Strategies for health promotion

PREVENTIVE

MEDICINE

15,

492-507

(1986)

Strategies

for Health Promotion

S.LEONARDSYME, Department

of Epidemiology,

School of Public Berkeley, California

PH.D. Health, 94720

University

of

California,

A key element in most efforts to prevent disease and promote health is behavioral change to lower risk. One-to-one programs to help people change their behavior are seriously limited because of the difficulty people have in making behavioral changes and because oneto-one programs do little to modify those forces in the community that continually produce new people at risk. In addition to one-to-one programs, therefore, environmental strategies for disease prevention are needed. Several clues regarding environmental interventions can be gleaned from the study of patterns of disease distributions. Not only are environmental approaches to prevention more efficient and practical than one-to-one programs, they also may shed new light on our understanding of disease etiology. 0 1986 Academic Press, Inc. INTRODUCTION

A key element in most programs directed toward the prevention of disease and the promotion of health is the identification of risk factors for disease. The rationale behind this is that individuals, once informed of their risk, will act in their own best interests to reduce that risk. While there can be no question that this is important in efforts to prevent disease, it is also necessary to be aware that this approach is only one very limited dimension of a prevention program. One reason why this approach is limited is that so many people find it difficult to change behavior, even when they are aware of their risk status; a second reason is that many diseases of concern today involve so many people that a one-to-one risk factor approach simply is not an efficient way to deal with the problem. As these limitations of one-to-one risk factor programs have been recognized, increasing interest has been paid to environmental approaches to prevention. The purpose of this article is to discuss in some detail the concept of environmental approaches to health promotion. The term environment is a very general one, of course, and it describes many different conditions and influences under which people live and develop. The term has been used to describe many phenomena including the air we breathe, the water we drink, the geographic regions and buildings in which we live, the groups to which we belong, and the climatic conditions we experience. In this article, particular attention will be given to the social environment. This limited focus is not meant to imply that other aspects of the environment are unimportant, but rather to emphasize that the social environment has received relatively less attention than other aspects of the environment. Even though the social, man-made, natural, and symbolic environments are interconnected, it is nevertheless useful on occasion to examine one component in more detail, espe492 0091-7435/86

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Copyright 0 1986 by Academic Press. Inc. All rights of reproduction in any form reserved.

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The way we behave as individuals affects both disease occurrence and treatment outcome. A wide variety of behaviors have been shown by research over the last 30 years to contribute to the etiology of many diseases and conditions (12, 20). As these behavioral risk factors have been identified, intervention programs have been developed to modify or eliminate them. The rationale for these intervention programs is that if a behavior increases the risk of disease, it should be changed to lower risk. In addition to changing old behaviors, many treatment and control programs require also that people begin for the first time to initiate new behaviors, such as taking medications, introducing substantial dietary changes, or beginning exercise programs. These behavioral approaches to disease contrast with activities that consist primarily of doing something “to” people. While some diseases and conditions can perhaps best be treated by injection, surgery, or other nonbehavioral interventions, most chronic diseases and conditions of concern today cannot. Noninfectious diseases-such as cancer, diseases of the cardiovascular system, cirrhosis, chronic respiratory disease, and injuries caused by accidents and other forms of violence-are caused, to a greater or lesser degree, by particular behaviors and, hopefully, can be prevented or treated by behavioral change. Even when direct, nonbehavioral interventions are possible, they often are not effective or efficient in the long run. Thus, while a dietary deficiency could perhaps be treated by long-term injection of missing nutrients, it is probably more useful to teach better eating habits to persons with such a deficiency. To ensure successful behavior change, we also must involve people as active partners rather than as passive recipients. Behavior modification is necessary to the treatment, control, and prevention of disease. In treatment, we ask that people recognize the need for medical help, that they seek such help in timely fashion, that they listen to advice given, and, finally, that they follow that advice. Without the cooperation of patients, treatment plans are of little value. With regard to the control of disease, treatment programs must be continued either permanently or, at least, for long periods of time. The prevention of disease similarly involves the active compliance and cooperation of people. People must become aware of health hazards associated with particular behaviors, they must accept that this information is personally relevant, and they must be willing to change that behavior in the interest of some future gain. While these concepts of behavior change are important and useful, it is important to recognize that encouraging individuals to change behavior can have only a very limited impact on the distribution of disease in the community. Two reasons for this limited impact are (a) the difficulty of getting people to maintain behavior changes over time, and (b) the prevalence of the diseases with which we are concerned.

