Follow-up study on mitochondrial DNA copy number in workers exposed to low concentration benzene in China

Objective To explore the changes of the mitochondrial DNA copy number in workers exposed to low concentration benzene and the factors associated with such change.

Methods A total of 150 workers exposed to low concentration of benzene in a chemical plant in Shanghai were studied, and the mitochondrial DNA copy number for the indicators of oxidative stress were measured twice in a follow-up study during year 2018 and 2019. The repeated measurement analysis and generalized estimation model were used to investigate the changes of the mitochondrial DNA copy number and the relationship between the mitochondrial DNA copy number and low concentration of benzene exposure in the working environment.

Results The median of benzene exposure concentration level of the workers was 0.46 mg/m³, the 25th percentile was 0.14 mg/m³, and the 75th percentile was 0.50 mg/m³. Compared with the relative mitochondrial DNA copy number of workers exposed to benzene in 2018 (5.79±0.84), the relative mitochondrial DNA copy number in 2019 (4.66±0.58) was significantly lower (P < 0.01). The results of repeated measurement ANOVA showed that the relative mitochondrial DNA copy number of workers with different exposure concentrations was significantly different(P < 0.05);the mitochondrial DNA copy number observed at these two years was not the same, and the difference was statistically significant (P < 0.05). The results of generalized estimation model analysis showed that compared with high exposure group, the relative mitochondrial DNA copy number of workers exposed to medium concentration group decreased by 0.25 (P < 0.05). No effect of employment time in this plant, age, smoking and drinking habits on relative mitochondrial DNA copy number was found.

Conclusions In the workplaces with the concentration of benzene lower than the current occupational exposure limits in China, it can still observed the change of the relative copy number of mitochondrial DNA among these workers, suggesting that low occupational benzene exposure may lead to oxidative stress and mitochondrial damage, and its mechanism needs further study.