Open access peer-reviewed chapter

Pathological Conditons Related to Bisphenols and It’s Compounds

Written By

Geethamani Palanisamy and Divya Palanisamy

Submitted: May 21st, 2021 Reviewed: October 7th, 2021 Published: March 23rd, 2022

DOI: 10.5772/intechopen.101114

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Abstract

Bisphenols (BP) is one of the most important and highest volumes of chemicals produced in the universe. Each year, around 100 tons of bisphenol compounds are released into the atmosphere. In general, bisphenol is most widely used for production of polycarbonate (making plastic bottles like baby bottles and nursing products, dental sealants, CDs, DVDs, eye glasses, medical equipment’s, plasticizers etc.) and polymeric resins (epoxy resins, impact resistant safety materials like sports goods etc.). Due to these unavoidable chemicals, human beings are affected by human chronic diseases like obesity, toxicity, neuro disorder, reproductivity disorders, diabetes, cardio related issues, birth defects, metabolic syndrome, breathing issues, digestive related issues, cancer, genetic mutation etc., Children are easily affecting due to the multi dose consumption of packed food containing BP (canned foods) than adults. Women are affecting polycystic ovaries due to the high-level deposition of BP.

Keywords

  • metabolic syndrome
  • bisphenols
  • obesity
  • toxicity
  • disruption of endocrine
  • disorders

1. Introduction to bisphenol compounds

The commercial production of Bisphenol compounds (BP) initiated by late 1950’s, after the first epoxy resin was developed. A synthetically man-made chemical which is a polymeric monomer named bisphenol (BP) is widely used for the manufacture of plastic things and goods for the usage of daily life need for the human beings (food packages, drink containers, body lotions, playing toys, house hold plastic things, nursing products, decorators and water pipe lines, etc.) and industrial usages. Also, Bisphenol compounds are used for the manufacture of unsaturated polyester, polysulphones and polyetherimide. BP compounds of non-polymer are also used as an additive in flame retardants, thermal papers and brake fluids. The usage of BP is increasing more in more from last few decades in the universe, resulting BP is finding throughout the environment and also in human body [1] through their diet. A huge number of journals published based on the studies of BP and its compounds.

Chemically, BPA has two large phenyl groups with two electron rich hydroxyl group (alcohol and two methyl group). It forms lipophilic (associates with lipids), through the conjugation process, it makes a substance more water soluble. BPA is slightly more hydrophilic (associate with water), found in Adipose tissues and in breast milk too. The hydrophilic form is seen in urine and excrement. From the obtained information [2], BPA has a moderate potential for bioaccumulation and not found that to readily biodegrade.

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2. Bisphenol A

It was discovered by the Chemist A.P.Dianin in the year of 1891. These compounds are basically a carbon based synthesised compound belongs to the group of derivatives of diphenyl methane and bisphenols, which is colourless in nature called polycarbonate and are mostly stable and very strong in nature. The BPA components can withstand up to moderate to very high temperature even it is exposed to oven or furnace. Due to these properties, they can be used to manufacturing safety equipment’s components, glassware, bullet proof windows, doors, etc. As one of the main component of epoxy resins in protective coatings or layers of those lining the inner surfaces of plastic tins or cans, BPA supposed to extend the shelf life of food and beverage products. Figure 1 shows the structure of Bisphenol A. The toughness of BPA plastics has led to their use in medical equipment’s like cardiopulmonary (heart-lung) machines, incubators, hemodialyzers (artificial kidneys) and dental sealants and dental fillers and their light weight and optical clarity glasses which has made for eyeglasses [3, 4, 5]. Also, the chemicals are found in a variety of other products, including compact discs (CD’s) and other paper receipts.

Figure 1.

Structure of BPA.

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3. Adverse health effects

In 1930s, the first studies indicated that, the BPA to be a weakly estrogenic molecule but later [6] confirmed that it has harmful effects through the animal research. The cancer like breast cancer, prostate cancer, Uro genital abnormalities (in Male babies), early onset of puberty in girls, metabolic disorders like Obesity and type-two diabetics, decreases in semen quality in men and neuro-behaviour problems including attention deficit hyperactivity disorder etc. are the possible diseases and disorder of BPA from the exposures during the critical periods.

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4. Biological effects of bisphenol A

During 20th century, it was found it in only plastics even though scientists had developed BFA in 1930’s as a man-made estrogens and its cancer causing (Carcinogenic) properties. The American endocrinologist led by his team in the early 1990’s, unexpectedly found out, the BPA growth is medium in polycarbonate flask which is used to culture yeast cells. Further, they proceeded to isolate BP samples from the water in the flask and had been autoclaved, where they confirmed the chemical which was found same in the earlier detection (during 1930’s). They also confirm that, BPA produced estrogenic effects in cells at the level of 5–10 times lower than who used for safety assessments companies where polycarbonate plastics are manufactured [7].

