# Maternal-Foetal Effects of Exposure to Bisphenol A: Outcomes and Long-Term Consequences
## 5 Maternal-Foetal Effects of BPA  
The Developmental Origins of Health and Disease (DOHaD) theory introduced the concept that maternal diet, environmental stimuli and lifestyle can harm foetus-placental development and promote several diseases in adulthood. In this context, endocrine disruptors such as BPA may play an important role in changes in foetal development [21]. The placenta is not a very effective barrier against EDCs, and exposure in pregnant women is associated with the entry of these compounds into the foetal circulation [21].  
One of the actions of BPA in altering maternal-foetal physiology is related to epigenetic processes. Epigenetics is defined as inherited changes in the phenotype that involve changes in gene expression rather than in the DNA sequence. DNA methylation and acetylation are some of the modifications that modulate the accessibility of DNA to transcription factors and regulatory proteins, altering the structure of chromatin [33]. Early foetal development is particularly sensitive to these mechanisms due to the high rate of DNA synthesis. Epigenetics thus constitute an important means by which the environment and genetics influence foetal development, and BPA has been shown to have the ability to disrupt this homeostasis [33]. In addition to epigenetics as a promoter of maternal-foetal dysfunction,placental morphology is also affected by BPA. The success of pregnancy depends largely on placentation, a process that begins immediately after implantation of the blastocyst in the uterus and continues until a mature placenta is formed with the purpose of mediating physiological communication between the mother and the foetus [34]. As placentation occurs, superfluous, infected, damaged, or dysfunctional cells are eliminated through apoptosis. Therefore, the proliferation, fusion, invasion and apoptosis of trophoblasts are essential in this process. Cytotrophoblasts (CTBs), syncytiotrophoblasts (STBs) and extravillous trophoblasts (EVTs) are the main subtypes of trophoblasts that form the mature placenta [34]. These processes are regulated by transcription factors and signalling pathways. Thus, the presence of BPA can interfere with trophoblastic cells, impairing placentation and pregnancy. The placenta of rats exposed to BPA showed a reduction in its layers and erroneous remodelling of the spiral artery [34].  
These are some of the impacts of BPA on the morphology, the metabolic state of the placenta, and its epigenetic impact on maternal-foetal development. Although these models do not fully reflect human placental conditions in vivo, their use is considered acceptable, as it is unethical to experimentally expose pregnant women to BPA. Thus, epidemiological studies have been a great advantage in understanding the levels of BPA exposure and its effects on both the mother and the foetus. Exposure to BPA has been shown to be harmful to foetal and post-natal development, with possible consequences later in life for both the mother and the baby. The main changes already described in the literature are analysed throughout this section and summarised in Figure 3.