Stress and Health

Stress and Health 24: 231–238 (2008)

Published online 14 July 2008 in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/smi.1203
Received 16 November 2007; Accepted 29 February 2008

Occupational stress and

cardiovascular disease
D.G. Byrne1,*,† and Geir Arild Espnes2
1
School of Psychology, The Australian National University
2
School of Social Work and Health Sciences, The Norwegian University of Science and
Technology

Summary
Links between occupational stress and cardiovascular risk have long been asserted. This paper
reviews the evidence from the simple notion of occupational level and type as a risk through to
the more theoretically sophisticated models of occupational stress as a determinant of cardiovas-
cular risk and disease. It maps measures of occupational stress against the three related end points
of coronary risk profiles, hypertension and clinical cardiovascular disease. Taken broadly, the
evidence is supportive of postulated links. The persuasiveness of the evidence now points to inter-
vention studies in the workplace as the next major focus of research. Copyright © 2008 John
Wiley & Sons, Ltd.

Key Words
occupation, stress, cardiovascular disease

Introduction Despite evidence for a recent decline in car-

Occupational stress (OS) is experienced when an
individual is exposed to an overload of stressors
originating wholly (or largely) from the occupa-
tional environment, but this grossly over-simpli-
fies a complex bio-psycho-social situation. The
cumulative literature on OS (or work, or job
stress) is substantial both in volume and breadth,
covering domains as far apart as the physical
characteristics of occupational environments (e.g.
heat, noise and crowding) and the personal char-
acteristics of those working within those environ-
ments (e.g. coping styles, beliefs and cognitive
capacities); and recognizes the interdependence of
OS and other arenas of life stressors.
* Correspondence to: D.G. Byrne, School of Psychol-
ogy, The Australian National University, Canberra
ACT 0200, Australia
†
E-mail: don.byrne@anu.edu.au
diovascular disease (CVD)1 mortality (Taylor,
Dobson, & Mirzaei, 2006), CVD remains a major
cause of death and disability in Western societies.
An interest in the presence of CVD risk factors is
therefore not surprising, and attempts to link the
psychological characteristics of both individuals
and their social environments to CVD risk has
formed a good part of that research. It is inevi-
table then, that attention has turned to OS as an
explanatory factor in the search to explain CVD
risk.
1
A number of terms could be used to refer to the
clinical end-points discussed in this paper; CVD, coro-
nary heart disease (CHD), ischaemic heart disease
(IHD), myocardial infarction (MI) and others are all
relevant. For the sake of consistency however, the
paper will use the standard descriptive term CVD, since
this captures the broadest range of end-points and
allows the most inclusive consideration of the
evidence.

Copyright © 2008 John Wiley & Sons, Ltd.

 D. G. Byrne and G. A. Espnes
Comprehensive reviews of evidence linking OS
to CVD are available to cover the period to the
end of the 20th century (see for example, Byrne,
2000; Smith & Ruiz, 2002; Melamed, Shiron,
Toker, Berliner, & Shapira, 2006). This paper
focuses, therefore, largely on the evidence accu-
mulating from the beginning of this century,
accessed either through Pub Med or PsycINFO
databases, and favouring studies with large
samples, robust designs and theory-driven
measures.
Definitions and models of OS
Definitions of OS are completely consistent with
more general definitions of stress—OS is seen,
either singly or collectively, as exposure to a set
of unique stressors, the operation of an interpre-
tive process, or a pattern of individual responses,
both biological (arousal) and psychological (strain
or distress) (Sulsky & Smith. 2005), However,
Hart and Cooper (2001) have eloquently
highlighted the difficulty in providing a truly
satisfactory definition for such a patently
complex construct. They note that ‘. . . the scien-
tific community has still not reached an agreed
position on the meaning and definition of occu-
pational stress’ (p. 94), and indicate instead the
importance of focusing attention on integrated
models to explain the phenomenon. This review
will therefore organize itself largely around
the usefulness of the dominant theoretical
models of OS.
While Lazarus’s (1991) transactional model of
stress theoretically underpins many approaches to
conceptualising OS, Sulsky and Smith (2005)
note its substantial focus on the individual and
therefore caution against an over-reliance on its
use in empirical studies of OS. But two more
specific models of OS have captured the greatest
research attention in recent times.
• The Demand/Control Model—which views
OS (and its consequences) as arising from a
tension between the demands an occupational
environment imposes on an individual and the
level of perceived control that person has over
the environment (Karasek, 1979). This model
was subsequently updated by Johnson and
Hall (1988) to include a component of social
support.
• Effort/Reward Imbalance Model—where OS
(and its consequences) is related to the balance
232 Copyright © 2008 John Wiley & Sons, Ltd.
between the degree of effort put into the job
and the level of reward resulting from that
effort (Siegrist, et al., 2004).
While these models clearly overlap both themati-
cally and in terms of their capacities to predict
CVD risk (Bosma, Peter, Siegrist, & Marmot.
1998).they both represent conceptually strong
and theoretically coherent approaches to explain-
ing that risk, and both have been backed by a
wealth of empirical evidence. For this reason,
many of the studies chosen for review in this
paper have been based on either one or other of
these models.
