Environmental Disease: Bisphenol A - Literature review Example

Bisphenol A (BPA): Literature review Name: Institution: Bisphenol A (BPA): Literature review Introduction Bisphenol A, also known as BPA, is a chemical compound that is produced in large quantities primarily to be used in the manufacture of epoxy resins and polycarbonate plastics (Ubelacker, 2008; Kroschwitz, n.d). At room temperature, its appearance is white, and it has a placid hospital odor. Polycarbonate plastics are used in the manufacture of specific food and drink packages, including infant and water bottles, medical devices, impact-resistant protection equipment, and compact discs (European Food Safety Authority, 2010). In general, they are clear and hard, and have the letters “PC” or a “7” symbol close to the recycle symbol. On the other hand, epoxy resins are employed as lacquers, which are used in coating metal products, for instance, water supply pipes, bottle tops, and food cans. Bisphenol A-derived substances can also be found in a number of polymers that are used in dental composites or sealants. In the United States, the production of BPA was estimated at around 2.3 billion pounds in 2004 (NTP, 2008). Most of what was produced was used in the production of polycarbonate plastics and resins. Dianin, a Russian scientist, was the first person to synthesize bisphenol A in 1891 (Dianin, 1891; Zincke, 1905). In 1984, the Scientific Committee on Food (SCF) conducted its first evaluation on BPA with regard to its use in plastic articles and materials used together with foodstuffs. In 2002, the SCF re-evaluated the substance using information that had emerged up to 2001. This re-evaluation was based on inclusive studies in rats, which had been exposed to BPA (NTP, 2008). Later in 2006, the European Food Safety Authority (EFSA) used new information to establish a tolerable daily intake of 0.05 mg/kg body weight using findings from studies conducted on rodents (NTP, 2008). Later on in 2008, another study was conducted by AFC Panel on Bisphenol’s toxicokinetics with the help of rats. Bisphenol A was selected for evaluation given that it has elicited a considerable amount of interest in recent times. This is attributed to its extensive human exposures, as well as the anxiety over its effects on reproduction and development as seen in studies involving laboratory animals. BPA has been frequently illustrated as being “faintly” estrogenic from the mid 1930s (NTP, 2008). On the other hand, the emergence of cellular and molecular studies is a sign of the impending supplementary biological activities. These activities range from relations involving cellular elements with unknown biological functions, to those that assist in reconciling the acts of hormones that are non-estrogenic (NTP, 2008). The media has been at the forefront in reporting concerns related to the utilization of bisphenol A in end user products. This was prompted by the action of a number of governments that questioned the safety of BPA, thus forcing several retailers to take away products containing the chemical from the market. A report by Food and Drug Administration (FDA) in 2010 gave rise to additional concerns as regards exposure of young children, infants, and fetuses (Food and Drug Administration, 2010). Canada became the first nation to proclaim that BPA was a toxic chemical in September of the same year (Mittelstaedt, 2010). Routes of Absorption and Modes of Action: Exposures, Outcomes and Toxicity Levels The question on the lips of many people is, “Are people exposed to bisphenol A?” This question has several answers; Yes, most likely, perhaps, probably not, no or even unknown. In this report, we shall examine the yes answer. A good number of people are primarily exposed to bisphenol A through diet (Wilson et al., 2007). In addition, people may also be exposed to BPA via air, dust and water, with the inclusion of skin contact through swimming and bathing. However, the most prevalent source of human exposure remains food and beverages (Chapin et al., 2007; Vandenberg et al., 2007). BPA easily migrates from food and beverages containers, and into food. This happens on containers that are internally coated with epoxy resin, or the containers are made using polycarbonate plastics. Higher temperatures of the liquid accelerate the migration of BPA from polycarbonate containers (Le et al., 2008). BPA has also been discovered in breast milk (Ye et al., 2006). Dental patients can have short-term exposures as a result of application of some dental composites or sealants made from BPA. In addition, workers may also be prone to exposure during the production of BPA or BPA associated products. Human exposure to bisphenol A is usually estimated using two methods (NTP, 2008). These are bio-monitoring and aggregating. Bio-monitoring using breast milk, urine, blood, and other fluids, can be used to estimate the concentration of bisphenol A the total intake of all known and unknown exposure sources. In aggregating, scientists add, or combine, the quantities of BPA that has been detected in food, dust, air, beverage, and water. The bio-monitoring technique is preferred given that all exposure sources are incorporated into the tissue or fluid measurement; hence, there is no need of prior identification (NTP, 2008). Studies on Reproductive Toxicity These studies usually involve evaluation of sperm counts, fertility, cellular growth or damage, and estrous cycling in reproductive tissues. As a result, reproductive toxicity in exposed animals is usually studied during development, or during adulthood, or both (NTP, 2008). Reproductive system and sexual behavior research In 2007, a study using pregnant