4.6 Article

Early-life and adult socioeconomic status and inflammatory risk markers in adulthood

期刊

EUROPEAN JOURNAL OF EPIDEMIOLOGY
卷 22, 期 1, 页码 55-66

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SPRINGER
DOI: 10.1007/s10654-006-9082-1

关键词

childhood; CRP; inflammation; life-course; SES; socioeconomic status

资金

  1. NHLBI NIH HHS [N01 HC 55016, N01 HC 55018, N01 HC 55019, N01 HC 55020, N01 HC 55015, N01 HC 55022, N01 HC 55021] Funding Source: Medline

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Background: Associations between childhood and adult socioeconomic status (SES) and adult levels of inflammatory markers (C-reactive protein [CRP], fibrinogen, white blood cell count [WBC], and von Willebrand factor [vWF]) were examined in the Atherosclerosis Risk in Communities (ARIC) Study cohort. Methods: A total of 12,681 white and African-American participants provided information on SES (via education and social class) and place of residence in childhood and adulthood. Residences were linked to census data for neighborhood SES information. Multiple imputation was used to impute missing data. Hierarchical and linear regression were used to estimate the effects of SES and possible mediation by adult cardiovascular disease (CVD) risk factors. Findings: Low childhood social class and education were associated with elevated levels of CRP, fibrinogen, WBC, and vWF (increments of 17%, 2%, 4% and 3% for lowest versus highest education in childhood, respectively) among whites. Findings were less consistent among African-Americans. Adult SES was more strongly associated with inflammation than childhood SES. Individual-level SES measures were more consistently associated with inflammation than neighborhood-level measures. Fibrinogen and WBC showed the most consistent associations with SES; the largest changes in inflammation by SES were observed for CRP. Covariate adjustment strongly attenuated these associations. Mediation of the SES-inflammation associations by BMI, smoking and HDL cholesterol (HDL-C) are suggested by these data. Conclusion: Low individual- and neighborhood-level SES in childhood and adulthood are associated with modest increments in adult inflammatory burden. These associations may operate through the influence of low SES on traditional CVD risk factors, especially BMI, smoking and HDL-C.

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