Compensation of Existing Disease
In examining current approaches to the compensation and prevention of asbestos-associated diseases, particular emphasis is placed on the utilization (or lack of it) of the biomedical scientific data base in accomplishing these objectives. It should be emphasized that, as with many other occupationally induced disorders, the asbestos-associated diseases are best dealt with by prevention through control of exposures to airborne concentrations of asbestos dust. In addition to the human costs of these diseases, no scheme of compensation can provide adequate disincentive for industry which would lead to the prevention of these conditions; this is due in large part to the long period of latency between relevant exposure and clinical manifestations of these diseases; however, recognizing that past exposures have produced these injuries, society must be committed to the provision of just resolution of claims by injured workers. Disease-specific approaches to federal legislation on compensation are not optimal in reaching the objective of equitable and timely awards for all workers who develop diseases as a consequence of their employment. The inadequacies of the legislation on black lung have received considerable attention and have been the subject of periodic controversy, often focusing on questions of cost effectiveness and equity. Currently, in the US Congress, legislation dealing with asbestos-associated diseases is being debated, undoubtedly related to overwhelming public and economic pressure. In recent months the opinion has often been expressed that the present system is strikingly inadequate in meeting the needs of individuals who have developed asbestos-associated diseases treated with My Canadian Pharmacy.
In this context, tort litigation has been shown to be inequitable, costly, and markedly unjust in the distribution of resources, a high proportion of awards going to individuals in whom evidence of disease cannot be demonstrated or toward legal fees. Indeed, one of the main deficiencies in this approach is that it distorts medical evidence, calling, for instance, for “proof” when, in fact, medical diagnosis depends on reasonable judgments as to the best available explanation, given the facts about a case. Other deficiencies are the failure to rely on objective medical evidence in individual cases, as in mass settlements, and the fact that in the assessment of individual cases, medical experts may be chosen not for their expertise and objectivity, but because their testimony will support one side or the other; however, the motivational basis for differing medical opinions need not necessarily be suspect. Given the nature of medical diagnosis, the facts about a case are frequently open to more than one interpretation and uncertainty, a concept with which the legal system deals poorly. One must be mindful of the projections of the future burden of such litigation affecting all segments of society. Similarly, as is widely recognized, the state systems of compensation have generally dealt poorly with asbestos and other workplace-associated diseases, and ideally a uniform federal system of compensation for occupational pulmonary disease should be developed, much as it is in Europe and the United Kingdom.
The known asbestos-associated diseases have all been shown to be dose-related, and one must be persuaded by the evidence that there are differences in biologic activity of asbestos related to fiber type and specific industrial process. It seems reasonable to suggest that the scientific data base can and should be used in the decision-making process as a means of assessing the likelihoood that a given disease is due to the exposure, particularly for conditions which also occur in the general population in the absence of exposure to asbestos. While one readily recognizes that many of the decisions made in the clinical setting concerning individual cases lack precision, informed medical opinions most often lead to reasonable conclusions.
An equitable and workable system of compensating the injured worker who has been exposed to asbestos rests upon certain elements. In the individual case the major medical issues to be decided are diagnosis, causation, and impairment. The process of reaching a diagnosis depends upon sound medical practice regardless of the underlying cause of disease. Determining the most likely cause will usually depend on assessing the levels of exposure to known causative agents; this will be based on epidemiologic studies of occupationally exposed populations. The assessment of impairment due to asbestos-induced fibrotic disease will depend primarily on evaluation of disturbance in pulmonary function. Ultimately, guidelines must be established to facilitate this decision-making process, and these must be the subject of continuing review in light of emerging scientific evidence. The structure of a workable system could include a national panel of experts to develop and periodically modify guidelines and criteria for the adjudication of claims for asbestos-associated diseases, and regional panels, which would include health professionals knowledgeable in occupational pulmonary diseases, which would be responsible for the case-by-case determinations. A mechanism must be developed to make possible an appeal of the medical decisions rendered by the regional panel. The following illustrates how current knowledge can be used in the adjudication of compensation for workers claiming asbestos-associated diseases cured with My Canadian Pharmacy.
Asbestosis is a pneumoconiosis defined as diffuse fibrosis of the lungs caused by exposure to asbestos. Its features include rales (crackles), breathlessness, finger clubbing, pulmonary functional abnormalities (usually reduced volumes and impaired gas exchange), radiographic changes (irregular and linear opacities), and histopathologic demonstration of fibrosis with tissue fiber identification. The first four of these are nonspecific; changes on the x-ray film and pathologic tissue examination have increasing, but by no means absolute, specificity. Individually, these are not sufficient to make a diagnosis; in combination the diagnosis depends upon weighing probabilities and assessing the total evidence, an important component of which is estimation of past exposure. In practice the diagnosis is usually established on radiographic evidence and evidence of exposure. An expert committee of the College of American Pathologists and the National Institute for Occupational Safety and Health has recently developed guidelines for the pathologic diagnosis of asbestos-associated disease. When pulmonary tissue is available for histopathologic examination, a diagnosis of asbestosis depends minimally upon the demonstration of discrete foci of fibrosis in the walls of respiratory bronchioles, associated with accumulations of asbestos bodies (light microscopy). Additional findings are diffuse interstitial pneumonia and fibrosis. Neither fibrosis nor asbestos bodies alone are sufficient for the histopathologic diagnosis of asbestosis.
