The Science of the total environment · 2025
Associations of volatile organic compounds with accelerated epigenetic aging in the lungs of smokers and electronic cigarette users.
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Khan Ajmal, Richardson Carson, McElroy Joseph P, Singh Amarnath, Weng Daniel Y, Kamel Sahar, Reisinger Sarah A, Wewers Mark D, Shields Peter G, Song Min-Ae
Аннотация
BACKGROUND: Cigarette smoke and electronic cigarettes (EC) contain volatile organic compounds (VOCs) that can irritate the respiratory tract and affect pulmonary health. No studies have reported relationships between VOCs from smokers and EC users and pulmonary cellular behavior, such as lung biological aging.
METHODS: Using urinary total nicotine equivalent (TNE) and propylene glycol, the primarily E-liquid constituent, the tobacco use status of smokers (SM, n = 13), EC users (n = 12), and never-smokers (NS, n = 31) was confirmed. In the lungs of SM and EC, we assessed methylation age (mAge) estimates and cellular senescence-related gene expression. Ten urinary metabolites of VOCs with and without adjusting for nicotine intake, TNE, were associated with mAge estimates and gene expression.
RESULTS: Compared to EC users, SM had a significantly higher level of TNE-adjusted metabolites of acrylonitrile and 1,3-butadiene, while showing a lower level of a metabolite of benzene. TNE-adjusted metabolites of 1,3 butadiene, ethylene oxide, and acrylonitrile were overall positively associated with Pheno-mAge (an epigenetic clock for lifespan/mortality), with different patterns of the associations by smoking group. IFNG and STAT1 showed an overall positive association with TNE-adjusted metabolites of propylene oxide and acrylamide, with a stronger association in SM compared to EC. Without controlling for TNE, a benzene metabolite was the only significant associated with POU5F1.
CONCLUSIONS: This is the first study reporting associations between smoking/EC-related VOCs and lung biological aging with strong associations in SM, supporting the need for further research on the roles of VOCs-related epigenetic aging and cell senescence genes in pulmonary diseases.
METHODS: Using urinary total nicotine equivalent (TNE) and propylene glycol, the primarily E-liquid constituent, the tobacco use status of smokers (SM, n = 13), EC users (n = 12), and never-smokers (NS, n = 31) was confirmed. In the lungs of SM and EC, we assessed methylation age (mAge) estimates and cellular senescence-related gene expression. Ten urinary metabolites of VOCs with and without adjusting for nicotine intake, TNE, were associated with mAge estimates and gene expression.
RESULTS: Compared to EC users, SM had a significantly higher level of TNE-adjusted metabolites of acrylonitrile and 1,3-butadiene, while showing a lower level of a metabolite of benzene. TNE-adjusted metabolites of 1,3 butadiene, ethylene oxide, and acrylonitrile were overall positively associated with Pheno-mAge (an epigenetic clock for lifespan/mortality), with different patterns of the associations by smoking group. IFNG and STAT1 showed an overall positive association with TNE-adjusted metabolites of propylene oxide and acrylamide, with a stronger association in SM compared to EC. Without controlling for TNE, a benzene metabolite was the only significant associated with POU5F1.
CONCLUSIONS: This is the first study reporting associations between smoking/EC-related VOCs and lung biological aging with strong associations in SM, supporting the need for further research on the roles of VOCs-related epigenetic aging and cell senescence genes in pulmonary diseases.