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OF INDIVIDUALLY ORIENTED PREVENTION CHANGE BEHAVIOR

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The Difjculty of Changing Behavior Much of the emphasis on individual behavior, individual risk factors, and behavior change is based on the implicit assumption that it is easier to change individual behaviors than it is to change the community or environment. In fact, it has proven to be extraordinarily difficult to bring about these behavior changes, and it is even more diflicult to maintain those changes once achieved. This difficulty is dramatically illustrated by behavior changes observed in the Multiple Risk Factor Intervention Trial (MRFIT) (31). This trial was the most ambitious effort ever organized to test the hypothesis that mortality rates from coronary heart disease (CHD) could be reduced if people changed their behavior. After 7 years of follow-up, disappointingly few people had made and maintained these recommended changes. These findings are of particular importance because this trial contained all the elements one would desire in an intervention program, and for this reason, one would have anticipated better results than were in fact achieved. Three special features of the trial are of special importance: First, the 6,428 men randomized to the special intervention (SI) group had been carefully and clearly informed of the fact that they were in the top 15% of risk for CHD. They knew also that their risk was due to high serum cholesterol levels, high blood pressure, and/or cigarette smoking. Indeed, before being selected for the trial, each man had agreed to change his eating and smoking behavior and to take antihypertensive medications if necessary. Thus, all of the men in the trial knew of their special risk and had volunteered to change behaviors to lower it. Second, an excellent intervention plan was devised to help people change their behavior. This plan was carefully developed to take account of individual circumstances, and it used a variety of approaches including group meetings, oneto-one counseling sessions, and opportunities to involve family members. Research findings from the behavioral literature were reviewed, and, wherever appropriate, successful strategies were included in the plan. Third, the staffing pattern at each of the 22 MRFIT clinics was designed to enable each participant to have close and continuing contact with well-trained professionals for the entire 7-year study period. In spite of these unique features, the behavior changes observed in MRFIT were of modest proportions (30). The best achievement was that in the SI group; 40% of smokers had stopped smoking at the end of the trial. Of those SI men with hypertension, 64% had achieved control by the fourth year. Only a 6.7% reduction was observed in serum cholesterol levels among SI participants. It should be noted that these results refer only to the men in the SI group and not to men receiving ordinary care [the usual care (UC) group]. The trial’s overall objective was to see if those in the SI would have a lower CHD mortality rate than those in the UC group. That the mortality results after 7 years of follow-up in MRFIT showed no statistically significant difference between the study groups (31) was due, in part, to the fact that many of the men in the UC group changed their behavior on their own. Indeed, they changed to such an extent that the contrast between the two groups was much smaller than had been anticipated. Why men

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in the UC group changed behavior on their own so dramatically is an important topic in its own right; for purposes of the present discussion, however, it is noteworthy that SI men changed much less than was hoped. In an ordinary study, the results achieved in the SI group would have been quite acceptable. In MRFIT, however, they were disappointing because this trial included so many of the elements needed for 100% success: an informed and highly motivated group of participants, a superb intervention plan, excellent staff in sufficient numbers, and enough time to bring about behavioral change. The less-than-loo% success is disappointing because these results are probably the best we can hope to achieve in one-to-one programs; it would be hard to imagine a situation better suited to complete success. Two lessons can be drawn from this experience: (a) we Carl achieve some success in one-to-one efforts, but (b) even under the best circumstances, results cannot be perfect or even close to perfection. Although many different factors need to be considered in helping people to change their behavior and maintain these changes over time, one factor rarely considered is that of environment. It may not be surprising that people find it difficult to maintain behavior changes when many forces in the social, cultural, and physical environment conspire against such change. A classic example of this problem is provided by reference to cigarette smoking. The argument against smoking is overwhelming. First, the health consequences of smoking are clear, and no serious question exists about this: smoking increases the risk of many diseases, and there is evidence that smoking cessation lowers that risk (1). Second, there is some evidence that “passive smoking” also may be harmful to health (7, 8, 14). Third, the economic burden imposed on all of us because of smoking is great, due to the higher cost of absenteeism and lower productivity among smokers and costs of accidents and fire (53, 54). Finally, the majority of smokers want to quit, and most wish there was a simple and painless way to do so (52).