OS and CVD risk profiles
One of the central issues surrounding the link
between OS and CVD has to do with whether OS
directly compromises cardiovascular function
and precipitates clinical events or is linked indi-
rectly through intervening factors. CVD risk is
predicted by an array of recognized risk factors,
most prominently cholesterol, cigarette smoking
and hypertension. Relationships between OS and
recognized CVD risk factors will therefore first be
considered.
Cigarette smoking
Cigarette smoking poses an established and potent
risk for CVD (Leone, 2007). Regardless of setting,
stress increases cigarette consumption among
established smokers (Byrne & Mazanov, 2007).
Associations between OS and CVD risk may
therefore be mediated through smoking.
The presence of work-related stress (including
high concentration demand and work dissatisfac-
tion) predicted smoking status in middle-aged
women (Jonsson, Johansson, Rosengren, Lappas,
& Wilhelmsen, 2003), and OS has been associated
with a broad range of smoking measures in both
men and women (Ng & Jeffery, 2003). Associa-
tions between OS and levels of cigarette consump-
tion particularly have emerged (Metcalfe, et al.,
2003). Smoking appears more prevalent amongst
blue- than amongst white-collar workers (Rose,
Kumlin, Dimberg, Bengtsson, Orth-Gomer, &
Cai, 2006), supposedly reflecting the negative
effects of OS. And those who perceive poor
involvement in decision making in the workplace
are more likely to be heavy smokers than those
Stress and Health 24: 231–238 (2008)
DOI: 10.1002/smi
 Occupational stress and cardiovascular disease
without such perceptions (Kouvonen, et al., 2007),
with this finding unaffected either by adjustments
for job strain or effort/reward imbalance.
Both the Demand/Control and Effort/Reward
Imbalance Models have also been more systemati-
cally applied to OS and smoking. High job demand
has been related to smoking in middle-aged rural
workers (Tsutsumi, et al., 2003), and it appears to
influence smoking irrespective of job strain (Kang,
et al., 2005). But job strain (high demand and low
control) too has been linked to smoking (John,
Riedel, Rumpf, Hapke, & Meyer, 2006). And both
high job strain and high effort/reward imbalance
have been independently associated with smoking
intensity (Kouvonen, Kivimaki, Virtanen, Pentti,
& Vahtera, 2005), with lower levels of effort in the
workplace also predicting ex-smoking status. Suf-
ficient evidence therefore now links OS and
smoking that it must be seen as one credible
pathway through which OS influences CVD risk.
The mechanisms for this are less clear—smoking
may operate through interactions with other risk
factors (Leone, 2007) or it may exert a more inde-
pendent influence through excitatory neural pro-
cesses (Byrne & Mazanov, 2007)—but these are
issues for further investigation.
Blood pressure
Elevated blood pressure (BP), particularly if it is
chronic (hypertension), poses an established risk
for CVD (Mendis, et al., 2007). Possible associa-
tions between OS and BP have therefore been
targeted to elucidate the link between OS and
CVD. However, it is important to distinguish
between evidence relating OS and BP per se (even
if measured repeatedly and/or in the work situa-
tion) and evidence linking OS and diagnosed
hypertension—the former may indicate future
hypertension but only the latter reliably predicts
CVD.
Although the idea that OS may influence blood
pressure has existed for some decades, Siegrist
and Klein (1990) first demonstrated a co-varia-
tion between chronic OS and BP reactivity under
challenge. Job strain has been specifically linked
to BP, although Theorell, Ahlberg-Hulten, Jodko,
and Sigala (1993) restricted this to diastolic BP,
and then largely in the work setting. Job strain
based on both demand and control has also been
associated with diastolic BP, but only in men
(Tsutsumi, et al., 1998), or when diastolic BP was
measured at night after work (Rau, Georgiades,
Copyright © 2008 John Wiley & Sons, Ltd.
Fredrikson, Lemne, & de Faire, 2001). Relation-
ships between OS and diastolic BP appear to hold
even after controlling for such possible confound-
ers as age, smoking and alcohol consumption (Su,
et al., 2001).
By contrast, OS specific to medical practitio-
ners was related to elevation of both diastolic and
systolic BP, but maximally only during the
working day (O’Connor, O’Connor, White, &
Bundred, 2001). Elevations in both diastolic and
systolic BP have also been reported in relation to
job strain using ambulatory BP measures in the
workplace (Landsbergis, Schnall, Pickering,
Warren, & Schwartz, 2003) but the association
was only evident in those with low socio-eco-
nomic status. Moving from low to high job strain
occupations significantly elevates systolic BP
(Cesana, Sega, Ferrario, Chiodini, Corrao &
Mancia, 2003), while the same effect has been
observed over time where high job strain prevails
(Kjeldsen, et al., 2006).
