Ferri – Asbestosis

Asbestosis

  • Imrana Qawi, M.D.

 Basic Information

Definition

Asbestosis is a slow, progressive diffuse interstitial fibrosis as a consequence of dose-related inhalation exposure to fibers of asbestos in miners, millers, workers of asbestos textiles, and insulators. Clinically, the lung involvement is characterized by bilateral diffuse interstitial fibrosis, more pronounced in the lower lobes, and pleural thickening, leading to shortness of breath and dry cough.

Asbestos exposure can lead to the spectrum of pulmonary pathology, including pulmonary fibrosis; asbestos-related pleural plaque (ARPD), both focal and diffuse; and malignancies (small cell carcinoma, non–small cell carcinoma, or mesothelioma).

ICD-10CM CODES
J61 Pneumoconiosis due to asbestos and other mineral fibers

Epidemiology & Demographics

  1. Five to 10 new cases per 100,000 persons per year in the U.S.

  2. Prolonged interval (20 to 30 yr) between exposures to inhaled fibers and clinical manifestations of disease

  3. Most common in workers over age 40 years involved in the primary extraction of asbestos from rock deposits and in those involved in the fabrication and installation of products containing asbestos (e.g., naval shipyards in World War II; installation of floor tiles, ceiling tiles, acoustic ceiling coverings, wall insulation, and pipe coverings in public buildings).

  4. Smokers and heavy drinkers have the greatest risk of developing this disease.

Physical Findings & Clinical Presentation

  1. Insidious onset of shortness of breath and dry cough with exertion is usually the first sign of asbestosis.

  2. Dyspnea becomes more severe as the disease advances; with time, progressively less exertion is tolerated.

  3. Cough is frequent and usually paroxysmal, dry, and nonproductive. Hemoptysis is rare but reported.

  4. Scant mucoid sputum may accompany the cough in the later stages of the disease.

  5. Fine end-respiratory crackles (rales, crepitations) are heard more predominantly in the lung bases.

  6. Digital clubbing, edema, jugular venous distention are present.

  7. Advanced cases may have signs of right heart failure.

Etiology/Pathogenesis

Inhalation of asbestos fibers. Recent work has shown that pathogenesis of pulmonary interstitial inflammation and fibrosis is related to immune mechanisms. Asbestosis is known to be associated with positive serum antinuclear antibody (ANA) and rheumatoid factor (RF). Recently, an important role of interleukin-1beta (IL-1beta) in the pathogenesis of asbestosis and its systemic autoimmune manifestations has been reported.

Diagnosis

Differential Diagnosis

  1. Silicosis

  2. Siderosis, other pneumonoconioses

  3. Lung cancer

  4. Atelectasis

Workup

Documentation of exposure history, diagnostic imaging, pulmonary function testing

Laboratory Tests

  1. Generally not helpful

  2. Possible mild elevation of erythrocyte sedimentation rate (ESR), positive antinuclear antibody (ANA), and rheumatoid factor (RF) (these tests are nonspecific and do not correlate with disease severity or activity)

  3. Pulmonary function testing: with decreased vital capacity (VC), decreased total lung capacity (TLC), decreased carbon monoxide gas transfer (DLco)

  4. FEV1 might be reduced in concomitant smokers

  5. Arterial blood gases: hypoxemia, hypercarbia in advanced stages

Imaging Studies

Chest radiograph (Fig. E1):

FIG.E1 

Asbestosis. Posteroanterior radiograph shows coarse linear opacities at both lung bases obscuring the cardiac borders.
From McLoud TC: Thoracic radiology: the requisites, St Louis, 1998, Mosby.

Small, irregular shadows in lower lung zones.

The imaging findings vary from benign pleural disease (including discrete plaques, pleural calcification, diffuse pleural thickening with blunting of costophrenic angles, and thickening of the interlobar fissure) to asbestosis (diffuse interstitial pulmonary fibrosis.

  1. Thickened pleura, calcified plaques (present under diaphragm and lateral chest wall).

  2. CT scan of chest (Fig. E2) confirms diagnosis. Typical findings on high-resolution CT of the chest include increased interstitial markings found mainly at the bases. As the disease progresses, honeycombing is noted.

FIG.E2 

Asbestos-related pleural plaques.
Typical calcified pleural plaques (arrows

Treatment

Nonpharmacologic Therapy

  1. Smoking cessation, proper nutrition, exercise program to maximize available lung function

  2. Home oxygen therapy PRN

  3. Removal of patient from further asbestos fiber exposure

General Rx

  1. Prompt identification and treatment of respiratory infections

  2. Supplemental oxygen on a PRN basis

  3. Annual influenza vaccination, pneumococcal vaccination every 6 years

  4. Pulmonary rehabilitation can be considered in advanced cases for improved cardiopulmonary capacity.

Some new data are coming out targeting IL-1 beta therapy on the progression of lung fibrosis that suggest a new perspective for the treatment of systemic autoimmune features of asbestosis and, possibly, of lung involvement.1

Disposition

  1. There is no specific treatment for asbestosis.

  2. Death is usually from respiratory failure from cor pulmonale.

  3. Diffuse pleural thickening and asbestosis are associated with increased risks of malignant peritoneal mesothelioma beyond the risk calculated to be associated with the degree of asbestos exposure.2

  4. None of the benign pleural diseases or ARPD was associated with an increased risk of malignant pleural mesothelioma.

  5. Asbestos increases lung cancer mortality among nonsmokers.

  6. Asbestos exposure without asbestosis and smoking increases the risk of lung cancer. The joint effect of asbestos and smoking is additive and depends in part on the presence of asbestosis. Asbestos workers who stop smoking experience a dramatic decline in lung cancer risk, which approaches that of nonsmokers after 30 years.

  7. Low-dose chest CT scanning offers an excellent opportunity to detect early-stage lung cancers in asbestos-exposed workers.

  8. Computed tomography is more sensitive than radiography, computed tomography without contrast generally suffices for evaluation, and PET scan (fluorodeoxyglucose-positron emission tomography) may have utility in patients with mesothelioma.

  9. Survival in patients after development of mesothelioma is 4 to 6 yr.

Suggested Readings

  • American Thoracic SocietyDiagnosis and initial management of nonmalignant diseases related to asbestos. Am J Respir Crit Care Med. 170 (691)2014

  • Expert Panel on Thoracic Imaging, et al.ACR appropriateness criteria review ACR Appropriateness Criteria® occupational lung diseases. J Thorac Imaging. 31 (1)2016 W1-3, 2016

Related Content

  1. Asbestosis (Patient Information)