Traffic-Related Air Pollution Linked to Higher Risk of Chronic Rhinosinusitis: JAMA
USA: A case-control study published in JAMA Otolaryngology–Head & Neck Surgery found that long-term exposure to traffic- and industry-related air pollutants was linked to chronic rhinosinusitis (CRS) and was associated with distinct patterns of sinonasal inflammation. The findings suggest that different pollutants may influence separate inflammatory pathways in the upper airway, although causality could not be established.
Chronic rhinosinusitis is a persistent inflammatory condition of the nasal and sinus passages that significantly affects quality of life. While environmental pollution has long been suspected of contributing, the biological mechanisms underlying this association remain unclear. Researchers led by Hong-Ho Yang aimed to examine how long-term exposure to specific air pollutants relates to both disease risk and immune responses within sinonasal tissues.
The study included 92 participants undergoing endoscopic sinus or skull base surgery at a tertiary care center between 2018 and 2021. Of these, 62 patients had chronic rhinosinusitis, while 30 served as controls without the condition. Sinonasal epithelial samples were collected during surgery and analyzed for cytokine expression.
Researchers estimated five-year average exposure to multiple pollutants, including nitrogen dioxide (NO₂), benzene, 1,3-butadiene, and various metal pollutants such as lead, chromium, nickel, and zinc. Residential exposure levels were calculated using geocoded addresses and a validated land-use regression model.
Cytokine activity was measured using flow cytometry and multiplex immunoassays. Statistical models were then applied to assess the association between pollutant exposure, CRS risk, and inflammatory profiles.
The following were the key findings:
- Higher exposure to nitrogen dioxide, a traffic-related pollutant, was significantly associated with increased odds of chronic rhinosinusitis.
- Increased exposure to benzene and lead was also linked to a higher risk of chronic rhinosinusitis.
- These associations remained significant even after adjusting for smoking status, steroid use, comorbidities, and demographic factors.
- Nitrogen dioxide exposure was associated with elevated type 2 inflammatory cytokines, including interleukin (IL)-4, IL-5, and IL-13, as well as tumor necrosis factor alpha.
- This cytokine pattern suggests a type 2–dominant inflammatory response commonly seen in allergic airway disease.
- Benzene exposure was linked to reduced levels of IL-1 receptor antagonist, indicating altered immune regulatory activity.
- Lead exposure was associated with increased IL-8 and IL-1 receptor antagonist levels, suggesting a neutrophil-driven, innate immune inflammatory profile.
Overall, the findings suggest that long-term exposure to traffic-related and industrial pollutants may not only increase the risk of chronic rhinosinusitis but also shape distinct inflammatory endotypes within the disease. This points to the possibility that environmental pollutants contribute to heterogeneous disease mechanisms through different biological pathways.
However, the authors noted that the study design does not allow for causal inference. They emphasized the need for larger and longitudinal studies to understand better how specific pollutants contribute to the development and progression of chronic rhinosinusitis.
Reference:
Yang H, O’Sharkey K, Paul K, et al. Traffic and Industrial Pollutants and Chronic Rhinosinusitis. JAMA Otolaryngol Head Neck Surg. Published online May 28, 2026. doi:10.1001/jamaoto.2026.1176
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