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This study characterized the joint effects of nPM (diameter\u2009\u2264\u2009200\u2009nm) and CCH secondary to bilateral carotid artery stenosis (BCAS) exposure on neuronal and white matter injury in a murine model. nPM was collected near a highway and re\u2010aerosolized for exposure. Ten\u2010week\u2010old C57BL\/6 male mice were randomized into four groups: filtered air (FA), nPM, FA\u2009+\u2009BCAS, and nPM\u2009+\u2009BCAS. Mice were exposed to FA or nPM for 10\u2009weeks. BCAS surgeries were performed. Markers of inflammation, oxidative stress, and apoptosis were examined. nPM\u2009+\u2009BCAS exposure increased brain hemisphere TNF\u03b1 protein compared to FA. iNOS and HNE immunofluorescence were increased in the corpus callosum and cerebral cortex of nPM\u2009+\u2009BCAS mice compared to FA. While nPM exposure alone did not decrease cortical neuronal cell count, nPM decreased corpus callosum oligodendrocyte cell count. nPM exposure decreased mature oligodendrocyte cell count and increased oligodendrocyte precursor cell count in the corpus callosum. nPM\u2009+\u2009BCAS mice exhibited a 200% increase in cortical neuronal TUNEL staining and a 700% increase in corpus callosum oligodendrocyte TUNEL staining compared to FA. There was a supra\u2010additive interaction between nPM and BCAS on cortical neuronal TUNEL staining (2.6\u00d7 the additive effects of nPM\u2009+\u2009BCAS). nPM\u2009+\u2009BCAS exposure increased apoptosis, neuroinflammation, and oxidative stress in the cerebral cortex and corpus callosum. nPM\u2009+\u2009BCAS exposure increased neuronal apoptosis above the separate responses to each exposure. However, oligodendrocytes in the corpus callosum demonstrated a greater susceptibility to the combined neurotoxic effects of nPM\u2009+\u2009BCAS exposure.<\/jats:p>","DOI":"10.1002\/jnr.25153","type":"journal-article","created":{"date-parts":[[2022,12,4]],"date-time":"2022-12-04T23:40:53Z","timestamp":1670197253000},"page":"384-402","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Particulate matter exposure and chronic cerebral hypoperfusion promote oxidative stress and induce neuronal and oligodendrocyte apoptosis in male mice"],"prefix":"10.1002","volume":"101","author":[{"given":"Krista","family":"Lamorie\u2010Foote","sequence":"first","affiliation":[{"name":"Zilkha Neurogenetic Institute University of Southern California  Los Angeles California USA"},{"name":"Department of Neurological Surgery, Keck School of Medicine University of Southern California  Los Angeles California 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