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      Pleural plaques in smoking-associated fibrosis and pulmonary asbestosis

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          Abstract

          Dear editor Bledsoe et al presents an interesting study examining the disparities between radiologic and pathologic diagnoses of asbestosis in cases referred for consultation in pulmonary malignancy.1 The authors conclude that the clinical diagnosis of asbestosis cannot be reliably distinguished from interstitial fibrosis in heavy smokers. These findings highlight the confounding role of cigarette smoking in the diagnosis of asbestosis when it is based on non-pathologic criteria. Clinical and radiographic characteristics of lung injury following particle exposure (including fibers in which one diameter of the particle is 3× that of the other by definition) are often comparable.2 The results of this investigation1 support further evaluation of a role for cigarette smoking in interstitial fibrosis. Furthermore, asbestos exposure can cause several non-malignant diseases of the pleura and lungs (ie, pleural effusions, pleural plaques, diffuse pleural fibrosis, rounded atelectasis, and asbestosis). Malignancies are also associated with asbestos exposure (ie, lung and laryngeal cancers and mesothelioma).3,4 Relationships between the dose–response and prevalence of asbestos-related diseases are complex.3,5 The injury requiring the least exposure, and which accordingly demonstrates the highest prevalence, is pleural plaque; 80% of individuals significantly exposed to asbestos (total dose of 0.1 fiber-year or less) will have plaques on the chest X-ray while only 0.5%–8% of an unexposed population will reveal such findings.6 Mesothelioma impacts 2,500 to 3,000 workers annually in the United States and its risk is elevated at a total asbestos dose of between 0.1 and 1.0 fiber-year. Those diseases requiring the greatest asbestos exposure are lung cancer and asbestosis; the risk for both is considered elevated at approximately 25 fiber-years. Bledsoe et al identify 24 cases with International Labour Organization (ILO) profusion score of ≥1, out of which only six cases show histological evidence of asbestosis. Of the remaining 18 cases, 16 are identified to have significant smoking history whereas two subjects had unknown smoking status. They observe radiographic evidence of pleural plaques in 82 (44%) of the cases included in the study. It would strengthen the conclusions of the study to know if those diagnosed with asbestosis demonstrated a higher prevalence of pleural plaques than those with cigarette smoking-related fibrosis.1

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          Most cited references 11

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          Diagnosis and initial management of nonmalignant diseases related to asbestos.

            (2004)
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            Mesothelioma trends in the United States: an update based on Surveillance, Epidemiology, and End Results Program data for 1973 through 2003.

            Using 1973-2000 mesothelioma incidence data released by the Surveillance, Epidemiology, and End Results Program in April 2003, the authors estimated the parameters of a birth-cohort and age model to determine whether previously reported patterns of mesothelioma in the United States have changed. Compared with analyses based on data through 1992, a slower decline was found in male cases immediately after a peak in 2000-2004, but no other notable changes in the time pattern were detected. Analysis confirmed that the annual number of male mesothelioma cases, which increased steeply from the 1970s through the mid-1990s, has leveled off in terms of both the age-adjusted rate and the absolute numbers of cases. After a peak of approximately 2,000 cases, a return to background levels is expected by 2055. The total projected number of male mesothelioma cases in 2003-2054 is approximately 71,000. The maximum lifetime risk for males, which occurs for the 1925-1929 birth cohort, is 1.8 x 10(-3). The age-adjusted rate for females is constant, as are the female lifetime mesothelioma risk across birth cohorts (3.6 x 10(-4)) and the annual risk (3.9 x 10(-6)). The time pattern of cases for females supports the existence of a threshold exposure for mesothelioma and a quantifiable background rate.
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              Pathology of asbestosis- An update of the diagnostic criteria: Report of the asbestosis committee of the college of american pathologists and pulmonary pathology society.

              Asbestosis is defined as diffuse pulmonary fibrosis caused by the inhalation of excessive amounts of asbestos fibers. Pathologically, both pulmonary fibrosis of a particular pattern and evidence of excess asbestos in the lungs must be present. Clinically, the disease usually progresses slowly, with a typical latent period of more than 20 years from first exposure to onset of symptoms. IDIOPATHIC PULMONARY FIBROSIS: The pulmonary fibrosis of asbestosis is interstitial and has a basal subpleural distribution, similar to that seen in idiopathic pulmonary fibrosis, which is the principal differential diagnosis. However, there are differences between the 2 diseases apart from the presence or absence of asbestos. First, the interstitial fibrosis of asbestosis is accompanied by very little inflammation, which, although not marked, is better developed in idiopathic pulmonary fibrosis. Second, in keeping with the slow tempo of the disease, the fibroblastic foci that characterize idiopathic pulmonary fibrosis are infrequent in asbestosis. Third, asbestosis is almost always accompanied by mild fibrosis of the visceral pleura, a feature that is rare in idiopathic pulmonary fibrosis. RESPIRATORY BRONCHIOLITIS: Asbestosis is believed to start in the region of the respiratory bronchiole and gradually extends outward to involve more and more of the lung acinus, until the separate foci of fibrosis link, resulting in the characteristically diffuse pattern of the disease. These early stages of the disease are diagnostically problematic because similar centriacinar fibrosis is often seen in cigarette smokers and is characteristic of mixed-dust pneumoconiosis. Fibrosis limited to the walls of the bronchioles does not represent asbestosis. Histologic evidence of asbestos inhalation is provided by the identification of asbestos bodies either lying freely in the air spaces or embedded in the interstitial fibrosis. Asbestos bodies are distinguished from other ferruginous bodies by their thin, transparent core. Two or more asbestos bodies per square centimeter of a 5- mu m-thick lung section, in combination with interstitial fibrosis of the appropriate pattern, are indicative of asbestosis. Fewer asbestos bodies do not necessarily exclude a diagnosis of asbestosis, but evidence of excess asbestos would then require quantitative studies performed on lung digests. Quantification of asbestos load may be performed on lung digests or bronchoalveolar lavage material, employing either light microscopy, scanning electron microscopy, or transmission electron microscopy. Whichever technique is employed, the results are only dependable if the laboratory is well practiced in the method chosen, frequently performs such analyses, and the results are compared with those obtained by the same laboratory applying the same technique to a control population.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2015
                02 May 2015
                : 10
                : 869-871
                Affiliations
                [1 ]Department of Pulmonary and Critical Care Medicine, West Virginia University, Morgantown, WV, USA
                [2 ]Environmental Public Health Division, National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Chapel Hill, NC, USA
                [1 ]Department of Pathology, Massachusetts General Hospital, Boston, MA, USA
                [2 ]Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
                Author notes
                Correspondence: Rahul G Sangani, Department of Pulmonary and Critical Care Medicine, West Virginia University, Robert C Byrd Health Science Center, 1 Medical Center Drive, Morgantown, WV 26505, USA, Tel +1 304 293 4661, Fax +1 304 293 3724, Email rgsangani@ 123456hsc.wvu.edu
                Correspondence: Richard L Kradin, Department of Pathology, Massachusetts General Hospital, Warren Building 253, 55 Fruit Street, Boston, MA 02114, USA, Tel +1 617 726 9029, Fax +1 617 726 7474, Email rkradin@ 123456partners.org
                Article
                copd-10-869
                10.2147/COPD.S83564
                4427072
                25999705
                © 2015 Sangani et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Letter

                Respiratory medicine

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