IJOMEH 2010;23(3) 279

R E V I E W P A P E R S
International Journal of Occupational Medicine and Environmental Health 2010;23(3):279 285
DOI 10.2478/v10001-010-0013-8
EFFORT-REWARD IMBALANCE AT WORK
AND CARDIOVASCULAR DISEASES
JOHANNES SIEGRIST
University of Duesseldorf, Duesseldorf, Germany
Department of Medical Sociology
Abstract
Working conditions and employment arrangements make a signifcant contribution to the burden of cardiovascular disease,
in particular in modern societies where mental and emotional demands and threats are becoming widespread. Occupa-
tional research has identifed health-adverse features of modern work with the help of theoretical models. One such model,
effort-reward imbalance, has been developed by this author and his group and has been widely tested in epidemiological
and experimental studies. The model claims that stressful experience at work is elicited by a lack of reciprocity between
efforts spent at work and rewards received in return, where rewards include money, promotion prospects, job security, and
esteem. Results demonstrate elevated risks of coronary heart disease among employees exposed to effort-reward imbal-
ance. Moreover, in ambulatory and experimental investigations, elevated heart rate and blood pressure and altered secre-
tion of stress hormones were observed under these conditions.
Although additional scientifc evidence is needed, available fndings call for practical measures towards improving quality
of work, most importantly at the level of single companies and organisations. This conclusion is supported by frst results
from intervention studies that are guided by this theoretical approach. In view of the burden of cardiovascular disease at-
tributable to unfavourable working conditions, such efforts are well justifed and need to be extended in order to promote
healthy work.
Key words:
Work stress, Effort-reward imbalance, Cardiovascular diseases, Epidemiology, Intervention
Address reprint request to J. Siegrist, Department of Medical Sociology, University of Duesseldorf, PO-Box 10 10 07; D-40001 Duesseldorf, Germany
(e-mail: [email protected]).
This contribution is a revised version of a keynote presentation given at the Fifth International Conference on Work Environment and Cardiovascular Diseases,
2730 September 2009, Krakw, Poland. Some parts of the text were modifed from my chapter Work and cardiovascular diseases to be published in Waldstein S,
editor. Handbook of Cardiovascular Behavioural Medicine. New York: Springer Science. In press.
INTRODUCTION
The nature of work has undergone rather fundamental
changes in economically advanced societies. Industrial
mass production no longer dominates the labour market.
This is due, in part, to technological progress, and in part
to a growing number of jobs available in the service sector.
Many jobs are confned to information processing, con-
trolling, and coordination. Sedentary rather than physi-
cally strenuous work is becoming more and more domi-
nant. Moreover, the traditional separation of the spheres
of work and home is vanishing. Homework, participation
in virtual networks, and an unprecedented degree of fex-
ibility in local and temporal work arrangements contrib-
ute to this process. Traditional continuous occupational
careers are increasingly being replaced by job change, fx-
term contract, temporary work, or self-employment. With
the advent of economic globalisation, pressure towards an
increase in return on investment has been growing over
the past two decades. As a consequence, work pressure
increased considerably in private, and increasingly in pub-
lic sectors, due to fnancial cuts [1]. Another consequence
of economic globalisation concerns the segmentation of
the labour market, a related increase in income inequality
and a substantial loss of jobs. A large part of the work-
force in advanced societies suffers from job insecurity, low
wages and salaries, and a low level of safety at work. With
the globalisation of labour markets, competition among
employees has been increasing, and a growing proportion
has been exposed to mergers, downsizing, outsourcing, or
redundancy [2].
R E V I E W P A P E R S J. SIEGRIST
IJOMEH 2010;23(3) 280
the demand-control model and the effort-reward imba-
lance model.
The demand-control model [7] posits that stressful experi-
ence at work results from a distinct job task profle defned
by two dimensions, the psychological demands put on the
working person and the degree of control or decision
latitude available to the person to perform the required
tasks. Jobs defned by high demands in combination with
low control are stressful because they limit the individuals
autonomy and sense of control while generating contin-
ued pressure (high job strain). A third dimension, social
support at work, was added to the original formulation. In
this formulation, the highest level of strain would be ex-
pected in jobs that are characterized by high demand, low
control and low social support at work or social isolation
(iso-strain jobs) [8].
