The present study relied on prospective cohort composed of men and women followed over 24 years. In this study, repeated exposure to long working hours at midlife was associated with increased arterial stiffness among participants who remained actively employed over the whole study period. This association was robust to adjustment for socio-demographics, lifestyle-related risk factors, clinical risk factors and psychosocial stressors at work. The magnitude of this association (+ 1.54 m/s) is of clinical importance. For instance, a meta-analysis has reported a 15% increased CVD risk for each 1 m/s increase in PWV (2).
To our knowledge, the current study is the first to examine the association between repeated exposure to long working hours and arterial stiffness. It is also the first to use carotid-femoral PWV, which is recognized as the reference standard measurement for arterial stiffness. One previous prospective study has reported an association between long working hours, as defined as working 55 hours or more per week, and arterial stiffness progression over 5 years (+ 0.32 m/s) (15). The present study showed association of comparable magnitude to that reported in this previous study, using baseline exposure (+ 0.54 m/s). The association was of higher magnitude using repeated exposure to long working hours. Therefore, results are consistent with the hypothesis of a potential underestimation of the association between long working hours and arterial stiffness using a single assessment. As a summary measure of vascular aging, arterial stiffness may capture vascular damage accumulated over the life course. Our results are consistent with this hypothesis and suggest that long working hours exert its effect on arterial stiffness over the working life and may be especially harmful among older workers exposed to long work hours over a prolonged period of time.
Pathophysiological mechanisms could explain the adverse effect of long working hours on arterial stiffness. Repeated exposure to long working hours may lead to increased activity of the sympathetic nervous system (catecholamines) and the hypothalamic-pituitary-adrenal axis (glucocorticoids). Moreover, the sympathetic nervous system is one of the pathways activating the renin-angiotensin system. Therefore, in conjunction with other risk factors, exposure to long working hours can trigger vasoconstriction, endothelial dysfunction, cellular proliferation, and inflammation that promote arterial stiffness (29–31). Indirect mechanisms could also explain the observed association. First, evidence suggests that long working hours could be associated with sleep deprivation, which could in turn increase cardiovascular risk (32, 33). Second, individuals working long hours might be more likely to adopt or maintain unhealthy behaviors (34). Third, long working hours could also be associated with prolonged exposure to psychosocial stressors at work (35). In a recent study conducted by our research team, job strain at midlife was associated with increased PWV among workers with high BP (36). In the present study, association between long working hours and arterial stiffness was observed following adjustment for lifestyle-related risk factors and psychosocial stressors at work from the job strain model. Therefore, lifestyle-related risk factors and psychosocial stressors at work unlikely explain the observed association.
Our study has limitations. First, exposure assessment at baseline and follow-up were spaced by approximately 8 years, which could have led to non-differential misclassification of the exposure. However, most workers (82%) remained in the same occupation between T1 and T2, in favor of exposure stability (37). Second, 7.4% of the study population worked more than 40 hours per week and only 2.8% were repeatedly exposed at both times. Therefore, the association between long working hours and arterial stiffness could not be examined using of higher thresholds of exposure to long working hours and the investigation of a potential dose-response relationship. Third, arterial stiffness was available at the last follow-up only. Therefore longitudinal progression could not be assessed. Adjusting for BP changes over the study period led to similar estimates suggesting that the longitudinal progression of BP could not explain the observed association. Future studies using multiple assessment of PWV are needed to examine the adverse effect of long working hours on arterial stiffness longitudinal progression. Finally, the generalizability of our findings might be limited to white-collar workers. More specifically, results might not be generalizable to blue-collar workers, who are more frequently exposed to different working arrangements including shift work and night work. However, the restriction to a white-collar population minimized the possibility for a large amount of unmeasured worked hours that could be more frequent in populations with different occupational profile.
Our study also has important strengths. First, carotid-femoral PWV was used, which is considered as the gold standard measurement for arterial stiffness. Moreover, the present study relied on a prospective cohort and long working hours were assessed at two different time points. The 24-year follow-up also allowed to examine the long-term association between long working hours at midlife and arterial stiffness at older age. The high participation proportion at each time, and the use of random sample for PWV assessment minimized the potential for selection bias. Finally, a large number of potential confounders were assessed and were adjusted for in the analyses.