Although the mechanisms linking cardiopulmonary diseases to ambient fine particles (PM_2.5) are still unclear, inflammation and oxidative stress play important roles in PM_2.5-induced injury. It is well known that inflammation and oxidative stress could be restricted by vitamin E (Ve) or omega-3 fatty acids (Ω-3 FA) consumption. This study investigated the effects of Ve and Ω-3 FA on PM_2.5-induced inflammation and oxidative stress in vascular endothelial cells. The underlying mechanisms linking PM_2.5 to vascular endothelial injury were also explored. Human umbilical vein endothelial cells (HUVECs) were treated with 50 μg/mL PM_2.5 in the presence or absence of different concentrations of Ve and Ω-3 FA. The inflammatory cytokines and oxidative stress markers were determined. The results showed that Ve induced a significant decrease in PM_2.5-induced inflammation and oxidative stress. Malondialdehyde (MDA) in supernatant and reactive oxygen species (ROS) in cytoplasm decreased by Ve, while the superoxide dismutase (SOD) activity elevated. The inflammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) also reduced by Ve. Moreover, Ω-3 FA played the same role on decreasing the inflammation and oxidative stress. IL-6 and TNF-α expressions were significantly lower in combined Ve with Ω-3 FA than treatment with Ve or Ω-3 FA alone. The Ve and Ω-3 FA intervention might abolish the PM_2.5-induced oxidative stress and inflammation in vascular endothelial cells. There might be an additive effect of these two nutrients in mediating the PM_2.5-induced injury in vascular endothelial cells. The results suggested that inflammation and oxidative stress might be parts of the mechanisms linking PM_2.5 to vascular endothelial injury.

Air pollution causes a great disease burden worldwide. Recent evidences suggested that PM_2.5 contributes to intestinal disease. The objective of present study was to investigate the influence of ambient PM_2.5 on intestinal tissue and microbiome via whole-body inhalation exposure. The results showed that high levels and prolonged periods exposure to concentrated ambient PM_2.5 (CAPM) could destroy the mucous layer of the colon, and significantly alter the mRNA expression of tight junction (Occludin and ZO-1) and inflammation-related (IL-6, IL-10 and IL-1β) genes in the colon, comparing with exposure to the filtered air (FA). The composition of intestinal microbiome at the phylum and genus levels also varied along with the exposure time and PM_2.5 levels. At the phylum level, Bacteroidetes was greatly decreased, while Proteobacteria was increased after exposure to CAPM, comparing with exposure to FA. At the genus level, Clostridium XlVa, Akkermansia and Acetatifactor, were significantly elevated exposure to CAPM, comparing with exposure to FA. Our results also indicated that high levels and prolonged periods exposure to CAPM altered metabolic functional pathways. The correlation analysis showed that the intestinal inflammation was related to the alteration of gut microbiome induced by CAPM exposure, which may be a potential mechanism that elucidates PM_2.5-induced intestinal diseases. These results extend our knowledge on the toxicology and health effects of ambient PM_2.5.

Aim: In this study, we aimed to explore the toxic mechanisms of cardiovascular injuries induced by ambient fine particulate matter (PM_2.5) in atherosclerotic-susceptible ApoE^−/− mice. An acute toxicological animal experiment was designed with PM_2.5 exposure once a day, every other day, for three days. Methods: ApoE^−/− and C57BL/6 mice were randomly categorized into four groups, respectively (n = 6): one control group, three groups exposed to PM_2.5 alone at low-, mid-, and high-dose (3, 10, or 30 mg/kg b.w.). Heart rate (HR) and electrocardiogram (ECG) were monitored before instillation of PM_2.5 and 24 h after the last instillation, respectively. Cardiac function was monitored by echocardiography (Echo) after the last instillation. Biomarkers of systemic oxidative injuries (MDA, SOD), heart oxidative stress (MDA, SOD), and NAD(P)H oxidase subunits (p22phox, p47phox) mRNA and protein expression were analyzed in mice. The results showed that PM_2.5 exposure could trigger the significant increase of MDA, and induce the decrease of heart rate variability (HRV), a marker of cardiac autonomic nervous system (ANS) function with a dose–response manner. Meanwhile, abnormal ECG types were monitored in mice after exposure to PM_2.5. The expression of cytokines related with oxidative injuries, and mRNA and protein expression of NADPH, increased significantly in ApoE^−/− mice in the high-dose group when compared with the dose-matched C57BL6 mice, but no significant difference was observed at Echo. In conclusion, PM_2.5 exposure could cause oxidative and ANS injuries, and ApoE^−/− mice displayed more severe oxidative effects induced by PM_2.5.