Depleted Housing Elicits Cardiopulmonary Dysfunction After a Single Flaming Eucalyptus Wildfire Smoke Exposure in a Sex-Specific Manner in ApoE Knockout Mice

• Published in: Cardiovascular toxicology Vol. 24; no. 9; pp. 852 - 869
• Main Authors: Fiamingo, Michelle, Toler, Sydnie, Lee, Kaleb, Oshiro, Wendy, Krantz, Todd, Evansky, Paul, Davies, David, Gilmour, M. Ian, Farraj, Aimen, Hazari, Mehdi S.
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.09.2024; Springer Nature B.V
• Subjects: Apolipoprotein E; Arteriosclerosis; Atherosclerosis; Biomedical and Life Sciences; Biomedicine; Cardiology; Cardiovascular diseases; Cardiovascular system; Housing; Morbidity; Pharmacology/Toxicology; Phenotypes; Smoke; Social interactions; Ventilatory behavior; Wildfires; Wildfires; Resiliency; Housing; Cardiovascular; Atherosclerosis
• ISSN: 1530-7905; 1559-0259; 1559-0259
• DOI: 10.1007/s12012-024-09897-8

Although it is well established that wildfire smoke exposure can increase cardiovascular morbidity and mortality, the combined effects of non-chemical stressors and wildfire smoke remains understudied. Housing is a non-chemical stressor that is a major determinant of cardiovascular health, however, disparities in neighborhood and social status have exacerbated the cardiovascular health gaps within the United States. Further, pre-existing cardiovascular morbidities, such as atherosclerosis, can worsen the response to wildfire smoke exposures. This represents a potentially hazardous interaction between inadequate housing and stress, cardiovascular morbidities, and worsened responses to wildfire smoke exposures. The purpose of this study was to examine the effects of enriched (EH) versus depleted (DH) housing on pulmonary and cardiovascular responses to a single flaming eucalyptus wildfire smoke (WS) exposure in male and female apolipoprotein E (ApoE) knockout mice, which develop an atherosclerosis-like phenotype. The results of this study show that cardiopulmonary responses to WS exposure occur in a sex-specific manner. EH blunts adverse WS-induced ventilatory responses, specifically an increase in tidal volume (TV), expiratory time (Te), and relaxation time (RT) after a WS exposure, but only in females. EH also blunted an increase in isovolumic relaxation time (IVRT) and the myocardial performance index (MPI) 1-week after exposures, also only in females. Our results suggest that housing alters the cardiovascular response to a single WS exposure, and that DH might cause increased susceptibility to environmental exposures that manifest in altered ventilation patterns and diastolic dysfunction in a sex-specific manner.