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
1. Adams SL, Roxe DM, Weiss J, Zhang F, Rosenthal JE. Ambulatory blood pressure and Holter monitoring of emergency physicians before, during, and after a night shift. Academic Emergency Medicine 1998; 5: 871-877.

2.Arstall MA, Wuttke RD, Arthur J, Whitford JA, Horowitz JD. The prevalence of ST segment depression on ambulatory electrocardiographic monitoring during daily life in high-risk police officers. Journal of Cardiovascular Risk 1994; 1: 143-148.

3. Asmar R, Benetos A, Pannier B, Agnes E, Topouchian J, Laloux B, Safar M. Prevalence and circadian variations of ST-segment depression and its concomitant blood pressure changes in asymptomatic systemic hypertension. Am J Cardiol 1996; 77: 384-390.

4. Barry J, Selwin AP, Nabel EG. Frequency of ST.segment depression produced by mental stress in stable angina pectoris from CAD. Am J Cardiol 1988; 61: 989-993.

5. Bartley M, Marmot M. Social class and power relations at the workplace. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease.2000; 15 (1): 73-78.

6. Belkic, K; Ercegovac, D; Savic, C; Panic, B; Djordjevic, M; Savic S. EEG arousal and cardiovascular reactivity in professional drivers. The glare pressor test. Eur Heart J. 1992; 13: 304-309.

7. Belkic K, Savic C, Theorell T, Cizinsky S. Work Stressors and Cardiovascular Risk: Assessment for Clinical Practice. Part I. Stockholm (Sweden): Stress Research Reports. National Institute for Psychosocial Factors and Health. Section for Stress Research, Karolinska Institute, WHO Psychosocial Center; 1995. Report No.: 256.

8. Belkic K. Psychosocial triggers of myocardial ischemia in women. Research Report to the Swedish Medical Research Council. 1995.

9. Belkic K, Emdad R, Theorell T. Occupational profile and cardiac risk: possible mechanisms and implications for professional drivers. International Journal of Occupational Medicine and Environmental Health. 1998; 11: 37-57.

10.Belkic K, Landsbergis P, Schnall P, Baker D, Theorell T, Siegrist J, Peter R, Karasek R. Psychosocial factors: Review of the empirical data among men. . In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 24-40.

11. Belkic K, Schnall P, Savic C, Landsbergis P. Multiple exposures: Towards a model of total occupational burden. .In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease.2000; 15: 94-105.

12. Belkic K. Cardiac electrical stability and environmental stress. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000;15 (1): 117-120.

13.Belkic K. Myocardial oxygen supply and demand: Environmental triggers of imbalance. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1):132-136.

14. Belkic K, Schnall P, Uglješic M. Cardiovascular evaluation of the work and workplace: A practical guide for clinicians.. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 213-222.

15. Belkic K, Schnall P, Landsbergis P, Baker D. The workplace and cardiovascular health: Conclusions and thoughts for a future agenda. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 307-321.

16. Belkic K, Schnall P, Landsbergis P, Schwartz JE, Gerber LM, Baker D, Pickering TG. Hypertension at the workplace-An occult disease? The need for worksite surveillance. Adv. Psychosom Med. In Press.

16a. Blumenthal JA, Bradley W, Dimsdale JE, Kasl SV, Powell LH, Taylor CB. Assessment of psychological status in patients with ischemic heart disease. J Am Coll Cardiol 1989; 14: 1039-1041.

17.Boggild H, Knutsson A. Shift work, risk factors and cardiovascular disease. Scand J Work Environ Health. 1999; 25: 85-99.

17a. Bond JT, Galinsky E, Swanberg JE. The 1997 National Study of the changing workforce. New York, Families and Work Institute, 1998.

18.Brisson C. Women, work and CVD .In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease.2000; 15(1):49-57.

18a. DeBusk RF. Determination of cardiac impairment and disability JACC 1989a; 14: 1043-4.

19.De Gaudemaris R. Clinical issues: return to work and public safety. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 223-230.

20.Denolin H, Feruglio GA, Gobbato F, Maisano G. Guidelines for return to work after myocardial infarction and/or revascularization. Eur Heart J 1988; 9 (Suppl. L): 130-131.

