Air Pollution Particulate Matter Exposure and Chronic Cerebral Hypoperfusion and Measures of White Matter Injury in a Murine Model
Qinghai Liu, Kristina Shkirkova, Krista Lamorie‐Foote, Michelle Connor, Arati Patel, Robin Babadjouni, Mikko T. Huuskonen, Axel Montagne, Hans Baertsch, Hongqiao Zhang, Jiu-Chiuan Chen, Wendy J. Mack, Brian P. Walcott, Berislav V. Zloković, Constantinos Sioutas, Todd E. Morgan, Caleb E. Finch, William J. Mack
Abstract
BACKGROUND: Exposure to ambient air pollution particulate matter (PM) is associated with increased risk of dementia and accelerated cognitive loss. Vascular contributions to cognitive impairment are well recognized. Chronic cerebral hypoperfusion (CCH) promotes neuroinflammation and blood-brain barrier weakening, which may augment neurotoxic effects of PM. OBJECTIVES: ) and CCH secondary to bilateral carotid artery stenosis (BCAS) in a murine model to produce white matter injury. Based on other air pollution interactions, we predicted synergies of nPM with BCAS. METHODS: . Behavioral outcomes, white matter injury, glial cell activation, inflammation, and oxidative stress were assessed. RESULTS: group. DISCUSSION: Our data suggest that nPM and CCH contribute to white matter injury in a synergistic manner in a mouse model. Adverse neurological effects may be aggravated in a susceptible population exposed to air pollution. https://doi.org/10.1289/EHP8792.