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Coal miner's pneumoconiosis

  Coal miner's pneumoconiosis refers to a general term for pulmonary lesions caused by long-term inhalation of dust in the production environment of coal mines. It includes coal lung caused by the inhalation of pure coal dust by coal mining and coal-making workers, accounting for about 10%; silicosis caused by the inhalation of silica dust by rock drilling workers, accounting for less than 10%; and coal-silicosis caused by the inhalation of mixed dust such as coal dust and silica dust, mainly occurring in mixed trades that both drill and mine coal, accounting for more than 80%. Coal-silicosis is the most common in coal mines. Coal miner's pneumoconiosis mainly occurs in underground mining workers, with a very low incidence rate in open-pit coal mine workers. Coal lung can also occur in other workers who have a large amount of contact with coal powder, such as dock coal unloading workers and coal ball makers. Due to the minor impact on labor capacity, there is not much research on this topic at present.

Table of Contents

1. What are the causes of coal worker's pneumoconiosis?
2. What complications can coal worker's pneumoconiosis lead to?
3. What are the typical symptoms of coal worker's pneumoconiosis?
4. How to prevent coal worker's pneumoconiosis?
5. What laboratory tests are needed for coal worker's pneumoconiosis?
6. Diet taboos for coal worker's pneumoconiosis patients
7. Conventional methods of Western medicine for the treatment of coal worker's pneumoconiosis

1. What are the causes of coal worker's pneumoconiosis?

  One: Etiology

  Coal is formed from the sedimentation of decomposed plants in peat bogs, with geological conditions causing chemical changes due to high pressure and high temperature. Different geological conditions produce different types of coal. It takes about 250 million years for peat to gradually transform into lignite, then into anthracite, and finally into anthracite coal. The origin of coal is closely related to sedimentary rock layers, such as sandstone, mudstone, shale, silt, refractory stone, and limestone. Different rocks result in different dust compositions in different coal mines or in different coal seams of the same coal mine. The free silicon dioxide content in coal itself is usually low, but there may be a small amount of other associated minerals. The air dust composition is also not the same when mining different rock strata in the same coal mine. During the coal mining process, both coal dust and silica dust coexist, and there have been different views on their effects over the years. Initially, it was mostly believed that coal dust only settled in the lungs, and the fibrotic change in coal miner's pneumoconiosis was caused by the presence of silica dust in coal dust. Later, some people observed progressive large-scale fibrosis in dock workers engaged solely in coal unloading, in addition to coal dust deposition, thus considering that coal dust itself could cause pneumoconiosis.

  Two: Pathogenesis

  1. The gross anatomical appearance of simple coal miner's pneumoconiosis varies with the duration of exposure to coal dust. Usually, there are no obvious abnormalities in the lungs except for melanotic deposits on the pleura surface. The trachea and bronchi also show no significant abnormalities unless there is concurrent chronic bronchitis. Lymph nodes often enlarge, showing uniform pigmentation and hardness without fibrosis. The lung sections show many pigmented foci adjacent to terminal and respiratory bronchioles. The air spaces adjacent to dust accumulation often undergo mild expansion, known as focal emphysema.

  2. Under the microscope, the basic pathological changes of coal lung include coal dust foci (or coal spots, which are 5mm of pigmented changes), perifocal emphysema or diffuse interstitial fibrosis. Coal dust and macrophages phagocytizing coal dust aggregate in the alveolar spaces, alveolar walls, bronchi, and vascular surrounding tissues, forming coal dust foci and coal dust cell foci, mostly around the second-order respiratory bronchioles. With the progression of the lesion, irregularly arranged reticular fibers appear, and a small amount of collagen fibers can be interwoven in the later stage, forming coal dust fibrosis foci. Perifocal emphysema is one of the main pathological features of coal worker's pneumoconiosis. There is varying degrees of fibrous tissue proliferation in the pulmonary interstitium.

