2026 Proffered Presentations
S107: IN VIVO EFFECTS OF CHRONIC INHALATIONAL EXPOSURE TO ULTRAFINE PARTICULATE MATTER ON SINONASAL EPITHELIA IN A MURINE MODEL
Jivianne T Lee, MD1; Saroj Basak, PhD2; Eri Srivatsan, PhD2; Sydney Lam, BS1; Thomas Issa, BS1; Rajat Gupta, BS1; Jesus Araujo, MD, PhD1; 1UCLA; 2Greater Los Angeles VA Healthcare System
Background: Although the precise etiology of chronic rhinosinusitis (CRS) remains unknown, environmental factors are understood to be involved in its pathogenesis. Clinical studies using spatial modeling from pollutant monitoring sites suggest particulate matter (PM) exposure exacerbates CRS symptom severity and is associated with worse clinical outcomes. However, the underlying pathomechanisms with which PM exposure contributes to CRS have not been fully characterized
Objective: The purpose of this study is to determine the impact of chronic inhalational exposure to ultrafine particulate matter on the upper airway utiilizing an in vivo murine experimental model.
Methods: Twenty-two male C57BL/6J mice (8 weeks old) were randomized to receive either filtered air (controls n=11) or ultrafine nPM at 300-350µg/m3(n=11) for 6 hours/day, 4 days/week, for 14 weeks. Mice were placed in whole body exposure chambers that could house up to 22 mice. PM was collected from ambient air, and a compressor pump was used to push HEPA-filtered air through a Hope nebulizer (B&B Medical Technologies, USA) to re-aerosolize PM-containing solutions into ultrafine fractions. A vacuum pump was then used to direct the re-aerosolized ultrafine PM into a silica gel diffusion dryer (Model 3620, TSI, USA) as well as a Po-210 neutralizer (Model 2U500, NRD Inc. USA) to remove excess water and particle electrical charges. The flow rate of the air stream into the exposure chamber was 2.5 lpm. Prior to each exposure session, a scanning mobility particle sizer (Model 3080 TSI, USA), condensation particle counter (Model 3022 TSI, USA), and optical particle sizer (Model 3330 TSI, USA). were used to measure particle number concentration distribution and size in the range of 0.013-2.5µm. An optical mass monitor (Dustrak TSI, USA) was used to assess mass concentration, with a target of 300-350µg/m3. Re-aerosolized PM were collected on Quartz (37-mm, Pall Life Sciences, 2-μm pore, Ann Arbor, MI) and PTFE (Teflon) filters for chemical characterization. For filtered air exposures, a vacuum was used to draw ambient air through a HEPA-filter into control mice exposure chambers. Following the exposure period, mice were euthanized and sinonasal tissue harvested. Specimens were placed in formalin for histopathologic analysis.
Results: Seven of the 11 (64%) exposed mice demonstrated signs of inflammation including increased secretory glands, submucosal mucin, subepithelial basement membrane thickening, squamous metaplasia, fibrosis and/or lymphocytic infiltration . Control mice exposed to filtered air showed normal ciliated pseudostratified columnar epithelium with no evidence of inflammation nor any other pathology.
Conclusion: Chronic (14 weeks) inhalational exposure to ultrafine particulate matter induced sinonasal inflammation in a majority of exposed mice relative to controls. These findings support the role of airborne environmental pollutants in contributing to the pathogenesis of chronic rhinosinusitis.