The Job Strain Model has been widely used to evaluate the impact
of the psychosocial work environment upon cardiovascular disease
(CVD). Many studies report positive findings, but non-confirmatory
results have spurred questions concerning the strength and consistency
of the evidence. We systematically examine the empirical studies
on job strain and CVD, using 15 pre-defined criteria to assess
methodological issues affecting internal validity, identifying
the likely direction in which the results were affected. Other
elements of causal inference are also reviewed. We thereby seek
to provide a more definitive answer to the question: Is job strain
a major CVD risk factor?
The 14 longitudinal studies had the highest validity ratings.
In all but 1, biases towards the null were predominant. This
was due most often to use of the imputation method and long follow-up
times during which there was no assessment of exposure or even
employment status. Viewed in this light, the 6 investigations,
including several of the largest, showing significant positive
results, plus another 3 with positive, though NS findings, provide
strong and consistent evidence, particularly among men, that exposure
to job strain is associated with an increased risk of future cardiac
events and death from CVD. The magnitude of this association
appears to be substantially underestimated, since bias towards
the null was present in nearly all of these longitudinal studies.
Six of 9 case-control studies had significant positive findings.
None had major threats to internal validity, and recall bias
possibly leading to overestimation appears to be minimal. Four
of 8 cross-sectional studies had significant positive results,
although biases leading to over-estimation, as well as to the
null, may have been present.
We conclude that among men, there is strong and consistent evidence
of an association between exposure to job strain and CVD across
study designs. The data among women are more sparse, not as
consistent, but, as among men, the majority of studies probably
underestimated existing effects. Other elements of causal inference
are also supportive, particularly biological plausibility. Still
needed are randomized clinical trials to examine whether ameliorating
exposure to job strain can impact upon hard CVD outcomes. These
would provide the needed link in etiological research, as well
as exploring possibilities for prevention.
CORRESPONDING AUTHOR: Dr. Karen Belkic, IPR, USC School of Medicine, 1000 So. Fremont, Unit 8, Alhambra, California 91803 USA, kbelkic@hsc.usc.edu