Purpose of the Review: Some physiopathological mechanisms that could support the relationship between tobacco and silicosis have been postulated but exact pathogenesis remains unknown. Recent Findings: Local inflammation in workers with silicosis is a complex process characterized by an infiltration of inflammatory cells in the respiratory alveolus, accompanied by an increase in the expression of cytokines, chemokines, enzymes, growth factors and adhesion molecules. Although in smokers without silicosis a similar pattern of inflammation can be observed, in workers with silicosis this process seems to be characterized by more pronounced increases in structural damage in the lungs. Altered balance of innate and adaptive immunity both play key roles in the pathogenesis of extensive fibrosis in a molecular level, influenced by individual susceptibilities and genetic traits. Conclusion: The identification of the molecular mechanism and a potential protective genotype for silicosis opens a window for the eradication of this occupational respiratory disease. This should encourage us to continue exploring and searching for the relation between the genetic polymorphism and the inorganic silica particle.
References
[1]
Abdelaziz, R. R., Elkashef, W. F., & Said, E. (2017). Tadalafil Reduces Airway Hyperactivity and Protects against Lung and Respiratory Airways Dysfunction in a Rat Model of Silicosis. International Immunopharmacology, 40, 530-541. https://doi.org/10.1016/j.intimp.2016.10.007
[2]
Adage, T. et al. (2015). Targeting Glycosaminoglycans in the Lung by an Engineered CXCL8 as a Novel Therapeutic Approach to Lung Inflammation. European Journal of Pharmacology, 748, 83-92. https://doi.org/10.1016/j.ejphar.2014.12.019
[3]
Baumgartner, K. B., Samet, J. M., Stidley, C. A., Colby, T. V., & Waldron, J. A. (1997). Cigarette Smoking: A Risk Factor for Idiopathic Pulmonary Fibrosis. American Journal of Respiratory and Critical Care Medicine, 155, 242-248. https://doi.org/10.1164/ajrccm.155.1.9001319
[4]
Borges, V. M. et al. (2002). Apoptosis Underlies Immunopathogenic Mechanisms in Acute Silicosis. American Journal of Respiratory Cell and Molecular Biology, 27, 78-84. https://www.ncbi.nlm.nih.gov/pubmed/12091249 https://doi.org/10.1165/ajrcmb.27.1.4717
[5]
Chan, J. W. et al. (2018). RNA-Seq Revealed ATF3-Regulated Inflammation Induced by Silica. Toxicology, 393, 34-41. https://doi.org/10.1016/j.tox.2017.11.001
[6]
Churg, A., Zhou, S., Preobrazhenska, O., Tai, H., Wang, R., & Wright, J. L. (2009). Expression of Profibrotic Mediators in Small Airways versus Parenchyma after Cigarette Smoke Exposure. American Journal of Respiratory Cell and Molecular Biology, 40, 268-276. https://www.ncbi.nlm.nih.gov/pubmed/18723441 https://doi.org/10.1165/rcmb.2007-0367OC
[7]
Delgado, D., Aguilera, M. A., Delgado, F., & Rug, A. (2012). The Experience of Miners Relocated to Alternative Positions due to Silicosis in the Andean of CODELCO, Chile, 2010. Safety and Health at Work, 3, 140-145. https://doi.org/10.5491/SHAW.2012.3.2.140
[8]
Delgado, L., Parra, E. R., & Capelozzi, V. L. (2006). Apoptosis and Extracellular Matrix Remodeling in Human Silicosis. Histopathology, 49, 283-289. https://www.ncbi.nlm.nih.gov/pubmed/16918975 https://doi.org/10.1111/j.1365-2559.2006.02477.x