While this model is focused on specifc workplace charac-
teristics, the effort-reward imbalance model is concerned
with stressful features of the work contract [9]. This model
builds on the notion of social reciprocity, a fundamental
principle of all types of transactions that are characterized
by some form of utility. Social reciprocity lies at the core
of the work contract which defnes distinct obligations or
tasks to be performed in exchange for adequate rewards.
These rewards include money, esteem and career oppor-
tunities (promotion, job security). Contractual reciproc-
ity operates through norms of return expectancy, where
effort spent by employees is reciprocated by equitable
rewards from employers. The effort-reward imbalance
model claims that lack of reciprocity occurs frequently un-
der specifc conditions. Failed reciprocity, in terms of high
cost and low gain, elicits strong negative emotions and
associated stress reactions with adverse long-term health
consequences. High cost-low gain conditions at work
occur frequently if employed people have no alternative
choice in the labour market (e.g. due to low qualifcation)
or if they make strategic choices to spend additional ef-
forts in order to improve their career prospects in highly
competitive professions. Moreover, there are psychologi-
cal reasons for a recurrent mismatch between efforts and
reward at work. People characterized by a motivational
pattern of excessive work-related overcommitment may
How do these changes relate to the occurrence of cardio-
vascular diseases?
Occupational health research has clearly demonstrated
that working conditions and employment arrangements
make a signifcant contribution to the burden of cardiovas-
cular disease [3,4]. While specifc physical and chemical
occupational hazards with direct impact on cardiovascular
pathology that are identifed by occupational medicine are
still relevant in distinct occupational groups, large propor-
tions of the work force in modern economies are exposed
to mental and emotional demands and threats at work,
rather than material demands and hazards. As a result,
psychological and social stressors (often termed psycho-
social stressors) are becoming more frequent, and their
contribution to cardiovascular disease at work is likely to
parallel or even outweigh the contribution of more tradi-
tional occupational stressors.
Although psychosocial adversity at work has become an
important concern of research and policy, conceptual clar-
ifcation and valid measurement are major challenges to
science. In a stress-theoretical perspective, occupational
demands, threats and conficts act as psychosocial stres-
sors if active coping efforts are required that cannot be
easily resolved.
These conditions cannot be identifed by direct physical or
biological measurement. Rather, theoretical concepts are
needed to delineate particular stressful job characteristics
so that they can be identifed at a level of generalization
that allows for their use in a wide range of different occu-
pations. These concepts can be translated into measures
with the help of social science research methods (stan-
dardized questionnaires, observation techniques, etc.)
that meet the criteria of adequate reliability and validity
of data collection. A variety of concepts that encapsulate
adverse psychosocial work environments have been de-
veloped in occupational health psychology and sociology,
social epidemiology and organisational sciences [for re-
views, see 5,6]. However, only a few have been tested with
convincing study designs (e.g. longitudinal observational
investigations of initially healthy employed populations)
and have addressed the social gradient in work and health.
Among these, two models have received special attention,
WORK AND CARDIOVASCULAR DISEASES R E V I E W P A P E R S
IJOMEH 2010;23(3) 281
(effort, reward, overcommitment, where reward is
further specifed into three theoretically relevant subcom-
ponents) loading on a general third factor that represents
the latent (theoretical) construct. Based on these prem-
ises, a short version containing 16 instead of 23 items was
developed more recently [12]. Both versions are available
in a number of languages.
In epidemiological studies it is often convenient to repre-
sent the independent variable in terms of a single binary
or continuous measure. Therefore, a ratio of the two vari-
ables effort and reward was constructed to represent
the core theoretical notion in a quantitative way, with
a possible cut-point of 1.0 representing a balance between
efforts and rewards, and higher values representing the
risk condition [10].
Quantitative self-report data have received methodologi-
cal criticisms given their limited validity. Yet, despite obvi-
ous limitations, satisfying correlations with more objective
measures and with computerized ambulatory diaries were
reported [13,14]. It should also be noted that in a stress-
theoretical perspective, subjective appraisals are an im-
portant source of information when estimating their po-
tential emotional and psychobiological impact.
Given the advantage of a short, standardized quantitative
measure with comparable scores the ERI questionnaire
has been applied in a large number of prospective epide-
miological studies, cross-sectional studies, case-control
studies and experimental investigations. Study populations
include industrial and service sectors, both gender and all
age groups, and participants from Western industrialised
societies as well as from rapidly developing Asian societ-
ies [for reviews 15,16].
