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A Proposal for an Agenda for Occupational Cardiology: How do we move from Epidemiological Evidence to Prevention-oriented Clinical Practice?

Karen Belkic and Peter Schnall


Epidemiological Evidence-Convergent Validation of the Role of Workplace Factors in the Etiology of Hypertension and IHD

There is a burgeoning body of empirical investigation concerning the role played by workplace factors in the risk of hypertension and of ischemic heart disease (IHD) morbidity and mortality. The epidemiological evidence is most abundant and convincing with respect to psychosocial factors, especially job strain or its major components: high psychological demands and low decision-making latitude, as reviewed in: Ref. (10, 18, 40, 68, 69, 118). The association between exposure to job strain and cardiovascular disease is particularly pronounced among those with lower occupational status (37,49b, 136). Consistent data are also found for work requiring intensive effort, but providing relatively few rewards (“effort-reward imbalance”) (10, 81, 124,141). Furthermore, the combined effects of exposure to job strain and to effort-reward imbalance appear to be much stronger than the separate effects of each model (96). Night shift work (17, 59, 61, 88), long work hours (38, 49a, 127), exposure to noise (22, 29, 72, 132), temperature extremes (77, 145), as well as chemicals such as carbon monoxide, lead and carbon disulfide (43, 45, 63, 89, 93), inter alia, are also implicated, on the basis of positive epidemiological studies, as possible risk factors for hypertension and/or IHD.

Certain occupational groups with exposure to a large number of workplace stressors are found to be at high risk for developing hypertension and IHD. Here the evidence is strongest with respect to professional drivers (9, 139, 148), whose work requires the maintenance of sustained vigilance, whereby an error or momentary lapse of attention can have serious, potentially fatal consequences (“threat-avoidant vigilant work”), and who face a heavy overall burden from potentially cardio-deleterious workplace factors (7). Rosengren, Anderson & Wilhelmsen (109) found that the increased risk of coronary heart disease was independent of standard risk factor status. After a mean of 11.8 years of prospective study, these authors reported an odds-ratio (OR) of 3.3 (95% Confidence Interval (CI)=2.0-5.5) for coronary heart disease among 103 middle-aged male mass transit drivers in Gothenberg with respect to 6596 men from other occupational groups. After accounting for age, serum cholesterol, blood pressure, smoking, body mass index, diabetes, positive parental history of CHD and physical activity, as well as socio-demographic factors, the risk decreased only slightly (OR=3.0, 95% CI=1.8-5.2).

Finally, epidemiological studies among working people reveal that systolic ambulatory blood pressure (AmBP) is on the average 5mmHg higher during the hours on the job compared to leisure time (33, 117, 120) and that mean 24-hour AmBP is lower on non-work days compared to work days (101, 102). There is also evidence of a septadian overrepresentation of acute cardiac events on Mondays (106, 147), and automatic implantable cardioverter-defibrillators are seen to fire significantly more on Mondays (97). These findings corroborate the statements of Lown (78) that “the stress of work after a weekend of respite may have been the precipitants of lethal arrhythmias” (p. I-188) and of Willich and colleagues (147) that “an increase in physical and mental burden from leisurely weekend activities to stressful work on Monday in the majority of working patients” could be causally related to the occurrence of acute MI (p.90).

In the above paragraphs, we have very briefly highlighted some of the key epidemiological data concerning the relation of workplace factors to hypertension and ischemic heart disease. This is a complex topic with numerous methodological challenges (42, 60, 67, 71, 86, 104, 112, 128), and there are some major longitudinal studies that report null findings, e.g. Ref. (44, 87, 94, 107). However, taken as a whole, the large body of empirical data confirms this relationship. Furthermore, the theoretical constructs of how workplace factors affect the development of hypertension and IHD (5, 54, 56, 75, 124, 135), together with a rich store of mediating biological mechanisms by which social factors such as work stress are perceived and processed by the central nervous system, and can lead to cardio-deleterious changes, as reviewed e.g. in Ref. (12, 13, 30, 35, 41, 64, 79, 99, 113, 121, 122, 129a, 137, 149), provide convergent validation for the conclusion that environmental stressors from the workplace play an important role in the development of cardiovascular disease (15). Please also see Occupational Medicine: State of the Art Reviews; Chapter 1. Why the Workplace and Cardiovascular Disease? , Chapter 14. The Workplace and Cardiovascular Health: Conclusions and Thoughts for a Future Agenda.

