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Children whose parents have lower income and education are at risk for obesity and later-life health risks. Explanations of enduring associations of early-life socioeconomic status (SES) with adult health have focused on stress and behavioral factors, but the biological mechanisms linking these are poorly understood. DNA methylation is the most studied epigenetic mechanism in epidemiologic studies, but social differences in methylation of particular genes are understudied, particularly at birth. We focus on a cluster of particularly well-studied genes, in which methylation is linked to gestational growth, increases childhood obesity risk, and predicts multiple health problems in adulthood. We measured methylation at differentially methylated regions (DMRs) regulating genomically-imprinted genes (IGF2, H19, DLK1, MEG3, PEG1/MEST, PEG3, PEG10/SGCE, NNAT, and PLAGL1) using umbilical cord blood from 619 infants in Durham, North Carolina in 2010-2011. We examined disparities in DMR methylation levels by race/ethnicity of both parents, and the role that maternal SES may play in explaining race/ethnic epigenetic differences. Unadjusted race/ethnic differences were evident only at the IGF2, H19, MEG3, and NNAT DMRs (e.g. a 0.83SD (p<0.001) difference in IGF2 methylation between Black and White fathers). An inverse pattern appeared by race/ethnicity of mothers vs. fathers for NNAT. With SES adjustment, race/ethnic differences persisted for the IGF2 and NNAT DMRs. Results suggest social factors may not only influence DNA methylation, but do so in ways that vary by DMR. These findings support the hypothesis that epigenetics is one path through which prenatal social conditions may influence health and health disparities across the lifecourse.