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Air pollution exposure increases type 2 inflammation-related markers and reduces ZO-1 in rodent modelsAir Pollution Worsens Allergic Rhinitis in Rodent Studies

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Key Takeaway
Note that rodent models show increased type 2 inflammatory markers following air pollution exposure.

This meta-analysis synthesized data from 18 rodent studies to evaluate the impact of air pollution on allergic rhinitis markers. The analysis focused on type 2 inflammation-related markers, including eosinophils, IL-4, IL-5, IL-13, and OVA-specific IgE, all of which were found to increase following exposure. Additionally, the study reported a reduction in ZO-1 levels and an increase in IL-1β/NLRP3 markers.

Secondary outcomes such as total IgE, neutrophils, lymphocytes, and IL-17 showed varying results, while IFN-γ showed no consistent effect. The authors noted that the evidence is not considered definitive causal pathways due to considerable heterogeneity and a lack of mechanistic markers for certain factors.

Clinical application of these findings is currently limited by the use of experimental animal models rather than human clinical trials. While the results suggest a link between environmental pollutants and inflammatory markers in allergic rhinitis, the high level of heterogeneity necessitates cautious interpretation regarding direct clinical implications.

How this fits prior evidence

This meta-analysis extends the understanding of eosinophils as dual pro-inflammatory and immunoregulatory cells in allergic rhinitis by identifying their increase following air pollution exposure. It also builds upon findings that calcium homeostasis dysregulation serves as an integrative regulatory node in allergic rhinitis inflammation by providing further data on inflammatory markers like IL-1β/NLRP3.

A new analysis of 18 rodent studies suggests that air pollution exposure may worsen allergic rhinitis, a common condition that causes sneezing, a runny or stuffy nose, and itchy eyes. The review looked at how air pollution affects markers of type 2 inflammation, which is a key driver of allergic responses. In the animals, exposure to air pollution increased levels of eosinophils (a type of white blood cell) and several inflammatory proteins, including IL-4, IL-5, and IL-13. It also raised levels of OVA-specific IgE, an antibody linked to allergies. At the same time, it reduced ZO-1, a protein that helps keep the nasal lining healthy, and increased other inflammatory markers like NLRP3 and IL-1β. These changes suggest that air pollution might make allergic rhinitis worse by ramping up inflammation and damaging the nasal barrier.

However, this evidence comes from animal studies, not human trials. The findings are not definitive because the studies varied widely, and the analysis did not report exact numbers or statistical details. Also, the review did not look at other potential mechanisms or report any safety concerns. So, while the link is plausible, we cannot say for sure that air pollution causes these effects in people.

For everyday readers, the takeaway is that reducing exposure to air pollution might help manage allergic rhinitis symptoms, but this is not proven. If you have allergic rhinitis and are concerned about air quality, talk to your doctor about ways to minimize exposure and manage your symptoms.

What this means for you:
Air pollution may worsen allergic rhinitis by increasing inflammation, but evidence is from animals and not definitive.

Common questions

Does air pollution cause allergic rhinitis?

This review of 18 rodent studies found that air pollution exposure increased markers of allergy inflammation, like eosinophils and IgE. However, this does not prove that air pollution causes allergic rhinitis in people. The evidence is from animals and not definitive, so more research is needed.

Who might be affected by air pollution and allergic rhinitis?

People with allergic rhinitis might be affected if air pollution worsens their symptoms. The studies were in rodents, but the findings suggest a possible link. If you have allergic rhinitis, talk to your doctor about how to reduce your exposure to air pollution.

What did the study find about inflammation?

The study found that air pollution increased several inflammatory markers in rodents, including IL-4, IL-5, IL-13, and OVA-specific IgE. It also reduced ZO-1, a protein important for the nasal barrier. These changes suggest air pollution might make allergic inflammation worse.

Study Details

Study typeMeta analysis
EvidenceLevel 1
PublishedJul 2026
View Original Abstract ↓
Although air pollution is associated with the onset and exacerbation of allergic rhinitis (AR), epidemiological studies alone cannot reveal the tissue-level immune mechanisms because factors such as the strength of exposure, duration of exposure, presence of co-pollutants and individual susceptibility are all difficult to control. Experiments on animals have provided support for research on the immune response in the nasal mucosa under controlled conditions. A systematic review and meta-analysis were conducted to quantify changes in nasal mucosal immune-inflammatory markers and to assess the strength of mechanistic evidence from various experiments. According to PRISMA, PubMed, Web of Science, Embase and the Cochrane Library were searched from the beginning until December 2025. Eighteen eligible rodent studies were included. As the primary outcomes, type 2 inflammation-related markers were selected because they had been reported frequently and were biologically central to asthma (asthma/AR), such as eosinophils, IL-4, IL-5, IL-13 and OVA-specific IgE. Other markers included ZO-1, NLRP3, IL-1β, IL-17, IL-33, IFN-γ, neutrophils, lymphocytes and total IgE, and were used as secondary or exploratory outcomes. Pooled effects were expressed as standardised mean differences (SMDs) with 95% confidence intervals, and a random-effects model was used. Exposure to air pollutants was associated with an increase in eosinophils, elevated IL-4, IL-5, IL-13, and OVA-specific IgE; thus, a type 2 inflammatory response had been enhanced. A few studies have also indicated that there may be defects in the epithelial barrier and activation of the innate immune system, as shown by reduced ZO-1 and increased IL-1β/NLRP3. The available evidence did not show a consistent effect on IFN-γ expression. Due to considerable heterogeneity and a lack of mechanistic markers for some other reasons, these results should be interpreted cautiously and are not considered definitive causal pathways.Systematic Review Registration: Identifier: CRD420251265574.
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