In spite of this evidence that smoking is undesirable behavior, and in spite of the recent decline in smoking prevalence in some countries, a very substantial number of people still smoke a large quantity of cigarettes (50). The record of smoking cessation programs is modest, with an average of about 25% of participants still off cigarettes at the end of 1 year (35, 42, 43). One of the major problems of these cessation programs (and of trials like the MRFIT) is that we have viewed risk behaviors almost exclusively as a problem of the individual: Virtually all smoking cessation programs have been directed only at the individual smoker (22). While it is true that only individuals can begin and quit smoking, a wide variety of environmental factors influence smoking behavior (8). These factors include cultural themes associated with smoking, such as relaxation, adulthood, sexual attractiveness, and emancipation; the socioeconomic structure of tobacco production, processing, distribution, and legislation; explicit and continual advertising by the smoking industry depicting values that favor smoking; subtle advertising by recording, TV, and movie stars; and the influence of siblings, peers, and other significant persons. In addition, cigarettes are almost always easily accessible and available to everyone. Unless these components are

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considered in smoking cessation programs, we ignore an environment that implicitly and explicitly encourages people to start and continue smoking (44). The problems associated with cigarette smoking cessation are similar to those involved in changing many other unhealthful behaviors. If behavior change programs are to be developed to prevent disease, more attention will need to be given not only to the behavior and risk profiles of individuals, but also to the environmental context within which people live. The Prevalence of Diseases in the Community The second reason for the consideration of environmental factors in efforts to prevent disease is based on the sheer prevalence of many of the diseases with which we are concerned (including CHD, cancer of various sites, arthritis, mental illness, diabetes, and stroke). Consider, for example, the case of CHD, a disease of substantial prevalence in all of the developed nations of the world. In the United States, approximately 7 million people have one form or another of atherosclerotic disease (49). If a permanent cure were available for this disease that was 100% effective (with no relapses) requiring 12 hr of physician time per patient during a l-year period, the treatment of these 7 million patients would require 28% of available physician time during that year. This estimate assumes that of the 390,000 professionally active physicians in the United States (49), only 150,000 would likely treat heart disease (removing from consideration such physicians as pediatricians, dermatologists, surgeons, anethesiologists, pathologists, radiologists, and psychiatrists), and it assumes that all physicians who do treat heart disease would do so 40 hr each week, 50 weeks a year. While the cost of this program in terms of physician time is relatively high, it nevertheless would be acceptable except for one problem: Enormous numbers of new people would continue to develop heart disease for the first time, since the treatment program would do nothing to deal with people “at risk” for becoming ill. If these at-risk people were included in the treatment program, and if each of these people required 6 hr of physician time in a year, this expanded program would require 91% of available physician time. This figure is based on the fact that about 40% of people over the age of 30 in the United States (about 45 million people) are estimated to be at risk for heart disease because of high blood pressure, high serum cholesterol, high blood glucose, excess body weight, cigarette smoking, and so on. Even the higher cost of this expanded program might be considered acceptable, since it could achieve a permanent and completely effective cure for a major disease. It must be noted, however, that while this program virtually exhausts all available physician resources, it does not solve the problem because it has not dealt with those forces in the community that brought about the problem in the first place: About 1% of healthy people over the age of 30 in the United States (about 1,130,OOO people) are expected to become part of the at-risk population for the first time each year because they start smoking, become overweight, or develop elevated levels of some other risk factor. While a one-to-one approach to diseases of great prevalence clearly is of value to patients, families, and friends, it does little to alter the distribution of disease in

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the population because new people develop disease even as sick people are cured and because new people enter the “at risk” population as others leave it. Thus, an individual approach exhausts substantial medical-care resources but does little to address those environmental factors that have initiated the problem. In this circumstance, an environmental approach to prevention clearly is needed and is likely to be more efficient than a one-to-one approach. IDENTIFICATION

