silicosis

—silicotic /sil'i kot"ik/, adj.

/sil'i koh"sis/, n. Pathol.

a disease of the lungs caused by the inhaling of siliceous particles, as by stonecutters.

[1890-95; SILIC(A) + -OSIS]

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Common pneumoconiosis caused by long-term inhalation of silica mineral dust.

Known since the 18th century, it usually occurs after 10–20 years of exposure in jobs such as mining, stonecutting, grinding, or polishing. The smallest particles do the most damage, killing macrophages (see reticuloendothelial system) that engulf them in the pulmonary alveoli. Dead cells accumulate, forming fibrous masses that reduce lung elasticity. Decreased lung volume and poor gas exchange lead to shortness of breath and then to coughing, difficulty in breathing, and weakness. Patients are vulnerable to tuberculosis, emphysema, and pneumonia. In the absence of effective treatment, control of silicosis depends on prevention with face masks, proper ventilation, and X-ray monitoring of workers' lungs.

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▪ disease

      a chronic disease of the lungs that is caused by the inhalation of silica dust over long periods of time. (Silica is the chief mineral constituent of sand and of many kinds of rock.) Silicosis is a form of pneumoconiosis. The disease occurs most commonly in miners, quarry workers, stonecutters, tunnelers, and workers whose jobs involve grinding, sandblasting, polishing, and buffing. Silicosis is one of the oldest industrial diseases, having been recognized in knife grinders and potters in the 18th century, and it remains one of the most common dust-induced respiratory diseases in the developed world.

      In most instances, 10 to 20 years of occupational exposure to silica dust are needed for silicosis to develop. The disease rarely occurs with exposures to concentrations of less than 6,000,000 particles of silica per cubic foot (about 210,000 per litre) of air. Only very small silica particles less than 10 microns (0.0004 inch) in diameter penetrate to the finer air passages of the lungs, and particles of one to three microns do the most damage.

      The symptoms of silicosis are shortness of breath that is followed by coughing, difficulty in breathing, and weakness. These symptoms are all related to a fibrosis that reduces the elasticity of the lung. In the actual disease process, the tiny particles of inhaled silica are taken up in the lungs by scavenger cells, called macrophages, that serve to protect the body from bacterial invasion. Silica particles, however, cannot be digested by the macrophages and instead kill them. The killed cells accumulate and form nodules of fibrous tissue that gradually enlarge to form fibrotic masses. These whorls of fibrous tissue may spread to involve the area around the heart, the openings to the lungs, and the abdominal lymph nodes. Lung volume is reduced, and gas exchange is poor. Silicosis predisposes a person to tuberculosis, emphysema, and pneumonia. In the past a large proportion of sufferers of silicosis died of tuberculosis, though this has changed with the availability of drug therapies for that disease.

      There is no cure for silicosis, and, since there is no effective treatment, control of the disease lies mainly in prevention. The use of protective face masks and proper ventilation in the workplace and periodic X-ray monitoring of workers' lungs has helped lessen the incidence of the disease.

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