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The relation of asbestosis to lung cancer - The important questions here are: firstly, is there an excess risk of bronchial cancer only in those who also have some degree of asbestosis? Secondly, if the dust exposures are low enough to eliminate asbestosis, will the excess lung cancer risk also be reduced to an acceptably low level? Neither question can be answered at present, and so disagreement is likely. It is known that there is a close association between asbestosis and lung cancer, about 50% of those dying from or with asbestosis have a lung cancer at post mortem. Among those knowledgeable about details of the dose-response data there would probably be agreement that dust exposures low enough to eliminate asbestosis will also reduce the ex- cess bronchial cancer risk to a very low value. This does not extend to the risk to a very low value. This nearly so closely related to that of asbestosis (see ASBESTOS (MESOTHELIMO AND LUNG CANCER).

The various components of the bronchial lining may undergo malignant transformation and consequently the carcinoma may be composed of various cells and have various histological appearances such as adenocar-cinoma or squamous, or oat-cell carcinoma.
There are no histological or other characterstics winch would specify the individual lung cancer as cancer caused by asbestos.
In many cases of asbestos-linked pulmonary cancers the lungs also show pulmonary fibrosis-asbestosis microscopically, and often macroscopically, and on x-ray. examination. Some scientists believe that so-called "asbestos lung cancer" can only develop on a pathologically changed terrain of asbestotic fibrosis. There is evidence of such a possibility in human pathology: the scar-carci- noma. Others believe that exposure to. asbestos alone, particularly in a smoker, may provoke cancerous growth without also causing asbestosis. The decision between the two opinions is difficult to reach because in individual clinical cases of bronchogenic carcinoma we cannot dis- tinguish what is an "asbestos cancer", a "ciprette cancer"
or lung cancer from yet another cause. Thus, in most coun- tries bronchogenic carcinoma is considered an occupational disease due to asbestos, e.g. for workmen's compensation, only in the presence of coexisting asbestosis. If pulmonary fibrosis were a prerequisite for development of asbestos- linked lung cancer, it would follow that lowering exposures to asbestos to levels which effectively prevent asbestosis would automatically eliminate "asbestos lung cancer".

Epidemiological data In man the link of lung cancer with asbestos has been mainly epidemiological. while asbestosis cannot occur without ex- posure to asbestos mad consequenty every case of asbbestoses must be linked with such exposure, with pulmonary cancer the situation is quite different. It is a rather common disease in the general population. The link with exposure to asbestos is based on finding whether in those exposed to asbestos is based on finding whether in those exposed to asbestos bang cancer occurs more frequently than in those unexposed, i.e. whether in those exposed there is an excess incidence of lung cancers.

Since Doll's study a number of other epidemilogical studies, of various levels of excellence, have been carried out which confirm that indeed there is an excess of bronchogenic carcinoma in persons exposed to asbestos, under certain circumstances, and thus that asbestos must be considered one of a number of carcinogenic substance.

What are the circumstances of a manifest risk of cancer in asbestos exposure? It has been established that smoking cigarettes greatly increases this risk. In fact the large majority of lung cancers attributed to asbestos exposure have occurred in smokers. A lung cancer in an asbestos- exposed non-smoker has been a rarity. Table 1 shows the effect of both exposures together while each of the two exposures also carries a risk by itself. A particular exposure to asbestos in the reported group of workers increased the basis risk of pulmonary cancer in nonsmokers. However, since the risk in nonsmokers was very small, its further increase still meant only very few cases, if any at all. On the other hand, when the basic risk of exposure to asbestos was combined with the 11. 8 time higher risk of a smoker, this combination necessarily produced a serious risk leading to an excess of incidence of pulmonary cancer. This experience has an important practical implication: most "asbestos cancers of the lungs" could be prevented if the workers did not smoke. In fact it was found that the risk for the asbestos workers who had stopped smoking declined after 10 years to the low level existing for non-smokers. The bronchogenic carcinoma has a long latent period, usually 20 years or more. Consequently, what excesses of incidence of pulmonary carcinoma linked with asbestos have been found to date must be linked with exposures 20 years or more development of the tumour. It is known that exposures in those days were generally very high. But we usually do not have any precise measurements. Thus in most existing epidemiological studies it has not been easy, and in some not possible, to establish a relation between the incidence of cancer and a certain quantitative level of exposure, other than that the exposure had been high.