BPA fetal exposures affect male and female development and quality of life as adults - Research Paper Example

In essence, early exposure to BPA, as well as other chemicals, especially in the foetal stage signifies an increase in the risk of disease later in life. This paper will examine the impact of BPA in adults following foetal exposure. Health Concerns Some of the risks involved with foetal exposure to BPA include increased risk for prostate cancer in adult men and breast cancer in both women (Okada et al 32). In addition, foetal exposure to BPA results in adverse metabolic changes, early onset of puberty and decreased fertility.

Furthermore, immunological changes are also a major consequence of foetal exposure to BPA (Rubin 30). Whenever foetal exposure to BPA occurs, the chemical infiltrates the body in an active fashion. BPA binds to the body’s oestrogen receptors replicating the functions of oestrogen. Furthermore, in both male and female adults, BPA causes adverse reproductive effects, particularly in populations exposed to BPA due to their occupations. During the initial 11 weeks of gestation, which is a time when most pregnant women are unaware of their pregnancy, the internal communication systems, and organs of the foetus develop quite rapidly, thus are extremely sensitive to external pressures.

Organs such as the brain and mammary glands develop during gestation, thus experience a prolonged period of vulnerability to the effects of BPA, especially since foetal development of such organs is susceptible to oestrogen fluctuations. Additionally, in certain instances, BPA has been shown to cause obesity. When BPA binds to oestrogen receptors in the human body, it causes alternative estrogenic effects, which start outside the nucleus. The alternate path caused by BPA ultimately alters lipid and glucose metabolism, resulting in weight gain (Rubin 31).

This is primarily since the alternative oestrogen receptors trigger pathways that result from exposure to BPA to rework the functions of vital components that play a significant role in metabolism, for instance, adiposities and pancreatic B cells. In a recent study, it was confirmed that foetal exposure to BPA has the capacity to potentiate the systems inherent in the central dopaminergy. This is bound to result in marked super sensitivity to the drugs linked to abuse-induced reward implications.

In essence, by affecting mesolimbic dopamine activity, BPA causes adverse effects such as attention deficits, hypersensitivity and an increased sensitivity to drugs linked to abuse. Furthermore, BPA is also known to bind to receptors of the thyroid hormone, and possibly cause certain side effects on its functions. For instance, BPA impacts triiodothyronine in adults following exposure to the chemical during the prenatal development phase (Rubin 33). Researchers now consider that there are actually two ways through which BPA interrupts the regular endocrine function (Okada et al 32).

The compound can perform as a weak estrogen, which binds to the estrogen receptor. It also can, on the other hand, impede the impact of stronger natural estrogens, restraining estrogen function. They are usually considered performing in the cell nucleus via the estrogen receptors, which control gene expression. Many other ways of BPA action are considered to be related to its biological