Job Strain, Inflammatory Biomarkers and Coronary Events in Healthy Workers of the MONICA/KORA Augsburg Case-Cohort Study

Abstract

Whether job strain contributes to the aetiology of coronary heart disease (CHD) is uncertain, and mechanisms underlying this relationship unknown. We investigated associations between job strain and biomarkers of subclinical inflammation and endothelial dysfunction with CHD, and examined whether these biomarkers provide mechanistic links between job strain and CHD. Study participants (n=1,027; age 35–64, 68% male) were selected from employed participants of the prospective, population-based MONICA/KORA Augsburg study (1984–2002). The case-cohort sample contained 951 non-cases and 114 incident CHD cases. Work stress, assessed by Karasek’s Job Strain Index, and 9 biomarkers were measured at baseline, and the main outcome (CHD), reported as sudden cardiac death or myocardial infarction (fatal and non fatal), was obtained after an average of 13 years. Baseline levels of C reactive protein (CRP), interleukin (IL)–6 and sICAM were significantly increased in all cases. In the high job strain group only, cases had significantly increased IL–18, IL–8 and monocyte chemoattractant protein (MCP)–1 compared to non-cases. In crude, Cox proportional hazard models, increased job strain significantly predicted CHD (hazard ratio 2.57, 95%CI 1.09–6.07, P-value=0.032). Depression and physical acitivty are considered as moderators or buffers, respectively, of stress-associated inflammation. These results suggest that work stress associated inflammatory burden may contribute to CHD pathogenesis.