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Publications (3 of 3) Show all publications
Clark, A., Stenholm, S., Pentti, J., Salo, P., Lange, T., Török, E., . . . Rod, N. H. (2021). Workplace discrimination as risk factor for long-term sickness absence: Longitudinal analyses of onset and changes in workplace adversity. PLOS ONE, 16(8), Article ID e0255697.
Open this publication in new window or tab >>Workplace discrimination as risk factor for long-term sickness absence: Longitudinal analyses of onset and changes in workplace adversity
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2021 (English)In: PLOS ONE, E-ISSN 1932-6203, Vol. 16, no 8, article id e0255697Article in journal (Refereed) Published
Abstract [en]

Workplace discrimination may affect the health of the exposed employees, but it is not known whether workplace discrimination is also associated with an increased risk of long-term sickness absence. The aim of this study was to examine the longitudinal associations of changes in and onset of workplace discrimination with the risk of long-term sickness absence. Data on workplace discrimination were obtained from 29,597 employees participating in survey waves 2004, 2006, 2008 and/or 2010 of the Finnish Public Sector Study. Four-year changes in long-term sickness absence (>= 10 days of medically certified absence with a mental or non-mental diagnosis) were assessed. This covered successive study waves in analyses of onset of workplace discrimination as well as fixed effect analyses of change in workplace discrimination (concurrent i.e. during the exposure year and 1-year lagged i.e. within one year following exposure), by using each employee as his/her own control. The risk of long-term sickness absence due to mental disorders was greater for employees with vs. without onset of workplace discrimination throughout the 4-year period, reaching a peak at the year when the onset of discrimination was reported (adjusted risk ratio 2.13; 95% confidence interval (CI) 1.80-2.52). The fixed effects analyses showed that workplace discrimination was associated with higher odds of concurrent, but not 1-year lagged, long-term sickness absence due to mental disorders (adjusted odds ratio 1.61; 95% CI 1.33-1.96 and adjusted odds ratio 1.02; 95% CI 0.83-1.25, respectively). Long-term sickness absence due to non-mental conditions was not associated with workplace discrimination. In conclusion, these findings suggest that workplace discrimination is associated with an elevated risk of long-term sickness absence due to mental disorders. Supporting an acute effect, the excess risk was confined to the year when workplace discrimination occurred.

National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:su:diva-198388 (URN)10.1371/journal.pone.0255697 (DOI)000685265700091 ()34351965 (PubMedID)
Available from: 2021-11-11 Created: 2021-11-11 Last updated: 2022-02-25Bibliographically approved
Lai, E. T. C., Schlüter, D. K., Lange, T., Straatmann, V., Nybo Andersen, A.-M., Strandberg-Larsen, K. & Taylor-Robinson, D. (2020). Understanding pathways to inequalities in child mental health: a counterfactual mediation analysis in two national birth cohorts in the UK and Denmark. BMJ Open, 10(10), Article ID e040056.
Open this publication in new window or tab >>Understanding pathways to inequalities in child mental health: a counterfactual mediation analysis in two national birth cohorts in the UK and Denmark
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2020 (English)In: BMJ Open, E-ISSN 2044-6055, Vol. 10, no 10, article id e040056Article in journal (Refereed) Published
Abstract [en]

Objectives We assessed social inequalities in child mental health problems (MHPs) and how they are mediated by perinatal factors, childhood illness and maternal mental health in two national birth cohorts.

Design Longitudinal cohort study

Setting We used data from the UK Millennium Cohort Study and the Danish National Birth Cohort.

Primary and secondary outcome measures We applied causal mediation analysis to longitudinal cohort data. Socioeconomic conditions (SECs) at birth were measured by maternal education. Our outcome was child MHPs measured by the Strength and Difficulty Questionnaire at age 11. We estimated natural direct, indirect and total effects (TEs) of SECs on MHPs. We calculated the proportion mediated (PM) via three blocks of mediators—perinatal factors (smoking/alcohol use during pregnancy, birth weight and gestational age), childhood illness and maternal mental health.

