Background: Peanut allergy affects 0.6% of the US population. At the present time, allergen avoidance is the only therapeutic option. Animal models of food-induced anaphylaxis would facilitate attempts to design novel immunotherapeutic strategies for the treatment of peanut allergy. Objective: The purpose of this study was to develop a murine model of IgE-mediated peanut hypersensitivity that closely mimics human peanut allergy. Methods: C3H/HeJ mice sensitized orally with freshly ground whole peanut and cholera toxin as adjuvant were challenged orally 3 and 5 weeks later with crude peanut extract. Anaphylactic reactions were determined. T-and B-cell responses to Ara h 1 and Ara h 2, the major peanut allergens, were characterized by evaluating splenocyte proliferative responses and IgE antibody concentrations. Furthermore, IgE antibodies in the sera of patients with peanut allergy and mice were compared for antibody binding to Ara h 2 isoforms and allergenic epitopes. Results: Peanut-specific IgE was induced by oral peanut sensitization, and hypersensitivity reactions were provoked by feeding peanut to sensitized mice. The symptoms were similar to those seen in human subjects. Ara h 1-and Ara h 2-specific antibodies were present in the sera of mice with peanut allergy. Furthermore, these Ara h 2-specific IgE antibodies bound the same Ara h 2 isoforms and major allergenic epitopes as antibodies in the sera of human subjects with peanut allergy.

Rationale: Air pollution is a known asthma trigger and has been associated with short-term asthma symptoms, airway inflammation, decreased lung function, and reduced response to asthma rescue medications. Objectives: To assess a causal relationship between air pollution and childhood asthma using data that address temporality by estimating air pollution exposures before the development of asthma and to establish the generalizability of the association by studying diverse racial/ethnic populations in different geographic regions. Methods: This study included Latino (n ¼ 3,343) and African American (n ¼ 977) participants with and without asthma from five urban regions in the mainland United States and Puerto Rico. Residential history and data from local ambient air monitoring stations were used to estimate average annual exposure to five air pollutants: ozone, nitrogen dioxide (NO 2 ), sulfur dioxide, particulate matter not greater than 10 mm in diameter, and particulate matter not greater than 2.5 mm in diameter. Within each region, we performed logistic regression to determine the relationship between early-life exposure to air pollutants and subsequent asthma diagnosis. Arandom-effectsmodelwasusedtocombinetheregionspecific effects and generate summary odds ratios for each pollutant. Measurements and Main Results: After adjustment for confounders, a 5-ppb increase in average NO 2 during the first year of life was associated with an odds ratio of 1.17 for physician-diagnosed asthma (95% confidence interval, 1.04-1.31). Conclusions: Early-life NO 2 exposure is associated with childhood asthma in Latinos and African Americans. These results add to a growing body of evidence that traffic-related pollutants may be causally related to childhood asthma.

Introduction Pediatric asthma is a serious public health problem around the world. The World Health Organization estimated that approximately 300 million people currently have asthma worldwide, and with current trends rising, it is expected to reach 400 million by 2025 [1]. Nearly 250,000 people die prematurely each year from asthma, and most of all these deaths are preventable. Globally, death rates from asthma in children range from 0 to 0.7 per 100,000 people [2]. Among children, asthma is the most common chronic disease, ranking among the top 20 conditions worldwide for disability-adjusted life years in children [3]. Increasing Prevalence The most accurate information regarding the prevalence of asthma in children around the world is available from the International Study of Asthma and Allergies in Childhood (ISAAC). Phase I of this study was completed in 1994-1995 and involved over 700,000 schoolchildren aged 6-7 and 13-14 years from 56 countries. The study revealed marked geographic variations in the prevalence of asthma. Countries with low prevalence of asthma (2-4%) were mostly in Asia, Northern Africa, Eastern Europe, and Eastern Mediterranean regions, whereas countries with high prevalence (29-32%) were located in South East Asia, North America and Latin America [4, 5] Phase III of ISAAC was conducted during 2000-2003 and involved over 1,100,000 school children from 98 countries [5-7].