RESULTS
The relatively strongest evidence on associations of psycho-
social stress at work with cardiovascular risk and disease is
obtained from prospective epidemiological observational
studies. This is due to the temporal sequence (exposure
assessment precedes disease onset), the usual sample
size (based on statistical power calculation and allowing
for adjustment for confounding variables in multivariate
strive towards continuously high achievement because of
their underlying need for approval and esteem at work.
Although these excessive efforts often are not met by ad-
equate rewards, overcommitted people tend to maintain
their level of involvement.
In summary, the model of effort-reward imbalance at
work maintains that people experiencing dependency,
strategic choice, and overcommitment, either separately
or in combination, are often exposed to failed contractual
reciprocity at work and its health-adverse consequences.
The model combines organisational features with person-
al coping characteristics.
The demand-control and the effortreward imbalance
models complement each other by focusing on toxic com-
ponents of job task profles and employment contracts,
respectively. Low control and low reward are assumed
to be equally stressful experiences in the context of work
that requires high levels of effort. They both elicit nega-
tive emotions and enhanced stress responses with adverse
long-term health consequences including cardiovascular
diseases. In the following parts of this contribution, the
current state of empirical evidence linking psychosocial
stress at work (specifcally in terms of the effort-reward
imbalance model) with cardiovascular risk and disease is
briefy summarized and discussed.
METHODS
Effortreward imbalance (ERI) at work is measured
by a standardised, psychometrically validated self-re-
port questionnaire containing the three scales: effort
(6 items), reward (11 items that represent the three
dimensions of fnancial and career-related rewards, of
esteem and of job security in respective subscales), and
overcommitment (6 items representing the intrinsic mod-
el component) [10]. The Likert-scaled items are rated by
respondents, and a total score of each scale is calculated.
Psychometric properties of these scales were extensively
assessed, including internal consistency, discriminant and
criterion validity, sensitivity to change, and factorial in-
variance [10,11]. Moreover, confrmatory factor analysis
revealed three moderately correlated second-order factors
R E V I E W P A P E R S J. SIEGRIST
IJOMEH 2010;23(3) 282
neuroendocrine, immune and infammatory responses
via the organisms stress axes. There is extensive evidence
from animal and human research that prolonged stimula-
tion of these psychobiological processes contributes to the
development of cardiovascular disease [2931].
Several studies were conducted so far testing effortreward
imbalance at work and its impact on cardiovascular, stress
hormone and immune parameters. Two such studies con-
cern ambulatory blood pressure monitoring where over-
committed, low status men were shown to exhibit elevated
systolic blood pressure throughout the workday [32] and
where stressed healthy computer employees were shown
to manifest elevated heart rate, systolic blood pressure
and a tendency towards reduced heart rate variability [33].
Additional studies explored associations of ERI with se-
cretion of stress hormones, e.g. cortisol, adrenalin and no-
radrenalin. A dysregulated secretion pattern was observed
in a majority of these studies [32,3436]. In view of the
importance of infammation for the development of car-
diovascular disease [37] a recent experimental study is of
particular interest documenting higher concentrations of
C-reactive protein (a marker of infammation) following
exposure to a standardized mental stress test in participants
scoring high on ERI measures, compared to participants
with less or no work stress [38]. Finally, a summary index
of stress-related biological markers of allostatic load has
been proposed by McEwen [31], indicating increased sus-
ceptibility to cardiovascular risk and disease. In a study on
female teachers it was demonstrated that the group scor-
ing high on ERI measures exhibited a signifcantly higher
mean score than the less stressed group [39].
Taken together, naturalistic and experimental studies
supplement epidemiological evidence by demonstrating
psychobiological processes that possibly mediate the ob-
served associations of psychosocial adversity at work with
cardiovascular disease.
DISCUSSION
This contribution documents available evidence on
the contribution of an adverse (in terms of effortre-
ward imbalance) psychosocial work environment to the
analysis), and the quantifcation of subsequent disease
risk following exposure (odds ratio of disease in exposed
vs. non exposed individuals). Additional evidence comes
from case-control studies, cross-sectional studies, ambu-
latory monitoring studies, and experimental or quasi-ex-
perimental investigations including intervention trials. All
these types of study designs were applied to analyse asso-
ciations of ERI with cardiovascular risk and disease.