BP in the workplace has been related to occu-
pational over-commitment, independent of job
control (Steptoe, Siegrist, Kirschbaum, & Marmot,
2004), and to expressions of workplace anger
(Bongard & al’Absi, 2005). And very recently it
has been reported that job strain may actually
interact with a genetic factor (I/D polymorphism
in the adrenergic alpha2B-receptor) to elevate
both systolic and diastolic BP (Ohlin, Berglund,
Nilsson, & Melander, 2007).
Broad evidence therefore links OS with BP,
largely through the experience of job strain. The
evidence indicates an effect of OS on both systolic
and diastolic BP, and may possibly be mediated
through a genetic interaction. But elevated BP is
not hypertension, and only the latter constitutes
an established risk for CVD.
Hypertension
A combination of high effort and low reward in
the workplace has been associated with a diagno-
sis of hypertension in middle managers (Peter &
Siegrist, 1997) and shift workers (Peter, Alfreds-
son, Knutsson, Siegrist & Westerholm, 1999).
Job strain too has been related to hypertension,
but curiously one study reported this only in men
(Tsutsumi, Kayaba, Tsutsumi, Igarashi, & Jichi,
2001), and another only in women (Alfredsson,
et al., 2002).
However, beyond the strict confines of theo-
retical models of OS, the prevalence of hyperten-
Stress and Health 24: 231–238 (2008) 233
DOI: 10.1002/smi
 D. G. Byrne and G. A. Espnes
sion have also been associated with organizational
job constraints (Radi, et al., 2005), excessive
work hours (Yang, Schnall, Jauregui, Su, &
Baker, 2006), job insecurity and low occupational
prestige, but only in men (Levenstein, Smith, &
Kaplan, 2001), covert coping with unfair treat-
ment at work, but only in men (Theorell, Alfreds-
son, Westerholm, & Falck, 2000), perceived job
barriers and job intensity (Greiner, Krause,
Ragland, & Fisher, 2004), and race-related work-
place stress (Din-Dzietham, Nembhard, Collins,
& Davis, 2004). The evidence implicating OS in
the genesis of hypertension is therefore persuasive
though much of it goes beyond the framework of
established theoretical models.
Blood lipids
Levels of blood lipids, and particularly levels of
LDL cholesterol, have long been associated with
elevated CVD risk (Campbell, et al., 2007). Recent
studies have established reliable links between OS
and this component of CVD risk. OS conceptu-
alised specifically within the Demand/Control
Model has been linked with elevated blood lipids
(Kang, et al., 2005). Curiously, elevated choles-
terol was related only to low decision latitude
(control) and not to job strain. The index of job
strain has been related to elevated lipids (Tsut-
sumi, et al., 1998), but only in working females.
Within the Effort/Reward Imbalance Model the
most persuasive link between OS and blood lipids
comes from the WOLF (Work, Lipids and Fibrin-
ogen) Study (Peter, et al., 1998). Examination of
baseline data from employed males and females
showed that in men, effort/reward imbalance was
significantly related both to high total cholesterol
and to a total cholesterol : HDL ratio; in women,
high effort was related both to increased LDL
levels and to a cholesterol : LDL ratio. Westerlund,
Theorell and Alfredsson (2004) extended analyses
of the WOLF Study data to include indices of
employment stability, reporting elevated choles-
terol amongst employees of companies where
organizational instability was evident. Evidence
associating OS with potentially harmful levels of
blood lipids is therefore well established.
Metabolic syndrome
An interesting extension of this work focuses on
OS and the metabolic syndrome (Melamed, et al.,
234 Copyright © 2008 John Wiley & Sons, Ltd.
2006), which has been linked with CVD risk. Job
strain is strongly associated with rates of meta-
bolic syndrome (Kang, et al., 2004); this relation-
ship follows a dose-response function (Chandola,
Brunner, & Marmot, 2006). However, women
with low long-term job strain were reported to
have high levels of metabolic syndrome, whereas
men with high long-term job strain showed low
levels of metabolic syndrome (Kinnunen, Feldt,
Kinnunen, Kaprio, & Pulkkinen, 2006). And at
least one recent study found no relationship
between job strain and metabolic syndrome
(Demiral, et al., 2006). This area must therefore
be considered to require further exploration.
Fibrinogen
While the evidence here is by no means uncon-
tested, plasma fibrinogen has been implicated as
a predictor of CVD (Woodward, Rumley, Welsh,
McMahon, & Lowe, 2007) and this too may
mediate a link between OS and CVD risk (Theo-
rell, 2002). A number of studies have reported
associations between plasma fibrinogen and low
job control generally (Clays, et al., 2005), low job
control in female workers only (Tsutsumi, Theo-
rell, Hallqvist, Reuterwall, & de Faire, 1999),
and job strain in males but not females (Kittel, et
al., 2002). Unsupportive evidence, however
(Alfredsson, et al., 2002), indicates that some
caution must be exercised until further evidence
is available.
OS and incidence of clinical CVD
Both the Demand/Control (Theorell & Karasek,
1996) and Effort/Reward Imbalance (Siegrist,
2005; van Vegchel, se Jonge, Bosma, & Schaufeli,
2005) models have been persuasively linked to
clinical CVD. Largely atheoretical constructs
have also driven many studies in this area, and
while the evidence is more difficult to interpret, it
is also persuasive.
