Air pollution and allergic diseases: Mechanistic pathways,  clinical phenotypes, and public health implications

Nunnaphat Wongsuwan; Arunat Suwanvoradit; Napinprapa Angkanavis; Thanunchanok Tosomsakul; Khwanchai Pramoonsap

Authors

Nunnaphat Wongsuwan Anglo Singapore International School
Arunat Suwanvoradit Singapore International School of Bangkok
Napinprapa Angkanavis Benchamaracharungsarit School
Thanunchanok Tosomsakul Patumwan Demonstration School
Khwanchai Pramoonsap Independent Researcher

Keywords:

Air Pollution, Allergic Sensitization, Asthma, Epithelial Barrier Dysfunction, Type 2 Inflammation

Abstract

Allergic diseases—including asthma, allergic rhinitis, atopic dermatitis, food allergy, and allergic conjunctivitis—affect ~30–40% of the global population and are rising rapidly. Air pollution (PM₂.₅, PM₁₀, NO₂, O₃, and PAHs) is a major, modifiable environmental driver that contributes to allergic sensitization and worsens disease severity, with disproportionate impacts in children and underserved populations. This narrative review critically synthesizes epidemiological, mechanistic, and clinical evidence linking air pollution to allergic disease, with emphasis on shared mechanisms across organ systems, life-course and gene–environment vulnerability, and implications for prevention and policy.

A structured literature search of PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar identified English-language studies addressing major pollutants, allergic outcomes, and mechanistic pathways. Epidemiological, experimental, clinical, and high-quality reviews were included; non–peer-reviewed and occupational-only reports were excluded. Evidence was synthesized thematically with critical appraisal of relevance and study quality. Across respiratory, cutaneous, ocular, and gastrointestinal phenotypes, air pollution acts as an immune adjuvant via oxidative stress, epithelial barrier dysfunction, and type 2 (Th2) immune polarization mediated by epithelial alarmins (TSLP, IL-33, IL-25). Associations are strongest and most consistent for asthma and allergic rhinitis, with growing coherence for atopic dermatitis; evidence for food allergy and allergic conjunctivitis remains emerging and heterogeneous. Early-life exposure represents a critical window, with gene–environment interactions (e.g., antioxidant and barrier gene variants) contributing to heterogeneity.

Climate change amplifies risk through increased ozone formation, wildfire smoke, extended pollen seasons, and extreme events such as thunderstorm asthma. Pollution-related allergic disease reflects a multisystem “barrier–alarmin–Th2” framework shaped by exposure timing, susceptibility, and climate stressors. While individual mitigation can reduce acute risk, durable prevention requires upstream emission reduction and equity-centered implementation. Future priorities include longitudinal multi-omics, precision prevention, improved exposure assessment, and policy translation that explicitly considers allergic outcomes.

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