21.Devereux RB, Pickering TG, Harshfield GA, Kleinert HD, Denby L, Clark L, Pregibon D, Jason MN, Kleiner B, Borer JS, Laragh JH. Left ventricular hypertrophy in patients with hypertension: Importance of blood pressure response to regularly recurring stress. Circulation. 1983; 68: 476-479.

22.Deyanov C, Mincheva L, Hadjiolova I, Ivanovich E. Study on the level of blood pressure and prevalence of arterial hypertension depending on the duration of occupational exposure to industrial noise. Central European Journal of Occupational and Environmental Medicine 1995; 1: 109-116.

23.Dilaveris PE, Zervopoulos GA, Psomadaki ZD, Michaelides AP, Gialofos JE, Toutouzas PK. Assessment of time domain and spectral components of heart rate variability immediately before ischemic ST segment depression episodes. PACE 1996; 19: 1337-1345.

24.Drever F, Whitehead M, Roden M. Current patterns and trends in male mortality by social class (based on occupation). Population Trends 1996; 86: 15-20.

25. Emdad R, Belkic K, Theorell T, Cizinsky S, Savic C, Olsson K. Psychophysiologic sensitization to headlight glare among professional drivers with and without cardiovascular disease. Journal of Occupational Health Psychology 1998; 3: 147-160.

26.Epstein AE, Miles WM, Benditt DG, Camm AJ, Darling EJ, et al. Personal and public safety issues related to arrhythmias that may affect consciousness: Implications for regulation and physician recommendations. American Heart Association Scientific Statement, 1996.

27.European Foundation. Time constraints and autonomy at work in the European Union. Dublin, European Foundation for the Improvement of Living and Working Conditions, 1997.

28.Fisher J, Belkic K. A public health approach in clinical practice. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 245-253.

29.Fogari R, Zoppi A, Vanasia A, Marasi G, Villa G. Occupational noise exposure and blood pressure. J Hypertension 1994; 12: 475-479.

30.Folkow B. Autonomic Nervous System in Hypertension. In: (Ed) Swales JD Textbook of Hypertension. London: Blackwell Scientific Publications, 1994, pp.427-438.

31.Freeman LJ,, Nixon PGF, Sallabank P, etal. Psychological stress and silent myocardial ischemia. Am Heart J 1987; 114: 447-482.

32.Gabbay FH, Krantz DS, Kop WJ et al. Triggers of myocardial ischemia during daily life in patients with coronary artery disease. Physical and mental activities, anger and smoking. J Am Coll Cardiol 1996; 27:585-592.

33. Gerber LM, Schwartz JE, Schnall PL, Devereux RB, Warren K, Pickering TG. Effect of body weight changes on changes in ambulatory and standardized non-physician blood pressures over three years. Ann Epidemiology 1999; 9: 489-497.

34.Gobbato F, Maisano G. Outcome from the questionnaire adopted for the consensus conference. Eur Heart J 1988; 9 Suppl L: 123-129.

35. Goldstein DS. Stress, Catecholamines and Cardiovascular Disease. New York: Oxford University Press, 1995.

36. Green MS, Schwartz K, Harari G, Najenson T. Industrial noise exposure and ambulatory blood pressure and heart rate. J Occup Med 1991; 33: 879-883.

36a. Guillette W, Judge RD, Koehn E, Miller JE, Palmer RK, Tremblay JLGT. Committee report on economic, administrative and legal factors influencing the insurability and employability of patients with ischemic heart disease. J Am Coll Cardiol 1989; 14: 1010-1015.

37. Hallqvist J, Diderichsen F, Theorell T, et al. The SHEEP Study Group: Is the effect of job strain on myocardial infarction due to interaction between high psychological demands and low decision latitude? Results from Stockholm Health Epidemiology Program (SHEEP). Soc Sci Med 1998; 46: 1405-1415.

37a. Haskell WL, Brachfeld N, Bruce RA, Davis PO, Dennis CA, Fox SM, Hanson P, Leon AS. Determination of occupational working capacity in patients with ischemic heart disease. JACC 1989; 14: 1016-1042.

38.Hayashi T, Kobayashi Y, Yamaoka K, Yano E. Effect of overtime work on 24-hour ambulatory blood pressure. JOEM. 1996; 38: 1007-1011.