Case-control studies (theoretically based)
Job strain as an index of OS has been related to
a significant elevation in CVD amongst middle-
aged men, independent of other risk factors
(Alfredsson & Theorell, 1983), though a syner-
gistic interaction between demands and decision
Stress and Health 24: 231–238 (2008)
DOI: 10.1002/smi
 Occupational stress and cardiovascular disease
latitude strengthened associations (Hallqvist,
et al., 1998). A more recent study of job
strain strongly associated it with heart disease
in a large sample of men, again independent of
other CVD risk factors, however heart disease
here was self-reported (Sacker, Bartley, Frith,
Fitzpatrick, & Marmot, 2001). The relationship,
however, was also evident in a sample of men
who survived a clinically diagnosed CVD event
(Malinauskiene, et al., 2005). Over-commitment
to work (high effort) was also strongly related to
CVD in women occupying male-dominated jobs
(Peter, Hammarstrom, Hallqvist, Siegrist, & The-
orell, 2006). And interestingly, recent work sug-
gests that a combination of the demand/control
and effort/reward imbalance models further
strengthens the capacity of OS to predict clinical
CVD (Peter, Siegrist, Hallqvist, Reuterwall, &
Theorell, 2002).
Case-control studies (atheoretical)
Chronic high workload has been associated with
the prevalence of CVD (Siegrist, Dittmann,
Rittner, & Weber, 1982), as has shift work
(Alfredsson, Karasek, & Theorell. 1982), Self-
reported OS, again focussing on the workplace
structure, significantly predicted clinical CVD in
a sample of patients experiencing their first clini-
cal event (Panagiotakas, et al., 2003). Moreover,
perceived unfairness in the workplace has been
linked with an elevated risk of clinical CVD (De
Vogli, Ferrie, Chandola, Kivimaki, & Marmot,
2007).
Prospective studies (theoretically based)
However, prospective studies are crucial to
exploring links between OS and CVD. Lee,
Colditz, Berkman and Kawachi (2002) found no
evidence to causally associate job strain with the
emerging incidence of CVD in a sample of women
over four years. By contrast, Kivimaki, et al.
(2002) found both job strain and effort/reward
imbalance to significantly predict risk of CVD
mortality over 25 years. High demand and low
decision latitude also predicted the incidence of
CVD over an 11-year follow-up (Kuper &
Marmot, 2003). And in women, job strain has
been linked to progression of coronary athero-
sclerosis over a 3-year period (Wang, et al.,
2007).
Copyright © 2008 John Wiley & Sons, Ltd.
Prospective studies (atheoretical)
Job dissatisfaction was only slightly associated
with age-adjusted CVD risk in men over time, but
not in women, and there was no evidence linking
it with evolving CVD mortality (Heslop, Smith,
Metcalfe, Macleod, & Hart, 2002). However,
high perceived justice in the workplace related to
a lower risk of CVD in men followed-up over
more than 8 years (Kivimaki, et al., 2005).
Conclusions
This review has been selective and not exhaustive,
focussing largely on recent material. Empirical evi-
dence from studies with robust research designs
broadly—but not universally—support links
between OS and CVD. Studies relating OS and
CVD risk factors particularly support a link
between OS and eventual CVD—and evidence
focusing on BP and hypertension is perhaps stron-
gest. Evidence from both case-control and pro-
spective studies also persuasively support a link
between OS and clinical CVD, although prospec-
tive studies are fewer in number. Both the Demand/
Control (Job Strain) and Effort/Reward Imbalance
Models offer powerful conceptual frameworks
linking OS with CVD; a combination of the two
achieves demonstrable synergies in predicting
CVD. And, even atheoretical approaches provide
convincing evidence for the link. Strengths of asso-
ciation between OS and CVD are typically modest,
and obviously, not all studies have supported the
proposed link—to comprehensively discuss these
studies, and the reasons why they do not offer that
support, would go beyond the scope of this brief
review. The collective evidence now available,
however, must be viewed as sufficiently consistent
and robust to support the conclusion that OS is
linked, either indirectly or directly, with CVD.
This being so, the next generation of research
may well need to focus both on psycho-biological
mechanisms of influence and on interventions to
reduce OS in the workplace. Again, a detailed
discussion either of mediating mechanisms or of
specific workplace interventions goes well beyond
the scope of this review. In regard to the latter
however, future research will almost inevitably
need to address the legal and political realm of
industrial relations. The provision of a safe work-
place needs to encompass freedom from OS and
if this lowers the population risk of CVD it is a
freedom well worth seeking.
Stress and Health 24: 231–238 (2008) 235
DOI: 10.1002/smi
 D. G. Byrne and G. A. Espnes
References
Alfredsson, L., Hammar, N., Fransson, E., de Faire, U., Hal-
lqvist, J., Knutsson, A., Nilsson, T., Theorell, T., & Wester-
holm, P. (2002). Job strain and major risk factors for
coronary heart disease among employed males and females
in a Swedish study on work, lipids and fibrinogen. Scandi-
navian Journal of Work, Environment and Health, 28(4),
238–248.
