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      Descriptive Characteristics of Coal Workers' Pneumoconiosis Cases in Turkey

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          Abstract

          Dear Editor-in-Chief Working condition in underground mining are associated with many important risk factors for workers' health such as work injuries and occupational diseases. Coal workers' pneumoconiosis (CWP) is a preventable lung disease caused by occupational exposure to coal mine dust and was observed highly common in coal miners. Respirable coal dust concentration in working area, duration of exposure and free slica content play major role for CWP. Clinical form of CWP may be simple or complicated. In this evaluation, categories were determined with radiographs classified according to International Labour Office International Classification of Pneumoconiosis, and category 2 and 3 (subcategory ≥2/1) was considered advanced CWP (1,2). The most of CWP cases in Turkey were reported from Zonguldak Hard Coal Basin. According to national statistics of Ministry of Labor and Social Security, 429 occupational diseases were reported in 2009; of all cases, 230 (53.6%) were reported to have respiratory occupational disease and 201 of 230 cases were recorded from coal and lignit production workforce and 191 cases were reported from Zonguldak. In our study, hospital records of 457 coal mine workers who applied to Zonguldak Uzunmehmet Chest and Occupational Diseases Hospital and diagnosed with CWP in 2008 were evaluated retrospectively. Category 2 and 3 cases were considered simple CWP and the others were considered simple CWP. Of all cases, 58% were found to have simple and 42% to have advanced CWP. There were not statistically significant difference between simple and advanced cases in accordance with smoking status, tuberculosis, respiratory functions, spirometric parameters, underground working day and opacity type in chest radiographs. However mean age (P=0.008), disability (P=0.001), disability ratio (P=0.001) in advanced CWP cases were significantly higher than simple cases. Although there were significant difference between simple and advanced cases in accordance with underground working day, age at first exposure in simple CWP cases and tenure in advanced cases were significantly higher than the others (P=0.002 and P=0.021). In all groups, 446 cases (97.6%) were diagnosed as CWP at 10.8±4.7 years after their retirement, and time interval between diagnosis and retirement in advanced cases was significantly higher than simple cases (P=0.001). Disability and disability ratio are correlated with the present situation of the disease and should be improved with the clinical progression. According the Turkish regulations, when the calculation of permanent impairment of an occupational disease gives the “disability ratio” less than 10%, there is no obligation to pay pecuniary compensation for employers. This creates a distinct disadvantage for category-1 CWP patients. Results of our study are similar with other studies in accordance with prevalence of abnormal spirometric parameters, age at first exposure, tenure and underground working days (3, 4). Our investigation also shows that 97.6% of all cases were retired and they were diagnosed with CWP at 10.8±4.7 years after their retirement. Because of this unexpected situation three probabilities should be take into consideration: 1) Basic mechanism of CWP is inflammatory reaction (5, 6) and inflammatory process can be seamlessly continuing after starting of dust exposure, 2) Periodic follow-up examination and medical evaluation at the end of working of miners can be insufficient to determine the CWP cases, 3) It is known that there are some relatively small mines in the basin, and miners can work in different mines informally after retirement and cumulative effect of coal dust exposure can be continuing. Although first probability is relevant with pathogenesis of CWP, second and third probabilities are relevant with basin realities and problems of particular urgency. As a conclusion, prevention and control of CWP need not only engineering practices such as ventilation or wet operation but also good medical practices such as follow-up and severance medical examinations. Furthermore, countries should support the engineering and medical practices with auditing of occupational health and safety applications in the workplace and legal arrangement for reduction of dust levels in mines, impediment of informal working and higher education of occupational physicians.

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          Most cited references 5

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          Pneumoconiosis and advanced occupational lung disease among surface coal miners--16 states, 2010-2011.

