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It should be noted, however, that with adequate medical surveillance throughout employment in our field of respiratory diseases, using simple techniques, such as chest radiography and ventilatory function studies-spirometry—early small opacities appearing on the chest film will often be detectable at a time before pulmonary functional impairment is present. This may allow transfer of a worker before he has received an incremental exposure that could increase the risk of disabling illness. This is particularly true in most workplaces of industrialized nations today, since exposures are far lower than in past decades, and the effects of long latency disorders are much more slowly progressive. And many of the conditions we are discussing are such disorders-that is, it takes a long time for the clinical and laboratory evidence of the disease to appear. These are very slowly progressive. It gives us an opportunity, with careful surveillance begun at the onset of exposure, to detect early effects, preclinical effects, if you will, and presumably intervene in order to prevent more serious and established disease.

Now occupational asthma has become of substantial interest to people interested in occupational health generally. It's characterized-asthma generally-by variable airflow obstruction associated with certain types of workplace exposures. The list of occupations that cause occupational asthma is increasing all the time. There are a variety of them. Some of these are materials known to produce a classical allergic response, but some are chemicals for which sensitization is more difficult to determine, but quite as surely they also can produce occupational asthma.

Let me give you an example. In a castor bean oil processing plant there's a very potent allergen. If one is atopic—that is, has a predisposition to developing a certain type of antibody—that individual's risk may be two, three or four times that of a nonatopic or nonallergic individual for developing sensitization and symptoms related to this allergic or respiratory disorder. This risk, as I say, can be quantified. The question arises, is that a substantial enough risk to preclude employment? And that's a decision that I think must be shared widely and not made just by the medical profession.

Bronchial hyperresponsiveness may be a genetically determined factor leading to increased risk of developing occupational asthma, or may be acquired as the result of such an exposure prior to the onset of clinically overt asthma. Certainly this measurement may be useful in preemployment assessment in selected industries; we and others are looking at that to see whether or not we can identify, by hyperresponsiveness of the airways, those individuals who are most likely to develop occupational asthma. We don't know yet and it's too early to use that measurement as a screening technique.

Finally, in regard to occupational asthma where immunologic methods can provide information on specific immunoreactivity. That is, has a person become sensitized to a workplace allergen? There may be reasons to remove sensitized workers-detected by skin or blood tests—from further exposure prior to the time that clinical symptoms appear. Also, if sensitization is occurring, there may also be very good reason to lower airborne concentrations of these allergens in order to reduce sensitization risk in others. Industrial bronchitis has been recognized in certain dusty industries and is receiving some attention in other workplace conditions where irritant inhalants may be present, such as in the chemical industry. Since bronchitis is importantly causally associated with cigarette smoking and is a common condition in the general population, the ascertainment of industrial bronchitis—that is, the part of bronchitis that we would attribute to the workplace-is difficult, and predictors of this condition are therefore not available. Bronchitis may be associated only with cough and expectoration, but produces disability and shortened life span if it causes progressive airways obstruction. Let me emphasize that point. If in fact we are dealing with workplace exposure that may produce chronic airways obstruction, early monitoring of lung function over time, measured in a standardized way probably will allow us, as our investigations have shown, to detect rather modest increases in decline which may identify those individuals who are on the fast track downward and are presumably responding adversely to the environment. . Rapid decliners have been detected in smoking populations. Surveillance then, in a sense, early in the course of employment is a surrogate, if you will, of preemployment screening, but just as useful and certainly much more available. As has been demonstrated in longitudinal studies of smokers, intervention at these early times when one of these fast decliners is identified, can in fact prevent further accelerated decline in function.

In summary, it must be conceded that the "state of the art” in most areas of medicine, including lung diseases, does not often permit us to predict and quantify increased risk for developing work-related lung disorders. I have mentioned some exceptions. However, careful surveillance of respiratory health, using simple methods, in workers exposed to known or potentially hazardous inhalants, will often meet the objective of prevention of serious disease. Carcinogenesis may be the exception, with our present state of knowledge. In regard to the question of whether permissible workplace exposure standards can protect all workers, even those who ultimately prove to be susceptible, it is unlikely that this can be achieved, but we will come closer to this objective as we improve capability of identifying susceptible individuals and minimizing or preventing their exposure. In this regard we must be reminded that even susceptibility does not preclude does relatedness, and there may often be levels of exposure which can be tolerated by individuals who are susceptible to a particular agent, a fact recently demonstrated in our studies of workers exposed to isocyanates. While this may be demonstrable for acute responses, such as asthma, it is much more difficult to assess in the short term for chronic effects. This would become possible in the airways disorders if one could correlate the acute and chronic effects, a subject of considerable interest in cotton dust exposure. Whoever makes judgments concerning the acceptance or nonacceptance of various risks attendant upon occupational exposure, the judgments must be made on the basis of the best scientific information. It is the responsibility of groups like ours to provide accurate data and subsequent analyses on which public policy decisions can be made. There will always be an implicit, if not explicit, balancing of health effects and economic considerations. These judgments are best

spread widely over segments of society which have legitimate concern. Risk assessment will lead to rational prioritizing of our limited resources.