Up to now, six reports from prospective epidemiological
studies tested whether and to what extent components of
the ERI model are associated with incident coronary heart
or cardiovascular disease. In fve of these reports the odds
ratios or hazard ratios varied between 1.3 and 4.5, with an
overall doubling of the risk of exposed people [1721; for
review 22]. Even if the reported odds ratios are not large,
their effects in absolute terms are considerable, given the
fact that between 10 and 25 percent of the samples were
exposed to work stress in terms of this model. One report
was negative [for review 23]. Five additional reports from
cohort studies concern signifcant associations of ERI with
depression as disease outcome which is now considered an
established cardiovascular risk factor. In these studies ele-
vated depression risks of exposed people varied between 1.4
and 3.6 [24,25]. In the British Whitehall II study, an elevated
risk of type 2 diabetes, a further established cardiovascular
risk factor, was observed in men, but not in women [26]. Sev-
eral case-control studies with cardiac patients and healthy
controls were conducted, most recently an interesting study
in China where working men and women reporting high ef-
fort, low reward and high overcommitment were about fve
times more likely to belong to the group of myocardial in-
farction cases than those with low or no work stress [27].
Despite their methodological strengths, epidemiological
studies provide little insight into the mechanisms underly-
ing the observed statistical associations. Two such mecha-
nisms are generally considered: the mediation by health-
adverse behaviours, such as smoking, poor diet, or lack of
physical exercise [28], and the mediation by chronic stress
reactions that contribute to the development of disease
via psychobiological mechanisms. Psychobiological pro-
cesses are the pathways through which a health-adverse
psychosocial work environment activates autonomic,
WORK AND CARDIOVASCULAR DISEASES R E V I E W P A P E R S
IJOMEH 2010;23(3) 283
savings within companies. This has been highlighted by a US
study that documented a set of common organizational fea-
tures among those companies that were most successful in
terms of shareholder value over a couple of yeas [47]. These
features included employment security, selective hiring of
new personnel, comparatively high compensation contin-
gent on organizational performance and reduced status
distinctions, among other things. It is evident that several
of these features are similar to those which result as recom-
mendations from the scientifc fndings summarized above.
Yet, a third level of policy implications is needed: national
and international regulations that ensure and enhance
healthy work and fair employment contracts and that sup-
port welfare measures to protect workers against the risks
of unemployment, sickness absence, disability pensions, and
occupational injuries and diseases. Therefore, joint efforts
are required from stakeholders, professionals and national/
international organizations to improve healthy work and, by
doing so, to reduce a relevant part of the burden of cardio-
vascular disease.
REFERENCES
1. Ostry AS, Spiegel JM. Labor markets and employment inse-
curity: Impacts of globalization on the healthcare workforce.
Int J Occup Environ Health 2004;10:36874.
2. Landsbergis PA. The changing organization of work and the
safety and health of working people: A commentary. J Occup
Environ Med 2003;11:6171.
3. Schnall PL, Belkic K, Landsbergis PA, Baker D. Why the work-
place and cardiovascular disease? Occup Med 2000;15:116.
4. Schnall PL, Dobson M, Rosskam E, editors. Unhealthy work:
Causes, consequences and cures. Amityville, NY: Baywood
Press; 2009.
5. Antoniou AG, Cooper, CL, editors. Research companion to
organizational health psychology. Cheltenam: Edward El-
gar; 2005.
6. Cartwright S, Cooper CC, editors. The Oxford handbook
of organizational well-being. Oxford: Oxford University
Press; 2009.
7. Karasek RA, Theorell T. Healthy work. New York: Basic
Books; 1990.
development of cardiovascular risk and disease. Evidence
may be even stronger if supplemented by available research
on complementary work stress models, in particular the
demand-control model [40,3,4] or the organisational jus-
tice model [22]. Moreover, psychosocial adversity at work
often manifests itself in combination with noxious physi-
cal conditions (e.g. noise) and work time-related stressors
(shift work, overtime work), thus precipitating respective
health risks [4144]. Clearly, there are further challenges
concerning the robustness of scientifc evidence, the gen-
eralisation of fndings to other occupational groups and
socio-cultural contexts, and the need of conducting inter-
vention trials with documented health benefts.
Despite these limitations, several policy implications of
the current state of evidence are obvious. First, there is
a need of documenting, assessing and comparing the prev-
alence of critical aspects of an adverse psychosocial work
environment within and between companies and organi-
sations. By this approach, special employment groups at
elevated risk can be identifed, and preventive efforts can
be developed on this basis. A second practical implication
concerns the development, implementation and evaluation
of theory-guided interventions within single companies
and organisations. In this respect, the ERI model offers
options to develop activities at three levels, the individual
level (e.g. reduction of overcommitment), the interper-
sonal level (e.g. improvement of leadership, of providing
esteem reward), and the structural level (e.g. compensa-
tory wage systems, models of gain sharing, and strengthen-
ing of non-monetary gratifcations).
