Occupational Airborne Particulates
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Dust Exposure and Byssinosis Among Cotton Textile Workers in Dar Es Salaam, Tanzania
MOJ Public Health Research Article Open Access Dust exposure and byssinosis among cotton textile workers in Dar es salaam, Tanzania Abstract Volume 9 Issue 6 - 2020 Background: Cotton dust exposure increases the risk of developing lung diseases including Luco P Mwelange, Simon Mamuya, Gloria Byssinosis. The prevalence of byssinosis is more in developing countries compare to developed countries. For the past forty years there are little information known about the Sakwari, Witness John Axwesso Department of Environmental and Occupational Health, prevalence of byssinosis and its associated risk factors among textile workers in Tanzania. Muhimbili University of Health and Allied Sciences, Tanzania Objective: The study aimed to assess dust exposure and associated risk factors among textile workers, in Dar es Salaam, Tanzania. Correspondence: Luco P Mwelange, Muhimbili University of Health and Allied Sciences, Tanzania, Tel+255655049524, Material and methods: The study design was descriptive cross sectional study conducted Email from March to August 2019. Stratified sampling technique was used to obtain 325 participants (exposed 164 and control 161) respectively. A modified British Medical Received: October 29, 2020 | Published: November 30, 2020 Research Council (BMRC) questionnaire and Side Kick Casella Pump were used for data collection. Data were analyzed using Statistical Package for Social Science software 23 versions. Chi square test and Binary logistic regression were performed to check for association. A 95% confidence Interval with a significance expressed in P˂0.05 was used. Results: Prevalence of byssinosis in the exposed group was 18.9% and 6.2% in the control group. Respiratory symptoms such as Coughing more days in three consecutive months (P˂0.001), wheezing (P˂0.02), dyspnoea I (P˂0.03), dyspnoea II (P˂0.007), and dyspnoea III (P˂0.002), were higher among exposed group compare to control group and the differences were statistically significant. -
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. -
Occupational Lung Diseases
24 Occupational lung diseases Introduction i Occupational diseases are often thought to be Key points uniquely and specifically related to factors in the work environment; examples of such diseases are • Systematic under-reporting and the pneumoconioses. However, in addition to other difficulties in attributing causation both contribute to underappreciation of the factors (usually related to lifestyle), occupational burden of occupational respiratory exposures also contribute to the development or diseases. worsening of common respiratory diseases, such • Work-related exposures are estimated as chronic obstructive pulmonary disease (COPD), to account for about 15% of all adult asthma and lung cancer. asthma cases. • Boththe accumulation of toxic dust in the Information about the occurrence of occupational lungs and immunological sensitisation respiratory diseases and their contribution to to inhaled occupational agents can morbidity and mortality in the general population is cause interstitial lung disease. provided by different sources of varying quality. Some • Despite asbestos use being phased European countries do not register occupational out, mesothelioma rates are forecast diseases and in these countries, information about to continue rising owing to the long latency of the disease. the burden of such diseases is completely absent. • The emergence of novel occupational In others, registration is limited to cases where causes of respiratory disease in compensation is awarded, which have to fulfil specific recent years emphasises the need for administrative or legal criteria as well as strict continuing vigilance. medical criteria; this leads to biased information and underestimation of the real prevalence. Under- reporting of occupational disease is most likely to occur in older patients who are no longer at work but whose condition may well be due to their previous job. -
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. -
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 -
National Occupational Research Agenda (Nora)
NATIONAL OCCUPATIONAL RESEARCH AGENDA (NORA) NATIONAL OCCUPATIONAL RESEARCH AGENDA FOR HEALTHCARE AND SOCIAL ASSISTANCE (HCSA) February 2019 Developed by the NORA HCSA Council 1 . For more information about the National Occupational Research Agenda (NORA), visit the web site: https://www.cdc.gov/niosh/nora/ For monthly updates on NORA, subscribe to NIOSH eNews at www.cdc.gov/niosh/eNews Disclaimer This is a product of the National Occupational Research Agenda (NORA) Healthcare and Social Assistance Sector Council. It does not necessarily represent the official position of the National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, or U.S. Department of Health and Human Services. 2 INTRODUCTION What is the National Occupational Research Agenda? The National Occupational Research Agenda (NORA) is a partnership program to stimulate innovative research and workplace interventions. In combination with other initiatives, the products of this program are expected to reduce the occurrence of injuries and illnesses at work. Unveiled in 1996, NORA has become a research framework for the Nation and the National Institute for Occupational Safety and Health (NIOSH). Diverse parties collaborate to identify the most critical issues in workplace safety and health and develop research objectives for addressing those needs. NORA enters its third decade in 2016 with an enhanced structure. The ten sectors formed for the second decade will continue to prioritize occupational safety and health research by major areas of the U.S. economy. In addition, there are seven cross-sectors organized according the major health and safety issues affecting the U.S. working population. While NIOSH is serving as the steward to move this effort forward, it is truly a national effort. -
