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Background: The prevalence of food allergy is thought to be increasing, but data from the United States have not been systematically synthesized., Objective: To summarize the data on prevalence of food allergy in the US pediatric population and to estimate the effects of time, race/ethnicity, and method of assessing food allergy on the estimated prevalence., Methods: Embase, MEDLINE, bibliographies of identified reports, and data from publically available data sets were searched. Studies were limited to those in English with data from the general pediatric US population. Study synthesis was performed by meta-analysis and meta-regression to estimate the effect of study- and participant-level covariates. Meta-regression was limited to nationally representative surveys conducted by the Centers for Disease Control and Prevention., Results: A total of 10,090 publications were identified, from which 27 different survey administrations, representing 452,237 children, were identified, covering the period of 1988 to 2011. Because of heterogeneity among surveys in the estimated food allergy prevalence, a summary estimate of food allergy prevalence was not possible. Meta-regression was performed using 20 of these surveys. Temporal trends were pronounced, with an estimated increased prevalence of self-reported food allergy of 1.2 percentage points per decade (95% confidence interval [CI], 0.7-1.6). The increase per decade varied by race/ethnicity: 2.1% among non-Hispanic blacks (95% CI, 1.5%-2.7%), 1.2% among Hispanics (95% CI, 0.7%-1.7%), and 1.0% among non-Hispanic whites (95% CI, 0.4%-1.6%)., Conclusion: Self-report of food allergy among US children has sharply increased in the past 2 decades. The increase has been greatest among non-Hispanic black children, a disparity that needs to be investigated., (Copyright © 2014 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Background: Peanut allergy affects 1% of children, and for those with persistent disease, few data have been published on trends in peanut-specific immunoglobulin E (P-IgE) levels or the value of P-IgE in predicting reaction severity., Objective: The primary outcome was the frequency of inadvertent peanut exposure. Secondary outcomes included clinical characteristics, trends in P-IgE, characteristics of accidental exposures, and predictors of reaction severity in patients with persistent peanut allergy., Methods: Records of patients with persistent peanut allergy were reviewed. Other allergic conditions, P-IgE levels, and peanut exposures were documented., Results: Seven hundred eighty-two patients were studied, 524 of them male. The median age at initial observation was 1.4 years; the median duration of follow-up was 5.3 years. Of the 782 patients, 93.1% were avoiding other foods, 70.8% had atopic dermatitis, 57.3% allergic rhinitis, and 55.8% asthma. The median initial P-IgE was 28.0 kU/L, and the median peak P-IgE was 68.1. Six hundred eighty-five exposures were seen among 455 patients: 75.9% ingestion, 13.6% contact, 4.5% airborne. 73.7% resulted in urticaria/angioedema, 22.2% lower respiratory symptoms, 21.2% gastrointestinal symptoms, and 7.7% oral erythema/pruritus. Treatment included antihistamines (33.4%), emergency department visits (16.5%), epinephrine (13.1%), corticosteroids (7.7%), albuterol (3.2%), no treatment (26.3%), and not recorded (29.6%). The rate of postdiagnosis ingestion was 4.7%/year; exposures with severe reactions, 1.6%/year; reactions treated with epinephrine, 1.1%/year. Reaction severity did not change with repeated exposure. Severe reactions were associated with higher P-IgE, but not with age, sex, or asthma., Conclusion: In this referral population, the rates of accidental peanut exposures and severe reactions were low. There was a strong association between higher P-IgE levels and reaction severity., (Copyright © 2012 American College of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Background: Compared with atopic asthma, fewer environmental modifications are recommended for non-atopic asthma in children., Objective: To better understand the role of indoor pollutants in provoking non-atopic asthma, we investigated the effect of in-home particulate matter on asthma symptoms among non-atopic and atopic children living in inner-city Baltimore., Methods: A cohort of 150 children ages 2 to 6 years with asthma underwent home environmental monitoring for 3-day intervals at baseline, 3, and 6 months. Children were classified as non-atopic if they were skin test negative to a panel of 14 aeroallergens. Caregivers completed questionnaires assessing symptoms and rescue medication use. Longitudinal data analysis included regression models with generalized estimating equations., Results: Children were primarily African American from lower socioeconomic backgrounds and spent most of their time in the home. Thirty-one percent were non-atopic, and 69% were atopic. Among non-atopic and atopic children, increased in-home fine (PM2.5) and coarse (PM2.5-10) particle concentrations were associated with significant increases in asthma symptoms and rescue medication use ranging from 7% (95% confidence interval [CI], 0-15) to 14% (95% CI, 1-27) per 10 μg/m(3) increase in particle concentration after adjustment for confounders., Conclusions: In-home particles similarly cause increased symptoms of asthma in non-atopic and atopic children. Environmental control strategies that reduce particle concentrations may prove to be an effective means of improving asthma outcomes, especially for non-atopic asthma, for which there are few environmental control practice recommendations., (Copyright © 2011. Published by Elsevier Inc.)