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      Artificial stone‐associated silicosis in China: A prospective comparison with natural stone‐associated silicosis

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          ABSTRACT

          Background and objective

          We recently noted a dramatic increase in the number of patients with accelerated silicosis associated with exposure to artificial stone dust. Therefore, the natural history of artificial stone‐associated silicosis was compared with that of natural stone‐associated silicosis.

          Methods

          A total of 18 patients with artificial stone‐associated silicosis and 63 with natural stone‐associated silicosis were diagnosed sequentially in 2018 and followed up for a period of 6–12 months. Data were collected from clinical charts.

          Results

          The median duration of exposure prior to onset of symptoms of silicosis was shorter for patients who had been exposed to artificial stone dust (6.4 vs 29.3 years, P < 0.01). Four of the 18 patients experienced rapid deterioration in lung function over the follow‐up period, with declines in pre‐bronchodilator FVC of 587 (210–960) mL/year and FEV 1 of 625 (360–860) mL/year. GGO, PMF, emphysema and pulmonary artery widening were more frequently observed on computed tomography scans of patients with artificial stone‐associated silicosis than of those with natural stone‐associated silicosis. Approximately 38.9% of the patients with artificial stone‐associated silicosis were lung transplant candidates and 27.8% died, both rates being significantly higher than in patients with natural stone‐associated silicosis (3.2% and 0%, both P < 0.01).

          Conclusion

          Compared to natural stone‐associated silicosis, artificial stone‐associated silicosis was characterized by short latency, rapid radiological progression, accelerated decline in lung function and high mortality.

          Abstract

          High silica content of artificial stone and uncontrolled dry cutting and grinding presents as a high risk of developing accelerated silicosis. Compared to natural stone‐associated silicosis, artificial stone‐associated silicosis was characterized by short latency, rapid radiological progression, accelerated decline in lung function and high mortality in this study.

          See related https://onlinelibrary.wiley.com/doi/10.1111/resp.13766

          See https://onlinelibrary.wiley.com/doi/10.1111/resp.13594

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          Most cited references22

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          Silicosis.

          Silicosis is a fibrotic lung disease caused by inhalation of free crystalline silicon dioxide or silica. Occupational exposure to respirable crystalline silica dust particles occurs in many industries. Phagocytosis of crystalline silica in the lung causes lysosomal damage, activating the NALP3 inflammasome and triggering the inflammatory cascade with subsequent fibrosis. Impairment of lung function increases with disease progression, even after the patient is no longer exposed. Diagnosis of silicosis needs carefully documented records of occupational exposure and radiological features, with exclusion of other competing diagnoses. Mycobacterial diseases, airway obstruction, and lung cancer are associated with silica dust exposure. As yet, no curative treatment exists, but comprehensive management strategies help to improve quality of life and slow deterioration. Further efforts are needed for recognition and control of silica hazards, especially in developing countries. Copyright © 2012 Elsevier Ltd. All rights reserved.
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            Basic pathogenetic mechanisms in silicosis: current understanding.

            Silicosis continues to be a common cause of chronic lung diseases, despite evidence that these diseases can be prevented by environmental dust control. Silicosis has been studied extensively by basic and clinical scientists, yet little is known about the crucial cellular and molecular mechanisms that initiate and propagate the process of inflammation and scarring. Recent in vivo, in vitro, and human studies have focused on several main areas of investigation into the causes and processes of the development of silicosis. These areas of investigation include the variability of pathogenic potential of different varieties of silica; the role of activated alveolar macrophages products in the development and progression of silicosis; and the direct role played by the silica particle surface in triggering adverse biologic reactions, such as generating ROS and RNS. The generation of oxidants by silica particles and by silica-activated cells results in cell and lung damage; increased expression of inflammatory cytokines, including TNF-alpha, IL 1 beta, and TGF-beta; activation of cell signaling pathways, including the MAP kinase pathways; and phosphorylation and activation of specific transcription factors (e.g., NFkB). The ROS, RNS, and NO generated by the silica particles also induce apoptosis in macrophages and other cells. Further research on the molecular mechanisms involved in the inflammatory processes important for progression to fibrotic diseases is needed for the development of effective treatment of silicosis. Potential therapeutic strategies include inhibition of cytokines such as IL-1, TNF alpha, the use of anti-oxidants, and the inhibition of apoptosis.
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              Artificial stone-associated silicosis: a rapidly emerging occupational lung disease

              Artificial stone is an increasingly popular material used to fabricate kitchen and bathroom benchtops. Cutting and grinding artificial stone is associated with generation of very high levels of respirable crystalline silica, and the frequency of cases of severe silicosis associated with this exposure is rapidly increasing.
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                Author and article information

                Contributors
                yeqiao_chaoyang@sina.com
                Journal
                Respirology
                Respirology
                10.1111/(ISSN)1440-1843
                RESP
                Respirology (Carlton, Vic.)
                John Wiley & Sons, Ltd (Chichester, UK )
                1323-7799
                1440-1843
                11 December 2019
                May 2020
                : 25
                : 5 ( doiID: 10.1111/resp.v25.5 )
                : 518-524
                Affiliations
                [ 1 ] Department of Occupational Medicine and Toxicology, Clinical Center for Interstitial Lung Diseases Beijing Chao‐Yang Hospital, Capital Medical University Beijing China
                Author notes
                [*] [* ]Correspondence: Qiao Ye, Department of Occupational Medicine and Toxicology, Clinical Center for Interstitial Lung Diseases, Beijing Chao‐Yang Hospital, Capital Medical University, Worker's Stadium No. 8, Chao‐Yang District, Beijing 100020, China. Email: yeqiao_chaoyang@ 123456sina.com
                Author information
                https://orcid.org/0000-0002-0617-0241
                Article
                RESP13744
                10.1111/resp.13744
                7187561
                31828940
                00eb778d-6736-406b-8e62-4c3b7767d3ac
                © 2019 The Authors. Respirology published by John Wiley & Sons Australia, Ltd on behalf of Asian Pacific Society of Respirology.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 26 June 2019
                : 23 October 2019
                : 28 October 2019
                Page count
                Figures: 2, Tables: 4, Pages: 7, Words: 4743
                Funding
                Funded by: Application of Clinical Characteristics in Capital
                Award ID: Z181100001718118
                Funded by: National Natural Science Foundation of China , open-funder-registry 10.13039/501100001809;
                Award ID: 81970061
                Categories
                Original Article
                ORIGINAL ARTICLES
                Environmental and Occupational Lung Disease
                Custom metadata
                2.0
                May 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.1 mode:remove_FC converted:28.04.2020

                Respiratory medicine
                artificial stone,progressive massive fibrosis,pulmonary function,respirable crystalline silica,silicosis

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