The World Health Organization (WHO) and the International Labour Organization (ILO) are developing Joint Estimates of the work-related burden of disease and injury (WHO/ILO Joint Estimates), with contributions from a large network of experts. Evidence from mechanistic data suggests that exposure to long working hours may cause ischaemic heart disease (IHD). In this paper, we present a systematic review and meta-analysis of parameters for estimating the number of deaths and disability-adjusted life years from IHD that are attributable to exposure to long working hours, for the development of the WHO/ILO Joint Estimates.We aimed to systematically review and meta-analyse estimates of the effect of exposure to long working hours (three categories: 41-48, 49-54 and ≥55 h/week), compared with exposure to standard working hours (35-40 h/week), on IHD (three outcomes: prevalence, incidence and mortality).We developed and published a protocol, applying the Navigation Guide as an organizing systematic review framework where feasible. We searched electronic databases for potentially relevant records from published and unpublished studies, including MEDLINE, Scopus, Web of Science, CISDOC, PsycINFO, and WHO ICTRP. We also searched grey literature databases, Internet search engines and organizational websites; hand-searched reference lists of previous systematic reviews; and consulted additional experts.We included working-age (≥15 years) workers in the formal and informal economy in any WHO and/or ILO Member State but excluded children (aged < 15 years) and unpaid domestic workers. We included randomized controlled trials, cohort studies, case-control studies and other non-randomized intervention studies which contained an estimate of the effect of exposure to long working hours (41-48, 49-54 and ≥55 h/week), compared with exposure to standard working hours (35-40 h/week), on IHD (prevalence, incidence or mortality).At least two review authors independently screened titles and abstracts against the eligibility criteria at a first stage and full texts of potentially eligible records at a second stage, followed by extraction of data from qualifying studies. Missing data were requested from principal study authors. We combined relative risks using random-effect meta-analysis. Two or more review authors assessed the risk of bias, quality of evidence and strength of evidence, using Navigation Guide and GRADE tools and approaches adapted to this project.Thirty-seven studies (26 prospective cohort studies and 11 case-control studies) met the inclusion criteria, comprising a total of 768,751 participants (310,954 females) in 13 countries in three WHO regions (Americas, Europe and Western Pacific). The exposure was measured using self-reports in all studies, and the outcome was assessed with administrative health records (30 studies) or self-reported physician diagnosis (7 studies). The outcome was defined as incident non-fatal IHD event in 19 studies (8 cohort studies, 11 case-control studies), incident fatal IHD event in two studies (both cohort studies), and incident non-fatal or fatal ("mixed") event in 16 studies (all cohort studies). Because we judged cohort studies to have a relatively lower risk of bias, we prioritized evidence from these studies and treated evidence from case-control studies as supporting evidence. For the bodies of evidence for both outcomes with any eligible studies (i.e. IHD incidence and mortality), we did not have serious concerns for risk of bias (at least for the cohort studies). No eligible study was found on the effect of long working hours on IHD prevalence. Compared with working 35-40 h/week, we are uncertain about the effect on acquiring (or incidence of) IHD of working 41-48 h/week (relative risk (RR) 0.98, 95% confidence interval (CI) 0.91 to 1.07, 20 studies, 312,209 participants, I2 0%, low quality of evidence) and 49-54 h/week (RR 1.05, 95% CI 0.94 to 1.17, 18 studies, 308,405 participants, I2 0%, low quality of evidence). Compared with working 35-40 h/week, working ≥55 h/week may have led to a moderately, clinically meaningful increase in the risk of acquiring IHD, when followed up between one year and 20 years (RR 1.13, 95% CI 1.02 to 1.26, 22 studies, 339,680 participants, I2 5%, moderate quality of evidence). Compared with working 35-40 h/week, we are very uncertain about the effect on dying (mortality) from IHD of working 41-48 h/week (RR 0.99, 95% CI 0.88 to 1.12, 13 studies, 288,278 participants, I2 8%, low quality of evidence) and 49-54 h/week (RR 1.01, 95% CI 0.82 to 1.25, 11 studies, 284,474 participants, I2 