1 Department of Primary Care and Population Sciences, Royal Free and University College Medical School, London, NW3 2PF, UK
2 Department of Public Health Sciences, St. George's Hospital Medical School, London, SW17 0RE, UK
Correspondence: Mr Jonathan Emberson, Department of Primary Care and Population Sciences, Royal Free and University College Medical School, London NW3 2PF, UK. E-mail: j.emberson{at}pcps.ucl.ac.uk
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Abstract |
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Methods Prospective observational study of the relationship between occupational social class (assessed at baseline and after 20 years), major CHD (coronary death and non-fatal myocardial infarction) and all-cause mortality rates over 20 years among 5628 middle-aged British men with no previous evidence of CHD.
Results The age-adjusted hazard of major CHD for manual men relative to non-manual men was 1.41 (95% CI: 1.21, 1.64) before correction and 1.50 (95% CI: 1.25, 1.79) after correction for imprecision of social class measurement. The imprecision-corrected estimate was attenuated to 1.28 (95% CI: 1.06, 1.54) after adjustment for the adult coronary risk factors (blood cholesterol, blood pressure, body mass index, cigarette smoking, alcohol, physical activity, and lung function) and to 1.20 (95% CI: 0.99, 1.45) following further adjustment for height. The population attributable risk fraction of major CHD for social class (manual versus non-manual) was 22% after correction for imprecision in social class, which was reduced to 14% after adjustment for the adult coronary risk factors, and 10% after further adjustment for height. Similar results were obtained for all-cause mortality.
Conclusions Even taking account of measurement imprecision, the contribution of social class to overall CHD risk is modest. Population-wide strategies to reduce major CHD risk factors are likely to have greater potential benefits for CHD prevention than strategies designed specifically to reduce social inequalities in CHD.
Accepted 15 July 2003
Social inequalities in the incidence of coronary heart disease (CHD) in the UK are well documented,1,2 but while absolute CHD rates have fallen during the last 20 years,3,4 the fall has been concentrated among the highest social class groups so that the relative differences between those at the top and those at the bottom of the social scale have widened.5 In epidemiological studies that relate social conditions to subsequent disease risk, social class (as determined by job occupation) is often used as a convenient and available indicator of the underlying socioeconomic factors. However, despite considerable emphasis being placed in recent public health policies on reducing social class inequalities in CHD,5,6 several important aspects of social class differences remain unresolved.
First, even as an approximate index of socioeconomic status, adult social class is not always precisely estimated and may change over time. Though these factors will lead to underestimation of the true extent of social class differences in CHD, the extent of such underestimation has not been established.7 Furthermore, the relative contribution of adult and early life factors to social inequalities in CHD, as well as the likely value of identifying further factors influencing social inequalities, remains uncertain.
In this study, using a cohort of 5628 middle-aged British men with no previous evidence of CHD followed for 20 years between 1978 and 2000, we examine how wide social class differences in CHD are, before and after correction for imprecision in the measurement of social class. We estimate the amount that can be explained by the established coronary risk factors, and present estimates of population attributable risk for social class before and after adjustment for the established coronary risk factors. Parallel analyses for all-cause mortality are shown.
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Methods |
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Baseline risk factors
Height without shoes and weight in trousers and socks were measured, to the nearest millimetre and 0.1 kg respectively. Blood pressure was measured twice in succession in the right arm using the London School of Hygiene and Tropical Medicine sphygmomanometer, with the subject seated and the arm supported. Adjustment for observer variation within each town was performed10 and the mean of the two blood pressure measurements was used in analyses. Serum total cholesterol was measured by a modified Liebermann-Burchard method on a Technicon SMA 12/60 analyser,11 and body mass index (BMI) calculated as weight in kilograms divided by height in metres squared (kg/m2). Cigarette smoking status (current, ex, or never), alcohol intake (none, occasional, light, moderate, heavy) and level of leisure time physical activity (none, occasional, light, at least moderate) were ascertained through a questionnaire completed at the same time as the physical examination.12,13 Forced expiratory volume in one second (FEV1) was measured using a Vitalograph spirometer. Values were height standardized to 1.73 m, the average height of the men in the study.
Social class
At baseline, each man was asked about his longest held occupation in terms of type, designation, and status. The social class distribution observed in the study participants was almost exactly the same as that obtained from national census data recorded around the same time.14 After 20 years, all surviving men were invited for a re-screening where they were asked to record their current or most recent occupation and the duration of that occupation. Social class was determined using the Registrar General's six-category classification on both occasions and categorized as non-manual (I, II and IIINM) or manual (IIIM, IV and V).15 Men in the armed forces at baseline were excluded from this analysis.
Pre-existing coronary disease
At baseline, men were identified as having a possible history of CHD if: (1) they had ever been told by a doctor that they had angina or a heart attack; (2) their answers to the Rose angina questionnaire indicated that they had had definite or possible angina; (3) they had electrocardiographic evidence of definite or possible myocardial infarction or ischaemia; or (4) they had ever had a history of severe chest pain lasting half an hour or more that caused them to consult a doctor.
Major CHD events during follow-up
Subjects were followed up for mortality and cardiovascular morbidity, with 99.5% of subjects successfully traced over a 20-year follow-up period.9 Information on all deaths was collected through the established flagging procedures provided by the National Health Service registers in Southport (England and Wales) and Edinburgh (Scotland). Fatal CHD events were defined as deaths with ischaemic heart disease (International Classification of Diseases, Ninth Revision [ICD-9] 410414) as the underlying cause including sudden death of presumed cardiac origin. Evidence regarding non-fatal heart attacks was obtained by reports from general practitioners and by biennial reviews of the patients' notes, through to the end of the study period. Diagnosis was based on WHO criteria, (any report of myocardial infarction accompanied by at least two of: history of severe chest pain, electrocardiographic evidence of myocardial infarction, and cardiac enzyme changes associated with myocardial infarction). Major CHD was defined as non-fatal myocardial infarction or death from CHD.
