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Introduction. Pneumoconiosis and chronic obstructive pulmonary disease (COPD) of occupational origin result from prolonged exposure to industrial pollutants, each bearing distinct pathogenetic mechanisms leading to characteristic clinical manifestations and functional impairments. Crucial in the progression of inflammation in these disorders are imbalances in the production of inflammatory mediators and alterations in humoral and cellular components of general immunity. The investigation of pathogenetic mechanisms underlying pneumoconiosis in conjunction with COPD among mining and metallurgical industry workers gains paramount significance, particularly concerning the cellular link of general immunity. This exploration unveils insights into the unique formation of this occupational pathology, objectively evaluates the nature and direction of inflammatory processes, predicts potential complications, and devises strategies for timely diagnosis, treatment, and prevention of combined diseases.
The aim of the research – to study the condition of the cellular link of the general immunity among workers of the mining and metallurgical industry, suffering from pneumoconiosis in combination with chronic obstructive pulmonary disease, to assess the nature of the inflammatory bronchopulmonary process, to develop measures aimed at treatment and prevention of this occupational disease.
Objective. This study aims to assess the cellular link of general immunity in mining and metallurgical industry workers afflicted with pneumoconiosis in combination with COPD; to understand the inflammatory bronchopulmonary process and develop measures for effective treatment and prevention of this occupational disease.
Materials and methods. To comprehend the nature of bronchopulmonary inflammation, devise treatment strategies, and implement preventive measures, we examined the cellular immunity status of 99 patients with pneumoconiosis and COPD, 21 with pneumoconiosis, 515 with occupational COPD, and a control group of 21 healthy workers. The average age of employees was 58.6±2.4 years, the length of work in adverse conditions was 18.9±0.8 years. Among them, indicators of the cellular link of general immunity were determined in 33 patients with pneumoconiosis and COPD, 16 with pneumoconiosis, 69 with occupational COPD, and 10 healthy controls. We evaluated leukocyte count, leukocyte subpopulations (segmented neutrophils, rod-nucleated neutrophils, monocytes, eosinophils, lymphocytes), and erythrocyte sedimentation rate. Moreover, relative indicators of systemic cellular immunity were assessed, including T-lymphocytes (CD3+CD19), T-helpers/inducers (CD4+CD8-), cytotoxic cells (CD3+CD56+), T-suppressors/T-cytotoxic cells (CD4+CD8-\CD4-CD8+), natural killer cells (CD3-CD56+), specific markers of monocytes/macrophages (CD14), common leukocyte antigen (CD45), and immunoregulatory index.
Results. Through a comprehensive comparative analysis of collected data concerning the cellular component of general immunity, including parallel assessments with the control group, followed by a comparison with individuals afflicted by pneumoconiosis in combination with COPD and those solely diagnosed with pneumoconiosis. Our findings substantiated that individuals with pneumoconiosis combined with COPD showcased elevated levels of rod-nuclear leukocytes and eosinophils, alongside an increased erythrocyte sedimentation rate, indicating the activity of non-specific systemic inflammation. Enhanced CD3+CD19 content indicated immune system hyperreactivity, while diminished CD4+CD8 percentages (from 4.1% to 7.0%) alluded to chronicity. Excessive activity of the suppressor link of cellular immunity (CD4+CD8-\CD4-CD8+), ranging from 5.5% to 13.0%, implied the formation of "immune tolerance" - a tendency in extending bronchopulmonary inflammation, elevating the risk of infectious complications. A decrease in the immunoregulatory index from 11.1% to 16.6% contributed to immune "deficiency". The elevation in CD3+CD56 content from 6.1% to 28.8% marked heightened antiviral protection and the establishment of "tense" effector T-killer cell immunity. These identified changes unveiled novel perspectives on the pathogenetic mechanisms underlying pneumoconiosis combined with COPD, creating the basis for the development of a comprehensive framework of interventions targeted at treating and preventing this occupational ailment among mining and metallurgical industry workers.
Conclusions. In the mining and metallurgical industry workforce, individuals with pneumoconiosis combined with COPD exhibited significant elevations in rod-nuclear leukocytes (6.0% to 40.0%), eosinophils (7.8% to 11.8%), and erythrocyte sedimentation rate, with values exceeding their counterparts by up to 2.6 times, indicating the activity of non-specific systemic inflammation. Furthermore, substantial shifts emerged in the cellular immunity context. Increased CD3+CD19 content suggested immune hyperreactivity, while the decrease in CD4+CD8 indicators (from 4.1% to 7.0%) pointed towards chronicity; an excessive activity in suppressor cellular immunity CD4+CD8-\CD4-CD8+, ranging from 5.4% to 13.0%, indicated a tendency for chronic bronchopulmonary inflammation. The increase in CD3+CD56+ content (6.1% to 28.8%) reflected enhanced antiviral protection and the establishment of "tense" effector T-killer cellular immunity. Simultaneously, the elevation in CD3+CD56 content and a substantial (from 7.4% to 22.4%) decrease in CD14 content suggested a moderate immune response to the protracted course of bronchopulmonary inflammation.
Keywords: employees, pneumoconiosis, chronic obstructive pulmonary disease, cellular immunity.