Air pollution is associated with persistent peanut allergy in the first 10 years.

Background: The role of air pollution in eczema and food allergy development remains understudied.
Objective: We aimed to assess whether exposure to air pollution is associated with eczema and food allergies in the first 10 years of life.
Methods: HealthNuts recruited a population-based sample of 1-year-old infants who were followed up at ages 4, 6, and 10 years. Annual average fine particulate matter (particulate matter with diameter of 2.5 μm or less, or PM _2.5 ) and nitrogen dioxide (NO ₂ ) exposures were assigned to geocoded residential addresses. Eczema was defined by parent report. Oral food challenges to peanut, egg, and sesame were used to measure food allergy. Multilevel logistic regression models were fitted, and estimates were reported as adjusted odds ratios.
Results: Those exposed to high concentration of NO ₂ (<10 ppb) at age 1 year had higher peanut allergy prevalence at ages 1 (adjusted odds ratio [95% confidence interval], 2.21 [1.40-3.48]) and 4 (2.29 [1.28-4.11]) years. High exposure to NO ₂ at 6 years old were associated with higher peanut allergy prevalence at age 6 (1.34 [1.00-1.82] per 2.7 ppb NO ₂ increase) years. Similarly, increased PM _2.5 at age 1 year was associated with peanut allergy at ages 4, 6, and 10 years (respectively, 1.27 [1.01-1.60], 1.27 [1.01-1.56], and 1.46 [1.05-2.04] per 1.2 μg/m PM _2.5 increase) years. We found that increased concentrations of NO ₂ or PM _2.5 at age 1 year were associated with persistent peanut allergy at later ages. Little evidence of associations was observed with eczema or with egg allergy.
Conclusions: Early-life exposure to PM _2.5 and NO ₂ was associated with peanut allergy prevalence and persistence. Policies aiming at reducing air pollution could potentially reduce presence and persistence of peanut allergy.
Competing Interests: Disclosure statement Supported by funding from the National Health and Medical Research Council (NHMRC) of Australia, the Ilhan Food Allergy Foundation, AnaphylaxiStop, the Charles and Sylvia Viertel Medical Research Foundation, and the Victorian government’s Operational Infrastructure Support Program. R.P., C.L., K.P.P., and A.L. are supported by NHMRC awards. K.P.P. is also funded by a Melbourne Children’s Clinician-Scientist Fellowship. D.L. was supported by the University of Melbourne and Becas Carlos Antonio Lopez scholarship. The funding agencies had no direct role in the conduct of the study; the collection, management, statistical analysis, and interpretation of the data; decision to submit the report for publication; or the preparation and approval of the report. Disclosure of potential conflict of interest: C. J. Lodge, S. C. Dharmage, and A. J. Lowe have received research funds from GSK’s competitively awarded Investigator sponsored studies program for unrelated research. A. J. Lowe has received grant funding from SanofiRegeneron for unrelated research; and has received donations of interventional product (EpiCeram) from Primus Pharmaceuticals for unrelated research. J. C. Su has been consultant/speaker/investigator for AbbVie, Amgen, Bioderma, Bristol Myers Squibb, Ego Pharmaceuticals, Eli Lilly, Janssen, LEO Pharma, L’Oreal, Mayne, Novartis, Pfizer, Pierre-Fabre, and Sanofi. K. P. Perrett has received research grants from Aravax, DBV Technologies, Novartis, and Siolta; and consultant fees from Aravax, paid to Perrett’s institution, outside the submitted work. The rest of the authors declare that they have no relevant conflicts of interest.
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