OF ENVIRONMENTAL

RISK FACTORS

In thinking about environmental approaches to disease prevention, it is important to have knowledge about those environmental risk factors that might be intervened upon. While this issue has not received much research attention, some clues exist from available data that merit our attention. These clues derive from the fact that groups often have a characteristic pattern of disease over time even though individuals come and go from these groups. If groups have different rates over time, there may be something about the group that either promotes or discourages disease among individuals in those groups. The research that has been done on this problem has been directed toward the identification of environmental risk factors in the hope that environmental interventions might be developed to prevent or control disease. The search for causes in the environment is especially important because we have not been completely successful in pinpointing the causes of disease using conventional, individually oriented, epidemiologic models. For example, longterm community studies in the United States among several thousand middleaged people have clearly demonstrated that high serum cholesterol, high blood pressure, and cigarette smoking are important risk factors for the development of CHD (37). After adjustment for age, men with all three of these risk factors have over six times the chance of developing a first major coronary attack compared with men having none of these risk factors; the relative risks for people having one or two of these risk factors (compared with men with none) are 2.4 and 4.5, respectively (IS). On the other hand, only 14% of people with all three of these risk factors actually developed CHD during 10 years of observation in these community studies (25); 86% did not have a coronary event. Of people with one or two risk factors, only 5 and 9%, respectively, had an event in the lo-year study period. Thus, even though these three risk factors clearly are associated with an increased relative risk of disease, few people with the risk factors actually developed disease. Looked at another way, of all the people who developed CHD in these community studies over the lo-year follow-up period, only 17% had all three risk factors, and only 58% had two or more risk factors. Therefore, many people develop CHD for reasons not entirely explainable by the risk factors. While this observation should not lead to reduced emphasis on the importance of these risk factors, it does suggest that other factors also may be involved in CHD etiology. This circumstance is similar for most other noninfectious diseases, as well. And, of all the risk factors to be considered, the role of the environment must be of major importance. That environmental factors might be involved in the etiology of a broad range

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of diseases has been forcefully suggested both by McKeown (26) and by McKinlay and McKinlay (27). These scholars have concluded that the dramatic decline since 1900 in overall mortality in both Britain and the United States cannot be explained by the introduction and use of medical interventions. Indeed, many medical measures against disease (both chemotherapeutic and prophylactic) were introduced only several decades after a marked decline in mortality from those diseases had already taken place. McKinlay and McKinlay cite five diseases that, in their view, did benefit from medical intervention: influenza, pneumonia, diphtheria, whooping cough, and poliomyelitis. They note, however, that even if all of the declines in these diseases were attributable to medical measures, at best they account for only 3.5% of the total decline in mortality. In assessing these statistics, McKeown has argued that most of the decline in mortality since the second half of the 19th century was primarily due to improvements in hygiene and to rising standards of living, especially improved nutrition. As Rosen (39) has noted, this emphasis on the importance of environmental factors in the etiology and control of diseases has a long history, especially in reference to the study of infectious diseases. Rosen points out that in the 19th century in Germany, Virchow, Neumann, and Lebuscher all recognized the importance of social and environmental factors in the etiology of disease, and all believed that preventive efforts should be aimed at those factors. Rosen also has described the role of Chadwick in England and of Shattuck, Sydenstricker, and Sigerist in the United States in emphasizing the importance of social components in disease prevention and control programs. In spite of this long concern with the environment in reference to infectious diseases, most work on the prevention, treatment, and control of noninfectious diseases has focused, in one way or another, on the individual. As a consequence, while we may make mention of the importance of an environmental perspective for noninfectious diseases, we have very little specific or precise information about how the environment affects the incidence, severity, and persistence of the diseases and even less about how they can be prevented by environmental interventions. The first modern argument for the inclusion of social factors in environmental studies of disease etiology was offered by Emile Durkheim in his classic research on suicide. Durkheim’s book, Le Suicide, was published in France in 1897, although it was not translated into English until 1951 (9). This work is among the very first examples of the systematic and organized use of statistical methods to further the sociocultural investigation of disease. In this research, Durkheim noted that while suicide is one of the most individualistic acts imaginable, it can be understood only in terms of the social setting within which it takes place. At the time Durkheim wrote, it was known that suicide varied among different groups and among different time periods. Suicide rates were higher for Protestants than for Catholics, higher for the unmarried than for the married, higher for soldiers than for civilians, higher for noncommissioned officers than for enlisted men, higher in times of peace than in times of war and revolution, and higher in times of both prosperity and recession than in times of economic stability. Durkheim acknowledged that there were many different individual reasons for committing suicide (e.g., economic problems, sickness, personal failure); he

