Linda L. Magnusson Hanson

Dr. Linda L. Magnusson Hanson


Research Focus & Metrics

Academic Career Length

13Years (2014-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 September 2020 in Environment International
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Journal Article
Open access
ADAlexis Descatha
Alexis Descatha
GSGrace Sembajwe
Grace Sembajwe
FPFrank Pega
Frank Pega
YUYuka Ujita
Yuka Ujita
MBMichael Baer
Michael Baer
SERGIO IAVICOLISERGIO IAVICOLI
SERGIO IAVICOLI
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 individual experts. Evidence from mechanistic data and prior studies suggests that exposure to long working hours may cause stroke. 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 stroke 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 stroke (three outcomes: prevalence, incidence, and mortality). A protocol was developed and published, applying the Navigation Guide to systematic reviews as an organizing framework where feasible. We searched electronic databases for potentially relevant records from published and unpublished studies, including Ovid MEDLINE, PubMed, EMBASE, Scopus, Web of Science, CISDOC, PsycINFO, and WHO ICTRP.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) individuals 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 with 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 stroke (prevalence, incidence or mortality). At least two review authors independently screened titles and abstracts against the eligibility criteria at a first review 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-effects meta-analysis. Two or more review authors assessed the risk of bias, quality of evidence and strength of evidence, using the Navigation Guide and GRADE tools and approaches adapted to this project. Twenty-two studies (20 cohort studies, 2 case-control studies) met the inclusion criteria, comprising a total of 839,680 participants (364,616 females) in eight countries from 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 (13 studies), self-reported physician diagnosis (7 studies), direct diagnosis by a physician (1 study) or during a medical interview (1 study). The outcome was defined as an incident non-fatal stroke event in nine studies (7 cohort studies, 2 case-control studies), incident fatal stroke event in one cohort study and incident non-fatal or fatal ("mixed") event in 12 studies (all cohort studies). Cohort studies were judged to have a relatively low risk of bias; therefore, we prioritized evidence from these studies, but synthesised evidence from case-control studies as supporting evidence. For the bodies of evidence for both outcomes with any eligible studies (i.e. stroke incidence and mortality), we did not have serious concerns for risk of bias (at least for the cohort studies). Eligible studies were found on the effects of long working hours on stroke incidence and mortality, but not prevalence. Compared with working 35-40 h/week, we were uncertain about the effect on incidence of stroke due to working 41-48 h/week (relative risk (RR) 1.04, 95% confidence interval (CI) 0.94-1.14, 18 studies, 277,202 participants, I2 0%, low quality of evidence). There may have been an increased risk for acquiring stroke when working 49-54 h/week compared with 35-40 h/week (RR 1.13, 95% CI 1.00-1.28, 17 studies, 275,181participants, I2 0%, p 0.04, moderate 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 acquiring stroke, when followed up between one year and 20 years (RR 1.35, 95% CI 1.13 to 1.61, 7 studies, 162,644 participants, I2 3%, moderate quality of evidence). Compared with working 35-40 h/week, we were very uncertain about the effect on dying (mortality) of stroke due to working 41-48 h/week (RR 1.01, 95% CI 0.91-1.12, 12 studies, 265,937 participants, I2 0%, low quality of evidence), 49-54 h/week (RR 1.13, 95% CI 0.99-1.29, 11 studies, 256,129 participants, I2 0%, low quality of evidence) and 55 h/week (RR 1.08, 95% CI 0.89-1.31, 10 studies, 664,647 participants, I2 20%, low quality of evidence). Subgroup analyses found no evidence for differences by WHO region, age, sex, socioeconomic status and type of stroke. Sensitivity analyses found no differences by outcome definition (exclusively non-fatal or fatal versus "mixed") except for the comparison working ≥55 h/week versus 35-40 h/week for stroke incidence (p for subgroup differences: 0.05), risk of bias ("high"/"probably high" ratings in any domain versus "low"/"probably low" in all domains), effect estimate measures (risk versus hazard versus odds ratios) and comparator (exact versus approximate definition). We judged the existing bodies of evidence for human evidence as "inadequate evidence for harmfulness" for all exposure categories for stroke prevalence and mortality and for exposure to 41-48 h/week for stroke incidence. Evidence on exposure to 48-54 h/week and ≥55 h/week was judged as "limited evidence for harmfulness" and "sufficient evidence for harmfulness" for stroke...

