• Silica exposure increases risk for Scleroderma (see [[Scleroderma]])
    • Silicosis increases risk even further over exposure alone


  • Mining/ tunneling/ excavating: underground (gold, copper, iron, tin, uranium, civil enginerring projects)/ surface (coal, iron, excavation of foundations)
  • Quarrying: granite/ sandstone/ slate/ sand/ china stone or clay
  • Stonework: granite sheds/ monumental masonry
  • Foundries: ferrous and non-ferrous metals
  • Abrasives: production (silica flour/ metal polish and sandpapers/ filler in paint, rubbers, and plastics)/ sandblasting (oil rigs/ tombstones)
  • Ceramics: manufacture of pottery, stoneware/ reafractory bricks for ovens or kilns
  • Other: glass making/ boiler scaling/ traditional crafts/ stonegrinders/ gemstone workers/ dental technicians


  • Inhalation of silicon dioxide (silica) in crystalline form (usually as quartz but also as cristobalite or tridymite)
  • Combined silica: occurs as silicates in asbestos, talc, and mica (these cause different pulmonary responses)
  • Amorphous or non-crystalline silica (diatomite or vitreous silica) is relatively non-toxic

Pathologic Patterns

  • Acute silicosis: alveoloproteinosis (air spaces filled with PMN, epithelial cells, and proteinaceous material)/ interstitial reaction/ early loosely organized nodules
  • Chronic silicosis: classic silicotic islet or nodule (usually involving hilar nodes first, then upper lobes, to which it may be limited)
  • Accelerated silicosis: numerous nodules at various stages of development (sometimes with irregular interstitial fibrosis)


-Acute silicosis:
-Chronic silicosis: usually obstruction or combined obstruction-restriction (decreased flow rates/ decreased VC, TLC, RV/ usually normal FRC/ variable DLCO)
-Accelerated silicosis:

-BAL: silica detected suggests diagnosis/
-TBB: silica dust detected

OLB: may be necessary in some cases

CXR/Chest CT patterns:
1) Acute silicosis: alveolar (or interstitial) infiltrates
2) Chronic silicosis: small, rounded opacities (SRO)
-“Eggshell” calcifications of mediastinal/ hilar lymph nodes: strongly suggestive of silicosis
-Pleural plaques: occur but are not common in silicosis
3) Accelerated silicosis: irregular upper zone fibrosis with nodular component

Hypergammaglobulinemia: may be seen

Serum autoantibodies: may be seen

ACE level: may be elevated


Clinical Patterns:
1) Acute Silicosis:
-Exposure: usually intense exposure to fine dust (usually with high quartz content) for months
-Absence of clubbing
-Course: rapid progression to ALI/ARDS
-Complications: fulminating TB (common)

2) Chronic Silicosis:
-Exposure: occurs after >20 years of exposure to respirable dust (usually with <30% quartz)
-Impaired pulmonary function may occur (not always)/ absence of clubbing
-Course: not necessarily associated with increased morbidity or mortality
-Complications: progressive massive fibrosis (PMF)/ TB (especially in high-prevalence areas)

3) Accelerated Silicosis:
-Exposure: usually occurs after 5-15 year of heavy exposure (usually higher quartz content fiber dust)
-Symptomatic with pulmonary impairment / absence of clubbing
-Course: progression to respiratory failure and death
-Complications: PMF with cavitation (this usually indicates infection by atypical TB)


  • Treatment of Acute silicosis: lung lavage for alveolar proteinosis may not be effective (despite removal of large amounts of silica dust)
  • Treatment of TB: when present


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