39.Hellerstein HK. Work Evaluation. In: NK Wenger, HK Hellerstein (eds.) Rehabilitation of the coronary patient. Churchill Livingstone, 3d Edition, New York, 1992, pp.523542.

40.Hemingway H, Marmot M. Psychosocial factors in the aetiology and prognosis of coronary heart disease: systematic review of prospective cohort studies. BMJ 1999; 318: 1460-1467.

41.Henry JP, Cassell Psychological factors in essential hypertension. Am J Epidemiology 1969; 90: 171-200.

42.Hernberg S. Work related disease-Some problems in study design. Scand J Work Environ Health 1984; 10: 3267-372.

43.Hertz-Piccioto I, Croft J. Review of the relation between blood lead and blood pressure. Epidemiologic Reviews. 1993; 15: 352-373.

44. Hlatky MA, Lam LC, Lee KL, Clapp-Channing NE, Williams RB, Pryor DB, Califf RM, Mark DB. Job strain and the prevalence and outcome of coronary artery disease. Circulation 1995; 92: 327-333.

45. Hobbesland A, Kjuus H, Thelle DS. Mortality from cardiovascular diseases and sudden death in ferroalloy. Scand J Work Environ Health 1997; 23:334-341.

46. Hoffmann A. Psychosocial job demands of cardiac patients in Hungary Eur Heart J 1988; 9 Suppl L: 20-25.

47. Hoffmann A, Pfiffner D, Hornung R, Niederhauser H. Psychosocial factors predict medical outcome following a first myocardial infarction. Working Group on Cardiac Rehabilitation of the Swiss Society of Cardiology. Coronary Artery Disease 1995; 6: 147-152.

48. Hu H, Speizer FE. Influence of environmental and occupational hazards on disease. In Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, Hauser DL, Longo D (eds.)Harrison’s Principles of Internal Medicine. 14th Edition. New York: McGraw-Hill, Inc., 1998, pp. 18-21.

49a.Iwasaki K, Sasaki T, Oka T, Hisanaga N. Effect of working hours on biological functions related to cardiovascular system among salesmen in a machinery manufacturing company. Industrial Health 1998; 36: 361-367.

49b.Johnson JV, Hall EM. Job strain, workplace social support and cardiovascular disease: A cross-sectional study of a random sample of the Swedish working population. Am J Public Health 1988; 78:1336-1342

50.Johnson JV. Empowerment in future working life. Scand J Work Environ Health. 1997; 23 (Suppl. 4): 23-28.

51.Jorna PGAM. Heart rate and workload variation in actual and simulated flight. Ergonomics 1993; 36: 1043-1054.

52. Kageyama T, Kabuto M. Combined effects of mental workload and following exposure to road traffic noise on sympathetic activities assessed by a spectral component of heart rate variability. Archives of Complex Environmental Studies 1995; 7: 13-19.

53. Kalsbeek JWH. Do you believe in sinus arrhythmia? Ergonomics 1973; 16: 99-104.

54. Karasek RA, Theorell T. Healthy Work: Stress, productivity and the reconstruction of working life. New York. Basic Books, Inc., 1990.

55. Karasek R, Brisson C, Kawakami N, Houtman I, Bongers P, Amick B. The Job Content Questionnaire (JCQ): An instrument for internationally comparative assessments of psychosocial job characteristics. J Occup Health Psychology 1998; 3: 322-355.

56. Kasl SV. The influence of the work environment on cardiovascular health: A historical, conceptual and methodological perspective. J Occup Health Psychol. 1996; 1:42-56.

57. Kavanagh T, Matosevic V. Assessment of work capactiy in patients with ischaemic heart disease: methods and practices. Eur Heart J 1988; 9 (Suppl L): 67-73.

58. Kavanagh T, Matosevic V, Thacker L, Belliard R, shaphard RJ. On-site evaluation of bus drivers with coronary heart disease. J Cardiopulmonary Rehabilitation. 1998; 18: 209-215,

59. Kawachi I, Colditz GA, Hennekens CH. Prospective study of shift work and risk of coronary heart disease in women. Circulation 1995; 92: 3178-3183.

