E-Poster Presentation ESA-SRB-ANZBMS 2021

Long-term exposure of mice to 890 ppm atmospheric CO2 increases birth weight, modifies growth trajectories, and alters behaviour in young adulthood (#570)

Caitlin S Wyrwoll 1 , Melissa Papini 1 , Emily Chivers 2 , Alexander Larcombe 2
  1. The University of Western Australia, Nedlands, WA, Australia
  2. Telethon Kids, Perth, WA, Australia

Atmospheric carbon dioxide (CO2) levels are currently at 418 parts per million (ppm), and by 2100 may exceed 900 ppm. The biological effects of lifetime exposure to CO2 at these levels is unknown. We have previously shown that mouse lung function is altered by long-term exposure to 890 ppm CO2. Here, we assess the effects of exposure on pregnancy parameters, postnatal growth, and broader systemic responses to this exposure. Mice were exposed to either 460 ppm or 890 ppm from preconception to 3 months of age, and assessed for effects on maternal weight gain, litter size, sex ratio, birth weight, and postnatal growth. As young adults, renal and osteological parameters, locomotion, memory, learning, and anxiety-like behaviours were assessed. Exposure to 890 ppm CO2 increased birthweight by 15% (p<0.05) in comparison to controls but did not alter any other pregnancy outcomes.  From postnatal day 7 onwards, there were no differences in body weight until after weaning when female body weight was decreased by exposure to 890 ppm CO2. As young adults, life-long exposure to 890 ppm CO2 resulted in reduced engagement in memory/learning tasks, and hyperactivity in both sexes in comparison to controls. There were no clear anxiety, learning, or memory changes. Renal and osteological parameters were minimally affected. Overall, this study shows that exposure of mice to 890 ppm CO2 from preconception to young adulthood increases birthweight, alters growth and some behaviours, with limited evidence of compensatory changes in acid-base balance. The increased birth weight due to elevated CO2 exposure during conception and pregnancy were unexpected. The drivers of this change may be due to alterations in maternal adaptations to CO2 and/or placental function. These findings highlight the potential for a direct effect of increased atmospheric CO2 on mammalian health outcomes.