Work-Related Lung Disease Surveillance Report 1999
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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]). -
Siphoning Diesel: a Fatal Mistake
CASE REPORT Siphoning diesel: a fatal mistake Leong Wei Cheng, MRCP, Brian Cheong Mun Keong, FRCP Department of Medicine, Hospital Teluk Intan cervical lymphadenopathy and auscultation of his lungs SUMMARY revealed normal findings. Examination of other systems did Diesel is commonly used as fuel for engines and is distilled not reveal any abnormalities. from petroleum. Diesel has toxic potential and can affect multiple organs. Exposure can occur after ingestion, Initial blood investigations showed evidence of acute kidney inhalation or through the dermal route. The practice of injury (urea: 16.7 mmol/l, sodium 129 mmol/l, potassium 3.7 siphoning diesel using a rubber tubing and the mouth is mmol/l and creatinine 937 µmol/l). There was presence of common in rural communities. This can lead to accidental protein and erythrocytes (2+) in his urine. His full blood count ingestion and aspiration. Here we report a case of a patient showed elevated white cell count of 11,600/µl (neutrophil who accidentally ingested diesel during siphoning, which 85%) with normal haemoglobin concentration (15.9 g/dl) caused extensive erosion of the oral cavity and oesophagus and platelets (185,000/µl). Liver transaminases were normal. leading to pneumomediastinum and severe chemical lung Chest radiograph showed clear lung fields. His provisional injury. The patient responded well initially to steroids and diagnosis was acute tonsillitis with post- infectious Rapidly supportive care but required prolonged hospitalisation. He Progressive Glomerolonephritis (RPGN). Intravenous (IV) developed complications of nosocomial infection and Ceftriaxone 2 g daily was started. succumbed 23 days after admission. He became progressively more tachypnoeic in the ward with KEY WORDS: Diesel; siphon; chemical pneumonitis; oesophageal perforation; worsening renal function and metabolic acidosis. -
Ep001476158b1*
(19) *EP001476158B1* (11) EP 1 476 158 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: A61K 31/455 (2006.01) A61P 29/00 (2006.01) 14.11.2007 Bulletin 2007/46 A61P 11/00 (2006.01) C07D 405/12 (2006.01) C07D 213/82 (2006.01) C07D 401/12 (2006.01) (2006.01) (21) Application number: 03739392.3 C07D 451/04 (22) Date of filing: 03.02.2003 (86) International application number: PCT/IB2003/000439 (87) International publication number: WO 2003/068235 (21.08.2003 Gazette 2003/34) (54) NICOTINAMIDE DERIVATIVES USEFUL AS PDE4 INHIBITORS NICOTINAMID-DERIVATE ALS PDE4-HEMMER DERIVES DE NICOTINAMIDE UTILES COMME INHIBITEURS DE PDE4 (84) Designated Contracting States: • HENDERSON, A.J., AT BE BG CH CY CZ DE DK EE ES FI FR GB GR c/o UK Patent Dept., HU IE IT LI LU MC NL PT SE SI SK TR Pfizer Ltd. Designated Extension States: Sandwich, Kent CT13 9NJ (GB) AL LT LV MK RO • MAGEE, T.V., c/o Pfizer Global Res. and Develop. (30) Priority: 11.02.2002 GB 0203196 Groton, CT 06340 (US) 10.09.2002 GB 0220999 • MARFAT, A., 21.10.2002 GB 0224453 c/o Pfizer Global Res. and Develop. 20.11.2002 GB 0227139 Groton, CT 06340 (US) • MATHIAS, J.P., (43) Date of publication of application: c/o Pfizer Global Res. and Develop. 17.11.2004 Bulletin 2004/47 Sandwich, Kent CT13 9NJ (GB) (73) Proprietors: • MCLEOD, D.G., • Pfizer Limited c/o Pfizer Global Res. -
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. -
Are Serum Aluminum Levels a Risk Factor in the Appearance of Spontaneous Pneumothorax?
