Job strain associated CRP is mediated by leisure time physical activity: Results from the MONICA/KORA study

Abstract

Background

Psychological stress at work is considered a cardiac risk factor, yet whether it acts directly through neuroimmune processes, or indirectly by increasing behavioral risk factors, is uncertain. Cross-sectional associations between job strain and serum biomarkers of inflammation and endothelial dysfunction were investigated. Secondary analyses explored the role of psychosocial/cardiometabolic risk factors as mediators of job stress associated inflammation in healthy workers.

Methods

Information on risk factors was obtained in standardized personal interviews of a subcohort of working participants in the MONICA/KORA population (n = 951). Work stress was measured by the Karasek job strain index. Biomarkers were measured from non-fasting venous blood. Multivariate regression analyses were used to examine the association of job strain with inflammatory biomarkers. Mediation analysis (Sobel test) was used to determine the effect of psychosocial risk factors on the association between job strain and C-reactive protein (CRP).

Results

High job strain was reported by half (n = 482, 50.7%) of the study participants. While workers with high job strain were more likely to have adverse workplace conditions (competition with coworkers, job dissatisfaction and insecurity), sleeping problems, depressive symptoms, a Type A personality, and be physically inactive, no differences in cardiometabolic risk factors were detected. A strong and robust association between job strain and CRP was observed in age and sex adjusted models, as well as models adjusted for classic coronary heart disease risk factors (β = 0.39, p = 0.006 and β = 0.27, p = 0.03, respectively). Adjustment for physical activity abrogated this effect (β = 0.23, p = 0.07), and a mediating effect of physical activity on stress-associated inflammation was demonstrated (p = 0.04).

Conclusions

The analyses provide evidence for both a direct and an indirect effect of job strain on inflammation.

Introduction

The psychological stress associated with an individual’s work environment has long been considered as a risk factor in coronary heart disease (CHD) Eaker et al., 2004, Hallqvist et al., 1998, Kuper and Marmot, 2003. However, the inclusion of job strain into the Framingham risk algorithm for CHD did not significantly improve the performance of the model (Kivimaki et al., 2011). Nonetheless, the contribution of job strain as an upstream risk factor in the etiology of CHD is still plausible via direct modification of biochemical pathways or indirectly, by modifying behavioral CHD risk factors. While it is well documented that work stress significantly influences smoking (Hellerstedt and Jeffery, 1997, Radi et al., 2007), obesity (Brunner et al., 2007) and physical inactivity (Hellerstedt and Jeffery, 1997), psychophysiological consequences of work stress point towards sympatho–adrenal and hypothalamic–pituitary adrenal (HPA) pathways, yet these direct biomechanisms are not entirely understood (Chandola et al., 2010).

We therefore utilized the MONICA/KORA (Monitoring of trends and determinants in Cardiovascular disease/Cooperative Health Research in the region of Augsburg) population to investigate cross-sectional associations of work related stress with a panel of serum biomarkers of inflammation and endothelial dysfunction. Secondary analyses explored the role of psychosocial/cardiometabolic risk factors as mediators of job stress associated inflammation. Several conceptualisations of stress in a working environment are well published (Karasek, 1979, Kivimaki et al., 2005, Siegrist, 1996), the MONICA/KORA surveys utilized the Karasek job strain index to assess self-reported, work-associated stress in employed study participants.