Psychosocial stressors at work and inflammatory biomarkers: PROspective Quebec Study on Work and Health. (November 2021)

• Record Type: Journal Article
• Authors: Duchaine, Caroline S.; Brisson, Chantal; Talbot, Denis; Gilbert-Ouimet, Mahée; Trudel, Xavier; Vézina, Michel; Milot, Alain; Diorio, Caroline; Ndjaboué, Ruth; Giguère, Yves; Mâsse, Benoît; Dionne, Clermont E.; Maunsell, Elizabeth; Laurin, Danielle
• Is Part Of: Psychoneuroendocrinology. Volume 133(2021)
• Publication Date: 2021-11
• Subjects: Job strain -- Effort-reward imbalance -- Inflammatory biomarkers -- Low-grade inflammation -- CRP -- IL-6; Psychoneuroendocrinology -- Periodicals; Endocrinology -- Periodicals; Neurology -- Periodicals; Psychiatry -- Periodicals; Neuropsychoendocrinologie -- Périodiques; 616.8
• DOI: 10.1016/j.psyneuen.2021.105400
• Languages: English
• ISSNs: 0306-4530

Abstract

Abstract: Background: Chronic low-grade inflammation has been associated with high risk of several chronic diseases such as cardiovascular diseases, diabetes, depression, and dementia. As low-grade inflammation could be present long before the apparition of the disease, identifying modifiable risk factors could allow to act upstream. Psychosocial stressors at work have been suggested as modifiable risk factors of low-grade inflammation, but few longitudinal studies have evaluated the association between these stressors and inflammatory biomarkers, such as C-reactive protein (CRP) and interleukin-6 (IL-6). Objective: This longitudinal study evaluate the associations between exposure to psychosocial stressors at work and CRP and IL-6, separately and combined into an inflammatory index. Methods: Data came from a cohort of 9188 white-collar workers recruited in 1991–1993 (T1) and followed-up after 8 (T2, 1999–2000) and 24 (T3, 2015–2018) years. Participants included in this study were randomly selected at T3 for serum biomarkers studies (n = 2557). CRP and IL-6 were measured using standardized protocols. Psychosocial stressors at work were assessed at T2 according to recognized models: Karasek's Demand-Control-Support model and Siegrist's Effort-Reward Imbalance (ERI) model, using validated questionnaires. High job strain was defined by an exposure to high psychological demand combined with low job control, and iso-strain was defined by an exposure to high job strain combined with low social support at work. ERI was defined by an imbalance between psychological demand and social, economic, and organizational reward. Several covariates were considered including sociodemographic, anthropometric, and lifestyle characteristics, and comorbidities. Prevalence ratios (PRs) and 95% confidence interval (CI) for the highest quartile of CRP, IL-6 and inflammatory index at T3 according to psychosocial stressors at work measured at T2 were calculated using generalized estimating equations. Multiple imputation and inverse probability of censoring weighting were done. Results: In men, an association was observed between exposure to iso-strain and the inflammatory index (PR of 1.42 (95% CI: 1.06;1.90)), mainly among men aged less than 65 years (PR of 2.00 (95% CI: 1.37;2.92)). In this same age group, associations with inflammatory biomarkers were also observed among men with exposure to ERI, and among women with exposure to low reward at work or moderate social support at work. Conclusion: These results suggest that psychosocial stressors at work may increase low-grade inflammation. However, further studies are needed to corroborate these results and to clarify the potential differences between men and women. As these stressors are frequent and modifiable, their reduction is important for public health and could play a role in the primary prevention of chronic diseases. Highlights: Psychosocial stressors were associated with higher inflammatory biomarkers. Associations were higher among participants aged less than 65 years. In men, associations were with iso-strain, high strain and effort-reward imbalance. In women, associations were with low reward and medium social support. These stressors are modifiable and could prevent low-grade inflammation.