Traffic and Industrial Pollutants and Chronic Rhinosinusitis.

IMPORTANCE

Air pollution has been implicated in the pathogenesis of chronic rhinosinusitis (CRS).

OBJECTIVE

To investigate the association between long-term residential exposure to traffic-related and industry-related pollutants and CRS risk and sinonasal cytokine expression.

DESIGN, SETTING, AND

PARTICIPANTS

This case-control study was conducted at a tertiary center and examined sinonasal epithelial specimens that were collected 2018 to 2021 from 92 human participants during endoscopic sinus surgery (62 CRS case patients) and skull base surgeries (30 controls). Data were analyzed from 2022 to 2025.

EXPOSURES: Five-year average pollutant exposures were assigned to geocoded residential addresses using a validated land use regression model for nitrogen dioxide (NO2), benzene, 1,3-butadiene, chromium, lead, nickel, and zinc.

MAIN OUTCOMES AND MEASURES: Cytokine expression was quantified by flow cytometry and Luminex assays. CRS odds were estimated with a logistic regression, and cytokine levels were modeled with a generalized linear regression with a log link, using pollutant concentrations as predictors.

RESULTS

Of 92 participants, 44 (47.8%) were female, 48 (52.2%) were male, and the mean (SD) age was 50 (15) years. Adjusting for demographic characteristics, smoking history, steroid use, and comorbidities, each SD increase in NO2 levels was independently associated with a 132% rise in odds of CRS (adjusted odds ratio [aOR], 2.32, 95% CI, 1.09-4.93). Benzene levels were associated with an 115% rise (aOR, 2.15; 95% CI, 1.05-4.38), and lead levels were associated with a 248% rise (aOR, 3.48; 95% CI, 1.36-8.88). Controlling for CRS status and copollutant levels, NO2 exposure was associated with elevated interleukin (IL)-4, IL-5, IL-13, and tumor necrosis factor α levels, benzene with suppressed IL-1 receptor agonist levels, and lead with elevated IL-8 and IL-1 receptor agonist levels.

CONCLUSIONS AND RELEVANCE: The results of this case-control study suggest that long-term residential exposure to traffic-related and industry-related pollutants was associated with increased CRS risk and distinct cytokine signatures. Traffic-related NO2 was associated with elevated type 2 cytokines, which was consistent with a barrier alarmin type 2 pattern. Benzene and lead levels were associated with non-type 2 cytokine profiles that were characterized by innate and neutrophilic markers.