PREVENTIVE

MEDICINE

5,

106-121 (1976)

Behavioral

Issues in Prevention

of Cancer

BERNARD H. Fox Manager, Social Science Field Studies & Statistics Program, National Cancer Institute, Bethesda, Maryland 20014 AND

JOHN R. GOLDSMITH' Epidemiology Studies Laboratory, California State Department of Health, Berkeley, California 94704 At present, the most feasible way of preventing cancer is by reducing exposure to carcinogens. Conditions and behaviors having certain, likely, and possible association with increased risk are tabulated. Psychological characteristics as potential risk factors are reviewed, but the data are inconclusive. A classification of preventive measures is presented, as well as a model of secondary prevention needs and what agents can implement them. Some principles that might affect the policy of prevention are outlined. In occupational cancer, an example of slow progress toward major preventive activity is given by reviewing the history of reducing exposure to arsenic in industry. Three interactions are examined: company medical departments and government epidemiologists; regulations proposed by government agencies and company disclosure of hazards; and experimental vs epidemiologic scientists. The role of labor unions, while small up to this time, is increasing. Finally, the increase in and association among the following are described for uranium mining: knowledge about the amount and source of hazard, government inspection, sanctions, compensation claims, press articles, hazard “visibility,” and industry safetyimprovement actions. As the first group of items increases, the last one improves Safety. Coercion between organizations seems to be the most potent factor in safety improvement.

INTRODUCTION

Currently, both prevention of cancer (primary prevention) and removal or arrest of the disease once it has appeared (secondary prevention) are accomplished through behavior change in two major social entities, individuals and institutions. The latter include organizations such as industries, unions, government agencies, and public interest groups. Different kinds of carcinogenic exposure require different preventive approaches. For example, reduction of smoking is now primarily accomplished by convincing the individual to stop or not to begin, although some institutional and regulatory action is beginning to be taken. On the other hand, most industrial exposure to carcinogens is being reduced by institutional activity-regulations about manufacturing methods, exposure in the work space and different types of pollution control; and industry action associated with various influential events (see section below, Prevention of Occupational Cancer). Evidence about carcinogenesis (often a matter of dispute among industry, gov’ This paper is based on discussions held during a stay as environmental cancer epidemiologist at the Field Studies and Statistics Program, National Cancer Institute, Bethesda, Md. I06 Copyright @ 1976 by Academic Press. Inc. All rights of reproduction in any form reserved.

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ernment, and scientists) is required for action on specific preventive measures. Hearings that led to the recent ban on aldrin and dieldrin produced many variant views on the potential danger of these substances. More importantly, however, many variant views were expressed about the criteria that should govern a decision to ban a substance from widespread commercial use. We shall describe the evidence about carcinogenesis mentioned above in respect to behaviors and conditions associated with exposure rather than, as has been done in the past, in respect to cancer sites. With this as a factual basis, categorization and choice of preventive measures will be addressed. Because of the recent greatly increased interest in industrial carcinogenesis, we shall devote considerable space to this topic, focusing mostly on occupational carcinogenesis in workers, but also remarking on its effects on their families. Several reviews have described increased cancer risk by site of disease and have examined conditions associated with such risk that might account for it (21, 42, 51). Also, specific topics relating to preventive aspects of epidemiology have been reviewed briefly (1, 10, 11, 21, 39) and, from a program point of view, early detection of cancer and its precursors (47). If one assessesthese reviews, it is clear that different cancer sites are associated with different risk factors. Moreover, the latter require different preventive actions, which will yield different rates of cancer control for the various sites. BEHAVIORS AND CONDITIONS ASSOCIATED WITH INCREASED RISK OF CANCER

