Relationships among prenatal aeroallergen exposure and maternal and cord blood IgE: Project ACCESS

Abstract

Background While some evidence suggests that antigen sensitization may begin prenatally, the influence of maternal allergen exposure during pregnancy has not been fully elucidated. Objectives We examined the relationship between prenatal maternal aeroallergen exposure and cord blood total immunoglobulin E (IgE) and the potential mediating/indirect effect of maternal immune response. Methods This study was performed in 301 mother-infant pairs enrolled in the Asthma Coalition on Community, Environment, and Social Stress (ACCESS) project, a study examining the effects of prenatal and early life social and physical environmental exposures on urban asthma risk. Dust samples collected prenatally from mothers’ bedrooms were analyzed for cockroach and dust mite allergens. Cord blood was analyzed for total IgE and maternal serum collected during pregnancy for total and specific IgE. We assessed the relationship between prenatal exposure and cord blood total IgE and the potential mediation effect adjusting for maternal age, race, education, smoking status and dust collection season; and child’s gender and season of birth. Results In multivariate models, elevated prenatal dust mite levels (> 0.2 µg/g) increased cord blood IgE concentrations by 29% (p=0.08) and continuous dust mite concentration was associated with a significant non-linear increase in cord blood IgE (p=0.02). Elevated prenatal exposure to cockroach allergen (> 2 U/g) was not associated with cord blood IgE, but showed a significant indirect relationship through maternal total IgE (β=0.23; 95% CI: 0.08, 0.41). Conclusions These results demonstrate that maternal prenatal exposure to household allergens may impact cord blood IgE albeit the underlying mechanism may be allergen-specific. Clinical Implications Maternal prenatal inhalant allergen exposure may precipitate infant immune response although the pathway of the effect may differ by allergen. Capsule Summary Prenatal exposure to dust mite was associated with increased cord blood total IgE whereas the relationship between prenatal cockroach exposure and total cord blood IgE was only observed through the indirect effect of maternal allergic response.

Lifetime prevalence of childhood eczema and the effect of indoor environmental factors: Analysis in Hispanic and non-Hispanic white children

“…Prenatal exposures may influence the programming and development of neonatal immune response. 26,27 Maternal smoking is a frequently cited early life exposure that has been shown to have an effect on the development of atopic disorders. 9,28,29 Tobacco smoke exacerbates the T-helper 2 response by increasing production of interleukin 4, interleukin 5, and other proinflammatory cytokines that result in increased allergic responses, whereas it reduces the T-helper 1 response by altering natural killer T-cell function and suppressing interferon-␥ production.…”

Prenatal Maternal Stress and Cord Blood Innate and Adaptive Cytokine Responses in an Inner-City Cohort

“…Prior studies have demonstrated evidence for the transfer of house dust mite through the placenta or in amniotic fluid (56) as well as a dose-related association between prenatal dust mite and cord blood immune response (IgE) (57,58). Data supporting maternal-fetal transfer of cockroach antigen or the role of cockroach in sensitization at birth are less clear (58). Alternatively, antigenic stimulation can cause low-level activation of recent thymic T-cell emigrants in a nonspecific fashion (59).…”

Intrauterine sensitization of allergen-specific IgE analyzed by a highly sensitive new allergen microarray

“…[1][2][3][4][5][19][20][21][22] However, there is conflicting evidence on whether allergen-specific IgE in CB is a reflection of fetal immunity or the result of transfer of maternal IgE to the fetus. The controversy is probably related, at least in part, to the low sensitivity of the methods used for the detection of allergen-specific IgE in CB, and precise allergen-specific IgE profiling patterns against food and inhalant allergens are not available at present.…”

“…[1][2][3][4][5] The latter conclusion is supported by the detection of allergen-specific IgE 6,7 and allergen-specific T-cell memory [8][9][10] in CB and suggests that primary sensitization can occur transplacentally in utero. However, the timing of allergen sensitization is still controversial, with conflicting evidence suggesting transplacental priming 6 versus postnatal priming.…”