Silicosis

Silicosis is a chronic fibrotic occupational lung disease caused by inhalation of crystalline silica dust leading to inflammation, nodular pulmonary fibrosis, and progressive lung damage.

It is the most common pneumoconiosis worldwide and remains highly prevalent in mining, stone cutting, sandblasting, quarrying, construction, ceramics, and artificial stone industries.

Silica exposure can also produce:

  • Chronic obstructive lung disease
  • Tuberculosis predisposition
  • Lung cancer
  • Autoimmune diseases
  • Chronic kidney disease

Types of Silicosis

Type of Silicosis

Exposure / Pathogenesis

Clinical Features / Prognosis

Chronic (Classic) Silicosis

Most common form.


Occurs after low to moderate silica exposure usually over >10–20 years.


Pathology includes:

• Upper lobe nodules

• Pulmonary fibrosis

• Eggshell hilar lymph node calcification

Slowly progressive disease.


Symptoms include:

• Chronic cough

• Dyspnea

• Fatigue

Accelerated Silicosis

Occurs due to higher-intensity silica exposure.


Develops within 5–10 years of exposure.

Features include:

• Faster disease progression

• Earlier development of fibrosis

• Higher risk of tuberculosis (TB)

Acute Silicosis (Silicoproteinosis)

Caused by massive silica exposure over months to a few years.


Seen commonly in:

• Sandblasters

• Artificial stone workers


Pathogenesis:

• Proteinaceous material fills alveoli resembling pulmonary alveolar proteinosis

Rapidly progressive illness.


Symptoms include:

• Severe dyspnea

• Weight loss

• Hypoxemia

• Respiratory failure


Prognosis:

• Poor

• Often fatal

Gross pathology

  • Upper lobe predominance
  • Firm fibrotic nodules
  • Hilar lymph node calcification

Progressive Massive Fibrosis (PMF)

Coalescence of silicotic nodules into large fibrotic masses.

Usually:1 cm lesions,Upper lobes

Consequences

  • Severe restriction
  • Pulmonary hypertension
  • Respiratory failure
  • Cor pulmonale

Clinical Features

Early disease

May be asymptomatic.

Progressive disease

  • Exertional dyspnea/Chronic cough/Sputum/Wheeze/Chest tightness/Fatigue

Advanced disease

  • Severe hypoxemia/Cyanosis/Weight loss/Respiratory failure

Physical Examination

May be normal early.

Findings

  • Crackles
  • Reduced breath sounds
  • Clubbing (late)
  • Signs of pulmonary hypertension
  • Cor pulmonale

Silicotuberculosis

Silica impairs macrophage function causing major susceptibility to tuberculosis.

Silica:

  • Inhibits macrophage killing
  • Reduces cellular immunity

Clues

  • Fever
  • Weight loss
  • Cavitary lesions
  • Upper lobe infiltrates

Other Complications

Pulmonary complications

  • COPD
  • Emphysema
  • Bronchiectasis
  • Spontaneous pneumothorax
  • Respiratory failure
  • Pulmonary hypertension

Malignancy

Crystalline silica is carcinogenic.

Associated with:

  • Lung cancer

Autoimmune diseases

Silica exposure associated with:

  • Rheumatoid arthritis
  • Systemic sclerosis
  • SLE
  • ANCA vasculitis

Caplan syndrome

Combination of:

  • Pneumoconiosis
  • Rheumatoid arthritis

Renal disease

Associated with:

  • CKD
  • Glomerulonephritis

Diagnosis

1. Occupational History

2. Imaging-Chest X-ray

Typical findings

  • Small rounded opacities
  • Upper zone predominance
  • Bilateral nodules

ILO classification used for grading.

Eggshell calcification

Thin peripheral hilar node calcification.Characteristic but not exclusive.


HRCT Thorax

More sensitive than X-ray.

Findings

  • Centrilobular nodules
  • Perilymphatic nodules
  • Upper lobe fibrosis
  • Conglomerate masses
  • Mediastinal node calcification
  • PMF

Pulmonary Function Tests

Early-May be normal.

Later

  • Restrictive pattern common
  • Reduced DLCO
  • Mixed obstructive/restrictive possible

Bronchoscopy/BAL

Usually not diagnostic.

May help:

  • Rule out TB
  • Exclude malignancy

Histopathology

Rarely needed if:

  • Exposure history clear
  • Imaging typical

Differential Diagnosis

  • Tuberculosis
  • Sarcoidosis
  • Coal workers’ pneumoconiosis
  • Chronic berylliosis
  • Hypersensitivity pneumonitis
  • Metastatic nodules
  • Fungal infections

Acute Silicosis Differential

  • Pulmonary alveolar proteinosis
  • ARDS
  • PCP pneumonia

Management

Fundamental principle

No cure exists.

Management focuses on:

  • Preventing progression
  • Symptom control
  • Complication management

1. Remove Exposure

Most important intervention.


2. Smoking Cessation

Reduces:COPD progression/Lung cancer risk


3. Vaccination

  • Influenza vaccine/Pneumococcal vaccine/COVID vaccination


4. Bronchodilators

Useful if:Obstructive airway disease/COPD overlap


5. Oxygen Therapy

For chronic hypoxemia.


6. Pulmonary Rehabilitation

Improves:Exercise tolerance/Quality of life


7. Tuberculosis Screening

Very important.

Recommended evaluation

  • TB symptom screening
  • Chest imaging
  • Sputum testing when indicated

Latent TB treatment may be indicated according to guidelines.


8. Management of Acute Silicosis

Supportive care:

  • Oxygen
  • Ventilatory support

Some patients:

  • Whole lung lavage
  • Corticosteroids (limited evidence)

9. Lung Transplantation

For:

  • End-stage disease
  • Severe respiratory failure

Antifibrotic Therapy

Research ongoing for:

  • Pirfenidone
  • Nintedanib

No established guideline-approved routine role yet.

  • Nintedanib is a tyrosine kinase inhibitor with antifibrotic activity.
  • It inhibits PDGFR, FGFR, and VEGFR.
  • Main approved use: idiopathic pulmonary fibrosis.
  • Major adverse effect: diarrhea.( therefore Take with food)
  • Important toxicity: hepatotoxicity.
  • It slows FVC decline but does not reverse fibrosis.
  • INPULSIS, SENSCIS, and INBUILD are landmark trials.
  • Antifibrotic therapies are being explored in occupational fibrotic lung diseases including silicosis.
  • Contraindicated in Pregnancy

Prevention

Personal protective equipment

  • N95 respirators
  • Air-purifying respirators

Monitoring

  • Air silica monitoring
  • Periodic health surveillance