60. Kleinbaum DG, Morgenstern H, Kupper LL. Selection bias in epidemiologic studies. Am J Epidemiol. 1981; 113: 452-463.

61. Knutsson A, Åkerstedt T, Jonsson BG, Orth-Gomér K. Increased risk of ischaemic heart disease in shift workers. Lancet 1986; 89-92.

62. Kobayashi F, Furui H, Akamatsu Y, et al. Changes in psychophysiological functions during night shift in nurses: Influences of changing from a full-day to a half-day work shift before night duty. Int Arch Occup Environ Health 1997; 69: 83-90.

63. Koskela RS. Cardiovascular diseases among foundry workers exposed to carbon monoxide. Scand J Work Environ Health 1994; 20:286-293.

64. Krantz DS, Kop WJ, Santiago HT, Gottdiener JS. Mental stress as a trigger of myocardial ischemia and infarction. Cardiology Clinics 1996; 14: 271-287.

65. Kristal-Boneh E, Raifel M, Froom P, Ribak J. Heart rate variability in health and disease. Scand J Work Environ Health 1995; 21: 85-95.

66. Kristensen TS. Cardiovascular disease and the work environment; A critical review of the epidemiologic literature on chemical factors. Scand. J Work Environ Health 1989; 15: 245-265.

67. Kristensen TS. The demand-control-support model: methodological challenges for future research. Stress Medicine. 1995; 11:17-26.

68. Kristensen TS, Kornitzer M, Alfredsson L. Social factors, work, stress, and cardiovascular disease prevention. Brussels, The European Heart Network, 1998.

69. Landsbergis PA, Schnall PL, Schwartz JE, Warren K, Pickering TG, Schwartz JE. Association between ambulatory blood pressure and alternative formulations of job strain Scand J Work Environ Health. 1994; 20: 349-363.

70. Landsbergis PA, Cahill J, Schnall PL. The impact of lean production and related new systems of work organization on worker health. J Occup Health Psychol 1999; 4: 1-23.

71. Landsbergis PA, Theorell T. Measurement of psychosocial workplace exposure variables: Self-report questionnaires In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 163-175.

72. Lang T, Fouriaud C, Jacquinet-Salord M-C. Length of occupational noise exposure and blood pressure. Int Arch Occup Environ Health 1992; 63: 369-372.

73. Lee DH, Park KS. Multivariate analysis of mental and physical load components in sinus arrhythmia scores. Ergonomics 1990; 33: 35-47.

74. Levi L. Preventing Work Stress. Reading: Addison-Wesley Publishing Co., 1981.

75. Levi L. Stressors at the Workplace: Theoretical Models-An Historical Overview. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 69-73.

76. Liu J, Roman M, Pini R, Schwartz JE, Pickering TG, Devereux RB. Cardiac and arterial target organ damage in adults with elevated ambulatory and normal office blood pressure. Ann Intern Med 1999; 131: 564-572.

77. Lloyd EL. The role of cold in ischaemic heart disease: A review. Public Health 1991; 105: 205-215.

78. Lown B. Sudden cardiac death: biobehavioral perspective. Circulation 1987; 76 (suppl I): I-186–I195.

79. Lown B. Role of higher nervous activity in sudden cardiac death. Jpn Circ J. 1990; 54: 581-602.

80. Luczak H, Laurig W. An analysis of heart rate variability. Ergonomics 1973; 16: 85-97.

81. Lynch J, Krause N, Kaplan GA, Tuomilehto J, Salonen JT. Workplace conditions, socioeconomic status and the risk of mortality and acute myocardial infarction: The Kuopio Ischemic Heart Disease Risk Factor Study. Am J Public Health. 1997; 87: 617-622.

82. Maisano G. Summary and conclusions towards guidelines for return to work after myocardial infarction and myocardial revascularization. Eur Heart J 1988 (Suppl. L):9: 120-122.

83. Markowitz SB. The role of surveillance in occupational health. In: Rom WN (ed): Environmental and Occupational Medicine. Philadelphia, Lippincott-Raven Publishers, 1998; pp. 19-29.

84. Marmot M. Social class, occupational status and CVD. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 46-49.

85. Matsuzaki I, Nishimura A, Morita N, Satoh S, Kobayashi T, Murakami M. Autonomic nervous activity changes due to shift-work: an evaluation by spectral components of heart rate variability. J Occup Health 1996; 38: 80-81.

