CC BY
0«COyyOMUM-JMTMaL» 2023 / MEDICAL SCIENCES
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UDC: 616
Mandryk Olha Yevhenivna
PhD in Medicine, Associate Professor of the Department of Internal Medicine, Clinical Pharmacology and
Occupational Diseases
Bukovinian State Medical University Cherniievych Bohdan Oleksandrovych
student
Bukovinian State Medical University
Nykoliuk Mariia Volodymirivna
student
Bukovinian State Medical University DOI: 10.24412/2520-6990-2023-12171-15-17 SILICOSIS. STRUCTURED ABOUT THE MAIN THING.
Abstract:
Silicosis, a significant form of pneumoconiosis, causes progressive and irreversible damage starting from inflammation and fibrosis. Information on the worldwide prevalence of silicosis and long-term trends has been limited. In 2019, there were over 12.9 thousand (95% Uncertainty Intervals (UI): 10.9, 16.2) reported deaths worldwide due to silicosis, with 655.7 thousand (95% UI: 519.3, 828.0) disability-adjusted life years (DALYs) attributed to this disease. From 1990 to 2019, the number of deaths and DALYs in countries with high Socio-DemographicIndex (SDI) quintile decreased by 0.35% (95% UI: -0.45, -0.17) and 0.32% (95% UI: -0.45, -0.01) per year, respectively. However, there was a higher burden of silicosis in low- and middle-income countries, as estimated in 2019 based on age-standardized rates (ASRs). Males accounted for over 95% of all reported deaths and DALYs globally in 2019. Mortality and DALYs rates increased with age and peaked in the 85-89 age group. Over the past 30 years, there has been a decreasing trend in age-standardized mortality and DALYs rates with an average annual percentage change of -3.0% (95% Confidence Intervals (CI): -3.2, -2.9) and -2.0% (95% CI: -1.7, -2.2), respectively.
Keywords: Silicosis, silicon dioxide, an occupational disease.
Introduction: Silicosis is an occupational pneumoconiosis caused by inhaling crystalline silicon dioxide. It is one of several well-documented pulmonary complications associated with toxic exposures in the workplace, such as asbestos-related lung diseases, berylliosis, coal worker's pneumoconiosis, hard metal pneumoconiosis, among others. It is considered an occupational disease as it results from prolonged inhalation of airborne silica particles in work environments.
Etiology: There are two forms of silicon dioxide found in nature: amorphous and crystalline. Crystalline silicon dioxide is a common mineral abundant in substances like sandstone, quartz, and granite. Inhalation of the amorphous form does not typically cause significant health issues, but inhalation of crystalline silicon dioxide can result in pulmonary disease. When silica particles deposit in the airways, they come into contact with alveolar and endobronchial surfaces, leading to the generation of reactive oxygen species. Smaller particles are taken up by macrophages through phagocytosis, which then produce more free radicals. This oxidative damage caused by activated macrophages and silica particles results in the release of inflammatory cytokines, increased cell signaling, and apoptosis of paren-chymal cells and macrophages. As the disease progresses, fibroblast infiltration occurs in a nodular pattern.
Epidemiology: There are numerous occupations in various industries that may expose workers to silica dust, putting them at risk for silicosis. High-risk occupations include road repair, concrete manufacturing, coal mining, brick working, and rock excavation, as well as jobs in stone cutting, petroleum extraction,
steel working, sandblasting, and others. According to the Occupational Safety and Health Administration (OSHA), there are over two million workers who are regularly exposed to respirable crystalline silica in their workplaces. Although improved awareness and safety measures in the workplace have led to a significant decrease in the prevalence of silicosis over the past few decades, safeguards are not perfect and new cases of silicosis still occur.
Pathophysiology: Inhaling crystalline silicon dioxide leads to the formation of mineral deposits in the terminal bronchioles and alveoli of the lungs. These deposits activate alveolar macrophages and also have direct toxic effects on the surrounding lung tissue. This cellular damage triggers the release of inflammatory cytokines such as IL-1 and TNF-alpha, generation of free radicals, and activation of cell-signaling pathways, resulting in promotion of fibrosis. Mast cells in the tissue may also play a role in this process. Additionally, silica has been shown to interfere with the ability of macrophages to inhibit the growth of mycobacteria, which may explain the common association between silicosis and tuberculosis. In acute forms of silicosis, direct toxic effects on alveolar type 2 cells and macrophages may also occur. Although immunologic factors have been postulated as potential contributors to silicosis, their role has not been proven conclusively.
