Stress and Health Stress and Health 24: 231–238 (2008) Published online 14 July 2008 in Wiley InterScience (www.interscience.wiley.com). DOI: 10.1002/smi.1203 Received 16 November 2007; Accepted 29 February 2008

Occupational stress and cardiovascular disease D.G. Byrne1,*,† and Geir Arild Espnes2 1

School of Psychology, The Australian National University School of Social Work and Health Sciences, The Norwegian University of Science and Technology 2

Summary Links between occupational stress and cardiovascular risk have long been asserted. This paper reviews the evidence from the simple notion of occupational level and type as a risk through to the more theoretically sophisticated models of occupational stress as a determinant of cardiovascular risk and disease. It maps measures of occupational stress against the three related end points of coronary risk profiles, hypertension and clinical cardiovascular disease. Taken broadly, the evidence is supportive of postulated links. The persuasiveness of the evidence now points to intervention studies in the workplace as the next major focus of research. Copyright © 2008 John Wiley & Sons, Ltd.

Key Words occupation, stress, cardiovascular disease Introduction Occupational stress (OS) is experienced when an individual is exposed to an overload of stressors originating wholly (or largely) from the occupational environment, but this grossly over-simplifies a complex bio-psycho-social situation. The cumulative literature on OS (or work, or job stress) is substantial both in volume and breadth, covering domains as far apart as the physical characteristics of occupational environments (e.g. heat, noise and crowding) and the personal characteristics of those working within those environments (e.g. coping styles, beliefs and cognitive capacities); and recognizes the interdependence of OS and other arenas of life stressors.

* Correspondence to: D.G. Byrne, School of Psychology, The Australian National University, Canberra ACT 0200, Australia † E-mail: [email protected] Copyright © 2008 John Wiley & Sons, Ltd.

Despite evidence for a recent decline in cardiovascular disease (CVD)1 mortality (Taylor, Dobson, & Mirzaei, 2006), CVD remains a major cause of death and disability in Western societies. An interest in the presence of CVD risk factors is therefore not surprising, and attempts to link the psychological characteristics of both individuals and their social environments to CVD risk has formed a good part of that research. It is inevitable then, that attention has turned to OS as an explanatory factor in the search to explain CVD risk. 1

A number of terms could be used to refer to the clinical end-points discussed in this paper; CVD, coronary heart disease (CHD), ischaemic heart disease (IHD), myocardial infarction (MI) and others are all relevant. For the sake of consistency however, the paper will use the standard descriptive term CVD, since this captures the broadest range of end-points and allows the most inclusive consideration of the evidence.

D. G. Byrne and G. A. Espnes Comprehensive reviews of evidence linking OS to CVD are available to cover the period to the end of the 20th century (see for example, Byrne, 2000; Smith & Ruiz, 2002; Melamed, Shiron, Toker, Berliner, & Shapira, 2006). This paper focuses, therefore, largely on the evidence accumulating from the beginning of this century, accessed either through Pub Med or PsycINFO databases, and favouring studies with large samples, robust designs and theory-driven measures. Definitions and models of OS Definitions of OS are completely consistent with more general definitions of stress—OS is seen, either singly or collectively, as exposure to a set of unique stressors, the operation of an interpretive process, or a pattern of individual responses, both biological (arousal) and psychological (strain or distress) (Sulsky & Smith. 2005), However, Hart and Cooper (2001) have eloquently highlighted the difficulty in providing a truly satisfactory definition for such a patently complex construct. They note that ‘. . . the scientific community has still not reached an agreed position on the meaning and definition of occupational stress’ (p. 94), and indicate instead the importance of focusing attention on integrated models to explain the phenomenon. This review will therefore organize itself largely around the usefulness of the dominant theoretical models of OS. While Lazarus’s (1991) transactional model of stress theoretically underpins many approaches to conceptualising OS, Sulsky and Smith (2005) note its substantial focus on the individual and therefore caution against an over-reliance on its use in empirical studies of OS. But two more specific models of OS have captured the greatest research attention in recent times. • The Demand/Control Model—which views OS (and its consequences) as arising from a tension between the demands an occupational environment imposes on an individual and the level of perceived control that person has over the environment (Karasek, 1979). This model was subsequently updated by Johnson and Hall (1988) to include a component of social support. • Effort/Reward Imbalance Model—where OS (and its consequences) is related to the balance 232