In many cases, not only is there a large variety of cancer-enhancing and -producing agents, but the conditions and behaviors that result in the person’s being at higher risk of cancer are also many and varied. Fox has classified the more important of the latter, with a few examples (10). Table 1 shows a version of his tabulation, combining conditions subject to both primary and secondary prevention, and omitting cancer site. Obviously the classifications are arbitrary, and obviously they overlap, yet they are convenient. The important conditions and behaviors associatedwith increased risk of cancer that affect many people have been included, but only examples have been given of a large number of less important conditions. Many conditions whose potential for affecting risk of cancer is unproven or in dispute have been included becauseof their importance if this potential were indeed proven. In that category, only those conditions in which primary prevention is possible have been named. For example, the keeping of sick birds is suspected of being associated with leukemia (6)-suspected because only a few studies, needing verification, have been done on the matter. Since behavioral science is the theme of the present forum, it is appropriate to review briefly psychological characteristics as possible precursors to cancer. Psychosis, especially schizophrenia, has been said to protect against cancer (38, 40). Evidence against such protection is stronger than evidence for it (13, 41). Life stress is suspected of increasing risk of cancer, although at unspecified sites, through mechanisms of hormonal disturbance, possibly leading to immunosuppression. A word should be said about two studies purporting to show no

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TABLE 1 CONDITIONS

THAT

HAVE BEEN ASSOCIATED

WITH

INCREASED

RISK OF CANCER“

Conditions A. What people are, or what happens to them personally 1. Psychological characteristics Life stresses Personality Knowledge Attitudes Mental illnessr 2. Physical characteristics Obesity Complexion, eye color Somatotype 3. Congenital and genetic traits Family history of cancer Age at menarched Age at menopause Presence of diseases associated with cancer Congenital deficiency or anomaly Blood group 4. Other diseases and pathology Villous polyps Kidney or bladder stones Skin keratoses Tissue dysplasia, e.g., cervix Trauma, irritation, deep bums, scars Some communicable diseases, e.g., schistosomiasis Leukoplakia 5. Demographic and social characteristics Husband’s occupation (See D. 2. below) Sex, age, socioeconomic level, marriage, race, religion, ethnicity, geographic location B. What people do to themselves 1. Habits Drinking Use of tobacco 2. Customs and cultural behavior Sun-cult Age of marriage Age at first birth Circumcision Sick pets Eating habits Mouth cleanliness (In women) eariy intercourse, many partners Delay in physican contact Health practices C. Diet 1. Natural components and lacks Amount eaten Fat, protein content

Range of confidenceb

4 4 14 I-4 4 2-l l-2 4 l-4 3 34 14 l-4 4 1 3 2 l-4 2-4 2-4 2-3

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TABLE I (continued) Vitamin or mineral deficiencies Specific carcinogens Salt, coffee, tea, spices, milk (protection against tannin) 2. Processing effects Refined food Lost bulk Preservatives and colorants Water purifiers Caffeine removers D. What is done to people 1. Environmental pollution Pesticides, herbicides Air pollution Water pollution Ionizing radiation Commercial products, e.g., spray can propellants, hair dye 2. Occupation Carcinogen known: X-ray, uranium, asbestos, chromates, polyvinyl arsenic, benz[a]pyrene, many organic compounds Carcinogen unknown 3. Iatrogenic effects Drugs X-ray therapy X-ray diagnosis Transplantation Errors in diagnosing precancerous and cancerous states

1-4 4 4 c 4 4 4 4

2-3 4 4 4 4 chloride, 1-2 2-t 2-4 2-4 4 l-2 2-4

0 Adapted from Fox (10). b Confidence that condition is associated with high risk of cancer in one or more sites. l-certain; 2-high to moderate; 3-moderate to low; 4-just a suspicion, based on either theoretical grounds or one or more studies with suspicious findings. All confidence ratings reflect personal opinion only. c Suspected of protection. Evidence against is stronger than evidence for protection. d It is possible that nutritional level or social conditions affect age at menarche, hence it may not be altogether genetic.

