Introduction
This topic covers pneumoconiosis, the group of chronic lung diseases caused by inhaling mineral dusts, and in particular silicosis, the most important of them. Students should be able to classify the pneumoconioses, explain how dust causes lung injury, and describe the clinical picture, diagnosis, differential diagnosis, treatment and expertise assessment of silicosis.
Definition and classification
Pneumoconiosis is a diffuse interstitial and/or nodular lung disease caused by long-term inhalation of mineral dust and by the tissue reaction to its retention in the lung. Dusts are classified pathologically as fibrogenic (collagenous) or non-fibrogenic (non-collagenous), and etiologically by the mineral involved.
Etiology and pathogenesis
Disease depends on the dose and the properties of the dust. Only respirable particles of about 0.5 to 5 µm reach the alveoli. Their size, shape, surface chemistry and solubility determine how much harm they do. Crystalline silica is strongly fibrogenic because its sharp, reactive surface is toxic to cells.
- Inhalation and deposition: particles settle in the alveoli and are taken up by alveolar macrophages.
- Macrophage activation: the particle damages the phagolysosome and the cell dies, releasing the particle and more free radicals.
- Inflammation: activated macrophages release cytokines such as interleukin-1 and TNF-alpha, and chemotactic signals that attract further inflammatory cells.
- Fibroblast stimulation: growth factors such as TGF-beta drive fibroblast proliferation and collagen deposition.
- Result: the lesion is a hyalinised collagen nodule, and in advanced disease the nodules coalesce into fibrosis that impairs gas exchange.