Introduction

Recent studies suggest that organisational justice, that is, the decision-making rules and managerial behaviours within the organisation that affect the employees' experience of fairness, may influence the health of employees. The experience of lower levels of justice has been found to be associated with an increased risk of psychological distress, sickness absence and coronary heart disease.1–3 However, the mechanisms underlying these associations remain unclear.

Prolonged (chronic) inflammation is part of the atherosclerotic process4 and is a predictor of chronic conditions, such as coronary heart disease and some respiratory and musculoskeletal diseases.4–6 There is also evidence that plasma levels of circulating inflammatory markers, such as interleukin-6 (IL-6) and C-reactive protein (CRP) are associated with depression and distress,7 8 possibly because such states may diminish the immune system’s sensitivity to the glucocorticoid hormones responsible for terminating the inflammatory response.9 Although organisational injustice has been shown to be associated with depression10 and psychological distress,1 3 11 12 no previous studies are available on the association between perceived organisational injustice and long-term inflammation.

In this study, we examined the relationship between organisational justice and markers of inflammation (IL-6 and CRP) in a cohort of British civil servants, the Whitehall II study. Data on conventional risk factors for inflammation enabled us to determine whether organisational justice predicts inflammation over a 14-year follow-up independently of age, sex, occupational grade, body mass index (BMI), smoking, depressive symptoms and alcohol consumption, which are all covariates known to be associated with inflammatory markers.13–17

Methods

Participants and design

The target population for the Whitehall II Study was all office staff aged 35–55 years based in 20 civil service departments in London, England. With a 73% participation rate, the baseline cohort comprised 6895 men and 3413 women. The present study included the 3205 men (46.5% of all male participants) and 1204 women (35.3% of all women participants) who responded to questions on organisational justice at phases 1 (1985–1988) and 2 (1989–1990) and were tested for markers of inflammation at phases 3 (1991–1993) and 7 (2003–2004). The 3690 men and 2209 women excluded were older (44.9 years compared to 43.8 years, p<0.001) and more likely to be in the lower employment grades (20% vs 31%, p<0.001). We restricted the analyses to men and women with complete data of exposure and outcomes.

Measures

During the clinical examination fasting serum was collected between 8 am and 1 pm at study phases 3 and 7 and was stored at −70°C until analysis. Samples from both phases were analysed at the same time. CRP was measured using a high-sensitivity immunonephelometric assay in a BN ProSpec nephelometer (Dade Behring, Milton Keynes, UK). IL-6 was measured using a high-sensitivity ELISA assay (R & D Systems, Oxford, UK). Values lower than the detection limit (0.154 mg/l for CRP and 0.08 pg/ml for IL-6) were assigned a value equal to half the detection limit. To measure short-term biological variation and laboratory error, a repeated sample was taken from a subset of 150 participants for CRP and 241 for IL-6 at phase 3 (average elapsed time between samples was 32 (SD 10.5) days), and 533 for CRP and 329 for IL-6 at phase 7 (average elapsed time between samples was 24 (SD 11.0) days). Intra- and inter-assay coefficients of variation were 4.7% and 8.3% for CRP, and 7.5% and 8.9% for IL-6 at phases 3 and 7, respectively. Test–retest reliability between samples was assessed with Pearson's correlation coefficients: r=0.77 at phase 3 and r=0.72 at phase 7 for CRP, and r=0.61 and r=0.63, respectively, for IL-6.

We used a self-reported scale that tapped into the relational component of organisational justice (five items; Cronbach's α for internal consistency was 0.72 at phases 1 and 2), as in earlier studies in the Whitehall II cohort.12 18 This scale includes the following items: (1) Do you ever get criticised unfairly? (2) Do you get consistent information from line management (your superior)? (3) Do you get sufficient information from line management (your superior)? (4) How often is your superior willing to listen to your problems? and (5) Do you ever get praised for your work? Participants rated their response to each of these items on a four-point scale where 1 indicates never, 2 seldom, 3 sometimes and 4 often. For item 1, we recoded the responses, 1 to indicate often, 2 sometimes, 3 seldom and 4 never, to reflect the reversed wording of the item. For each participant, we averaged the scores of the five items at phases 1 and 2 and then calculated the mean of these averaged scores. The mean scores were scaled from 0 to 100 and treated as a continuous variable.