relationship between recent stressful events and presence of cancer (17, 45). Unfortunately, in both of these studies the control group contained patients with cancers at other sites. Moreover, since the proportion of such cases in the control group was not mentioned, the importance of this contamination is not known. There is, however, evidence both in rats (49) and in humans (14) that psychosomatic reaction to certain kinds of stress is dependent on local circumstances that do or do not allow them to anticipate or apparently control the stressful stimulus. If this is true about cancer, then on the basis of other evidence (27), one might hypothesize several things: (a) specific kinds of stress-responders would have different risks of cancer; (b) different types of cancer would be differently susceptible to initiating or promoting effects of stress; and (c) different studies would show different results when addressing the life-stress situation, depending on the attributes of the imposed stress and the site examined. All three of these hypotheses have been supported in animal studies (27). If the hypotheses were verified for humans one could seek out high-risk people by psychological tests and focus

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countermeasures on them. Here the attempt at behavior change could be individually targeted, and therefore more successful than if it were populationtargeted through the mass media. The individual, the physician, private agencies, government, and industry could all enter into such an effort. Even if verified, however, prospects for success under present social conditions would be rather tenuous and certainly long-term. People with different personalities have been said to be differentially prone to cancer (19). But both supportive (15) and controverting (36) reviews have appeared. The difftculty is that the studies have all been retrospective in principle; that is, cancer patients were chosen as cases and questions were asked about differences in personality between them and controls. Even when measures were taken long before the cancer (20), only in the necessary and important elimination of effect of cancer on test results are they superior to other retrospective studies. The definitive study, predicting cancer from personality, has not been done. It is, truly, a most difficult type of research (10). We are thus not yet able to prevent cancer by identifying persons with high-risk psychological characteristics. The successful prospective association of these characteristics and cancer, that is, the ability to identify presumptive susceptibles, must be shown first. Beyond the possible association of behavior, condition, and personal characteristics with increased risk of cancer, at least two things are missing from Table 1. For primary prevention, can we show which conditions associated with increased cancer risk are, in part, causes of that risk? Second, for both primary and secondary prevention, what types of countermeasures might prevent, remove or reduce the carcinogenic exposure, given that cause has been demonstrated? PREVENTIVE

MEASURES

Assuming that epidemiologic investigation has established partial or total causation, preventive measures are to be chosen and implemented. These fall into two general classes: changing the physical environment and changing the individual’s behavior. They include such diverse areas as incentives, regulations, and cultural patterns, and relate to several possible sources of change: the individual and his society, the physician, industry, government, and private agencies. One can set down the more important of the types of preventive measures, noting their relevance to primary or secondary prevention or both (Table 2). Choice of preventive measures is not straightforward, since each type of riskincreasing condition demands its own complex of countermeasures. Contrast, for example, two kinds of behavior changes: (a) some combination of measures that might cause a company to stop dissemination of waste products throughout the work space (union, government regulation, industry self-policing, media publicity, suits for damage) and (b), some combination that might increase consumption of roughage in food (education, physician advice, media information, activity of opinion molders in the community). The discussion SO far has not distinguished prevention of cancer by avoiding exposure to carcinogens from prophylaxis against cancer even in their presence. The main reason is that from our knowledge of current progress, the latter deals with activities now only in the early research stage+.g., vaccines against vir-

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TABLE 2 CLASSES OF PREVENTIVE ACTIOND

Preventive action

Change A.

P p, s P P p, s p, s p, s p, s P, s

p, s P, s P, s p, p, P, p,

s s s s

In physical environment

1. Change in laws or government regulations (a) Product regulation-food (additives, preparation, preservation); tobacco (composition, filters); other (e.g., hair dye, tear gas, if shown to be carcinogenic). (b) Work situation changes-substance enclosure, shielding, cleanliness, smoking, masking requirements; periodic precancer or early cancer screening. (c) Industrial regulation-manufacturing methods; release into air, water, or earth of wastes or by-products (d) Local environments-smoking or pollution in airplanes, movies, offices, government premises, homes (radiation emission requirements). (e) Medical regulations-screening controls, use of X-ray, use of carcinogens, required screening. 2. Institutional regulations (a) Self-regulation by industry (b) Rules by medical associations or hospitals (c) Insurance requirements (d) Union contract requirements B. In the individual’s behavior (by informing, changing attitudes) 1. By personal lay communication or behavior (friends, significant others, prestige or authority figures) 2. By mass media 3. By formal education (e.g., leading to improved practice of wearing masks in the work space) 4. By orienting local cultures to prevention 5. By changing the doctor’s behavior 6. By physician affecting the individual’s behavior 7. By specific incentives (e.g., insurance premium differences (50); money given to individual for being screened (7); saliva tests for smoking (9); damage suits (35)).

