In this urban, multiethnic, birth cohort, we found that self-identified black ethnicity was associated with a more than twofold increased likelihood of sensitization to foods, as well as sensitization to a greater number of foods, with controlling for both SES and early-life atopy-associated factors. African ancestry also was positively associated with the probability of sensitization to food and with a greater likelihood of being sensitized to multiple (≥3) foods. Lastly, although we did not corroborate recent findings in which peanut sensitization of ≥5 kUA/L was more common among black children (on the basis of self-reported race),4
we found that each 10% increment in African ancestry was associated with a 24% to 25% increase in the likelihood of having a peanut sIgE level beyond a cutoff point associated with increased likelihood of clinical reactivity.16
The results of our study are in keeping with recent findings that black children were at higher risk of both food allergy and peanut sensitization in 2 national cohorts.1,4
Although prospective studies with large, population-based, European cohorts have evaluated risk factors for food allergy,17,18
our study and the National Health and Nutrition Examination Survey study1
are the first multiethnic US studies. Furthermore, our study and the National Health and Nutrition Examination Survey were conducted with cohorts not selected according to high-risk status, which allows for better evaluation of the effects of race and ethnicity on food sensitization.
Study of the association of genetic ancestry with food sensitization is especially important for the US population. According to National Center for Health Statistics regulations,14
infant race is recorded as the mother's race. With more interracial people and marriages, traditional ethnic classifications will become increasingly imprecise, compared with genetic ancestry. Furthermore, as demonstrated in the recent US Census,8,19
there are increasing proportions of minority groups with admixed ancestral origins in the US population, particularly black20–22
groups. Self-identified race for these populations would underestimate the degree of genetic variation within these populations. Genetic factors influence the development of food allergy.25
As has been shown with susceptibility alleles for multiple other diseases,7
genetic factors that affect food sensitization may be distributed differently across ancestral groups. The association of ancestry with food sensitization is consistent with the findings of studies that found associations with other atopic diseases, such as asthma, and total IgE levels.26,27
The presence of ancestry associations across atopic diseases may represent population differences in genotypes associated with IgE production.28
In our sample, self-identified race was not associated with increased likelihood of peanut sensitization or peanut sIgE levels of ≥5 kUA/L. This may be attributable to several possible factors. Our sample was not selected on the basis of a history of milk or egg allergy, compared with the aforementioned study by Sicherer et al.4
It also is possible that, with an increase in sample size, particularly with more white subjects, our study might have greater power to detect an association with self-identified race and peanut allergy phenotypes.
It was interesting that African ancestry but not self-identified black race was associated with peanut sIgE levels. The opposite was seen for milk and egg. These different associations with ancestry are clearly seen in , in which milk does not display a pattern of association similar to seen for sensitization in general or sensitization to peanut or egg. One potential explanation for these discrepancies is that there may be ethnocultural factors, such as differences in diet and early-life feeding practices, that may have more relevance than genetic factors for milk sensitization. In contrast, genetic factors associated with ancestry may have more relevance for peanut sensitization, which was found to be greater among black children in 2 other studies.1,4
However, it is important to clarify that the associations with ancestry do not necessarily represent racially distributed genetic factors.29
It is possible that these associations are attributable to environmental factors that vary with ancestry and influence sensitization, such as early-life dietary patterns and vitamin D levels.30–34
Our study has several limitations. First, it is possible that some residual confounding from subtle socioeconomic factors or unmeasured early-life exposures remains. However, it would be harder to attribute the linear association of African ancestry with sensitization rates to this type of residual confounding. Second, our ancestry variable was derived from a panel of 150 AIMs and not genome-wide association study data. Panels of AIMs smaller than ours are sufficient to control for population stratification attributable to African ancestry,35
and accuracy similar to that of ancestry estimates from genome-wide association study data may be obtained with a dramatically smaller number of AIMs.36
Furthermore, ancestry has been used as a covariate across multiple self-identified ethnicities for multiethnic populations,37,38
and the results were shown to be highly correlated with the results of a principal component-based analysis.37
Third, this study involves a young cohort. It remains to be determined whether these disparities in food sensitization will persist as the children grow older and whether they will translate into disparities in clinical reactivity to food. However, the children had a mean age of 2.7 years. Before 1 year of age there can be some cyclical variations in sIgE levels.39
The mean age of the cohort makes these findings more likely to be representative of persistent sensitization.
The clinical relevance of sensitization at a level of ≥0.35 kUA/L to any of the foods tested needs to be considered. The association with being multiply sensitized was stronger for both self-identified race and African ancestry. Another group that found African ancestry generally increased total IgE levels.27
Although it is possible that African ancestry simply may increase sIgE levels beyond the level of detection for a number of foods, we also found associations with peanut sIgE levels of ≥5 kUA/L. This suggests that race and ancestry not only are associated with minimal increases in sIgE levels but also may be associated with clinical reactivity, in keeping with the findings of 2 other studies that evaluated race and food allergy.1,4
However, it should be noted that these cutoff points (which currently are used clinically regardless of patient ethnicity) were established with primarily white populations. Other populations might have different predictive values. In National Health Interview Survey data, black people had higher rates of detectable sIgE but did not report food allergy at higher rates.40
Although this discrepancy may represent differences in reporting, additional rigorous study of food allergy in minority populations is necessary.