Misclassification of Occupational Disease in Lung Transplant Recipients
HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author J Heart Manuscript Author Lung Transplant Manuscript Author . Author manuscript; available in PMC 2017 November 13. Published in final edited form as: J Heart Lung Transplant. 2017 May ; 36(5): 588–590. doi:10.1016/j.healun.2017.02.021. Misclassification of occupational disease in lung transplant recipients David J. Blackley, DrPHa, Cara N. Halldin, PhDa, Robert A. Cohen, MDa,b, Kristin J. Cummings, MDa, Eileen Storey, MDa, and A. Scott Laney, PhDa aRespiratory Health Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, West Virginia, USA bSchool of Public Health, University of Illinois at Chicago, Chicago, Illinois, USA Data from the United States Organ Procurement and Transplantation Network (OPTN) registry have been analyzed in recent years to assess post–lung transplant (LT) survival in occupational lung disease patients.1–3 Registry data include diagnosis codes with limited specificity; each patient is assigned a diagnosis code at waitlist candidacy, at listing, and at LT, and these codes can differ. The use of both numeric and free-text data can produce incompatible or unlikely diagnosis code pairings (such as a numeric code for idiopathic pulmonary fibrosis with a paired free-text entry of “silicosis”). The resulting misclassification could bias findings related to patient characteristics, post-LT survival comparisons and other measures used to summarize outcomes. Diagnosis codes from OPTN data could be inadequate for case finding and may result in missed occupational lung disease cases. Our objective was to identify and describe adult LT recipients documented as having conditions known to be entirely attributable to occupational exposure, and to calculate the proportion of those patients who were assigned an occupational lung disease diagnosis code at LT. -
European Respiratory Society Classification of the Idiopathic
This copy is for personal use only. To order printed copies, contact [email protected] 1849 CHEST IMAGING American Thoracic Society– European Respiratory Society Classification of the Idiopathic Interstitial Pneumonias: Advances in Knowledge since 20021 Nicola Sverzellati, MD, PhD David A. Lynch, MB In the updated American Thoracic Society–European Respira- David M. Hansell, MD, FRCP, FRCR tory Society classification of the idiopathic interstitial pneumonias Takeshi Johkoh, MD, PhD (IIPs), the major entities have been preserved and grouped into Talmadge E. King, Jr, MD (a) “chronic fibrosing IIPs” (idiopathic pulmonary fibrosis and id- William D. Travis, MD iopathic nonspecific interstitial pneumonia), (b) “smoking-related IIPs” (respiratory bronchiolitis–associated interstitial lung disease Abbreviations: H-E = hematoxylin-eosin, and desquamative interstitial pneumonia), (c) “acute or subacute IIP = idiopathic interstitial pneumonia, IPF = IIPs” (cryptogenic organizing pneumonia and acute interstitial idiopathic pulmonary fibrosis, NSIP = nonspe- cific interstitial pneumonia, RB-ILD = respi- pneumonia), and (d) “rare IIPs” (lymphoid interstitial pneumonia ratory bronchiolitis–associated interstitial lung and idiopathic pleuroparenchymal fibroelastosis). Furthermore, it disease, UIP = usual interstitial pneumonia has been acknowledged that a final diagnosis is not always achiev- RadioGraphics 2015; 35:1849–1872 able, and the category “unclassifiable IIP” has been proposed. The Published online 10.1148/rg.2015140334 diagnostic interpretation of -
A Breathless Builder
case presentations no03.qxd 17/05/2007 15:38 Page 2 CASE PRESENTATION A breathless builder J.J. Lyons1 P.J. Sime1 Case report hand-grinder, a common task known as "tuck- D. Ward2 The patient was a 30-year-old male mason whose pointing" (figure 2), while intermittently using a T. Watson3 work frequently involved cutting and grinding disposable particle mask. After completing this J.L. Abraham4 brick and cement with powered tools. He was an job, he felt well for ~2 months and then gradu- R. Evans5 active smoker (1–1.5 packs per day). He had ally began to develop a nonproductive cough, 6 M. Budev worked in building construction since the age of dyspnoea on exertion and an 11 kg weight loss K. Costas3 W.S. Beckett1 14 yrs, as a labourer then as a mason and had without fever. Serial pulmonary function testing been a mason for the previous 13 years. He showed restriction and a marked reduction in dif- reported frequent exposure to cement and brick fusing capacity. Chest computed tomography 1Division of Pulmonary and dust while removing stone floors with a jackham- (CT) showed bilateral diffuse infiltrates. A purified Critical Care Medicine, 2Dept of mer. From 8–2 months prior to presentation, he protein derivative test was negative. Anesthesiology and Biomedical had been employed repairing exterior brick on Bronchoalveolar lavage fluid was mucoid, and 3 Engineering and Division of three large apartment buildings (figure 1). This culture was negative. A transbronchial biopsy Thoracic/Foregut Surgery, University of Rochester, Rochester, required cutting through brick and mortar with a was nondiagnostic and the post-bronchoscopy 4Dept of Pathology, SUNY Upstate powered, high-speed demolition saw and grind- chest film showed a very small right apical pneu- Medical University, Syracuse, ing mortar from between bricks with a powered mothorax.