mice illustrated how bisphenol A altered the appearance of key developmental genes, which formed the uterus. This exposure would affect both the female fetus’ fertility, and the development of the female reproductive tract (science daily, 2007). According to Tyl et al., (2002) and Ema et al., (2001), when the dose levels given to rats is less than 500 mg/kg body weight/day, bisphenol A does not affect the fertility of exposed animals in adulthood or during development. However, NTP (1985) notes that dietary doses exceeding 875 mg/kg body weight/day negatively affects the fertility of exposed adult mice. This is indicated by a reduction in the number of litters. Exposure of rats to high oral dosage levels (not less than 600 mg/kg body weight/day) of BPA led to alteration of estrous cycling in female rats (Yamasaki et al., 2002). Dosage levels of 235 mg/kg body weight/day, led to cellular effects on the male rats’ testes (Takahashi & Oishi, 2001). Another 2009 rodent study was in agreement with the findings that low-dose BPA exposures revealed no effects on a number of behavioral activities and reproductive functions of female rats (Ryan et al., 2010). In another study, exposure to bisphenol A during pregnancy led to a lifelong effect on one gene, which is accountable for development of the uterine, as well as ensuing fertility in both humans and mice. It was therefore advisable to prevent pregnant women from being exposed to BPA given that scientists are not aware of the safe levels of BPA exposure (science daily, 2009). Dose levels, which the NTP defines as being high, have adverse effects on the growth and survival of pup. Kim et al. (2001) and Tyl et al. (2002) report that rats experience a decrease of between 20-30 per cent in the number of pups per litter, in case the maternal dosing was 500 mg/kg body weight/day or more. Pregnant rats that are treated with 1000 mg/kg body weight/day experience increase in post-implantation loss and fetal death (Kim et al., 2001). Rats’ female offspring that were treated orally with 50 mg/kg body weight/day experienced delayed puberty onset (Tinwell et al., 2002). On the other hand, male rats that were treated with 600 mg/kg body weight/day had a 1.8 day delay in puberty (Tyl, Myers & Marr, 2006). Mammary Gland Changes in tissues in the mammary glands occur where rodents are exposed to BPA doses ranging from 0.0025 mg/kg body weight/day to 1 mg/kg body weight/day (Durando et al., 2007). When exposed as adults, BPA does not cause cancer or cellular changes to rats’ and mice’s mammary glands (NTP, 1982). However, when exposed during gestation, lesions may develop during adulthood (Murray et al., 2007). In general, we can note that these discoveries are an interpretation of the indication that developmental exposure to BPA leads to different effects on the maturation process of the stromal and epithelial components in the breast tissues. This may set in motion a tendency for occurrence of diseases later on in life. Obesity Several studies do not provide conclusive results regarding the effects of low doses of BPA on body weight (Chapin et al., 2007). Numerous rats’ and mice’ studies have reported that oral doses ranging from 0.0024 to 1.2 mg/kg body weight/day have increased post-natal growth (Howdeshell et al., 1999; Akingbemi et al., 2004; Rubin et al., 2001). On the other hand, studies by did not detect any noteworthy effect on body weight, while those by Tyl et al. (2002), Negishi et al. (2003), and Talsness et al. (2000) did not report reduction in growth. A study by Rubin and Soto (2009) noted that perinatal bisphenol A exposure exerted unrelenting effects on adiposity and body weight. In view of this fact, Heindel and Vom Saal (2009), suggested that elimination of BPA exposures, in addition to improving nutrition throughout development, offered some possibility of minimizing obesity and related diseases. Sperm Quality and Sperm Count Although several studies have looked into this issue, the results are inconsistent and cannot be easily resolved. According to Tyl et al. (2002) and Tinwell et al. (2002), exposure to high amounts of oral dosages of BPA during young adulthood or development, impacted on the quantity of sperms. When adult male rats were exposed to bisphenol A, their levels of testosterone and sperm count reduced, when compared to that of those males that were unexposed. In another study, it was observed that these exposed mice behaved like their female counterparts, and were demasculinized. This made them less desirable to the female companions (Science Daily, 2011). Neurological issues As noted by National Toxicology Program (NTP) (2007), exposure to BPA has effects on the development and behavior of fetus’ and infant’s brains. In 2008, the National Toxicology Program expressed a number of concerns regarding the effects of BPA on the brain. Richter et al., (2007) argued that low dosages of bisphenol A during development had unrelenting effects on the structure, behavior and function of the brain in mice and rats. In addition, Palanza et al., (2008) stated that maternal exposure to low doses of BPA led to long lasting effects with regard to the neurobehavioral development of mice. When non-human primates were frequently exposed to BPA doses of 50 µg/kg each day, they demonstrated hostile neurological consequences (Leranth et al., 2008). As a result, this research unearthed a relationship between bisphenol A and hindrance with brain cell links that are essential to learning, memory and mood. Thyroid function A study conducted by Zoeller (2007) found out that BPA had the ability to attach to thyroid hormone receptors, and possibly have selective consequences on the