Influence of different concentrations of ozone on the alteration of mitochondrial DNA copy numbers in human peripheral blood

By now, O3 pollution has become a main environmental problem. O3 is a prevalent risk factor for many diseases, but the regulatory factors linking O3 and diseases remain ambiguous. Mitochondrial DNA (mtDNA) is the genetic material in mitochondria, which plays a key role in the production of respiratory ATP. Due to a lack of histone protection, mtDNA is easily damaged by ROS, and O3 is an important source to stimulate the production of endogenous ROS in vivo. Therefore, we logically speculate that O3 exposure can alter mtDNA copy number by the induction of ROS. In the present study, we performed a panel study of 65 MSc students at the Chinese research academy of environmental sciences (CRAES) with 3 rounds of follow-up visits from August 2021 to January 2022. We examined the mtDNA copy numbers in the peripheral blood of subjects using quantitative polymerase chain reaction. Linear mixed-effect (LME) model and stratified analysis were used to investigate the association between O3 exposure and mtDNA copy numbers. We found a dynamic process of the association between the concentration of O3 exposure and the mtDNA copy number in the peripheral blood. The lower concentration of O3 exposure did not affect the mtDNA copy number. As the concentration of O3 exposure increased, the mtDNA copy number also increased. While, when O3 exposure reached a certain concentration, a decrease in mtDNA copy number was found. This correlation between the concentration of O3 and the mtDNA copy number could be ascribed to the severity of cellular damage induced by O3 exposure. Our results provide a new perspective for the discovery of a biomarker of O3 exposure and health response, as well as for the prevention and treatment of adverse health effects caused by different concentrations of O3.