Thank you, Mr. Chairman.
[The prepared statement of Dr. Weill follows:]

PREPARED STATEMENT OF HANS WEILL, M.D. At Tulane, I direct a multidisciplinary research unit in occupational lung diseases funded by the National Heart, Lung and Blood Institute through a Specialized Center of Research grant. Our interests in hazardous exposures found in the workplace vary widely and include mineral dusts (e.g., silica and asbestos), organic dusts (e.g., cotton), and irritant gases and chemical vapors (e.g., chlorine, isocyanates and formaldehyde). It is the intention of my colleagues and me that the scientific product of our research efforts be utilized in the prevention of occupational lung diseases, acute and chronic disorders which are all potentially preventable. Much of the scientific approach that we employ depends upon the investigation of working populations, quantification of their respiratory health, and characterization of their environmental exposures. Correlations of the biological and environmental data lead to information concerning dose-response relationships, and how these may be modified by personal or host factors of the worker. The respiratory diseases that we study are invariably multifactorial in cause and are likely to have as determinants both genetic and environmental (used in the broad sense) factors. Among the former are included a few specific genetic aberrations that increase the risk of developing certain respiratory diseases, and among the latter are such heterogeneous factors as smoking and infection, as well as the specific occupational inhalants which are generally the focus of our attention. It is clear that the most effective approach to the prevention of these disorders would be a determination of susceptibility to developing the respiratory disorder and, if that susceptibility could be dichotomized (i.e., yes or no), the preclusion or exclusion prior to employment of all those found to be susceptible. Regrettably, such is not often the case in the real world.

However, epidemiologic studies of populations exposed to workplace inhalants may identify both exposure and host characteristics which result in increased risk for the development of the adverse respiratory effect, and such risk is quantifiable. While occasionally this may be possible with our present state of knowledge prior to the time of exposure, therefore leading to the possibility of pre-employment screening for high risk individuals, most often indicators of increase risk emerge following initial exposure which may, however, still lead to removal from such exposure before advanced or possibly irreversible respiratory injury has taken place. My first point, therefore, is that while pre-employment screening is currently at a very early stage of development in meeting the objectives of occupational lung disease prevention, careful medical surveillance of employed (and exposed) populations may serve a similar function.

In our investigative field, there are three major exposure-related respiratory health effects of concern: (1) diffuse pulmonary fibrosis, such as the pneumoconioses, silicosis and asbestosis; (2) acute and chronic airways responses, the former represented either by occupational asthma or acute bronchitis, and the latter by chronic industrial bronchitis; and (3) respiratory malignancies.

Dealing with the third category first, it is reasonably safe to indicate to you that we currently have no method to predict which individuals are at increased risk due to genetic factors of developing respiratory cancer. We know, however, that in essentially all occupational causes of respiratory cancer this risk is importantly influenced by cigarette smoking. The interaction between the occupational agent and smoking is substantial, and it is widely agreed that the risk of occupational lung cancer would be strikingly diminished in the absence of smoking. The scientific community can produce quantitative estimates of risk, but society and their representatives must decide how to intervene in minimizing these risks.

The risk of developing pneumoconiosis is invariably dose-related in that the higher the average and cumulative exposure, the greater the prevalence and severity of diffuse pulmonary fibrosis associated with this exposure. This has been demonstrated by our group and others in asbestosis and silicosis, but it has not been possible to identify immuonologic or personal factors which lead to susceptibility to these conditions. While certain immunologic markers are noted with increased prevalence in workers who have mineral dust diseases, there is no evidence that these serve to predict the condition rather than appearing after the disease is well established. It should be noted, however, that with adequate medical surveillance throughout employment using simple techniques, such as chest radiography and

ventilatory function studies (spirometry), early small opacities appearing on the chest film will often be detectable at a time before pulmonary functional impairment is present. This may allow transfer of a worker before he has received an incremental exposure that could increase the risk of disabling illness. This is particularly true in most workplaces of industrialized nations today, since exposures are far lower than in past decades, and the effects of long latency disorders are much more slowly progressive.

Occupational asthma is characterized by variable air flow obstruction associated with certain types of workplace exposures. This condition can be caused not only by materials known to produce a classical allergic response, but by simple chemicals for which sensitization is more difficult to determine. For some causes an atopic (classically allergic) predisposition constitutes a risk factor for developing sensitization to the workplace allergen. This risk is quantifiable, and again the question must be raised whether such individuals can or should be excluded from certain of these jobs. The biomedical investigator can provide the data quantifying risk; others must participate in the important social and economic decisions. Bronchial hyperresponsiveness may be a genetically determined factor leading to increased risk of developing occupational asthma, or may be acquired as the result of such an exposure prior to the onset of clinically overt asthma. Certainly this measurement may be useful both in pre-employment assessment in selected industries, as well as serial measurement for the earliest signs of variable air flow limitation. Finally, in regard to occupational asthma where immunologic methods can provide information on specific immunoreactivity, i.e., that a person has become sensitized to a workplace allergen, there may be reasons, even in an asymptomatic but sensitized individual, to first remove that person from further exposure to the sensitizing agent, and to then reduce exposures in order to prevent sensitization of others.

