Long-Term Particulate Matter Exposure May Increase Risk of Chronic Rhinosinusitis with Nasal Polyposis: Results from an Exposure-Matched Study

CLINICAL QUESTION

Does long-term exposure to fine particulate matter (PM2.5) increase the risk of developing chronic rhinosinusitis with nasal polyposis (CRSwNP)?

BOTTOM LINE

Patients with higher year-long PM2.5 exposure were more than seven times as likely to have CRSwNP compared to matched controls. This association was not seen in patients with CRS without polyps (CRSsNP). Reduced levels of the anti-inflammatory cytokine IL-10 in pollution-exposed controls suggest a possible biologic link between fine particulate matter and sinonasal inflammation.

BACKGROUND: Chronic rhinosinusitis is a complex inflammatory condition shaped by genetics, immunity, and environmental factors. Air pollution—and especially fine particulate matter under 2.5 microns in size—has long been tied to asthma and lower airway disease. Prior studies suggested pollution could push the sinonasal mucosa toward a type 2 inflammatory state, but its relationship to different CRS phenotypes has been unclear.

STUDY DESIGN: Researchers at Vanderbilt University Medical Center retrospectively analyzed 376 surgical patients between 2015 and 2021 (308 with CRS, 68 controls). Using a machine learning model, they estimated average PM2.5 exposure for the 12 months before surgery. Cytokine levels were measured from middle meatus mucus, and exposure-matched logistic regression was applied to control for confounders like age, income, asthma, allergic rhinitis, and rurality.

SETTING: Single tertiary-care academic center, southeastern U.S.

SYNOPSIS: Patients were grouped as having CRSwNP or CRSsNP. Average PM2.5 exposure across the cohort was 8.1 µg/m³, close to U.S. national levels. Among controls, higher PM2.5 exposure correlated with reduced IL-10 (β = –0.735, p = 0.0196), a key immune regulator that normally suppresses inflammation. In exposure-matched analysis, high PM2.5 levels were an independent predictor of CRSwNP (OR 7.22, p = 0.0001). The effect size was strikingly similar to that of asthma (OR 7.7) and allergic rhinitis (OR 8.7), both well-established CRS risk factors. High PM2.5 exposure did not increase the odds of CRSsNP (OR 1.42), but allergic rhinitis (β = 1.85; OR 6.41, p < 0.0001) and asthma β = 1.18; OR 3.26, p = 0.0254) remained strong independent predictors of this phenotype. Limitations of the study included a single-center design, a relatively small control group, and reliance on home zip codes (not individual-level monitoring) to estimate pollution exposure. Because only surgically managed CRS patients were included, findings may not apply to milder cases. Still, the results point to long-term particulate pollution as a potential driver of CRSwNP.

CITATION: Lubner RJ, et al. Long-term particulate matter exposure may increase risk of chronic rhinosinusitis with nasal polyposis: results from an exposure-matched study. Int Forum Allergy Rhinol. 2025;15:926-933. doi: 10.1002/alr.23589.

COMMENT: While we would intuitively suspect that pollution may contribute to more severe sinonasal inflammatory disease, progressive interest in PM2.5 (or particulate matter≤2.5 µm in diameter) has begun to produce clearer evidence of the association. This study took the investigation a step further, focusing specifically on cytokine changes and manifestations in chronic rhinosinusitis without nasal polyps (CRSsNP) versus chronic rhinosinusitis with nasal polyps (CRSwNP) phenotypes in the context of PM2.5. They found that reduced IL-10 levels were associated with higher PM2.5 exposure, and PM2.5 exposure was an independent risk factor for CRSwNP in regression analysis. Interestingly, this relationship was not identified in CRSsNP.—Ashoke Khanwalkar, MD