Abstract
Inhaled inorganic dusts such as coal can cause inflammation and fibrosis in the lung called pneumoconiosis. Chronic inflammatory process in the lung is associated with various cytokines and reactive oxygen species (ROS) formation. Expression of some cytokines mediates inflammation and leads to tissue damage or fibrosis. The aim of the present study was to compare the levels of blood cytokines interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor (TNF)-α and monocyte chemoattractant protein (MCP)-1 among 124 subjects (control 38 and pneumoconiosis patient 86) with category of chest x-ray according to International Labor Organization (ILO) classification. The levels of serum IL-8 (p = 0.003), TNF-α (p = 0.026), and MCP-1 (p = 0.010) of pneumoconiosis patients were higher than those of subjects with the control. The level of serum IL-8 in the severe group with the small opacity (ILO category II or III) was higher than that of the control (p = 0.035). There was significant correlation between the profusion of radiological findings with small opacity and serum levels of IL-1β (rho = 0.218, p < 0.05), IL-8 (rho = 0.224, p < 0.05), TNF-α (rho = 0.306, p < 0.01), and MCP-1 (rho = 0.213, p < 0.01). The serum levels of IL-6 and IL-8, however, did not show significant difference between pneumoconiosis patients and the control. There was no significant correlation between serum levels of measured cytokines and other associated variables such as lung function, age, BMI, and exposure period of dusts. Future studies will be required to investigate the cytokine profile that is present in pneumoconiosis patient using lung specific specimens such as bronchoalveolar lavage fluid (BALF), exhaled breath condensate, and lung tissue.
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Ates, I., Suzen, H.S., Yucesoy, B., Tekin, I.O. and Karakaya, A. (2008). Association of cytokine gene polymorphisms in CWP and its severity in Turkish coal workers. Am. J. Ind. Med., 51, 741–747.
Becker, S., Soukup, J.M., Gilmour, M.I. and Devlin, R.B. (1996). Stimulation of human and rat alveolar macrophages by urban air particles: effects on oxidant radical generation and cytokine production. Toxicol. Appl. Pharmacol., 141, 637–648.
Biswas, S.K. and Sodhi, A. (2002). In vitro activation of murine peritoneal macrophages by monocytes chemoattractant protein upregulation of CD11b, production of proinflammatory cytokines, and the signal transduction pathway. J. Interferon Cytokine Res., 22, 527–538.
Boitelle, A., Gosset, P., Copin, M.C., Vanhee, D., Marquette, C.H., Wallaert, B., Gosselin, B. and Tonnel, A.B. (1997). MCP-1 secretion in lung from nonsmoking patients with coal worker’s pneumoconiosis. Eur. Respir. J., 10, 557–562.
Brunzel, N.A. (2003). Clinical Chemistry-Concepts & applications: Renal function-Nonprotein, nitrogen compounds, function tests, and renal disease (Anderson, S.C. and Cockayne, S. Eds.), The McGraw-Hill Co. New York, pp. 373–399.
Brusasco, V., Crapo, R. and Viegi, G. (2005). Series “ATS/ERS Task Force: Standardisation of lung function testing”. Eur. Respir. J., 26, 319–338.
Castranova, V., Vallyathan, V., Ramsey, D.M., McLaurin, J.L., Pack, D., Leonard, S., Barger, M.W., Ma, J.Y., Dalai, N.S. and Teass, A. (1997). Augmentation of pulmonary reactions to quartz inhalation by trace amounts of iron-containing particles. Environ. Health Perspect., 105, 1319–1324.
Dalai, N.S., Jafari, B., Peterson, M., Green, F.H. and Vallyathan, V. (1991). Presence of stable coal radicals in autopsied coal miners’ lungs and its possible correlation to coal worker’s pneumoconiosis. Arch. Environ. Health, 46, 366–372.
Donalson, K., Brown, G.M., Brown, D.M., Robertson, M.D., Slight, J., Cowie, H., Jones, A.D., Bolton, R.E. and Davis, J.M.G. (1990). Contrasting brochoalveolar leukocyte in rat s inhaling coal mine dust, quartz, or titanium dioxide: effects of coal rank, airborne mass concentration, and cessation of exposure. Environ. Res., 52, 62–76.
Elias, J.A. and Zitnik, R.J. (1992). Cytokine-cytokine interactions in the context of cytokine networking. Am. J. Respir. Cell Mol. Biol., 7, 365–367.