Covariates included age, employment grade, smoking, alcohol consumption, depressive symptoms and BMI. Grade was measured as civil service employment grade (administrative, professional, clerical/support). Smoking (never/former/current smoker), alcohol consumption (none, 1–14 units, 15–21 units, 22+ units per week with the highest two categories being combined in women), depressive symptoms and BMI (under 18.5, 18.5–24.9, 25–29.9, ≥30 kg/m²) were all measured at both phases 3 and 7. Depressive symptoms were measured using a four-item depression scale (Cronbach's α=0.88), derived from the 30-item General Health Questionnaire based on principal component analysis.19 The four items requested whether the participant has recently: been thinking of him/herself as a worthless person; felt that life is entirely hopeless; felt that life isn't worth living; and, found at times (s)he couldn't do anything because his/her nerves were too bad. Response options were “not at all”=0, “no more than usual”=1, “rather more than usual”=2, and “much more than usual”=3. Depressive symptoms were defined as a summary score. As previously, the summary score derived from this subscale was dichotomised, with a score of 4 or higher defining depression cases.20

We considered age and employment grade only as potential confounding factors for the association between organisational justice and inflammatory markers. In contrast, the role of health behaviours, BMI and depressive symptoms may vary and they may represent both confounding and mediating factors for this association.21 22

Statistical analysis

The relationships between organisational justice at phases 1 and 2 and inflammatory markers at phase 3 and phase 7 were analysed using linear regression. As the distribution of CRP and IL-6 was skewed, the log-transformed CRP and IL-6 levels at phase 3 and at phase 7 were used as the dependent variables. The regression coefficients are presented for percentage change in CRP and IL-6 levels per one standard deviation change in organisational justice. Statistical models were adjusted for age, employment grade, BMI, alcohol consumption and smoking status obtained from the same phase as the outcome. When testing the associations of justice with CRP and IL-6 at phase 7, the models were additionally adjusted for CRP and IL-6 at phase 3. The statistical tests were performed with Statistical Analysis System (SAS) v 9.01, and statistical significance was inferred at a two-tailed p value <0.05.

Results

Characteristics of the men and women participating in the study are shown in table 1. The mean age of the participants at phase 1 was 43.9 years. The majority worked in the professional grades, only 7%–10% of both sexes were current smokers and men consumed more alcohol than women at phases 3 and 7. There was a small difference in BMI at phase 7 between men and women, but no sex differences in justice perception (table 1).

Age-adjusted models showed lower employment grade to be associated with lower justice in men (t(1)=−4.63, p<0.001). In men, lower organisational justice was also related to higher BMI at phase 3 (t(1)=−3.90, p<0.001) and at phase 7 (t(1)=−5.20, p<0.001) and increased depressive symptoms at phase 3 (t(1)=−8.53, p<0.001) and phase 7 (t(1)=−6.14, p<0.001). Similar associations between justice and BMI at phase 3 (t(1)=−3.42, p<0.001) and at phase 7 (t(1)=−2.77, p=0.006) and between justice and depressive symptoms at phase 3 (t(1)=−4.72, p<0.001) and at phase 7 (t(1)=−5.19, p<0.001) were found in women. BMI was a strong correlate of the inflammation markers in men and women, but the same was not true for depressive symptoms although there was some evidence of an association with IL-6 in men (table 2).

The levels of inflammatory markers (at phase 7) in men as a function of the quintiles of organisational justice are presented in figure 1. A similar linear relationship is also seen for CRP in men at phase 3 (not shown).

• Download figure
• Open in new tab
• Download powerpoint

Figure 1

Mean levels of CRP (mg/l) and IL-6 (pg/ml) at phase 7 in men (n=3204).

