Pulmonary Dysfunction in Silica-Exposed Workers: A Relationship to Oxidant/Antioxidant State and Soluble Interleukin-2 Receptors

Document Type : Original Article

Authors

1 Department of Physiology, Medical Research Institute, Alexandria University, Egypt

2 Department of Biochemistry , Medical Research Institute, Alexandria University, Egypt

3 Department of Immunology, Medical Research Institute, Alexandria University, Egypt

Abstract

Silicosis is a chronic progressive granulomatous and fibrotic lung disease caused by inhalation of quartz [SiO2] that leads to the formation of complex substances containing phosphosilicate with a single oxygen atom which is highly catalytic and reactive. Twenty male workers exposed to silica and 11 control subjects were studied in a trial to clarify the role of oxidant/antioxidant state, soluble interleukin 2 receptors in relation to pulmonary performance. A restrictive ventilatory impairment was detected in the present study as assessed by significant decrease in flow rates [FVC, FEV., FEV, , FVC%, FEF25%-75% and MVV] and in VE and VA values compared to their respective values of controls, P< 0.05. Significant negative correlations were observed between duration of exposure to silica and FVC, FEV,1: FEF25%-75% [r= -0.857, -0.695 and -0.582 respectively, P = 0.001].The oxidant/ antioxidant balance of silicotic cases was disturbed as shown by significant high levels of oxidants [Lipid peroxides] P = 0.001 and significant low levels of antioxidant enzymes [superoxide dismutase and catalase], P < 0.05. The antioxidant vitamins [A,C and E] were as well significantly decreased compared to those of controls, P < 0.01. We observed positive correlations between FVC and plasma levels of vitamin C and E [r= 0.878 and 0.915, P = 0.001]. Serum soluble interleukin-2 receptors [sIL-2r] were elevated in patient's serum indicating that activation of T-lymphocytes might have a role in initiating and sustaining symptoms in patients with silicosis. These data suggest that exposure to silica causes increase oxidant burden which could lead to imbalance of the oxidant/ antioxidant state ending with enhanced pulmonary injury and fibrosis. Abbreviations: FVC: Forced vital capacity FEV1 :Forced expiratory volume in one second. FEF25%-75%* MVV: Maximum voluntary ventilation VE: Minute ventilation VA: Alveolar ventilation :Maximum mid expiratory flow rate

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