Asbestos


Etiology


Clinical Presentations

Pulmonary Manifestations

Tobacco: 13x increased risk of asbestosis in smokers (compared to non-smoking asbestos-exposed cohort)
– Household exposure to clothes of spouse or parent: increases risk of asbestosis
– Latency:
– Benign Asbestos Pleural Effusion: may occur within 10 years of exposure (this is the shortest latency period for any of the asbestos-related lung manifestations)
– Asbestosis, pleural plaques, and asbestos-related lung cancer: typically occur 20 years or more after exposure
– Malignant mesothelioma: usually occurs 30 years of more after exposure

Diagnosis
– Pleural fluid: exudate
– Appearance:
– pH:
– Cell count/diff: PMN or mononuclear-predominant/eosinophilia seen in 52% of cases
– Culture:
– FOB: >1 asbestos bodies/hpf suggests asbestos exposure (but does not confirm asbestosis)
– Should do BAL in basilar segments to obtain asbestos bodies (due to gravity effect of deposition)
– CXR/Chest CT patterns:
– Interstital infiltrates: lower-lobe predominance
– Honeycombing: small cystic changes (seen best in lower fields) seen late in course
– Radiographic honeycombing correlates well with pathologic honeycombing
– Diaphragmatic pleural calcifications/ asbestos plaques: indicate history of asbestos exposure only and have no significance (they may become more numerous or grow over time)
– Asbestos pleural effusion: usually small-moderate and unilateral (bilateral in only 10% of cases)
– Rounded atelectasis:
– HRCT: picture mimics that of IPF
– More sensitive than CXR, especially in patients with subtle ILD and non-calcified pleural plaques
– Serum autoantibodies: may be seen
– Hypergammaglobulinemia: may be seen

Pathologic Patterns
– Desquamative Interstitial Pneumonia (DIP):
– Usual Interstitial Pneumonitis (UIP):

Other Manifestations


Treatment


References