With some effort we were finally able to retrieve an article (click here for pdf) written by Peter Schnall and Michael Alderman in 1984 making available evidence from the Hypertension, Detection and Follow-up Program (HDFP) clinical trial of hypertension drugs. This paper demonstrates that white men and white women with very elevated blood pressure did poorly in response to treatment in the HDFP trial. Please keep in mind that this remains a controversial issue as significant side effects occur from the treatment of mild hypertension (blood pressures of 140/90 remains undemonstrated, see 2010 Cochrane report on mild hypertension).
Peter Schnall MD, MPH
Professor of Medicine, U.C. at Irvine
Director, Center for Social Epidemiology
Controversy surrounding recent IPD Consortium Publications 2012-2014 about Job strain, CVD risk factors and CVD
A number of publications authored by the IPD consortium (a collective group of nearly 40 European researchers from 8 Northern and Western European countries, the “IPD-work consortium”, PI Dr. Mika Kivimäki) as well as critical letters to the editor have appeared in various medical and epidemiological journals in the past year and a half. (see http://unhealthywork.org/category/is-job-strain-a-risk-factor-for-cvd/) The conclusions drawn in many of the IPD Work Consortium publications seriously undermine public health efforts to improve the work environment worldwide, especially in countries where job strain and other work stressors may be far more prevalent than in Europe. Additionally, preventing job stress from occurring may be, in the long run be far more cost-effective than medicating millions of people who develop hypertension and high cholesterol, or trying to fund expensive behavioral modification programs, which have only had marginal success.
The IPD research is based on a large “pooled, individual-participant meta-analysis” combining 13 cohort studies. The possibilities and potential benefits of such a large dataset (almost 200,000 individuals) for exploring the effects of job strain on several health outcomes is obviously enormous. The lead PI Dr. Mika Kivimäki proposes that it as an example of a “new epidemiology” that resolves “longstanding debates” in the field and is more “scientifically rigorous” than previous research ([Kivimaki and Kawachi 2012]). The initial goal of the IPD research and analysis was to examine if “job strain” (a widely utilized psychosocial work stress variable which measures demands and control at work) is substantially and significantly related to CVD. The study confirmed this relationship and also found the PAR% for job strain was 3.4%. They conclude in the Lancet paper of September 14 2012 that: “Our findings suggest that prevention of workplace stress might decrease disease incidence; however, this strategy would have a much smaller effect than would tackling of standard risk factors, such as smoking.”[Kivimaki, et al. 2012]
A number of researchers in the field have noted several potentially serious methodological problems with the IPD studies, including issues with the assembling of the sample, lack of representativeness of the study population, unstated limitations with the process of exposure harmonization, and faulty protocol operationalization . Taken together these issues support a conclusion there is a strong likelihood that the strength of association between job strain and CVD, and the resulting PAR% for job strain, has been underestimated.
Also problematic was an unfortunate error made by the authors (recently acknowledged in the Jan 2014 issue of the SJWEH by one of the IPD consortiums PI’s Dr. Tores Theorell) in drawing conclusions about their findings in The Lancet. They erroneously equate job strain with all workplace stressors. Note the quote above says “… prevention of workplace stress…. “ when the authors should have stated “…prevention of job strain…” as this was the only workplace stressor being analyzed and discussed. As is well known, job strain is only one of a number of workplace stressors that include long work hours, shiftwork, ERI, social support/social isolation, and job insecurity (threat of unemployment), ,– to name a few of the most important ones – which have been identified as contributing to CVD risk factors and to CVD incidence and prevalence (see review below). If all of these variables were to be included in a calculation of the PAR% of workplace stress and CVD this might well lead to a larger PAR% than does job strain when taken alone. To date, the IPD consortium has not yet examined these additional factors.
The conclusions reached by the IPD consortium undermine decades of scientific research and evidence linking work with cardiovascular disease and run contrary to a collective assessment of the scientific evidence by a large group of researchers which support a substantially larger role for work stressors in the development of CVD ( (see Conference statement attached1 from the 6th ICOH on Work Environment and Cardiovascular Disease held March 27-30 2013). Additionally, the IPD conclusions may have a negative impact on the future health of working people if policy makers downgrade the important role of work stress and the possibly ameliorating aspects of work organization change.
1 According to research data about 10 to 20% of all causes of CVD deaths among the working age populations can be attributed to work, i.e. are work-related. The loss of work days and work ability is likely to be substantially greater.