[9]
Deng, H. et al. (2016). Protective Effect of Ac-SDKP on Alveolar Epithelial Cells through Inhibition of EMT via TGF-β1/ROCK1 Pathway in Silicosis in Rat. Toxicology and Applied Pharmacology, 294, 1-10. https://doi.org/10.1016/j.taap.2016.01.010
[10]
Emad, A., & Emad, Y. (2007). Increased in CD8 T lymphocytes in the BAL Fluid of Patients with Sulfur Mustard Gas-Induced Pulmonary Fibrosis. Respiratory Medicine, 101, 786-792. https://doi.org/10.1016/j.rmed.2006.08.003
[11]
Fang, G. F., Fan, X. Y., & Shen, F. H. (2011). The Relationship between Polymorphisms of Interleukin-4 Gene and Silicosis. Biomedical and Environmental Sciences, 24, 678-682. https://www.ncbi.nlm.nih.gov/pubmed/22365405
[12]
Fang, S. C., Zhang, H. T., Wang, C. Y., & Zhang, Y. M. (2014). Serum CA125 and NSE: Biomarkers of Disease Severity in Patients with Silicosis. Clinica Chimica Acta, 433, 123-127. https://doi.org/10.1016/j.cca.2014.03.005
[13]
Gardiner, C. M., & Mills, K. H. (2016). The Cells That Mediate Innate Immune Memory and Their Functional Significance in Inflammatory and Infectious Diseases. Seminars in Immunology, 28, 343-350. https://doi.org/10.1016/j.smim.2016.03.001
[14]
Katzenstein, A. L., Mukhopadhyay, S., Zanardi, C., & Dexter, E. (2010). Clinically Occult Interstitial Fibrosis in Smokers: Classification and Significance of a Surprisingly Common Finding in Lobectomy Specimens. Human Pathology, 41, 316-325. https://doi.org/10.1016/j.humpath.2009.09.003
[15]
Leung, C. C., Yu, I. T., & Chen, W. (2012). Silicosis. The Lancet, 379, 2008-2018. https://doi.org/10.1016/S0140-6736(12)60235-9
[16]
Li, J. et al. (2017). Crystalline Silica Promotes Rat Fibrocyte Differentiation in Vitro, and Fibrocytes Participate in Silicosis in Vivo. Biomedical and Environmental Sciences, 30, 649-660.
[17]
Li, X. et al. (2017). Bone Marrow Mesenchymal Stem Cells Attenuate Silica-Induced Pulmonary Fibrosis via Paracrine Mechanisms. Toxicology Letters, 27, 96-107. https://doi.org/10.1016/j.toxlet.2017.02.016
[18]
Liu, D. D. et al. (2018). Progress in Pharmacological Research of Chemokine like Factor 1 (CKLF1). Cytokine, 102, 41-50. https://doi.org/10.1016/j.cyto.2017.12.002
[19]
Liu, X. et al. (2015). Role of Human Pulmonary Fibroblast-Derived MCP-1 in Cell Activation and Migration in Experimental Silicosis. Toxicology and Applied Pharmacology, 288, 152-160. https://doi.org/10.1016/j.taap.2015.07.002
[20]
Naghadehi, M. Z., Sereshki, F., & Mohammadi, F. (2014). Pathological Study of the Prevalence of Silicosis among Coal Miners in Iran: A Case History. Atmospheric Environment, 83, 1-5. https://doi.org/10.1016/j.atmosenv.2013.10.053
[21]
Nicod, L. P. (2005). Lung Defenses: An Overview. European Respiratory, 14, 45-50. http://err.ersjournals.com/content/14/95/45
[22]
Perkins, T. N. et al. (2015). Indications for Distinct Pathogenic Mechanisms of Asbestos and Silica through Gene Expression Profiling of the Response of Lung Epithelial Cells. Human Molecular Genetics, 24, 1374-1389. https://doi.org/10.1093/hmg/ddu551 https://www.ncbi.nlm.nih.gov/pubmed/25351596
[23]
