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Race, ancestry, and development of food-allergen sensitization in early childhood.

ABSTRACT: We examined whether the risk of food-allergen sensitization varied according to self-identified race or genetic ancestry.We studied 1104 children (mean age: 2.7 years) from an urban multiethnic birth cohort. Food sensitization was defined as specific immunoglobulin E (sIgE) levels of ? 0.35 kilo-units of allergen (kUA)/L for any of 8 common food allergens. Multivariate logistic regression analyses were used to evaluate the associations of self-identified race and genetic ancestry with food sensitization. Analyses also examined associations with numbers of food sensitizations (0, 1 or 2, and ? 3 foods) and with logarithmically transformed allergen sIgE levels.In this predominantly minority cohort (60.9% black and 22.5% Hispanic), 35.5% of subjects exhibited food sensitizations. In multivariate models, both self-reported black race (odds ratio [OR]: 2.34 [95% confidence interval [CI]: 1.24-4.44]) and African ancestry (in 10% increments; OR: 1.07 [95% CI: 1.02-1.14]) were associated with food sensitization. Self-reported black race (OR: 3.76 [95% CI: 1.09-12.97]) and African ancestry (OR: 1.19 [95% CI: 1.07-1.32]) were associated with a high number (? 3) of food sensitizations. African ancestry was associated with increased odds of peanut sIgE levels of ? 5 kUA/L (OR: 1.25 [95% CI: 1.01-1.52]). Similar ancestry associations were seen for egg sIgE levels of ? 2 kUA/L (OR: 1.13 [95% CI: 1.01-1.27]) and milk sIgE levels of ? 5 kUA/L (OR: 1.24 [95% CI: 0.94-1.63]), although findings were not significant for milk.Black children were more likely to be sensitized to food allergens and were sensitized to more foods. African ancestry was associated with peanut sensitization.

SUBMITTER: Kumar R

PROVIDER: S-EPMC3182844 | biostudies-other | 2011 Oct

REPOSITORIES: biostudies-other

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Race, ancestry, and development of food-allergen sensitization in early childhood.

Kumar Rajesh R Tsai Hui-Ju HJ Hong Xiumei X Liu Xin X Wang Guoying G Pearson Colleen C Ortiz Katherin K Fu Melanie M Pongracic Jacqueline A JA Bauchner Howard H Wang Xiaobin X

Pediatrics 20110902 4

<h4>Objective</h4>We examined whether the risk of food-allergen sensitization varied according to self-identified race or genetic ancestry.<h4>Methods</h4>We studied 1104 children (mean age: 2.7 years) from an urban multiethnic birth cohort. Food sensitization was defined as specific immunoglobulin E (sIgE) levels of ≥ 0.35 kilo-units of allergen (kUA)/L for any of 8 common food allergens. Multivariate logistic regression analyses were used to evaluate the associations of self-identified race an ...[more]

PMID: 21890831

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Project description:BackgroundThe effect of breast-feeding on the development of allergic disease is uncertain. There are no data that show whether this relationship varies by individual genotypes.ObjectiveWe sought to evaluate the effect of breast-feeding and gene-breast-feeding interactions on food sensitization (FS) in a prospective US birth cohort.MethodsThis study included 970 children who were prospectively followed since birth. Breast-feeding history was obtained from a standardized questionnaire interview. FS was defined as a specific IgE level of 0.35 kU(A)/L or greater to any of 8 common food allergens. Eighty-eight potentially functional single nucleotide polymorphisms (SNPs) were genotyped from 18 genes involved in innate immunity or T(H)1/T(H)2 balance. Logistic regression models were used to test the effects of breast-feeding and gene-breast-feeding interactions on FS, with adjustment for pertinent covariates.ResultsChildren who were ever breast-fed (n = 739), including exclusively breast-fed children, were at a 1.5 (95% CI, 1.1-2.1; P = .019) times higher risk of FS than never breast-fed children (n = 231). This association was significantly modified by rs425648 in the IL-12 receptor ?1 gene (IL12RB1; P for interaction = .0007): breast-feeding increased the risk of FS (odds ratio, 2.0; 95% CI, 1.4-3.1; P = .0005) in children carrying the GG genotype but decreased the risk (odds ratio, 0.6; 95% CI, 0.3-1.4; P = .252) in children carrying the GT/TT genotype. Similar interactions were observed for SNPs in the Toll-like receptor 9 (TLR9; rs352140) and thymic stromal lymphopoietin (TSLP; rs3806933) genes. The interaction between the combined genotypes of the 3 SNPs and breast-feeding on FS was even stronger (P for interaction < 10??).ConclusionOur data suggest that the effect of breast-feeding on FS was modified by SNPs in the IL12RB1, TLR9, and TSLP genes both individually and jointly. Our findings underscore the importance of considering individual genetic variations in assessing this relationship.

Project description:BackgroundHousehold endotoxin levels have been variably associated with risk for asthma and atopy.MethodsWe studied participants from the 2005-2006 National Health and Nutrition Examination Survey (NHANES, n = 6963), a large cohort representative of the US population (aged 1-84 years). We built logistic regression models to test for associations between house dust endotoxin and sensitization to specific foods (milk, egg, and peanut). To experimentally explore the detected epidemiologic associations, peripheral blood mononuclear cells (PBMCs) were collected from 21 children (aged 1-19 years) mono-food allergic (ie, sensitized and clinically reactive) to milk, egg, or peanut and nonallergic controls for stimulation with endotoxin and secreted cytokine measurement. For each food allergy, linear mixed-effects models were built to test the association between endotoxin stimulation and cytokine level.ResultsAmong NHANES subjects, the geometric mean household endotoxin level was 15.5 EU/mg (GSE 0.5). Prevalence of food allergen sensitization (sIgE ≥ 0.35 kUA /L) varied by food: milk 5.7%, egg 4.0%, and peanut 7.9%. In models adjusted for potential confounders (age, race, country of birth, total people per household, US region, and history of wheezing in the past year), household endotoxin level was associated with sensitization to milk (OR 1.7, 95% CI 1.2-2.1) and egg (OR 1.4, 95% CI 1.01-1.9), but not peanut (OR 0.98, 95% CI 0.8-1.2). Interferon-γ levels of endotoxin-stimulated PBMCs from children allergic to milk or egg, but not peanut, were significantly lower compared to controls in linear mixed-effects models adjusted for repeated measures, experimental variables, age, and inter-individual variability (P-values .007, .018, and .058, respectively).ConclusionHigher household endotoxin is associated with increased odds of milk and egg sensitization. Altered cytokine responsiveness to endotoxin is also observed in PBMCs from individuals with milk and egg allergy.

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Race, ancestry, and development of food-allergen sensitization in early childhood.

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Race, ancestry, and development of food-allergen sensitization in early childhood.

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