Asbestosis pathophysiology


 * Associate Editor(s)-In-Chief: Kim-Son H. Nguyen, M.D., M.P.A., Beth Israel Deaconess Medical Center, Harvard Medical School, Boston MA,

Overview
Asbestosis is the scarring of lung tissue (around terminal bronchioles and alveolar ducts) resulting from the inhalation of asbestos fibers. There are two types of fibers, amphibole (thin and straight) and serpentine (curved). The former are primarily responsible for human disease as they are able to penetrate deeply into the lungs. When such fibers reach the alveoli (air sacs) in the lung, where oxygen is transferred into the blood, the foreign bodies (asbestos fibers) cause the activation of the lung's local immune system and provoke an inflammatory reaction. This inflammatory reaction can be described as chronic rather than acute, with a slow ongoing progression of the immune system in an attempt to eliminate the foreign fibres. Macrophages phagocytose (ingest) the fibers and stimulate fibroblasts to deposit connective tissue. Due to the asbestos fibres' natural resistance to digestion, the macrophage will die off, releasing certain cytokines and attracting further lung macrophages and fibrolastic cells to lay down fibrous tissue, which eventually forms a fibrous mass. The result is interstitial fibrosis. The fibrotic scar tissue causes alveolar walls to thicken, which reduces elasticity and gas diffusion, reducing oxygen transfer to the blood as well as the removal of carbon dioxide.

Asbestos presents as a restrictive lung disease. The total lung capacity (TLC) may be reduced through alveolar wall thickening. In the more severe cases, the drastic reduction in lung function due to the stiffening of the lungs and reduced TLC may induce right-sided heart failure (cor pulmonale).

More than 50% of people affected with asbestos develop plaques in the parietal pleura, in the space between the chest wall and lungs. Clinically, patients present with dry inspiratory crackles, clubbing of the fingers, and a diffuse fibrotic pattern in the lower lung lobes (where asbestosis is most prevalent).

In general;


 * Asbestos is a useful product because of its thermal, electric and sound-insulating qualities, and has been used in many settings for these reasons.
 * Asbestos refers to a group of naturally-occurring fibers composed of hydrated magnesium silicates.
 * World production and consumption peaked in the mid-1970s around 5.0 million tons, and has fallen thereafter to about 2.5 million tons today. Use has fallen in Europe and America, but has risen in countries with rapidly growing economies.
 * As many as 8 million persons living in the U.S. have been occupationally exposed in the last 50 years.
 * Asbestosis is a fibrotic interstitial lung disease.
 * The asbestos fibers are inhaled into the pulmonary tree.
 * The fibers tend to deposit at the level of the respiratory bronchiole and alveolar duct bifurcans. Most are removed by mucociliary clearance, but some are taken up by alveolar macrophages and alveolar cells.
 * Alveolar macrophages accumulate and inflammation develops, and there is movement of other inflammatory cells into the lung.
 * Various mediators including proteases, cytokines, growth factors and reactive oxygen species are released by inflammatory cells in response to the fibers. As alveolar and interstitial macrophages, neutrophils, lymphocytes, and eosinophils accumulate, normal alveolar cells are lost.
 * The asbestos fibers probably have a direct toxic effect on the lung as well.
 * Fibroblast proliferation and collagen accumulation eventually develop resulting in pulmonary fibrosis.
 * Onset of fibrosis occurs 15-30 years after first exposure.