Wednesday, April 25, 2007

Asbestos Cancer




Asbestosis is a chronic inflammatory medical condition affecting the parenchymal tissue of the lungs. It occurs after long-term, heavy exposure to asbestos, e.g. in mining, and is therefore regarded as an occupational lung disease. Sufferers have severe dyspnea (shortness of breath) and are at an increased risk regarding several different types of lung cancer.
As clear explanations are not always stressed in non-technical literature, care should be taken to distinguish between several forms of relevant diseases. According to the World Health Organisation (WHO), these may defined as; asbestosis, lung cancer, and mesothelioma (generally a very rare form of cancer, but increasing in frequency as people exposed to asbestos age).

Signs and symptoms:

The primary symptom of asbestosis is generally the slow, insidious onset of shortness of breath on exertion. In severe, advanced cases, this may lead to respiratory failure. Coughing is not usually a typical symptom, unless the patient has other, concomitant respiratory tract diseases.
People with extensive occupational exposure to the mining, manufacturing, handling or removal of asbestos are at risk of developing asbestosis. There is also an increased risk of lung cancer and mesothelioma. Asbestosis and lung cancer require prolonged exposure to asbestos. However, cases of mesothelioma have been documented with even 1-3 months of exposure, and only indirect exposure (through air ventilation system.) Most cases of asbestosis do not present until 5-10 years after exposure to the material.
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).