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between the degree of effort put into the job and the level of reward resulting from that effort (Siegrist, et al., 2004). While these models clearly overlap both thematically and in terms of their capacities to predict CVD risk (Bosma, Peter, Siegrist, & Marmot. 1998).they both represent conceptually strong and theoretically coherent approaches to explaining that risk, and both have been backed by a wealth of empirical evidence. For this reason, many of the studies chosen for review in this paper have been based on either one or other of these models. OS and CVD risk profiles One of the central issues surrounding the link between OS and CVD has to do with whether OS directly compromises cardiovascular function and precipitates clinical events or is linked indirectly through intervening factors. CVD risk is predicted by an array of recognized risk factors, most prominently cholesterol, cigarette smoking and hypertension. Relationships between OS and recognized CVD risk factors will therefore first be considered. Cigarette smoking Cigarette smoking poses an established and potent risk for CVD (Leone, 2007). Regardless of setting, stress increases cigarette consumption among established smokers (Byrne & Mazanov, 2007). Associations between OS and CVD risk may therefore be mediated through smoking. The presence of work-related stress (including high concentration demand and work dissatisfaction) predicted smoking status in middle-aged women (Jonsson, Johansson, Rosengren, Lappas, & Wilhelmsen, 2003), and OS has been associated with a broad range of smoking measures in both men and women (Ng & Jeffery, 2003). Associations between OS and levels of cigarette consumption particularly have emerged (Metcalfe, et al., 2003). Smoking appears more prevalent amongst blue- than amongst white-collar workers (Rose, Kumlin, Dimberg, Bengtsson, Orth-Gomer, & Cai, 2006), supposedly reflecting the negative effects of OS. And those who perceive poor involvement in decision making in the workplace are more likely to be heavy smokers than those Stress and Health 24: 231–238 (2008) DOI: 10.1002/smi

Occupational stress and cardiovascular disease without such perceptions (Kouvonen, et al., 2007), with this finding unaffected either by adjustments for job strain or effort/reward imbalance. Both the Demand/Control and Effort/Reward Imbalance Models have also been more systematically applied to OS and smoking. High job demand has been related to smoking in middle-aged rural workers (Tsutsumi, et al., 2003), and it appears to influence smoking irrespective of job strain (Kang, et al., 2005). But job strain (high demand and low control) too has been linked to smoking (John, Riedel, Rumpf, Hapke, & Meyer, 2006). And both high job strain and high effort/reward imbalance have been independently associated with smoking intensity (Kouvonen, Kivimaki, Virtanen, Pentti, & Vahtera, 2005), with lower levels of effort in the workplace also predicting ex-smoking status. Sufficient evidence therefore now links OS and smoking that it must be seen as one credible pathway through which OS influences CVD risk. The mechanisms for this are less clear—smoking may operate through interactions with other risk factors (Leone, 2007) or it may exert a more independent influence through excitatory neural processes (Byrne & Mazanov, 2007)—but these are issues for further investigation. Blood pressure Elevated blood pressure (BP), particularly if it is chronic (hypertension), poses an established risk for CVD (Mendis, et al., 2007). Possible associations between OS and BP have therefore been targeted to elucidate the link between OS and CVD. However, it is important to distinguish between evidence relating OS and BP per se (even if measured repeatedly and/or in the work situation) and evidence linking OS and diagnosed hypertension—the former may indicate future hypertension but only the latter reliably predicts CVD. Although the idea that OS may influence blood pressure has existed for some decades, Siegrist and Klein (1990) first demonstrated a co-variation between chronic OS and BP reactivity under challenge. Job strain has been specifically linked to BP, although Theorell, Ahlberg-Hulten, Jodko, and Sigala (1993) restricted this to diastolic BP, and then largely in the work setting. Job strain based on both demand and control has also been associated with diastolic BP, but only in men (Tsutsumi, et al., 1998), or when diastolic BP was measured at night after work (Rau, Georgiades, Copyright © 2008 John Wiley & Sons, Ltd.

