Pneumoconiosis Medical Panel
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Risk Factors for Malignant Mesothelioma
cancer.org | 1.800.227.2345 Malignant Mesothelioma Causes, Risk Factors, and Prevention Risk Factors A risk factor is anything that affects your chance of getting a disease such as cancer. Learn more about the risk factors for malignant mesothelioma. ● Risk Factors for Malignant Mesothelioma ● What Causes Malignant Mesothelioma? Prevention There's no way to completely prevent mesothelioma. But there are things you can do that might lower your risk. Learn more. ● Can Malignant Mesothelioma Be Prevented? Risk Factors for Malignant Mesothelioma A risk factor is anything that increases your chance of getting a disease such as cancer. Different cancers have different risk factors. Some risk factors, like smoking, can be changed. Others, like a person’s age or family history, can’t be changed. But having a 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 known risk factor, or even many, does not mean that you will get the disease. And some people who get the disease may have few or no known risk factors. Researchers have found some factors that increase a person’s risk of mesothelioma. Asbestos The main risk factor for pleural mesothelioma is exposure to asbestos. In fact, most cases of pleural mesothelioma have been linked to high levels of asbestos exposure, usually in the workplace. Asbestos is a group of minerals that occur naturally as bundles of tiny fibers. These fibers are found in soil and rocks in many parts of the world. When asbestos fibers in the air are inhaled, they can get into the lungs. Fibers that stay in the lungs can travel to the ends of the small airways and enter the pleural lining of the lung and chest wall. -
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]). -
Solitary Fibrous Tumor of the Pleura: Histology, CT Scan Images and Review of Literature Over the Last Twenty Years
DOI: 10.26717/BJSTR.2017.01.000150 Flavio Colaut. ISSN: 2574-1241 Biomed J Sci & Tech Res Case Report Open Access Solitary Fibrous Tumor of the Pleura: Histology, CT Scan Images and Review of Literature over the Last Twenty Years Giulia Bora1, Flavio Colaut2*, Gianni Segato3, Luisa Delsedime4 and Alberto Oliaro1 1Department of Thoracic Surgery, University of Turin, Italy 2Department of General Surgery and Thoracic, City Hospital , Montebelluna, (Treviso), Italy 3Department of General Surgery, S. Bortolo City Hospital, Vicenza, Italy 4Department of Pathology, University of Turin, Italy Received: June 14, 2017; Published: June 26, 2017 *Corresponding author: Flavio Colaut, Department of General Surgery, City Hospital Montebelluna, Thoracic City Hospital, via Montegrappa 1, 31044 Montebelluna (Treviso), Italy, Tel: ; Fax: 0499367643; Email: Introduction Literature up to 800 cases [1-3] have been reported, and these in case of recurrence [10,16,17]. In less than 5% of patients with Solitary fibrous tumor of the pleura is a rare neoplasm. In numbers show its rarity, despite of mesotheliomas, the most pleural SFPTs an increase of insulin-like factor II type occur and this causes refractory to therapy hypoglycaemia (Doege-Potter syndrome) similar in both sexes and there no differences in both benign and [10,18,19]. The incidence of Doege-Potter syndrome in SFPT is tumors represented. Males and females are equal distributed asbestos, tobacco or others environmental agents, were found for and the same is true for age. No correlation with exposure to malignantSome patients forms. may also present gynecomastia or galactorrhoea its development. Solitary fibrous tumor of the pleura occurs as localized neoplasms of the pleura and was initially classified as microscope and immunohistochemistry, has been possible [1]. -
Global Mesothelioma Deaths Reported
