahrendorf, J. Preisler, R. Luther, D. Scheuler, W. Reimer, W. Schilling. ABSTRACT: The aim of our prospective multicentric study was to develop a Correspondence: H. Evers Chest Clinic screening method for pulmonary hypertension in patients with chronic lung diseases. Str. nach Fichtenwalde 16 We investigated 710 patients in 10 hospitals: 315 males and 109 females with chronic D(o)·1504 Beelitz-Heilstiitten obstructive pulmonary disease, and 286 males with silicosis. Manifest pulmonary Germany. hypertension was defined as pulmonary artery pressure > 20 mmHg (2.7 kPa) at rest. The multivariate statistical method used was a stepwise discriminant analysis. In males with chronic obstructive pulmonary disease, the diameter of the right Keywords: descending pulmonary artery, forced expiratory volume in one second {FEV ) Chronic obstructive pulmonary disease 1 discriminant analysis ) arterial oxygen tension (Pao1 at rest, and age turned out to be relevant for dis crimilllltion of groups with and without manifest pulmonary hypertension. For pulmonary hypertension screening females the FEV/FVC (forced vital capacity) ratio replaced the absolute value of silicosis. FEV1 in the calculated discriminant function. -
08-0205: N.M. and DEPARTMENT of the NAVY, PUGET S
United States Department of Labor Employees’ Compensation Appeals Board __________________________________________ ) N.M., Appellant ) ) and ) Docket No. 08-205 ) Issued: September 2, 2008 DEPARTMENT OF THE NAVY, PUGET ) SOUND NAVAL SHIPYARD, Bremerton, WA, ) Employer ) __________________________________________ ) Appearances: Oral Argument July 16, 2008 John Eiler Goodwin, Esq., for the appellant No appearance, for the Director DECISION AND ORDER Before: DAVID S. GERSON, Judge COLLEEN DUFFY KIKO, Judge JAMES A. HAYNES, Alternate Judge JURISDICTION On October 30, 2007 appellant filed a timely appeal from a November 17, 2006 decision of the Office of Workers’ Compensation Programs denying his occupational disease claim. Pursuant to 20 C.F.R. §§ 501.2(c) and 501.3, the Board has jurisdiction over the merits of the claim. ISSUE The issue is whether appellant has established that he sustained occupational asthma in the performance of duty due to accepted workplace exposures. On appeal, he, through his attorney, asserts that the Office did not provide Dr. William C. Stewart, the impartial medical examiner, with a complete, accurate statement of accepted facts. FACTUAL HISTORY On December 8, 2004 appellant, then a 57-year-old insulator, filed an occupational disease claim (Form CA-2) asserting that he sustained occupational asthma and increasing shortness of breath due to workplace exposures to fiberglass, silicates, welding smoke, polychlorobenzenes, rubber, dusts, gases, fumes and smoke from “burning out” submarines from 1991 through January -
Concurrent Silicosis and Pulmonary Mycosis at Death
DISPATCHES B35–B49 (any mycosis). We defi ned pulmonary myco- Concurrent sis as death with ICD-9 and ICD-10 codes 112.4/B37.1 (candidiasis); 114/B38.0, B38.1, B38.2, B38.9 (coccid- Silicosis and ioidomycosis); 115/B39.0, B39.1, B39.2, B39.4, B39.9 (histoplasmosis); 116.0/B40.0, B40.1, B40.2, B40.9 (blas- Pulmonary tomycosis); 116.1/B41.0, B41.9 (paracoccidioidomyco- sis); 117.1/B42.0, B42.9 (sporotrichosis); 117.7/B46.0, Mycosis at Death B46.5, B46.9 (zygomycosis); 117.3/B44.0, B44.1, B44.9 Yulia Iossifova,1 Rachel Bailey, John Wood, (aspergillosis); 117.5/B45.0, B45.9 (cryptococcosis); and and Kathleen Kreiss 118/B48.7 (opportunistic mycoses). For many mycoses, ICD-9 codes do not differentiate pulmonary from other To examine risk for mycosis among persons with sili- types of mycoses. For ICD-10 codes, we limited data to cosis, we examined US mortality data for 1979–2004. Per- mycoses coded as pulmonary, opportunistic, and some sons with silicosis were more likely to die with pulmonary unspecifi ed type of mycoses (e.g., B38.9, B39.4, B39.9, mycosis than were those without pneumoconiosis or those with more common pneumoconioses. Health profession- B40.9, B41.9, B42.9, B44.9, B45.9, B46.5, and B46.9). als should consider enhanced risk for mycosis for silica- We provided results with and without ICD-9 code for op- exposed patients. portunistic mycoses and ICD-10 codes for unspecifi ed mycoses and opportunistic mycoses. We computed prevalence rate ratios and 95% con- he pneumoconioses are a group of irreversible but fi dence intervals (CIs) to separately compare pulmonary Tpreventable interstitial lung diseases, most commonly mycosis prevalence at death among persons with silicosis, associated with inhalation of asbestos fi bers, coal mine asbestosis, and CWP with that for persons in the refer- dust, or crystalline silica dust. -
Cryptococcus Pneumonia Presenting in an Immunocompetent Host with Pulmonary Asbestosis
Guy et al. Journal of Medical Case Reports 2012, 6:170 JOURNAL OF MEDICAL http://www.jmedicalcasereports.com/content/6/1/170 CASE REPORTS CASE REPORT Open Access Cryptococcus pneumonia presenting in an immunocompetent host with pulmonary asbestosis: a case report Judah P Guy1, Shahzad Raza1,2*, Elliot Bondi1, Yale Rosen2, Dong-Sung Kim2 and Barbara J Berger1 Abstract Introduction: Cryptococcal infections pose a diagnostic challenge in an immunocompetent host. Asbestos exposure has been associated with pulmonary aspergillosis. This case highlights an interesting presentation of cryptococcal lung inflammation with underlying asbestosis. Case presentation: A 63-year-old Mediterranean Caucasian woman presented with progressive dry cough of nine months duration. A computed tomography (CT) scan of her chest revealed multiple foci in the right infra-hilar region, which were seen as hot lung masses on a positron emission tomography (PET) scan. These multiple foci appeared metastatic in nature throughout both lung fields with early mediastinal invasion. A computed tomography (CT)-guided core biopsy was obtained from a dominant right lower lobe lung mass. Histology showed chronic granulomatous inflammation with numerous budding yeast forms that were GMS-, PAS-, and mucin- positive, consistent with cryptococcosis together with asbestos bodies (ferruginous). She was managed with fluconazole (400mg (6mg/kg) per day orally) daily. At her six-month follow up, she had marked improvement in her general condition along with a diminution of the lower lobe lung mass. Conclusion: We report a clinical and radiological improvement in a patient treated for cryptococcal pneumonia. Asbestos exposure was likely to have been an important pathophysiological precursor to infection by environmental fungi.