86. McMichael AJ. Standardized mortality ratios and the “healthy worker effect”. Scratching the surface. J Occup Med 1976; 18: 165-168.

87. McNamee R, Binks K, Jones S, et al.Shiftwork and mortality from ischaemic heart disease. Occ Env Med 1996; 53: 367-373.

88. Morikawa Y, Nakagawa H, Miura K, Ishizaki M, Tabata M, Nishijo M, Higashiguchi K, Yoshita K, Sagara T, Kido T, Naruse Y, Nogawa K. Relationship between shift work and onset of hypertension in a cohort of manual workers. Scand J Work Environ Health 1999; 25: 100-104.

89. Morvai V. Cardiovascular effects of metals. Central European Journal of Occupational and Environmental Medicine. 1996; 2: 115-145.
90. Mulcahy R, Kennedy C, Conroy R. The long-term work record of post-infarction patients subjected to an informal rehabilitation and secondary prevention programme. Eur Heart J 1988; 9: 84-88.

91. Mulder, G., Mulder-Hajonides van der Meulen WREH. Mental load and the measurement of heart rate variability. Ergonomics. 1973; 16: 69-83.

92. Mullan RJ, Murthy LK. Occupational sentinel health events: an updated list for physician recognition and public health surveillance. Am J Industrial Med 1991; 19:775-799.

93. Nurminen H, Hernberg S. Effects of intervention on the cardiovascular mortality of workers exposed to carbon disulfide. A 15-year follow-up. Br J Industrial Med 1985; 42: 32-35.

94. Paradis G, Theriault G, Tremblay C. Mortality in a historical cohort of bus drivers. Int J Epidemiol 1989: 18:397-402.

95. Perloff D, Sokolow M, Cowan R. The prognostic value of AMB monitoring in treated hypertensive patients. J Hypertension 1991; 9 (SUPPL. 1): S33-S40.

96. Peter R, Hallqvist J, Reuterwall C, et al. Psychosocial work environment and myocardial infarction: Improving risk prediction by combining two alternative job stress models in the SHEEP Study. Submitted.

97. Peters RW, McQuillan S, Resnick SK, Gold MR: Increased Monday incidence of life-threatening ventricular arrhythmias: Experience with a third-generation implantable defibrillator. Circulation 1996: 94: 1346-1349.

98. Petronio L. Chemical and physical agents of work-related cardiovascular disease. Eur Heart J 1988; 9 (Suppl. L): 26-34.

99. Pickering TG. Psychosocial stress and hypertension. B: Clinical and Experimental Evidence. In Textbook of Hypertension. (Edited by Swales JD) London: Blackwell Scientific Publications, 1994, pp. 641-654.

100. Pickering TG, Alpert BS, de Swiet M, Harshfield G, O’Brien E, Shennan AH. Ambulatory blood pressure. Redmond, SpaceLabs Medical, Inc., 1994.

101. Pickering TG. The effects of environmental and lifestyle factors on blood pressure and the intermediary role of the sympathetic nervous system. J Hum Hypertens 1997; 11 (Suppl 1): S9-S18.

102. Pieper C, Schnall PL, Warren K, Pickering TH. A comparison of ambulatory blood pressure and heart rate at home and work on work and non-work days. J Hypertension 1993; 11: 177-183.

103. The Psychophsyiological Investigations of Myocardial Ischemia (PIMI) Study: Objective, methods, and variability of measures. Psychosomatic Medicine 1998; 60: 56-63.

104. Punnett L. Adjusting for the healthy worker selection effect in cross-sectional studies. Int J Epidemiol. 1996; 25: 1068-1076.

105. Quinlan M. The implications of labour market restructuring in industrialized societies for occupational health and safety. Economic and Industrial Democracy. 1999; 20: 427-460.

106. Rabkin SW, Mathewson FAL, Tate RB. Chronobiology of cardiac sudden death in men. JAMA 1980; 44: 1357-1358.

107. Reed DM, LaCroix AZ, Karasek RA, Miller D, McLean CA. Occupational strain and the incidence of coronary heart disease. Am J Epidemiol 1989; 129: 495-502.