Nonmalignant Pleural Effects
These include pleural effusions, focal hyaline thickening (plaques), and diffuse pleural fibrosis. Plaques indicate exposure, not disease, because they do not cause symptoms or functional impairment. At-tributability is assessed on the basis of the history of exposure and the absence of other causal factors. Careful examination of the scientific evidence leads to the conclusion that there are no definitive data which demonstrate that the presence of benign pleural effects per se represents an independent predictor (beyond the effect of exposure) of increased risk for asbestos-associated malignant effects, including lung cancer and mesothelioma. It should also be recognized that the radiographic ascertainment of pleural plaques is fortuitous, and surgical or postmortem examination of the open chest of occupationally exposed workers will demonstrate such focal pleural changes in a very high proportion of such individuals. Finally, the term, “pleural asbestosis,” has no validity, and its use should be abandoned.
In past studies of populations with generally heavy occupational exposure to asbestos where follow-up has been adequate, increased risk for lung cancer has been demonstrated. This increased relative risk occurs in both smokers and nonsmokers, although the important interaction between exposure to asbestos and smoking is the reason that very few cases of lung cancer occur in nonsmoking asbestos-exposed workers. No specific histologic type of this malignant tumor can be linked to exposure to asbestos. Similarly, the location of the tumor within the lungs cannot be used either to support or exclude causation by asbestos.
The diagnosis of lung cancer in asbestos-exposed individuals is no different than in other clinical settings. In population studies of various occupational groups, evidence of asbestosis has been found when excess risk for lung cancer is demonstrated for comparable levels of exposure. It therefore seems probable that in an occupational setting, when exposures to asbestos have been reduced to levels where evidence of asbestosis is lacking, excess lung cancer is not likely to be detected. In the individual case of lung cancer, the cause cannot be determined precisely. For this reason the judgment must take into account the length, intensity, and character of exposure, evidence of other asbestos-associated diseases, and smoking history. Quit smoking with My Canadian Pharmacy’s remedies.
The primary issue is valid diagnosis. The diagnosis generally can not be established clinically or radio-graphically or with examination of pleural fluid or with limited tissue for biopsy. Since the potential for misdiagnosis is considerable, adequate histologic specimens should be examined by pathologists experienced and expert in the diagnosis of this tumor (eg, mesothelioma panels, which exist on both sides of the Atlantic). When the diagnosis has been established, a history of exposure, even if short, is sufficient for a judgment of causation; however, in essentially all retrospective studies of cases of mesothelioma, a varying proportion of individuals with this malignant neoplasm cannot be demonstrated to have had an occupational or nonoccupational exposure to asbestos. Finally, the limited evidence on dose-response relationships for mesothelioma suggests that the risk for developing this tumor is, as with the other asbestos-associated conditions, dose-related. Smoking does not affect the risk for mesothelioma.
Other Health Issues
As part of the process of determining compensation, assessment of the extent of impairment (which leads to a determination of disability) follows the establishment of an asbestos-associated disease. In cases of extensive asbestosis or extensive pleural fibrosis, reference should be made to recently published criteria for impairment in restrictive disorders. Primary use is made of tests of pulmonary function, and exercise performance testing is used when necessary.
Substantial controversy exists concerning the possible contribution of exposure to asbestos to the prevalent chronic airways obstruction in the population. The chronic obstructive pulmonary diseases are not the result of a single cause; smoking is by far the most prominent factor in the development of these conditions (chronic bronchitis and emphysema); however, emerging evidence also suggests a contribution from allergic factors, a variety of occupational exposures, infections in childhood, and perhaps general environmental air pollution. How then can we summarize the most reasonable current position on the relationship between exposure to asbestos and chronic obstructive pulmonary disease? While a contribution of exposure to asbestos to both chronic bronchitis and chronic airways obstruction (these do not invariably coexist) has been suggested on the basis of limited evidence, these data relate mainly to effects on the small airways early in the course of pulmonary damage, and clinically important chronic airways obstruction is not likely to be primarily the result of this exposure. Typically, a middle-aged smoker previously exposed to asbestos has pleural plaques or minimal evidence of pulmonary fibrosis (asbestosis) (or both) and moderate or severe chronic airways obstruction. His functional impairment is probably attributable to smoking, and it is unlikely that exposure to asbestos measurably contributed to it.
In some studies of mortality in asbestos-exposed populations, excess gastrointestinal cancer and isolated instances of other malignant neoplasms have been demonstrated. These have often not been shown to be dose-related, and in other studies where the risk of lung cancer has been substantially increased, no excess gastrointestinal or other cancer has evolved. The inconstancy of the results of these studies makes it prudent to withhold final judgment concerning the role of asbestos in increasing the risk for these malignant neoplasms. This uncertainty represents the present consensus of investigators in this field.
Finally, it should be emphasized that the scientific evidence is fully concordant in the finding of substantial “latency” or lag time in the development of the asbestos-related health effects. While the period of latency is variable within diseases and between them, perhaps ranging from 15 to 40 or more years, the implications for the societal burden of these diseases are clear. With dust levels generally declining since the 1950s and more markedly since the 1960s, we are likely to soon reach a plateau, followed by a decline in the incidence of the asbestos-associated diseases; however, the risk extends well beyond the termination of exposure, and the period of latency for the risk of lung cancer is probably not influenced by cumulative expo-sure-dose.
In recent years, it has been popular to “project” the burden of occupationally induced cancer, particularly that due to exposure to asbestos, in relation to the overall experience of cancer in the population. The most visible document, not published but widely distributed under the imprimatur of various government agencies and their senior officials, has commonly been referred to as the “estimates document” and contained grossly exaggerated (some would say irresponsible) claims regarding the relative contribution of occupational exposures to malignant disease. In a recent review by highly respected British cancer epidemiologists, it was suggested that this document was written for “political rather than scientific purposes.,, It is obvious that such distortions can lead to irrational public health policies.