Results At age 11 years, 9% of children in the UK and 3.8% in Denmark had MHPs. Compared with high SECs, children in low SECs had a higher risk of MHPs (relative risk (RR)=4.3, 95% CI 3.3 to 5.5 in the UK, n=13 112; and RR=6.2, 95% CI 4.9 to 7.8 in Denmark, n=35 764). In the UK, perinatal factors mediated 10.2% (95% CI 4.5 to 15.9) of the TE, and adding maternal mental health tripled the PM to 32.2% (95% CI 25.4 to 39.1). In Denmark, perinatal factors mediated 16.5% (95% CI 11.9 to 21.1) of the TE, and including maternal mental health increased the PM to 16.9% (95% CI 11.2 to 22.6). Adding childhood illness made little difference in either country.

Conclusion Social inequalities in child mental health are partially explained by perinatal factors in the UK and Denmark. Maternal mental health partially explained inequalities in the UK but not in Denmark.

Keywords
mental health, social medicine, epidemiology
National Category
Public Health, Global Health and Social Medicine
Identifiers
urn:nbn:se:su:diva-188647 (URN)10.1136/bmjopen-2020-040056 (DOI)000582256700025 ()33046476 (PubMedID)
Available from: 2021-01-11 Created: 2021-01-11 Last updated: 2025-02-20Bibliographically approved
Magnusson Hanson, L. L., Hulvej Rod, N., Vahtera, J., Peristera, P., Pentti, J., Rugulies, R., . . . Westerlund, H. (2019). Multicohort study of change in job strain, poor mental health and incident cardiometabolic disease. Occupational and Environmental Medicine, 76(11), 785-792
Open this publication in new window or tab >>Multicohort study of change in job strain, poor mental health and incident cardiometabolic disease
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2019 (English)In: Occupational and Environmental Medicine, ISSN 1351-0711, E-ISSN 1470-7926, Vol. 76, no 11, p. 785-792Article in journal (Refereed) Published
Abstract [en]

Objectives Several recent large-scale studies have indicated a prospective association between job strain and coronary heart disease, stroke and diabetes. Job strain is also associated with poorer mental health, a risk factor for cardiometabolic disease. This study investigates the prospective relationships between change in job strain, poor mental health and cardiometabolic disease, and whether poor mental health is a potential mediator of the relationship between job strain and cardiometabolic disease.

Methods We used data from five cohort studies from Australia, Finland, Sweden and UK, including 47 757 men and women. Data on job strain across two measurements 1-5 years apart (time 1 (T1)-time 2 (T2)) were used to define increase or decrease in job strain. Poor mental health (symptoms in the top 25% of the distribution of the scales) at T2 was considered a potential mediator in relation to incident cardiometabolic disease, including cardiovascular disease and diabetes, following T2 for a mean of 5-18 years.

Results An increase in job strain was associated with poor mental health (HR 1.56, 95% CI 1.38 to 1.76), and a decrease in job strain was associated with lower risk in women (HR 0.70, 95% CI 0.60-0.84). However, no clear association was observed between poor mental health and incident cardiometabolic disease (HR 1.08, 95% CI 0.96-1.23), nor between increase (HR 1.01, 95% CI 0.90-1.14) and decrease (HR 1.08, 95% CI 0.96-1.22) in job strain and cardiometabolic disease.

Conclusions The results did not support that change in job strain is a risk factor for cardiometabolic disease and yielded no support for poor mental health as a mediator.

Keywords
mental health, cardiovascular, diabetes mellitus, stress, meta-analysis
National Category
Public Health, Global Health and Social Medicine
Identifiers
urn:nbn:se:su:diva-176576 (URN)10.1136/oemed-2018-105595 (DOI)000497712200002 ()31488605 (PubMedID)
Available from: 2019-12-12 Created: 2019-12-12 Last updated: 2025-02-20Bibliographically approved
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0001-6807-8347

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