10 January 2018 in International Journal of Epidemiology
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Journal Article
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LHLinda L. Magnusson Hanson
Linda L. Magnusson Hanson
CLConstanze Leineweber
Constanze Leineweber
VPViktor Persson
Viktor Persson
MHMartin Hyde
Martin Hyde
TTTöres Theorell
Töres Theorell
HWHugo Westerlund
Hugo Westerlund
Sweden has played a major role in the development of psychosocial work environment research.1 In addition, Sweden, along with the other Nordic countries, has unique possibilities to link questionnaire data to administrative registers on demographics, employment and health. Despite this, the country has not previously had a prospective cohort with regularly repeated measures of work environment and health. The strengths of longitudinal studies in epidemiological research, as opposed to cross-sectional studies, are well known. Still, a significant part of the available evidence on associations between psychosocial work characteristics and health has been based on cross-sectional studies, making it difficult to separate cause and effect. Both selection and reverse causation are often plausible alternatives to a causal interpretation.2,3 Associations may also be inflated by common method bias, since self-ratings are often used for both exposures and outcomes.4 Repeated measures of both psychosocial work factors and health outcomes have become more common, but are often treated with cross-sectional methodologies using information on exposure variables from one time point to predict outcome variables from the next.5 Although preferable to cross-sectional studies, such approaches do not rule out reverse causation and contribute little or no understanding of causal mechanisms. Longitudinal studies with multiple repeat measures of both exposures and outcomes are therefore needed to advance our understanding of causality.

13 November 2017 in Diabetologia
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Journal Article
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TXTianwei Xu
Tianwei Xu
LHLinda L. Magnusson Hanson
Linda L. Magnusson Hanson
TLTheis Lange
Theis Lange
LSLiis Starkopf
Liis Starkopf
HWHugo Westerlund
Hugo Westerlund
NRNaja H. Rod
Naja H. Rod
Aims/hypothesis The aim of this multicohort study was to examine whether employees exposed to social stressors at work, such as workplace bullying and violence, have an increased risk of type 2 diabetes. Methods The study included 45,905 men and women (40–65 years of age and free of diabetes at baseline) from four studies in Sweden, Denmark and Finland. Workplace bullying and violence were self-reported at baseline. Incident diabetes was ascertained through national health and medication records and death registers. Marginal structural Cox models adjusted for age, sex, country of birth, marital status and educational level were used for the analyses. Results Nine per cent of the population reported being bullied at work and 12% were exposed to workplace violence or threats of violence. Bullied participants had a 1.46 (95% CI 1.23, 1.74) times higher risk of developing diabetes compared with non-bullied participants. Exposure to violence or threats of violence was also associated with a higher risk of diabetes (HR 1.26 [95% CI 1.02, 1.56]). The risk estimates attenuated slightly when taking BMI into account, especially for bullying. The results were similar for men and women, and were consistent across cohorts. Conclusions/interpretation We found a higher risk of incident type 2 diabetes among employees exposed to bullying or violence in the workplace. Further research is needed to determine whether policies to reduce bullying and violence at work may reduce the incidence of type 2 diabetes in working populations. Research on the mechanisms is also highly warranted.

12 October 2015 in BMC Public Health
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EAElena Andreeva
Elena Andreeva
LHLinda L. Magnusson Hanson
Linda L. Magnusson Hanson
HWHugo Westerlund
Hugo Westerlund
TTTores Theorell
Tores Theorell
MBM. Harvey Brenner
M. Harvey Brenner
Few studies have examined depression as both a cause and effect of unemployment, but no prior work investigated these relationships in the context of organisational downsizing. We explored whether the exposure to downsizing is associated with subsequent depression (social causation), and whether pre-existing depression increases the risk of being laid off when organisations downsize (health selection). Two successive waves of the nationally representative Swedish Longitudinal Occupational Survey of Health represented the baseline (2008) and follow-up (2010) of this study. Analyses included 196 workers who lost their jobs through downsizing, 1462 layoff survivors remaining in downsized organisations and 1845 employees of non-downsized workplaces. The main outcomes were: (1) Depressive symptoms at follow-up, assessed with a brief subscale from the Symptom Checklist 90, categorised by severity levels (“major depression”, “less severe symptoms” and “no depression”) and analysed in relation to earlier downsizing exposure; (2) Job loss in persons with downsizing in relation to earlier depressive symptoms. The associations were assessed by means of multinomial logistic regression. Job loss consistently predicted subsequent major depression among men and women, with a somewhat greater effect size in men. Surviving a layoff was significantly associated with subsequent major depression in women but not in men. Women with major depression have increased risks of exclusion from employment when organisations downsize, whereas job loss in men was not significantly influenced by their health. The evidence from this study suggests that the relative importance of social causation and health selection varies by gender in the context of organisational downsizing. Strategies for handling depression among employees should be sensitive to gender-specific risks during layoffs. Policies preventing social exclusion can be important for female workers at higher risk of depression.

