Silicosis

Silicosis is irreversible fibronodular lung disease caused by inhalation of dust containing crystalline silica (alpha-quartz or silicon dioxide) during occupational exposure.

Currently, >1,000,000 workers are exposed, with 200–300 deaths/y; protection devices decrease incidence.

Mostly >65 y of age

Incidence higher in males than females.

No racial predilection.

Hypoxemia, CO ₂ retention with chronic respiratory acidosis, bronchospasm, pneumothorax, atelectasis, mycobacterium (30-fold increased risk for TB) and fungal infection, bacterial pneumonia, chronic bronchitis exacerbation

Periop respiratory failure, especially following thoracic and upper-abdominal surgery

Pulm Htn; cor pulmonale

Renal insufficiency (tubular nephropathy)

Steroid-induced diabetes (in cases of chronic steroid treatment)

In cases of associated scleroderma and/or rheumatoid arthritis, possible difficult intubation

Bronchospasm and chronic bronchitis exacerbation

Respiratory failure

Cor pulmonale

Silicosis-pulmonary fibrosis commonly occurs after 4–5 (acute, very rare), 5–10 (accelerated), or >10 y (chronic) of occupational exposure.

In advanced stage, both obstructive (graduate loss of FEV ₁ , FVC and decrease of FEV ₁ /FVC ratio) and restrictive ventilatory defects, as well as decreases in diffusing capacity, are common; exertional dyspnea is the predominant symptom.

CO ₂ retention, pulm Htn, or cor pulmonale late in the course.

Associated TB, lung cancer, connective tissue diseases (scleroderma, rheumatoid arthritis, Sjögren’s syndrome), nephritic syndrome, and renal failure.

Prolonged occupational exposure may occur from mining, stone cutting, sandblasting, abrasive industries, granite quarrying, packing silica flour; this causes dose- and time-related development of pulmonary fibrosis.

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

Initial lesions are silicotic nodule mostly located near the respiratory bronchiole. The nodule is composed of refractile particles of silica surrounded by whorled collagen in concentric layers, with macrophages, lymphocytes, and fibroblasts in the periphery. Emphysematous blebs surround the silicotic nodule, especially in the subpleural area. Bleb and bulla formation, and airways and vascular bed distortion by these nodules complicate advanced disease.