13%, low quality of evidence). Compared with working 35-40 h/week, working ≥55 h/week may have led to a moderate, clinically meaningful increase in the risk of dying from IHD when followed up between eight and 30 years (RR 1.17, 95% CI 1.05 to 1.31, 16 studies, 726,803 participants, I2 0%, moderate quality of evidence). Subgroup analyses found no evidence for differences by WHO region and sex, but RRs were higher among persons with lower SES. Sensitivity analyses found no differences by outcome definition (exclusively non-fatal or fatal versus "mixed"), outcome measurement (health records versus self-reports) and risk of bias ("high"/"probably high" ratings in any domain versus "low"/"probably low" in all domains).We judged the existing bodies of evidence for human evidence as "inadequate evidence for harmfulness" for the exposure categories 41-48 and 49-54 h/week for IHD prevalence, incidence and mortality, and for the exposure category ≥55 h/week for IHD prevalence. Evidence on exposure to working ≥55 h/week was judged as "sufficient evidence of harmfulness" for IHD incidence and mortality. Producing estimates for the burden of IHD attributable to exposure to working ≥55 h/week appears evidence-based, and the pooled effect estimates presented in this systematic review could be used as input data for the WHO/ILO Joint Estimates.
Abstract Background By 2050, an estimated 152 million people will be living with dementia. Prospective studies suggest that exposure to psychosocial stressors at work could be associated with a higher risk of mild cognitive impairment or dementia, but the evidence is still not clear. Method This study aimed to evaluate the effect of cumulative exposure to psychosocial stressors at work on global cognitive function in a cohort followed for over 25 years. At baseline in 1991‐1993 (T1), 9,188 white‐collar workers were recruited. Two follow‐ups were carried out in 1999‐2001 (T2) and 2015‐2019 (T3). This analysis was done among 5,728 participants working in T2, which participated in T3. Global cognitive function was evaluated with the validated Montreal Cognitive Assessment test (Nasreddine, 2005) and categorized in three groups according to standardized cut‐offs. Psychosocial stressors at work were evaluated with the validated Job Content Questionnaire (Karasek, 1979) at each time. The effect of cumulative exposure to psychosocial stressors at work at T1 and T2 on cognitive function categories at T3 was estimated with marginal structural models using inverse probability of treatment and censoring weights. Each observation was weighted for the inverse of the probability of death and lost to follow‐up and adjusted for potential confounders measured at T1 (age, sex, education, number of years in the same job, comorbidities, and lifestyle habits). Multiple imputation of missing data was performed. Result Workers exposed to low job demand and those exposed to a passive job (low job demand combined with low job control) at both T1 and T2 were at higher risk of moderate to severe cognitive impairment than non‐exposed workers (prevalence ratios (PR) and 95% confidence intervals (CI) of 1.34 (1.10;1.63), p=0.003, and 1.27 (1.05;1.54), p=0.012 respectively). Men, but not women, exposed to low job control at both T1 and T2 were at higher risk of moderate to severe cognitive impairment than non‐exposed workers (PR and 95% CI: 1.38 (1.07;1.79), p=0.015). No statistically significant associations were observed with the risk of mild cognitive impairment. Conclusion Primary prevention of cognitive impairment could be possible with the reduction of these frequent and modifiable psychosocial stressors at work.
Marginal structural models (MSMs) allow estimating the causal effect of a time‐varying exposure on an outcome in the presence of time‐dependent confounding. The parameters of MSMs can be estimated utilizing an inverse probability of treatment weight estimator under certain assumptions. One of these assumptions is that the proposed causal model relating the outcome to exposure history is correctly specified. However, in practice, the true model is unknown. We propose a test that employs the observed data to attempt validating the assumption that the model is correctly specified. The performance of the proposed test is investigated with a simulation study. We illustrate our approach by estimating the effect of repeated exposure to psychosocial stressors at work on ambulatory blood pressure in a large cohort of white‐collar workers in Québec City, Canada. Code examples in SAS and R are provided to facilitate the implementation of the test.
