The Lancet, Volume 380, Issue 9852, Pages 1491 - 1497, 27 October 2012

Job strain as a risk factor for coronary heart disease: a collaborative meta-analysis of individual participant data

Prof Mika Kivimäki PhD ,Solja T Nyberg MSc, G David Batty PhD , Eleonor I Fransson PhD, Katriina Heikkilä PhD, Prof Lars Alfredsson PhD , Prof Jakob B Bjorner MD, Marianne Borritz MD,Hermann Burr PhD, Annalisa Casini PhD , Els Clays PhD , Prof Dirk De Bacquer PhD, Prof Nico Dragano PhD , Jane E Ferrie PhD  Goedele A Geuskens PhD, Prof Marcel Goldberg MD , Mark Hamer PhD, Wendela E Hooftman PhD , Irene L Houtman PhD , Matti Joensuu MSc, Markus Jokela PhD , Prof France Kittel PhD , Prof Anders Knutsson PhD

Summary

Background

Published work assessing psychosocial stress (job strain) as a risk factor for coronary heart disease is inconsistent and subject to publication bias and reverse causation bias. We analysed the relation between job strain and coronary heart disease with a meta-analysis of published and unpublished studies.

Methods

We used individual records from 13 European cohort studies (1985—2006) of men and women without coronary heart disease who were employed at time of baseline assessment. We measured job strain with questions from validated job-content and demand-control questionnaires. We extracted data in two stages such that acquisition and harmonisation of job strain measure and covariables occurred before linkage to records for coronary heart disease. We defined incident coronary heart disease as the first non-fatal myocardial infarction or coronary death.

Findings

30 214 (15%) of 197 473 participants reported job strain. In 1·49 million person-years at risk (mean follow-up 7·5 years [SD 1·7]), we recorded 2358 events of incident coronary heart disease. After adjustment for sex and age, the hazard ratio for job strain versus no job strain was 1·23 (95% CI 1·10—1·37). This effect estimate was higher in published (1·43, 1·15—1·77) than unpublished (1·16, 1·02—1·32) studies. Hazard ratios were likewise raised in analyses addressing reverse causality by exclusion of events of coronary heart disease that occurred in the first 3 years (1·31, 1·15—1·48) and 5 years (1·30, 1·13—1·50) of follow-up. We noted an association between job strain and coronary heart disease for sex, age groups, socioeconomic strata, and region, and after adjustments for socioeconomic status, and lifestyle and conventional risk factors. The population attributable risk for job strain was 3·4%.

Interpretation

Our findings suggest that prevention of workplace stress might decrease disease incidence; however, this strategy would have a much smaller effect than would tackling of standard risk factors, such as smoking.