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The Consequences of Early Gestational Ozone Exposure On Uterine Arterial Flow And Placental Efficiency In Long-Evans Rats#
Citation:
Miller, C., U. Kodavanti, A. Ledbetter, M. Schladweiler, A. Henriquez, K. Lavrich, D. Freeborn, S. Snow, P. Kodavanti, L. Thompson, A. Farraj, M. Hazari, AND J. Dye. The Consequences of Early Gestational Ozone Exposure On Uterine Arterial Flow And Placental Efficiency In Long-Evans Rats#. Keystone Symposium on Maternal-Fetal Crosstalk: Harmony vs. Conflict, Washington DC, Washington DC, October 04 - 08, 2017.
Impact/Purpose:
Exposure to air pollutants during gestation have been epidemiologically linked to adverse pregnancy outcomes and impaired fetal growth. Despite this, limited experimental evidence exists on the toxicological impacts of ozone in pregnancy and fetal development.
Description:
Exposure to air pollutants during gestation have been epidemiologically linked to adverse pregnancy outcomes and impaired fetal growth. Despite this, limited experimental evidence exists on the toxicological impacts of ozone in pregnancy and fetal development. Pregnant Long-Evans rats were exposed to filtered air or ozone (0.8 ppm) for four hours on gestational days 5 and 6. Uterine arterial blood flow was measured by Doppler ultrasonography on gestational days 15 and 21 and dams were then euthanized on day 21. Various growth parameters in the offspring were examined and markers of mitochondrial health were measured in the placenta. Offspring from dams exposed to ozone in early gestation were growth restricted at gestational day 21. Resistance in the uterine artery was increased as pregnancy advanced in ozone-exposed dams, resulting in reduced blood flow. As a consequence of reduced blood flow to the fetoplacental unit, placental efficiency (as measured by placenta-to-pup weight ratio) was impaired in ozone-exposed pregnancies. Furthermore, mitochondrial number and biogenesis were increased in placentas of both male and female offspring compared to control placentas. Elevated oxygen consumption rate was found in male placentas from ozone-exposed pregnancies. Although this bioenergetic perturbation was not observed in female placentas, ozone-exposed females had evidence of increased autophagy compared to controls. Together these findings show that early ozone exposure in gestation compromises uterine blood flow and energy efficiency of the placenta. Such maladaptations may have likely contributed to the resultant fetal growth restriction as demonstrated in our model. (Does not reflect US EPA policy).