Effects of ozone and fine particulate matter (PM2.5) on rat system inflammation and cardiac function

In order to understand the toxic mechanisms of cardiovascular system injuries induced by ambient PM_2.5 and/or ozone, a subacute toxicological animal experiment was designed with exposure twice a week for 3 continuous weeks. Wistar rats were randomly categorized into 8 groups (n = 6): 1 control group, 3 groups exposed to fine particulate matters (PM_2.5) alone at 3 doses (0.2, 0.8, or 3.2 mg/rat), 1 group to ozone (0.81 ppm) alone and 3 groups to ozone plus PM_2.5 at 3 doses (0.2, 0.8, or 3.2 mg/rat). Heart rate (HR) and electrocardiogram (ECG) was monitored at approximately 24-h both after the 3rd exposure and the last (6th) exposure, and systolic blood pressure (SBP) was monitored at approximately 24-h after the 6th exposure. Biomarkers of systemic inflammation and injuries (CRP, IL-6, LDH, CK), heart oxidative stress (MDA, SOD) and endothelial function (ET-1, VEGF) were analyzed after the 6th exposure. Additionally, myocardial ultrastructural alterations were observed under transmission electron microscopy (TEM) for histopathological analyses. Results showed that PM_2.5 alone exposure could trigger the significant increase of CRP, MDA, CK, ET-1 and SBP and decrease of heart rate variability (HRV), a marker of cardiac autonomic nervous system (ANS) function. Ozone alone exposure in rats did not show significant alterations in any indicators. Ozone plus PM_2.5 exposure, however, induced CRP, IL-6, CK, LDH and MDA increase, SOD and HRV decrease significantly in a dose–response way. Meanwhile, abnormal ECG types were monitored in rats exposed to PM_2.5 with and without ozone and obvious myocardial ultrastructural changes were observed by TEM. In conclusion, PM_2.5 alone exposure could cause inflammation, endothelial function and ANS injuries, and ozone potentiated these effects induced by PM_2.5.