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Silicosis

Chronic silicosis develops slowly, with symptoms often appearing years after initial exposure. These symptoms include:

  • Dyspnea (shortness of breath), especially on exertion
  • Persistent cough
  • Fatigue
  • Rapid and laboured breathing (tachypnea)
  • Appetite and weight loss
  • Chest pain
  • Fever
  • Cyanosis and darkening of the skin
  • Nail changes, including dark shallow rifts and cracks
Miner's lung with silicosis and tuberculosis
Miner's lung with silicosis and tuberculosis (Basque Museum of the History of Medicine and Science, Spain)

Advanced cases might present cyanosis, cor pulmonale (right ventricular heart disease), and respiratory insufficiency. Patients are particularly susceptible to tuberculosis, chronic bronchitis, airflow limitation, and other pulmonary complications.

Silica dust particles, when inhaled, embed deep into the alveolar sacs of the lungs. Macrophages ingest these particles, triggering an inflammatory response that leads to fibrosis and the formation of nodular lesions. The inflammatory effects are mediated by the NLRP3 inflammasome, resulting in specific fibrotic nodules with concentric collagen fibres.

Diagnosis of silicosis involves three key elements: a history of silica dust exposure, chest imaging consistent with silicosis, and exclusion of other conditions. Chest x-rays are very important, revealing small nodules in the upper lung zones. Advanced cases show large opacities and possibly calcified nodules. CT scans offer detailed lung analysis, showing cavitation due to infections.

Chest X-ray showing uncomplicated silicosis
Chest X-ray showing uncomplicated silicosis
Complicated silicosis
Complicated silicosis

Silicosis is classified into:

  • Chronic simple silicosis: Appears 10-30 years post-exposure to low dust concentrations.
  • Accelerated silicosis: Develops 5-10 years after high dust exposure.
  • Complicated silicosis: Features severe scarring and lung disease.
  • Acute silicosis: Rapid onset post high-concentration exposure, leading to severe symptoms and often death.

Preventing silicosis involves avoiding dust exposure and controlling dust generation. Methods include using water-integrated tools, industrial vacuums, and personal protective equipment (PPE). Regulations mandate dust control measures, including local exhaust ventilation in industries like ceramics.

Workers in a cloud of concrete dust containing respirable crystalline silica
Workers in a cloud of concrete dust containing respirable crystalline silica with no controls in place

Silicosis is incurable, with treatment focusing on symptom relief and disease progression prevention:

  • Whole lung lavage: Flushing lungs with saline to remove dust.
  • Avoidance: Stopping further exposure to silica dust and other lung irritants.
  • Medications: Cough suppressants, antibiotics, and bronchodilators.
  • Therapies: Chest physiotherapy and oxygen administration.
  • Surgery: Lung transplantation in severe cases.

Silicosis remains the most common occupational lung disease globally, with significant prevalence in developing countries. While incidences in developed nations like the US have declined, occupational exposure still poses a significant risk, particularly in industries involving mining, sandblasting, and manufacturing.

Fibrothorax and pleural effusion caused by silicosis
Fibrothorax and pleural effusion caused by silicosis

In 2016, OSHA mandated safety measures to prevent silicosis, including reducing the permissible exposure limit (PEL) for respirable crystalline silica and emphasising engineering controls over PPE. Employers must limit worker access to high exposure areas, develop exposure control plans, and provide medical exams and training.

Silicosis ILO Classification 2-2 R-R
Silicosis ILO Classification 2-2 R-R

Self-assessment MCQs (single best answer)

What triggers the development of silicosis?



Which of the following is NOT a common symptom of chronic silicosis?



What is the main diagnostic tool used to identify silicosis?



Silicosis is classified into several types. Which type develops 10-30 years post-exposure to low dust concentrations?



Which of the following is an effective prevention measure for silicosis?



Which complication is NOT typically associated with advanced silicosis?



What is the role of macrophages in the pathophysiology of silicosis?



Which treatment option for silicosis involves flushing the lungs with saline?



In the United States, what organisation mandated safety measures to prevent silicosis in 2016?



What is a key characteristic of accelerated silicosis?



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