Exploring racial differences in IgE-mediated food allergy in the WHEALS birth cohort.

BACKGROUND: Suspected food allergies are the cause of more than 200,000 visits to the emergency department annually. Racial differences in the prevalence of food allergy have also been reported, but the evidence is less conclusive. Researchers continue to struggle with the identification of food allergy for epidemiologic studies. OBJECTIVE: To explore racial differences in IgE-mediated food allergy (IgE-FA) in a birth cohort. METHODS: We used a panel of board-certified allergists to systematically identify IgE-FA to egg, milk, or peanut in a multiethnic birth cohort in which patient medical history, patient symptoms, and clinical data were available through 36 months of age. RESULTS: Of the 590 infants analyzed, 52.9% were male and 65.8% African American. Sensitization (serum specific IgE >0.35 IU/mL) to the food allergens was significantly higher for African American children compared with non-African American children as has been previously reported. No statistically significant racial/ethnic differences in IgE-FA were observed; however, a higher proportion of African American children were designated as having peanut allergy, and the percentage of African American children with an IgE level greater than 95% predictive decision points for peanut was 1.7% vs 0.5% for non-African American children. With the use of logistic regression, race/ethnicity was not significantly associated with IgE-FA (adjusted odds ratio, 1.12; 95% confidence interval, 0.58-2.17; P = .75) but was associated with sensitization to more than 1 of the food allergens (adjusted odds ratio, 1.80; 95% confidence interval, 1.22-2.65; P = .003). CONCLUSION: We did not observe an elevated risk of IgE-FA for African American children, although established differences in sensitization were observed. Racial/ethnic differences in sensitization must be taken into consideration when investigating disparities in asthma and allergy.

Transforming growth factor beta (TGFß1) in breast milk and indicators of infant atopy in a birth cohort.

BACKGROUND: The infant gut's ability to suppress immunologic reactions to food proteins could be influenced by levels of TGFß in breast milk. We hypothesized that lower levels of TGFß(1) in the breast milk (BM) of mothers in the WHEALS birth cohort are associated with atopy at infant age 2-3 yrs. METHODS: We used data collected during infancy in addition to the results of skin prick tests (SPT+) and measures of specific IgE >0.35 IU/ml (spIgE) to milk, egg, and peanut at infant age 2-3 years. Infants were classified as food allergic (FA) based on parental report of infant symptoms/diagnoses and information from clinical assessments. RESULTS: Data for 304 cohort members were analyzed. Among non-black infants, BM-TGFß(1) was lower for those classified as FA (vs. no FA) and those SPT+ (vs., SPT-), geometric mean = 1100 pg/ml vs. 1417pg/ml, p = 0.081; and 1100 pg/ml vs. 1415pg/ml, p = 0.064, respectively. Among infants of non-atopic mothers, BM-TGFß(1) was lower for those with elevated (vs. not elevated) sIgE, geometric mean = 1347 pg/ml vs. 1651 pg/ml, p = 0.047. Using logistic regression, adjusted odds ratios describing the association of BM-TGFß1 to the presence of atopic indicators in the infant were in the hypothesized direction only for non-black infants of non-atopic mothers: aORs for FA, sIgE and SPT+ were 0.08, 0.34, and 0.26 respectively; p = 0.091, 0.13, and 0.23. CONCLUSION: Immune benefit of BM-TGFß(1) could inform prevention strategies. Evidence of an association appears greatly influenced by infant race and maternal atopy. More research can determine if these relationships represent a modifiable risk factor for the development of food allergy in certain subgroups.

Relationship between childhood body mass index and young adult asthma.

BACKGROUND: The relationship between obesity and asthma is an area of debate. OBJECTIVE: To investigate the association of elevated body mass index (BMI) at a young age and young adult asthma. METHODS: BMI, questionnaires, and serologic tests results were analyzed in participants of a predominantly white, middle-class, population-based birth cohort from Detroit, Michigan at 6 to 8 and 18 years of age. Asthma diagnosis was based on medical record data. Allergen specific IgE was analyzed using UniCAP, with atopy defined as 1 or more allergen specific IgE levels of 0.35 kU/L or higher. Overweight was defined as a BMI in 85th percentile or higher. RESULTS: A total of 10.6% of overweight males at 6 to 8 years of age had current asthma at 18 to 20 years of age compared with 3.2% of males who were normal or underweight (relative risk [RR], 3.3; 95% confidence interval [CI], 1.0-11.0; P=.048). A total of 19.6% of females who were overweight at 6 to 8 years of age had asthma compared with 10.3% of females who were normal or underweight (RR, 1.9; 95% CI, 0.9-3.9; P=.09). After adjustment for atopy at 6 to 8 years of age, overweight males had an adjusted RR of 4.7 (95% CI, 1.4-16.2; P=.01), and overweight females had an adjusted RR of 1.7 (95% CI, 0.8-3.3; P=.15). Change in BMI between 6 to 8 years of age and 18 to 20 years of age was also examined. Patients with persistently elevated BMI exhibited increased risk of asthma as young adults (RR, 2.4; 95% CI, 1.2-4.7) but not with an increasing BMI (RR, 0.8; 95% CI, 0.3-2.2) or a decreasing BMI (RR, 0.8; 95% CI, 0.3-2.2). CONCLUSION: Overweight males 6 to 8 years of age have increased risk of asthma as young adults. Being overweight remains a predictor of asthma after adjustment for early atopy. A similar but not statistically significant trend was also seen among overweight females. Overweight body habitus throughout childhood is a risk factor for young adult asthma.

The association of maternal prenatal IgE and eczema in offspring is restricted to non-atopic mothers.

The risk of developing eczema is thought to be influenced by both genetic and environmental factors. Prenatal factors including the intrauterine environment may influence risk. We examined the relationship of maternal total IgE obtained during pregnancy to the incidence of atopic dermatitis in their 2-yr-old offspring. Subjects were participants in an unselected Detroit area birth cohort. Serum IgE was measured from 458 mothers in the third trimester of pregnancy along with prenatal family and environmental histories. Children were evaluated at approximately 2 yr of age for current or past eczema by maternal questionnaire and physician examination. Among the 458 children, 20.3% (n = 93) had a doctor confirmed diagnosis of eczema. Prenatal IgE was higher among women whose children developed AD vs. women whose children did not [Geometric means and 95% confidence intervals 52.7 IU/ml (40.9-68.0) vs. 32.9 IU/ml (28.0-38.7), p = 0.010]. The association was only seen in a subgroup of 181 women without allergic sensitization (specific IgE >0.35 IU/ml) to a panel of eight common allergens. Of the women without allergic sensitization, the mean serum IgE was 24.1 IU/ml (15.5-37.6) among those whose children had a diagnosis of eczema. The mean serum IgE was 11.2 IU/ml (9.2-13.6) among those whose children did not have a diagnosis of eczema (p-value 0.002). Maternal prenatal IgE level among women who are not sensitized to common allergens is associated with increased risk of eczema in offspring.