Statistical methods
Time to major CHD events by social class status
For men with no baseline evidence of CHD, Kaplan Meier curves stratified by social class (manual versus non-manual) were used to display the differences in major CHD and all-cause mortality rates by social class over 20 years (Figure 1). The 20-year event rates were calculated per 1000 person years of exposure and directly standardized to the age distribution of the entire cohort. Relative hazards were estimated using Cox proportional hazards regression. The relative difference between social classes explained by the coronary risk factors was estimated by the equation (ß0ß1)/ß0, where ß0 is the age-adjusted log hazard ratio for social class, and ß1 the fully adjusted coefficient. Approximate 95% CI were calculated using bias-corrected bootstrap re-sampling of size 1000 to estimate the upper and lower limits.16
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Population attributable risk fraction (AR)
The population attributable risk fraction (AR) for manual social class is the proportion of all disease events in the population that can be attributed to the excess risks experienced by manual men over those of non-manual men, and is calculated through the equation p(RR 1)/(1 + p(RR 1)), where p is the proportion of manual men in the population and RR is the relative risk of major CHD for manual men relative to non-manual men (approximated in this paper by the relative hazard from the Cox regression20). The 95% CI for the AR were calculated by assuming that p was fixed and calculating the AR values corresponding to the lower and upper confidence limits of the RR. This method of estimation yielded virtually exactly the same estimates and CI as methods based on logistic regression prediction.
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Results |
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For total mortality, the age-adjusted hazard ratio for social class was 1.75 (95% CI: 1.52, 2.01) after correction for imprecision in social class. Taking into account the adult coronary risk factors (as before), this attenuated to 1.34 (95% CI: 1.16, 1.55), a 48% reduction in magnitude. Cigarette smoking explained the greatest amount of the social class divide (24%), whilst FEV1 explained 16%. The remaining coronary risk factors explained little or none of the difference in mortality rates between manual and non-manual men. Height made no additional contribution to explaining the differences in all-cause mortality.
Effects of imprecision and changes in established coronary risk factors
The multivariate effects that regression dilution of total cholesterol, systolic blood pressure, and BMI over 20 years may have on the estimated relative hazard for social class were assessed. The simultaneous influence on the hazard ratio was found to be negligible, due mainly to the fact that BMI was fairly insensitive to the effects of regression dilution and the effects for blood pressure and blood cholesterol were acting in opposite directions (since manual men had higher blood pressure but lower total cholesterol levels than non-manual men). Furthermore, taking changes in cigarette smoking, physical activity, and alcohol intake over the study period into account (by fitting time updated covariates in the Cox model) had virtually no effect on the adjusted social class effect.
Population attributable risk fraction (AR) estimates
For major CHD and total mortality, Table 4 shows the AR for social class (manual versus non-manual) before and after correction for imprecision in social class status and before and after adjustment for the adult coronary risk factors. For major CHD events, the age-adjusted AR for social class was 22% (95% CI: 13%, 31%) after correction for social class imprecision. Assuming manual men had the same average levels of total cholesterol, systolic blood pressure, BMI, physical activity, FEV1, alcohol intake, and smoking rates as non-manual men, the age- and imprecision-adjusted AR for social class would have been 14% (95% CI: 3%, 24%). Further adjustment for height at baseline reduced this estimate to 10% (95% CI: 2%, 21%). For all-cause mortality, the age-adjusted AR for social class was 30% (95% CI: 23%, 37%) after correction for social class imprecision, which decreased to 16% (95% CI: 8%, 23%) after adjustment for the adult coronary risk factors. Further adjustment for height had no additional effect. Including men with baseline evidence of CHD in analyses had little effect on the estimated AR for all-cause mortality.
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Discussion |
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Strengths and weaknesses of analyses |
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Estimating the social inequalities remaining after adjustment for baseline risk factors depends on the assumption that imprecision of assessment and changes in risk factors over time does not differ by social class. This would not be true for cigarette smoking, where differential rates of quitting exist.26 In our study 33% of non-manual smokers had given up by 5 years compared with 24% of manual smokers. The effect of this on the corrected relative hazard for social class after adjustment for the adult risk factors was small (decreasing it marginally). Similarly, other differential changes in risk factors would tend to lead to overestimation, rather than underestimation, of the real social class differences in CHD, as they are more likely to result in improvements in the risk profile of non-manual men over manual men.
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Explanations for the social gradient in CHD risk |
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Implications for CHD prevention |
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Although these conclusions only apply directly to the period 19802000 on which the data are based, they are still likely to be relevant to CHD prevention in the early 21st century. Current patterns of blood cholesterol and blood pressure (as measured in the Health Survey for England44) show less evidence of a social class gradient than was observed in the British Regional Heart Study at baseline in 19781980, so that the case for population-wide prevention by reducing total cholesterol and blood pressure levels remains compelling. However, to secure both effectiveness and equity in CHD prevention (and in the reduction of all-cause mortality), these population-wide measures would logically include measures to encourage smoking cessation among socially disadvantaged groups.
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Conclusions |
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KEY MESSAGES
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Acknowledgments |
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References |
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