We are most strongly in disagreement with the IPD consortium authors where they have made what we believe to be overly strong conclusions in recent publications. These conclusions are essentially public policy recommendations that deemphasize the importance of job strain or work stress intervention. Some examples,
“Our findings suggest that prevention of workplace stress might decrease disease incidence; however, this strategy would have a much smaller effect than would tackling of standard risk factors, such as smoking” (Kivimäki et al Lancet, 2013).
“…reducing work-related psychosocial stress, operationalized as job strain … is unlikely to be an important target for any policy or intervention aiming to influence health-related lifestyle factors or overall lifestyle.” (Heikkila et al AJPH, 2013)
“…it is unlikely that intervention to reduce job strain would be effective in combating obesity at a population level.” (Nyberg et al. JIM, 2012)
“For many people, avoidance of stress at work is unrealistic. The absence of strong evidence for effective interventions to reduce job strain therefore raises the challenge of identifying additional approaches for dealing with the health impact of stress in the workplace.” (Kivimäki et al CMAJ, 2013)
We have published our reasons for the disagreement with these conclusions in several letters to the editor (see www.unhealthywork.org for refs) and in email exchanges with IPD-work authors. Our disagreement and concern over these conclusions is based on several central arguments 1) these conclusions overstate the data based on some evident methodological limitations in the IPD-work analyses, and 2) the conclusions are not limited in the discussions of these articles to the Northern European, largely white collar populations represented by the study samples included in the IPD-work studies and so may have negative repercussions for other countries with poorer working conditions and health 3) they are not consistent with current public policy in Europe and in the United States which address the complex, synergistic relationship between work stress, health behaviors and illness,.
What follows is a brief summary of our arguments in opposition to the IPD consortium’s conclusions quoted above.
1) Their conclusions overstate the data because of evident methodological problems that may lead to bias towards the null and an underestimation of work stress effects on CVD and other health outcomes or behaviors.
C. There are problems with the conduct of their meta-analysis
2) The conclusions are not limited in the discussions of these articles to the Northern European, largely white collar populations represented by the IPD-work cohort studies but are easily misinterpretable as applying to all working people worldwide.
3) Conclusions about preventing standard risk factors rather than preventing work stress through workplace interventions are not in concert with current public policy efforts in the United States or Europe.
The conclusion that intervening on standard risk factors for CVD will be more effective than addressing workplace job stress prevention efforts is premature and problematic. The Job Strain PAR% is 3.4% (but not insignificant!). Even this low PAR% of 3.4% of CVD cases means millions of people have job strain related CVD.
There are numerous questions to be answered before public policy is determined. Among them:
We would like to add to this discussion that the goal of reducing standard risk factors may well benefit from interventions at the workplace that reduce work stressors. Recent policies on Total Worker Health from NIOSH in the United States suggest that workplace health promotion programs (i.e., to reduce smoking, encourage healthy eating, physical activity and reduce
weight etc.) may be more effective when they also “address the physical and organizational work environment”. NIOSH’s approach is consistent with the WHO Healthy Workplace Framework and the European Network for Workplace Health Promotion’s Luxembourg Declaration.
Kivimaki M, Kawachi I. 2012. Need for More Individual-level Meta-Analyses in Social Epidemiology: Example of Job Strain and Coronary Heart Disease. American Journal of Epidemiology: DOI: 10.1093/aje/kws1407.
Kivimaki M, Nyberg ST, Batty GD, Fransson EI, Heikkila K, Alfredsson L, Bjorner JB, Borritz M, Burr H, Casini A, Clays E, De Bacquer D, Dragano N, Ferrie JE, Geuskens GA, Goldberg M, Hamer M, Hooftman WE, Houtman IL, Joensuu M, Jokela M, Kittel F, Knutsson A, Koskenvuo M, Koskinen A, Kouvonen A, Kumari M, Madsen IE, Marmot MG, Nielsen ML, Nordin M, Oksanen T, Pentti J, Rugulies R, Salo P, Siegrist J, Singh-Manoux A, Suominen SB, Vaananen A, Vahtera J, Virtanen M, Westerholm PJ, Westerlund H, Zins M, Steptoe A, Theorell T. 2012. Job strain as a risk factor for coronary heart disease: a collaborative meta-analysis of individual participant data. Lancet 380: 1491–1497.
Choi B, Schnall P, Ko S, Dobson M, Baker D. 2013. Job strain and coronary heart disease ([letter]. Lancet 381: 448.