Several intervention studies were conducted along these
lines. For instance, in a trial involving urban bus drivers,
skills of coping with stressful work were improved, over-
commitment was reduced, superiors were trained to appre-
ciate the bus drivers work more closely and group sizes of
subordinates were reduced to enhance communication and
collaboration across hierarchies [45]. Another intervention
was implemented in two Canadian hospitals to reduce burn-
out and to improve occupational rewards among nurses and
physicians [46]. Resistance against such interventions from
the part of management may be overcome by expected in-
creases in return on investment due to medium-term cost
R E V I E W P A P E R S J. SIEGRIST
IJOMEH 2010;23(3) 284
heart disease and health functioning within the Whitehall II
Study. Occup Environ Med 2002;59:77784.
20. Lynch J, Krause N, Kaplan GA, Tuomilehto J, Salonen JT. Work
place conditions, socioeconomic status, and the risk of mortality
and acute myocardial infarction: The Kuopio ischemic heart dis-
ease risk factor study. Am J Public Health 1997b;87:61722.
21. Siegrist J, Peter R, Junge A, Cremer P, Seidel D. Low
status control, high effort at work and ischemic heart dis-
ease: Prospective evidence from blue-collar men. Soc Sci
Med 1990;31:112734.
22. Kivimki M, Virtanen M, Elovainio M, Kouvonen A,
Vn nen A, Vahtera J. Work stress in the etiology of coro-
nary heart disease A meta-analysis. Scand J Work Environ
Health 2006;32:43142.
23. Eller NH, Netterstrom B, Gyntelberg F, Kristensen TS,
Nielsen F, Steptoe A, et al. Work-related psychosocial fac-
tors and the development of ischemic heart disease. Cardiol
Rev 2009;17:8397.
24. Siegrist J. Unfair exchange and health: Social bases of stress-
related diseases. Soc Theory Health 2009;7(4):30517.
25. Stansfeld SA, Candy B. Psychosocial work environment and
mental health A meta-analytic review. Scand J Work Environ
Health 2006;32:44362.
26. Kumari M, Head J, Marmot M. Prospective study of social
and other risk factors for incidence of type II diabetes in White-
hall 2 study. Ann Intern Med 2004;164:187380.
27. Xu W, Zhao Y, Guo L, Guo Y, Gao W. Job stress and coro-
nary heart disease: A case-control study using a Chinese popu-
lation. J Occup Health 2009;51 10713.
28. Siegrist J, Rdel A. Work stress and health risk behaviour.
Scand J Work Environ Health 2006;32:47381.
29. Chandola T, Britton A, Brunner E, Hemingway H, Malik M,
Kumari M, et al. Work stress and coronary heart disease: What
are the mechanisms? Eur Heart J 2008;29:6408.
30. Weiner H. Perturbing the organism. The biology of stressful ex-
perience. Chicago: Chicago University Press; 1992.
31. McEwen B. Protective and damaging effects of stress media-
tors. New Engl J Med 1998;338:1719.
32. Steptoe A, Siegrist J, Kirschbaum C, Marmot M. Effort
reward imbalance, overcommitment, and measures of cor-
tisol and blood pressure over the working day. Psychosom
Med 2004;66:3239.
8. Johnson JV, Hall EM. Job strain, workplace social support
and cardiovascular disease: A cross sectional study of a ran-
dom sample of the Swedish working population. Am J Public
Health 1988;78:133642.
9. Siegrist J. Adverse health effects of high-effort/low-reward con-
ditions. J Occup Health Psychol 1996;1:2741.
10. Siegrist J, Starke D, Chandola T, Godin I, Marmot M,
Niedhammer I. The measurement of effortreward imbal-
ance at work: European comparisons. Soc Sci Med 2004;58:
148399.
11. Jonge J de, Linden S van der, Schaufeli W, Peter R, Siegrist J.
Factorial invariance and stability of the EffortReward Im-
balance Scales: A longitudinal analysis of two samples with
different time lags. Int J Behav Med 2008;15(1):6272.
12. Siegrist J, Wege N, Phlhofer F, Wahrendorf M. A short
generic measure of work stress in the era of globalisa-
tion: Effortreward imbalance. Int Arch Occup Environ
Health 2008;82:100513.