Alfredsson, L., Karasek, R., & Theorell, T. (1982). Myocar-
dial infarction risk and psychosocial work environment: An
analysis of the male Swedish working force. Social Science
and Medicine, 16, 463–467.
Alfredsson, L., & Theorell, T. (1983). Job characteristics of
occupations and myocardial infarction risk: Effect of pos-
sible confounding factors. Social Science and Medicine,
17(20), 1497–1503.
Bongard, S., & al’Absi, M. (2005). Domain-specific anger
expression and blood pressure in an occupational setting.
Journal of Psychosomatic Research, 58(1), 43–49.
Bosma, H., Peter, R., Siegrist, J., & Marmot, M. (1998).
Two alternative job stress models and the risk of coronary
heart disease. American Journal of Public Health, 88(1),
68–74.
Brunner, E.J., Kivimaki, M., Siegrist, J., Theorell, T., Luuk-
konen, R., Riihimaki, H., Vahtera, J., Kirjonen, J., & Leino-
Arjas, P. (2004). Is the effect of work stress on
cardiovascular mortality confounded by socioeconomic
factors in the Valmet study? Journal of Epidemiology and
Community Health, 58(12), 1019–1020.
Byrne, D.G. (2000). The frustration of success: Type A behav-
ior, occupational stress and cardiovascular disease. In D.T.
Kenny, J.G. Carlson, F.J. McGuigan & J.L. Sheppard (Eds),
Stress and health. research and clinical applications. Amster-
dam, The Netherlands: Harwood Academic Publishers.
Byrne, D.G., & Mazanov, J. (2007). Personality, stress and
the determination of smoking behaviour in adolescents. In
G. Boyle, G. Matthews & D. Saklofske (Eds), Handbook
of personality theory and testing. London: Sage.
Campbell, C.Y., Nasir, K., Sarwar, A., Meneghelo, R.S., Car-
valho, J.A., Blumenthal, R.S., et al. (2007). Combined effect
of high low-density lipoprotein cholesterol and metabolic
syndrome on subclinical coronary atherosclerosis in white
men without clinical evidence of myocardial ischemia.
American Journal of Cardiology, 100(5), 840–843.
Cesana, G., Sega, R., Ferrario, M., Chiodini, P., Corrao, G.
& Mancia, G. (2003) Job strain and blood pressure in
employed men and women: A pooled analysis of the four
northern Italian population samples. Psychosomatic Medi-
cine, 65, 558–563.
Chandola, T., Brunner, E., & Marmot, M. (2006). Chronic
stress at work and the metabolic syndrome: Prospective
study. British Medical Journal, 332(7540), 521–525.
Clays, E., De Bacquer, D., Delanghe, J., Kittel, F., Van Rent-
erghem, L., & De Backer, G. (2005). Associations between
dimensions of job stress and biomarkers of inflammation
and infection. Journal of Occupational & Environmental
Medicine, 47(9), 878–883.
De Vogli, R., Ferrie, J.E., Chandola, T., Kivimaki, M., &
Marmot, M.G. (2007). Unfairness and health: Evidence
from the Whitehall II Study. Journal of Epidemiology and
Community Health, 61(6), 513–518.
Demiral, Y., Soysal, A., Can Bilgin, A., Kilic, B., Unal, B.,
Ucku, R., & Theorell, T. (2006). The association of job
strain with coronary heart disease and metabolic syndrome
in municipal workers in Turkey. Journal of Occupational
Health, 48(5), 332–338.
236 Copyright © 2008 John Wiley & Sons, Ltd.
Din-Dzietham, R., Nembhard, W.N., Collins, R., & Davis,
S.K. (2004). Perceived stress following race-based discrimi-
nation at work is associated with hypertension in African-
Americans. The Metro Atlanta Heart Disease Study,
1999–2001. Social Science and Medicine, 58(3), 449–461.
Greiner, B.A., Krause, N., Ragland, D., & Fisher, J.M. (2004).
Occupational stressors and hypertension: A multi-method
study using observer-based job analysis and self-reports in
urban transit operators. Social Science and Medicine, 59(5),
1081–1094.
Hallqvist, J., Diderichsen, F., Theorell, T., Reuterwall, C.,
Ahlbom, A., & Sheep Study Group. (1998). Is the effect of
job strain on myocardial infarction risk due to interaction
between high psychological demands and low decision
latitude? Results from Stockholm Heart Epidemiology
Program (SHEEP). Social Science and Medicine, 46(11),
1405–1415.
Hart, P.M. & Cooper, C.L. (2001). Occupational stress:
Toward a more integrated framework. In N. Anderson,
D.S. Ones, H.K. Sinangil & C. Viswesvaran (Eds), Hand-
book of Industrial, Work and Organizational Psychology
(Vol. 2. Personnel Psychology, pp 93–114). London:
Sage.
Heslop, P., Smith, G.D., Metcalfe, C., Macleod, J., & Hart,
C. (2002). Change in job satisfaction, and its association
with self-reported stress, cardiovascular risk factors and
mortality. Social Science and Medicine, 54, 1589–1599.
