Acute Silicosis (Silicoproteinosis)

Acute silicosis (silicoproteinosis) is a rapidly progressive variant of silicosis that develops within weeks to a few years (typically < 5 years) following intense exposure to high concentrations of fine respirable crystalline silica particles (< 5 µm). High-risk occupations include sandblasting (especially Turkish denim jeans sandblasting epidemic 2005–2010), engineered (artificial) stone bench-top fabrication, tunnel boring, abrasive cleaning and silica flour production.

Pathologically, alveolar macrophages overwhelmed by silica release surfactant components and proteinaceous material into the alveoli, producing a pattern indistinguishable from primary pulmonary alveolar proteinosis (PAP). Histology shows PAS-positive eosinophilic intra-alveolar material with refractile silica crystals on polarized microscopy. Concurrent inflammation, type II pneumocyte hyperplasia, and rapid fibrosis distinguish it from chronic silicosis.

Clinically presents with progressive dyspnea, dry cough, weight loss and hypoxemia developing over months. HRCT shows bilateral mid-lower zone ground-glass opacities, crazy-paving pattern, consolidation, and absence of the characteristic upper-lobe rounded nodules of chronic silicosis. Diagnosis combines exposure history, imaging, and BAL (milky lavage with PAS-positive material). Mortality is 50–80% within 1–2 years; current therapies include whole-lung lavage, systemic corticosteroids, GM-CSF therapy, and ultimately lung transplantation.