13. Tsutsumi A, Nagami M, Morimoto K, Matoba T. Responsive-
ness of measures in the effortreward imbalance questionnaire
to organisational change: A validation study. J Psychosom Re-
search 2002;52:24956.
14. Johnston DW, Beedie A, Jones MC. Using computerized
ambulatory diaries for the assessment of job characteristics
and work-related stress in nurses. Work & Stress 2006;20(2):
16372.
15. Tsutsumi A, Kawakami A. A review of empirical studies on
the model of effortreward imbalance at work: Reducing oc-
cupational stress by implementing a new theory. Soc Sci
Med 2004;59:233559.
16. Vegchel N van, Jonge J de, Bosma H, Schaufeli W. Reviewing
the effortreward imbalancwe model: Drawing up the balance
of 45 empirical studies. Soc Sci Med 2005;60:111731.
17. Bosma H, Peter R, Siegrist J, Marmot M. Two alternative job
stress models and the risk of coronary heart disease. Am J Pub-
lic Health 1998;88:6874.
18. Kivimki M, Leino-Arjas P, Luukkonen R, Riihimki H,
Vahtera J, Kirjonen J. Work stress and risk of cardiovascular
mortality: Prospective cohort study of industrial employees. Brit
Med J 2002;325:85761.
19. Kuper H, Singh-Manoux A, Siegrist J, Marmot M. When reci-
procity fails: Effortreward imbalance in relation to coronary
WORK AND CARDIOVASCULAR DISEASES R E V I E W P A P E R S
IJOMEH 2010;23(3) 285
41. Hrm M. Work hours in relation to work stress, recovery, and
health. Scand J Work Environ Health 2006;32:50214.
42. Peter R, Alfredsson L, Knutsson A, Siegrist J, Wester-
holm P. Does a stressful psychosocial work environment
mediate the effects of shiftwork on cardiovascular factors
in men? Scand J Work Environ Health 1999;25:37681.
43. Krause N, Brand RJ, Kauhanen J, Kaplan GA, Syme SL,
Wong CC, et al. Work time and 11-year progression of carotid
atherosclerosis in middle-aged Finnish men. Prev Chronic
Dis 2009;6:120.
44. Hulst M van der. Long work hours and health. Scand J Work
Environ Health 2003;29:17188.
45. Aust B, Peter R, Siegrist J. Stress management in bus drivers:
A pilot study based on the model of effortreward imbalance.
Int J Stress Manage 1997;4:297305.
46. Bourbonnais R, Brisson C, Vinet A, Vzina M, Lower A.
Development and implementation of a participative inter-
vention to improve the psychosocial work environment and
mental health in an acute care hospital. Occup Environ
Med 2006;63:32634.
47. Pfeffer J. Human equation: Building proft by putting people
frst. Boston: Harvard Business School Press; 1998.
33. Vrijkotte DGM, Doornen LJP van, Geus EJC de. Effect of
work stress on ambulatory blood pressure, heart rate, and heart
rate variability. Hypertension 2000;35:8806.
34. Bellingrath S, Weigl T, Kudielka BM. Cortisol dysregulation
in school teachers in relation to burnout, vital exhaustion, and
effortreward imbalance. Biol Psychol 2008;78:10413.
35. Hurwitz Eller N, Netterstrom B, Hansen AM. Psychosocial
factors at home and at work and levels of salivary cortisol. Biol
Psychol 2006;73:2807.
36. Wirtz PH, Siegrist J, Rimmele U, Ehlert U. Higher overcom-
mitment to work is associated with lower norepinephrine se-
cretion before and after acute psychosocial stress in men. Psy-
choneuroendocrino 2008;33:929.
37. Stansfeld SA, Marmot M, editors. Stress and the Heart. Lon-
don: BMJ Publishing Company; 2002.
38. Hamer M, Williams E, Vuonovirta R, Giacobazzi P, Gib-
son EL, Steptoe A. The effects of effortreward imbalance on
infammatory and cardiovascular responses to mental stress.
Psychosom Med 2006;68:40813.
39. Bellingrath S, Weigl T, Kudielka BM. Chronic work stress and
exhaustion is associated with higher allostatic load in female
school teachers. Stress: Int J Biol Stress 2009;12:3748.
40. Belkic KL, Landsbergis PA, Schnall PL, Baker D. Is job strain
a major source of cardiovascular disease risk? Scand J Work
Environ Health 2004;30:85128.