John, U., Riedel, J., Rumpf, H.J., Hapke, U., & Meyer, C.
(2006). Associations of perceived work strain with nicotine
dependence in a community sample. Occupational & Envi-
ronmental Medicine, 63(3), 207–211.
Johnson, J.V. & Hall, E.M. (1988). Job strain, workplace,
social support and cardiovascular disease: A cross-sectional
study of a random sample of the Swedish working popula-
tion. American Journal of Public Health, 78, 1336–1342.
Jonsson, D., Johansson, S., Rosengren, A., Lappas, G., &
Wilhelmsen, L. (2003). Self-perceived psychological stress
in relation to psychosocial factors and work in a random
population sample of women. Stress and Health, 19(3),
149–162.
Kang, M.G., Koh, S.B., Cha, B.S., Park, J.K., Baik, S.K., &
Chang, S.J. (2005). Job stress and cardiovascular risk
factors in male workers. Preventive Medicine, 40, 583–
588.
Kang, M.G., Koh, S.B., Cha, B.S., Park, J.K., Woo, J.M., &
Chang, S.J. (2004). Association between job stress on heart
rate variability and metabolic syndrome in shipyard male
workers. Yonsei Medical Journal, 45(5), 838–846.
Karasek, R. (1979). Job demands, job decision latitude and
mental strain: Implications for job redesign. Administrative
Science Quarterly, 24, 285–308.
Kinnunen, M.L., Feldt, T., Kinnunen, U., Kaprio, J., & Pulk-
kinen, L. (2006). Association between long-term job strain
and metabolic syndrome factor across sex and occupation.
Journal of Individual Differences, 27(3), 151–161.
Kittel, F., Leynen, F., Stam, M., Dramaix, M., de Smet, P.,
Mak, R., De Backer, G. & Kornitzer, M. (2002). Job
conditions and fibrinogen in 14,226 Belgian workers. The
Belstress study. European Heart Journal, 23, 1841–1848.
Kivimaki, M., Ferrie, J.E., Brunner, E., Head, J., Shipley, M.J.,
Vahtera, J., & Marmot, M.G. (2005). Justice at work and
reduced risk of coronary heart disease among employees:
The Whitehall II Study. Archives of Internal Medicine,
165(19), 2245–2251.
Kjeldsen, S.E., Knudsen, K., Ekrem, G., Fure, T.O., Mov-
inckel, P., & Erikssen, J.E. (2006). Is there an association
between severe job strain, transient rise in blood pressure
Stress and Health 24: 231–238 (2008)
DOI: 10.1002/smi
 Occupational stress and cardiovascular disease
and increased mortality? Journal of Blood Pressure, 15(2),
93–100.
Kouvonen, A., Kivimaki, M., Virtanen, M., Pentti, J., &
Vahtera, J. (2005). Work stress, smoking status, and
smoking intensity: An observational study of 46,190
employees. Journal of Epidemiology and Community
Health, 59(1), 63–69.
Kouvonen, A., Vahtera, J., Elovainio, M., Cox, S.J., Cox, T.,
Linna, A., et al. (2007). Organisational justice and smoking:
The Finnish Public Sector Study. Journal of Epidemiology
and Community Health, 61(5), 427–433.
Kuper, H., & Marmot, M. (2003). Job strain, job demands,
decision latitude, and risk of coronary heart disease within
the Whitehall II study. Journal of Epidemiology and Com-
munity Health, 57, 147–153.
Landsbergis, P.A., Schnall, P.L., Pickering, T.G., Warren, K.,
& Schwartz, J.E. (2003). Lower socioeconomic status
among men in relation to the association between job strain
and blood pressure. Scandinavian Journal of Work, Envi-
ronment and Health, 29(3), 206–215.
Lazarus, R.S. (1991). Psychological stress in the workplace.
Journal of Social Behavior and Personality, 6, 1–13.
Lee, S., Colditz, G., Berkman, L., & Kawachi, I. (2002). A
prospective study of job strain and coronary heart disease
in US women. International Journal of Epidemiology,
31(6), 1147–1153.
Leone, A. (2007). Smoking, haemostatic factors, and cardio-
vascular risk. Current Pharmaceutical Design, 13(16),
1661–1667.
Levenstein, S., Smith, M.W., & Kaplan, G.A. (2001). Psycho-
social predictors of hypertension in men and women.
Archives of Internal Medicine, 161(10), 1341–1346.
Malinauskiene, V., Theorell, T., Grazuleviciene, R., Azara-
viciene, A., Obelenis, V., & Azelis, V. (2005). Psychosocial
factors at work and myocardial infarction among men in
Kaunas, Lithuania. Scandinavian Journal of Work, Envi-
ronment and Health, 31(3), 218–223.
Melamed, S., Shirom, A., Toker, S., Berliner, S., & Shapira,
I. (2006). Burnout and risk of cardiovascular disease: Evi-
dence, possible causal paths, and promising research direc-
tions. Psychological Bulletin, 132(3), 327–353.