Background Childhood asthma prevalence and morbidity varies among Latinos in the United States, with Puerto Ricans having the highest and Mexicans the lowest. Objective To determine whether genetic ancestry is associated with the odds of asthma among Latinos, and secondarily whether genetic ancestry is associated with lung function among Latino children. Methods We analyzed 5,493 Latinos with and without asthma from three independent studies. For each participant we estimated the proportion of African, European, and Native American ancestry using genome-wide data. We tested whether genetic ancestry was associated with the presence of asthma and lung function among subjects with and without asthma. Odds ratios (OR) and effect sizes were assessed for every 20% increase in each ancestry. Results Native American ancestry was associated with lower odds of asthma (OR=0.72, 95% confidence interval [CI]: 0.66–0.78, p=8.0×10−15), while African ancestry was associated with higher odds of asthma (OR=1.40, 95%CI: 1.14–1.72, p=0.001). These associations were robust to adjustment for covariates related to early life exposures, air pollution and socioeconomic status. Among children with asthma, African ancestry was associated with lower lung function, including both pre- and post-bronchodilator measures of forced expiratory volume in the first second (−77±19 ml, p=5.8×10−5 and −83±19 ml, p=1.1×10−5, respectively) and forced vital capacity (−100±21 ml, p=2.7×10−6 and −107±22 ml, p=1.0×10−6, respectively). Conclusion Differences in the proportions of genetic ancestry can partially explain disparities in asthma susceptibility and lung function among Latinos.

Rationale: Obesity is associated with increased asthma morbidity, lower drug responsiveness to inhaled corticosteroids, and worse asthma control. However, most prior investigations on obesity and asthma control have not focused on pediatric populations, considered environmental exposures, or included minority children. Objectives: To examine the association between body mass index categories and asthma control among boys and girls; and whether these associations are modified by age and race/ethnicity. Methods: Children and adolescents ages 8-19 years (n ¼ 2,174) with asthma were recruited from the Genes-environments and Admixture in Latino Americans (GALA II) Study and the Study of African Americans, Asthma, Genes, and Environments (SAGE II). Ordinal logistic regression was used to estimate odds ratios (OR) and their confidence intervals (95% CI) for worse asthma control. Measurements and Main Results: In adjusted analyses, boys who were obese had a 33% greater chance of having worse asthma control than their normal-weight counterparts (OR, 1.33; 95% CI, 1.04-1.71). However, for girls this association varied with race and ethnicity (P interaction ¼ 0.008). When compared with their normal-weight counterparts, obese African American girls (OR, 0.65; 95% CI, 0.41-1.05) were more likely to have better controlled asthma, whereas Mexican American girls had a 1.91 (95% CI, 1.12-3.28) greater odds of worse asthma control. Conclusions: Worse asthma control is uniformly associated with increased body mass index in boys. Among girls, the direction of this association varied with race/ethnicity. Keywords: obesity; asthma control; race and ethnicity; age; sex Obesity and asthma are among the most challenging health conditions affecting children and adolescents in the United States. Among this segment of the population, obesity (1) and asthma (2) prevalence vary by sex. For example, obesity is more common among boys (18.6%) than among girls (15%) aged 2-19 years old (1). This is also true for asthma with boys (10.5%) being more likely to have asthma than girls (8.2%) (2). Given these sex differences, obesity and asthma should be examined among boys and girls separately.Further variations on obesity and asthma are observed across age and race/ethnicity (1, 2). It is estimated that 32.6% of US children ages 6-11 years and 33.6% of adolescents ages 12-19 are overweight or obese (1). The prevalence of obesity is significantly higher among Mexican (23.9%) and African American (23.7%) children compared with non-Hispanic whites (16.1%) (1). Moreover, there are sex-specific differences in Obesity and asthma are common health conditions among US children. Obesity is associated with asthma control, although the mechanism is not well-understood. What This Study Adds to the FieldWorse asthma control is uniformly associated with increased body mass index in boys. Boys who were obese had increased odds of having worse asthma control than their normal-weight counterparts after adjusting for selected characteristics. For girls, this associat...