Current trends in working life: A Challenge for Cardiology

Reflecting the pressures of global competition, current trends in working life, are characterized by increasing job demands, longer working hours, and job instability (50, 70,105, 133). In 1996, 23% of employed Europeans worked more than 45 hours/week (142) and those working under time constraints increased markedly from 1977 to 1996 (27). In the U.S., the average number of hours worked per week rose by 3.5 hours from 1977 to 1997, being now 47.1 hours/week. Increased psychological work demands have also increased dramatically in the over this period (17a). Taking a longer historical view, these trends reflect the transformation in working life during the past century, away from agricultural work and relatively autonomous craftwork towards machine-based labor, as is characteristic of e.g. mass production. In particular, the growing dependence upon computer technology, while potentially offering the chance to improve working life (54) has de facto lead to greater workload and pressure for increased productivity, together with other untoward consequences (125).

There is also a widening income gap among occupational strata, which appears to place those in the low socio-economic sectors at greatest vulnerability with respect to cardiovascular disease. Drever, Whitehead and Roden (24) have demonstrated a dramatically increased social class gradient in ischemic heart disease in England and Wales from 1970 to the early 1990’s. According to Marmot (84), “the evidence from the Whitehall and Whitehall II studies is that …lifestyle factors may account for some, but by no means all, of the social gradient in CVD…Among non-smokers the social gradient in CHD incidence and mortality was similar to the gradient in smokers. In Whitehall II, low control in the workplace was related to CHD incidence and accounted for about half of the social gradient” (p.47-48).

These trends suggest that work-related hypertension and IHD will become an increasingly important problem in the years to come. The clinician is often called upon to judge the cardiovascular work fitness of patients. Given the rising prevalence of working conditions that are potentially harmful to the cardiovascular system, this type of judgment will be ever more frequently sought, and ever more difficult to render. Further complicating the issue is that the very jobs in which public safety could be compromised with the occurrence of an acute cardiac event (19,26) are often those in which exposure to potentially cardio-deleterious factors is the greatest (28).

Occupational Cardiology: Progress and Potential

Earlier Workshops relating to Occupational Cardiology

Over a decade ago, a Workshop on Occupational Cardiology was held in Udine, Italy, with the proceedings published in the European Heart Journal. The focus of that workshop was return-to-work for coronary patients, and a number of seminal concepts were put forward at that time. An appreciation was expressed for the special importance of psychosocial workplace factors among coronary patients, and this was quantitatively demonstrated by a comparison to patients with valvular heart disease (46). Mulcahy, Kennedy and Conroy (1988) cited type of occupation and social class, e.g., as important factors influencing return-to-work post-infarction. Denolin, Feruglio, Gobbato and Maisano (90), emphasized the need for more systematic research and analysis concerning various aspects of return to work for cardiac patients, including, inter alia, the effect on prognosis. In addition to the diagnostic and prognostic value of exercise testing at the end of cardiac rehabilitation, the importance of ambulatory monitoring to “check on the infarcted patient after his return to work, i.e. in the workplace” was underscored (34, p. 125). Stolz and Erdelyi (130) noted that cardiovascular responses to most types of work activities are markedly different from those during exercise testing, with a non-linear increase in heart rate and BP. Kavanagh and Matosevic (57) provided descriptive reports of several post-MI patients in whom exercise testing was normal, but who developed significant ST segment depression during specific physically and mentally stressful work activities.

“The cornerstones of a preventative strategy of CVD” were put forward as “environmental monitoring and medical surveillance, but at the same time on multidisciplinary and multicentred scientific research” (98, p. 26). Some clinical guidelines besides those relating to heavy physical work were specified. Namely, it was stated that certain exposures should be forbidden for coronary patients, i.e. “shift work, impulse noise, exposure to hot and humid environments, electromagnetic fields (for infarcted patients with a pacemaker), carbon monoxide, carbon disulphide, halogenated hydrocarbons and lead, cadmium, mercury and arsenic” (20, p. 131). Summarizing the goals of the Workshop, Dr. Giorgio Maisano (82) eloquently articulated the clinician’s challenge of offering the cardiac patient a style of life and of work that protects both his or her health and right to be productive. Dr. Maisano insisted that in order to achieve the aforementioned goal, understanding of the job and the work environment, in addition to a functional evaluation of the patient, is absolutely essential.