Fredrikson, Lemne, & de Faire, 2001). Relationships between OS and diastolic BP appear to hold even after controlling for such possible confounders as age, smoking and alcohol consumption (Su, et al., 2001). By contrast, OS specific to medical practitioners was related to elevation of both diastolic and systolic BP, but maximally only during the working day (O’Connor, O’Connor, White, & Bundred, 2001). Elevations in both diastolic and systolic BP have also been reported in relation to job strain using ambulatory BP measures in the workplace (Landsbergis, Schnall, Pickering, Warren, & Schwartz, 2003) but the association was only evident in those with low socio-economic status. Moving from low to high job strain occupations significantly elevates systolic BP (Cesana, Sega, Ferrario, Chiodini, Corrao & Mancia, 2003), while the same effect has been observed over time where high job strain prevails (Kjeldsen, et al., 2006). BP in the workplace has been related to occupational over-commitment, independent of job control (Steptoe, Siegrist, Kirschbaum, & Marmot, 2004), and to expressions of workplace anger (Bongard & al’Absi, 2005). And very recently it has been reported that job strain may actually interact with a genetic factor (I/D polymorphism in the adrenergic alpha2B-receptor) to elevate both systolic and diastolic BP (Ohlin, Berglund, Nilsson, & Melander, 2007). Broad evidence therefore links OS with BP, largely through the experience of job strain. The evidence indicates an effect of OS on both systolic and diastolic BP, and may possibly be mediated through a genetic interaction. But elevated BP is not hypertension, and only the latter constitutes an established risk for CVD. Hypertension A combination of high effort and low reward in the workplace has been associated with a diagnosis of hypertension in middle managers (Peter & Siegrist, 1997) and shift workers (Peter, Alfredsson, Knutsson, Siegrist & Westerholm, 1999). Job strain too has been related to hypertension, but curiously one study reported this only in men (Tsutsumi, Kayaba, Tsutsumi, Igarashi, & Jichi, 2001), and another only in women (Alfredsson, et al., 2002). However, beyond the strict confines of theoretical models of OS, the prevalence of hypertenStress and Health 24: 231–238 (2008) DOI: 10.1002/smi

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D. G. Byrne and G. A. Espnes sion have also been associated with organizational job constraints (Radi, et al., 2005), excessive work hours (Yang, Schnall, Jauregui, Su, & Baker, 2006), job insecurity and low occupational prestige, but only in men (Levenstein, Smith, & Kaplan, 2001), covert coping with unfair treatment at work, but only in men (Theorell, Alfredsson, Westerholm, & Falck, 2000), perceived job barriers and job intensity (Greiner, Krause, Ragland, & Fisher, 2004), and race-related workplace stress (Din-Dzietham, Nembhard, Collins, & Davis, 2004). The evidence implicating OS in the genesis of hypertension is therefore persuasive though much of it goes beyond the framework of established theoretical models.

2006), which has been linked with CVD risk. Job strain is strongly associated with rates of metabolic syndrome (Kang, et al., 2004); this relationship follows a dose-response function (Chandola, Brunner, & Marmot, 2006). However, women with low long-term job strain were reported to have high levels of metabolic syndrome, whereas men with high long-term job strain showed low levels of metabolic syndrome (Kinnunen, Feldt, Kinnunen, Kaprio, & Pulkkinen, 2006). And at least one recent study found no relationship between job strain and metabolic syndrome (Demiral, et al., 2006). This area must therefore be considered to require further exploration. Fibrinogen

Blood lipids Levels of blood lipids, and particularly levels of LDL cholesterol, have long been associated with elevated CVD risk (Campbell, et al., 2007). Recent studies have established reliable links between OS and this component of CVD risk. OS conceptualised specifically within the Demand/Control Model has been linked with elevated blood lipids (Kang, et al., 2005). Curiously, elevated cholesterol was related only to low decision latitude (control) and not to job strain. The index of job strain has been related to elevated lipids (Tsutsumi, et al., 1998), but only in working females. Within the Effort/Reward Imbalance Model the most persuasive link between OS and blood lipids comes from the WOLF (Work, Lipids and Fibrinogen) Study (Peter, et al., 1998). Examination of baseline data from employed males and females showed that in men, effort/reward imbalance was significantly related both to high total cholesterol and to a total cholesterol : HDL ratio; in women, high effort was related both to increased LDL levels and to a cholesterol : LDL ratio. Westerlund, Theorell and Alfredsson (2004) extended analyses of the WOLF Study data to include indices of employment stability, reporting elevated cholesterol amongst employees of companies where organizational instability was evident. Evidence associating OS with potentially harmful levels of blood lipids is therefore well established. Metabolic syndrome An interesting extension of this work focuses on OS and the metabolic syndrome (Melamed, et al., 234

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While the evidence here is by no means uncontested, plasma fibrinogen has been implicated as a predictor of CVD (Woodward, Rumley, Welsh, McMahon, & Lowe, 2007) and this too may mediate a link between OS and CVD risk (Theorell, 2002). A number of studies have reported associations between plasma fibrinogen and low job control generally (Clays, et al., 2005), low job control in female workers only (Tsutsumi, Theorell, Hallqvist, Reuterwall, & de Faire, 1999), and job strain in males but not females (Kittel, et al., 2002). Unsupportive evidence, however (Alfredsson, et al., 2002), indicates that some caution must be exercised until further evidence is available. OS and incidence of clinical CVD Both the Demand/Control (Theorell & Karasek, 1996) and Effort/Reward Imbalance (Siegrist, 2005; van Vegchel, se Jonge, Bosma, & Schaufeli, 2005) models have been persuasively linked to clinical CVD. Largely atheoretical constructs have also driven many studies in this area, and while the evidence is more difficult to interpret, it is also persuasive. Case-control studies (theoretically based) Job strain as an index of OS has been related to a significant elevation in CVD amongst middleaged men, independent of other risk factors (Alfredsson & Theorell, 1983), though a synergistic interaction between demands and decision Stress and Health 24: 231–238 (2008) DOI: 10.1002/smi

