Ambient air pollutants increase the risk of immunoglobulin E-mediated allergic diseases: a systematic review and meta-analysis
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Updated: Sep 22, 2025

Flow Cytometric Analysis of Particle-bound Bet v 1 Allergen in PM10
Published on: November 19, 2016
Hua Wang1,2, Xian-Bao Li1,2, Xiu-Jie Chu1,2
1Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, Anhui, China.
Abstract:
Immunoglobulin E (IgE)-mediated allergic diseases, including eczema, atopic dermatitis (AD), and allergic rhinitis (AR), have increased prevalence in recent decades. Recent studies have proved that environmental pollution might have correlations with IgE-mediated allergic diseases, but existing research findings were controversial. Thus, we performed a comprehensive meta-analysis from published observational studies to evaluate the risk of long-term and short-term exposure to air pollutants on eczema, AD, and AR in the population (per 10-μg/m3 increase in PM2.5 and PM10; per 1-ppb increase in SO2, NO2, CO, and O3). PubMed, Embase, and Web of Science were searched to identify qualified literatures. The Cochran Q test was used to assess heterogeneity and quantified with the I2 statistic. Pooled effects and the 95% confidence intervals (CIs) were used to evaluate outcome effects. A total of 55 articles were included in the study. The results showed that long-term and short-term exposure to PM10 increased the risk of eczema (PM10, RRlong = 1.583, 95% CI: 1.328, 1.888; RRshort = 1.006, 95% CI: 1.003-1.008) and short-term exposure to NO2 (RRshort = 1.009, 95% CI: 1.008-1.011) was associated with eczema. Short-term exposure to SO2 (RRshort: 1.008, 95% CI: 1.001-1.015) was associated with the risk of AD. For AR, PM2.5 (RRlong = 1.058, 95% CI: 1.014-1.222) was harmful in the long term, and short-term exposure to PM10 (RRshort: 1.028, 95% CI: 1.008-1.049) and NO2 (RRshort: 1.018, 95% CI: 1.007-1.029) were risk factors. The findings indicated that exposure to air pollutants might increase the risk of IgE-mediated allergic diseases. Further studies are warranted to illustrate the potential mechanism for air pollutants and allergic diseases.
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