Background: Pathophysiology of rhinitis in older adults is largely unknown. We tested whether air pollution is associated with this condition and how immune mechanisms may play a role in this relationship.

Methods: We analyzed cross-sectional data from the National Social Life, Health, and Aging Project, a nationally representative study of older adults born between 1920 and 1947. Particulate matter ≤2.5 μm (PM_2.5) air pollution exposure estimates were generated using validated spatiotemporal models. Presence of rhinitis was defined based on medication use (≥1: intranasal medications: steroids, antihistamines, lubricants, and/or decongestants, and/or oral medications: antihistamines and/or decongestants). K-means cluster analysis (Jaccard method) was used to group 13 peripheral blood cytokines into 3 clusters to facilitate functional determination. We fitted multivariate logistic regressions to correlate PM_2.5 exposure with presence of rhinitis, controlling for confounders, and then determined the role of cytokines in this relationship.

Results: Long- (but not short-) term exposure to PM_2.5 was associated with presence of rhinitis: 3-year exposure window, odds ratio (OR) = 1.32, 95% confidence interval (CI): 0.98, 1.80, per 1 standard deviation (SD) PM_2.5 increase. Inclusion of cytokine cluster in the model led to a modestly stronger effect of PM_2.5 exposure on rhinitis (OR = 1.37; 95% CI: 1.00, 1.87; 3-year exposure window). The particular immune profile responsible for this result was composed of elevated IL-3, IL-12, and IFN-γ (OR = 4.86, 95% CI: 1.10, 21.58, immune profile-PM_2.5 exposure interaction term).

Conclusion: We show for the first time that IL-3, IL-12, and IFN-γ explain in part the relationship between PM_2.5 exposure and rhinitis in older US adults. If confirmed, these immune pathways may be used as therapeutic targets.