SummaryBackgroundPublished 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 We analysed the relation between job strain and coronary heart disease with a meta-analysis of published and unpublished studies.MethodsWe used individual records from 13 European cohort studies (1985–2006) of men and women without coronary heart disease who were employed at time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.Findings30 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 This effect estimate was higher in published (1·43, 1·15–1·77) than unpublished (1·16, 1·02–1·32) studies.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%.InterpretationOur 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.FundingFinnish 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.

Kivimäki M, Virtanen M, Elovainio M, Kouvonen A, Väänänen A, Vahtera J. Work stress in the etiology of coronary heart disease-a meta-analysis. Scand J Work Environ Health 2006;32(6 special issue):431-442.Objectives This study focused on estimating the relative risk of coronary heart disease (CHD) in association with work stress, as indicated by the job-strain model, the effort-reward imbalance model, and the organizational injustice model. MethodsA systematic review and meta-analysis of prospective cohort studies were carried out. Studies were eligible if they had published a quantitative estimate of the association between work stress and incident CHD or cardiovascular mortality by January 2006.Results Fourteen prospective cohort studies were identified. For a total of 83 014 employees, the age-and gender-adjusted relative ratio of CHD for high versus low job strain was 1.43 [95% confidence interval (95% CI) 1.15-1.84], but the ratio decreased to 1.16 (95% CI 0.94-1.43) after adjustment for risk factors and potential mediators. The age-and gender-adjusted risk ratio for a combination of high efforts and low rewards was 1.58 (95% CI 0.84-2.97) for 11 528 employees, and no reduction in the risk ratio was seen after further adjustments. For organizational injustice, the age-and gender-adjusted, and multiple-adjusted relative risks were 1.62 (95% CI 1.24-2.13) and 1.47 (95% CI 1.12-1.95), respectively, for a population of 7246 men and women. There was little standardization in the assessment of work stress within all three stress models, and significant heterogeneity in the effects of stress was observed between studies. Few studies were available for female samples. ConclusionsObservational data suggest an average 50% excess risk for CHD among employees with work stress. Further research is needed to confirm that a reduction in work stress will lead to a reduction in CHD risk.Key terms cardiovascular disease; effort-reward imbalance; job strain; mortality; organizational justice; prospective cohort study; psychosocial factors; systematic review; working population. Activation of the stress system in the hypothalamus and the brain stem helps the body to overcome the influence of short-term physical stressors. However, prolonged overactivity of these systems may cause wear and tear and play a role in coronary heart disease (CHD), infection, and accelerated aging (1). The recognition that the physiological reactions to stress cannot only protect, but also damage the body has provided a basis for epidemiologic research on work stress.Three models for work stress and coronary heart disease Work-stress models aim at describing factors that are likely to elicit harmful stress at work in a large proportion of employees. These factors are conceptualized at a level of generalization that allows for their identification in a wide range of occupations. The stress model most often cited and most widely tested is the two-dimensional job-strain model (2-4) ( Work stress in the etiology of coronary heart disease strain model adds...

The evidence indicates an association between temporary employment and psychological morbidity. The health risk may depend on instability of temporary employment and the context. Confounding by occupation may have biased some of the studies. Additional research to clarify the role of employment instability, hazard accumulation, and selection is recommended.