Mika Kivimäki a , b , c , * , Solja T Nyberg c , G David Batty a , d , Eleonor I Fransson e , f , g , Katriina Heikkilä c , Lars Alfredsson e , Jakob B Bjorner h , Marianne Borritz i , Hermann Burr j , Annalisa Casini k , Els Clays l , Dirk De Bacquer l , Nico Dragano m , Jane E Ferrie a , n , Goedele A Geuskens o , Marcel Goldberg p , q , Mark Hamer a , Wendela E Hooftman o , Irene L Houtman o , Matti Joensuu c , Markus Jokela b , France Kittel k , Anders Knutsson r , Markku Koskenvuo s , Aki Koskinen c , Anne Kouvonen t , Meena Kumari a , Ida EH Madsen h , Michael G Marmot a , Martin L Nielsen i , Maria Nordin u , Tuula Oksanen v , Jaana Pentti v , Reiner Rugulies h , w , Paula Salo v , x , Johannes Siegrist m , Archana Singh-Manoux a , q , Sakari B Suominen y , z , Ari Väänänen c , Jussi Vahtera v , y , aa , Marianna Virtanen c , Peter JM Westerholm ab , Hugo Westerlund g , Marie Zins p , q , Andrew Steptoe a , Töres Theorell g , for the IPD-Work Consortium
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 We analysed the relation between job strain and coronary heart disease with a meta-analysis of published and unpublished studies.
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.
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 This effect estimate was higher in published (1·43, 1·15–1·77) than unpublished (1·16, 1·02–1·32) studies.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%.
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.
Finnish Work Environment Fund, the Academy of Finland, the Swedish Research Council for Working Life and Social Research, the German Social Accident Insurance, the Danish National Research Centre for the Working Environment, the BUPA Foundation, the Ministry of Social Affairs and Employment, the Medical Research Council, the Wellcome Trust, and the US National Institutes of Health.