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. Methods A 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. Conclusions Observational 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.

Objectives We aimed to review evidence on the relationship between temporary employment and health, and to see whether the association is dependent on outcome measure, instability of employment, and contextual factors. Method We systematically searched for studies of temporary employment and various health outcomes and critically appraised 27 studies. Results The review suggests higher psychological morbidity among temporary workers compared with permanent employees. According to some studies, temporary workers also have a higher risk of occupational injuries but their sickness absence is lower. Morbidity may be higher in temporary jobs with high employment instability and in countries with a lower number of temporary workers and unemployed workers. Conclusions 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.

Objectives. This study examined the justice of decision-making procedures and interpersonal relations as a psychosocial predictor of health. Methods. Regression analyses were used to examine the relationship between levels of perceived justice and self-rated health, minor psychiatric disorders, and recorded absences due to sickness in a cohort of 506 male and 3570 female hospital employees aged 19 to 63 years. Results. The odds ratios of poor self-rated health and minor psychiatric disorders associated with low vs high levels of perceived justice ranged from 1.7 to 2.4. The rates of absence due to sickness among those perceiving low justice were 1.2 to 1.9 times higher than among those perceiving high justice. These associations remained significant after adjustment for behavioral risks, workload, job control, and social support. Conclusions. Low organizational justice is a risk to the health of employees.

Background: A lack of longitudinal studies has made it difficult to establish the direction of associations between circulating concentrations of low-grade chronic inflammatory markers, such as C-reactive protein and interleukin-6, and cognitive symptoms of depression. The present study sought to assess whether C-reactive protein and interleukin-6 predict cognitive symptoms of depression or whether these symptoms predict inflammatory markers.Method: In a prospective occupational cohort study of British white-collar civil servants (the Whitehall II study), serum C-reactive protein, interleukin-6 and cognitive symptoms of depression were measured at baseline in 1991–1993 and at follow-up in 2002–2004, an average follow-up of 11.8 years. Symptoms of depression were measured with four items describing cognitive symptoms of depression from the General Health Questionnaire. The number of participants varied between 3339 and 3070 (mean age 50 years, 30% women) depending on the analysis.Results: Baseline C-reactive protein (β=0.046, p=0.004) and interleukin-6 (β=0.046, p=0.005) predicted cognitive symptoms of depression at follow-up, while baseline symptoms of depression did not predict inflammatory markers at follow-up. After full adjustment for sociodemographic, behavioural and biological risk factors, health conditions, medication use and baseline cognitive systems of depression, baseline C-reactive protein (β=0.038, p=0.036) and interleukin-6 (β=0.041, p=0.018) remained predictive of cognitive symptoms of depression at follow-up.Conclusions: These findings suggest that inflammation precedes depression at least with regard to the cognitive symptoms of depression.

The associations of social isolation and loneliness with premature mortality are well known, but the risk factors linking them remain unclear. We sought to identify risk factors that might explain the increased mortality in socially isolated and lonely individuals. We used prospective follow-up data from the UK Biobank cohort study to assess self-reported isolation (a three-item scale) and loneliness (two questions). The main outcomes were all-cause and cause-specific mortality. We calculated the percentage of excess risk mediated by risk factors to assess the extent to which the associations of social isolation and loneliness with mortality were attributable to differences between isolated and lonely individuals and others in biological (body-mass index, systolic and diastolic blood pressure, and handgrip strength), behavioural (smoking, alcohol consumption, and physical activity), socioeconomic (education, neighbourhood deprivation, and household income), and psychological (depressive symptoms and cognitive capacity) risk factors. 466 901 men and women (mean age at baseline 56·5 years [SD 8·1]) were included in the analyses, with a mean follow-up of 6·5 years (SD 0·8). The hazard ratio for all-cause mortality for social isolation compared with no social isolation was 1·73 (95% CI 1·65–1·82) after adjustment for age, sex, ethnic origin, and chronic disease (ie, minimally adjusted), and was 1·26 (95% CI 1·20–1·33) after further adjustment for socioeconomic factors, health-related behaviours, depressive symptoms, biological factors, cognitive performance, and self-rated health (ie, fully adjusted). The minimally adjusted hazard ratio for mortality risk related to loneliness was 1·38 (95% CI 1·30–1·47), which reduced to 0·99 (95% CI 0·93–1·06) after full adjustment for baseline risks. Isolated and lonely people are at increased risk of death. Health policies addressing risk factors such as adverse socioeconomic conditions, unhealthy lifestyle, and lower mental wellbeing might reduce excess mortality among the isolated and the lonely. Academy of Finland, NordForsk, and the UK Medical Research Council.