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

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.