Landsbergis P, Schnall P. 2013. Job strain and coronary heart disease (letter). The Lancet 381: 449.
Below are links to the articles that have sparked this controversy and subsequent letters to the editor.
Job strain as a risk factor for coronary heart disease: a collaborative meta-analysis of individual participant data
Mika Kivimäki, Solja T Nyberg, G David Batty, Eleonor I Fransson, Katriina Heikkilä, Lars Alfredsson, Jakob B Bjorner, Marianne Borritz, Hermann Burr, Annalisa Casini, Els Clays, Dirk De Bacquer, Nico Dragano, Jane E Ferrie, Goedele A Geuskens, Marcel Goldberg, Mark Hamer, Wendela E Hooftman, Irene L Houtman, Matti Joensuu, Markus Jokela, France Kittel, Anders Knutsson, Markku Koskenvuo, Aki Koskinen, Anne Kouvonen, Meena Kumari, Ida E H Madsen, Michael G Marmot, Martin L Nielsen, Maria Nordin, Tuula Oksanen, Jaana Pentti, Reiner Rugulies, Paula Salo, Johannes Siegrist, Archana Singh-Manoux, Sakari B Suominen, Ari Väänänen, Jussi Vahtera, Marianna Virtanen, Peter J M Westerholm, Hugo Westerlund, Marie Zins, Andrew Steptoe, Töres Theorell, for the IPD-Work Consortium
Background: Published work assessing psychosocial stress (job strain) as a risk factor for coronary heart disease is inconsistent and subject to publication bias and reverse causation bias. We analysed the relation between job strain and coronary heart disease with a meta-analysis of published and unpublished studies.
Methods: We used individual records from 13 European cohort studies (1985–2006) of men and women without coronary heart disease who were employed at time of baseline assessment. We measured job strain with questions from validated job-content and demand-control questionnaires. We extracted data in two stages such that acquisition and harmonisation of job strain measure and covariables occurred before linkage to records for coronary heart disease. We defined incident coronary heart disease as the first non-fatal myocardial infarction or coronary death.
Findings: 30 214 (15%) of 197 473 participants reported job strain. In 1·49 million person-years at risk (mean follow-up 7·5 years [SD 1·7]), we recorded 2358 events of incident coronary heart disease. After adjustment for sex and age, the hazard ratio for job strain versus no job strain was 1·23 (95% CI 1·10–1·37). This effect estimate was higher in published (1·43, 1·15−1·77) than unpublished (1·16, 1·02−1·32) studies. Hazard ratios were likewise raised in analyses addressing reverse causality by exclusion of events of coronary heart disease that occurred in the first 3 years (1·31, 1·15−1·48) and 5 years (1·30, 1·13−1·50) of follow-up. We noted an association between job strain and coronary heart disease for sex, age groups, socioeconomic strata, and region, and after adjustments for socioeconomic status, and lifestyle and conventional risk factors. The population attributable risk for job strain was 3·4%.
Interpretation: Our findings suggest that prevention of workplace stress might decrease disease incidence; however, this strategy would have a much smaller effect than would tackling of standard risk factors, such as smoking.
A PDF of our Letter to the Editor, as well as the author’s response can be found HERE.
To: IPD Work Consortium Authors
From: Peter Schnall, BongKyoo Choi, Marnie Dobson, Paul Landsbergis
Date: October 7, 2013
Re: Publication Concerns
We would like to congratulate all of the IPD Consortium authors for their extensive efforts in exploring the relationship between job strain and cardiovascular disease as well as the many intervening variables that contribute to cardiovascular disease, such as obesity (or BMI) and physical inactivity. The collaborative effort in bringing together so many cohort datasets is very impressive. Nonetheless, we have numerous concerns that are expressed in the attached letters about the IPD Consortium sample, methods and the conclusions of the papers. Herein we would like to share some thoughts with you in the hope that this will lead to further dialogue.
In the attached letters to the editor (all published), we have raised a number of methodological and interpretational problems with the meta-analyses, including the measurement and analysis of job strain (e.g. use of unqualified samples in the harmonization of job strain and ERI measures), and the restriction of range during sample selection (e.g. Northern European samples, and weighted towards white collar samples), leading to a likely underestimation of the true associations. Given the limitations of these meta-analyses, we think the interpretations made and the sweeping conclusions drawn in the publications are deeply concerning (Kivimäki et al, Lancet 2012, Kivimäki et al, CMAJ 2013, Kivimäki and Kawachi AJE 2013, Nyberg et al Plos One, 2013, Siegrist et al IAOEH 2013).