The leached plastics, resins in tin cans contains BPA products by various conditions including the photochemical break down, exposure of various temperature range (Low to high), maturity of plastics cans and/or resins and the presence of ethanol. In the middle of 1990’s, number of studies confirms that, the main adverse effect due to BPA was reproductive system and development in animals by the interfering with their endocrine systems (energy balance and stress response) by the exposure level of BPA (both high and low level). The studies confirm that, due to the accumulation of BPA, it retards sexual behaviour in animals [8, 9, 10]. Also, it has been identified that the crossed placental barrier in animals (mammals) like mice and rats has been detected in human beings maternal and fetal serum which was also coincident with in human placental tissues. Thus, Bisphenol compounds found its way into tissues and fluids in the human womb. The chemical reaction attack and its effects in human fetal development is still not-clear. Similarly, the function of the human endocrine system is a matter to discuss. Much more speculation centres on whether BPA is a true endocrine disruptor chemical (EDC) in humans. The substituted Endocrine disruptor like DichloroDiphenylTrichloroEthane (DDT) & diethylstilbestrol, had been combined with birth defects, reduced fertility (infertility), and diseases such as obesity, diabetes, and carcinoma in humans. Derivatives of Bisphenol compounds (BPA, BPS and BPF) are used as alternatives to BPA, are associated with obesity, particularly in children [11, 12].

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5. BPA with in the environment

From the industries like chemical, plastics coat and staining manufactures, paper mills or material recycling companies, foundries (casting sand) or any direct or indirect leaching from the above and landfills (waste metal dumping), BPA might enter in to the environment directly. The accumulation of BPA, totally affects the growth, reproduction and life time of aquatic organisms. The United States Environmental Protection Agency (EPA) reported in 2010 that more than 1,000,000 pounds (454,000 kilogrammes) of BPA were released into environmental reservoirs each year, including soil, rivers, lakes, and oceans. Leaching from landfills and release from municipal water supplies, such as those associated with wastewater-treatment plants and paper mills, are the primary sources of environmental contamination. Plastic pollution is a major source of BPA in the world’s oceans. Despite the fact that seawater accelerates the breakdown of BPA plastics, the likelihood of leached BPA accumulating in the tissues of marine species is quite low. On the other hand, studies on terrestrial and freshwater species have shown that even low concentrations of the chemical can cause abnormalities when exposed for an extended period of time. BPA exposure, for example, causes an increase in micronuclei in root tip cells, indicating DNA damage in plants. BPA exposure causes sex ratios to become biased toward females in certain species of reptiles whose sex determination is normally influenced by temperature [13, 14, 15, 16].

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6. Effects of BP in human body

6.1 Neurotoxic, neuro behavioural and its effects

The developmental exposure of BP & BPA are does not appear to affects the sensory system, the spontaneous or Laboratory animals’ self-activity or sexual behaviour. At dietary doses below 5 mg/kg bw per day, changes in brain biochemical signalling, morphometric and cellular end-points within sexually dimorphic anatomical structures, and neuro-endocrine end-points were described. The most significant restriction is that methodological flaws cause uncertainty in the interpretation of results. Changes in anxiety and convergence of structural brain sex differences were identified as end-points suggestive of effects with possible human relevance based on the available data, although more research is needed to clarify uncertainties [17].

6.2 Cardiovascular effects

The toxicological evidence suggests that BPA has no discernible effect on cardiovascular function. The expert meeting is aware of upcoming cardiovascular function research that will soon inform judgements about cardiac end-points [18].

6.3 Metabolic disorders

Metabolic diseases are a new field of study, and the evidence currently available is insufficient to draw any conclusions about the possible harm to humans. However, the present evidence suggests that more research into the effects of BPA on adiposity, glucose or insulin control, lipids, and other diabetes or metabolic syndrome end-points is needed [19].

6.4 Effects on child and infants

Generally, the conservative assumptions made by the estimated international exposures reported are higher than comparable national estimates. The average and main exposure of exclusively breastfed babies (infants 0–6 months) to BPA was 0.3 μg/kg/day and exposure at the 95% was 1.3 μg/kg/day. When solid foods are introduced, exposure to BPA reduces after 6 months (at 6–36 months). For formula-fed newborns, there is a wide range of exposure estimates. Infants (0–6 months) fed liquid formula have a higher exposure than infants fed powdered formula, and infants fed polycarbonate (PC) bottles have a higher exposure than infants fed non PC bottles [20, 21, 22, 23].

Infants (0–6 months) who are fed liquid formula out of PC bottles have the highest estimated exposure are 2.4 μg/kg/day and 4.5 μg/kg /day at the 95th percentile. For children older than 3 years, highest exposure estimates did not exceed 0.7 μg/kg / day and 1.9 μg/kg /day at the optimum. For adults, highest exposure estimates did not exceed 1.4 μg/kg/day and 4.2 μg/kg bw/day at the maximum.

For most subgroups evaluated, exposure to BPA through non-food sources is at least one order of magnitude lower than that from food, based on the limited data available. Food, on the other hand, is by far the most significant source of overall BPA exposure in the majority of demographic groups. In addition, possible sources of exposure have been identified (unpackaged food and thermal paper). However, due to a lack of data, researchers were unable to produce exposure estimates. BPA concentrations in unpackaged foods and data on the consumer use patterns for materials and products containing BPA, including specific geographical differences; and the contribution of dermal exposure to overall exposure are furnished from the data over the exposure of BPAs [24, 25, 26, 27, 28, 29].

