PERINATAL EPIDEMIOLOGY Early-life and adult socioeconomic status and inﬂammatory risk markers in adulthood Ricardo A. Pollitt 1 , Jay S. Kaufman 2 , Kathryn M. Rose 1 , Ana V. Diez-Roux 3 , Donglin Zeng 4 & Gerardo Heiss 1 1 Department of Epidemiology, School of Public Health, The University of North Carolina at Chapel Hill, 137 E. Franklin S Suite 306, Bank of America Center, Chapel Hill, NC, 27514, USA; 2 Department of Epidemiology, School of Public Health, The University of North Carolina at Chapel Hill, CB#7435, 2104C McGravran-Greenberg Bldg, Chapel Hill, NC, 27599-7 USA; 3 The University of Michigan at Ann Arbor School of Public Heath, Ann Arbor, MI, USA; 4 Department of Biostatistics, School of Public Health, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA Accepted in revised form 7 November 2006 Abstract. Background: Associationsbetween child- hood and adult socioeconomic status (SES) and adult levelsof 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 Afri- can-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 estimatetheeﬀectsof SES and possible mediation by adult cardiovascular disease (CVD) risk factors.Findings:Low childhood socialclassand education wereassociated with elevated levels of CRP, ﬁbrinogen,WBC, and vWF (incrementsof 17%, 2%, 4% and 3% for lowestversushighest education in childhood, respectively) among whites. Findings were less consistent among African-Ameri- cans.Adult SES was more strongly associated with inﬂammation than childhood SES. Individual-level SES measures were more consistently associated with inﬂammationthan neighborhood-level measures. Fibrinogen and WBC showed the most consistent associations with SES; the largest changes in inﬂam- mation by SES were observed for CRP. Covariate adjustmentstrongly 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 tradi- tional CVD risk factors, especially BMI,smoking and HDL-C. Key words:Childhood, CRP, Inﬂammation, Life-course, SES, Socioeconomic status Introduction Low individualand contextual (neighborhood-level) socioeconomicstatus(SES) has been repeatedly associated with worse cardiovascular disease (CVD) risk factor proﬁles, health behaviors and CVD out- comes [1–5]. Inquiries into the possible mechanisms that underlie such associations have recently reported that elevated levelsof inﬂammatory markers are associated with lower levels of adult SES, suggesting that inﬂammation may be one of the mediators of social diﬀerences in cardiovascular risk [6–9]. In recent years, studies have more closely examined the inﬂuence of socioeconomic conditions in early life on the development of CVD [10–17]. Interest in early- life SES research was stimulated by the development of the fetaloriginsof adult disease hypothesis by David Barker [18]. Later theories and studies expanded the scope of inquiry beyond the neonatal period to include the putativeeﬀectsof adverse socioeconomic conditions and events during sensitive early-life periods on adult chronic diseaserisk, operating through various physiologicaland/or psychosocialmechanisms[19–21].Thisliterature providessupportfor an association between low early-life SES and elevated CVD risk, likely mediated by adult behavioralor biologic CVD risk factors [22, 23]. One potential link between low early-life SES and CVD risk is a sustained,elevated systemic inﬂam- matory burden. Laboratory and epidemiologic evi- dence indicate that a chronic and systemic inﬂammatory up-regulation plays a centralrole in atherosclerosis and its sequelae [24–26]. Associations between inﬂammatory markers such as ﬁbrinogen and white blood cell (WBC) countand CVD have European Journal of Epidemiology (2007) 22:55–66 Springer 2007 DOI 10.1007/s10654-006-9082-1