The most problematic issues in the IPD consortium publications are twofold; first is the equation of job strain with all work stressors and second the subsequent conclusion that because of the small calculated PAR% for job strain that the prevention of workplace stress would have a much smaller effect than would the tackling of standard risk factors, such as smoking or physical inactivity (Kivimäki et al Lancet 2012, Kivimäki et al CMAJ 2013, Nyberg et al Plos One, 2013). Most importantly, we are concerned that the conclusions drawn in many of the IPD Work Consortium publications could detrimentally affect public health efforts to improve the work environment worldwide, especially in countries where job strain and other work stressors may be far more prevalent than in Europe. The conclusion that “…prevention of workplace stress might decrease disease incidence; however, this strategy would have a much smaller effect than would tackling of standard risk factors, such as smoking” may well turn out to be incorrect. Preventing work stress(ors) and the subsequent development of heart disease from occurring may be, in the long run, far more beneficial to the health of working people and more cost-effective than medicating millions of people who develop hypertension and high cholesterol, or trying to fund expensive behavioral modification programs, which have only had marginal success.
Prevention and treatment are not mutually exclusive approaches.
We hope that all of you will take the time to read our letters carefully and give serious consideration to our concerns. We look forward to continuing this discussion at the earliest possible time.
RE: Response to the email from Dr. Schnall and colleagues (9th October, 2013)
From: Investigators of the IPD-Work Consortium – Kivimaki et al
Date: 17th October, 2013
On the 9th of October, Drs. Schnall, Choi, Landsbergis and Dobson sent an email (copy below) via various yahoogroups, in which they raised concerns about the publications from the IPD-Work Consortium. They also attached several letters to the editors detailing their concerns. The discussion evolved from a publication by the IPD-Work group in the Lancet that found a pooled hazard ratio (HR) of 1.23 (95% CI 1.10-1.37) for the prospective association of job strain with onset of coronary heart disease in 13 European cohort studies (Kivimäki et al., 2012, http://pmid.us/22981903). The analysis was based on 197,473 participants.
As the Principal Investigators of the IPD-Work Project, we are delighted about the interest in our publications and we welcome the critical reading of our work. We attach our published response letters to this email. In addition we have the following reply to Dr. Schnall and colleagues (our reply is also attached as a pdf file for more convenient reading):
1) Dr. Schnall and colleagues are concerned that our sample was weighted to white collar workers which they believe would lead to an underestimation of the association between job strain and cardiovascular disease (CVD) and coronary heart disease (CHD). We disagree. First, of the 13 IPD-Work cohorts included in the Lancet paper, 5 were population-based samples from the general workforce (DWECS, COPSOQ-I, POLS, NWCS, HeSSup, see the Lancet paper for an explanation of the study name acronyms). Further, blue collar workers constituted the majority of participants in Still Working, the majority of the male participants in Wolf-N and a considerable proportion (about 30%) of the male participants in Wolf-S. Moreover, IPAW and FPS included a substantial number of (mainly female) low socioeconomic status (SES) human service workers such as health care helpers. Thus, Choi et al. appear to be misinformed when they wrote in one of their letters to the editors that, apart from a few exceptions, most of the samples “were recruited from white collar organizations” (Choi et al. 2013a, http://pmid.us/23399069). To the contrary, the IPD-Work dataset includes one of the largest samples of blue collar workers and low SES service workers ever analyzed in the job strain literature.
Second, the assumption by Dr. Schnall and colleagues that the association of job strain with CHD is stronger in blue collar workers compared to white collar workers is not supported by our analyses. The large study sample allowed us not only to adjust for SES, but also stratify by SES (Figure 3 in the Lancet paper, http://pmid.us/22981903). The hazard ratios for the association of job strain with CHD were 1.65 (95% CI 1.08-2.52), 1.31 (95% CI 1.05-1.64), and 1.24 (95% CI 1.05-1.47) for the high, intermediate and low SES groups, respectively. Thus, there was no statistically significant difference between the SES groups. Recently, Dr. Schnall and colleagues have used this finding as an argument against our study, speculating that the lack of a stronger association in the low SES groups is an indication that something is wrong with the data (Choi et al. 2013b, http://pmid.us/23956098; Landsbergis et al. 2013, http://pmid.us/23956099). We find this argument unconvincing. Instead, we would like to emphasize that our stratification by SES addressed one of the major criticisms of the job strain model during the last decade, i.e. the possibility that the association of job strain with risk of CHD/CVD might be biased due to confounding by SES (Macleod & Davey Smith, 2003,http://pmid.us/12883057). According to our analyses, there is no evidence for such a confounding, which we regard as an important contribution to the job strain literature.