Mendis, S., Lindholm, L.H., Mancia, G., Whitworth, J.,
Alderman, M., Lim, S., et al. (2007). World Health Orga-
nization (WHO) and International Society of Hypertension
(ISH) risk prediction charts: Assessment of cardiovascular
risk for prevention and control of cardiovascular disease in
low and middle-income countries. Journal of Hypertension,
25(8), 1578–1582.
Metcalfe, C., Smith, G.D., Wadsworth, E., Sterne, J.A. C.,
Heslop, P., Macleod, J., et al. (2003). A contemporary
validation of the Reeder Stress Inventory. British Journal of
Health Psychology, 8(1), 83–94.
Ng, D.M., & Jeffery, R.W. (2003). Relationships between
perceived stress and health behaviors in a sample of working
adults. Health Psychology, 22(6), 638–642.
O’Connor, D.B., O’Connor, R.C., White, B.L., & Bundred,
P.E. (2001). Are occupational stress levels predictive of
ambulatory blood pressure in British GP’s? An exploratory
study. Family Practice, 18(1), 92–94.
Ohlin, B., Berglund, G., Nilsson, P.M., & Melander, O.
(2007). Job strain, decision latitude and alpha2B-adrenergic
receptor polymorphism significantly interact, and associate
with higher blood pressure in men. Journal of Hyperten-
sion, 25(8), 1613–1619.
Panagiotakos, D.B., Chrysohoou, C., Pitsavos, C., Antoniou,
S., Vavouranakis, E., Stravopodis, P., Morairi, A.D., Stefa-
nadis, C.I., & Toutouzas, P.K. (2003). The association
Copyright © 2008 John Wiley & Sons, Ltd.
between occupational stress and the risk of developing
acute coronary syndromes: The CARDIO2000 Study.
Central European Journal of Public Health, 11(1), 25–30.
Peter, R., Alfredsson, L., Hammar, N., Siegrist, J., Theorell,
T., & Westerholm, P. (1998). High effort, low reward, and
cardiovascular risk factors in employed Swedish men and
women: Baseline results from WOLF study. Journal of Epi-
demiology and Community Health, 52, 540–547.
Peter, R., Alfredsson, L., Knutsson, A., Siegrist, J., & Wester-
holm, P. (1999). Does a stressful psychosocial work envi-
ronment mediate the effects of shift work on cardiovascular
risk factors? Scandinavian Journal of Work, Environment
and Health, 25(4), 376–381.
Peter, R., Hammarstrom, A., Hallqvist, J., Siegrist, J., &
Theorell, T. (2006). Does occupational gender segregation
influence the association of effort-reward imbalance with
myocardial infarction in the SHEEP study? International
Journal of Behavioral Medicine, 13(1), 34–43.
Peter, R., & Siegrist, J. (1997). Chronic work stress, sickness
absence, and hypertension in middle managers: General or
specific sociological explanations? Social Science and Med-
icine, 45(7), 1111–1120.
Peter, R., Siegrist, J., Hallqvist, J., Reuterwall, C., & Theorell,
T. (2002). Psychosocial work environment and myocardial
infarction: Improving risk estimation by combining two
complementary job stress models in the SHEEP study.
Journal of Epidemiology and Community Health, 56, 294–
300.
Radi, S., Lang, T., Lauwers-Cances, V., Diene, E., Chatellier,
G., Larabi, L., et al. (2005). Job constraints and arterial
hypertension: Different effects in men and women: The
IHPAF II case control study. Occupational & Environmen-
tal Medicine, 62(10), 711–717.
Rau, R., Georgiades, A., Fredrikson, M., Lemne, C., & de
Faire, U. (2001). Psychosocial work characteristics and per-
ceived control in relation to cardiovascular rewind at night.
Journal of Occupational Health Psychology, 6(3), 171–
181.
Rose, G., Kumlin, L., Dimberg, L., Bengtsson, C., Orth-
Gomer, K., & Cai, X. (2006). Work-related life events,
psychological well-being and cardiovascular risk factors in
male Swedish automotive workers. Occupational Medicine,
56(6), 386–392.
Sacker, A., Bartley, M.J., Frith, D., Fitzpatrick, R.M., &
Marmot, M.G. (2001). The relationship between job strain
and coronary heart disease: Evidence from an English
sample of the working male population. Psychological
Medicine, 31, 279–290.
Siegrist, J. (2005). Social reciprocity and health: New scientific
evidence and policy implications. Psychoneuroendocrinol-
ogy, 30, 1033–1038.
Siegrist, J., Dittmann, K., Rittner, K., & Weber, I. (1982). The
social context of active distress in patients with early myo-
cardial infarction. Social Science and Medicine, 16, 443–
453.
Siegrist, J., & Klein, D. (1990). Occupational stress and car-
diovascular reactivity in blue-collar workers. Work and
Stress, 4(4), 295–304.
Siegrist, J., Dagmar Starke, D., Chandola, T., Godin, I.,
Marmot, M., Niedhammer, I., Peter, R. (2004). The mea-
surement of effort-reward imbalance at work: European
comparisons. Social Science and Medicine, 58, 1483–1499.