ResearchResearch Global mesothelioma deaths reported to the World Health Organization between 1994 and 2008 Vanya Delgermaa,a Ken Takahashi,a Eun-Kee Park,a Giang Vinh Le,a Toshiyuki Haraa & Tom Sorahanb Objective To carry out a descriptive analysis of mesothelioma deaths reported worldwide between 1994 and 2008. Methods We extracted data on mesothelioma deaths reported to the World Health Organization mortality database since 1994, when the disease was first recorded. We also sought information from other English-language sources. Crude and age-adjusted mortality rates were calculated and mortality trends were assessed from the annual percentage change in the age-adjusted mortality rate. Findings In total, 92 253 mesothelioma deaths were reported by 83 countries. Crude and age-adjusted mortality rates were 6.2 and 4.9 per million population, respectively. The age-adjusted mortality rate increased by 5.37% per year and consequently more than doubled during the study period. The mean age at death was 70 years and the male-to-female ratio was 3.6:1. The disease distribution by anatomical site was: pleura, 41.3%; peritoneum, 4.5%; pericardium, 0.3%; and unspecified sites, 43.1%. The geographical distribution of deaths was skewed towards high-income countries: the United States of America reported the highest number, while over 50% of all deaths occurred in Europe. In contrast, less than 12% occurred in middle- and low-income countries. The overall trend in the age- adjusted mortality rate was increasing in Europe and Japan but decreasing in the United States. Conclusion The number of mesothelioma deaths reported and the number of countries reporting deaths increased during the study period, probably due to better disease recognition and an increase in incidence. -
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. -
Epidemiology and Clinical Aspects of Malignant Pleural Mesothelioma
cancers Review Epidemiology and Clinical Aspects of Malignant Pleural Mesothelioma Fraser Brims 1,2,3 1 Curtin Medical School, Curtin University, Perth, WA 6845, Australia; [email protected] 2 Department of Respiratory Medicine, Sir Charles Gairdner Hospital, Perth, WA 6009, Australia 3 National Centre for Asbestos Related Diseases, Institute for Respiratory Health, Perth, WA 6009, Australia Simple Summary: Mesothelioma is a cancer of the lining of the lungs caused by breathing in asbestos fibres. Asbestos was widely used in industry in the last century in most developed countries and is still present in many older buildings to this day. There is no known safe level of asbestos exposure. Symptoms of mesothelioma can include worsening breathlessness, chest pain and loss of weight. There is no cure, and the treatment of mesothelioma is limited, although there have been some recent improvements in therapy. Survival is very variable although most people live for around one year after diagnosis. Efforts to improve and maintain the quality of life for patients with mesothelioma remain a priority. Abstract: Mesothelioma is a cancer predominantly of the pleural cavity. There is a clear association of exposure to asbestos with a dose dependent risk of mesothelioma. The incidence of mesothelioma in different countries reflect the historical patterns of commercial asbestos utilisation in the last century and predominant occupational exposures mean that mesothelioma is mostly seen in males. Modern imaging techniques and advances in immunohistochemical staining have contributed to an improved diagnosis of mesothelioma. There have also been recent advances in immune checkpoint inhibition, however, mesothelioma remains very challenging to manage, especially Citation: Brims, F. -
Pneumoconiosis in Coalminers
6I8 POSTGRADUATE MEDICAL JOURNAL December I949 Postgrad Med J: first published as 10.1136/pgmj.25.290.618 on 1 December 1949. Downloaded from IRVINE, L. G., SIMSON, F. W., and STRACHAN, A. S. (1930), NEW YORK STATE DEPARTMENT OF LABOUR (1949), Proc. Intern. Conf. on Silicosis in Johannesburg, I.L.O. Studies Monthly Review, 28, No. 4, April. and Reports, Series F. (Industrial Hygiene), No. I3, p. 259. PERRY, K. M. A. (1948), Proc. Ninth Intern. Cong. of Ind. Med., JONES, W. R. (I933), ,. of Hyg., 33, 307. London (in the press). KETTLE, E. H. (I932), Y. Path. and Bat., 35, 395. KETTLE, E. H. (I934), Ibid., 38, 20o. POLICARD, A. (1947), Proc. Conf. of the Institution of Mining KING, E. J. (I945), M.R.C. Special Report Series, No. 250, p. 73. Engineers and Institution of Mining and Metalurgy, London, KING, E. J. (I947) Occ. Med., 4, 26. P. 24. KING, E. J., WRI6HT, B. M., and RAY, S. C. (I949), Paper read ROGERS, E. (i944), Paper read to the British Tuberculosis Associa- to the Path. Soc., Great Britain, January, 1949. tion. McLAUGHLIN, A. I. G., ROGERS, E., and DUNHAM, K. C. (I949), Brit. 3Y. Ind. Med., 6, I84. SHAVER, C. G. (1948), Radiology, 50, 760. MINERS' PHTHISIS MEDICAL BUREAU OF SOUTH SHAVER, C. G., and RIDDELL, A. R. (I947), J. Id. Hyg. and AFRICA (1946), Report for the Three Years ending Jy 31, Tox., 29, 145. I944 (South African Government Printer). VORWALD, A. J., and CARR, J. W. (1938), Amer. J7. Path., 14,49. PNEUMOCONIOSIS IN COAL MINERS By J. -
