Edited by Peter Schnall, Karen Belkic, Paul Landsbergis and Dean Baker
Published by Hanley & Belfus, Inc. Occup Med 15(1), 2000
1. Anders Knutsson, MD
Scand J Work Environ Health 2000;26(5):455
2. Hazards: April/June 2000
3. Norman M. Kaplan in Hypertension
WHY THE WORKPLACE AND CARDIOVASCULAR DISEASE? (1)
By Peter Schnall, MD, Karen Belkic, MD, PhD, Paul Landsbergis, PhD, Dean Baker, MD Reproduced with the permission of Hanley & Belfus, Inc., 210 South 13th Street, Philadelphia, PA, 19107. Phone: 215-546-7293.Web site: www.hanleyandbelfus.com
(1) Schnall PL, et al. Why the workplace and cardiovascular disease? In: Schnall PL, Belkic KL, Landsbergis PA,
Baker DB, eds: The Workplace and Cardiovascular Disease. Occup Med 15(1), 2000, pp 1-5.
Cardiovascular disease (CVD) is the major cause of morbidity and mortality in the industrialized world.* While there have been trends towards lowered rates of CVD mortality in North America and Western Europe, CVD still represents a significant public health problem – indeed, a pandemic. In the former Soviet Union and other eastern European countries, CVD morbidity and mortality have increased dramatically over the last 30 years.(7) Rising prevalence rates also have been observed in many developing countries. Thus, “it has been projected that CVD worldwide will climb from the second most common cause of death . . . in 1990, to first place, with more than 36% of all deaths in 2020.”(5)
In the U.S. alone, CVD is the cause of 41% of all deaths.(2) An estimated 250,000-350,000 people annually die suddenly of heart disease in the U.S.,(3,6,10,18,20,21) and at least the same number lose their lives more slowly due to manifest CVD from which they have chronically suffered.
The dominant focus of research and intervention in the medical community has been on individual traits, especially genetic susceptibility and risky behaviors (e.g., smoking, over-eating, sedentary lifestyle) as playing a primary role in the etiology of CVD. The underpinnings of this explanation of the CVD epidemic lie in the development of powerful engineering models. Modern advances in the physical sciences lend themselves particularly well to the study of the cardiovascular system. Namely, it has appeared that CVD could be characterized as a disturbance in hydraulic (hemodynamic) and/or electrical (electrophysiologic) function.(5) Coronary atherosclerosis (i.e., vascular obstruction) has been designated as the “prime mover” of cardiovascular disorders, such that a series of atherogenic risk factors were sought, and many were identified (e.g., hypercholesterolemia, hypertension, diabetes, obesity). According to this view, the CVD epidemic can be curtailed by: 1. better management of atherogenic risk factors, 2. use of available medical treatments and more technological advances, and 3. additional research into the molecular biology of atherogenic and other cardiodegenerative processes.
It is indisputable that this approach represents an invaluable advance in our battle against CVD. Millions of people have been protected by quitting smoking, eating a “heart-healthy” diet, and exercising. And countless patients with manifest coronary heart disease (CHD) have been saved by percutaneous transluminal coronary angioplasty and coronary artery by-pass surgery, not to mention the life-saving armamentarium of pharmacologic agents we now have at our disposal. Cardiac pacemakers and automatic implantable cardioverter defibrillators provide hope for a normal life to many patients suffering from life-threatening cardiac rhythm and conduction disturbances. Only 50 years ago, nearly all of these patients would have been doomed.
Despite the optimism engendered by these achievements, we believe that a closer look at the overall public health impact of this traditional medical approach to CVD is in order. While these methods of electrical and hemodynamic systems are highly sophisticated, the etiology and pathogenesis of CVD cannot be reduced to a series of disordered pumps and electrical circuits. Furthermore, the intimate connections between the social environment and the central nervous system (CNS), and the CNS and the cardiovascular system via the autonomic nervous system, compel one to look beyond the cardiovascular system in isolation to fully appreciate how CVD develops.