D P, relevant to primary prevention; S, relevant to secondary prevention.

uses, anti-oxidants and other substances (4, 48)--and hence cannot be applied in the field, in view of the requirement stated above that secure evidence must be present before widespread active prevention is undertaken. For some time to come, preventing cancer even in the presence of carcinogens will remain a challenge to research rather than a set of procedures that is ready for application. Activities aimed at reducing mortality from cancer by detection of localized cancers (secondary prevention) and of precursors are very promising and have already shown impressive payoff (44). We have amended Green’s schema (18) of factors affecting secondary prevention and have associated with each of the improvements suggested the agencies that could bring them about (Table 3). The potential payoff value of these changes has not been addressed, nor the weight of effort that should be applied to each. Value and weights depend, of course, not only on the probable successof the changes if applied, but upon the value of that

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success, the probability that they could be applied, that they would be implemented if one attempted to apply them, and the cost-financial, social, political-of applying them (8, 12, 31). Failure to evaluate the countermeasures tabulated in the beginning of this section and mistaken estimates of their worth have led to vast expenditure of money and effort that could better have been devoted to activities with greater ultimate payoff. Before dealing specifically with occupation as an area with high payoff potential, it will be of value to make several observations that might affect policy in cancer prevention. 1. Permanent changes are less costly, in the long run, than temporary changes or changes that affect only a single generation where there is turnover. For example, industrial changes affect all generations of workers, whether there is turnover or not. Anti-smoking education must be repeated in each school class and reinforced as the person grows older. Permanent changes in cultural pattern TABLE 3 RELATION OF IMPROVEMENTS IN SECONDARY PREVENTION TO AGENTS THAT CAN BRING THEM

ABOUT’

Improvement of predisposing factors

Improvement of enabling factors

Improvement of reinforcing factors

Provide knowledge about recognition of symptoms susceptibility seriousness curability Change attitudes shame relative worth of health vs. other life aspects cultural attitudes toward preventive health behavior Make available medical and related personnel medical facilities laws or rules requiring screening Improve medical skills physician attitudes toward prevention Adjust insurance coverage Provide a better system for dealing with patients in the medical environment, leading to better patient experience (e.g., in clinics) Results of previous tests on patient Doctor-patient relationship

a Adapted from Green (18).

x x x x

x x x x

x x x x

x x x x

x x x x

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x x

x x X

x x

x X

x x X

x x

x x X

x x

x x X

x

x X

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or outlook would have the efficiency of a permanent change since they would be built into the system. 2. While knowledge alone is not enough (26), one cannot expect any change at all among people without knowledge (28). It is important to assess the value of knowledge properly. 3. People forget and need to be re-educated and reminded. 4. Some cultures do not accept prevention as an objective on which they should spend much effort. 5. In secondary prevention, informing some persons at high risk may produce psychic damage greater than they would be willing to suffer even in the face of such risk. 6. A major positive incentive to action (e.g., antismoking ads on TV) is likely to be relatively more effective than removal of a minor incentive to the opposite action (TV cigarette ads). 7. The aggregate payoff is the ultimate criterion. A highly potent preventive measure acting on a few (e.g., 70% of 1,000 people affected) is less cost-effective than a less potent one acting on many (e.g., 10% of 10,000 people affected). 8. An epidemiologic finding does not necessarily mean that the preventive measure must be addressed to the variable itself (e.g., having children late in life or not at all increases breast cancer chances, but preventive measures could focus on the hormonal basis of such a finding, not early childbirth). 9. Preventive measures on closed systems (e.g., individual schools, companies, factories, communities, buildings, agencies) are more likely to be successful than preventive measures on open systems (e.g., societies, unspecified radio audiences, specific demographic groups). 10. The placebo effect can provide valuable information, even though it may involve mechanisms as yet undefined. But proof of its effectiveness is mandatory. 11. Certain epidemiologic suspicions about cause could lead to preventive action if verified, but have not because preliminary indications have not been followed up with definitive research. We desperately need verification of preliminary findings and confirmation of cause. Without them prevention in respect to suspected causes is itself suspect. In that case the cry for prevention in these areas is useless. PREVENTION

