期刊
ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
卷 29, 期 56, 页码 84180-84190出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s11356-022-20921-8
关键词
Tobacco smoke; Neurological performance; Mitochondrial DNA copy number
资金
- National Natural Science Foundation of China [81673143, 81072279, 30800899]
- Shanxi Province Natural Science Foundation [2010021034-3, 2015011128]
- Shanxi Scholarship Council [2016-057]
This study investigates the dose-response relationships between tobacco smoke and neurological performance, and finds that mtDNAcn acts as a mediator between cotinine levels and auditory memory, indicating a negative impact of tobacco smoke on neurobehavioral changes.
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.
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