Poster Presentation ESA-SRB-ANZBMS 2024 in conjunction with ENSA

PFAS Exposure and its Impacts on the Placenta and on Offspring development; Who is to Blame, Mum or Dad?   (#489)

Leah Calvert 1 2 , Amanda L Anderson 1 2 , Ilana R Berntstein 1 2 , Natalie A Trigg 3 , John Schjenken 1 2 , Shaun Roman 4 , Brett Nixon 1 2 , Jacinta Martin 1 2
  1. The University of Newcastle, Callaghan, NSW, Australia
  2. Infertility and Reproduction Program, Hunter Medical Research Institute, New Lambton Heights, Newcastle, NSW 2305, Australia, Newcastle, NSW
  3. Division of Neonatology, Children’s Hospital of Philadelphia., Philadelphia, PA, USA
  4. NSW Health Pathology, Newcastle, NSW, Australia

Per- and polyfluoroalkyl substances (PFAS) are a diverse family of fluorinated organic chemicals that were used widely in consumer products and industrial applications for many years. Given their widespread use and chemical stability, PFAS are now considered ubiquitously persistent environmental contaminants. Once absorbed into the body, PFAS bioaccumulate and take many years to be excreted. Concerningly epidemiological studies now identify associations between PFAS exposure and numerous adverse perinatal health outcomes.
To define the influence of parental PFAS exposure on these perinatal effects, we generated two models. The first model explored the consequences of a 12-week paternal PFAS exposure prior to conception. To ensure this model was reflective of human exposure, PFAS pups continued to receive PFAS via their mother for the duration of gestation. This model revealed that combination paternal and maternal PFAS exposure led to significant consequences for offspring at 17.5 days gestation. Specifically, these fetuses were heavier and their placentae smaller than their control counterparts. These data were indicative of an increased placental efficiency which is likely attributable to the observed increased in junctional area of these PFAS placenta. Additional, measurement of the fetuses also revealed that PFAS offspring (both sexes) had an increased crown-rump length and co-concomitant increase in stomach girth (female only), reflective of fetal growth restriction and a brain sparing phenotype. In our second study, only adult females were exposed to PFAS during gestation after mating with previously unexposed males. Here, at 17.5 days none of those aforementioned phenotypes were evident. These data indicate that paternal and maternal PFAS exposure has differential effects on offspring outcomes, adding critical new understanding about the effects of parental PFAS exposure on offspring health and development. Our future studies will focus on examining the longer-term consequences of these effects after birth.