108.Rohmert W, Laurig W,Philipp U, Luczak H.Heart rate variability and work-load measurement. Ergonomics 1973: 16: 33-44.

109. Rosengren A, Anderson K, Wilhelmsen L. Risk of coronary heart disease in middle-aged male bus and tram drivers compared to men in other occupations: A prospective study. Int J Epidemiol 1991; 20: 82-87.

110. Rosenman KD. Occupational heart disease. In: W.N. Rom (ed). Environmental and Occupational Medicine. 3d Edition, Lippincott-Raven Publishers, Philadelphia, 1998, pp. 733-741.

111. Rosenstock L, Cullen MR. Clinical Occupational Medicine. Philadelphia: WB Saunders, 1986.

112. Rothman KJ, Greenland S. Modern Epidemiology. Philadelphia, Lippincott-Raven, 1998.

113. Rozanski A, Blumenthal JA, Kaplan J. Impact of psychological factors on the pathogenesis of cardiovascular diseaes and implications for therapy. Circulation 1999; 99: 2192-2217.

114. Sammer G. Heart period variability and respiratory changs associated with physical and mental load: Non-linear analysis. Ergonomics. 1998; 41: 746-755.

115. Sayers BM. Analysis of heart rate variability. Ergonomics 1973; 16: 17-32.

116. Schnall PS, Pieper C, Schwartz JE, Karasek RA, Schlussel Y, Devereux RB, Ganau A, Alderman M, Warren K, Pickering T. The relationship between “job strain”, workplace diastolic blood pressure, and left ventricular mass index. Results of a case-control study. JAMA. 1990; 263: 1929-1935.

117. Schnall PL, Schwartz JE, Landsbergis PA, Warren K, Pickering TG. Relation between job strain, alcohol and ambulatory blood pressure. Hypertension 1992; 19: 488-494.

118. Schnall PL, Landsbergis PA, Baker D. Job strain and cardiovascular disease. Annu Rev Public Health 1994; 15: 381-411.

119. Schnall PL, Landsbergis PA, Schwartz J, Warren K, Pickering TG. A longitudinal study of job strain and ambulatory blood pressure: results of a three year follow-up. Psychosom Med 1998; 60: 697-706.

120. Schwartz JE, Warren K, Pickering TG. Mood, location and physical position as predictors of ambulatory blood pressure and heart rate: application of a multi-level random effects model. Ann Behav Med 1994; 16: 210-220.

121. Schwartz JE, Pickering TG, Landsbergis PA. Work-related stress and blood pressure: Current theoretical models and consideration from a behavioral medicine perspective. J Occup Health Psychol. 1996; 1:287-310.

122. Schwartz JE, Belkic K, Schnall PL, Pickering TG. Evidence for mediating econeurocardiologic mechanisms: Mechanisms leading to hypertension and CV morbidity. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 121-132.

123. Schwartz JE. Imputation of job characteristics scores. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 172-175.

124. Siegrist J. Adverse health effects of high-effort/low-reward conditions. J Occup Health Psychol. 1996; 1: 27-41.

125. Smith MJ, Conway FT, Harsh B-T. Occupational stress in hyman computer interaction. Industrial Health 1999; 37: 157-173.

126. Spiezer FE.Environmental lung diseases.In Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, Hauser DL, Longo D(eds.)Harrison’s Principles of Internal Medicine. 14th Edition. New York: McGraw-Hill, Inc., 1998, pp. 1429-1436.

127. Spurgeon A, Harrington JM, Cooper CL. Health and safety problems associated with long working hours: a review of the current position Occupational & Environmental Medicine 1997; 54: 367-375.

128. Steenland K, Deddens J, Salvan A, Stayner L. Negative bias in exposure-response trends in occupational studies: modeling the healthy worker survivor effect. Am J Epidemiol. 1996; 143: 202-210.

129a. Steptoe A, Marmot M. Atherogenesis, coagulation and stress mechanisms. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 136-138.

129b. Steptoe A, Vögele C.Methodology of mental stress testing in cardiovascular research.Circulation. 1991Suppl II; 83: II 14-II 24.

130. Stolz I, Erdélyi A. Practical aspects of identifying and correcting worksite stress in post-infarction patients returning to work. Eur Heart J 1988 (Suppl. L); 9: 82-83.

