Enhanced Cerebral Microbleeds by Long-Term Air Pollution Exposure in Spontaneously Hypertensive Rats

Background Cerebral microbleeds (CMBs) are associated with a high risk for stroke . The present study determined whether long-term exposure to PM2.5 results in progressive worsening of CMBs and induction of systemic inflammation and microvascular oxidative stress. Methods Sixteen male Spontaneously hypertensive rats (SHR) and eight Wistar-Kyoto (WKY) rats were exposed to either filtered air or PM2.5 for 12 months. To detect CMBs, rats were imaged using a 7-T MRI. To determine systemic inflammation and oxidative stress, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), monocyte chemoattractant protein-1 (MCP-1), as well as reactive oxygen species (ROS), NADPH activity and its subunits p22/47/67phox & gp91phox were measured. Results During the exposure period, the mean daily concentration of PM2.5 was 59.2 +/- 1.0 mu g/m(3). PM2.5 exposure significantly increased the incidence of CMBs compared to the PM2.5 (-) group (37.5% vs 12.5% incidence rate, p < 0.001). Animals exposed to PM2.5 also had significantly increased systolic blood pressures (SBPs) at 3 months (173 +/- 5 vs 157 +/- 5 mmHg, p < 0.05), 6 months (218 +/- 6 vs 193 +/- 7 mmHg, p < 0.01), 9 months (222 +/- 6 vs 203 +/- 8 mmHg, p < 0.05), and 12 months (231 +/- 4 vs 207 +/- 5 mmHg, p = 0.01). Additionally, there were significant elevations in IL-6, MCP-1, and TNF-alpha in the exposed group. Furthermore, PM2.5 significantly increased NOX activity and protein levels of gp91phox and p22/47/67phox. Conclusion In the SHR model, long-term exposure to PM2.5 worsened CMBs, increased SBPs, induced systemic inflammation and oxidative stress. Therefore, PM2.5 is potentially a controllable risk factor that promotes CMBs in certain patients, such as those with hypertension.

Automated summary

In the SHR model, long-term exposure to PM2.5 worsened CMBs, increased SBPs, induced systemic inflammation and oxidative stress. PM2.5 is potentially a controllable risk factor that promotes CMBs in certain patients, such as those with hypertension.