- pneumoconiosis: causes
- pneumoconiosis: symptoms
- pneumoconiosis: types
- pneumoconiosis: diagnosis
- pneumoconiosis: treatment
- pneumoconiosis: prophylaxis
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Pneumonia is one of the occupational diseases associated with exposure to harmful dust. In response to the ingress of dust particles, the pulmonary parenchyma becomes fibrotic, and the lungs irreversibly lose their elasticity and functionality. What are the symptoms of pneumoconiosis? How to prevent the disease?
Pneumoniais a chronic respiratory disease in which chronic bronchitis and progressive emphysema lead to the development of the pulmonary heart and circulatory failure.
Our respiratory system has a number of defense mechanisms: mucus captures most of the dust, and the movement of the cilia removes them. Unfortunately, this is not always enough. Many factors affect the response of lung tissue to dust, including: shape, solubility, particle reactivity, and size.
- particles larger than 5-10 um have a chance of reaching the end of the airways
- particles smaller than 0.5 um behave like gases, they enter and leave the respiratory tract without significantly damaging them
- particles l-5 um are the most dangerous as they hit the bifurcation of the distal airways.
In the case of chronic exposure to harmful dusts, some particles remain in the bifurcations of the vesicular conductors, they are absorbed and collected in macrophages.
Remember that smoking increases the negative effects of all mineral dusts inhaled, especially asbestos.
Macrophages release inflammatory mediators and substances that stimulate fibroblast proliferation and collagen production. Lung tissue is damaged. Some particles enter the lymphatic vessels, either through direct run-off or through macrophages. They trigger an immune reaction that leads to the intensification and spread of local changes. The overgrowth of the pulmonary parenchyma with fibrous tissue limits the functional parenchyma of the lungs and limits the possibility of gas exchange. Symptoms of respiratory failure gradually increase.
- shortness of breath
- removal of mucous or mucopurulent sputum
- chronic fever
- symptoms of the pulmonary heart - failurerespiratory, heart failure
- complications in the form of chronic bronchitis, emphysema
- sometimes stick fingers are present
Classification of dusts by the causative agent:
- carbon dioxide (anthracosis)
Coal dust is relatively neutral and only large amounts of it remain in the lungs revealing clinical changes. Therefore, it typically occurs in hard coal miners. However, residents of large urban agglomerations and smokers are also at risk of developing the disease. Silicon and asbestos are more reactive than coal dust, so even low concentrations cause marked fibrous changes in the lungs.
The picture of fibrosis in the anthers may vary. Silica leads to nodular changes. Fibrosis occurs as a result of the breakdown of macrophages containing silica particles. Occupational exposure occurs in people working in the construction of tunnels and shafts, in quarries, in the steel and porcelain industries, in the production of refractory and abrasive materials.
Like other pneumoconiosis, asbestosis leads to macrophage-related pulmonary fibrosis. However, in this case diffuse interstitial fibrosis occurs.
It should be noted that an increased incidence of asbestos-related cancers has also been shown in family members of occupational asbestos exposure.
It is not clear why this is happening. The reasons are the ability of asbestos fibers to deposit more uniformly in the alveoli and the ability to penetrate epithelial cells. It is a particularly dangerous form of pneumoconiosis, because exposure to asbestos also predisposes to the occurrence of: pleural changes, lung cancer, pleural mesothelioma.
- Caplan syndrome (silicoarthritis)
In addition to the symptoms of silicosis (silicosis, carbonic or asbestosis), there are changes typical of rheumatoid arthritis. The earlier appearance of symptoms is characteristic than in isolated pneumoconiosis. Microscopically, the changes in the lungs resemble subcutaneous rheumatoid nodules. They appear in the form of hard tumors with fibrous necrosis foci in the center and an intense inflammatory infiltrate on the periphery. The cause of Caplan's syndrome is unknown.
The basic examination is a chest X-ray, but a detailed examination is necessary to establish a correct diagnosisprofessional and community interview and physical examination.
Unfortunately, the lesions are irreversible. All that can be done is symptomatic treatment. Bronchodilators are given to improve gas exchange. It is important to combat comorbidities that may exacerbate the patient's condition, e.g. bronchiectasis, bronchiectasis, infections. It is also advisable to check for infection with mycobacterium tuberculosis, because patients with pneumoconiosis are particularly predisposed to its occurrence. Complications, including heart failure, should also be treated to alleviate symptoms, but most importantly, the harmful factor should be removed from the environment and, in the case of smokers, encouraged to quit.
Prevention plays a very important role in the absence of effective treatment. Everyone exposed to harmful dust in the workplace should use protective clothing and masks. Asbestos removal workers should receive adequate training. Since the onset of the disease is secretive and the changes are irreversible when symptoms appear, regular checkups should be performed to detect possible changes in the lungs early and to stop dust exposure.