Progressive Plasterer's Pneumoconiosis Complicated By
Kurosaki et al. BMC Pulmonary Medicine (2019) 19:6 https://doi.org/10.1186/s12890-018-0776-4 CASEREPORT Open Access Progressive plasterer’s pneumoconiosis complicated by fibrotic interstitial pneumonia: a case report Fumio Kurosaki1,2*, Tamiko Takemura3, Masashi Bando1, Tomonori Kuroki1,2, Toshio Numao2, Hiroshi Moriyama4 and Koichi Hagiwara1 Abstract Background: Although the prevalence of pneumoconiosis has been decreasing due to improvements in working conditions and regular health examinations, occupational hygiene measures are still being established. Plasterers encounter a number of hazardous materials that may be inhaled in the absence of sufficient protection. Case presentation: A 64-year-old man who plastered without any dust protection for more than 40 years was referred to our hospital with suspected interstitial pneumonia. Mixed dust pneumoconiosis and an unusual interstitial pneumonia (UIP) pattern with fibroblastic foci were diagnosed by video-assisted thoracoscopic surgery, and an elemental analysis detected elements included in plaster work materials. Despite the cessation of plaster work and administration of nintedanib, the patient developed advanced respiratory failure. Conclusion: Plasterers are at an increased risk of pneumoconiosis and may have a poor prognosis when complicated by the UIP pattern. Thorough dust protection and careful monitoring are needed. Keywords: Plasterer, Pneumoconiosis, Usual interstitial pneumonia, Elemental analysis Background unusual interstitial pneumonia (UIP) pattern, the cause of With energy transition from coal to oil and nuclear power, which was identified as plaster work by an elemental coal mines completely disappeared by the early first analysis. Therefore, plasterers need to take proper coun- decade of the 2000s in Japan. Furthermore, improvements termeasures for dust prevention and undergo regular in industrial hygiene and vocational education have examinations. -
Chrysotile Asbestos As a Cause of Mesothelioma: Application of the Hill Causation Model
Commentary Chrysotile Asbestos as a Cause of Mesothelioma: Application of the Hill Causation Model RICHARD A. LEMEN, PHD Chrysotile comprises over 95% of the asbestos used this method, researchers are asked to evaluate nine today. Some have contended that the majority of areas of consideration: strength of association, tempo- asbestos-related diseases have resulted from exposures rality, biologic gradient, consistency, specificity, bio- to the amphiboles. In fact, chrysotile is being touted as logic plausibility, coherence, experimental evidence, the form of asbestos which can be used safely. Causa- and analogy. None of these considerations, in and of tion is a controversial issue for the epidemiologist. How itself, is determinative for establishing a causal rela- much proof is needed before causation can be estab- tionship. As Hill himself noted, “[n]one of my nine lished? This paper examines one proposed model for establishing causation as presented by Sir Austin Brad- view points can bring indisputable evidence for or ford Hill in 1965. Many policymakers have relied upon against the cause and effect hypothesis, and none can this model in forming public health policy as well as be required as a sine qua non.” In the same vein, it is deciding litigation issues. Chrysotile asbestos meets not necessary for all nine considerations to be met Hill’s nine proposed criteria, establishing chrysotile before causation is established. Instead, Hill empha- asbestos as a cause of mesothelioma. Key words: sized that the responsibility for making causal judg- asbestos; chrysotile; amphiboles; causation; mesothe- ments rested with a scientific evaluation of the totality lioma; Hill model. of the data. -
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). -
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