Wood smoke exposure affects lung aging, quality of life, and all-cause mortality in New Mexican smokers

Author:

Leng Shuguang,Picchi Maria A.,Meek Paula M.,Jiang Menghui,Bayliss Samuel H.,Zhai Ting,Bayliyev Ruslan I.,Tesfaigzi Yohannes,Campen Matthew J.,Kang Huining,Zhu Yiliang,Lan Qing,Sood Akshay,Belinsky Steven A.

Abstract

Abstract Background The role of wood smoke (WS) exposure in the etiology of chronic obstructive pulmonary disease (COPD), lung cancer (LC), and mortality remains elusive in adults from countries with low ambient levels of combustion-emitted particulate matter. This study aims to delineate the impact of WS exposure on lung health and mortality in adults age 40 and older who ever smoked. Methods We assessed health impact of self-reported “ever WS exposure for over a year” in the Lovelace Smokers Cohort using both objective measures (i.e., lung function decline, LC incidence, and deaths) and two health related quality-of-life questionnaires (i.e., lung disease-specific St. George's Respiratory Questionnaire [SGRQ] and the generic 36-item short-form health survey). Results Compared to subjects without WS exposure, subjects with WS exposure had a more rapid decline of FEV1 (− 4.3 ml/s, P = 0.025) and FEV1/FVC ratio (− 0.093%, P = 0.015), but not of FVC (− 2.4 ml, P = 0.30). Age modified the impacts of WS exposure on lung function decline. WS exposure impaired all health domains with the increase in SGRQ scores exceeding the minimal clinically important difference. WS exposure increased hazard for incidence of LC and death of all-cause, cardiopulmonary diseases, and cancers by > 50% and shortened the lifespan by 3.5 year. We found no evidence for differential misclassification or confounding from socioeconomic status for the health effects of WS exposure. Conclusions We identified epidemiological evidence supporting WS exposure as an independent etiological factor for the development of COPD through accelerating lung function decline in an obstructive pattern. Time-to-event analyses of LC incidence and cancer-specific mortality provide human evidence supporting the carcinogenicity of WS exposure.

Funder

National Institute of General Medical Sciences

National Cancer Institute

National Cancer Institute, United States

Publisher

Springer Science and Business Media LLC

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