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pointed out, however, that suicide rates are patterned and consistent over time among social groups even though individuals come and go. To explain this difference in group rates, Durkheim argued, one must refer to social factors. He reasoned that if different groups have different suicide rates, there must be something about the social organization of the groups that encourages or deters individuals from suicide. Durkheim’s research led him to conclude that the major factor affecting suicide rates was the degree of social integration of groups. He suggested that the extent to which the individual was integrated into group life determined whether he would be motivated to commit suicide. In addition to Durkheim’s substantive contribution regarding suicide, however, is the important epidemiological observation that systematic, patterned differences in disease rates among groups must be explainable in group terms. This idea continues to be the major rationale for research on social factors in disease etiology today. Many patterned differences in disease rates exist, but few have been studied carefully and little is known about the reason for their consistency. Three factors that exhibit such characteristics disease patterns, for example, are socioeconomic status, marital status, and gender. Socioeconomic Status One of the most persistent disease patterns observd in public health research is that people in the lowest socioeconomic groups have the highest rates of morbidity and mortality. In a comprehensive review of 30 studies on this topic, Antonovsky noted the consistency of this finding dating from the 12th century (2). Further, this differential has been observed in many places in the world, regardless of whether the dominant diseases causing death and disability were attributed to infectious or noninfectious causes and regardless of the specific methods used to assess socioeconomic status (SES) (45). In a massive nationwide survey of mortality in the United States, Kitagawa and Hauser (18) found that mortality rates varied dramatically among socioeconomic groups for both men and women, whether SES was studied in terms of education, income, or occupation: the lower the socioeconomic level, the higher the death rate. In addition, these researchers found that those in lower socioeconomic groups had higher death rates for every cause of death except, among women, cancer of the breast and motor vehicle accidents. Higher rates of morbidity also have been observed among those in lower socioeconomic groups. These higher morbidity rates include virtually every disease, as well as mental illnesses and conditions such as schizophrenia, depression, unhappiness, worry, anxiety, and hopelessness (45). These higher rates of morbidity and mortality cannot simply be attributed to poverty. The lower ranks of many of the hierarchies studied have included people earning relatively substantial incomes; in spite of this relative affluence, the disease rates of these people nevertheless are higher than the rates of those above them in status. For example, Marmot and colleagues (24) have shown in the United Kingdom that those in top administrative civil service positions have the lowest CHD rate and that this rate increases progressively as one descends the civil service hierarchy. Similarly, Lee and Schneider (21) have observed that

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those in top management positions have the lowest blood pressures and that blood pressures rise progressively as one moves down the occupational ladder. The question, then, is not simply one of explaining why poor people have higher rates of disease but why even those fairly high in a rank ordering system have higher disease rates than those above them. Many possible explanations for this phenomenon have been studied, including inadequate medical care, unemployment, low income, racial factors, poor nutrition, poor housing, and poor education. While some of these explanations perhaps account for the excess of disease in the very lowest socioeconomic levels, they do not account for the fact that disease rates progressively increase from the highest to the lowest ranks of the socioeconomic hierarchy. Nor do these explanations easily account for the fact that so many different diseases and conditions of all organ systems are ranked in this way. An important study recently conducted by Haan and colleagues (10) provides an example of the difficulty we have in explaining socioeconomic differentials in disease incidence in a simple or straightforward way. These investigators compared death rates among persons living in defined poverty and nonpoverty areas in Oakland, California, from 1965 to 1974. As might be expected, persons living in poverty areas had death rates 50% higher than those living in nonpoverty areas. A long list of factors that might have explained this rate difference was examined, but none could account for it. Thus, after the effects of income, lack of medical care, unemployment, race and ethnicity, health practices, and such psychological factors as depression and personal uncertainty were removed, rates in the poverty area were still 50% higher than in the nonpoverty area. The explanation for these findings is not clear. It is possible that the measurement of such factors as income and medical care was not sufficiently accurate in this study or, as Haan and associates note, other as yet unidentified factors are involved (such as quality of the social or physical environment and higher levels of social stressors). It is surprising that one of the most persistent and pervasive observations in public health remains so little understood. One of the reasons for this may be that SES so powerfully influences disease rates that most researchers statistically remove it from analysis so that other factors can be studied without its overwhelming influence. In consequence, the role of SES itself often remains unexamined. The studies by Haan and colleagues (10) and by Marmot and colleagues (24) stand out as important first steps in clarifying the meaning of these socioeconomic differentials. Marital