In point of fact, both our understanding of the etiology of CVD and our ability to manage the epidemic are still limited. For example, the Framingham Heart Study used epidemiologic techniques to identify important risk factors (smoking, diabetes, hypertension, and cholesterol). However, these traditional risk factors explained only part of the risk for CHD.11 In practical terms, this means that these standard risk factors fail to predict many of the new CHD cases. Note that one of these factors – essential hypertension – is of practically unknown etiology. Moreover, these traditional risk factors represent relatively “proximate” causes of CVD; each of them, in turn, has a complex set of determinants, many of which are of psychosocial origin.
New developments expand and challenge the focus on these traditional, proximate risk factors. One of these is the emergence of research into behavioral factors that might influence the development of CVD. A notable example has been the formulation of the concept of CVD-prone behavior – the Type A behavior pattern (TABP).(9) While initial study results from the Western Collaborate Group Study indicated that TABP was a strong independent predictor of CHD mortality,(24) subsequent research has failed to substantiate these findings.(22) More recently, hostility – a component of Type A behavior – has emerged as a possible risk factor for CVD.(30)
The importance of the TABP is not so much its contribution to the explanation of CVD, but its laying the groundwork for social psychology to examine the impact of the social and psychological environment on CVD. TABP was a stepping-stone to the investigation of the role of the workplace in CVD.
This formulation regarding TABP is complemented by a body of epidemiologic literature which documents the strong role of social experiences, beginning in childhood and extending through working life and beyond, in shaping human behavior. For example, recent research has demonstrated that characteristics of people’s jobs, such as high or low decision-making authority, are associated with the development of specific complex behaviors and personality attributes.(4,14-16,27)
Another development that has expanded traditional cardiovascular epidemiology has been the field of social epidemiology, which examines factors such as social networks, social support, and social class as potential causes or modifiers of disease processes.(8,17,23,28) For example, social epidemiologists have demonstrated that lower socioeconomic status is an important risk factor for CVD.(12,19) Nonetheless, even with the inclusion of these social and behavioral factors, there is still a large amount of unexplained variance in CVD, as well as in essential hypertension.
We wish to argue that to better understand the CVD epidemic, social epidemiology needs to incorporate, in a much more prominent manner, a heretofore relatively neglected realm of social life – the workplace. We briefly present the case of essential hypertension (EH) as an illustration of our argument. EH is a major risk factor not only for CHD, but also for left ventricular hypertrophy, stroke, renal disease, and many other major pathologic processes. This disease afflicts 60 million Americans and 600 million people worldwide. The identified risk factors (i.e., obesity, salt intake, genetics, age, alcohol intake) explain only a small part of the risk.
Occupational Medicine: State of the Art Reviews; Chapter 2: Research Findings Linking Workplace Factors to CVD Outcomes Authors: Paul Landsbergis, Kyle Steenland, Lawrence Fine, Karen Belkic, Peter Schnall, Dean Baker, Tores Theorell, Johannes Siegrist, Richard Peter, Robert Karasek, Michael Marmot, Chantal Brisson, Finn Tuchsen
A variety of workplace conditions have been implicated as risk factors for cardiovascular disease (CVD). These include shift work, long work hours, and chemical (e.g., carbon disulfide, nitrate esters, carbon monoxide, methylene chloride, solvents), physical (e.g., cold, heat, noise, passive smoking, sedentary work) and psychosocial conditions. The most consistent evidence is provided by sources of psychosocial stress at work. The evidence strongly suggests a causal association between job strain (a combination of high psychological demands and low job decision latitude, or low job control) and hypertension and CVD. Low decision latitude is also a risk factor for CVD. As yet limited but convincing evidence exists for a role of another psychosocial factor effort-reward imbalance (ERI) with similar observed effect sizes as job strain. In addition, threat-avoidant vigilant work (TAV) has been identified through studies of single occupations as a potentially helpful explanatory variable as to why groups such as professional drivers — whose work is characterized by high TAV, — have the most consistent evidence of elevated risk of CVD and hypertension.