Occupational stress and cardiovascular disease latitude strengthened associations (Hallqvist, et al., 1998). A more recent study of job strain strongly associated it with heart disease in a large sample of men, again independent of other CVD risk factors, however heart disease here was self-reported (Sacker, Bartley, Frith, Fitzpatrick, & Marmot, 2001). The relationship, however, was also evident in a sample of men who survived a clinically diagnosed CVD event (Malinauskiene, et al., 2005). Over-commitment to work (high effort) was also strongly related to CVD in women occupying male-dominated jobs (Peter, Hammarstrom, Hallqvist, Siegrist, & Theorell, 2006). And interestingly, recent work suggests that a combination of the demand/control and effort/reward imbalance models further strengthens the capacity of OS to predict clinical CVD (Peter, Siegrist, Hallqvist, Reuterwall, & Theorell, 2002). Case-control studies (atheoretical) Chronic high workload has been associated with the prevalence of CVD (Siegrist, Dittmann, Rittner, & Weber, 1982), as has shift work (Alfredsson, Karasek, & Theorell. 1982), Selfreported OS, again focussing on the workplace structure, significantly predicted clinical CVD in a sample of patients experiencing their first clinical event (Panagiotakas, et al., 2003). Moreover, perceived unfairness in the workplace has been linked with an elevated risk of clinical CVD (De Vogli, Ferrie, Chandola, Kivimaki, & Marmot, 2007). Prospective studies (theoretically based) However, prospective studies are crucial to exploring links between OS and CVD. Lee, Colditz, Berkman and Kawachi (2002) found no evidence to causally associate job strain with the emerging incidence of CVD in a sample of women over four years. By contrast, Kivimaki, et al. (2002) found both job strain and effort/reward imbalance to significantly predict risk of CVD mortality over 25 years. High demand and low decision latitude also predicted the incidence of CVD over an 11-year follow-up (Kuper & Marmot, 2003). And in women, job strain has been linked to progression of coronary atherosclerosis over a 3-year period (Wang, et al., 2007). Copyright © 2008 John Wiley & Sons, Ltd.

Prospective studies (atheoretical) Job dissatisfaction was only slightly associated with age-adjusted CVD risk in men over time, but not in women, and there was no evidence linking it with evolving CVD mortality (Heslop, Smith, Metcalfe, Macleod, & Hart, 2002). However, high perceived justice in the workplace related to a lower risk of CVD in men followed-up over more than 8 years (Kivimaki, et al., 2005). Conclusions This review has been selective and not exhaustive, focussing largely on recent material. Empirical evidence from studies with robust research designs broadly—but not universally—support links between OS and CVD. Studies relating OS and CVD risk factors particularly support a link between OS and eventual CVD—and evidence focusing on BP and hypertension is perhaps strongest. Evidence from both case-control and prospective studies also persuasively support a link between OS and clinical CVD, although prospective studies are fewer in number. Both the Demand/ Control (Job Strain) and Effort/Reward Imbalance Models offer powerful conceptual frameworks linking OS with CVD; a combination of the two achieves demonstrable synergies in predicting CVD. And, even atheoretical approaches provide convincing evidence for the link. Strengths of association between OS and CVD are typically modest, and obviously, not all studies have supported the proposed link—to comprehensively discuss these studies, and the reasons why they do not offer that support, would go beyond the scope of this brief review. The collective evidence now available, however, must be viewed as sufficiently consistent and robust to support the conclusion that OS is linked, either indirectly or directly, with CVD. This being so, the next generation of research may well need to focus both on psycho-biological mechanisms of influence and on interventions to reduce OS in the workplace. Again, a detailed discussion either of mediating mechanisms or of specific workplace interventions goes well beyond the scope of this review. In regard to the latter however, future research will almost inevitably need to address the legal and political realm of industrial relations. The provision of a safe workplace needs to encompass freedom from OS and if this lowers the population risk of CVD it is a freedom well worth seeking. Stress and Health 24: 231–238 (2008) DOI: 10.1002/smi

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