Status

It has been known for many years that people who are not married-whether single, separated, widowed, or divorced-have higher mortality rates than married people (4, 33, 46). These rate differences cannot be explained by an increase in any one cause of death. Ortmeyer (33), using U.S. national data, has reported that divorced and single white men have higher mortality rates for virtually every major cause of death (except leukemia for divorced men, and genital cancer for single men). Similarly, divorced and single white women, compared with those who are married, have higher death rates for almost all causes of death. While

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these differences conceivably could be accounted for by socioeconomic factors, three studies have now shown that the effect of marital status is independent of SES (13, 19, 46). In an effort to account for the fact that single, widowed, and divorced persons have more disease than married persons, Weiss (51) compared these groups in terms of a variety of disease risk factors. Using data from the U.S. Health Examination Survey, he studied a sample of 6,672 adults with and without CHD and found that after such risk factors as serum cholesterol, obesity, and systolic and diastolic blood pressure were accounted for, the observed disease differences among the various marital statuses were not diminished. Considerable attention is now being given to this issue, and especially to the effect of different types of work on women in differing marital circumstances and to the way in which these relationships are affected by variations in SES. At the moment, however, the effect of marital status on health remains largely unexplained. Gender

One of the most well-established facts among students of health and disease is that men have higher mortality rates than women (55). In 1980 in the United States, men had an age-adjusted death rate 80% higher than women, and, as would be expected, women live about 7.5 years longer than men. This excess of male deaths occurs for every age and major cause of death for which comparison is possible. The largest male excess occurs for suicide and homicide (age-adjusted ratios of 3.33 and 3.86, respectively) and the lowest for diabetes (age-adjusted ratio of 1.02). These patterns are generally similar in all of the developed nations of the world. Moreover, since 1900, the differential in mortality between the sexes has been increasing. Wingard (56, 57) examined two proposed explanations for this differential: a biological explanation that women are biologically more “fit” than men and a social or lifestyle explanation that men behave in ways more damaging to health. After a detailed review of such possible lifestyle explanations as marriage, parenthood, employment, hard-driving behavior, cigarette smoking, and physical activity, she concluded that none of these, singly or together, eliminated the sex differential in mortality. In fact, in one study, multivariate adjustments for all known risk factors actually increased the sex differential. Once again, then, a major factor known to influence rates of disease remains largely unexplained. These examples of patterned consistency of disease rates among socioeconomic, marital, and gender groups emphasize the importance of environmental factors in the study of disease etiology, and they illustrate also how little is known about these major issues. AN ENVIRONMENTAL

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The research to date on social factors leaves many questions unanswered. One explanation is that this area of research is still relatively new. Investigators have used different research designs in different populations, they have defined con-

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cepts in noncomparable ways, and they have used crude and imprecise assessment tools. These are problems typical of many new research fields, and they tend to be resolved in time as research experience accumulates. Nevertheless, it is interesting to note that in spite of these problems, the research that has been done in this area has yielded a remarkably consistent pattern of results. Another possible explanation for the uneven pattern of research findings concerning social factors is that an inappropriate disease classification system has been used. This problem was noted by Cassel (5) in his observation that a wide variety of disease outcomes was associated with similar circumstances. He cited the remarkably similar set of risk factors that characterize people who develop tuberculosis and schizophrenia, become alcoholics, and are victims of multiple accidents or commit suicide. Cassel pointed out that this phenomenon had generally escaped comment and, as a possible explanation, suggested that investigators usually are “concerned with only one clinical entity, so that features common to multiple disease manifestations have tended to be overlooked.” When researchers focus on one or another clinical entity, they are (consciously or unconsciously) adopting a clinical classification scheme that may be useful in clinical settings but that may not be as useful in studies of disease etiology. The clinician uses a scheme that has proven helpful in disease treatment and in making prognostic estimates for such diseases. However, when it is observed that several different clinical entities have one risk factor in common, it seems reasonable to consider alternative disease classifications that may unify these disparate clinical entities based on the features they have in common. This is not a new idea. Infectious disease epidemiologists have for many years grouped together different clinical entities based on their similarities in modes of transmission. Thus, different clinical conditions have been grouped together according to whether they were water-borne, air-borne, vector-borne, or foodborne. These environmental classifications may not be of direct value in the treatment of sick people, but they certainly are of value in identifying those aspects of the environment toward which interventions can be directed. A comparable set of environmental categories for noninfectious diseases does not exist. The reason for this is not clear, but it may be that diseases such as CHD, cancer, and arthritis often are viewed as being diseases “of the individual” and not as diseases influenced by environmental factors. As we have seen, the fact that so many diseases exhibit patterned consistencies in populations over time, even though individuals come and go from these populations, suggests that there may indeed by environmental factors associated with their occurrence. An illustration of this environmental perspective is provided by a research project we are conducting among bus drivers in San Francisco, California. Several previous studies have noted that bus drivers, compared with workers in other occupations, have a higher prevalence of hypertension, as well as diseases of the gastrointestinal tract and of the musculoskeletal system. These results have been obtained from studies in different transit systems, under different conditions, and in several countries (3, 11, 29, 32, 36). Based on these findings, it has been suggested that certain aspects of the bus drivers’ occupation may create an increased risk for disease among these workers.

