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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. 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-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), as well as reactive oxygen species (ROS), NADPH activity and its subunits p22/47/67phox &amp; gp91phox were measured. During the exposure period, the mean daily concentration of PM2.5 was 59.2 ± 1.0 μg/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 &lt; 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 &lt; 0.05), 6 months (218 ± 6 vs 193 ± 7 mmHg, p &lt; 0.01), 9 months (222 ± 6 vs 203 ± 8 mmHg, p &lt; 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-α in the exposed group. Furthermore, PM2.5 significantly increased NOX activity and protein levels of gp91phox and p22/47/67phox. 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.

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