Unadjusted and age-adjusted associations between CRP and IL-6 levels at phases 3 and 7 and organisational justice are presented in table 3. In men, high organisational justice was associated with lower CRP levels at both follow-up phases (3 and 7) and with lower IL-6 level at the later follow-up phase. In women, no associations were detected between inflammatory markers and justice perceptions.

In men, the associations between organisational justice and inflammatory markers at phase 7 were robust to adjustments for age, occupational grade, BMI and depressive symptoms and remained even after adjustments for inflammatory markers at phase 3 (table 4). However, the relationship between organisational justice and CRP at phase 3 attenuated after the model was adjusted for BMI.

We repeated the final set of analyses using one of the items of our scale, “Do you ever get criticised unfairly?” as a measure of organisational justice. This item, with the most face validity, permits a sensitivity analysis for the results using all five items of the scale. In men, there was an age-adjusted association between this one-item justice measure and IL-6 at phase 7 (p=0.025), but that association was attenuated in the fully adjusted model (p=0.44). No age-adjusted associations were seen with CRP (p=0.21) or IL-6 (p=0.36) at phase 3.

Discussion

We found a lower mean level of organisational justice on two occasions to be predictive of higher levels of CRP and IL-6 approximately 2.5 and 13.5 years later in men. Adjustment for demographic characteristics, obesity and depressive symptoms did not substantially attenuate the association with CRP and IL-6 at the later follow-up, providing evidence that low organisational justice may act as an independent risk factor for increased long-term levels of inflammatory markers. The association between organisational justice and the first measurement of CRP (about 2.5 years later) attenuated after controlling for the behavioural factors. To our knowledge, this is the first prospective study analysing the associations between organisational justice and inflammatory markers.

By characterising organisational justice with repeated measurements across two time points, we were able to test associations between a reliable measure of organisational justice and one of the potential physiological mechanisms explaining the association between organisational justice and health. This study benefits from using data from the Whitehall II study, a well-characterised cohort with sufficient power to detect effects within both sexes. The adjustment for levels of inflammatory markers at the first follow-up when testing the association between justice and inflammatory markers at the second follow-up reduced the likelihood that our findings were attributable to pre-existing inflammation.

It is possible that people who are more sensitive to stress tend to both report low justice at work and have higher levels of inflammatory markers, creating a spurious association between justice and inflammation. In our analyses, we took account of the effect of depressive tendencies which have previously been associated with both justice perceptions12 and inflammatory markers.23 However, this did not eliminate the association between justice and inflammation. In addition, previous studies testing the modifying effects of various stress-related personality factors suggest that such factors are not strong modifiers of justice perceptions and health outcomes.23 24

The present findings are in line with previous studies suggesting an association between depression and CRP25–29 and between negative emotions and inflammatory markers.23 More specifically, our results offer evidence suggesting that there may be a physiological link between the fairness of decision-making procedures and treatment of employees and their health.1 18 Previous studies found that perceived organisational injustice was associated with elevated ambulatory blood pressure30 and quantitative markers of cardiac dysregulation, including reduced heart rate variability and altered systolic arterial pressure variability.31 These mechanisms may also link organisational justice to disease end points.

It has been suggested that inflammation may be one of the mechanisms through which psychosocial factors, including justice, increase the risk of cardiovascular disease.32 This is especially the case for coronary artery disease, which is seen as a chronic inflammatory response to injuries of the vascular endothelium,33 although the aetiological role of CRP in the disease process remains controversial.34–37 Although the mean CRP levels in our data were not extremely high even in the lowest justice group, they may be biologically significant. It has been suggested that even low levels of chronically increased CRP is a risk factor for coronary heart disease (see review38). In one study, a baseline level of 2.4 mg/l, as compared with 1.0 mg/l, was associated with increased coronary risk.35 In our study, the crude mean level of CRP was 2.9 mg/l in the low justice group and 2.1 mg/l in the high justice group. The biological significance of such a difference is not clear, and thus more research is needed to determine whether such changes are part of the pathophysiological pathway leading to disease, or simply physiological changes related to maintaining homeostasis.