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From a clinical viewpoint, it is valuable to identify drivers with disease in order to treat them. To help drivers, it also would be of value to teach them about better posture, more healthful eating habits, and alternative ways of dealing with job stress. However, from an environmental perspective to prevent disease, it would perhaps be more useful to identify characteristics of the job itself that are associated with increased disease risk in order to change them. In our study of bus drivers, we are monitoring such environmental factors as exposure to noise, vibration, and carbon monoxide fumes, but we also are paying particular attention to the drivers’ social environment (38). For example, in preliminary studies of bus drivers, the “tyranny of the schedule” has been forcefully brought to our attention. Drivers must keep to a specific schedule, but, in almost every instance, this schedule is arranged without realistic reference to actual road conditions and, in fact, cannot be met. From the instant the bus drivers sit in the bus, they are behind schedule. Further, they are continually reprimanded for being behind schedule. We also have been struck by the social isolation and loneliness of drivers. Most work a very long shift without much opportunity to talk to other people all day long. In spite of this long and lonely work day, many drivers do not immediately go home after work, but remain instead at the bus yard for 1 to 3 additional hours to “wind down.” By the time they do get home, it is very late and they usually go directly to bed. Many drivers with whom we have talked have indicated that they have very limited interactions with their spouses, children, or friends. In addition to loneliness, we have observed that driving a bus often provokes inappropriate coping responses. In particular, we have observed hostile and impatient behavior being stimulated and provoked in situations that involve limited personal control, unpredictability, deadlines, and tight schedules. If in this research we can identify characteristics of the job of bus driving that are associated with disease, we may be able to introduce interventions, not merely among bus drivers, but directly on those environmental factors associated with the job. For example, it may be that by changing the way in which schedules are arranged, the bus company will be able to earn more money than it loses because of reduced rates of absenteeism among drivers as well as lower rates of sickness, accidents, and in particular, turnover. In addition, rest stops might be located in or near central cities so that drivers would be more likely to meet other drivers from time to time instead of the current practice of locating rest stops at remote and lonely places on the outer edges of the city. Further, it certainly might be possible to arrange work schedules so that more time is available for drivers to be with their families and to participate in outside community activities. One of the most important things that also might be done would be to initiate a campaign to inform the public of the difficult circumstances faced by drivers. As the situation exists at present, bus drivers feel themselves to be the objects of considerable negative affect from passengers, car drivers, and the media, and they feel blamed for problems that are not of their making. In the case of bus drivers, a clinical focus on either hypertension, gastrointestinal diseases, or musculoskeletal disorders clearly is useful. However, from an environmental and preventive perspective, it might be more useful to group together these different diseases and conditions associated with a common work