  3. In addition to the basic pathological changes of coal lung and silicosis, coal worker's pneumoconiosis also has pathological changes under the coexistence of coal dust and silica dust, forming coal-silica mixed nodules. In addition to the reticular fibrosis proliferation within the nodules, there is also a crisscrossing of collagen fibers, but the latter are arranged irregularly. Coal dust cells and quartz particles are present within the nodules. In the late stage, large areas of fibrosis can be seen. Other features include subpleural coal dust deposition, enlargement of hilar and mediastinal lymph nodes, and changes in the parietal pleura caused by coal dust.

2. What complications can coal worker's pneumoconiosis easily lead to?

  The main complications or complications of coal worker's pneumoconiosis are chronic bronchitis and emphysema, respiratory tract infections, spontaneous pneumothorax, and chronic pulmonary heart disease. Coal worker's pneumoconiosis with pulmonary tuberculosis is also common, with an incidence rate of about 22%. The occurrence of pulmonary tuberculosis often significantly aggravates the lesions, especially in simple coal worker's pneumoconiosis, which can rapidly progress to progressive massive fibrosis, and the therapeutic effect of anti-tuberculosis treatment is poor. Rheumatoid pneumoconiosis (Caplan syndrome) also has a higher incidence in coal worker's pneumoconiosis than in other pneumoconioses. Patients have rheumatoid arthritis, and chest X-rays show scattered, clear, round shadows in both lungs, with a diameter of 0.5 to 5 cm, appearing almost simultaneously and rapidly increasing. After 3 months, they no longer increase. Serum rheumatoid factor may be positive, but this complication is rare in China.

3. What are the typical symptoms of coal worker's pneumoconiosis?

  1. Firstly, attention should be paid to the duration of exposure to dust and the occupational history. Generally, the development of simple coal worker's pneumoconiosis requires 10 to 12 years of dust exposure in the mine, during which the lung function usually shows no abnormal changes. The clinical manifestations are non-specific, often asymptomatic in the early stage. Symptoms such as cough, usually mild dry cough, may appear when there is concurrent bronchitis or lung infection. Coughing may become more severe with sputum production, which may contain coal dust or cholesterol crystals. Hemoptysis is rare. Coal worker's pneumoconiosis patients often have varying degrees of chest tightness or chest pain, manifested as intermittent, hidden pain or pricking pain, which is more pronounced after labor or severe coughing. Sudden, severe chest pain accompanied by dyspnea should be considered as a possible spontaneous pneumothorax. Gradually, progressive and worsening dyspnea may occur. In some cases, respiratory symptoms may not be consistent with X-ray findings, with mild X-ray findings but severe dyspnea symptoms.

  2. With the increase of exposure time to dust, shortness of breath and worsened cough may occur, and the chest X-ray findings become more obvious. The worsening of respiratory difficulty is often consistent with the development of massive pulmonary fibrosis. Sputum is black and in large quantities. When the area of massive fibrosis develops ischemic necrosis and forms a cavity, a large amount of black sputum is often coughed up. When acute infection is complicated, a large amount of purulent sputum may also be coughed up.

  2. Most coal worker's pneumoconiosis patients even in stages II and III have no positive signs, occasionally cyanosis and clubbing fingers, a few patients may have rough or weakened breath sounds and dry wheezes in both lungs, and corresponding signs appear only when there are various complications.

4. How to prevent coal worker's pneumoconiosis?

  The preventive measures for coal worker's pneumoconiosis are the same as those for silicosis, and it must be emphasized that the standards for the maximum allowable dust concentration stipulated by the state must be strictly enforced. The current Chinese regulations stipulate that the maximum allowable concentration of coal dust containing less than 10% free silicon dioxide is 10mg/m3. The main measures include removing from the dust working environment, doing a good job of protective measures, reasonably protecting the environment, staying away from dust environments, reasonably improving lung function, actively exercising the body, not eating spicy foods, avoiding smoking and alcohol, and ensuring adequate sleep. Improving the environmental hygiene, doing a good job of personal labor protection, eliminating and avoiding the effects of smoke, dust, and irritating gases on the respiratory tract.

