Social deprivation is a major factor in health inequality. In the UK residence in a socially deprived area is associated with an increase in mortality from coronary heart disease (CHD).¹ A positive association between the incidence of CHD and residence in a socially deprived neighbourhood has also been observed in the USA.²

Inflammation is important in the development of atherosclerosis, plaque rupture, and thrombosis leading to myocardial infarction. An increase in the plasma concentration of C reactive protein (CRP), within the reference range for the population but below the threshold that indicates clinically significant inflammation, is an independent risk factor for CHD.³ It is also a predictor for the development of diabetes mellitus⁴—a major cause of vascular disease. We have investigated the relation between the plasma CRP concentration and social deprivation in two large study populations.

METHODS AND RESULTS

CRP was measured by an enzyme linked immunoassay, with a lower limit of the working range of 0.1 mg/l, calibrated with the international reference standard (CRM 470-CAP/IFCC; lot 91/0619) and thus yielded results comparable with other major studies.³ CRP measurements were available for 5245 men aged 45–64 years on recruitment in 1989–91 to the WOSCOPS (West of Scotland coronary prevention study).⁴ The second population were men (n  =  941) and women (n  =  1160) aged 30–59 years studied in 1996 for the Midspan family study.⁵

The deprivation status of the subjects was assessed from the postcode of residence, obtained from the 1991 census data, according to Carstairs and Morris, which defines seven categories of deprivation, category 1 being the most affluent.¹ The deprivation score (DEPCAT) for an area of residence is calculated from the population census data on car ownership, overcrowded housing, occupations of the household heads, and percentage of men unemployed. In the UK a national census is undertaken every decade. The DEPCATs derived from the 1991 national census were used in this study as it was closest in time to the recruitment for both population studies. Full details of the methods used to derive the DEPCATs are available on line from the Medical Research Council’s Social and Public Health Sciences Unit at the University of Glasgow (www.msoc-mrc.gla.ac.uk/Publications/pub/Carstairs_MAIN.html), which has reported that the DEPCATs of Scottish postcode sectors based on the 2001 census data are strongly correlated (r  =  0.955) with those derived from the 1991 census.

The plasma concentration of CRP was log normally distributed in the population. Table 1 gives the geometric mean CRP concentration for the WOSCOPS population grouped by deprivation and smoking status. The mean CRP concentration in current smokers was about twice that of the corresponding never smokers and in the most deprived was about double that observed in the most affluent. The trend was present among the former smokers though they were heterogeneous with regard to the time since they stopped smoking. The Midspan population data show an increase in CRP among both men and women with increasing deprivation. In both populations univariate analysis showed a highly significant correlation between plasma CRP and deprivation (p < 0.0001).

Table 2 gives the CRP concentration in the WOSCOPS population grouped by deprivation, smoking, and body mass index (BMI). The data show a highly significant increase in CRP (p < 0.0001) with increasing deprivation.

Inflammatory disorders, cigarette smoking, obesity (assessed by BMI), age, sex, and use of drugs such as aspirin, angiotensin converting enzyme inhibitors, and statins influence CRP. Table 3 gives the results of regression modelling, which showed that taking all these factors into account for the WOSCOPS population maintained a highly significant relation (p < 0.0001) between deprivation and CRP with an increase in CRP of 5.4% (95% confidence interval 3.6 to 7.1) for each unit of deprivation. In the Midspan population the relation was observed for both sexes combined, with each unit of deprivation associated with an increase in CRP of 3.7% (95% confidence interval 0.5 to 7.0%, p  =  0.024). Positive associations were observed for women and men separately (table 3), and though the association did not reach significance for men, this may have been a consequence of reduced sample size, since there was no evidence that the effect of deprivation was different for men and women (interaction test for heterogeneity, p  =  0.62).

DISCUSSION

Social and economic deprivation, assessed by place of residence, is associated with an aggregation of features that results in an increase in low grade background systemic inflammation indicated by an increase in the plasma concentration of CRP that is not fully explained by smoking and BMI. Background inflammation may partially explain the increase in morbidity and mortality from CHD observed in the socially and economically deprived sections of the population.

In this cross sectional study of two populations it is not possible to identify with any degree of confidence what factors associated with deprivation caused the observed increase in background inflammation. One could speculate that it may be due to low grade subclinical infections caused by factors such as over crowding in poor quality damp housing with suboptimal personal and dental hygiene.