Chronic Inhalation of Ultrafine Particulate Matter Results in a Peripartum Cardiomyopathy-like Phenotype in Pregnant Sprague Dawley Rats

Peripartum Cardiomyopathy (PPCM) is a leading cause of maternal death world-wide. It is diagnosed in the last month of pregnancy or 6 months after delivery as left ventricle systolic dysfunction, including significant (10 - 20%) reductions in ejection fraction and fractional shortening (-10%). While there is an association between particulate matter (PM) exposure and poor maternal cardiovascular health, little work has been done to elucidate PM’s role in the development of pregnancy-specific cardiovascular diseases like PPCM. Therefore, the purpose of this study was to characterize maternal cardiac structure and function and the risk of developing PPCM after gestational inhalation of nano-titanium dioxide (TiO 2 ), a surrogate for ultrafine PM. Using our custom whole-body rodent inhalation facility (IEStechno, Morgantown, WV), we exposed pregnant Sprague Dawley rats to nano-TiO 2 powder (Aeroxide, Parsippany, NJ) from gestational day (GD) 5 – GD 19 to occupationally-relevant concentrations of nano-TiO 2 (9.72 mg/m 3 ± 1.83). On GD 20, maternal heart structure and function were evaluated by cardiac ultrasound and morphometric analysis. Ultrasound of the maternal heart revealed significantly increased left ventricle mass (+22%) and length (+7%). Likewise, morphometric analysis revealed an enlargement of the left ventricle (97%), suggesting left ventricle dilation. Functionally, we identified left ventricle systolic dysfunction, reminiscent of the human PPCM phenotype, including clinically significant reductions in left ventricle ejection fraction (-10%) and fractional shortening (-14%).Overall, data demonstrates the development of a PPCM-like phenotype suggesting that gestational inhalation of PM may be a risk factor for disease development and/or progression. Future studies will aim to investigate the relationship between PM exposure and pregnancy driven hormonal changes in environmentally-induced PPCM to identify clinical biomarkers and therapeutic targets. Supported by: R01-ES-031285, P30-ES-005022, T32-ES-007148, Bristol Myers Squibb Fellowship, and Grover Foundation This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.