The 20th Bethesda Conference was devoted to the insurability and employability of the patient with ischemic heart disease, the proceedings of which were published in 1989 the Journal of the American College of Cardiology. This included a Committee Report on Economic, Administrative and Legal Factors influencing the insurability and employability of patients with ischemic heart disease (36a), together with several task force reports covering topics germane to occupational cardiology. Determination of Occupational Working Capacity in Patients with ischemic heart disease was the focus of one of the Task Forces (37a). While primarily concerned with physical exertion and exercise testing, there was also some discussion of work duration and rest cycle, physical and chemical exposures, and what was termed “psychological stress” at work. Occupations requiring special consideration were briefly reviewed: police officers and firefighters, commercial airline pilots, air traffic controllers, and drivers of commercial vehicles. The potential usefulness of simulated work testing was pointed out, as well as on-the-job monitoring. These two topics were explored further in the Executive Summary on Determination of Cardiac Impairment and Disability (18a). Another Task Force (16a) dealt with psychological status in patients with ischemic heart disease. The authors stated: “psychological assessment should be incorporated into the medical evaluation of every patient who has suffered from an acute myocardial infarction” (p. 1035). Within that context, the importance of “work stress” was mentioned. Dr. Robert DeBusk (18a) suggested that simulating the psychological, as well as physical and other stressors in the work environment, “might be helpful in evaluating the capacity for specific job tasks” (p. 1044).

Progress, Missing Data, and Dilemmas: Occupational Cardiology 2000

Since these Workshops were held, in addition to the overall breakthroughs in cardiovascular epidemiology, diagnosis and treatment, there have been many major advances directly pertinent to occupational cardiology. Much of the epidemiological evidence relating workplace factors to CVD has emerged since 1988. The armamentarium of tools for evaluating exposure to key psychosocial job stressors has been expanded, and these instruments are undergoing continuous refinement (55, 71, 123, 124). The possibilities for assessing cardiovascular function during work are much greater, due to progress in ambulatory monitoring techniques. The simultaneous recording of blood pressure and prognostically important electrocardiographic parameters (heart rate variability, ST segment, QT interval), as well as heart rate and arrhythmias per se, has now become much more feasible. Other non-invasive techniques, such as high-resolution carotid ultra-sound to quantitate intimal-medial thickening and plaque height, are now available for population-based screening.

Prognosis of Coronary Patients Returning to a Stressful Work Environment?

Despite this progress, not only does Dr. Maisano’s statement still apply, but, if anything, clinicians face an even greater challenge today, as indicated above. With the exception of those related to physical activity levels, there is a lack of evidence-based guidelines that would help clinicians make informed recommendations concerning levels of exposure to occupational factors, as these pertain to patients who have suffered cardiac events. There are, as yet, no controlled studies among cardiac patients in which amelioration of untoward working conditions was introduced as an interventional modality. Only two observational investigations have been published in which the role of exposure to workplace stressors was examined with respect to the prognosis of patients who have suffered cardiac events. In a one-year follow-up study of 222 men post first MI by Hoffman and colleagues (47), after adjusting for age, severity of MI and the results of exercise testing, high workload and low external locus of control were found to be significantly associated with all-cause mortality and IHD-related morbidity. The other study is by Theorell and colleagues (134a), which reveals that among 79 men who had survived a first myocardial infarction before the age of 45, return to work at a high strain job was a significant, independent predictor of IHD-related mortality after five years of follow-up. The predictive strength of return to high strain work was of comparable magnitude to degree of angiographically assessed coronary atheromatosis, and more powerful than left ventricular ejection fraction. This finding remained robust after adjustment for standard cardiac risk factors. On the basis of these data, together with the numerous cohort studies showing an excess risk of CHD morbidity and mortality among workers exposed to job strain or other untoward psychosocial work conditions, Theorell and Karasek (134b) raised the question: “should heart attack patients return to stressful jobs?” This question needs to be answered with the degree of precision that would be meaningful for clinical decision-making.

