Abstract Body (Do not enter title and authors here): Background: Cardiovascular disease (CVD) remains the leading cause of death in the U.S., with major influence by environmental factors (Particulate Matter PM_2.5 exposure), and psychosocial stress. These factors converge on shared biological pathways, including direct particle translocation, systemic inflammation, and oxidative stress, ultimately impacting cardiovascular and behavioral outcomes such as anxiety-like behavior and the hypothalamic-pituitary-adrenal (HPA) axis activation. Hypothesis: PM_2.5 or psychosocial stress exposures can both have significant effects on the cardiovascular system. Methods: Male C57BL/6 mice were exposed to filtered air (FA) or PM ≤2.5 μm at concentrations of 34.85 μg/m³ for six hours/day, five days/week for three weeks. Mice underwent 10 minutes of physical interaction with a retired FVB breeder, followed by 18 hours of sensory (non-physical) contact (SDSI) for 10 days. For the Daily Restraint (DR) group, mice were placed in perforated conical tubes for 2 hours over 7 days. Data was analyzed using one-way ANOVA with significance set at p<0.05. Results: DR exposure significantly increased corticosterone levels (p<0.0001). Tail-cuff measurements exhibited a statistically significant reduction in both systolic and diastolic blood pressure for the DR group (p<0.05). Echocardiography revealed that left ventricular mass was significantly increased for the SDSI and DR groups. Ejection Fraction and Fractional Shortening were both significantly increased from the DR exposure (p<0.05). Pressure-volume (PV) loop analyses demonstrated that SDSI exposure caused an increase in the End-diastolic PV-relationship (p<0.05). Functional analyses of isolated cardiac myocytes revealed that PM_2.5 and DR groups exhibited reduced contraction velocity under isoproterenol stimulation compared to FA (p<0.05). Additionally, these groups showed increased relaxation velocity under the same conditions (p<0.05). Conclusion: Chronic stress induced a compensatory cardiac response, marked by increased LV mass, elevated systolic function, and reduced blood pressure. Moreover, isolated cardiomyocytes showed impaired β-adrenergic contractility and relaxation. Elevated circulating corticosterone levels further indicate HPA axis activation; therefore, PM_2.5 could also be considered a stressor. These findings suggest that early maladaptive remodeling occurs in the heart under chronic stress, highlighting its potential role in increasing long-term risk for CVD.