Silicosis

Silicosis, the oldest known occupational pulmonary disease, is caused by inhalation of tiny particles of silicon dioxide in the form of unbound (free) crystalline silica (usually quartz) or, less commonly, by inhalation of silicates, minerals containing silicon dioxide bound to other elements, such as talc. Workers at greatest risk are those who move or blast rock and sand (miners, quarry workers, stonecutters) or who use silica-containing rock or sand abrasives (sand blasters; glass makers; foundry, gemstone, and ceramic workers; potters). Coal miners are at risk of mixed silicosis and coal workers’ pneumoconiosis Coal Workers’ Pneumoconiosis Coal workers’ pneumoconiosis is caused by inhalation of coal dust. Deposition of dust produces dust-laden macrophages around bronchioles (coal macules), occasionally causing focal bronchiolar... read more .

Factors that influence the likelihood of development of silicosis include

Alveolar macrophages engulf inhaled free silica particles and enter lymphatics and interstitial tissue. The macrophages cause release of cytokines (tumor necrosis factor-alpha, interleukin-1), growth factors (tumor growth factor-beta), and oxidants, stimulating parenchymal inflammation, collagen synthesis, and, ultimately, fibrosis.

When the macrophages die, they release the silica into interstitial tissue around the small bronchioles, causing formation of the pathognomonic silicotic nodule. These nodules initially contain macrophages, lymphocytes, mast cells, fibroblasts with disorganized patches of collagen, and scattered birefringent particles that are best seen with polarized light microscopy. As they mature, the centers of the nodules become dense balls of fibrotic scar with a classic onion-skin appearance and are surrounded by an outer layer of inflammatory cells.

In low-intensity or short-term exposures, these nodules remain discrete and do not compromise lung function (simple chronic silicosis). But with higher-intensity or more prolonged exposures (complicated chronic silicosis), these nodules coalesce and cause progressive fibrosis and reduction of lung volumes (total lung capacity, vital capacity) on pulmonary function tests, or they coalesce, sometimes forming large conglomerate masses (called progressive massive fibrosis).

Chronic silicosis is the most common form of the disorder and generally develops only after exposure over decades.

Acute silicosis, also known as acute silicoproteinosis, and the rarer accelerated silicosis are caused by intense silica dust exposure over short periods (several months or years). Mononuclear cells infiltrate alveolar septa, and alveolar spaces fill with a proteinaceous material that stains periodic acid-Schiff (PAS) positive and is similar to that found in pulmonary alveolar proteinosis Pulmonary Alveolar Proteinosis Pulmonary alveolar proteinosis is accumulation of surfactant in alveoli. Etiology is almost always unknown. Symptoms are dyspnea, fatigue, and malaise. Diagnosis is based on bronchoalveolar... read more . The occupational history of acute exposure is needed to distinguish silicoproteinosis from pulmonary alveolar proteinosis.

Conglomerate silicosis (also known as progressive massive fibrosis or complicated silicosis) is the advanced form of chronic or accelerated silicosis and is characterized by widespread masses of fibrosis, typically in the upper lung zones.

Chronic silicosis is often asymptomatic, but many patients eventually develop dyspnea during exertion that progresses to dyspnea at rest. Productive cough, when present, may be due to silicosis, coexisting chronic occupational (industrial) bronchitis, or smoking. Breath sounds diminish as the disorder progresses, and pulmonary consolidation, pulmonary hypertension Pulmonary Hypertension Pulmonary hypertension is increased pressure in the pulmonary circulation. It has many secondary causes; some cases are idiopathic. In pulmonary hypertension, pulmonary vessels may become constricted... read more , and respiratory failure Overview of Respiratory Failure Acute respiratory failure is a life-threatening impairment of oxygenation, carbon dioxide elimination, or both. Respiratory failure may occur because of impaired gas exchange, decreased ventilation... read more with or without right ventricular failure Cor Pulmonale Cor pulmonale is right ventricular (RV) enlargement secondary to a lung disorder that causes pulmonary artery hypertension. Right ventricular failure follows. Findings include peripheral edema... read more may develop in advanced disease.

Patients with accelerated silicosis experience the same symptoms as those with chronic silicosis, but symptoms develop over a shorter period.

Acute silicosis patients experience rapid progression of dyspnea, weight loss, and fatigue with diffuse bilateral crackles. Respiratory failure often develops within 2 years.

Conglomerate silicosis causes severe, chronic respiratory symptoms.

Silicosis initially causes no symptoms or only mild dyspnea. Over years, the development of increasing symptoms of dyspnea, hypoxemia, pulmonary hypertension, and respiratory impairment in a patient whose works puts them at risk, suggests the diagnosis of silicosis.

Patients with airway obstruction due to any form of silicosis may be treated empirically with bronchodilators and inhaled corticosteroids. Patients should be monitored and treated for hypoxemia to forestall pulmonary hypertension. Pulmonary rehabilitation Pulmonary Rehabilitation Pulmonary rehabilitation is the use of supervised exercise, education, support, and behavioral intervention to improve functional capacity and enhance quality of life in patients with chronic... read more may help patients carry out activities of daily living. Workers who develop silicosis should be removed from further exposure. Lung transplantation Lung and Heart-Lung Transplantation Lung or heart-lung transplantation is an option for patients who have respiratory insufficiency or failure and who remain at risk of death despite optimal medical treatment. (See also Overview... read more is a last resort. A number of experimental treatments have been proposed, but none have demonstrated effectiveness at altering the course of the disease.

Management of TB is the same as for other patients with TB except that longer courses are usually recommended because relapse is more common in patients with silicotuberculosis.

The most effective preventive interventions for silicosis occur at an industrial rather than clinical level and include dust suppression, process isolation, ventilation, and use of non–silica-containing abrasives. Respiratory masks provide imperfect protection and, although helpful, are not an adequate solution. Surveillance of exposed workers with respiratory questionnaires, spirometry, and chest x-rays is recommended. Frequency of surveillance depends to some degree on the expected intensity of the exposure. Other preventive measures include smoking cessation and pneumococcal and influenza vaccination.

Physicians must be alert to the risk of TB and nontuberculous mycobacterial infections in silica-exposed patients, especially miners. People exposed to silica should have annual tuberculin testing. Those with a positive skin test should have sputum culture for TB. In some cases, CT and bronchoscopy may be needed to confirm TB. Patients with a positive tuberculin test and negative TB cultures should be given isoniazid chemoprophylaxis in keeping with standard guidelines for tuberculin reactors.