TOPLINE:

Prophylactic nasal budesonide spray reduces nasal inflammation and modulates epigenetic age acceleration (EAA) in patients with allergic rhinitis before and after repeated acute exposures to an allergen and diesel exhaust.

METHODOLOGY:

• The study included 20 patients with allergic rhinitis (mean age, 31 years; 70% women; 85% nonsmokers) who received once‑daily budesonide (64 µg per spray; two sprays per naris [256 µg total]) or placebo for at least 4 weeks, with a washout of 4 or more weeks between treatment periods.
• All patients underwent a titrated nasal allergen challenge and separate 2‑hour exposures to diesel exhaust at a nominal concentration of particulate matter ≤ 2.5 µm in diameter (300 µg/m³); exposures were given at 0 and 24 hours.
• Researchers measured the peak nasal inspiratory flow (PNIF) to assess obstruction of nasal airways and the total nasal symptom score (TNSS) to assess the severity of nasal symptoms (higher scores indicated greater severity), both recorded preexposure and at 0.5 and 24 hours post‑exposure.

TAKEAWAY:

• Pretreatment with budesonide significantly lowered nasal levels of interleukin (IL)‑5 and IL‑17A at treatment baseline, and the reduction in IL‑5 level persisted through 24 hours after exposure to the allergen and diesel exhaust.
• Budesonide significantly increased the PNIF at 24 hours after initial exposure and re-exposure to the allergen compared with placebo; for diesel exhaust, the PNIF was significantly higher at baseline, 0.5 hour after initial exposure, and 24 hours after re-exposure (P ≤ .05 for all).
• A significant reduction in the allergen-induced increase in TNSS was observed with budesonide at 0.5 and 24 hours after reexposure (P < .05 for both).
• Budesonide treatment decreased Horvath 1 EAA epigenetic biomarker across the allergen exposure period and at the baseline of diesel exhaust exposure, while allergen exposure increased Horvath 1 EAA.

IN PRACTICE:

“These findings may inform the targeted use of budesonide to support patients disproportionately affected by particulate air pollution exposure as part of precision health approaches,” the authors of the study wrote. 

SOURCE:

Christopher Carlsten, MD, MPH, with The University of British Columbia, Vancouver, Canada, was the corresponding author of the study, which was published online on February 25, 2026, in Annals of Allergy, Asthma & Immunology.

LIMITATIONS:

This study was limited by the small sample size and differences in pretreatment timing between exposure groups. The diesel exhaust aerosol used in controlled exposures may not have fully represented real‑world traffic‑related air pollution, and logistical constraints prevented randomization of the allergen and diesel exhaust exposure order.

DISCLOSURES:

This study was funded by Kenvue and Genome BC. This study received support from a CANTRAIN-CTTP & Michael Smith Health Research BC Master’s Studentship Award, a British Columbia Graduate Scholarship, a Michael Smith Health Research BC Fellowship, Genome BC, and the Terry Fox Research Institute. The authors declared having no conflicts of interest.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.