Article record

野火空气污染暴露与头颈癌发病率

Wildfire Air Pollution Exposure and Head and Neck Cancer Incidence.

临床研究咽喉科IF 2.3Q2

文献信息

PMID	42870377
原文	在 PubMed 查看原文 ↗
发表日期	2026
作者	Youn Soo Jung 查看其他 8 位作者 Sophie E Yu；Kari C Nadeau；John Cramer；Mary Jue Xu；Margaret B Mitchell；Simon Chiang；Mengyuan Ruan；Stella E Lee
作者单位	T. H. Chan School of Public Health, Harvard University, Boston, Massachusetts, USA. 查看其他 7 条单位信息 Department of Otolaryngology-Head & Neck Surgery, University of California San Francisco, San Francisco, California, USA.；Department of Environmental Health, Harvard Chan School of Public Health and Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA.；Department of Otolaryngology, Head and Neck Surgery, Wayne State University, Detroit, Michigan, USA.；Department of Otolaryngology-Head & Neck Surgery, University of Pennsylvania, Philadelphia, Pennsylvania, USA.；Thomas Jefferson School of Medicine, Philadelphia, Pennsylvania, USA.；Center for Surgery and Public Health, Department of Surgery, Brigham and Women's Hospital, Boston, Massachusetts, USA.；Department of Otolaryngology-Head & Neck Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
期刊	The Laryngoscope
SCI 分区	Q2
IF	2.3
研究类型	临床研究 · 临床
所属专科	咽喉科

中文摘要

目的： 确定野火特异性细颗粒物2.5（wPM2.5）暴露与头颈及呼吸消化系统癌症（HNC）总体及部位特异性发病率之间的关联。
研究设计： 流行病学回顾性队列分析。
方法： HNC发病率数据来自监测、流行病学和最终结果计划（2016-2022年）。使用分布滞后非线性模型检查县级wPM2.5暴露指标与HNC发病率之间的关系，并调整健康行为（烟草/酒精使用、饮食、运动和性活动）、人口统计学特征（年龄、性别、种族/民族）、人口规模和年份，以县作为随机效应。滞后效应分析跨越10年。HNC亚部位包括鼻/鼻窦/耳、鼻咽、口腔、口咽（按p16状态分层）、下咽和喉。
结果： 较高的野火特异性PM2.5暴露与0-10年滞后期间累积HNC发病率增加相关，每增加一个烟雾超标日的累积相对风险（cRR）为1.06（95% CI：1.04-1.09），任何年度暴露为1.41（1.24-1.60），每增加一个高于5 μg/m3的天数百分比点为1.23（1.13-1.33）。在各亚部位中，口腔癌显示持续增加（cRR 1.03，95% CI：1.00-1.06），口咽癌风险增加至1.09（1.06-1.13），喉癌表现出最大效应，在10年滞后期间每增加一个超标日的cRR为1.13（1.07-1.19）。按p16状态分层时，p16阳性、p16阴性和p16未知肿瘤均观察到显著关联。
结论： 野火烟雾暴露的频率、强度或持续性越高，与HNC风险增加相关，其中最强的关联由长期暴露驱动。

英文摘要

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.