Turk J Med Sci 2010; 40 (3): 459-463 Original Article © TÜBİTAK E-mail: [email protected] doi:10.3906/sag-0901-11 Are serum aluminum levels a risk factor in the appearance of spontaneous pneumothorax? Serdar HAN1, Rasih YAZKAN2, Bülent KOÇER3,*, Gültekin GÜLBAHAR3, Serdal Kenan KÖSE4, Koray DURAL3, Ünal SAKINCI3 Aim: To investigate the relationship between aluminum and spontaneous pneumothorax (SP) development. Materials and methods: A patient group and a control group were formed with 100 individuals in each. The serum aluminum levels of the groups were determined and statistically compared. Results: The mean serum aluminum levels were 5.6 ± 2.4 μg/L (1.6-11.9) and 23.2 ± 15.4 μg/L (2-81) in the control and SP groups, respectively (P < 0.001). The specificity and sensitivity of the measurement of aluminum level were 74.4% and 86.4% in the SP group. The risk of SP development was found to be 18 times higher in individuals with high serum levels of aluminum compared to that in individuals with low serum levels of aluminum. Conclusion: A high level of aluminum is a risk factor for the development of SP. Key words: Aluminum, pneumothorax, public health Spontan pnömotoraks gelişiminde serum aluminyum seviyeleri bir risk faktörü müdür? Amaç: Bu çalışmada spontan pnömotoraks (SP) gelişimi ile serum aluminyum düzeyleri arasındaki ilişkinin analiz edilmesi amaçlandı. Yöntem ve gereç: Yüz SP hastasından oluşan hasta grubunun yanı sıra 100 kişiden oluşan sağlıklı kontrol grubu çalışmaya dahil edildi. Gruplar serum aluminyum düzeyleri açısından istatistiksel olarak kıyaslandı. Bulgular: Ortalama serum aluminyum düzeyleri SP ve kontrol grupları için sırasıyla 5,6 ± 2,4 μg/L (1,6-11,9) ve 23,2 ± 15,4 μg/L (2-81) bulundu (P < 0,001). -
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. -
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. -
Nebulizers: Diagnosis Codes – Medicare Advantage Policy Appendix
UnitedHealthcare® Medicare Advantage Policy Appendix: Applicable Code List Nebulizers: Diagnosis Codes This list of codes applies to the Medicare Advantage Policy Guideline titled Approval Date: September 8, 2021 Nebulizers. Applicable Codes The following list(s) of procedure and/or diagnosis codes is provided for reference purposes only and may not be all inclusive. The listing of a code does not imply that the service described by the code is a covered or non-covered health service. Benefit coverage for health services is determined by the member specific benefit plan document and applicable laws that may require coverage for a specific service. The inclusion of a code does not imply any right to reimbursement or guarantee claim payment. Other Policies and Guidelines may apply. Diagnosis Code Description For HCPCS Codes A7003, A7004, and E0570 A15.0 Tuberculosis of lung A22.1 Pulmonary anthrax A37.01 Whooping cough due to Bordetella pertussis with pneumonia A37.11 Whooping cough due to Bordetella parapertussis with pneumonia A37.81 Whooping cough due to other Bordetella species with pneumonia A37.91 Whooping cough, unspecified species with pneumonia A48.1 Legionnaires' disease B20 Human immunodeficiency virus [HIV] disease B25.0 Cytomegaloviral pneumonitis B44.0 Invasive pulmonary aspergillosis B59 Pneumocystosis B77.81 Ascariasis pneumonia E84.0 Cystic fibrosis with pulmonary manifestations J09.X1 Influenza due to identified novel influenza A virus with pneumonia J09.X2 Influenza due to identified novel influenza A virus with other -
Occupational Dusts Other Than Silica* by Kenneth M
Thorax: first published as 10.1136/thx.2.2.91 on 1 June 1947. Downloaded from Thorax (1947), 2, 91. DISEASES OF THE LUNG RESULTING FROM OCCUPATIONAL DUSTS OTHER THAN SILICA* BY KENNETH M. A. PERRY London It is only in recent years that considerable interest has been given to the dusts to which men are exposed at their work, even though silicosis is known to have occurred in prehistoric times. Many dusts are now recognized as dangerous, and in the extreme it may even be doubted whether any dust can be regarded as harmless. It is rational at least to suppose that the lung cannot become a physiological dust trap and yet retain its elasticity. It seems possible that any dust, no matter how innocuous in small concentrations, would in large enough quantity eventually overwhelm the defences of the lung and accumulate in such amounts as to impair function; such a form of lung disease would be the result of causes of a mechanical nature-the physical presence of large amounts of inert foreign material. The term "benign pneumoconiosis " has been given to this type of disease in order to contrast it with diseases resulting http://thorax.bmj.com/ from the inhalation of siliceous matter. But besides this group of conditions occupational dust may give rise to inflammatory lesions, allergic responses, and neoplastic changes. INFLAMMATORY CHANGES Inflammatory changes may be caused by inorganic metals, such as manganese, on September 24, 2021 by guest. Protected copyright. beryllium, vanadium, and osmium, giving.rise to a chemical pneumonitis; and by organic matter, such as decaying hay and grain, bagasse, cotton fibre, and similar substances where the aetiology is somewhat obscure, though fungi are frequently blamed.