Abstract
In order to understand the toxic mechanisms of cardiovascular system injuries induced by ambient PM2.5 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 (PM2.5) alone at 3 doses (0.2, 0.8, or 3.2mg/rat), 1 group to ozone (0.81ppm) alone and 3 groups to ozone plus PM2.5 at 3 doses (0.2, 0.8, or 3.2mg/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 PM2.5 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 PM2.5 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 PM2.5 with and without ozone and obvious myocardial ultrastructural changes were observed by TEM. In conclusion, PM2.5 alone exposure could cause inflammation, endothelial function and ANS injuries, and ozone potentiated these effects induced by PM2.5.
Published Version
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