2) Dr. Schnall and colleagues are concerned that we might have included “unqualified samples in the harmonization of job strain”. The rationale for this conclusion is unclear to us. Our consortium has set the pre-condition that the operationalization of job strain must be described in detail and published before any outcome analysis is conducted. Based on a scale harmonization analysis, conducted and published before the Lancet paper, we concluded that “all the partial scales in the present study (including the subscales comprising only two items), showed high to reasonable agreement with complete scales. In order to capture the theoretical background for job strain and to measure the same construct as the complete JCQ/DCQ, it is important that the abbreviated control scales cover both the skill discretion and the decision authority dimensions” (Fransson et al., 2012 http://pmid.us/22264402). The analysis in the Lancet paper supports this conclusion, as there was little heterogeneity between the studies with and without standard measures. Despite this, we agree that it is possible that the use of short scales may have decreased the precision of our predictions. However, within the published job strain literature, the study that showed one of the strongest associations with CVD was based on a non-standard measure for job strain (Kivimäki et al., 2002, http://pmid.us/12386034).
3) Dr. Schnall and colleagues are concerned that the high proportion of Northern European samples might have lead to an underestimation of associations. It is correct that eight of our studies came from the Nordic countries (Finland, Sweden, Denmark), four from Continental Western Europe (France, Netherlands, Belgium) and one from the UK. We agree that the association of job strain with CHD might be different in other countries and continents. However, it is unknown whether these associations would be stronger or weaker. Thus, it is speculation whether inclusion of studies from other countries or continents would have led to an increase or a decrease of the hazard ratios reported in our paper.
4) Dr. Schnall and colleagues are concerned that we may equate job strain with all work stressors. We are fully aware that job strain is only one of many potential health-hazardous psychosocial constellations at work. Some of the members of the IPD-Work consortium have been involved in the development and testing of comprehensive measurements of the psychosocial work environment (e.g., Bjorner & Rugulies 2010 eds., The Copenhagen Psychosocial Questionnaire,http://sjp.sagepub.com/content/38/3_suppl). Moreover, several of the members have been pioneers in examining the contribution of work stressors other than job strain to risk of cardiovascular disease. These include effort-reward imbalance (Siegrist, 1996, http://pmid.us/9547031), organizational justice (Kivimäki et al., 2005, http://pmid.us/16246990), bullying (Kivimäki et al., 2003,http://pmid.us/14504368), and long working hours (Virtanen et al., 2012, http://pmid.us/22952309) to name just a few examples. It is indeed well possible that using other work stressors or combining multiple work stressors might result in estimates that are different than the one we reported for job strain in the Lancet paper. To go from speculation to evidence, we will in the future IPD-Work analyses examine the contribution of other work stressors to CHD/CVD, to the extent our data allow this. We have already published an analysis on the association of job insecurity with CHD in the British Medical Journal (Virtanen et al., 2013, http://pmid.us/23929894) and a paper on scale harmonization of the effort-reward-imbalance model (Siegrist et al., 2013, http://pmid.us/23456220). We also plan to combine work stressors in an analysis of the “total” impact of available job conditions on CHD/CVD.
5) Based on the results from our analyses we believe that our conclusions in the Lancet paper are reasonable. Preventing job strain may decrease incidence of CHD, but the effect will likely be considerably smaller compared with preventing standard risk factors. However, we acknowledge that there might be complex relationships between work environment factors and standard risk factors. As discussed in previous literature, a favorable work environment may facilitate prevention based on standard risk factors and an unfavorable environment may correspondingly make such work difficult. For example, smoking may amplify the effects of stress on metabolic syndrome. Such mechanisms have not been sufficiently examined in the literature including the papers from the IPD-Work Consortium. We therefore agree that this discussion should be humble.
6) Dr. Schnall and colleagues are concerned that the publication of our research findings could undermine “public health efforts to improve the world environment worldwide”. We sympathize with the desire by Dr. Schnall and colleagues to improve the work environment and we would like to emphasize that we strongly believe that exposure to work stressors, including job strain, is morally wrong. However, as researchers, this belief cannot prevent us from publishing research findings that show no or only weak associations of work stressors with risk of ill-health.