OF OCCUPATIONAL

CANCER

Prevention of occupationally caused or aggravated cancer, to the extent that it involves individuals interacting with groups, involves the perceptions, the analysis, and the behavior of persons interacting with groups. The present weaknesses in prevention of cancer of industrial origin lie not in the motivation and actions of individuals alone, but perhaps more in the attitudes, behavior, and responsibilities of groups. Thus, following, in part, principles of payoff suggested above, we are led to suggest an alteration in the strategy of prevention of occupational cancer to one which seeks to develop and strengthen group involvement, rather than placing the primary burden on individual workers, physicians, and technicians. Consider, as an initial example, industrial exposures to arsenic, long suspected to be a carcinogen (23). The medical director of a major metal refiner published an

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analysis of mortality experience of workers employed in an arsenic-producing smelter in the state of Washington (37). The analysis showed no excess of lung cancer but an epidemiologist at the Washington State Health Department was at the same time conducting an analysis of all the state’s death certificates by occupation. He found that there was an excess of lung cance.r mortality among smelter workers in that county (32). Shortly afterward, in connection with proposed regulations to be based on criteria promulgated by the National Institute of Occupational Safety and Health (NIOSH), two large chemical firms reported the cancer experience of their long-term arsenic exposed workers (2,33). The report of one firm was based on an analysis by university scientists, and workmen from both firms were found to show an excess of cancer. In a recent analysis of 20-year cancer mortality by county in the United States, two National Cancer Institute scientists reported (3) that in counties containing copper, lead, or zinc smelters, both males and females had excess rates of lung cancer, suggesting not only that there was a workplace cancer hazard, but one affecting the community as well. An industry association employed a research firm to study the mortality of past employees in the smelting industry (46). qmitting short-term employees, a slight excess cancer risk was found. In a major Swedish arsenic producing plant, a review of the mortality data shows that arsenical workers had somewhat elevated lung cancer rates (22). The medical director has discussed this with the workers and their union, but the findings have not been published. In carcinogenesis tests, there is no convincing proof that arsenic is carcinogenic to laboratory animals under experimental conditions (24). In this abbreviated review covering only the problem of identifying an occupational carcinogenic hazard, the following mix of the five classes of organizations and individuals mentioned above (with subclasses) is relevant: industrial firms and their medical directors, governmental epidemiologists and toxicologists, university scientists, governmental regulatory agencies, labor organizations, industry associations, and research firms. Such a brief analysis, regrettably, may not give a fully adequate account of the scientific problem or provide a qualitatively adequate or a specified quantitative guide, but that is not the purpose of our discussion. The recognition of arsenic as a cancer hazard has involved organizations with different motivations, competencies, and constituencies. An understanding of the interaction of such groups is necessary for the control of occupational cancer hazards. Case follow-ups and procedural modeling will be a natural and necessary follow-up to outcomes of such interactions, regardless of their consequences. Three types of organizational interaction are indicated in the account of the arsenic hazard. First is the difference in interpretation of cause-of-death data by a company medical director and by a governmental epidemiologist. We would like to know how often this occurs, and how to avoid erroneous interpretations, possibly through changes in motivation and competencies of the individuals and groups. It can be seen that the issue of motivation is a delicate one, to say nothing of competency. The second important interaction is one by which the proposed NIOSH criteria statement and the implied regulations led two major chemical firms to disclose data on the existence of a hazard, one based on analyses