            (2012)
          Coal workers' pneumoconiosis (CWP) is a chronic occupational lung disease caused by long-term inhalation of dust, which triggers inflammation of the alveoli, eventually resulting in irreversible lung damage. CWP ranges in severity from simple to advanced; the most severe form is progressive massive fibrosis (PMF). Advanced CWP is debilitating and often fatal. To prevent CWP, the Coal Mine Health and Safety Act of 1969 established the current federal exposure limit for respirable dust in underground and surface coal mines. The Act also established a surveillance system for assessing prevalence of pneumoconiosis among underground coal miners, but this surveillance does not extend to surface coal miners. With enforcement of the exposure limit, the prevalence of CWP among underground coal miners declined from 11.2% during 1970-1974 to 2.0% during 1995-1999, before increasing unexpectedly in the last decade, particularly in Central Appalachia. Exposure to respirable dust is thought to be less in surface than underground coal miners. Although they comprise 48% of the coal mining workforce, surface coal miners have not been studied since 2002. To assess the prevalence, severity, and geographic distribution of pneumoconiosis among current surface coal miners, CDC obtained chest radiographs of 2,328 miners during 2010-2011 through the Coal Workers' Health Surveillance Program of the National Institute for Occupational Safety and Health (NIOSH). Forty-six (2.0%) of 2,257 miners with >1 year of surface mining experience had CWP, including 37 who had never worked underground. Twelve (0.5%) had PMF, including nine who had never worked underground. A high proportion of the radiographs suggested silicosis, a disease caused by inhalation of crystalline silica. Surface coal mine operators should monitor worker exposures closely to ensure that both respirable dust and silica are below recommended levels to prevent CWP. Clinicians should be aware of the risk for advanced pneumoconiosis among surface coal miners, in addition to underground coal miners, to facilitate prompt disease identification and intervention.
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            Lung-function impairment among US underground coal miners, 2005 to 2009: geographic patterns and association with coal workers' pneumoconiosis.

            To investigate contemporary geographic distributions of lung-function impairment and radiographic evidence of coal workers' pneumoconiosis (CWP) and their associations. From 2005 to 2009, 6373 underground coal miners completed a health survey, including spirometry testing and chest radiography. Coal workers' pneumoconiosis and progressive massive fibrosis were determined by NIOSH B readers, using the International Labour Office classification. Prevalences of CWP and spirometry less than lower normal limits were mapped by county, and their association assessed. The prevalences of abnormal spirometry results and CWP were 13.1% and 4.0%, respectively. Counties with elevated prevalences for both the outcomes were located in contiguous areas of southeastern Kentucky, western Virginia, southern West Virginia, and eastern Pennsylvania. Prevalence of abnormal spirometry results increases with increasing category of simple CWP and progressive massive fibrosis. Abnormal spirometry in coal miners is associated with CWP; these two health outcomes have similar geographic distributions.
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              The role of cell injury and the continuing inflammatory response in the generation of silicotic pulmonary fibrosis.

              The pathogenesis of silicosis involves interaction between pulmonary macrophages and fibroblasts. The consequences of direct injury to pulmonary cells and the role of inflammatory cells other than the macrophage have received little attention. These were studied over a 20 week period after instilling silica to mice by correlating the changing inflammatory response, as revealed by bronchoalveolar lavage and lung sections, with the cellular location of silica particles and the development and resolution of granulomatous lesions. Within 24 h, a massive concentration of particles and PMN was seen in centrilobular locations with acute focal necrosis of type 1 epithelial cells. Rapid epithelial repair occurred but PMN were recovered from the lung up to 20 weeks. In the alveoli, silica was ingested by PMN and AM, resulting in the death of some cells; free particles crossed the epithelium and were found predominantly in peribronchial macrophages. Silicotic granulomas formed within a week and consisted mainly of fibroblasts macrophages and some PMN. It is suggested that the necrosis of type 1 epithelium and the continuing efflux with serial destruction of PMN may be important factors in the generation of silicotic fibrosis.
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                Author and article information

                Affiliations
                1. Dept. of Public Health, School of Medicine, Bulent Ecevit University , Zonguldak, Turkey
                2. Ankara Occupational Diseases Hospital , Ankara, Turkey
                3. Zonguldak Uzunmehmet Chest and Occupational Diseases Hospital , Zonguldak, Turkey
                Author notes
                * Corresponding Author: Email: fayoglu@ 123456yahoo.com
                Journal
                Iran J Public Health
                Iran. J. Public Health
                IJPH
                Iranian Journal of Public Health
                Tehran University of Medical Sciences
                2251-6085
                2251-6093
                March 2014
                : 43
                : 3
                : 389-390
                IJPH-43-389
                4419183
                25988105
                Copyright © Iranian Public Health Association & Tehran University of Medical Sciences

                This work is licensed under a Creative Commons Attribution-Non Commercial 3.0 Unported License which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.

                Categories
                Letter to the Editor

                Public health

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