Abstract
OBJECTIVES: We aimed to find evidence of the inflammation-mediated mechanism by which long working hours contribute to cardiovascular disease (CVD). METHODS: This cohort study was performed in 56 953 Korean adults free of CVD who underwent a comprehensive screening examination and were followed for up to 7 years. An increase in blood high-sensitivity C-reactive protein (hsCRP) of 1 mg/L or more at the follow-up visit was defined as an incidence. The average weekly working hours in the past year were categorized as ≤40, 41-52, 53-60, and ≥60 h per week. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using generalized estimating equations to calculate the risk of an incidental increase of hsCRP. RESULTS: Participants with longer working hours had a higher incidence of hsCRP. Multivariable-adjusted ORs (95% CIs) of incident cases for ≥61 h compared with ≤40 h was 1.69 (1.04-2.75). In subgroup analyses according to sex and the presence of hypertension and diabetes, the risk of hsCRP incidence were highest in the group working more than 61 h in all subgroups, but none of them were statistically significant. CONCLUSIONS: Working hours are independently associated with increased risk of elevated hsCRP in a dose-response relationship. Excessive long-time work is a risk factor for CVD, and it was found that an increase in hsCRP was associated with the pathogenesis.