Biological Effects of Asbestos Dust Exposure

The radiological appearance of asbestosis is rather like that of other forms of pulmonary fibrosis, with irregular opacities, preponderantly in the lower lobes. The clue relating this interstitial change to asbestosis is the finding of pleural thickening or plaques. Careful search for calcification on the diaphragm can be rewarding. The textbook description of shaggy heart border and indistinct diaphragm is rarely seen and, then, only in advanced cases. A helpful practical point is that the chest radiograph in asbestosis generally looks more untidy, with more aggregation than that of, for example idiopathic pulmonary fibrosis.

Lung function tests classically reveal a restrictive pattern, with decreased lung volumes and decreased gas transfer. Those who have airway obstruction will show a mixed picture.

Asbestos bodies, now more correctly called ferruginous bodies, may be found in the sputum. They indicate exposure to asbestos, but are not a mark or disease.

The diagnostic criteria established by Parkes are as follows:

1. History of exposure (including presence of asbestos bodies)
2. Dyspnea on exertion
3. Persistent basal crackles, with or without clubbing
4. Radiological evidence of diffuse interstitial fibrosis or pleural plaques, or both
5. Restricted lung function and impairment

It is rarely necessary to obtain tissue to make the diagnosis, but if this is required, then an open-lung biopsy should be considered. Lung function changes may precede radiological and clinical evidence and, particularly, in the early stages, it is not uncommon to hear crackles, whereas the chest radiograph is still normal, although it is usually abnormal. Management should first revolve around persuading those who smoke to cease. This is imperative in all those exposed to asbestos, but particularly in those who show overt evidence of considerable exposure. Nonsmokers exposed to asbestos have a fivefold greater risk of lung cancer. The risk of developing lung cancer in smokers exposed to asbestos is about 50 times greater than in nonsmokers with no asbestos exposure.

The pathological appearance shows that inhaled asbestos fibers become trapped in the lung tissue, in the alveoli arising directly from the respiratory bronchioles. The fibers of more than 10 um in length lodge in these air spaces, either within the macrophages or lying loose; some of the fibers are coated and appear as asbestos bodies. At this stage, some of the macrophages disintegrate and release enzymes, attracting fibroblasts that start secreting thin stands of collagen that eventually form a fine net of scar tissue. Unable to escape, more macrophages die and release yet more enzymes; the process progresses until the alveoli all along the respiratory bronchioles are replaced with a layer of scar tissue. Initially, only occasional respiratory bronchioles are involved, but gradually more and more of these airways become scarred. The fibrous tissue then spreads farther down the walls of the air sacs, at first as a thin layer, but gradually thickening; the extensions of the scarring between the individual units link up so that increasingly more lung becomes involved. The scarred walls of the respiratory bronchioles then become stretched because of respiratory movement and appear as small, thick-walled cystic spaces. The amount of scar tissue thus increases, but eventually, if the patient lives long enough, the scarring which starts at the base of the lower lobe of the lungs may continue, resulting in a shrunken lung that is a mass of scar tissue surrounding collapsed and useless air spaces.

Asbestos bodies are golden-brown rods found in the sputum and lung tissue. They consist of asbestos fibers, usually of amphibole type, and coated with an iron-mucoprotein complex. These bodies were thought to be evidence of occupational exposure to asbestos dust. However, as techniques became more sophisticated, it was realized that these bodies can be found in the lungs of most people living in urban communities. Electron microscopy has shown that only a small proportion of the inhaled fibers become coated and that most, which are uncoated, are rarely observed under the light microscope. In the study of the general population, up to a million fibers can be recovered from 1 g of dried lung tissue, without any evidence of disease being discovered in the individual.