Alterations to gastrointestinal bacterial communities have been linked to the exacerbation of numerous diseases, including Alzheimer’s Disease (AD), via changes to bacterial‐derived metabolites. Community changes can result from antibiotic use, dietary changes, psychosocial stress, and possibly air particulate matter exposure. Previous studies from our group demonstrated that a transgenic mouse model predisposed to create amyloid‐β fibers similar to AD, namely APP/PS1 mice, exposed to air particulate matter (PM) led to significant increases in hippocampal amyloid‐β1‐40 (Aβ) and Aβ1‐42, as well as astrocytosis, microgliosis, and proinflammatory cytokines in the temporal cortex as compared to PM‐exposed non‐carrier mice. Such findings indicate the presence of PM2.5‐induced neuroinflammation in APP/PS1 mice; however, the mechanism by which this occurs is unknown. Recent data demonstrates PM‐induced alterations to the gut microbiome, prompting us to test the hypothesis that disruptions of microbial‐derived metabolites are present in PM‐exposed APP/PS1 mice. To test this hypothesis, APP/PS1 and non‐carrier, littermate wild type (WT) mice were exposed to filtered air (FA) or PM for 5 days/week, 6 hours/day, for 3 months. The average daily PM exposure is 90.0 μg/m3, which is a 5‐fold concentration above the ambient mean daily PM2.5 concentration (18.8 ±11.4 μg/m3) at the study site in Columbus, OH. At the end of the 3‐month exposure, fecal samples were collected to assess bacterial byproducts, i.e. short chain fatty acids (SCFAs), by gas chromatography/mass spectrometry. Serum samples were collected to characterize additional metabolites including the bacterial metabolite trimethylamine (TMA) by liquid chromatography/mass spectrometry. Results demonstrated that SCFA butyric acid was significantly reduced by PM‐exposure in both APP/PS1 and WT animals as compared to their FA‐exposed counterparts (p<0.01) and propionic acid was significantly increased in FA‐exposed APP/PS1 mice as compared to their WT counterparts (p<0.0001). Serum metabolite analyses revealed distinct principal component patterns among groups, demonstrating unique metabolic profiles associated with exposure and genotype. One such metabolite, TMA, was significantly increased by PM‐exposure (p<0.05). Taken together, these findings indicate that airborne particulate matter exposure alters metabolic profiles in a transgenic mouse model of AD.