Fitzgerald, S.P., Lamont, J.V., McConnell, R.I. and Benchikh, EL.O. (2005). Development of high-throuput automated analyzer using biochip array technology. Clin. Chem., 51, 1165–1176.
Gosset, P., Lassale, P., Vanhee, D., Wallaert, C., Aerts, C., Voisin, C. and Tonne, A.B. (1991). Production of tumor necrosis factor alpha and interleukin-6 by human alveolar marcrophages exposed in vitro to coal mine dust. Am. J. Resp. Cell Mol. Biol., 5, 431–436.
Griwatz, U. and Seemayer, N.H. (1994). 29 P 13 Release of cytokines by quartz and coal mine dust exposed macrophages. J. Aerosol Sci., 25, 495–496.
Griwatz, U., Seemayer, N.H., Jung, B. and Dehnen, W. (1994). Cytokine production of human marcrophages induced by quartz and coal mine dusts: Tuberculosis and lung disease. Int. J. Tuberc. Lung Dis., 75, 103–104.
Gulumian, M., Borm, P.J.A., Vallyathan, V., Castranova, V., Donaldson, K., Nelson, G. and Murray, J. (2006). Mechanistically identified suitable biomarkers of exposure, effect, and susceptibility for silicosis and coal-worker’s pneumoconiosis: a comprehensive review. J. Toxicol. Environ. Health, Part B, 9, 357–395.
IARC (1997). IARC Monograph on the evaluation of the carcinogenic risk of chemicals to humans. In: Silica, some silicates, coal dust and para-aramid fibrils, Vol. 68. IARC Press, Geneva, Switzerland.
ILO (2002). Guidelines for the use of the ILO international classification of radiographs of pneumoconiosis. Geneva, International Labor Organization.
Ingram, L.R. (2003). Clinical Chemistry-Concepts & applications: Liver function (Anderson, S.C. and Cockayne, S. Eds.), The McGraw-Hill Co. New York, pp. 285–321.
Kolb, M., Margetts, P., Anthony, D.C., Pitossi, F. and Gauldie, J. (2001). Transient expression of IL-1 beta induces acute lung injury and chronic repair leading to pulmonary fibrosis. J. Clin. Invest, 107, 1529–1536.
Lasky, J.A., Oritz, L.A. and Brady, A.R. (2005). Lung injury-Mechanisms, pathophysiology, and therapy: Mediators and mechanisms in chronic lung injury and fibrosis (Notter, R.H., et al. Eds.). Taylor & Franics group, FL, pp. 175–226.
Loetscher, P., Seitz, M., Clark-Lewis, I., Baggiolini, M. and Moser, B. (1994). Monocyte chemotactic proteins MCP-1, MCP-2, and MCP-3 are major attractants for human CD4+ and CD8+ T lymphocytes. FASEB J., 8, 1055–1060.
Lukacs, N.W. and Ward, P.A. (1996). Inflammatory mediators, cytokines, and adhesion molecules in pulmonary and injury. Adv. Immunol., 62, 257–304.
Molloy, R.M., McConnell, R.I., Lamont, J.V. and Fitzgerald, S.P. (2005). (Review) Automation of biochip array technology for quality results. Clin. Chem. Lab. Med., 43, 1303–1313.
Morris, J.F., Koski, A. and Johnson, L.C. (1971). Spirometric standards for healthy nonsmoking adults. Am. Rev. Respir. Dis., 103, 57–67.
Perlman, D., Bitterman, P.B. and Wendt, C.H. (2005). Lung injury-Mechanisms, pathophysiology, and therapy: Chronic lung injury-Basic features and clinical relevance (Notter, R.H., et al. Eds.). Taylor & Franics group, FL, pp. 151–173.
Porter, D.W., Hubbs, A.F., Mercer, R., Robinson, V.A., Ramsey, D., McLaurin, J., Khan, A., Battelli, L., Mrumbaugh, K., Teass, A. and Castranova, V. (2004). Progression of lung inflammation and damage in rats after cessation of silica inhalation. Toxicol. Sci., 79, 370–380.
Prince, P., Boulay, M.E., Page, N., Desmeules, M. and Boulet, L.P. (2008). Induced sputum markers of fibrosis and decline in pulmonary function in asbestosis and silicosis: a pilot study. Int. J. Tuberc. Lung. Dis., 12, 813–819.
Razzaque, M.S. and Taguchi, T. (2003). (Review article) Pulmonary fibrosis: Cellular and molecular events. Pathol. Int., 53, 133–145.