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exposure, so they can be studied together as related phenomena. If this is not done, the circumstances they share in common will not likely be appreciated. Despite the usefulness of looking at groups of diseases in this way, almost all research on noninfectious disease is directed more or less exclusively toward one or another clinical entity. While this is understandable (not only because of the enormous influence of the clinical tradition but also because funding for research is so firmly focused on well-established and recognized clinical entities), it has serious consequences. One such consequence is that the power of our research is compromised: If a risk factor is associated with several diseases, and if we study it only with reference to one disease, its greater general importance is not likely to be appreciated and, in fact, may be missed entirely. While our work with bus drivers focuses on the work environment, thought also has been given by others to the impact of the built environment on health and well-being in general (23), to the facilitation of social support networks for the prevention and treatment of a variety of diseases (6), and to the strengthening of community and social ties for the health of poor, elderly people living in cheap hotels in the center of the city (28). We now are involved in the design of a community-wide program in a low-income area to change the social climate regarding cigarette smoking with the hope that the benefits of this program will extend beyond that specific behavioral outcome. The fact that one risk factor is associated with higher rates of many different diseases and conditions may, at first glance, seem biologically plausible. However, two models that might account for this phenomenon come to mind. One model postulates that the risk factor under study includes many diverse elements and that each of these elements separately influences the likelihood of different diseases. This often is the explanation offered to account for the higher rate of so many diseases associated with cigarette smoking. The second model suggests that environmental stressors act to depress the body’s defense systems so that people exposed to them are more vulnerable to a wide range of disease agents (16, 17,40, 47). In this model, the presence of such specific disease agents as viruses, bacteria, or air pollutants would not result in disease unless the person was vulnerable to them. For this reason, the presence of environmental stressors would predict the likelihood of people getting sick, but not what disease they got. This latter model is attractive because it would account for (a) the fact that several social risk factors are related to many different diseases (involving many organ systems), as well as (b) the fact that most well-recognized disease-specific risk factors are only modestly predictive of those diseases. CONCLUSION

This article has been concerned primarily with strategies for the prevention of disease and the promotion of health. It has been argued that while disease prevention can and should be encouraged in individually oriented programs, more attention now must be given to an environmental approach to prevention. The environmental perspective of disease presented here has several advantages: It can help us think about alternative disease classification systems, it is useful in

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thinking about disease etiology in innovative ways, and it is important for targeting intervention programs more effectively. Environmental approaches have a long history in public health and have been of great importance in the control of infectious diseases; they have been much less prominent with reference to noninfectious diseases. There are many reasons for this, but one important factor may be our reluctance to encourage environmental interventions for fear they may preempt individual freedom and choice by limiting options and by allowing the few to dictate to the many. In fact, environmental interventions can be seen in precisely the opposite way-as increasing freedom of choice and options. For example, teenagers can hardly be considered free agents when the tobacco industry puts enormous pressure on them to smoke. By being provided with structural alternatives, teenagers would have more options for making choices than are now possible. Similarly, when a food market has a wide selection of unhealthful foods prominently and attractively displayed at reduced prices (while healthful foods are more expensive and hidden on the bottom or top shelf), the consumer hardly has a full range of options easily available. The environmental pressures now in place often favor unhealthful interests; the introduction of healthful environmental changes can be seen as redressing this imbalance by providing people with greater freedom of choice among a broader range of alternatives. The importance of social factors in the etiology of many diseases is becoming increasingly clear even though much of the evidence currently available is still quite preliminary. In spite of the substantial methodologic problems involved in research on these factors, an increasingly large body of consistent findings is being developed. Whatever the uncertainties in the data now available, it is clear that careful attention should be given to the social environment in the development of any programs to prevent disease and promote health. To increase the effectiveness of these considerations, it is clear also that continued research on social factors must become an important priority in the development of effective strategies for health promotion. REFERENCES I. Adams, E. E. Mortality, in “Smoking and Health-A Report of the Surgeon General.” pp. l-l-1-35. U.S. DHEW, PHS. National Institutes of Health, Washington, D.C., 1979. 2. Antonovsky, A. Social class, life expectancy and overall mortality. Milhank Mem. Fund Q. 45, 31-73 (1967). 3. Berlinguer, G. “Maladies and Industrial Health of Public Transportation Workers” (Translation). U.S. Dept. of Transportation, UMTA-VA-06-0034-82-2, Washington, D.C., 1962. 4. Carter, H., and Click, P. C. “Marriage and Divorce: A Social and Economic Study.” Harvard Univ. Press, Cambridge, Mass., 1970. 5. Cassel, J. The contribution of the social environment to host resistance. Anzer. J. Epiderniol. 104, 107-123 (1976). 6. Cohen, S., and Syme, S. L. (Eds.). “Social Support and Health.” Academic Press. Orlando. Fla., 1985. 7. Colley. J. R. T., Holland, W. W., and Corkhill, R. T. Influence of passive smoking and parental phlegm on pneumonia and bronchitis in early childhood. L~nce( 2, 103 1- 1034 (1974). 8. Dekker, E. Youth culture and influences on the smoking behavior of young people, in “Smoking and Health. Proceedings of the Third World Conference,” pp. 381-392. U.S. DHEW, PHS. National Institutes of Health, Washington, D.C., 1975.

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