Perkins, T. N., Peeters, P. M., Wouters, E. F. M., Reynaert, N. L., & Mossman, B. T. (2014). Pathogenesis and Mechanisms of Asbestosis and Silicosis. In L. M. McManus, & R. N. Mitchell (Eds.), Pathobiology of Human Disease (pp. 2654-2664). Cambridge, MA: Academic Press. https://doi.org/10.1016/B978-0-12-386456-7.05308-9
[24]
Rimal, B., Greenberg, A. K., & Rom, W. N. (2005). Basic Pathogenetic Mechanisms in Silicosis: Current Understanding. Current Opinion in Pulmonary Medicine, 11, 169-173. https://www.ncbi.nlm.nih.gov/pubmed/15699791 https://doi.org/10.1097/01.mcp.0000152998.11335.24
[25]
Shan, M. et al. (2012). Cigarette Smoke Induction of Osteopontin (SPP1) Mediates T(H)17 Inflammation in Human and Experimental Emphysema. Science Translational Medicine, 4, 117-119. https://www.ncbi.nlm.nih.gov/pubmed/22261033 https://doi.org/10.1126/scitranslmed.3003041
[26]
Skuland, T., Ovrevik, J., Lag, M., & Refsnes, M. (2014a). Role of Size and Surface Area for Pro-Inflammatory Responses to Silica Nanoparticles in Epithelial Lung Cells: Importance of Exposure Conditions. Toxicology in Vitro, 28, 146-155. https://doi.org/10.1016/j.tiv.2013.10.018
[27]
Skuland, T., Ovrevik, J., Lag, M., Schwarze, P., & Refsnes, M. (2014b). Silica Nanoparticles Induce Cytokine Responses in Lung Epithelial Cells through Activation of a p38/TACE/TGF-α/EGFR-Pathway and NF-κΒ Signaling. Toxicology and Applied Pharmacology, 279, 76-86.
[28]
Sultan, N. (2017a). The Silent Killer. Solids and Bulk Handling, 3, 17-18. http://www.academia.edu/32341180/The_Silent_Killer
[29]
Sultan, N. (2017b). The Silica Dust Hazard—Why I Should Be Concerned? Canadian Design and Construction Report, 8, 12-17. http://www.academia.edu/31084926/The_silica_dust_hazard_why_I_should_be_concerned
[30]
Truong, T. M., Li, H., Dhapare, S., Desai, U. R., Voelkel, N. F., & Sakagami, M. (2017). Sulfated Dehydropolymer of Caffeic Acid: In Vitro Anti-Lung Cell Death Activity and in Vivo Intervention in Emphysema Induced by VEGF Receptor Blockade. Pulmonary Pharmacology &Therapeutics, 45, 181-190. https://doi.org/10.1016/j.pupt.2017.06.007
[31]
Wang, Y. W., Lan, J. Y., Yang, L. Y., De J. W., & Kuang, J. (2012). TNF-α and IL-1RA Polymorphisms and Silicosis Susceptibility in Chinese Workers Exposed to Silica Particles: A Case-Control Study. Biomedical and Environmental Sciences, 25, 517-525.
[32]
World Health Organization (2015). Global Report on the Trends in Prevalence of Tobacco Smoking. http://www.who.int/tobacco/publications/surveillance/trends-tobacco-smoking-second-edition/en/
[33]
World Health Organization (2017). Report on the Global Tobacco Epidemic. http://www.who.int/tobacco/global_report/en/
[34]
Yuan, J. et al. (2017). Polymorphisms in Autophagy Related Genes and the Coal Workers’ Pneumoconiosis in a Chinese Population. Gene, 632, 36-42. https://doi.org/10.1016/j.gene.2017.08.017
[35]
Yucesoy, B. et al. (2001). Association of Tumor Necrosis Factor-Alpha and Interleukin-1 Gene Polymorphisms with Silicosis. Toxicology and Applied Pharmacology, 172, 75-82. https://doi.org/10.1006/taap.2001.9124
[36]
Zhang, L. et al. (2016). Combined Pulmonary Fibrosis and Emphysema: A Retrospective Analysis of Clinical Characteristics, Treatment and Prognosis. BMC Pulmonary Medicine, 16, 137. https://www.ncbi.nlm.nih.gov/pubmed/27809901 https://doi.org/10.1186/s12890-016-0300-7