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by its own staff, and one using university scientists. We will want to know whether the disclosure of still other hazards must await the regulatory threat. If so, how do we strengthen the validity of the disclosed information, its timeliness as far as prevention is concerned, and its acceptance and incorporation into preventive practice? (In the examples, the hazardous exposures reported by the two firms do not occur any longer, in contrast to the exposures to arsenic in the smelting industry.) In broader terms, what is the role of regulatory threat? Alternatively, under what circumstances can we expect or encourage industrial managers to identify cancer hazards and to report them in the absence of the prospect of regulation or the implied costs of compensation? If these circumstances are few or absent, what inferences can be drawn about the need for regulation and monitoring? A third important area of interaction is within the scientific community. Experimental scientists who have not been able to demonstrate carcinogenicity for arsenic in animals are reluctant to believe that it is an important carcinogen for humans. One of the strongest bases for suspicion of arsenical hazard was a study of smelter workers by Lee and Fraumeni (29) which could not exclude a role for the exposure to sulfur oxides that also occurs in smelters. A single epidemiological study could not isolate the role of arsenic, since epidemiologists approach a conclusion of causation differently from the experimental scientist, who is usually willing to draw conclusions from a single study. Almost always a group of epidemiological studies (and epidemiologists) is needed to draw together a critical mass of data for identification of a hazard. Behavioral science has little to say yet about how this is done, but could contribute to defining diverse criteria for action, motivation, and secure conclusions. A second aspect of the problem is the tendency not to analyze vital statistical data on the scale which is needed to detect a hazard. It was only with a large-scale analysis of all cancer mortality data for the years 1950-1969 that the excess community hazard in smelter counties was found. Can a county-based or other geographical cancer mortality monitoring program be developed to detect such problems earlier? The possibility of using cancer registries for this purpose was the topic of a recent meeting called by the International Agency for Research on Cancer, the U. S. National Cancer Institute, and the International Association of Cancer Registries. Such registries involve the cooperation of many groups and organizations, such as hospitals, pathologists, health care agencies and administrations, statisticians, and voluntary or other funding organizations. That implies a major social process, with many types of motivation and of secondary gain, and many types of intra-agency relationships to be worked out. The methods of accomplishing these things are less matters of science-even behavioral sciencethan practice and profiting from others’ experience. In this account, although possibly incomplete, the involvement of labor unions is not prominent, although they were informed about the problem in the Swedish smelter. Unions have been showing more interest in carcinogenic hazards recently, and have a great potential role in detecting and responding to occupational cancer threats. One of the problems of union leadership is to increase the level of interest of the rank-and-file union member. Often that becomes articulated only when the existence of hazard is already known, either formally through scientific

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or governmental publications, or informally from knowledge of occurrence of cancer in several members of a union local. Once hazard is detected, labor unions have been active in seeking adequate regulations, and protection or preventive measures for occupational cancer. The account of the Tyler, Texas, asbestos exposure problem (5) illustrates the important role of the labor union in forcing disclosure of the existence of a known cancer hazard problem and of the inadequacy of preventive programs. These disclosures led to the shutting down of the factory, although many problems remain. The Asbestos Insulation Workers Union, recognizing that high cancer rates among their own members required action (25), have supported a program of studies, development and application of preventive regulations, and an extensive educational effort having industry-wide implications, with “ripple” effects going out to detection and prevention of other cancer hazards. Another constructive example of union activity is the cooperative involvement of the United Rubber Workers Union and components of the rubber industry in the study and control of cancer and other occupational hazards in the industry (34). By placing contracts for a great deal of work to be done in two universities, the program is having a most constructive effect on training in occupational health, and in cancer prevention and detection. One task for the behavioral scientists is to attempt to describe the inhibitions and stimulations to active support for prevention of occupational cancer within unions and between unions and management. Sellivan and de Groot surveyed attitudes (43) toward health care among men employed at an asbestos mill where a dust problem was poorly controlled. The study was supported by the Industrial Union Department, A.F.LK.I.0. One finding was that 61.6% of the men did not have confidence in the company’s medical staff. Half the men surveyed reported they did not know enough about hazards on the job. About 85% said they take the precautions suggested to them. The men listed as a dangerous hazard the absence of a clean place to eat lunch or take a break (41%)-about half as often as dust was listed as a hazard (82%). The preceding analyses deal with detecting a hazard, and barely touch on the development of regulatory policies. The implementation of programs for reducing cancer hazards is the third major area in which behavioral science can make a useful contribution. A SOCIOLOGICAL

