Experimental data confirms that small-sized (0.5-5 μm) airborne aerosols deposit in significant concentrations within the olfactory epithelium, providing a compelling aerodynamic mechanism to explain atypical olfactory dysfunction in COVID-19 patients.
Introduction Olfactory dysfunction (OD) affects a majority of COVID-19 patients, is atypical in duration and recovery, and is associated with focal opacification and inflammation of the olfactory epithelium. Given recent increased emphasis on airborne transmission of SARS-CoV-2, the purpose of the present study was to experimentally characterize aerosol dispersion within olfactory epithelium (OE) and respiratory epithelium (RE) in human subjects, to determine if small (sub 5 mu m) airborne aerosols selectively deposit in the OE. Methods Healthy adult volunteers inhaled fluorescein-labeled nebulized 0.5-5 mu m airborne aerosol or atomized larger aerosolized droplets (30-100 mu m). Particulate deposition in the OE and RE was assessed by blue-light filter modified rigid endoscopic evaluation with subsequent image randomization, processing and quantification by a blinded reviewer. Results 0.5-5 mu m airborne aerosol deposition, as assessed by fluorescence gray value, was significantly higher in the OE than the RE bilaterally, with minimal to no deposition observed in the RE (maximum fluorescence: OE 19.5(IQR 22.5), RE 1(IQR 3.2), p<0.001; average fluorescence: OE 2.3(IQR 4.5), RE 0.1(IQR 0.2), p<0.01). Conversely, larger 30-100 mu m aerosolized droplet deposition was significantly greater in the RE than the OE (maximum fluorescence: OE 13(IQR 14.3), RE 38(IQR 45.5), p<0.01; average fluorescence: OE 1.9(IQR 2.1), RE 5.9(IQR 5.9), p<0.01). Conclusions Our data experimentally confirm that despite bypassing the majority of the upper airway, small-sized (0.5-5 mu m) airborne aerosols differentially deposit in significant concentrations within the olfactory epithelium. This provides a compelling aerodynamic mechanism to explain atypical OD in COVID-19.
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