Wildfire Smoke and the Human Larynx: Preliminary Evidence of Functional and Molecular Change

Air pollution is a major public health burden. Wildfires are a known source of air pollution in their production of smoke, containing fine particulate matter (PM2.5). PM2.5 is known to induce respiratory inflammation, but its effects on the human larynx remain poorly understood. This case report provides a preliminary investigation into the impact of wildfire-related air pollution on vocal function and laryngeal tissue biology in an adult participant exposed to elevated PM2.5 during a wildfire event.

Comprehensive voice and laryngeal assessments were conducted during a period of wildfire smoke exposure (PM2.5 > 100 µg/m³) and a subsequent period of normal air quality (PM2.5 < 10 µg/m³). Voice evaluation included acoustic and aerodynamic measures as well as laryngeal endoscopy with stroboscopy. Ventricular fold biopsies were also collected at each time point for gene expression analysis using quantitative PCR (qPCR) targeting extracellular matrix (ECM) remodeling and inflammatory markers.

During record breaking air pollution with PM2.5 levels up to 117 μg m-3 related to massive regional wildfires, the participant exhibited a reduction in speaking fundamental frequency compared to baseline under normal air quality conditions. Laryngeal endoscopy revealed visibly increased laryngeal mucus. qPCR analysis demonstrated approximately a twofold increase in MMP-1 expression, consistent with heightened ECM turnover. Other ECM and inflammatory genes showed variable expression patterns without consistent upregulation.

These preliminary findings suggest that acute exposure to wildfire-associated PM2.5 may alter vocal function and induce early molecular changes in the laryngeal tissue consistent with matrix remodeling. Further studies with larger cohorts are warranted to define the mechanisms by which wildfire smoke impacts the human larynx and voice.