Work-related Hypertension: Observational Data using Ambulatory Monitoring

With respect to patients with hypertension, or with IHD prior to cardiac events, an approach to the workplace is even less developed in clinical cardiologic practice. This is indeed unfortunate, since the possibility that amelioration of untoward workplace factors could be a cardio-protective modality for this population, remains unexplored. While controlled interventional study is needed to substantiate this suggestion, there are some initial promising observational data. Schnall and colleagues (119) demonstrated among men with hypertension followed over three years, that change from exposure to non-exposure to job strain (N=10), was associated with a mean fall in unmedicated ambulatory workplace blood pressure levels of – 11.3/-5.8 mmHg, after adjusting for age, body mass index, alcohol and smoking status. Those with hypertension who continued to work at high strain jobs for the three years showed persistently high BP levels.
A number of cross-sectional studies, especially among men, have found that exposure to job strain or its major dimensions is associated with significant elevations in work-place ambulatory blood pressure monitoring (AmBP), in particular during work, as reviewed in Ref. (10, 18). Published data from two-waves of cross-sectional results in one of the largest and most rigorously controlled of these, the Work-Site Blood Pressure Study from New York City (116,117,119) reveals that mean workplace systolic AmBP was consistently over 6 mmHg higher among men exposed to job strain compared to those not exposed. Three-year longitudinal results of those chronically exposed to job strain show a + 11.1 / + 9.1 mmHg adjusted difference in work systolic/diastolic AmBP, compared to those unexposed both at baseline and at three-year follow-up (119). In contrast, the relationship between job strain and blood pressure has been inconsistent when casual clinic BP measurements were used (10).
These discrepant findings with respect to casual versus ambulatory BP, lead us recently to investigate the possibility that blood pressure elevations during work may be under-detected. A re-examination of the initial case-control data from the Work-Site Blood Pressure Study (117) revealed that 36 of 181 men with normal casual clinic BP had elevated BP during work (diastolic BP > 85mmHg). In comparison, 27 of 86 men had white coat hypertension (elevated clinic BP but normal AmBP). These figures suggested that among working populations, the problem of occult workplace hypertension could be of even greater magnitude that that of white coat hypertension (16). In light of the prognostic significance of elevated ambulatory blood pressure (21, 76, 95, 100), making the diagnosis of occult workplace hypertension becomes a clinically important issue, with major public health implications that will require workplace surveillance.

Heart rate variability and myocardial ischemia: The impact of the work environment?

With respect to other clinically important endpoints that can be stress-mediated, such as myocardial ischemia and low heart rate variability (HRV), the application of ambulatory monitoring to assess the role workplace factors has been far more sporadic. There is a large body of laboratory investigation among healthy subjects demonstrating an association between mental workload and attenuation or disappearance of respiratory sinus arrhythmia (53, 73, 80, 91, 108, 114, 115). Kalsbeek (53) ascribed the complete suppression of respiratory sinus arrhythmia to performance at peak capacity with “no reserve capacity left unoccupied” (p.102). This contention is corroborated by field studies among pilots, who during the time of landing, exhibit a total loss of HRV. Among pilots learning to handle a new type of aircraft, there was a prolonged duration of attenuated HRV during the approach period, prior to touch down (51). Very recently, van Amelsvoort and colleagues (140) have reported an elevated %LF during work among employees in high strain jobs or exposed to high levels of noise. There are also data from these and other authors (62, 85) indicating that night shift work, especially coupled with long work hours, disrupts the normal circadian HRV patterns. Long work hours have also been associated with untoward short-term changes in HRV (52).
The above-cited study of Kobayashi and colleagues (62) also included repeat examination following a change in the work schedule. Specifically, prior to working the night shift, the nurses worked a half rather than the full day schedule and thereby had a chance to sleep for an average of four hours in the late afternoon and early evening, prior to going to work. A distinct drop in LF/HF lasting about seven hours was observed during this period, although these values were still not as low as seen during a normal night sleep after day shift work. These findings provide an empirical corroboration of the statement of Kristal-Boneh and colleagues (65) that “spectral analysis of HRV may be used to predict optimal work time under a combination of enhanced mental load and other stressors”(p. 90).

