Silicosis is the most common type of pneumoconiosis, caused by prolonged inhalation of large amounts of free silica dust, leading to extensive nodular fibrosis in the lungs. In severe cases, it impairs respiratory function and results in loss of labor capacity.

bubble_chart Etiology

Approximately 95% of ores contain varying proportions of quartz. In some industrial productions, raw materials also contain varying amounts of quartz sand, such as in glass, refractory materials, enamel, ceramics, etc. Quartz contains more than 97% free silica, so silicosis can occur among miners, workers, military engineers, and farmers (engaged in railway construction or exposed to dust in township industries) who are exposed to silica dust.

Whether exposure to quartz dust leads to illness depends on various factors. For instance, the higher the free silica content in the dust, the greater the concentration in the ambient air, the smaller the dust particles (0.5-2 μm), the longer the exposure time, and the poorer the respiratory defense function of the body (such as chronic rhinitis, bronchitis, pulmonary subcutaneous nodules, etc.), the faster the onset and progression of silicosis. Additionally, even after ceasing exposure, delayed-onset silicosis may still develop years later due to short-term inhalation of large amounts of free silica dust. Silicosis can occur as quickly as within 1 year or as slowly as over 10 years after exposure to dust.

bubble_chart Pathogenesis

Silica dust particles (silica dust) are engulfed by pulmonary macrophages (dust cells) after being inhaled into the alveoli. The phagosomes containing silica dust merge with lysosomes to form secondary lysosomes. Silica dioxide has a significant toxic effect on macrophages. The hydroxyl groups on the quartz surface form hydrogen bonds with phospholipids or proteins in the lysosomal membrane, leading to the disintegration of the phagocyte lysosome. Eventually, the cell membrane itself is also damaged, releasing the silica dust, which is then engulfed by other macrophages. This process repeats continuously. Damaged or destroyed macrophages release "fibrogenic factors," activating fibroblasts and causing collagen fiber proliferation. When macrophages disintegrate, they release antigens (silica dioxide), stimulating immunocompetent cells to produce antibodies. The antigen-antibody reaction forms complexes that, together with complement, deposit as hyaline material on collagen fibers, giving the newly formed connective tissue a glassy appearance. During the development of silicotic nodules, numerous plasma cells are present in the surrounding area.

Silicotic nodules are the characteristic lesions of silicosis, and the aggregation of dust cells is the foundation for the formation of silicotic nodules. After the dust cell clusters form, fibroblasts proliferate around them, and reticular fibers appear. The latter thicken and degenerate into collagen fibers, eventually forming collagen nodules, with central hyaline degeneration. Microscopically, silicotic nodules are located around bronchi and blood vessels, with diameters ranging from 0.3 to 1.5 mm. Typical silicotic nodules exhibit concentrically arranged hyalinized collagen fibers. Silica dust particles may be present between the collagen fibers, and the silica dust can migrate with tissue fluid to other sites, causing new silicotic nodules. Therefore, even after ceasing exposure to dust, silicosis can continue to progress. Multiple nodules may aggregate into larger nodules, and many large nodules can fuse into large hyalinized masses.

After silica dust enters the alveoli, it is phagocytosed by macrophages. The dust cells can enter the lymphatic system and reach the hilar lymph nodes. Due to the continuous accumulation of dust cells, lymphatic vessels become obstructed, and lymphatic fluid stagnates, counterflowing to the subpleural lymphatic vessels. This leads to the aggregation of dust cells in the alveolar septa and around blood vessels and bronchi, resulting in nodular fibrosis. The compression or contraction of fibrous masses distorts the pulmonary interstitium, deforms it, and narrows the lumens of small bronchi and capillaries, impairing ventilation and blood flow.

The accumulation of dust cells in the hilar lymph nodes causes fibrous tissue hyperplasia, forming silicotic nodules and leading to hilar lymph node enlargement and hardening. Calcification may occur within or around the lymph nodes, appearing as "eggshell calcification" on chest X-rays.

bubble_chart Clinical Manifestations

In the early stages, there may be no symptoms or only mild symptoms, but as the disease progresses, symptoms increase. Silica dust inhalation irritates the respiratory tract, causing reflexive cough, but the severity of cough and the amount of sputum are closely related to respiratory infections and do not necessarily correlate with the degree of silicosis. A few patients may have bloody sputum. If there is recurrent massive hemoptysis, the possibility of concurrent pulmonary subcutaneous nodules or bronchiectasis should be considered. In the early stages, patients often experience needle-like pain in the upper-middle part of the chest, unrelated to breathing posture or physical labor, which frequently occurs during weather changes. The severity of chest tightness and shortness of breath depends on the extent and nature of the lesions. If the lesions are widespread and progress rapidly, shortness of breath becomes pronounced and progressively worsens. Patients may also experience dizziness, lack of strength, insomnia, palpitations, and poor appetite.