CASE STUDY OF CANCER HAZARD CONTROL URANIUM MINES

IN

An excellent and careful analysis of the 25year involvement of the Federal Government in regulation of radon exposure in the country’s uranium mines has just been published by Pearson (35). As early as 1947, the U. S. Atomic Energy Commission, after sampling several uranium mines, found radon concentrations comparable to those of central European mines from which high lung cancer rates were reported. In 1951, industrial hygiene engineers visited the principal mining companies and stressed the need for better ventilation in order to prevent cancer. No excess cancer in U. S. miners had yet been reported. Measurements of exposures and of health status of miners started between 1950and 1953. In 1958, four uranium miners died of lung cancer,

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but the excess was said not to be statistically significant; one miner and his family received compensation. By 1960it was reported that there was a significant excess of lung cancer in men with 3 or more years of uranium mining. From this year on, the ventilation costs began to increase as the exposures to radon declined. The year of maximum A. E. C. purchases of uranium was 1960. Regulatory standards were proposed in 1967 by the Secretary of Labor, with gradual reductions to one-third the 1967 standard by 1971. A dose-response relationship was established in 1965, and the confounding effect of smoking was excluded in the relationship. In 1%8 the National Academy of Sciences and the National Research Council reviewed the matter and recommended that uranium miners should not smoke and that radon exposures should be kept low. Pearson traced and documented the tendency to assume that, as was assumed for industrial injury, industrial disease is attributable to the industrial worker’s carelessness. She reported “Numerous respondents to interviews administered in 1973 persisted in stressing the importance of smoking, drinking, and eating habits of the uranium miner to explain his exceptionally high incidence of lung cancer.” As she pointed out, the worker-carelessness argument has a shaky basis in industrial injury, but industrial diseases, certainly including cancer, are generally caused by pollutants of which workers are, at first, altogether ignorant. The reduction of hazardous radiation in mines was in fact achieved by relentless inspection, costly penalties for violating mandatory standards imposed by governmental agencies, and the expenditure of funds to implement ventilation. As a result, radiation levels dropped and the health of the miner was protected. The sociological approach used by Pearson was based on a technique of problem recognition and problem solving starting with the model shown in Fig. 1. A sample of mines in Colorado was used to generate data on production, exposure, inspection, ventilation, and for the miners, lung cancer experience. Governmental concern was “measured” by the annual number of inspections and sanctions issued by governmental enforcement agencies to mine operators. “Measurements” of company concern were based on yearly expenditures for ventilation by the largest uranium mining companies in Colorado. A variable called by Pearson “Hazard Visibility” consisted of evidence of cancer deaths among uranium miners, a mounting tide of compensation claims filed by afflicted workers and their families, and a series of articles in the popular press depicting official neglect of the lung cancer risk. It is possible that the (unfounded) premise was adopted that working conditions in European mines were much less satisfactory than in “our” mines, and thus the reported effect of radon exposure on lung cancer in European mines was not sufficient to lead to effective “visibility” of the hazard. Such selective blindness was a costly mistake, as can be seen from the actual projection that in 6,000 Colorado residents who have ever mined uranium, 1,150 deaths during the years 1967-1985 would be attributable to uranium mining and associated exposures. Figure 2 shows the trend in hazard visibility and organizational concern. Taking into account national uranium needs and the scale and structure of the industry (involving the tendency for larger companies to dominate the production with the passage of years), Pearson used a set of procedures called “path analysis” to

