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.
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