Aeroallergen Sensitization in Healthy Children: Racial and Socioeconomic Correlates

Stevenson, Michelle D.; Sellins, S.L.; Grube, Emilie; Schroer, Kathy T.; Gupta, Jayanta; Wang, Ning; Hershey, Gurjit K. Khurana

doi:10.1016/j.jpeds.2007.03.001

Cited by 35 publications

(28 citation statements)

References 21 publications

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“…Studies in older children suggest that African American subjects are at greater risk for allergen sensitization, and genetic studies have suggested racial differences in genes associated with asthma. 29-31 Because we did not find that PC 30 or eNO values were related to race and differences in baseline airway function and airway reactivity in the group sensitized to egg or milk persisted after adjusting for race, we believe that the observed differences were primarily related to sensitization to egg or milk.…”

Section: Discussionmentioning

confidence: 83%

Expired nitric oxide and airway reactivity in infants at risk for asthma

Tepper

Llapur

Jones

et al. 2008

Journal of Allergy and Clinical Immunology

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Background Family histories of atopy, as well as histories of atopic dermatitis and food allergy, are important risk factors for an infant to have asthma. Although atopic sensitization appears to contribute to the development of asthma, it is unclear when the airways become involved with the atopic process and whether airway function relates to the atopic characteristics of the infant. Objective We sought to evaluate whether atopic infants without prior episodes of wheezing have increased expired nitric oxide (eNO) levels and heightened airway reactivity. Methods Infants with eczema were recruited, and atopic status was defined by specific IgE levels to foods or aeroallergens and total IgE levels. eNO, forced expiratory flow at 75% exhaled volume (FEF75), and airway reactivity to inhaled methacholine were measured in sedated infants. Airway reactivity was quantified by using the provocative concentration to decrease FEF75 by 30%. Results Median age for the 114 infants evaluated was 10.7 months (range, 2.6–19.1 months). Infants sensitized to egg or milk compared with infants sensitized to neither egg nor milk had lower flows (FEF75: 336 vs 285 mL/s, P < .003) and lower lnPC30 (mg/mL) provocative concentrations to decrease FEF75 by 30% (−0.6 vs −1.2, P < .02) but no difference in eNO levels. Infants with total serum IgE levels of greater than 20 IU/mL had higher eNO levels compared with infants with IgE levels of 20 IU/mL or less (14.6 vs 11.2 ppb, P < .023) but no difference in forced flows or airway reactivity. Conclusions Our findings suggest that atopic characteristics of the infant might be important determinants of the airway physiology of forced expiratory flows, airway reactivity, and eNO.

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Section: Discussionmentioning

confidence: 83%

Expired nitric oxide and airway reactivity in infants at risk for asthma

Tepper

Llapur

Jones

et al. 2008

Journal of Allergy and Clinical Immunology

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“…This could be one of the reasons why people of African ancestry in western countries have higher prevalence and greater severity of allergic symptoms than natives of these host countries, indicating that African ancestry might be a risk factor for allergic disease. 219–221 Indeed, several candidate genes that encode for Th2-related molecules, such as IL-4 and IL-13 , show a higher frequency in people with African ancestry of alleles that have a strong Th2- promoting activity, 219 suggesting that these alleles, which have been conserved to combat parasitic infections in Africa are leading to increased prevalence of atopic disorders in African origin people settled in western countries.…”

Section: Patterns Of Ancestry Differentiation and Selection At Loci Amentioning

confidence: 99%

Resolving the etiology of atopic disorders by using genetic analysis of racial ancestry

Gupta

Johansson

Bernstein

et al. 2016

Journal of Allergy and Clinical Immunology

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Atopic dermatitis (AD), food allergy (FA), allergic rhinitis (AR) and asthma are common atopic disorders of complex etiology. The frequently observed “atopic march” from early AD to asthma and/or AR later in life as well as the extensive comorbidity of atopic disorders, suggests common causal mechanisms in addition to distinct ones. Indeed, both disease-specific and shared genomic regions exist for atopic disorders. Their prevalence also varies among races; for example, AD and asthma have a higher prevalence in African-Americans when compared to European-Americans. Whether this disparity stems from true genetic or race-specific environmental risk factors or both is unknown. Thus far, the majority of the genetic studies on atopic diseases have utilized populations of European ancestry, limiting their generalizability. Large cohort initiatives and new analytic methods such as admixture mapping are currently being employed to address this knowledge gap. Here we discuss the unique and shared genetic risk factors for atopic disorders in the context of ancestry variations, and the promise of high-throughput “-omics” based systems biology approach in providing greater insight to deconstruct into their genetic and non-genetic etiologies. Future research will also focus on deep phenotyping and genotyping of diverse racial ancestry, gene-environment, and gene-gene interactions.

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“…[17] (Table 2) The study population was 48% Caucasian and 46% African-American. Forty-eight percent of the African-American children and 30% of the Caucasian children had at least one positive skin prick test.…”

Section: What We Knowmentioning

confidence: 99%

Racial Differences in Allergic Sensitization: Recent Findings and Future Directions

Wegienka

Johnson

Zoratti

et al. 2013

Curr Allergy Asthma Rep

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Racial disparities are present in many facets of health and disease. Allergy and asthma are no exceptions. Secondary results from cross-sectional and cohort studies have provided information on the scope of racial disparities in allergic sensitization in the United States. African American/Black individuals tend to be sensitized more frequently than White individuals. Little is known about rates in other race groups. Genetics are unlikely to be the sole or major cause of the observed differences. Home dust allergen and endotoxin levels cannot explain the differences. Studies that have been designed to specifically address the sources of these racial disparities are needed. A “Multilevel Framework” that considers the roles of the individual, family and community presents an excellent approach to guide design of future studies of the causes of these disparities. Understanding the causes of the disparities could lead to interventions that would improve the health of all individuals.

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Aeroallergen Sensitization in Healthy Children: Racial and Socioeconomic Correlates

Cited by 35 publications

References 21 publications

Expired nitric oxide and airway reactivity in infants at risk for asthma

Expired nitric oxide and airway reactivity in infants at risk for asthma

Resolving the etiology of atopic disorders by using genetic analysis of racial ancestry

Racial Differences in Allergic Sensitization: Recent Findings and Future Directions

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