There has been substantial investigation of myocardial ischemia induced by mental stress in field and laboratory studies, as well as of transient ischemia during daily life. Reported mental stress during general daily activities has been found to be associated with ischemic electrocardiographic changes in patients with coronary heart disease (4, 31, 32). Gabbay and colleagues (32) found that among 63 patients with CAD, “mental activities [appeared] to be as potent as physical activities in triggering daily life ischemia” (p. 585). The psycho physiological determinants of myocardial ischemia are the topic of intensive examination in the on-going multicentred PIMI study (103). However, therein and elsewhere the potential role of exposure to workplace stressors in provoking myocardial ischemia has rarely been specifically addressed.
Considerable attention has been paid to the circadian pattern of myocardial ischemia. Transient electrocardiographic signs of myocardial ischemia show a nadir during sleep and a peak in the morning hours after waking. This peak corresponds to the time of maximum heart rate, and systolic blood pressure, catecholamine, as well as cortisol, which increases the sensitivity of coronary arteries to catecholamine-mediated vasoconstriction (8, 35, 138, 146). The relation of this circadian distribution of myocardial ischemia to work schedule and other occupational factors has not been described.
There are very few reports of ambulatory monitoring during work made among subjects without apparent IHD. Green and colleagues (36) made one-hour Holter recordings during work among 2508 factory workers without a history of IHD to examine the relation between ST segment depression and exposure to the physical factors of noise and cold. Female factory workers showed a significantly increased risk of ST segment depression during work in inverse relation to occupational temperature levels (OR=0.77, CI=0.62 – 0.95), after adjusting for age, type of work, smoking and relative weight. In relation to occupational noise exposure male factory workers showed a borderline significant increase in odds ratio for ST depression during work (1.07 CI=0.99 – 1.12), after adjusting for age, type of work, smoking and relative weight. Arstall and colleagues (2) reported that among male police officers 45 years or older with two or more cardiac risk factors but without known IHD, there was a 3.4% prevalence of ST segment depression during 24-hour ambulatory monitoring which included shift work; follow-up thallium perfusion scans were negative. Of eighteen precision casting factory workers examined by Taccola et al (131), five exhibited tachycardia and STT changes during physical exertion and radiant heat exposure. In a study of Asmar and colleagues (1996), self-rated work stress levels were significantly higher among asymptomatic patients with hypertension who had ST-segment depression during ambulatory monitoring, compared to those without signs of myocardial ischemia.
Overall, there is a paucity of systematic study on myocardial ischemia in relation to working activity. In particular, there is a lack of comprehensive examination of the psychosocial, ergonomic and physical-chemical work environment as this impacts upon the occurrence of myocardial ischemia. Especially surprising is the small amount of published data on this topic among series of patients who have returned to work after acute cardiac events.

Integrative Studies of CV Responses to the Work Environment using Ambulatory Monitoring

Not only is there a need for a comprehensive approach to assessing the relevant workplace factors, but the outcome measures, namely the physiologic parameters, need to be viewed integratively, as well. A study of Dilaveris and colleagues (23) illustrates this point. Therein diminished HRV preceded ST segment depression, and was significantly related to the magnitude and duration of myocardial ischemia. Seen in this light, the observations concerning abrupt and total loss of respiratory sinus arrhythmia with work performance at peak capacity might provoke greater attention among clinicians.
There are a few small series in which BP and electrocardiographic monitoring were simultaneously performed in relation to work activity. In a study by Adams et al. (1) among thirteen young, apparently healthy emergency department physicians, there was a significant elevation of diastolic BP during a night shift work against the backdrop of an elevated LF/HF ratio as well as HR, compared to pre- and post-work periods. The authors concluded: The elevation of DBP during a night shift suggests that these patterns of BP variability are activity-or stress-related rather than a result of a true diurnal variation. HRV analysis suggests that sympathetic tone is heightened both before work and during work.” (p. 871). A recent publication by Kavanagh and colleagues (58) reports on the results of ambulatory BP and Holter monitoring during a 4-hour work shift among 22 city bus drivers with IHD (19 post-MI, 2 post-coronary-artery bypass surgery and 1 with IHD) who had applied return to full duties. All testing was performed with the drivers on their usual medication. In general, driving elicited lower peak systolic BP, rate-pressure product, ST segment depression (in the single lead recorded) compared to a graded exercise test. However, in four cases, peak ST depression was highest during the driving shifts, and among these drivers there was less reduction of SBP from the laboratory to the work situation compared to the others.

What is the Future for Occupational Cardiology?