Histopathology: Nodular silicosis is characterized by the presence of silicotic nodules, which are firm, discrete, rounded lesions containing variable amounts of black pigment. These nodules typically occur around respiratory bronchioles, small pulmonary arteries, and in the subpleural and paraseptal areas of
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the lungs. Progressive expansion of these nodules leads to obliteration of small airways and pulmonary vessels. Histologically, silicotic nodules show concentrically arranged hyalinized collagen bundles surrounded by variable numbers of dust-filled histiocytes. In early nodules, fibroblasts and histiocytes are prominent with acellular collagen lamellae. Small, polarizable, doubly refractile, round or oval particles may be found within nodules, although their presence is not specific for silicosis and they may be absent in some cases. Granulom-atous reaction may be observed in the capsule of sili-cotic nodules, raising the possibility of coexisting my-cobacterial infection, such as tuberculosis. In acute silicosis, microscopic findings may resemble pulmonary alveolar proteinosis, but typically show additional features such as interstitial inflammation, fibrosis, irregular hyaline scars, and variable amounts of pigment. Silicotic nodules are usually poorly formed or absent in most cases. Microscopic examination may also reveal complications such as progressive massive fibrosis or tuberculosis and non-tuberculous infections. Progressive massive fibrosis is characterized by the presence of nodular fibrosis that is greater than 1 cm in size, with a large amorphous mass of fibrous tissue composed of conglomerated nodules causing obliteration and contracture of lung parenchyma. This type of lesion can also occur in other pneumoconioses, including asbesto-sis, coal workers' pneumoconiosis, or mixed dust fibro-sis. Tuberculosis and non-tuberculous mycobacteriosis may be suspected when encountering a granulomatous infection with necrosis in the lung tissue.
History and Physical: Silicosis can manifest in different clinical entities along a spectrum of disease severity. Chronic forms of silicosis typically occur after prolonged exposure to silica dust over 20 or more years in occupational settings. Accelerated forms of silicosis can develop after heavier exposure to silica dust for 5 to 10 years. Acute silicosis, on the other hand, is a rare reaction that occurs after heavy exposure to high levels of silica dust of small particle size over a short period of time. The severity of silicosis is dependent on the duration and intensity of exposure to silica dust.
Radiologic Findings: In simple silicosis, chest X-ray shows variable features consisting mainly in well-defined opacities ranging from 1 to 10 mm in diameter, located in the upper lobe and posterior portion of the lung. CT-scan findings consist of multiple small nodules with hilar and mediastinal lymphadenopathy. Some nodules may be calcified.
In acute silicosis, chest X-ray shows bilateral consolidation associated with ground-glass opacities. CT-scan findings consist of numerous centrilobular ground-glass opacities with consolidation.
Differential Diagnosis: Silicotic nodules can show features that mimic rheumatoid nodules, which are nodules that can develop in individuals with rheumatoid arthritis. Both silicotic nodules and rheumatoid nodules can show central areas of necrosis surrounded by histiocytes and inflammatory cells.
In rheumatoid arthritis, nodules typically develop in the subcutaneous tissues, often overlying bony prom-
inences such as the elbows or fingers. They are typically firm, mobile, and can range in size from a few millimeters to several centimeters. Microscopically, rheumatoid nodules show central areas of necrosis surrounded by a palisade of histiocytes, with a peripheral rim of lymphocytes and plasma cells.
In silicosis, silicotic nodules tend to occur in the lungs, specifically around respiratory bronchioles and small pulmonary arteries. Microscopically, silicotic nodules can also show central areas of necrosis surrounded by histiocytes and inflammatory cells, which can resemble rheumatoid nodules. However, the location of the nodules (in the lungs in silicosis versus subcutaneous tissues in rheumatoid arthritis) and the presence of other features such as dust-filled histiocytes and hyalinized collagen bundles in silicotic nodules can help differentiate between the two conditions.
A thorough clinical evaluation, including a detailed history of occupational exposure to silica and imaging studies such as chest X-rays or CT scans, along with microscopic examination of the nodules, can help differentiate between silicosis and rheumatoid arthritis or other conditions with similar features. Consultation with a qualified healthcare professional is essential for accurate diagnosis and appropriate management.
Treatment: The most important treatment for silicosis is to remove the source of exposure to silica dust. This typically involves implementing strict dust control measures in the workplace, such as proper ventilation, use of wet methods to suppress dust, and wearing appropriate personal protective equipment (PPE) such as respirators. In some cases, it may be necessary to modify work processes or provide alternative work assignments to minimize further exposure to silica dust.
There is no specific cure for silicosis, and treatment is primarily focused on managing symptoms and preventing further progression of the disease. This may involve medications to control symptoms such as cough, shortness of breath, and chest pain. In some cases, supplemental oxygen therapy may be necessary to improve oxygen levels in the blood. In severe cases, lung transplantation may be considered as a treatment option.
It's also important to provide supportive care to individuals with silicosis, including smoking cessation counseling, vaccinations against respiratory infections such as pneumonia and influenza, and regular monitoring of lung function to track disease progression.
Prevention: Through effective dust control measures in the workplace remains the key approach to managing silicosis, and early detection through regular health screenings and prompt removal from exposure are critical in preventing the progression of the disease.
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