Several theoretical models of workplace psychosocial stressors have been empirically validated, including the Demand-Control-Support (DCS) model and the Effort Reward Imbalance (ERI) model. The nature of these models –deeply rooted in social class relations–is explored in terms of their relationship to the organization of work. While gradations in degree of job strain (high demand, low control work) exist, the trend is for increasing demands with inadequate augmentation of control for more and more of the labor force. Demands are viewed in a broad context encompassing workload, time pressure, conflicts, requirements upon attentional resources, and the emotional dimensions of work-especially those involving threat avoidance–as well as long and unphysiologic work hours. In comparison to the DCS model with its emphasis on moment-to-moment control over the work process (i.e. decision latitude), the ERI model emphasizes macro-level rewards such as career opportunities, job security, esteem and income. The ERI model also integrates the exigencies and rewards of the job with the individual’s input and coping style. The insights provided by cognitive ergonomics and brain research complement the DCS and ERI models, and can be of practical use in efforts to humanize the labor process. The concept of total burden (risk) due to exposure to multiple occupational stressors is explored.
The concept of neurocardiology, introduced as an interdisciplinary area linking the neurosciences and cardiology, is expanded into a tripartite construct, which includes the environment as the potential stressor: “econeurocardiology”. Experimental animal studies provide empirical grounding for this construct; therein central stress mechanisms are implicated in cardiac electrical instability, as well as in hypertension, abnormalities of heart beat dynamics and atherogenesis. The defense response appears to play an important role in these processes, with the defeat reaction being activated in chronic stress, especially of a severe nature. In the worst case, both are operative: the defense-defeat response, activating the sympatho-adrenomedullary and hypophyseal-adrenocortical pathways, respectively. This appears to be a particularly deleterious combination for the cardiovascular system.
Workplace factors can impact upon many pathways leading to CVD, promoting underlying pathological processes, as well as triggering acute cardiac events. Neuroendocrine and autonomic mechanisms are the main mediators. Elevated catecholamines and cortisol have been demonstrated in relation to occupational stressors. Exposure to job strain has been directly linked to increased workplace ambulatory blood pressure (AmBP) and hypertension. The connection among chronic exposure to job strain, high workplace AmBP and increased left ventricular mass has also been empirically confirmed. Experimental data implicate stress mechanisms at several steps in the early and late stages of atherogenesis, with corroborative occupational epidemiologic evidence for some of these processes. Patterns consistent with the Cardiovascular Metabolic Syndrome have been reported in association with Effort-Reward Imbalance. In coronary patients laboratory mental stress can provoke myocardial ischemia, the biological determinants of which are frequently work-related. However, work-place field studies of myocardial ischemia are lacking. Stress mechanisms can also compromise cardiac electrical stability; several indicators of which can now be monitored during work. Circadian and septadian data suggest that workplace factors could precipitate myocardial infarction and sudden cardiac death at vulnerable time intervals in at-risk individuals.
An important empirical and methodologic issue is the determination whether it is primarily the objective characteristics of jobs or an individual’s subjective perception and evaluation of them (or some combination of these) that is most predictive of changes in blood pressure and the development of cvd. This chapter describes three main approaches for measurement of job characteristics: self-report questionnaires (e.g., Job Content Questionnaire, Effort-Reward Imbalance questionnaire, Occupational Stress Index); imputation of job characteristics scores based on aggregate data (e.g. national job title averages); and external assessment (e.g. supervisor or coworker ratings, job analysis by expert observers). Use of multiple methods of assessment of job characteristics allows for triangulation. We review important research results, highlight advantages and limitations of each method and discuss some issues to be resolved through future research. We recommend multi-method strategies, for convergent validation, using as many of these approaches as possible.
The obstacles and challenges of obtaining a cardiovascular disease history at the workplace are explored including the use and limitations of symptom data, the issue of false negatives and false positives, as well as the need for caution to avoid bias if symptoms are reported together with the self-report about exposure. A discussion of the various techniques of blood pressure (bp) measurement at the workplace is presented, including casual, self-measured, and ambulatory monitoring, their advantages and limitations, and their particular utility for the workplace. A new protocol for obtaining point estimates of bp at the worksite is outlined and its feasibility as an alternative to traditional measures of casual bp or ambulatory bp monitoring is assessed. In addition, other clinically-relevant endpoints which are sensitive, stress-mediated and measurable by ambulatory electrocardiographic monitoring are described.
Unlike several other branches of medicine, (e.g., pulmonology), primary cardiology has yet to fully develop a discipline of occupational cardiology. The authors outline an approach for including a focused occupational history in the CV work-up and present a graded, risk-stratified algorithm for occupational cardiologic assessment. This work-up can help clinicians make specific recommendations concerning working conditions, as these impact upon the patient’s CV status.