Psychosocial stressors at work, like job strain and effort-reward imbalance (ERI), can increase coronary heart disease (CHD) risk. ERI indicates an imbalance between the effort and received rewards. Evidence about the adverse effect of combined exposure to these work stressors on CHD risk is scarce. This study examines the separate and combined effect of job strain and ERI exposure on CHD incidence in a prospective cohort of white-collar workers in Quebec, Canada.Six thousand four hundred sixty-five white-collar workers without cardiovascular disease (mean age, 45.3±6.7) were followed for 18 years (from 2000 to 2018). Job strain and ERI were measured with validated questionnaires. CHD events were retrieved from medico-administrative databases using validated algorithms. Marginal Cox models were used to calculate hazard ratios (HR) stratified by sex. Multiple imputation and inverse probability weights were applied to minimize potential threats to internal validity.Among 3118 men, 571 had a first CHD event. Exposure to either job strain or ERI was associated with an adjusted 49% CHD risk increase (HR, 1.49 [95% CI, 1.07-2.09]). Combined exposure to job strain and ERI was associated with an adjusted 103% CHD risk increase (HR, 2.03 [95% CI, 1.38-2.97]). Exclusion of early CHD cases and censoring at retirement did not alter these associations. Among 3347 women, 265 had a first CHD event. Findings were inconclusive (passive job HR, 1.24 [95% CI, 0.80-1.91]; active job HR, 1.16 [95% CI, 0.70-1.94]; job strain HR, 1.08 [95% CI, 0.66-1.77]; ERI HR, 1.02 [95% CI, 0.72-1.45]).In this prospective cohort study, men exposed to job strain or ERI, separately and in combination, were at increased risk of CHD. Early interventions on these psychosocial stressors at work in men may be effective prevention strategies to reduce CHD burden. Among women, further investigation is required.
Mental health problems are associated with considerable occupational, medical, social, and economic burdens. Psychosocial stressors at work have been associated with a higher risk of mental disorders, but the risk of sickness absence due to a diagnosed mental disorder, indicating a more severe condition, has never been investigated in a systematic review and meta-analysis.To synthesize the evidence of the association of psychosocial stressors at work with sickness absence due to a diagnosed mental disorder among adult workers.Seven electronic databases (MEDLINE, Embase, PsycInfo, Web of Science, CINAHL, Sociological Abstracts, and International Bibliography of the Social Sciences), 3 gray literature databases (Grey Literature Report, WHO-IRIS and Open Grey), and the reference lists of all eligible studies and reviews were searched in January 2017 and updated in February 2019.Only original prospective studies evaluating the association of at least 1 psychosocial stressor at work from the 3 most recognized theoretical models were eligible: the job demand-control-support model, including exposure to job strain (high psychological demands with low job control); effort-reward imbalance model; and organizational justice model. Study selection was performed in duplicate by blinded independent reviewers. Among the 28 467 citations screened, 23 studies were eligible for systematic review.This meta-analysis followed the PRISMA and MOOSE guidelines. Data extraction and risk of bias evaluation, using the Risk of Bias in Nonrandomized Studies-Interventions tool, were performed in duplicate by blinded independent reviewers. Data were pooled using random-effect models.Sickness absence due to a mental disorder with a diagnosis obtained objectively.A total of 13 studies representing 130 056 participants were included in the 6 meta-analyses. Workers exposed to low reward were associated with a higher risk of sickness absence due to a diagnosed mental disorder compared with nonexposed workers (pooled risk ratio [RR], 1.76 [95% CI, 1.49-2.08]), as were those exposed to effort-reward imbalance (pooled RR, 1.66 [95% CI, 1.37-2.00]), job strain (pooled RR, 1.47 [95% CI, 1.24-1.74]), low job control (pooled RR, 1.25 [95% CI, 1.02-1.53]), and high psychological demands (pooled RR, 1.23 [95% CI, 1.04-1.45]).This meta-analysis found that workers exposed to psychosocial stressors at work were associated with a higher risk of sickness absence due to a mental disorder. A better understanding of the importance of these stressors could help physicians when evaluating their patients' mental health and work capacity.