The impact of occupational and other environmental hazards upon disease processes is becoming an increasingly important concern for clinical medicine. Hu and Spiezer in the most recent edition of Harrison’s Principles of Internal Medicine (48) state: “Exposures to hazardous materials and processes in the home, the workplace and the community can cause or exacerbate a multitude of diseases. Physicians commonly treat the sequelae of such disease in the practice of medicine; however, unless the underlying connection with hazardous exposures is identified and mitigated, treatment of the manifestations rather than the cause at best only ameliorates the condition. At worst, the neglect of hazardous exposures may lead to both failure of treatment and failure to recognize a public health problem with wide significance (p. 18).
These points are reflected in the concept of the “occupational sentinel health event” which “allow(s) health care providers and public health authorities to sort through health events of individuals and populations to determine a priori which health events and patterns of health events are most likely to be caused by occupation factors, given current knowledge…[This] concept transforms the health problems of individuals into the potential health problems of populations. To recognize the diagnosis of an occupational disease in an individual as a sentinel health event facilitates the identification of others at the workplace who are also ill or who may become ill if exposure continues…The occurrence of a sentinel health event may signify the failure of a system to control known occupational hazards and thereby to prevent cases of unnecessary occupational disease” (83 p. 20).
Implied here is that clinicians can play a proactive role, especially by recognizing unexpected patterns or clusters of disease. In other medical disciplines, the astute physician has often been the one to identify occupationally associated diseases, and then to develop diagnostic protocols for surveillance of exposed groups. Clinicians have also been instrumental in bringing about protection against these exposures.
One classic example is that of Dr. Irving Selikoff and colleagues in the relation between asbestos exposure and mesothelioma, as well as pulmonary interstitial fibrosis (asbestosis). Another example from pulmonary medicine is byssinosis, in which the pathognomonic symptom of Monday chest tightness among workers exposed to cotton dust, heralds the epidemiological finding that up to 80% of employees have a significant fall in their FEV1 during the course of a Monday work shift (126). In the chapter on Environmental Lung Disease in Harrison’s Principles of Internal Medicine (Ibid), not only is the need for an adequate occupational history and surveillance underscored, but also the key therapeutic measure is stated to be “reduction of dust exposure” (p. 1433).
Monday morning syndromes stemming from occupational exposure to toxic substances have also been described in cardiology. One of the best known is “Monday Morning Sudden Cardiac Death” among dynamite manufacturing workers, most likely due to acute re-exposure to nitrate esters upon return to work after a brief period of absence (66,110,111,143).
However, as discussed earlier, the occupational exposures that contribute to an increased risk of cardiac events, especially on Monday mornings, are not solely of a toxicological nature. The workplace factors that contribute to an increased risk of hypertension and IHD are prominently psychosocial, as well as physical, chemical and ergonomic, including long work hours and shift work. It may be that it is the total burden of these factors, which, as stated by Lennart Levi (74), “…become superimposed on each other in an additive way, or synergistically. In this way, the straw that breaks the camel’s back may be a very trivial environmental factor which, however, is added to a very considerable existing environmental load” (p. 58).
An approach has recently been elaborated for assessing multiple workplace exposures relevant to cardiovascular disease, with the aim of assessing this total occupational burden (11). This is operationalized in a practical guide for clinicians to aid in the cardiovascular evaluation of the worker and the workplace (14).
Heretofore, recognition of occupational sentinel health events (OCHE) has relied upon a deterministic approach of assessing causal relations between a single exposure and a given outcome. This is reflected in the most recent list of OCHE, which includes 64 diseases or conditions; with the exception of vibration-related Raynaud’s phenomenon, none of these OCHE is related to the cardiovascular system (28, 92). Furthermore, all of the listed exposures are physical or chemical in nature. It should also be noted that most of the disorders are fairly uncommon.

