Coal dust (Anthracosis)
Progressive massive fibrosis( PMF)
Caplan syndrome( with RA)
Silicosis, eg sandblasting
Asbestosis: Mining, milling, and fabrication; installation and removal of insulation
Pleural plaques
Caplan syndrome
Mesothelioma
Carcinoma of the lung, larynx, stomach, colon
Berylliosis
Iron oxide: Siderosis, eg Welding
Moldy hay: Farmer's lung
Bagassosis: wallboard, paper
Bird-breeder's lung due to bird droppings
Byssinosis : cotton in Textile manufacturing
Pathogenesis:
Particles that are 1 to 5 μm are the most dangerous, because they get lodged at the bifurcation of the distal airways.
particles greater than 5 to 10 μm are unlikely to reach distal airways
particles smaller than 0.5 μm tend to act like gases and move into and out of alveoli
Silica, asbestos, and beryllium are more reactive than coal dust, resulting in fibrotic reactions at lower concentrations
Usually these harmful particles are entrapped in the mucus blanket and rapidly removed from the lung by ciliary movement
The pulmonary alveolar macrophage mediate an inflammatory response and initiate fibroblast proliferation and collagen deposition
Tobacco smoking worsens the effects of all inhaled mineral dusts
Coal worker’s pneumoconiosis: spectrum of disease:
asymptomatic anthracosis
simple coal workers' pneumoconiosis (CWP
complicated CWP or progressive massive fibrosis (PMF)
Caplan syndrome if associated with Rheumatoid Arthritis
PMF has a tendency to progress even in the absence of further exposure
Morphology:
upper lobes are predominantly involved
coal macules and coal nodule
centrilobular emphysema.
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