Pneumoconiosis.



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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