131. Taccola A, Assandri J, Gotti GB.Dynamic electrocardiographic findings in a precision casting factory. Med Lav 1979; 70: 215-222.
132. Talbott EO, Gibson LB, Burks A, Engberg R, McHugh KP. Evidence for a dose-response relationship between occupational noise and blood pressure. Arch Environ Health 1999; 54: 71-78.

133. The Tokyo Declaration on Work-Related Stress and Health in Three Post-Industrial Settings-EU, Japan and USA. J Tokyo Med Univ 1998; 56: 760-767.

134a. Theorell T, Perski A, Orth-Gomér K, Hamsten A, de Faire U The effects of the strain of returning to work on the risk of death after a first myocardial infarction before age of 45. Int J Cardiol 1991; 30: 61-67.

134b. Theorell T, Karasek R. Should heart attack patients return to stressful jobs? Stress Medicine 1995; 11: 219-220.

135. Theorell T, Karasek R. Current issues relating to psychosocial job strain and cardiovascular disease research. J Occup Health Psychol. 1996; 1:9-26.

136. Theorell T, Tsutsumi A, Hallqvist J, Reuterwall C, Fredlund P, Emlund N, Johnson J, SHEEP Study Group. Decision latitude, job strain and myocardial infarction. Am J Public Health 1998; 88; 382-388.

137. Theorell T. Evidence for mediating econeurocardiologic mechanisms. Neuroendocrine mechanisms. In: Schnall PL, Belkic K, Landsbergis PA, Baker D (eds.) Occupational Medicine: State of the Art Review. The Workplace and Cardiovascular Disease. 2000; 15 (1): 139-146.

138. Tofler GH. Triggering and the pathophysiology of acute coronary syndromes. Am Heart J. 1997; 134: S55-S61.

139. van Amelsvoort LGPM. Coronary heart disease among truckdrivers. Report of the International Workshop on the Epidemiology of Coronary Heart Disease among European Truck Drivers. Bilthoven, European Commision, 1995.

140. van Amelsvoort LGPM, Schouten EG, Maan AC, Swenne CA, Kok FJ. Occupational determinants of heart rate variability. Int Arch Occup Environ Health. 2000; 73:255-262.

141. Vrijkotte TG, van Doornen LJ, de Geus EJ. Effects of work stress on ambulatory blood pressure, heart rate and heart rate variability. Hypertension 2000; 35: 880-886.

142. Walters D. Health and safety strategies in a changing Europe. Int J Health Services 1998; 28: 305-331.

143. Wenger NK. Occupation and cardiovascular disease. In (Ed) Hurst W, Schlant R, Rackley CE, Sonnenblick EH, Wenger NK. The Heart. New York: McGraw-Hill Services Company, 1990, pp. 1666-1669.

144. Wenger NK. Rehabilitation of the patient with coronary heart disease. In: Alexander RW, Schlant RC, Fuster V, O’Rourke RA, Roberts R, Sonnenblick EH (eds.). Hurst’s The Heart. 9th Edition. 1998, McGraw-Hill, New York, pp. 1619-1631.

145. Wild P, Moulin J-J, Ley F-X, Schaffer P. Mortality from cardiovascular diseases among potash miners exposed to heat. Epidemiology 1995; 6: 243-247.

146. Willich SN, Maclure M, Mittleman M, Arntz HR, Muller JE. Sudden cardiac death support for a role of triggering in causation. Circulation 1993; 87: 1442-1450.

147. Willich SN, Löwel H, Lewis M, Hörmann A, Arntz HR, Keil U. Weekly variation of acute myocardial infarction : Increased Monday risk in the working population. Circulation. 1994: 90: 87-93.

148. Winkleby, MA; Ragland, DR; Fisher, JM; Syme SL. Excess Risk of Sickness and Disease in Bus Drivers: A Review and Synthesis of Epidemiological Studies Int J Epidemiol 1988; 17: 255-262.

149. Wolf S. Psychosocial forces in myocardial infarction and sudden death. Circulation. 1969; 40: IV-74–IV-83.

For more information regarding this site, e-mail us at: cse@workhealth.org

Comments are closed.

© 2017 Unhealthy Work  |  For more information regarding this site, please contact us