2 December 2019 in Journal of Sleep Research
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Journal Article
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JGJohanna Garefelt
Johanna Garefelt
LPLoretta G. Platts
Loretta G. Platts
MHMartin Hyde
Martin Hyde
LHLinda L. Magnusson Hanson
Linda L. Magnusson Hanson
HWHugo Westerlund
Hugo Westerlund
TÅTorbjörn Åkerstedt
Torbjörn Åkerstedt
Summary: Work stress and poor sleep are closely related in cross‐sectional data, but evidence from prospective data is limited. We analysed how perceived stress and work stressors (work demands, decision authority and workplace social support) are related to key dimensions of insomnia over time, using structural equation modelling. Biennial measurements from a large sample of the working population in Sweden enabled us to analyse both the relationship from stress to sleep as well as that from sleep to stress. Overall, we found reciprocal relations between insomnia and all four stress measures. However, looking at the relation between each dimension of insomnia and each stress measure, there were some differences in direction of effects. In the direction from stress to sleep, all work stressors as well as perceived stress predicted both difficulties initiating sleep and difficulties maintaining sleep. The same was found for non‐restorative sleep, with the exception for decision authority. In the opposite direction, difficulties maintaining sleep predicted increased levels of work demands and perceived stress. Difficulties initiating sleep stood out among the insomnia symptoms as not predicting any of the stress measures, while non‐restorative sleep was the only symptom predicting all stress measures. The results advance the understanding of the stress−sleep relationship and indicate a potential vicious circle between insomnia and perceived stress as well as work stressors, suggesting that the workplace could be an arena for interventions to alleviate insomnia.

2 September 2020 in BMJ
Verified
Journal Article
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LHLinda L. Magnusson Hanson
Linda L. Magnusson Hanson
ANAnna Nyberg
Anna Nyberg
EMEllenor Mittendorfer-Rutz
Ellenor Mittendorfer-Rutz
FBFredrik Bondestam
Fredrik Bondestam
IMIda E H Madsen
Ida E H Madsen
Objective To analyse the relation between exposure to workplace sexual harassment and suicide, as well as suicide attempts. Design Prospective cohort study. Setting Sweden. Participants 86 451 men and women of working age in paid work across different occupations responded to a self-report questionnaire including exposure to work related sexual harassment between 1995 and 2013. The analytical sample included 85 205 people with valid data on sexual harassment, follow-up time, and age. Main outcome measures Suicide and suicide attempts ascertained from administrative registers (mean follow-up time 13 years). Results Among the people included in the respective analyses of suicide and suicide attempts, 125 (0.1%) died from suicide and 816 (1%) had a suicide attempt during follow-up (rate 0.1 and 0.8 cases per 1000 person years). Overall, 11 of 4095 participants exposed to workplace sexual harassment and 114 of 81 110 unexposed participants committed suicide, and 61/4043 exposed and 755/80 513 unexposed participants had a record of suicide attempt. In Cox regression analyses adjusted for a range of sociodemographic characteristics, workplace sexual harassment was associated with an excess risk of both suicide (hazard ratio 2.82, 95% confidence interval 1.49 to 5.34) and suicide attempts (1.59, 1.21 to 2.08), and risk estimates remained significantly increased after adjustment for baseline health and certain work characteristics. No obvious differences between men and women were found. Conclusions The results support the hypothesis that workplace sexual harassment is prospectively associated with suicidal behaviour. This suggests that suicide prevention considering the social work environment may be useful. More research is, however, needed to determine causality, risk factors for workplace sexual harassment, and explanations for an association between work related sexual harassment and suicidal behaviour.