Silicosis
The most common form of pneumoconiosis, silicosis is a progressive disease characterized by nodular lesions, which frequently progress to fibrosis. It’s classified according to the severity of the pulmonary disease and the rapidity of its onset and progression, although it usually occurs as a simple illness without symptoms.
Those who work around silica dust, such as foundry workers, boiler scalers, and stonecutters, have the highest incidence of the disease. Silica in its pure form occurs in the manufacture of ceramics (flint) and building materials (sandstone). It occurs in mixed form in the production of construction materials (cement). It’s also found in powder form (silica flour) in paints, porcelain, scouring soaps, and wood fillers, and in the mining of gold, lead, zinc, and iron.
Sand blasters, tunnel workers, and others exposed to high concentrations of respirable silica may develop acute silicosis after 1 to 3 years. Those exposed to lower concentrations of free silica can develop accelerated silicosis, usually after about 10 years of exposure.
The prognosis is good unless the disease progresses to the complicated fibrotic form.
Causes
Silicosis results from the inhalation and pulmonary deposition of respirable crystalline silica dust, mostly from quartz. The risk depends on the concentration of dust in the atmosphere, the percentage of respirable free silica particles in the dust, and the duration of exposure. Although particles up to 10 microns in diameter can be inhaled, the disease-causing particles deposited in the alveolar space usually have a diameter of only 1 to 3 microns.
Nodules result when alveolar macrophages ingest silica particles, which they can’t process. As a result, the macrophages die and release proteolytic enzymes into surrounding tissue. The enzymes inflame the tissue, attracting other macrophages and fibroblasts. These produce fibrous tissue to wall off the reaction, resulting in a nodule that has an onionskin appearance.
These nodules develop adjacent to the terminal and respiratory bronchioles. Although frequently accompanied by bullous changes in both lobes, nodules concentrate in upper lung lobes. If the disease doesn’t progress, the patient may experience only minimal physiologic disturbances with no disability. Occasionally, however, the fibrotic response accelerates, engulfing and destroying a large lung area.
Complications
Assessment
The patient has a history of long-term industrial exposure to silica dust. He may complain of dyspnea on exertion, which he’s likely to attribute to “being out of shape” or “slowing down.” If the disease has progressed to the chronic and complicated state, the patient may report a dry cough, especially in the morning.
When you inspect the patient, you may note decreased chest expansion and tachypnea. If he has advanced disease, he may also act lethargic and look confused. You may percuss areas of increased and decreased resonance. On auscultation, you may hear fine to medium crackles, diminished breath sounds, and an intensified ventricular gallop on inspiration—a hallmark of cor pulmonale.
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