Asbestos has been used in a limited way for thousands of years. However, it is only since the 1880’s that mining and the use of asbestos has risen dramatically. In England the first described case of asbestos-related lung disease was a worker who died in 1900 from pulmonary fibrosis but was not reported until 1907. Since then many studies have been made and the causes and patterns of asbestos-related diseases have become more apparent, although even today uncertainties still exist. Asbestos causes diseases by being inhaled into the lungs and aerodynamic studies have shown that fibres less than 3 microns in diameter are capable of penetrating the bronchial tree and reaching the alveoli. Coarser fibres will impact higher up and be eliminated by the ciliary ‘escalator’. Long chrysotile fibres, which tend to be curly, are less likely to penetrate through to the alveoli than the straight, more rigid amphiboles. Once in the lungs, amphibole fibres are less susceptible to clearance than chrysotile and may persist for many years. A proportion of asbestos fibres, almost always amphiboles, may become coated with an iron containing protein to form `Asbestos Bodies’, which may have bulbous ends and are found in lung tissue and sputum. They are an indication of asbestos exposure but not necessarily a sign of disease and can in-fact be found in a high proportion of urban dwellers.
Asbestosis usually occurs in those that have been exposed for many years to respirable Asbestos dust. It has a long latent period and is rarely seen less than 10 years after first exposure to asbestos. The likelihood of developing the disease is related to the degree of exposure. It is not known if there is a threshold exposure level at which asbestosis will not occur. Even after prolonged exposure, only a proportion of workers will show signs of the disease and individual metabolisms are obviously a factor. The first clinical evidence of the disease is scarring to the base of the lungs. As the disease progresses, the usual symptom is breathlessness. At first this is only on exertion but there may be breathlessness at rest in advanced cases. There may also be a dry cough. There is not usually any excess sputum except in smokers. In advanced cases there may be finger clubbing and central cyanosis that may only be apparent on exertion. There is no specific treatment that alters the progression of the disease. The patient should be strongly advised to stop smoking and chest infections should be promptly treated. Up to 40% of asbestotics who smoke may develop lung cancer. However the prognosis is not uniformed and some cases show slow signs of progression. The death rate from asbestosis has risen slowly since the 1970s to 186 deaths in 2000.
Mesothelioma, a malignant tumour of the pleura or peritoneum, was first definitely associated with Asbestos exposure during 1960 in workers at the Crocidolite mines in South Africa. Since then other studies have confirmed the link between mesothelioma and exposure to Crocidolite and Amosite Asbestos fibres. Cases of mesothelioma in workers exposed to Chrysotile asbestos alone seem to be rare. The latent period for the development of the disease is very long, between 15 and 40 years from first exposure. Cases have arisen after brief periods of exposure but these have usually been due to high levels of amphibole dust. One area of confusion is that a small proportions of sufferers, about 15% in this country, have reported no recognisable contact with asbestos. The usual gross appearance of a mesothelioma is a thick, whitish sheet of tumor tissue that encircles and compresses the thoracic or abdominal viscera. The normal clinical features of a mesothelioma are chest pains, breathlessness and abdominal distension and discomfort. Diagnosis may be difficult to establish during life and biopsy material can be difficult to obtain and interpret. Biopsy may also carry the risk of seeding of the tumour along the track of the needle.
Treatment is only applied for the relief of pain and the prognosis is uniformly fatal and usually within 18 months of development. Mesothelioma is now the leading asbestos related disease in Western Europe and reported cases are increasing due to the prolonged latent period and use of Amosite asbestos in a wide variety of building materials over the last 60 years. A small number of people who develop mesothelioma are unable to recall exposure to Asbestos, this may be because they don’t remember the exposure or because they weren’t aware that they had been exposed to asbestos at any time. Exposure to all asbestos types but especially of Crocidolite (blue) asbestos can cause mesothelioma, which is a cancer of the pleural lining to the lung or much less commonly of the peritoneum. This disease is essentially incurable, and commonly leads to a great deal of pain and other suffering. Hundreds of ex-workers still die of these diseases in the UK every year.
Bronchial cancer / Lung Cancer
There is a known association between Lung Cancer and exposure to Asbestos dust. People who have already developed Asbestosis have a greater risk of contracting Lung Cancer. Lung cancer is a frequent complication of asbestosis and as with asbestosis, there is a latent period from first exposure to the development of the disease. This is usually in excess of 10 years. Studies have shown a linear relationship between levels of exposure to asbestos and the risk of developing lung cancer. This relationship is only in workers who have had prolonged exposures to asbestos dust. Lung cancer is a common disease with a statistic of 1 in 12 male deaths in England and Wales. The risk to asbestos workers is further increased in cigarette smokers. There are no pathological features which distinguish the asbestos related lung cancer, although the tumour commonly arises in the lower lobes in association with the fibrosis. The effects of lung cancer are often greatly increased by cigarette smoking ( by about 50%). Cancer of the gastrointestinal tract can also be caused by asbestos. The latency period for cancer is often 15-30 years.
The pleura is a two layered smooth wet membrane which surrounds the lungs and lines the inside of the rib cage. The layers slide relative to each other as the lungs expand and contract. Asbestos fibres inhaled into the lungs can work their way out to the pleura and may cause fibrosis or scarring to develop. This causes the pleura to thicken. Pleural plaques are a form of localised thickening or calcification on the outer layer of the pleura that line the chest wall. Although usually without symptoms they can cause impairment of the lung and pain. They are a marker of asbestos exposure. They are present in approximately 40% of people with regular exposure to asbestos.
A non malignant collection of fluid between the lung and the chest wall. It may precede or predispose to diffuse bilateral pleural thickening.
Diffuse Pleural Thickening
Thickening of the lung walls due to scarring caused by Asbestos which may cause breathlessness. Exposure to asbestos can lead to generalised scarring (replacement and disruption of the normal cellular pattern by fibrous tissue) in the pleura. This involves the pleural membrane which covers the lungs. Usually affecting both lungs although not necessarily to the same extent. This thickening leads to constriction of the lung with consequent loss of lung volume and increasing breathlessness. There is often an episode of pleurisy which settles spontaneously or after treatment. This pleurisy may reoccur on the other side of the chest but does not usually affect the same side twice. There may be an associated pleural effusion (a collection of fluid in the pleural space between the lung and the chest wall). Further pleural thickening may occur leading to worsening breathlessness. This may worsen in either a stepped pattern or steady deterioration. It is usually not possible to give a firm prognosis for diffuse pleural thickening as the natural history of the disease is variable. Often the process is not progressive but it can result in an increasing restrictive pattern due to restriction or loss of lung elasticity from fibrosis.
The long latent period between first exposure to asbestos dust and the development of disease means that cases diagnosed today relate to conditions many years ago. Although the first asbestos regulations date from 1931, it was not until the 1969 Asbestos regulations that all areas of asbestos usage came under control. During the 1960’s, effective methods of monitoring the asbestos levels in the air were developed that permitted the establishment and enforcement of meaningful standards. Dust levels in industry today are a fraction of the levels that have occurred in the past. Chrysotile asbestos is the only fibre used to any extent in this country now. Imports of crocidolite ceased in 1969 and amosite in 1985.Whilst modern industrial practices should result in minimal risk of exposure, cases of asbestos related diseases will continue to escalate over the next 20 years due to past exposures. On the basis of deaths up to 1991, the number of male mesothelioma deaths is expected to go on rising and reaching a peak of between 1300 and 3300 annually. The lessons learned from asbestos should not be forgotten in the assessment of any future alternative materials.
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