Industrial bronchitis has been recognized in certain dusty industries and is receiving some attention in other workplace conditions where irritant inhalants may be present, such as in the chemical industry. Since bronchitis is importantly causally associated with cigarette smoking, and is a common condition in the general population, the ascertainment of industrial bronchitis is difficult, and predictors of this condition are therefore not available. Bronchitis may be associated only with cough and expectoration, but produces disability and shortened life span if it causes progressive airways obstruction. The latter can be ascertained early by serial lung function measurements available to those responsible for monitoring occupational health, and must be considered when there is excess annual decline in pulmonary function parameters. Again, as has been demonstrated with smoking, intervention can be expected to reverse the accelerated decline in function.

In summary, it must be conceded that the “state of the art” in most areas of medicine, including lung diseases, does not often permit us to predict and quantify increased risk for developing work-related lung disorders. I have mentioned some exceptions. However, careful surveillance of respiratory health, using simple methods, in workers exposed to known or potentially hazardous inhalants, will often meet the objective of prevention of serious disease. Carcinogenesis may be the exception, with our present state of knowledge. In regard to the question of whether permissible workplace exposure standards can protect all workers, even those who ultimately prove to be susceptible, it is unlikely that this can be achieved, but we will come closer to this objective as we improve capability of identifying susceptible individuals and minimizing or preventing their exposure. In this regard we must be reminded that even susceptibility does not preclude dose-relatedness, and there may often be levels of exposure which can be tolerated by individuals who are susceptible to a particular agent, a fact recently demonstrated in our studies of workers exposed to isocyanates. While this may be demonstrable for acute responses, such as asthma, it is much more difficult to assess in the short-term for chonic effects. This would become possible in the airways disorders if one could correlate the acute and chronic effects, a subject of considerable interest in cotton dust exposure. Whoever makes judgements concerning the acceptance or non-acceptance of various risks attendant upon occupational exposure, the judgements must be made on the basis of the best scientific information. It is the responsibility of groups like ours to provide accurate data and subsequent analyses on which public policy decisions can be made. There will always be an implicit, if not explicit, balancing of health effects and economic considerations. These judgements are best spread widely over seg. ments of society which have legitimate concern. Risk assessment will lead to rational prioritizing of our limited resources.

Mr. GORE. Thank you very much.

Mr. Samuels, welcome. And without objection, your entire text will be put in the record. We invite you to present any or all of it as you see fit.

STATEMENT OF SHELDON SAMUELS, DIRECTOR, HEALTH,

SAFETY, AND ENVIRONMENT INDUSTRIAL UNION DEPARTMENT, AFL-CIO, ON BEHALF OF HOWARD D. SAMUEL, PRESI. DENT OF THE DEPARTMENT

Mr. SAMUELS. Thank you, Mr. Gore and Mr. Walker. Let me thank you and your staff for putting light on what potentially poses the most difficult problem workers will have to face in the coming decade.

The genetic factor in occupationally related disease is one factor in a broader system of disease explanation. The system is useful if it bears fruit in prevention or intervention of disease development. There is nothing about such a system that demands that we characterize it as "The Truth” or “The Cause.” The system is simply a scientific model that either is or is not heuristic.

The model finds expression, whether in blood enzyme or anatomical differences, in the gene as a physiological agent, but “primarily," noted Sewall Wright, as a mere “hypothetical entity postulated to make sense out of the results of breeding experiments."

Because of the power of the genetic factor, partly a function of historical visibility, there is a rising tendency to isolate and favor it, especially since some of the other cofactors in the system of disease explanation-personal habits, lifestyle, diet, community environment-are wearing out their propagandic usefulness. For some, there is a need for new fads to rationalize the continuing tragedy in which the workplace is permitted-indeed, designed to uniquely and unnecessarily contribute to death and sickness. Placing the genetic factor in a socially and individually meaningful context at this stage in the management of risk and high risk populations is still possible, but not without congressional action.

There has been a long-held and strong consensus among scientists that the final expression of any gene depends upon the complex end results of physico-chemical reactions started by the gene and other factors. The reactions can be influenced by the internal and external environments of the organism and by other genes. Differences in environment result in marked differences in the expression of genes. Indeed, many geneticists hold that no statement about genetic differences has meaning unless the environment in which the gene manifests itself is specified.

If we understand the way in which a gene operates to exert its effects, we may be able-by monitoring genetic change and by controlling conditions-to limit the effect of the gene to some particular—or even no-effect.

Clearly, given this understanding, significant new tools can be developed in our struggle to control the environments created by man to prevent disease or to intervene when environmentally induced damage has already occurred.

A barrier to this understanding is the failure to understand concurrently that organisms are not pieces of putty, infinitely moldable by infinitestimal degrees in any direction, but are, rather, complex and resilient structures.

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