The concept of occupational sentinel health event needs to be expanded in order to be helpful vis-à-vis generic cardiovascular diagnoses: arterial hypertension, myocardial infarction, sudden cardiac death as well as other forms of IHD with and without symptoms. Given that these are highly common disorders, i.e. the major cause of morbidity and mortality in much of the world, and that the contributory occupational exposures are of a multi-factorial nature, the OSHE concept will only be helpful if placed within an epidemiological framework. This can be envisioned as an iterative process, whereby the cardiologic care-giver has immediate access to data concerning prevalence of cardionoxious workplace exposures, as well as of the physiological and disease outcomes, and through his or her clinical insights, would help to continuously upgrade and refine these data bases, especially by targeting high priority sites for surveillance.
The critical importance of the surveillance process has been underscored in the recent Tokyo Declaration, on Work-related Stress and Health in Three Post-Industrial Settings-E.U., Japan and the USA (133). Therein, it is stated that a program is needed for “surveillance at individual workplaces and monitoring at national and regional levels in order to identify the extent of work-related stress health problems and to provide baselines against which to evaluate effects at amelioration…[It is] recommended that workplaces assess both workplace stressors and health outcomes known to result form such exposures…on an annual basis” (p.5)
This type of approach could help us “move from epidemiological evidence to prevention-oriented clinical practice”. In other words, this could help bring the workplace into the realm of consideration for clinical cardiology. The discipline of Occupational Cardiology, as a link between primary cardiology and occupational and preventive medicine, and as introduced by the European Society of Cardiology in 1988, could be a vehicle for achieving this goal.

Topics on an Agenda for Occupational Cardiology might include:

(1) An in-depth review of the empirical evidence with respect to workplace factors and cardiovascular disease, with particular attention to the methodological quality-validity of the data. Recommendations for future study designs, especially those of an interventional nature, that would be the most helpful for clinical decision-making in occupational cardiology.

(2) How to incorporate occupational history taking into the standard cardiologic workup. Clinical examples of how this can facilitate an integrated Occupational Cardiologic Approach to Patients

(3) How could the concept of occupational sentinel health events be expanded, so as to be helpful for generic cardiovascular disease processes (as opposed to rare events), to which multiple (as opposed to single) workplace factors contribute? How could, in practice, a more epidemiological approach with surveillance as a cornerstone, become an integral part of cardiology? What can we learn from the experience of our colleagues in other disciplines, e.g. pulmonary medicine?

(4) Identification of target groups for whom application of ambulatory monitoring techniques during work should be prioritized. The judicious use of these techniques for improved detection of abnormalities such as occult workplace hypertension and silent myocardial ischemia. The use of integrative ambulatory monitoring to help find the safest working conditions for high-risk patients/ e.g. optimizing work-schedules and medication regimen.

(5) Could laboratory simulations of potential cardionoxins other than exercise, be useful in occupational cardiologic diagnostic evaluations? Some examples that might be discussed include the glare pressor test which has been applied in the research setting among professional drivers with IHD, hypertension as well as healthy drivers (6, 25); testing responses to other physical noxins, as well as psychosocial simulations, as discussed in Ref. (14). This could be placed within the context of “ecologically relevant” cardiovascular laboratory testing (129b).

(6) Development of evidence-based recommendations concerning levels of exposure to potentially cardionoxious occupational factors (other than physical activity levels), for
(a) Cardiac patient groups (e.g. post-acute MI, stable angina pectoris, post-PTCA etc.)
(b) High risk groups (e.g. silent myocardial ischemia, hypertension with LVH)
(c) The general working population
Since the 1988 and 1989 Workshops, there have been some publications, e.g. Ref. (14, 19, 39, 110,144), that discuss this issue and propose some guidelines that might serve as a starting point for discussions.

(7) How can occupational cardiology help clinicians tackle the following major dilemma: that jobs, such as truck driving, mass transit operation, etc. in which public safety could be compromised by sudden loss of consciousness or acute onset of a cardiac event, are also often those with heavy exposure to cardionoxious workplace factors?

(8) Ethical and legal issues. Protection of confidentiality, avoidance of iatrogenic deprivation of occupational activity, protecting public safety, workers compensation issues and dilemmas.

(9) The preferred setting(s) for occupational cardiologic practice?
Some possible settings to discuss include: occupational health services, health maintenance organizational (HMO) primary care contracting to a specific industry, regional-geographic clinical care, contracts for mandated examinations, workers’ compensation examinations, inter alia.
Within this framework, there might be a discussion of “other key players”, for cooperation and collaboration, e.g. occupational health specialists, epidemiologists, labor and management, inter alia.

(10) Dissemination of information about the workplace and CVD to the clinical community.

(11) What is the definition of a “heart healthy” work environment? What can be learned from interventions aimed at working conditions? How can this be integrated with efforts towards work-site Health promotion (e.g. smoking cessation, exercise, heart healthy diet)? How can clinicians help to bring about a “heart healthy” work environment?

Cited References
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