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American Heart Association

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Final ID: Mon035

Pre-conception Particulate Matter Exposure Causes Cardiac and Metabolic Phenotype in Female Offspring

Abstract Body: Introduction: Parental exposure to particulate matter (PM) represents a critical window influencing health outcomes in offspring. While the effects on male progeny are better characterized, whether a similar phenotype occurs in females remains under explored. Therefore, we investigated disease inheritance in female offspring and hypothesized a phenotype like that previously shown in males. Methods: Parent FVB sire and dam mice were exposed to either filtered air (FA) or PM with an aerodynamic diameter <2.5 in (PM2.5) for 6 h/day (avg of 36.0 μg/m3), 5 d/week for 3 months. Following exposure, mice were bred to produce female FAsFAd(both sire and dam exposure to FA) and PMsPMd (both sire and dam exposed to PM). Cardiovascular and metabolic health were measured at 18, 30, and 46 weeks via echocardiography, tail cuff plethysmography, and glucose tolerance testing (GTT). Lung mechanics (Flexivent) and cardiac pressure-volume (PV) loops were performed following 46-week measurements. Data were analyzed using mixed model analyses with comparisons between exposure and time via Sidak’s test. Significance was set at p<0.05. Results: Female PMsPMd left ventricle diastolic volume and diameter were elevated at 18 (both p=0.08) and 46 weeks (p=0.03). Ejection fraction (EF) and fractional shortening (FS) revealed transient deficits at 30 weeks (both p<0.01) which may have been influenced by reduced n at 46 weeks (n=3). Transient reductions at 18 weeks were also detected in blood pressures (all p<0.05) and GTT (AUC p=0.01) in PMsPMd. PV loop analysis revealed PMsPMd operating pressures did not differ (Ped and Pes, both p>0.05) despite an increased end-diastolic volume (p<0.01) and supported by reduced contractility (Ees) compared to FAsFAd (p=0.01). Conclusion: By limiting PM2.5 exposure to sire and dam prior to conception, an altered cardiac and metabolic phenotype was present in female offspring. Together with previous evidence in males, these data suggest potential for an epigenetically regulated pattern of disease that appears independent of sex.
  • Mohler, Eleanor  ( The Ohio State University , Powell , Ohio , United States )
  • Gibson, Brandon  ( Ohio State University , Grove City , Ohio , United States )
  • Gallego Perez, Mariana  ( The Ohio State University , Columbus , Ohio , United States )
  • Saldana, Sierra  ( The Ohio State University , Powell , Ohio , United States )
  • Citek, Noah  ( The Ohio State University , Columbus , Ohio , United States )
  • Schweiterman, Neill  ( The Ohio State University , Powell , Ohio , United States )
  • Saldana, Ty  ( The Ohio State University , Columbus , Ohio , United States )
  • Hookfin, Harrison  ( The Ohio State University , Powell , Ohio , United States )
  • Miller, Roy  ( The Ohio State University , Columbus , Ohio , United States )
  • Gorr, Matthew  ( The Ohio State University , Columbus , Ohio , United States )
  • Falvo, Michael  ( VA , East Orange , New Jersey , United States )
  • Wold, Loren  ( THE OHIO STATE UNIVERSITY , Columbus , Ohio , United States )
  • Author Disclosures:
Meeting Info:

Basic Cardiovascular Sciences 2026

2026

Boston, Massachusetts

Session Info:

Poster Session 1

Monday, 07/13/2026 , 04:30PM - 07:00PM

Poster Session and Reception

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