Epidemiology
- Silica exposure increases risk for Scleroderma (see [[Scleroderma]])
- Silicosis increases risk even further over exposure alone
Etiology
- 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
Physiology
- 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)
Diagnosis
PFT’s:
-Acute silicosis:
-Chronic silicosis: usually obstruction or combined obstruction-restriction (decreased flow rates/ decreased VC, TLC, RV/ usually normal FRC/ variable DLCO)
-Accelerated silicosis:
FOB:
-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
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
- 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
References
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