Early-stage silicosis may show no abnormal signs. In late-stage [third-stage] silicosis, massive fibrosis causes lung tissue contraction, leading to tracheal displacement and dullness on percussion. If complicated by chronic bronchitis, lung qi distension, or lung heart disease, corresponding signs may appear.

bubble_chart Auxiliary Examination

Due to the strong compensatory capacity of lung tissue, early-stage patients show no obvious impairment in pulmonary function. As pulmonary fibrosis increases and lung elasticity declines, restrictive ventilatory changes may occur, such as reductions in vital capacity, total lung capacity, and residual volume, while forced vital capacity and maximum ventilation remain normal. If accompanied by obstructive ventilation, vital capacity, forced vital capacity, and maximum ventilation all decrease, while residual volume and its percentage of total lung capacity increase, along with impaired diffusion function. In severe cases, hypoxemia and/or carbon dioxide retention may occur. Pulmonary function tests have limited diagnostic significance but serve primarily as a basis for assessing work capacity.

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The patient has a history of close exposure to silica dust and detailed occupational history. Combined with clinical manifestations and comprehensive analysis based on chest X-rays, a diagnostic staging is made.

The chest X-ray manifestations of silicosis in patients exposed to high levels of silica dust often show predominantly round or round-like shadows, initially appearing in the middle and lower lung zones and gradually extending upward. They may also first appear in the upper lung fields. For those exposed to low levels of silica dust or mixed dust, the shadows are mostly round-like or irregular. Large shadows are commonly seen in the middle and outer zones of the upper lung fields, often symmetrically distributed in a "V" shape across lobes, with increased translucency at the outer edges. Massive pulmonary fibrosis contraction may cause upward displacement of the hilar region. The density of hilar shadows increases, and sometimes "eggshell-like calcification" of lymph nodes can be observed. The pleura may show thickening, adhesions, or calcification.

In December 1986, China issued the "Diagnostic Criteria and Management Principles of Pneumoconiosis." The X-ray diagnostic staging criteria for pneumoconiosis are described as follows:

1. No pneumoconiosis (Code 0)
   (1) 0: No X-ray manifestations of pneumoconiosis.
   (2) 0+: X-ray manifestations insufficient for a diagnosis of "I."
2. Initial stage [first stage] pneumoconiosis (Code I)
   (1) I: Presence of density grade I, i.e., definite, round-like small shadows (＜1cm) numbering around 10 within a 2cm diameter range, distributed in at least two lung zones (a total of six zones in the upper, middle, and lower regions of both lungs), with each zone having at least one such shadow; or irregular small shadows of density grade I (a cluster of dense shadows varying in thickness, length, and shape), distributed in no fewer than two lung zones, with clearly visible lung markings.
   (2) I+: Significant increase in small shadows, but either the density or distribution range is insufficient for a diagnosis of "Ⅱ."
3. Intermediate stage [second stage] pneumoconiosis (Code Ⅱ)
   (1) Ⅱ: Presence of density grade 2, i.e., numerous round-like or irregular small shadows distributed over more than four lung zones, with lung markings still recognizable or partially obscured; or density grade 3, i.e., abundant round-like or irregular shadows distributed across four lung zones, with lung markings partially or completely obscured.
   (2) Ⅱ+: Small shadows of density grade 3 distributed over more than four lung zones; or presence of large shadows insufficient for a diagnosis of "Ⅲ."
4. Late stage [third stage] silicosis (Code Ⅲ)
   (1) Ⅲ: Presence of large shadows with a long diameter of at least 2cm and a short diameter of at least 1cm.
   (2) Ⅲ+: The area of a single large shadow or the combined area of multiple large shadows exceeds the area of the right upper lung zone.

bubble_chart Treatment Measures

For silicosis patients, comprehensive measures should be taken, including removal from dust-exposed work, reassignment to suitable jobs, enhanced nutrition, and proper rehabilitation exercises to strengthen the constitution. Prevention of respiratory infections and complications should also be emphasized.

Regarding drug treatment for silicosis, China has conducted extensive research over the years. Through animal experiments and clinical trials of certain drugs, certain therapeutic effects have been achieved.

(1) Poly-2-vinylpyridine-N-oxide (referred to as P204) is a high-molecular nitrogen oxide compound. Experiments have shown that it plays a protective role in the process of silica dust destroying macrophages and has the effect of preventing or delaying the progression of silicosis. Clinical trials of P204 have demonstrated delayed progression of lesions on chest X-rays, indicating certain efficacy for stage I and II silicosis, though its effect on stage III silicosis is less apparent. It shows noticeable improvement in patients' general condition and respiratory symptoms. Usage: 4% P204 aqueous solution, 8-10ml, administered once daily via aerosol inhalation. A treatment course lasts 3 months, followed by a 1-2 month interval before repeating 2-4 courses. Subsequently, two courses should be administered annually. This drug has minimal side effects when inhaled via aerosol.