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FIG. 1. Proposed model of the historical process by which a health hazard to uranium miners was solved. Based on Pearson (35).

show the time trend for the process of dealing with excess radiation hazards in uranium mines (Figure 3)“. Pearson’s analysis leads to the principle that prevention of lung cancer in uranium miners required coercion by one organization of another; in this example, governmental regulatory organizations needed to wield coercive power over mining companies. She notes . . . that the absence of union coercion probably caused the deterioration of the health picture of the uranium miner. It seems likely that if unions had overcome the practical and financial barriers that made the unionization of uranium workers uneconomical and difficult, they would have exercised the needed coercive force on management to achieve a healthy environment for miners sooner . . . as for the interests of the general public, the consumer and the unorganized worker, their hope lies in the independent advocacy actions of the enforcement

2iL Ill161412IO' Lb 6& 24

4,

FIG.

2. Trends in hazard visibility and organized concern. Based on Pearson (35).

* Path analysis refers to a set of procedures for ordering the relation among independent variables in a multivariate system and computing the numerical dependency of a dependent variable on one or more independent variables when these variables affect one another in both series and parallel paths. For example and discussion, see Goldsmith and Berglund (16) and Li (30).

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FIG. 3. Modified path model of the process of solving the hazard of excess radiation in mines. Based on Pearson (35).

agency which can coerce companies and unions whose actions threaten the public interest. Along with numerous other accounts, this study reiterates the urgent necessity for regulatory agencies that are uncompromisingly independent.

From this analysis, we can also conclude that the prevention of industrial cancer depends on an understanding of the role of organizations in demanding and requiring adequate preventive practices. In acquiring this understanding, the identification of processes, organizations, and the influence of one on the other is derivable from studies such as Pearson’s. We are aware of the parallelism of industry’s safety activity, and legal suits and intensity of regulatory requirements in other disease and injury programs; e.g., pollution control, EPA; air traffic accidents, FAA; hazardous radiation exposure, FDA and ERDA; and safety, potency, and efficacy of drugs, FDA. It is difficult to generalize about the complicated dynamics of the interaction of hazard-control by industry and hazard-related regulations in government, or the most valid and effective dimensions of involvement by the public, unions, and families. Among these dimensions are scientific as well as general knowledge, publicity, probability of legislative control, regulatory sanctions, attitude of workers, and quid-pro-quo views among management,unions, and government. Moreover, while coercion is needed in some industries, others are highly motivated toward prevention of disease and injury. Their motivations need to be studied as well as supported. REFERENCES I. Antonovsky, A., and Hartman, H. Delay in the detection of cancer: A review of the literature. Health Educ. Monogr. 2.98-128 (1974). 2. Baetjer, A. M., Lilienfeld, A. M., and Levin, M. L. “Cancer and occupational exposure to inorganic arsenic.” Abstracts of papers, XVIII International Congress on Occupational Health, 3. Blot, W. J., and Fraumeni, J. F. Arsenical air pollution and lung cancer. Lancet ii, 142-144(1975). 4. Bollag, W. Therapeutic effects of an aromatic retinoic acid analog on chemically induced skin papillomas and carcinomas of mice. Europ. J. Cancer 10, 731-737 (1974). 5. Brodeur, P. Annals of industry: Casualties of the workplace. The New Yorker, Oct. 29, NOV. 5, Nov. 12, Nov. 19, and Nov. 26, passim (1973). 6. Bross, I. D. J., Bertell, Sister Rosalie, and Gibson, R. Pets and adult leukemia. Amer. J. Pub. Heolrh 62, 1520-1531(1972). 7. Bryant, E. E., Kovar, M. G., and Miller.H. “A Study of Remuneration Upon Response in the Health and Nutrition Examination Survey.” Vital Health Statistics Series 2, No. 67, National

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