Reviews and feature articleRelationships among prenatal aeroallergen exposure and maternal and cord blood IgE: Project ACCESS
Section snippets
Study participants
Cross-sectional analyses were conducted in the Asthma Coalition on Community, Environment, and Social Stress (ACCESS) project, an ongoing prospective cohort of mother-child pairs originally funded to recruit 500 pregnant women and their children to study the main effects of prenatal maternal and early life stress and other environmental risk factors on urban childhood asthma risk (described in detail elsewhere21). Briefly, English-speaking or Spanish-speaking pregnant women who were at least 18
Sample characteristics
Characteristics of the study participants are shown in Table I. The mean maternal age was 26.6 years. The population was predominately Hispanic (61.8%), and 36% of the mothers had a history of allergic disease with symptoms.
The percent of homes with dust mite allergen concentrations >0.20 μg/g was 67.6%, and with concentrations >2 μg/g, 38.1%. The percent of homes with cockroach allergen concentrations >2 U/g was 18.5%, and with concentrations >8 U/g, 8.33%.
Cord blood IgE was detected in 82.4%
Discussion
In this study, we examined the impact of prenatal maternal exposure to dust mite and cockroach allergens on cord blood IgE and the relationships among allergen exposure, maternal immune response, and cord blood IgE. We found that elevated dust mite in household dust measured during pregnancy significantly affected cord blood IgE levels. Conversely, we observed no association of cockroach allergen with cord blood IgE concentrations, but instead found a significant indirect relationship operating
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Prenatal and postnatal stress and asthma in children: Temporal- and sex-specific associations
2016, Journal of Allergy and Clinical ImmunologyCitation Excerpt :Populations of lower socioeconomic status exposed to higher stress might also be exposed to increased levels of household allergens.44 Settled dust collected within 2 weeks of enrollment from the mother's bedroom using a standardized protocol45 was assayed for cockroach allergen (Blatella germanica, Bla g 1 and 2) by using an mAb-based ELISA (Indoor Biotechnologies, Charlottesville, Va). Social resources that might influence stress experiences and asthma among residents can also vary by neighborhood characteristics or quality.41
Immune mechanisms and development of childhood asthma
2014, The Lancet Respiratory MedicineEnvironmental assessment and exposure control of dust mites: A practice parameter
2013, Annals of Allergy, Asthma and ImmunologyCitation Excerpt :There is preliminary evidence that sensitization to dust mites may begin prenatally depending on maternal allergen exposure during pregnancy. In the Asthma Coalition on Community, Environment, and Social Stress (ACCESS) project, prenatal dust mite exposure to higher than 0.2 μg/g was associated with a 29% increase in cord blood total IgE and a significant nonlinear increase in mite-specific IgE.84 An important and to date unanswered question is whether a dust mite–laden environment that undergoes interventions to decrease exposure would have the same salutary effect on sensitization as an environment that is intrinsically free of dust mite allergen.
The association of month of birth with atopy in adult patients with asthma and rhinitis in Anatolia, Turkey
2012, Allergologia et ImmunopathologiaCitation Excerpt :High levels of allergen exposure also may lead not only to the development of respiratory disease but account for the severity of respiratory disease.13,14 The age of exposure was also investigated for its effect on the sensitisation and it was found that even in utero exposure affects the sensitisation.15 The dose and effect relationship seems to be more prominent when exposure occurs during early years of childhood.16
Intrauterine sensitization of allergen-specific IgE analyzed by a highly sensitive new allergen microarray
2012, Journal of Allergy and Clinical Immunology
Supported by the National Institutes of Health R01ES010932, U01HL072494, R01HL080674, A1-20565, R01A135786, T32MH073122.
Disclosure of potential conflict of interest: J. L. Peters has received research support from the National Institutes of Health and the Robert Wood Johnson Foundation. T. A. E. Platts-Mills serves on the scientific advisory board for Indoor Biotechnologies and has received research support from Indoor Biotechnologies, ImClone, and Phadia. D. R. Gold has received research support from the National Institutes of Health and the Environmental Protection Agency, and is a delegate to American Lung Association for the American Thoracic Society. R. J. Wright has received research support from the National Institutes of Health. The rest of the authors have declared that they have no conflict of interest.