Hard Metal Pneumoconiosis


Epidemiology


Etiology

1) Cobalt Exposure:
a) Diamond Polishing/Tooling:
b) Sharpening of Hard Metal Tools:
c) Hard Metal Production:
d) Oil-Well Drilling: using cemented tungsten carbide
e) Armored Plate Production: tanks, naval ships
f) Manufacture of Cutting Tools/Loops for Fishing Poles:


Physiology


Pathologic Patterns


Diagnosis


Clinical

Clinical Presentations: features from each of these presentations may co-exist in the same patient
1) Acute Hard Metal Disease: more common manifestation than ILD presentation
a) Rhinitis/Conjunctivitis: due to fact that cobalt is a skin sensitizer
b) Occupational Asthma:
c) Bronchitis:
d) Skin Symptoms: due to fact that cobalt is a skin sensitizer

2) Subacute Hard Metal Disease:
a) Fibrosing Alveolitis:

3) Chronic Hard Metal Disease: rare manifestation
a) Diffuse and Progressive Interstitial Fibrosis: dyspnea, hypoxemia
-FOB with BAL: multinucleated cannabilistic -appearing cells in BAL fluid ( cell within a cell apprearance)
–Multinucleated giant cells stain positive for cytokeratin (may represent epithelial cells)
–Multinucleated giant cells comprise up to 15% of total BAL cells
-OLB: giant cell interstitital pneumonia (GIP) is almost pathognomonic for Hard Metal Pneumoconiosis
–Tungsten carbide can be identified on biopsy (but due to solubility, cobalt is usually not detected)


Treatment