by Regis de Gaudemaris
Return to work after cardiac events is an especially delicate question for the clinician. The cardiologic caregiver must evaluate the full clinical picture, including symptoms and morphological and functional status, as well as address complex personal, psychological, social, economic, legal, and ethical issues. The importance of job characteristics is illustrated by the existing, albeit limited, longitudinal data showing that return to high-strain work is a significant independent predictor of mortality in young men post-myocardial infarction.
Practical information is provided for clinicians who may be called upon to evaluate and manage the workplace as a potential source of increased risk for cardiovascular disease (CVD). The possibilities and limitations of stress management programs focusing on the individual, as well as the need for complementary organizational job redesign approaches, are presented. We raise the question: could lowering of job strain be a specific therapeutic modality for workplace-related hypertension, and we view this in light of the efficacy of pharmacologic, as well as other individual-based approaches to managing elevated blood pressure. Guidelines for the clinician to help determine the effectiveness of work-based intervention trials focused upon CVD prevention and to define critical endpoints for various clinical groups, are discussed, together with some clinical-methodological caveats for interpretation of findings. Finally, an argument is presented that a public health perspective is needed to effectively tackle work-related CVD, with incorporation of the concept of “occupational sentinal health event” into the realm of cardiology. As the role and potential contribution of the clinician in this process become better defined, possibilities emerge for him or her to become a truly effective agent for change, in improving the work environment.
This chapter analyzes the overt and hidden economic costs of work-related cardiovascular diseases. Affected individuals and society at large, rather than employers, pay much of the costs. Economic interventions to motivate public health approaches to preventing CVD are explored.
A variety of legal and legislative measures have been employed to reduce employee exposure to workplace risk factors for cardiovascular disease. These include legislation (and accompanying regulations) and collective bargaining by labor unions and employers, both of which are designed to reduce exposure to workplace chemical, physical, ergonomic and psychosocial hazards. The costs of workers’ compensation for work-related cardiovascular disease may also provide an incentive to reduce workplace exposure to cardiovascular risk factors. The state of legislation (and regulations) in Europe, the United States and Japan is briefly reviewed. In addition, the use of workers’ compensation and collective bargaining as prevention strategies in the United States is discussed. These measures not only have the potential to reduce exposure to workplace cardiovascular risk factors but also can promote the development of a “heart healthy” work environment.
by Tage Kristensen
The author reviews and discusses several intervention studies with implications for CVD or CV risk. The studies address chemical exposures, work schedules and working hours, and psychosocial factors at work. Effective strategies for prevention of CVD at the workplace are based on intervention research and integrate prevention at different levels.
We argued in the introduction that to adequately address the CVD epidemic, there is a need for a social epidemiologic approach that focuses on the workplace. Here, we briefly review the empirical, theoretical, and biological evidence presented earlier to demonstrate “convergent” validation that the relationship between workplace stressors and CVD risk is causal. The empirical findings are consistent with and predicted by the theoretical models, and the linkage between them is demonstrated to be plausible via biological mechanisms and experimental research. We then elaborate on new strategies, presented in the latter part of this book, for enhanced prevention and clinical management, workplace interventions, and social policy to reduce the impact of CVD.
EMPIRICAL EVIDENCE OF WORKPLACE EFFECTS ON CVD
In Chapter 2, we presented a substantial body of findings concerning the impact of workplace psychosocial, chemical, and physical conditions on CVD. The most consistent evidence is provided by research on sources of psychosocial stress at work, which are also the most prevalent risk factors. The most highly studied of these is work with high psychological demands coupled with low decision latitude, i.e., job strain. On the basis of empirical reviews focused on men and on women, as well as the recent review by the European Heart Network, (34) and notwithstanding some studies with null results, the conclusion of Schnall, Landsbergis, and Baker that “a body of literature has accumulated that strongly suggests a causal association between job strain and cardiovascular disease” has been corroborated and strengthened. The data relating job strain to AmBP and decision latitude to CVD outcomes are particularly compelling.
Besides consistency of association among studies, other evidence supporting causality has emerged. There are now data, albeit limited, suggesting a dose-response relationship between exposure to job strain or its major dimension(s) and both CVD and BP. New job strain cohort studies further confirm that exposure precedes outcome in time. Overall, of ten such studies in men, six show an increased CVD risk due to job strain or its components, and an additional two provide mixed results. Of five cohort studies among women, four demonstrate an elevated CVD risk related to job strain or its components.
Epidemiologic evidence of the plausibility of the relationship between job strain and CVD has expanded. Cross-sectional, as well as some longitudinal data, linking exposure to job strain with elevated AmBP in men and women suggests one major mediating mechanism for this process. There are now cohort data demonstrating that a change in job strain exposure is associated with a change in BP.(58) Furthermore, some data suggests an association between job strain and/or its major dimensions and other CVD risk factors, primarily smoking intensity in men, and possibly increased coagulation tendencies.
The magnitude of association between job strain and CVD typically range from risk ratios (RR) of about 1.2-2.0 for studies using imputed job characteristics (with resulting nondifferential misclassification bias towards the null), to 1.3-4.0 for studies using self-reported job characteristics. Associations are more consistent and stronger among blue-collar workers, with RR as high as 10. Systolic BP at work (as measured with an ambulatory monitor) among employees facing job strain is typically 4-8 mmHg higher than among those without job strain.