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Prenatal exposure to environmental contaminants and newborn immune system biomarkers

Date

2014-12-12

Authors

Ashley-Martin, Jillian

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Abstract

Allergic disease are among the most common chronic childhood disease and a leading cause of hospitalization. Exposure to certain environmental contaminants has been hypothesized to be a risk factor for childhood allergies and asthma. Scientific understanding regarding the effect of prenatal contaminant exposure on fetal immune system development and subsequent susceptibility to allergic diseases is limited. Elevated levels of immunoglobulin E (IgE) are a hallmark sign of an allergic response. Elevated levels of interleukin-33 (IL-33) and thymic stromal lymphopoietin (TSLP) are implicated in inflammatory responses and early life manifestations of allergic disease but have not been measured in neonates. The objectives of this research were to 1) assess the levels of, correlation among and predictors of IgE, IL-33 and TSLP in umbilical cord blood and 2) determine the association between prenatal exposure to environmental contaminants and elevated levels of IgE, TSLP and IL-33. Concentrations of metals, phthalates, bisphenol A, pesticides, and polychlorinated biphenyls were measured in maternal urine, blood or plasma. IgE, IL-33 and TSLP were measured in umbilical cord blood samples. Data were obtained from the Maternal-Infant Research on Environmental Chemicals (MIREC) study, a Canadian cohort study of 2,001 women recruited from 10 sites between 2008 and 2011. TSLP and IL-33 were highly correlated with each other but neither was strongly correlated with IgE. Elevated levels of TSLP and IL-33 were significantly associated with maternal characteristics indicative of inflammatory responses. None of the environmental contaminants were associated with elevated immune system biomarker levels. These findings support the mechanistic hypothesis that IL-33 and TSLP are both operational in early life inflammatory pathways. Determination of whether the observed absence of environmental exposure-induced immunotoxicity persists into childhood requires follow-up in a cohort of children.

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Keywords

epidemiology, immunology

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