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Updated: Oct 15, 2026

Whole-Body Nanoparticle Aerosol Inhalation Exposures
Published on: May 7, 2013
Wildfire Air Pollution Exposure and Head and Neck Cancer Incidence
Youn Soo Jung1, Sophie E Yu2, Kari C Nadeau3
1T. H. Chan School of Public Health, Harvard University, Boston, Massachusetts, USA.
Objectives:
To determine the association between wildfire-specific particulate matter 2.5 (wPM2.5) exposure and the overall and site-specific incidences of head and neck and aerodigestive cancer (HNC).
Study Design:
Epidemiological retrospective cohort analysis.
Methods:
HNC incidence data were derived from the Surveillance, Epidemiology, and End Results Program (2016-2022). The relationship between county-level wPM2.5 exposure metrics and HNC incidence rates were examined using a distributed lag non-linear model, adjusting for health behaviors (tobacco/alcohol use, diet, exercise, and sexual activity), demographics (age, sex, race/ethnicity), population size, and year, with county as a random effect. Lag effects were analyzed over 10 years. HNC subsites included nasal/sinus/ear, nasopharynx, oral cavity, oropharynx (stratified by p16 status), hypopharynx, and larynx.
Results:
Higher wildfire-specific PM2.5 exposure was associated with increased cumulative HNC incidence over 0-10-year lags, with a cumulative relative risk (cRR) of 1.06 (95% CI: 1.04-1.09) per additional smoke exceedance day, 1.41 (1.24-1.60) for any annual exposure, and 1.23 (1.13-1.33) per percentage-point increase in days above 5 μg/m3. Among subsites, oral cavity cancer showed consistent increases (cRR 1.03, 95% CI: 1.00-1.06), oropharyngeal cancer risk increased to 1.09 (1.06-1.13), and laryngeal cancer exhibited the largest effect, with a cRR of 1.13 (1.07-1.19) per additional exceedance day over a 10-year lag period. When stratified by p16 status, significant associations were noted for p16-positive, p16-negative, and p16-unknown tumors.
Conclusions:
Higher frequency, intensity, or persistence of wildfire-smoke exposure is associated with increased HNC risk, with the strongest associations driven by long-term exposures.
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