Diffuse interstitial pulmonary fibrosis caused by inhalation of asbestos fibers.
Occupational exposure is a risk factor for development for cancer of the lung with an average increased risk of 16% over unexposed control patients.
The likelihood of the development of asbestosis, the rapidity of onset of the disease, and the severity of the disease depend on the intensity and duration of exposure to asbestos dust.
Lifetime threshold cumulative fiber exposure of 25 fibers per cubic centimeter-years (Mossman BT).
Present concentration of ambient asbestos in the workplace by OSHA is 0.1 fiber per milliliter of air.
Latency period often 20 years or more to develop asbestosis.
Pleural plaques do not correlate with the cumulative asbestos exposure.
Pleural plaques are unilateral in one third of cases asbestosis (Gevenois PA).
Can develop without pleural plaques (Aberle DR).
Chest x-ray typically shows increased interstitial markings but 15% of patients have a relatively normal radiographic appearance.
Sensitivity of chest radiographs is about 85-90%.
Patients may develop rheumatoid factor and anti-nuclear antibodies reflecting the presence of abnormal humoral immunity.
The prevalence of asbestosis in an at-risk population such as construction or petrochemical workers is 1-5%.
Patients are at increased risk of acute lung infections by bacteria, fungi, viruses, and opportunistic fungi, most commonly aspergillus species.
Susceptibility to infections may be related to lung scarring, impaired muco-ciliary clearance that may be associated with bronchiectasis, and the possible presence of chronic obstructive pulmonary disease.
Rales present in 70-90%.
Rate of death from asbestosis greatest among individuals with evidence of pulmonary disability at the time of initial diagnosis.
Smoking increases the mortality of asbestosis.
Mortality in asbestosis is twice that of individuals without asbestosis.
Most common cause of death with asbestosis is progressive asbestosis and the development of kung cancer (Huuskonen MS).