Silicosis and Coal Worker’s Pneumoconiosis (CWP)

Key Facts
  • Miners inhaling quartz (silica) or coal dust
  • Radiography of silicosis and CWP are similar:
    • Simple: micronodules < 1 cm, upper lungs, hilar/mediastinal lymphadenopathy, egg shell calcifications
    • Complicated known as progessive massive fibrosis (PMF): aggregation of nodules into large masses, may cavitate
    • As PMF worsens profusion of nodules decreases
    • Acute silicoproteinosis: resembles alveolar proteinosis, progresses to fibrosis
    • Caplans syndrome: CWP + rheumatoid arthritis + necrobiotic nodules
  • Silicosis: round lamellated collagen surrounding silica particles
  • CWP: coal macule composed of black pigmented macrophages in respiratory brnochioles
  • Increased risk for TB
  • Requires 20 or more years of high dust exposure, silicosis will progress, even after removal from dust in contrast to CWP
  • Increased mortality with PMF
Imaging Findings

Chest radiography

  • Findings seen 10 to 20 years after exposure
  • Silicosis and CWP similar, usually less severe in CWP
  • Simple silicosis
    • 1 – 3 mm nodules, posterior segments, upper lobes
    • Nodules may calcify
    • Reticular opacities
    • Nodules increase in size and number and may eventually involve all lobes
    • Hilar and mediastinal lymphadenopathy, egg shell calcification
  • Complicated silicosis (PMF)
    • Nodules coalesce and are > 1 cm
    • Usually bilateral, right > left
    • Usually located in dorsal aspect of lung
    • PMF may be lens shaped (wide PA and narrow lateral view)
    • Overall profusion of nodules decreases due to aggregation into PMF
    • May have foci of amorphous calcification, or calcified rim
    • Migrates centrally with time
    • May cavitate
    • Lung distal to PMF emphysematous
      • Risk for spontaneous pneumothorax
  • Acute silicoproteinosis
    • Butterfly edema pattern
    • Air bronchograms
    • Hilar/mediastinal lymphadenopathy
    • Progresses rapidly over months
    • Fibrosis, distortion, bullae, pneumothorax
  • Caplan’s syndrome
    • Multiple large nodules (may cavitate)
    • Nodular interstitial thickening (CWP)
    • Bone changes of rheumatoid arthritis
      • Humeral or clavicular erosions

CT/HRCT

  • HRCT – best imaging modality
  • Can detect disease with normal radiograph
  • Micronodules
    • Upper lobe and posterior segment predominance
    • Location in center and periphery of lobule
    • < 7 mm diameter
    • May calcify
  • Aggregation of nodules into PMF more readily detected
  • PMF
    • Lens shaped
    • Nodules > 7 mm
    • May cavitate,
    • Migrate to hila with time
    • May have punctate calcification
    • Lung distal to PMF emphysematous
  • Hilar/mediastinal lymphadenopathy, egg shell calcification,
Differential Diagnosis
  • Sarcoidosis
  • TB
  • Fungal infection
  • Langerhans cell histiocytosis
  • Hypersensitivity pneumonitis
  • Differentiation
    • History of occupational exposure
    • Egg shell calcification only seen with sarcoid
    • Langerhans cell histiocytosis or Farmers lung do not lead to PMF
Pathological Features
  • General
    • Upper lobe predominance
    • Increased risk of tuberculosis
    • Silica more fibrogenic
    • Progressive massive fibrosis - nodules aggregate, form small and large masses of fibrosis, sometimes with cavitation
  • Silicosis
    • Inhalation of silica dust, silicon dioxide (SiO2)
    • Silica particles within concentric lamellae of collagen in bronchioles, small vessels, and lymphatics
    • Birefringent silicate crystals (1 – 3 µ) in nodules by polarized microscopy
    • Silica laden macrophages carry particles to hilar and mediastinal nodes and form granulomas
    • May co-exist with TB
    • Silicoproteinosis high concentrations of silica, alveolar filling by lipoproteinaceous material, similar to alveolar proteinosis
  • Coal workers pneumonconiosis
    • Macule: stellate shaped collection of macrophages containing black particles, (1 – 5µ) in terminal and respiratory bronchioles and in pleural lymphatics
    • No or little fibrosis
Clinical Presentation
  • More common in men with occupational history of exposure
  • Silicosis progressive, even after removal from dust
  • CWP will not prgoress is removed from dust
  • Sandblasting, work in quarries, mining, glassblowing, pottery making
  • Silica often found in coal mines (silica most common element earth’s crust)
  • Acute silicoproteinosis
    • Massive exposure to silica dust
    • Usually seen in sandblasters
    • Marked cellular and exudative alveolar reaction
  • Chronic form requires 20 or more years of high dust exposure
  • Caplan’s Syndrome
    • CWP, rheumatoid arthritis, necrobiotic lung nodules
  • Symptoms
    • None with simple silicosis.
    • Miners commonly smoke and have symptoms related to bronchitis or emphysema
    • Cough, dyspnea, increased sputum in complicated disease
    • Black sputum in coal workers
  • Pulmonary hypertension, cor pulmonale
  • PFTs – decreased diffusion capacity, obstructive, then restrictive defect
  • Diagnosis by history of exposure, radiography/HRCT and/or lung biopsy
  • Slight increased risk of lung cancer, scleroderma
  • Prognosis
    • Simple, normal longevity
    • Complicated PMF, death from respiratory failure, pneumothorax, carcinoma, TB
    • Silicosisproteinosis: death within 2 to 3 years
References

Pendergrass EP. Some considerations concerning the roentgen diagnosis of pneujoconiosis and silicosis AJR 48:571-594, 1942
Remy-Jardin M, Degreef JM, Beuscart R, et al. Coal worker's pneumoconiosis: CT assessment in exposed workers and correlation with radiographic findings Radiology 177:363-371, 1990
Bergin CJ, Muller NL, Vedal S, et al. CT in silicosis: correlation with plain films and pulmonary function tests AJR 146:477-483, 1986