(2) Other drugs include piperaquine compounds (mainly piperaquine phosphate and hydroxy piperaquine phosphate), tetrandrine, aluminum preparations (such as aluminum citrate and aluminum sorbitol), etc. After treatment, silicosis patients show varying degrees of improvement in subjective symptoms, and some may experience delayed disease progression.

bubble_chart Prognosis

Once diagnosed with silicosis, patients should immediately cease exposure to dust and receive active comprehensive treatment. Their lifespan can be extended to the average life expectancy of the general population, but their working capacity may be impaired to varying degrees. Death from silicosis often results from complications such as severe pulmonary subcutaneous nodules, spontaneous pneumothorax, and respiratory failure.

bubble_chart Prevention

The key to controlling or reducing the incidence of silicosis lies in dust prevention. Industrial and mining enterprises should implement comprehensive dust control measures, including reforming production processes, wet operations, sealing dust sources, ventilation and dust removal, and equipment maintenance and repair. Strengthen personal protection and adhere to dust control operating procedures. Regularly monitor the concentration of dust in the production environment and enhance public awareness. Conduct pre-employment physical examinations, including chest X-rays. Individuals with active pulmonary or extrapulmonary tuberculosis, as well as those with various respiratory diseases, should not engage in silica dust-related work. Strengthen regular health check-ups for silica dust workers, including chest X-rays, with the interval determined by the exposure to silica content and airborne dust concentration. Additionally, enhance the prevention and treatment of tuberculosis in industrial and mining areas. Those with negative tuberculin tests should receive BCG vaccination, while those with positive results should undergo preventive anti-tuberculosis chemotherapy to reduce the incidence of silicosis complicated by tuberculosis.

bubble_chart Complications

1. Pulmonary subcutaneous node: A common complication of silicosis, occurring in up to 20–50% of cases, with autopsy findings being more frequent (approximately 36–75%). The complication rate increases with the progression of silicosis stages. In stages I–II, the incidence of pulmonary subcutaneous nodes is 20–40%, rising to 70–95% in stage III. Pulmonary subcutaneous nodes account for 45% of direct causes of death in silicosis. When silicosis is complicated by subcutaneous nodes, the conditions mutually exacerbate, accelerating deterioration. Symptoms of subcutaneous node toxicity may appear, and subcutaneous node bacteria can be found in sputum. Subcutaneous node cavities are often large, irregularly shaped, mostly eccentric, with papillary protrusions on the inner walls, resembling rock caves. The surrounding pleural membrane thickens in areas affected by subcutaneous node lesions.
2. Chronic bronchitis and obstructive pulmonary emphysema: Long-term inhalation of dust damages the ciliated epithelium of the bronchi. Due to diffuse nodular fibrosis in both lungs, bronchial narrowing and poor drainage occur, making viral and bacterial infections more likely, leading to complications such as chronic bronchitis and pulmonary emphysema. In severe cases, this can progress to pulmonary heart disease, often triggered by respiratory infections, resulting in respiratory failure and right heart failure.
3. Spontaneous pneumothorax: In advanced-stage silicosis, spontaneous pneumothorax may occur due to the rupture of pulmonary bullae during severe coughing or excessive exertion. Because of pleural adhesions, localized pneumothorax is more common and may be masked by preexisting dyspnea symptoms, only being detected during X-ray examination. Pneumothorax may recur or alternate between both sides. Due to fibrosis of lung tissue and the pleural membrane, the ruptures are difficult to heal, and gas absorption is slow.

bubble_chart Differentiation

1. Acute miliary pulmonary tuberculosis: Stage II silicosis must be differentiated from acute miliary pulmonary tuberculosis. The latter has no history of silica dust exposure, presents with obvious systemic toxic symptoms, and chest X-rays show dense, uniformly sized miliary lesions in both lungs, more concentrated in the upper lung apices, without reticular or lung texture changes. The miliary lesions can be absorbed with anti-tuberculosis treatment.
2. Bronchioloalveolar carcinoma: Alveolar carcinoma presenting as diffuse nodular shadows in both lungs should be differentiated from stages II and III silicosis. Alveolar carcinoma on X-ray appears as nodular or infiltrative lesions, unevenly distributed, varying in size, without mass formation or large-scale fusion, rarely showing reticular shadows or pulmonary emphysema. The disease progresses rapidly, and cancer cells can be found in sputum. Patients have no history of silica dust exposure.
3. Pulmonary hemosiderosis: This condition can occur in rheumatic heart disease with mitral stenosis, seen in patients with recurrent heart failure, and has no history of silica dust exposure. Its X-ray presentation shows diffuse small nodular shadows in both lungs, similar to stage II silicosis, but the shadows are denser near the hilum and sparser in the middle and outer zones, with the heart shadow showing left atrial enlargement.
4. Pulmonary alveolar microlithiasis: A rare disease of unknown cause, often with a family history. There is no history of dust exposure. Chest X-rays show both lungs covered with fine sand-like nodular shadows, about 1mm in size, with clear edges, more common in the inner lungs, without enlargement of the hilar shadow or changes in lung texture. The disease progresses slowly, potentially over decades.