5. What laboratory tests are needed for coal worker's pneumoconiosis?

  1. Pulmonary function examination

  Early coal worker's pneumoconiosis patients may have diffuse interstitial fibrosis and mild emphysema, but there are usually no significant changes in pulmonary function. Only in the late stage of pneumoconiosis can a decrease be seen, or a decrease trend can be observed earlier in dynamic observation. The type of ventilation dysfunction in early coal worker's pneumoconiosis is mainly restrictive, while in the middle and late stages, obstruction is most common, followed by mixed type. Usually, the mean values of FEV1, FVC, VC, and MMF in coal worker's pneumoconiosis patients are lower than those of normal people or dust-exposed workers, and basically decrease progressively with the progression of the lesions. Among all indicators, the predicted values of FEV1, FEV1/FVC, and FEV1/VC are most sensitive. When coal worker's pneumoconiosis patients have significant emphysema, the total lung capacity and lung compliance increase. In simple coal worker's pneumoconiosis, the diffusion function can be within the normal range, while in patients with progressive massive fibrosis, it can decrease to below 50% of the predicted value. The diffusion function shows progressive decrease, and the decrease may also be related to obstructive lung disease or associated with silicosis. In the Ⅲ stage and some Ⅱ stage coal worker's pneumoconiosis patients, the arterial blood oxygen partial pressure and oxygen saturation decrease at rest, while the arterial carbon dioxide partial pressure is usually within the normal range or slightly decreased.

  2. X-ray examination

  The chest X-ray findings of coal worker's pneumoconiosis include: reticular changes; nodular changes; nodular fusion; mass shadows and a large amount of fluffy changes.

6. Dietary taboos for coal worker's pneumoconiosis patients

  Coal worker's pneumoconiosis patients should increase the intake of high-quality protein, which should be 90-110 grams per day to supplement the consumption of the patient's body and increase the immune function of the body; it is appropriate to increase the intake of vitamin C and A, as vitamin C has antioxidant effects, and vitamin A can maintain the health of epithelial tissue, especially respiratory epithelial tissue. Abstain from smoking and alcohol, avoid spicy and stimulating foods. Avoid overexertion.

7. Conventional methods of Western medicine for the treatment of coal worker's pneumoconiosis

  I. Treatment

  1. Regular physical examinations for coal mine workers, and timely transfer of those with coal worker's pneumoconiosis. Coal worker's pneumoconiosis, like silicosis, is an irreversible disease, but if the dust exposure environment is left in time when there is simple coal worker's pneumoconiosis, it can prevent or slow down the progression to complex coal worker's pneumoconiosis. When it progresses to complex coal worker's pneumoconiosis, even if there is no longer contact with coal dust, the condition can still continue to worsen.

  2. Treatment principles can be referred to the treatment of silicosis.

  3. Whole-lung high-volume lavage (massive whole-lung lavage, MWLL) is a new method in the treatment of pneumoconiosis in recent years, but there are different opinions on this. Some people believe that lung lavage can only wash out part of the inert dust and dust cells inside the lung, but cannot wash out the dust that has formed fibrous encapsulation inside the lung, so it is not significant in preventing the fibrosis process of lung tissue. Most scholars believe that lung lavage can wash out a large amount of dust, dust-containing cells, and non-cellular components in alveolar spaces, which will play a beneficial role in alleviating and reducing the occurrence and progression of pneumoconiosis, and the effect of MWLL in the early stage of pneumoconiosis will be better. Its exact efficacy needs to be evaluated through prospective studies under strict control.

  4. It is necessary to actively handle the complications. Encourage smoking cessation to alleviate the symptoms of chronic bronchitis and delay the progression of emphysema. For those with tuberculosis, effective and regular anti-tuberculosis treatment should be provided. For those with pulmonary infection and heart failure, appropriate treatment should be given. For those with concurrent rheumatoid pneumoconiosis, glucocorticoid therapy can be used, with prednisone 40mg/d. After the efficacy is observed, it should be maintained for a longer time. If necessary, cyclophosphamide, azathioprine, and other immunosuppressants can be added.

  II. Prognosis

  Prognosis can be referred to silicosis.

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