While we much appreciate the critical reading of our work, we were surprised about the intensity of the critique by Dr. Schnall and colleagues in their letters to the editors. Moreover, in a letter Dr. Choi sent to all members of the IPD-Work Consortium, he asked us “why so many prominent researchers in European countries have produced so many problematic papers”. One answer we have to offer is the following: There might be different understandings of the sentence “job strain is a risk factor for CHD/CVD”. We do not regard this sentence as a statement of a fact that is proven beyond reasonable doubt, but as a hypothesis that needs to be rigorously tested according to accepted standards in the medical literature.
In 2004, Belkic, Landsbergis, Schnall and Baker published a comprehensive review on job strain and risk of CVD in the Scandinavian Journal of Work, Environment and Health (http://pmid.us/15127782). As other reviews in this field, they found mixed results from cohort studies. Of the 17 cohort studies, 8 supported the job strain hypothesis, 3 did not support the hypothesis but showed some non-statistically significantly tendencies for an association of job strain with CVD, and 6 did not support the job strain hypothesis at all. Belkic and colleagues decided not to calculate a pooled effect estimate, but instead conducted a detailed narrative review focused on potential biases in the literature. They concluded that the vast majority of studies were biased towards the null hypothesis, i.e. towards an underestimation of the job strain-CVD association. Together with some further findings from case- control and cross-sectional studies, this lead them to the conclusion that there is “…strong, consistent evidence of an association between exposure to job strain and CVD, especially among men…” (page 117).
We commend Belkic and colleagues for their thorough review of the literature and their detailed analyses of biases, although we believe that they showed a tendency to underestimate biases away from the null hypothesis. We also applaud the editors of SJWEH to publish this review. However, it also appears clear to us that the scientific arena has changed since the Belkic review was published. Today, such a review would not be acceptable for publication in high-ranking general medicine, cardiovascular disease or epidemiologic journals. Publications in such journals request an adherence to a different methodological standard. One may question those standards, one may be critical of the biomedical understanding of health and illness from which these standards evolved, and one may point out that these standards may not be well-suited for examining upstream factors, such as psychosocial and societal determinants of health and illness. But if one wants to bring the discussion of the possible contribution of work stressors to CVD to the attention of the biomedical and general epidemiologic scientific community, one has to play the game by the current established rules in these fields. These ever tighter rules focus, among other things, on cohort designs, pre-definition of the exposure, omission of or correcting for multiple testing for alternative exposure definitions, the careful and balanced consideration of confounders, and the use of transparent meta-analytic techniques, if the data allow this. Lengthy speculations about potential biases that are not testable in the analyses are usually not encouraged.
Because we adhered to the standards of rigorous hypothesis testing in mainstream biomedicine/epidemiology, we believe that the modest but statistically significant association of job strain with CHD shown in the Lancet paper provides stronger and more convincing evidence for a role of job strain in the etiology of CHD/CVD than most of the previous studies in this area. Importantly, the results in the Lancet paper are in line with the most recent state-of-the-art meta-analysis of all published literature on job strain and CHD that showed a 1.3-fold increased CHD risk among employees with job strain based on studies from Europe, the US and Asia (Steptoe & Kivimäki, 2013,http://pmid.us/23297662).
Dr. Schnall and Dr. Landsbergis have been on the forefront of research on job strain and CVD for decades. Together with others, their relentless effort and passion has kept work stressors in general and job strain in particular on the research agenda. We would like to encourage them to continue their effort. We would also encourage them and others to examine aspects that are more upstream, and that are usually not considered in mainstream biomedicine/epidemiology, such as the role of the societal context for the association of work stressors with health. Within the IPD-Work Consortium, our task is to rigorously test hypotheses about the association of work environment with health. We expect in the next few years further to contribute to this scientific debate with several important findings on the status of different work stressors as risk factors for different health endpoints.
Prof. Reiner Rugulies (Co-Principal Investigator, IPD-Work Consortium)
National Research Centre for the Working Environment, Denmark
Prof. emeritus Töres Theorell (Co-Principal Investigator, IPD-Work Consortium)
Stress Research Institute, University of Stockholm, Sweden
Prof. Nico Dragano (Co-Principal Investigator, IPD-Work Consortium)
Heinrich-Heine University of Düsseldorf, Germany
Prof. Mika Kivimäki (Principal Investigator, IPD-Work Consortium)
University College of London, UK, and Finnish Institute of Occupational Health