Abstract

Whether long-term exposure air to pollution has effects on allergic sensitization is controversial. Our aim was to investigate associations of air pollution exposure at birth and at the time of later biosampling with IgE sensitization against common food and inhalant allergens, or specific allergen molecules, in children aged up to 16 years. A total of 6163 children from 4 European birth cohorts participating in the Mechanisms of the Development of ALLergy [MeDALL] consortium were included in this meta-analysis of the following studies: Children, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) (Sweden), Influences of Lifestyle-Related Factors on the Human Immune System and Development of Allergies in Childhood (LISA)/German Infant Study on the Influence of Nutrition Intervention PLUS Environmental and Genetic Influences on Allergy Development (GINIplus) (Germany), and Prevention and Incidence of Asthma and Mite Allergy (PIAMA) (The Netherlands). The following indicators were modeled by land use regression: individual residential outdoor levels of particulate matter with aerodynamic diameters less than 2.5 μm, less than 10 μm, and between 2.5 and 10 μm; PM2.5 absorbance (a measurement of the blackness of PM2.5 filters); and nitrogen oxides levels. Blood samples drawn at ages 4 to 6 (n= 5989), 8 to 10 (n= 6603), and 15 to 16 (n= 5825) years were analyzed for IgE sensitization to allergen extracts by ImmunoCAP. Additionally, IgE against 132 allergen molecules was measured by using the MedALL microarray chip (n= 1021). Air pollution was not consistently associated with IgE sensitization to any common allergen extract up to age 16 years. However, allergen-specific analyses suggested increased risks of sensitization to birch (odds ratio [OR]= 1.12 [95% CI= 1.01-1.25] per 10-μg/m3 increase in NO2 exposure). In a subpopulation with microarray data, IgE to the major timothy grass allergen Phleum pratense 1 (Phl p 1) and the cat allergen Felis domesticus 1 (Fel d 1) greater than 3.5 Immuno Solid-phase Allergen Chip standardized units for detection of IgE antibodies were related to PM2.5 exposure at birth (OR= 3.33 [95% CI= 1.40-7.94] and OR= 4.98 [95% CI= 1.59-15.60], respectively, per 5-μg/m3 increase in exposure). Air pollution exposure does not seem to increase the overall risk of allergic sensitization; however, sensitization to birch as well as grass pollen Phl p 1 and cat Fel d 1 allergen molecules may be related to specific pollutants.

Highlights

  • Whether long-term exposure air to pollution has effects on allergic sensitization is controversial

  • Median air pollution levels ranged from 12.4 mg/m3 (BAMSE) to 23.2 mg/m3 (LISA/GINI North) for NO2 and from 8.1 mg/m3 (BAMSE) to 17.2 mg/m3 (LISA/GINI North) for PM2.5, whereas the concentrations of PMcoarse were largely comparable between the cohorts

  • Higher air pollution exposure at birth address appeared to be associated with elevated levels of the grass allergen molecule Phl p 1, as well as with the cat allergen molecule Fel d 1 in a subset of the study population with available data on IgE sensitization against allergen molecules

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Summary

Introduction

Whether long-term exposure air to pollution has effects on allergic sensitization is controversial. Objective: Our aim was to investigate associations of air pollution exposure at birth and at the time of later biosampling with IgE sensitization against common food and inhalant allergens, or specific allergen molecules, in children aged up to 16 years. Results: Air pollution was not consistently associated with IgE sensitization to any common allergen extract up to age 16 years. Conclusion: Air pollution exposure does not seem to increase the overall risk of allergic sensitization; sensitization to birch as well as grass pollen Phl p 1 and cat Fel d 1 allergen molecules may be related to specific pollutants. Conclusion: Air pollution exposure does not seem to increase the overall risk of allergic sensitization; sensitization to birch as well as grass pollen Phl p 1 and cat Fel d 1 allergen molecules may be related to specific pollutants. (J Allergy Clin Immunol 2021;147:713-22.)

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