receptor’s functions. According to Boas, Main, and Feldt-Rasmussen, (2009), there is need for governing institutions to control the use of thyroid-unsettling chemicals. They add that this should be emphasized particularly in cases where pregnant women, small children and neonates would be susceptible to exposure to the chemical’s agents. Another study by Kashiwagi et al. (2009), showed the adverse effects of bisphenol-A on the action of thyroid hormone. Research on Cancer There is no convincing evidence that exposure to bisphenol-A is a gateway to getting cancer ("BISPHENOL A (BPA) – Current state of knowledge and future actions by WHO and FAO", 2009). According to a research done at Tufts University Medical School, exposure to BPA is likely to cause an increase the risk of getting cancer (Soto & Sonnenschein, 2010). Breast Cancer According to Brisken (2008), exposure to low dosages of bisphenol-A modifies the development of the breast, and thus, increases the risk of getting breast cancer. In another study conducted by Soto et el., (2008), epidemiological data and animal experiments were proof that exposure of fetuses to BPA may be the primary source for the increased occurrence of breast cancer. In addition, BPA is capable of producing neo-plastic alterations in an individual’s breast epithelial cells (Fernandez & Russo, 2009). Lapensee and colleagues (2010) argue that exposure to BPA may minimize sensitivity of certain tumors to chemotherapy treatment. Prostate Cancer and Development There is an increase in the prostate weight of adult mice when they experienced neonatal exposure to BPA dosage of 2 μg/kg (Nagel et al., 1997). On the other hand, a neonatal exposure to BPA dosage of 10 μg/kg, led to disruption of the development of the prostate of the fetal mouse (Timms et al., 2005). When rats were subjected to neonatal exposures to BPA dosages of 10 μg/kg, there was an increase in the susceptibility of the prostate gland to adult-inception hormonal carcinogenesis and precancerous abrasions. There is a link between the current concentrations of BPA in human serum and a permanent increase in the size of the prostate. Exposure of newborn rats to low doses of BPA increases their susceptibility to prostate cancer when they become adults (Prins et al., 2008). Sensitive groups Children and infants may be more vulnerable to exposure to BPA than adults. This is attributed to the fact that children and infants have the highest amounts of daily intakes of BPA (NTP, 2008). This happens because children and infants tend to eat, drink and breathe more than adults. The fact that they spend most of the time on floors increases their susceptibility to activities such as ingestion of dirt, or mouthing plastic objects (NTP, 2008). These activities increase the risk for exposure. Under typical exposure conditions, the young children’s urine had higher concentrations of BPA than that for adults. Feeding infants using formula from polycarbonate bottles increases their exposure, while canned foods increase the exposure of teenagers and adults. The exposure of pregnant women to BPA also exposes the fetus. A study by NTP (2008) on pregnant mice revealed the presence of bisphenol-A in the amniotic fluid and the placenta. After birth, the baby may still be exposed via the transfer of bisphenol-A through the mother’s breast milk. Evaluation of Risk or Safety On the whole, different studies have revealed the effect of exposure to BPA on the growth, development and reproduction of organisms. Amongst freshwater aquatic organisms, fish is the most sensitive. Confirmation of the values of endocrine-related outcomes varies between 1μg per liter to 1 mg per liter (U.S. Environmental Protection Agency, 2010). The environment is at risk of direct contamination from BPA or by means of disintegration of substances or materials containing bisphenol-A, for instance ocean-borne plastic refuse. Exposure to BPA has an effect on the reproduction systems of animals such as fish, crustaceans, amphibians, annelids, insects and molluscs; it also impairs the development of amphibians and crustaceans; and it produces genetic aberrations (NTP, 2008). Summary of Findings It is worth noting that the existing levels of exposure of infants, children and fetuses to BPA have led to behavioral and neural consequences. In addition, exposure to BPA has impacts on the mammary glands, prostate glands, as well as a delay in puberty in females. People should show concern for pregnant women, since exposure to doses of BPA will give rise to fetal or neonatal death, birth defects, as well as a reduction in the growth and birth weight of their offspring. There should be an increase in the concern shown to workers who are exposed to high levels in work-related surroundings and non-professionally exposed adults, with regard to the reproductive effects caused by exposure to bisphenol A. As a result, there should be enactment of measures that should control the present exposures to BPA, in view of the fact that they are high enough to warrant concern. Lastly, it is important to estimate the daily intake or measure the concentration of free BPA in blood either by means of aggregating or by bio-monitoring. References Akingbemi, B.T., Sottas, C.M., Koulova, A.I., Klinefelter, G.R., and Hardy, M.P. (2004). Inhibition of testicular steroidogenesis by the xenoestrogen bisphenol A is associated with reduced pituitary luteinizing hormone secretion and decreased steroidogenic enzyme gene expression in rat Leydig cells. Endocrinology, 145 (2), 592-603. “Bisphenol A (BPA) – Current state of knowledge and future actions by WHO and FAO.” (2009). 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