A S B E S T O S

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A S B E S T O S

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The role of occupation in the development of chronic obstructive pulmonary disease (COPD)

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Types of Mesothelioma

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Because it is difficult to appreciate obstructive disease against a background of severe restrictive disease, the airways component of asbestosis has not received much attention until recently. Pleural fibrosis is particularly associated with these restrictive changes and probably represents the contribution of mechanical changes in the chest wall, but this is a relatively minor effect41-43). Pulmonary function studies also show a reduced diffusing capacity, both because of delayed diffusion across the thickened interstitium and mismatching of blood and air in the alveolar region due to the disruption of the fibrosis. This mismatching is also a reason for the progressive desaturation of oxygen in the blood that eventually results in hypoxemia and clinical respiratory insufficiency in severe cases. Mild cases of asbestosis may not necessarily show this interference with gas exchange and blood gases may be normal in such cases.

Unlike other outcomes associated with asbestos, there is no evidence that cigarette smoking plays any role in contributing to the onset of asbestosis, or that the effects of asbestos exposure and cigarette smoking are positively interactive in causing enhanced asbestosis44). There is some evidence that once established, asbestosis may be enhanced by cigarette smoking with an increased frequency of opacities detectable by HRCT for the same degree of asbestos exposure45). Since the frequency of opacities does not correlate closely with changes in pulmonary function and therefore impairment, it is not clear that this finding can be used as the basis for an apportionment formula.

Possible susceptibility states may contribute to risk of asbestosis, for example glutathione-S-transferase deficiency46). This is a common condition, affecting some 50% of Caucasian males, that might well be considered within the range of normal but that appears to predispose to asbestosis and may modify the outcome. However this observation is not helpful in apportionment. It is an inborn condition of the worker and so common that it may be considered a variant of normal.

The implications of these data simplify apportionment in most cases. Because asbestosis is a disease only caused by exposure to asbestos, and because other risk factors play only a minor role in modifying the outcome associated with the fibrosis (as opposed to complications such as cancer), there is no basis for apportionment by cause. If the diagnosis is asbestosis and causation can be established, the apportionment by cause is 100% attributable to asbestos and all respiratory impairment resulting from the fibrotic component of the disease is asbestos-related. Examiners often acknowledge the presence of asbestosis, but apportion the resulting respiratory impairment between asbestos and cigarette smoking, particularly when there is mixed obstructive/restrictive impairment. It is difficult to do this by cause for the obstructive component and the progression of mixed impairment makes separation of the restrictive and obstructive components uncertain. Given the caveat in workers' compensation that any substantial contribution by a workplace exposure is sufficient to consider the outcome to be work-related, the presence of any documentable asbestosis-related impairment, for example mild restrictive impairment, should be sufficient to apportion all impairment to the asbestos exposure.

The general rule that in the presence of asbestosis all respiratory impairment should be apportioned to asbestos. The exception may be a very mild case of asbestosis with minimal or no functional impairment associated with marked obstructive changes in a heavy smoker, a characteristic smoking-related respiratory impairment. In such a case, the restrictive component of the disease would be considered asbestos-related and the obstructive component, taken as FEV1/FVC(%) rather than FEV1 compared to predicted, would be more likely to reflect the influence of cigarette smoking. The treatment in such a case would then parallel that given below for chronic obstructive airways disease.

However, even in this case there is evidence that the asbestosrelated airways changes modify the effects of cigarette smoke, at least in experimental studies46, 47). The relative contribution by cigarette smoking may be overestimated by this approach in such cases.

Chronic Obstructive Airways Disease

It has been known for many years that exposure to asbestos is associated with obstruction to airflow as well as restrictive changes50-52). Functional changes are also correlated with respiratory symptoms such as cough, wheeze, and shortness of breath53). However, chronic obstructive airways disease (COAD) has not been emphasized as an asbestos-related outcome and has not been accepted by compensation agencies as a presumption or scheduled occupational disease. There are several reasons for this reluctance to recognize asbestosrelated chronic obstructive airways disease. The most influential has probably been that the effect of cigarette smoking is not easily separated from asbestos exposure and has confounded the association, influencing agencies and adjudicators to attribute all of the cause to the smoking50).

Another factor is that the predominant effect in advanced asbestosis is restrictive disease and the obstructive changes associated with lesser degrees of asbestosis have been largely overlooked37, 39). Yet another factor is that mandated surveillance for asbestos-exposed workers, such as the OSHA asbestos standard in the United States and the Alberta Fibrosis Program in Canada, have emphasized the early identification of restrictive changes and changes in the FEV1, which will reflect changes in the FVC, rather than an interpretation that emphasizes airflow taking changes in vital capacity into account.

Adults lose a fraction of their lung capacity and airflow velocity, as measured by routine spirometry, due to aging; this loss is predictable, and for FEV1 averages 30 ml/y. In theory, any person who lived long enough would develop obstructive disease, once the natural loss progressed far enough. Pulmonary injury may accelerate this loss and in cigarette smokers this rate of loss may easily double or triple, so that during their lifetime they dip well below the normal range and develop incapacity, the condition known as chronic obstructive pulmonary disease (COPD). (COPD and the less common term COAD are usually synonymous. Here, COAD is the more general term, and is used to avoid confusion with the complex illness associated with cigarette smoking that most clinicians have in mind when they refer to COPD.)

It is now well established that asbestos-exposed workers show accelerated loss of airflow and are at risk for obstructive airways disease54-59). Those with signs of early parenchymal fibrosis appear to be at higher risk for more rapid decline60).

Asbestos-exposed workers who develop persistent respiratory symptoms are at risk for even more rapid loss of pulmonary function61). There is also experimental evidence for a positive interaction (synergy) in airflow obstruction between asbestos exposure and cigarette smoking because of changes in compliance in the wall of small airways47).

Mesothelioma Info

Malignant mesothelioma is often confused with asbestos related lung cancer because the two diseases both affect similar regions of the body and are both caused by asbestos exposure. There are three distinct types of mesothelioma: pleural mesothelioma, peritoneal mesothelioma and pericardial mesothelioma.