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Health Outcomes

From a Life Course Theory Perspective

By Lauren & Lisa

Not only is your child's health affected after they are born, their health is also impacted from your health before and during pregnancy. The biological effects of EDC exposure accumulate over time from general reproductive health to pregnancy-related outcomes. Here we highlight current research on the health outcomes from EDC exposure on women's reproductive health, prenatal development, neonatal development, and childhood outcomes. The purpose behind covering these different stages of life is to emphasize the interconnectedness between the mother and child's level of exposure and potential for adverse health outcomes, justifying the need for more awareness and regulation of EDCs during pregnancy.

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Reproductive

When talking about pregnancy, it is important to first think about how factors prior to conception can influence reproductive health and therefore an individual's ability to have children. Endocrine disrupting chemicals commonly interfere with levels of estrogen and progesterone within the body. This leads to considerable risk for women in terms of fertility as the menstrual cycle is largely dependent on these hormones. For example, Bisphenol A (BPA) and phthalates can both alter the amount of these hormones and how the hormones affect the body. For more information about these specific EDCs and how they work, take a look at our “What are EDCs?” page HERE.

Endometriosis 

One of the effects of these chemicals includes the increased risk for endometriosis. According to the Mayo Clinic, endometriosis is a condition which causes intrauterine tissues to grow outside the uterus in places such as the fallopian tubes and the ovaries (3). This is often very painful for women and can result in significant infertility issues. EDCs are thought to potentially influence the risk of developing this disorder, as it has been seen that in uterine exposure to BPA in mice led to the occurrence of the condition (2). Additionally, one study showed that the average BPA concentrations in women with endometriosis were higher than in women without the condition. Phthalates have also been shown to be positively correlated with the incidence of endometriosis and women with endometriosis have been recorded to have higher levels of phthalates (2). 

Polycystic Ovary Syndrome

Another possible consequence of EDC exposure is the prevalence of Polycystic Ovarian Syndrome (PCOS). PCOS is characterized by an increase in androgen as well as the development of small fluid filled sacs around the ovaries (6). It also increases the risk for development of type 2 diabetes. Many studies have shown a positive correlation between levels of BPA and androgen and that women with PCOS exhibit higher levels of BPA than women without the disorder (2).

Prenatal

EDCs hold the potential to cross the bridge between maternal consequences and effects on fetal development, demonstrated through the detection of EDCs in amniotic fluid, umbilical blood, breast milk, and urine of pregnant individuals (10). In utero, research has illustrated associations between EDC exposure in mothers with fetal changes in DNA structure, placenta structure and function, and gene expression.

The Placenta

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Prenatal Outcomes

Although there are limited studies and conclusions about the effect of maternal EDC exposure on the placenta and prenatal development, here are a few preliminary research findings. BPA may alter early cell growth and cell death rates by changing protein, hormone, and enzyme levels. BPA also has effects on gene expression and DNA methylation,  later impacting growth and metabolism of newborns (9). DNA methylation is an epigenetic effect, meaning that it slightly modifies the DNA and gene expression without changing the sequence. EDC exposure during the first trimester of pregnancy was found to associate with differing maternal and fetal protein levels, resulting in changes to birth weight (5). DES exposure may cause DNA methylation in the fetal genome, but they may not be expressed until a certain period of time, explaining why the adverse health outcomes of DES were found much later in life (10). Phthalates may also alter gene expression in the fetus, impacting the function of important growth factors necessary for placental growth and development (10). 

The placenta is an important contributor to the discussion of EDCs and pregnancy because it serves as the connection between mother and fetus and the fetus’ protective barrier. The placenta facilitates the exchange of nutrients, gases, and waste (10). With intense periods of cellular growth and specialization where hormone levels must be controlled in a homeostatic or balanced environment, fetal development and the placenta lie in a critical window of exposure where EDC changes to hormone homeostasis have drastic effects (10). Additionally, the placenta is believed to have a large impact on diseases based on sex, explaining why EDC exposure during pregnancy may alter newborns’ reproductive anatomy (9). It is unknown still whether EDCs pass through the placental barrier through passive transport (not needing energy) or with specific transport mechanisms (9). Learn more about pregnancy as a critical window of exposure and how EDCs pass through the placental barrier HERE.

Neonatal

One of the most important considerations of EDCs is how their effects are seen in children, especially in newborns. As previously covered, fetuses are susceptible to physiological changes in utero due to exposures during development. Therefore, we can see the effects of EDCs right from birth. For example, there is a large amount of evidence suggesting that EDCs are correlated with physical abnormalities of the reproductive organs, altered hormone physiology as well as various adverse birth outcomes.

Reproductive Anatomy

Hormones

Birth Outcomes

One of the most common known effects of EDCs is the distortion of normal reproductive physiology. EDCs seem to target reproductive organs, and their effects on neonates are no different. Various studies have shown that phthalates are negatively correlated with penile size and maldevelopment (1). Alterations to general physiological traits can lead to more serious issues with infertility. 

As we know, EDCs affect how your body responds to hormones. This means that they can affect the way in which various glands function within a neonate and how their bodies produce hormones. For example, it has been found that EDCs such as organochlorine polyfluoroalkyl substances (PFAS) have been negatively associated with the amount of the thyroid hormone thyroxine or T4 produced (8). This hormone is very important to many physiological processes such as metabolism and reproduction therefore the abnormally low levels could cause developmental difficulties for the neonate. 

Since EDCs affect the fetus while in utero, there are various birth outcomes that can be influenced by the levels of exposure. The most common birth outcomes include small birth weights as well as the neonate being small for gestational age (4). Many different EDCs have been noted to have these effects such as metals, but also the general mixture of various EDCs can also cause these birth outcomes. Read more about this “cocktail” effect HERE. Unfortunately, EDCs have also been associated with extreme birth outcomes such as spontaneous abortions and stillbirths (7).

Childhood

We’ve already covered how EDCs can impact mothers’ reproductive health and cross the placental barrier to affect prenatal and neonatal development. As your baby grows up, EDCs continue to create long-term consequences in offspring through childhood into adulthood. Recent literature illustrates how the combination of in utero and childhood exposures generate outcomes in three main areas of health: reproductive, neurocognitive, and metabolic.

Reproductive

Literature focuses on male reproductive health in particular, observing abnormal growth of reproductive organs, low sperm count, and increased risk of testicular cancer due to the estrogen-mimicking effects of EDCs (11).

Neurocognitive

Function of the thyroid hormone system is crucial to the neurodevelopment of the offspring, especially to the central nervous system. Therefore, disruption to the mother’s thyroid hormone levels or transference of thyroid hormones via the placenta may alter normal neurocognitive development. Associations between EDC exposure and thyroid hormone levels have been found to increase risk of ADHD, anxiety, and depression (12).

Metabolic

From mice studies, researchers found that EDC exposure in pregnant mothers contributed to inflammation of adipose (fat) tissue and risks of metabolic disorders that could lead to obesity in offspring (13).

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