Tobacco smoke exposure and mitochondrial DNA copy number on neurobehavioural performance: A community study

被引：2

作者：

Wang, Huimin ^{[1
]}

Fu, Mengmeng ^{[1
]}

Ma, Yifei ^{[1
]}

Liu, Chenjuan ^{[1
]}

Wu, Min ^{[1
]}

Nie, Jisheng ^{[1
]}

机构：

[1] Shanxi Med Univ, Sch Publ Hlth, Dept Occupat Hlth, Taiyuan 030001, Shanxi, Peoples R China

来源：

ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH | 2022年 / 29卷 / 56期

基金：

中国国家自然科学基金;

关键词：

Tobacco smoke; Neurological performance; Mitochondrial DNA copy number; COGNITIVE IMPAIRMENT; ALZHEIMERS-DISEASE; CIGARETTE-SMOKING; OXIDATIVE STRESS; RISK-FACTORS; COTININE; ASSOCIATION; ALCOHOL; CONSUMPTION; DYSFUNCTION;

D O I：

10.1007/s11356-022-20921-8

中图分类号：

X [环境科学、安全科学];

学科分类号：

08 ; 0830 ;

摘要：

The influence of tobacco smoke has been a controversial and very questionable subject within the field of neurological behaviours. To examine the dose-response relationships between tobacco smoke and neurological performance, we investigated whether mitochondrial DNA copy number (mtDNAcn) mediates these relationships. We used restricted cubic spline models to estimate the dose-response relationships. A mediation model was also used to detect the mediating effect. Increased cotinine was negatively associated with auditory memory scores and a 0.51 decrease in mtDNAcn. MtDNAcn acts as a mediator between cotinine and auditory memory. Tobacco smoke levels were inversely associated with mtDNAcn and neurobehavioural changes, and there was a mediation effect between cotinine levels and auditory memory by mtDNAcn.

引用

页码：84180 / 84190

页数：11

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