Pathophysiology of asbestosis

Asbestosis is a chronic inflammatory medical condition affecting the parenchymal tissue of the lungs. It is essentially a fibrosis, or scarring, of the lung tissue.

The microscopic asbestos fibers enter the body when it is inhaled. Since these fibers are so thin and light, they are not filtered by the nose of bronchi, thus having easy access to the alveolus of the lungs. The alveolus are small sacs, that together, make up the lungs. They serve as the site of gas exchange – where oxygen is captured for the body. Since many materials can enter this region, the immune system has cells there to destroy any foreign materials and organisms. These cells, called macrophages, function by engulfing (phagocytosis) the materials. Once inside the macrophages, acidic digestive enzymes break down the foreign materials. However, therein lies the problem leading to asbestosis.

The macrophages gallantly perform their function by attempting to engulf the asbestos particles. However, this will prove detrimental to these cells because the fibers are too long. In trying to engulf these asbestos particles, the macrophage basically cuts itself open (lysis) and the digestive enzymes that were contained inside the macrophage are now released into the alveolus. These enzymes go on to injure the alveolus.

In addition, since the asbestos fibers are still free in the alveolus, more macrophages migrate to the area to attempt to destroy it. However, the problem compounds itself as more macrophages become destroyed and their enzymes released to harm the alveolus.

The damage caused by these enzymes lead to fibrosis (the scarring process). Fibrosis is a function of the immune system that aims to repair any tissue damage and to minimize the spread of an infected area. As one can imagine, scarring of the alveolus impairs their function in gas exchange. This leads to the problems that are associated with asbestosis, such as breathing problems.