RATIONALE: There are well known racial disparities in atopic diseases such as asthma. We sought to determine whether there are also early life disparities in atopic outcomes. In particular, we sought to determine whether cord blood IgE (cbIgE) differs by race independent of socio-economic (SES) factors. METHODS: We evaluated the cbIgE levels (Phadia) in infants in a prospective, multi-ethnic Boston birth cohort. Socio-demographic information including race and annual household income (≥ or <30K) was obtained via standardized interview. Cord blood was log transformed to normalize the data for linear regression. The limit of detection of IgE in the assay was 0.1 kUA/L. Linear (log IgE) and logistic regression models (for detectable IgE) assessed the association of cbIgE with race/ethnicity, controlling for SES, and maternal (including age, atopy, education and smoking) and infant (gender and firstborn status) variables. RESULTS: The median (IQR) for cbIgE (n = 1179 infants) was 0.25 kUA/L (0-0.75kUA/L). cbIgE was detectable in 70%, 55%, 67%, and 72% of blacks, whites, Latinos, and Asian/other subjects respectively. Compared to whites, logIgE was higher in blacks (β, SE = 0.94±0.36, p = 0.009), Latinos (β, SE = 0.88±0.40, p = 0.03), and Asian/others (β, SE = 0.91±0.42, p = 0.03). When adjusted for SES, the magnitude and significance of these estimates did not change. Compared to whites, the odds of detectable cbIgE was greater in blacks (OR, SE = 2.1±0.53, p = 0.005) and Asian/others (OR, SE = 2.2±0.65, p = 0.01). Again, adjusted for SES, these estimates showed minimal change. CONCLUSIONS: Race/ethnicity has effects on cbIgE independent of SES and other prenatal factors. This finding suggests that there may be genetic or unmeasured environmental factors modifying in-utero IgE production which are differentially distributed by race/ethnicity.