Reuben, J.S., Guo, R.F. and Ward, P.A. (2004). Oxygen/Nitrogen radicals-Lung injury and disease: Mediators of lung inflammation-Role of reactive oxygen and nitrogen species (Vallyathan et al., Ed.). Marcel Deckker, New York, pp. 91–110.
Schins, R.P.F. and Borm, P.J.A. (1995). Epidemiological evaluation of release of monocyte TNF-a as an exposure and effect marker in pneumoconiosis. Occup. Environ. Med., 52, 441–450.
Schins, R.P.F. and Borm, P.J.A. (1999). Mechanisms and mediators in coal dust induced toxicity: A review. Am. Occup. Hyg., 43, 7–33.
Shoemaker, D.A., Pretty, J.R., Ramsey, D.M., McLaurin, J.L., Khan, A., Teass, A.W., Castranova, V., Pailes, W.H., Dalai, N.S., Miles, P.R., Bowman, L., Leonard, S., Shumaker, J., Vallyathan, V. and Pack, D. (1995). Particle activity and in vivo pulmonary response to freshly milled and aged alpha-quartz. Scand. J. Work Environ. Health, 21, 15–18.
Strieter, R.M., Standiford, T.J., Rolfe, M.W. and Kunkel, S.L. (1993). Cytokines of lung: Interleukine-8 (Kelly, J., Ed.). Marcel Deckker, New York, pp. 281–305.
Toews, G.B. (2000). Cytokines and pulmonary host defense against microbes: Cytokines in pulmonary disease-Infection and inflammation (Neson, S. and Martin, T.S., Eds.). Marcel Deckker, New York, pp. 1–17.
Tourmann, J.L. and Kaufmann, R. (1994). Biopersistence of the mineral matter of coal mine dusts in silicotic human lungs: is there a preferential release of iron? Environ. Health Perspect, 102, 265–268.
Ulker, O., Yucesoy, B., Demir, O., Tekin, I. and Karakaya, A. (2008). Serum and BAL cytokine and antioxidant enzyme levels at different stages of pneumoconiosis in coal workers. Hum. Exp. Toxicol., 27, 871–877.
Vallyathan, V. (2004). Oxygen/nitrogen radicals-lung injury and disease: Oxidative stress: antioxidant status in health and disease (Vallyathan et al., Ed.). Marcel Deckker, New York, pp. 35–58.
Vallyathan, V., Goins, M., Lapp, L.N., Pack, D., Leonard, S., Shi, X. and Castranova, V. (2000). Changes in bronchoal-veolar lavage indices associated with radiographic classification in coal miners. Am. J. Respir. Crit. Care. Med., 162, 958–965.
Vanhee, D., Gosset, P., Boitelle, A., Wallaert, B. and Tonnel, A.B. (1995). Cytokines and cytokine network in silicosis and coal workers’ pneumoconiosis. Eur. Respir. J., 8, 834–842.
Wallaert, B., Lassalle, P., Fortin, F., Aerts, C., Bart, F., Fournier, E. and Voisin, C. (1990). Superoxide anion generation by alveolar inflammatory cells in simple pneumoconiosis and in progressive massive fibrosis of nonsmoking coal workers. Am. Rev. Respir. Dis., 141, 129–133.
Weber, S.L., Lapp, N.L., Vallyathan, V., Castranova, V., Shumaker, J. and Schwegler-Berry, D. (1996). Role of cytokines and mineral particle profile in the development of coal workers’ pneumoconiosis as assessed by bronchoal-veolar lavage. Appl. Occup. Environ. Hyg., 11, 923–927.
Yoshimura, T., Yuhki, N., Moore, S.K., Appella, E., Lerman, M.I. and Leonard, E.J. (1989). Human monocyte chemoat-tractant protein-1 (MCP-1). Full-length cDNA cloning, expression in mitogen-stimulated blood mononuclear leukocytes, and sequence similarity to mouse competence gene JE. FEBS Lett, 244, 487–493.
Zhai, R., Liu, G., Ge, X., Bao, W., Wu, C., Yang, C. and Liang, D. (2002). Serum levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and their soluble receptors in coal workers pneumoconiosis. Respir. Med., 96, 829–834.
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Lee, J.S., Shin, J.H., Lee, J.O. et al. Blood Levels of IL-Iβ, IL-6, IL-8, TNF-α, and MCP-1 in Pneumoconiosis Patients Exposed to Inorganic Dusts. Toxicol Res. 25, 217–224 (2009). https://doi.org/10.5487/TR.2009.25.4.217
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DOI: https://doi.org/10.5487/TR.2009.25.4.217