Töres Theorell and Jeffrey V. Johnson
The scientific evidence suggesting that exposure to job stress increases the risk for cardiovascular disease increased substantially beginning in the mid-1980s (Gardell 1981; Karasek and Theorell 1990; Johnson and Johansson 1991). Cardiovascular disease (CVD) remains the number one cause of death in economically developed societies, and contributes to increasing medical care costs. Diseases of the cardiovascular system include coronary heart disease (CHD), hypertensive disease, cerebrovascular disease and other disorders of the heart and circulatory system.
Most manifestations of coronary heart disease are caused partly by narrowing of the coronary arteries due to atherosclerosis. Coronary atherosclerosis is known to be influenced by a number of individual factors including: family history, dietary intake of saturated fat, high blood pressure, cigarette smoking and physical exercise. Except for heredity, all these factors could be influenced by the work environment. A poor work environment may decrease the willingness to stop smoking and adopt a healthy lifestyle. Thus, an adverse work environment could influence coronary heart disease via its effects on the classical risk factors.
There are also direct effects of stressful work environments on neurohormonal elevations as well as on heart metabolism. A combination of physiological mechanisms, shown to be related to stressful work activities, may increase the risk of myocardial infarction. The elevation of energy-mobilizing hormones, which increase during periods of excessive stress, may make the heart more vulnerable to the actual death of the muscle tissue. Conversely, energy-restoring and repairing hormones which protect the heart muscle from the adverse effects of energy-mobilizing hormones, decrease during periods of stress. During emotional (and physical) stress the heart beats faster and harder over an extended period of time, leading to excessive oxygen consumption in the heart muscle and the increased possibility of a heart attack. Stress may also disturb the cardiac rhythm of the heart. A disturbance associated with a fast heart rhythm is called tachyarrhythmia. When the heart rate is so fast that the heartbeat becomes inefficient a life-threatening ventricular fibrillation may result.
Early epidemiological studies of psychosocial working conditions associated with CVD suggested that high levels of work demands increased CHD risk. For example a prospective study of Belgian bank employees found that those in a privately owned bank had a significantly higher incidence of myocardial infarction than workers in public banks, even after adjustment was made for biomedical risk factors (Komitzer et al. 1982). This study indicated a possible relationship between work demands (which were higher in the private banks) and risk of myocardial infarction. Early studies also indicated a higher incidence of myocardial infarction among lower level employees in large companies (Pell and d’Alonzo 1963). This raised the possibility that psychosocial stress may not primarily be a problem for people with a high degree of responsibility, as had been assumed previously.
Since the early 1980s, many epidemiological studies have examined the specific hypothesis suggested by the Demand/ Control model developed by Karasek and others (Karasek and Theorell 1990; Johnson and Johansson 1991). This model states that job strain results from work organizations that combine high- performance demands with low levels of control over how the work is to be done. According to the model, work control can be understood as “job decision latitude”, or the task-related decision-making authority permitted by a given job or work organization. This model predicts that those workers who are exposed to high demand and low control over an extended period of time will have a higher risk of neurohormonal arousal which may result in adverse pathophysiological effects on the CVD system—which could eventually lead to increased risk of atherosclerotic heart disease and myocardial infarction.
Between 1981 and 1993, the majority of the 36 studies that examined the effects of high demands and low control on cardiovascular disease found significant and positive associations. These studies employed a variety of research designs and were performed in Sweden, Japan, the United States, Finland and Australia. A variety of outcomes was examined including CHD morbidity and mortality, as well as CHD risk factors including blood pressure, cigarette smoking, left ventricular mass index and CHD symptoms. Several recent review papers summarize these studies (Kristensen 1989; Baker et al. 1992; Schnall, Landsbergis and Baker 1994; Theorell and Karasek 1996). These reviewers note that the epidemiological quality of these studies is high and, moreover, that the stronger study designs have generally found greater support for the Demand/Control models. In general the adjustment for standard risk factors for cardiovascular disease does not eliminate nor significantly reduce the magnitude of the association between the high demand/low control combination and the risk of cardiovascular disease.
It is important to note, however, that the methodology in these studies varied considerably. The most important distinction is that some studies used the respondent’s own descriptions of their work situations, whereas others used an ‘average score’ method based on aggregating the responses of a nationally representative sample of workers within their respective job title groups. Studies utilizing self-reported work descriptions showed higher relative risks (2.0–4.0 versus 1.3–2.0). Psychological job demands were shown to be relatively more important in studies utilizing self-reported data than in studies utilizing aggregated data. The work control variables were more consistently found to be associated with excess CVD risk regardless of which exposure method was used.
Recently, work-related social support has been added to the demand-control formulation and workers with high demands, low control and low support, have been shown to have over a twofold risk for CVD morbidity and mortality compared to those with low demands, high control and high support (Johnson and Hall 1994). Currently efforts are being made to examine sustained exposure to demands, control and support over the course of the “psychosocial work career”. Descriptions of all the occupations during the whole work career are obtained for the participants and occupational scores are used for a calculation of the total lifetime exposure. The “total job control exposure” in relation to cardiovascular mortality incidence in working Swedes was studied and even after adjustment was made for age, smoking habits, exercise, ethnicity, education and social class, low total job control exposure was associated with a nearly twofold risk of dying a cardiovascular death over a 14-year follow-up period (Johnson et al. 1996).
A model similar to the Demand/Control model has been developed and tested by Siegrist and co-workers 1990 that uses “effort” and “social reward” as the crucial dimensions, the hypothesis being that high effort without social reward leads to increasing risk of cardiovascular disease. In a study of industrial workers it was shown that combinations of high effort and lack of reward predicted increased myocardial infarction risk independently of biomedical risk factors.
Other aspects of work organization, such as shift work, have also been shown to be associated with CVD risk. Constant rotation between night and day work has been found to be associated with increased risk of developing a myocardial infarction (Kristensen 1989; Theorell 1992).
Future research in this area particularly needs to focus on specifying the relationship between work stress exposure and CVD risk across different class, gender and ethnic groups.