Similarly, it has been suggested that higher levels of chronic inflammation may be one of the predecessors of depression,23 which has been shown to be associated with organisational injustice in a number of studies.1 12 39 Previous studies from the Whitehall II cohort have shown that a favourable change in justice perceptions was associated with a reduction in the immediate risk of psychiatric morbidity, while an adverse change increased both the immediate risk and the longer-term risk.12 Furthermore, because inflammation is a component in diseases that are responsible for a large share of sickness absence days, such as the common cold, it may also be one of the mechanisms through which low justice affects sickness absence.40 In the future, research is needed on the associations between low organisational justice and other inflammatory diseases, such as diabetes and arthritis.

We did not find an association between organisational justice and inflammation in women. It is possible that the substantially lower sample size of women is an explanation of the null finding. However, gender difference is also possible, as some previous studies suggest that the relationship between inflammatory markers and distress related psychological states, such as depression, are only apparent in men.23 41 Furthermore, our measure of organisational justice covers mainly the relational dimension of the theoretical construct. It has been suggested previously that the relational justice component may be more consistently related to mental health problems in men than in women. According to a previous study using Whitehall II data,12 low relational justice at baseline was a significant predictor of psychiatric morbidity in both sexes, but there was an indication that intermediate relational justice was also predictive in men.

Organisational justice perceptions and other psychosocial factors may contribute to inflammation in a number of other ways by promoting distress and maladaptive behaviour, such as smoking,42 and by triggering dysregulation of the neurohormonal systems responsible for cortisol and catecholamine secretion.43–45 Our results suggest that the effect of justice on inflammation is not attributable to smoking or alcohol consumption. In contrast, effect attenuations following adjustment for high BMI indicate that adiposity may be one of the underlying factors in the relationship between justice and health problems. This is plausible given that adipose tissue secretes cytokines.

In interpreting the present results, it is important to note some limitations. First, a drawback of this study is the lack of standard measures of organisational justice at the time of the baseline survey of the Whitehall II study. Using existing questions we were able to derive a five-item measure of organisational justice, especially its relational component. One of these items directly assessed the experience of unfairness. The items used in this study to measure organisational justice are comparable to those used in standard measures of organisational justice, such as the Moorman scale46 or the Colquitt scale.47 Both these scales include items measuring procedures such as getting information about decisions, hearing the concerns of all those affected by decisions, getting consistent and timely information, getting sufficient feedback, treating subordinates with kindness and consideration, and taking steps to deal with subordinates in a truthful manner. In addition, overall justice experience is requested in both scales. Our measure of justice does not allow us to capture more extreme sources of injustice (including coercion, intimidation, discrimination and denigration) that may also have effects on inflammation.

Second, a baseline measure for inflammation was lacking, with the time lag between justice perception and the first measure of the inflammatory markers being 2.5 years on average. However, we took into account the effects of the inflammatory markers at phase 3 when testing the association between organisational inflammatory markers 10 years later at phase 7. The robust association observed suggests long-term effects and that those exposed to low organisational justice at baseline continue to be exposed to low justice at follow-up.

Third, future studies need to analyse whether confounding or mediation is the more probable explanation for the attenuation of the association between organisational justice and CRP measured at the first follow-up (phase 3) after taking into account the effects of BMI. Diet and exercise may also have a role in the association between justice and inflammatory markers. Previous studies have offered some but not completely consistent support for the favourable effects of exercise and diet (rich in natural fibre or low fat Mediterranean) on circulating levels of CRP in middle-aged and elderly populations.21 22 48

Fourth, all the analyses were conducted using participants with complete data on the measured variables. This meant that more than half the original population was excluded and this is a potential source of selection bias. However, differences in baseline characteristics between the included and excluded civil servants were relatively small. Furthermore, these characteristics were adjusted for in the analyses and the associations were not substantially changed.

In conclusion, these findings suggest that in men organisational justice is associated with long-term inflammatory processes that are themselves potential mechanisms linking organisational justice to health.