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PH-RS22

Pneumoconioses

How inhaled mineral dust is cleared, why carbon is stored harmlessly while silica and asbestos kill macrophages and drive fibrosis, how coal, silica and asbestos scar the lung in different patterns, and why beryllium causes granulomas instead.

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  • 5 steps · 10 questions
  • 3D anatomy, affected parts marked

By the end, you can

  • Explain how particle size decides where dust settles and how the lung normally clears it.
  • Explain why inert dusts are stored harmlessly while fibrogenic dusts start a self-perpetuating cycle of macrophage injury and fibrosis.
  • Compare coal workers’ pneumoconiosis, silicosis and asbestosis in their lesions, distribution and complications, including progressive massive fibrosis, tuberculosis and cancer.
  • Explain why chronic beryllium disease is a granulomatous hypersensitivity rather than a dose-dependent dust disease.
  • Recognise the classic appearances and tests of the pneumoconioses, and explain how exposure control and each main treatment act on the mechanism.

What it is

A pneumoconiosis is a lung disease caused by inhaled mineral dust retained in the lung, usually after years of work exposure. Most are fibrosing diseases driven by injured macrophages (coal workers’ pneumoconiosis, silicosis, asbestosis); chronic beryllium disease is a granulomatous hypersensitivity to a metal. Some dusts, such as carbon or iron, are stored with little reaction.

4 types to tell apart
Inert dust deposits
Carbon (anthracosis), iron oxide in welders (siderosis) or tin: stored in macrophages and nodes with little fibrosis or loss of function.
Nodular fibrosing pneumoconioses
Coal mine dust and crystalline silica: nodules mostly in the upper zones that can merge into progressive massive fibrosis.
Fibre-related disease
Asbestos: diffuse interstitial fibrosis of the lower lobes (asbestosis), with pleural disease and cancers from the same exposure.
Hypersensitivity pneumoconiosis
Chronic beryllium disease: T-cell-mediated granulomas in sensitised people, even after small exposures.

US spelling: litres → liters.

Normal function

Where inhaled particles land and how they are cleared

Every day we inhale thousands of litres of air carrying particles, and their size decides where they land. Large particles, over about 10 micrometres, strike the nose and throat. Smaller ones settle on the bronchi, where mucus traps them and cilia sweep them up and out (the mucociliary escalator). Only respirable particles, roughly 1–5 micrometres, travel past the to the and , where airflow slows almost to a stop and they settle; many smaller particles are breathed out again.

Beyond the terminal bronchioles there are no cilia. Here alveolar macrophages engulf the particles. Most dust-laden macrophages then move up to the ciliated airways and are coughed or swallowed; some enter the lymphatics, which carry them to the lymph nodes at the hilum. Clearing the alveoli takes weeks to months, far slower than clearing the airways.

This system copes with the dust of daily life. A pneumoconiosis develops when years of heavy exposure overwhelm clearance, or when the dust injures the very macrophages meant to remove it.

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