Citation:

Nguyen, H., M. Moore, M. Schladweiler, W. Williams, L. Strader, G. Klinefelter, P. Evansky, Yong Ho Kim, Matthew Gilmour, J. Dye, AND C. Miller. Paternal Eucalyptus Smoke Exposure Alters Metabolic Responses to Heat in Offspring. Society of Toxicology, Nashville, TN, March 19 - 23, 2023.

Impact/Purpose:

Considering the expected increase in frequency and intensity of wildfire events, the objective of this study was to determine whether paternal smoke exposure alters metabolism in offspring exposed to heat, a prototypic metabolic stressor.

Description:

Paternal exposures to environmental stressors may program offspring susceptibility to metabolic deficits, in part, through epigenetic germ cell alterations. We have recently demonstrated that laboratory-generated wildfire smoke alters sperm motility and non-coding sperm RNAs. Considering the expected increase in frequency and intensity of wildfire events, the objective of this study was to determine whether paternal smoke exposure alters metabolism in offspring exposed to heat, a prototypic metabolic stressor. 14-week-old male Long-Evans rats were episodically exposed to either filtered air (FA) or eucalyptus smoke (WF; 4-5 mg/m3 PM, 10 ppm CO) for 1 hour/day over 2 weeks during sperm maturation. 24 hours following the final exposure, male rats were bred with estrus-synchronized female rats. Resulting offspring were litter-standardized on postnatal day (PND) 4 and weaned on PND 19. At approximately 5-months-old, offspring were exposed to either standard vivarium housing temperature (N; 72oF) or heat (H; 78oF) for 2 weeks. Offspring were then euthanized, and serum was collected for further assessments. Results revealed no significant differences in final rectal temperature, despite increased surface body temperature in both heat-exposed males and females. Individual pre- and post-heat exposure body weights were also not significantly different between groups. Body weight gain, however, was significantly reduced by 31% in WFH males compared to FAN controls after 1 week and was near significance at 2 weeks (p = 0.08). Furthermore, serum glucose levels were significantly higher in FAH (20%) and WFH (10%) males compared to FAN controls, suggesting that heat alone impacted offspring glucose metabolism. Serum low-density lipoprotein cholesterol, a marker of dyslipidemia, was 59% higher in WFH compared to FAN controls. Females showed no significant differences in body weight gain or serum clinical chemistry endpoints, regardless of paternal exposure or temperature condition. In summary, paternal smoke exposure resulted in sex-specific metabolic alterations in offspring exposed to heat. Our data suggest that paternal exposure to air pollutants may program metabolic risk related to additional postnatal stressors. Abstract does not reflect U.S. EPA policy.

Record Details: