Background: 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. Methods: 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). Results: 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). Conclusion: 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.
FörderungenBad Honnef Netherlands Organization for Scientific Research Netherlands Organization for Health Research and Development Megagrant of the Government of the Russian Federation Austrian Science Fund Swedish Research Council for Health, Working life and Welfare European Research Council Cancer and Allergy Foundation Swedish Asthma and Allergy Research Foundation Swedish Environment Protection Agency Swedish Research Council Formas Strategic Research Programme in Epidemiology at Karolinska Institutet Region Stockholm Swedish Heart-Lung Foundation Swedish Research Council Netherlands Asthma Fund Netherlands Ministry of Spatial Planning, Housing, and the Environment European Union from the European Regional Development Fund under the Smart Growth Operational Programme NeuroSmog: Determining the impact of air pollution on the developing brain Seventh Framework Program: MeDALL project Pediatric Practice Research Institute at Marien-Hospital Wesel Helmholtz Centre for Environmental Research-UFZ, Leipzig Federal Ministry for Education, Science, Research and Technology Nestle Mead Johnson Commission of the European Communities, the Seventh Framework Program: MeDALL project Federal Ministry for Environment (IUF Dusseldorf) IUF-Leibniz Research Institute for Environmental Medicine at the University of Dusseldorf Helmholtz Zentrum Munich Grant of The Netherlands Organization for Scientific Research Netherlands Ministry of Health, Welfare, and Sport European Community