Smith, T.W., & Ruiz, J.M. (2002). Psychosocial influences on
the development and cause of coronary heart disease:
Current status and implications for research and practice.
Journal of Consulting and Clinical Psychology, 70, 548–
568.
Stress and Health 24: 231–238 (2008) 237
DOI: 10.1002/smi
 D. G. Byrne and G. A. Espnes
Stanley, R.O., & Burrows, G.D. (2006). Editorial: It is
now the time to further help the professionals and
the public understand the nature, role and implications
of stress for ill-health. Stress and Health, 22(3), 139–
141.
Steptoe, A., Siegrist, J., Kirschbaum, C., & Marmot, M.
(2004). Effort-reward imbalance, overcommittment, and
measures of cortisol and blood pressure over the working
day. Psychosomatic Medicine, 66, 323–329.
Su, C.T., Yang, H.J., Lin, C.F., Tsai, M.C., Shieh, Y.H., &
Chiu, W.T. (2001). Arterial blood pressure and blood lipids
as cardiovascular risk factors and occupational stress in
Taiwan. International Journal of Cardiology, 81, 181–
187.
Sulsky, L. & Smith, C. (2005). Work stress. Belmont CA:
Thomson Wadsworth.
Taylor, R., Dobson, A., & Mirzaei, M. (2006). Contribution
of changes in risk factors to the decline of coronary heart
disease mortality in Australia over three decades. European
Journal of Cardiovascular Prevention & Rehabilitation,
13(5), 760–768.
Theorell, T. (2002). Job stress and fibrinogen. European
Heart Journal, 23, 1799–1801.
Theorell, T., Ahlberg-Hulten, G., Jodko, M., & Sigala, F.
(1993). Influence of job strain and emotion on blood pres-
sure in female hospital personnel during workhours. Scan-
dinavian Journal of Work, Environment and Health, 19(5),
313–318.
Theorell, T., Alfredsson, L., Westerholm, P., & Falck, B.
(2000). Coping with unfair treatment at work—what is the
relationship between coping and hypertension in middle-
aged men and women? Psychotherapy and Psychosomatics,
69(2), 86–94.
Theorell, T., & Karasek, R.A. (1996). Current issues relating
to psychosocial job strain and cardiovascular disease
research. Journal of Occupational Health Psychology, 1(1),
9–26.
Tsutsumi, A., Kayaba, K., Tsutsumi, K., Igarashi, M., & Jichi
Medical School Cohort Study Group. (2001). Association
between job strain and prevalence of hypertension: A cross-
sectional analysis in a Japanese working population with a
238 Copyright © 2008 John Wiley & Sons, Ltd.
wide range of occupations: The Jichi Medical School cohort
study. Occupational & Environmental Medicine, 58(6),
367–373.
Tsutsumi, A., Kayaba, K., Yoshimura, M., Sawada, M., Ishi-
kawa, S., Sakai, K., et al. (2003). Association between job
characteristics and health behaviors in Japanese rural
workers. International Journal of Behavioral Medicine,
10(2), 125–142.
Tsutsumi, A., Theorell, T., Hallqvist, J., Reuterwall, C., & de
Faire, U. (1999). Association between job characteristics
and plasma fibrinogen in a normal working populaton: A
cross sectional analysis in referents of the SHEEP study.
Journal of Epidemiology and Community Health, 53, 348–
354.
Tsutsumi, A., Tsutsumi, K., Kayaba, K., Theorell, T., Nago,
N., Kario, K., & Igarashi, M. (1998). Job strain and bio-
logical coronary risk factors: A cross-sectional study of
male and female workers in a Japanese rural district. Inter-
national Journal of Behavioral Medicine, 5(4), 295–311.
van Vegchel, N., de Jonge, J., Bosma, H., & Schaufeli, W.
(2005). Reviewing the effort-reward imbalance model:
Drawing up the balance of 45 empirical studies. Social
Science and Medicine, 60, 1117–1131.
Wang, H.W., Leineweber, C., Kirkeeide, R., Svane, B.,
Schenck-Gustafsson, K., Theorell, T., & Orth-Gomér, K.
(2007). Psychosocial stress and atherosclerosis: Family and
work stress accelerate progression of coronary disease in
women. The Stockholm Female Coronary Angiography
Study. Journal of Internal Medicine, 261(3), 245–254.
Westerlund, H., Theorell, T., & Alfredsson, L. (2004). Orga-
nizational instability and cardiovascular risk factors in
white-collar employees. European Journal of Public Health,
14, 37–42.
Woodward, M., Rumley, A., Welsh, P., MacMahon, S., &
Lowe, G. (2007). A comparison of the associations between
seven hemostatic or inflammatory variables and coronary
heart disease. Journal of Thrombosis and Haemostasis,
5(9), 1795–1800.
Yang, H., Schnall, P.L., Jaurequi, M., Su, T.C., & Baker, D.
(2006). Work hours and self-reported hypertension among
working people in California. Hypertension, 48(4), 744–750.
Stress and Health 24: 231–238 (2008)
DOI: 10.1002/smi