Differences in cellular and molecular processes in exposure to PM2.5 and O3

Epidemiological and toxicological studies have shown that PM_2.5 and O₃ could pose significant risks to human health, such as an increased incidence of respiratory and cardiovascular diseases. Usually, the adverse health outcomes induced by PM_2.5 and O₃ exposure are similar. However, PM_2.5 and O₃ have distinct physical and chemical properties, with PM_2.5 being a solid-liquid mixture and O₃ being a strongly oxidizing gaseous pollutant. Therefore, we speculated that there are some differences in biological processes induced by PM_2.5 and O₃ exposure. In the present study, we investigated the differences induced by PM_2.5 and O₃ exposure from the perspective of cellular and molecular processes. Firstly, the pulmonary epithelial cells (BEAS-2B) were exposed to different concentrations of PM_2.5 or O₃ at different durations. Then, we chose experimental models with the concentrations and duration at which the cell survival rate was 50 % after exposure to PM_2.5 and O₃, which were 100 μg/mL for 24 h for PM_2.5, and 200 ppb for 4 h for O₃. Our findings indicate that PM_2.5 infiltrates cells via endocytosis without causing significant damage to cell membranes, while O₃ induces lipid peroxidation at the cell surface. Moreover, the detection of mitochondrial function showed that the content of ATP was significantly reduced after exposure to both PM_2.5 and O₃. However, we found a significant difference in mtDNA copy number. PM_2.5 exposure increased the mtDNA copy number by up-regulating the expression of fission genes (Fis1, Mff, Dnm1). O₃ exposure decreased it by up-regulating the expression of fusion gene (Mfn1, Mfn2) and down-regulating the expression of fission gene (Fis1, Dnm1). These results indicate that although both PM_2.5 and O₃ exposure induced almost exactly similar adverse health outcomes, significant differences do exist in cellular and molecular processes.