6.5 Some studies on BPA and obesity

The studies of Serbian involve the 103 women aged, 19–50 years measured BPA in first morning urine and the number of anthropometric measures including height, weight, and waist and circumference (WC) were collected. Milosevic et al., described a positive suggestion between BPA and obesity [30]. However, limitations of this investigation were cross-sectional sample collection and the quantities of participants were very small. Also, there is no physical activity data were collected. The recent study in USA, involves 977 adult women were conducted; where BPA (urine) were monitored, anthropometric measures were collected (including weight and height). The recent study of BPA (urine) of children and pregnant women were also determined in USA [31]. Of these 408 children were 3 years, 518 children where 5 years were monitored until 7 years of age, along with 369 pregnant women who’s between the ages 18 and 35. The anthropometric measures consists of Fat mass index (FMI), body fat (BF) and WC were collected.

The study was to monitor the mothers and their children at different stages of their development. In this investigation, BPA concentration of pregnant women had a positive suggestion with FMI, BF and WC of children at age of 7 but not associated with birth mass and childhood body mass index z-scores (BMIZ) at age of 5 and 7 and there are changes in BMIZ from ages of 5 to 7. The physical activity information of participants was not provided in the limitation of this study. A study in China involving 1326 students aged between 9 and 12 also measured (BPA) urine where anthropometric measures were collected with weight, height, WC, hip circumference and skinfold thickness [32]. From this study, it shows that the BPA had positive relationship with obesity in girls but not in boys.

6.6 Obesity diagnosis

Generally, obesity can be defined by using body mass index (BMI) by WHO to identify the obesity in people. The diagnosis of obesity is represented in the Table 1. The child obesity is studied by the nomogram technique. If, BMI equal to or greater than the age- and gender-specific, the 95th percentile is considered as obese (Centre for disease control) [33, 34, 35]. An obese person accumulates excess BF in his or her muscle, bone, fat and water. Obese people were facing many health problems at high risk including hypertension, mortality, low high-density lipoprotein cholesterol or high or low-density lipoprotein cholesterol and high levels of triglycerides (dyslipidaemia), coronary heart disease, diabetes (Type II), osteoarthritis, gallbladder disease, stroke and some cancers including endometrial, breast, colon, kidney, and liver cancer and gallbladder [36, 37, 38, 39, 40].

S.NoParticularsReport
1less than 18.5 kg/m2underweight
2between 18.5 and 24.9 kg/m2normal
3between 25 and 29.9 kg/m2is overweight
4between 30.00 and 34.99 kg/m2class 1 obese
535.00 and 39.9 kg/m2class 2 obese
6above 40 kg/m2class 3 obese

Table 1.

The diagnosis of obesity (WHO., 2000).

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7. Effects of exposure to BPs

There is only inadequate information about the adverse effects of non-BPA. However, it is believed that they have similar effects to BPA [41]. In human fluids or tissues including placental tissue, serum, foetal plasma and breast milk, the concentration of BPA has been determined. Many studies have been focussed on children and pregnant women, where high BPA levels were linked with chromosomal abnormalities and miscarriages and infertility in women and abnormal karyotypes in foetuses [42]. The high BPA levels causes to more unilateral or bilateral blood-filled ovarian bursae in women.

7.1 Effect of BPA in biota

In comparison to non-biotic and biotic environmental compartments, biota contains a small amount of ambient BPA. BPA’s published bio-concentration factor (BCF) values are much below 1000, which the US Environmental Protection Agency deems to be the threshold for concern. BCFs for fish exposed to BPA have been reported to be quite low [32].

7.2 Effect of BP on wild life

Numbers of challenges are facing due to the exposure of BPA (high concentration) on wildlife now days. The complexities in the natural system including chemical mixture, spatial varying exposure levels with tropic interactions and related few studies investigated results, the effect of chemical exposure on wildlife in-situ [43]. Many BPA toxicity studies have been used endocrine related measurement endpoints which triggered by other toxicological modes of action that was identifying these mechanisms may/may not be necessary in order to characterise the response to the environmental toxicity [44].

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8. Relevance of the study to BFA

BPA metabolism takes place by glucuronidation once in the body, under the catalytic action of the enzymes. While uridine 5-diphospho-glucuronosyltransferase (UGT) catalyses the conversion of BPA-to-BPA glucuronide, sulfotransferase catalyses the conversion of BPA- to the BPA- sulphate. Both metabolites are very soluble and removed from the human body in urine. The biotransformation of BPF and BPS is still unclear, but reactions carried out in vivo and in vitro organisms indicate that BPF metabolism is similar to BPA, while published studies on the biodegradation of BPS are extremely scarce [45].

In response to the same negative health effects of BPA, the US Food and Drug Administration (FDA) banned the use of BPA in baby bottles, sippy cups, and infant formular containers in 2012 [46]. Obesity increases the risk of a number of debilitating and fatal diseases, including diabetes, heart disease, and some cancers (US National Heart, Lung and Blood Institute, 1998). Obesity reduces a person’s quality and length of life, raises an individual’s healthcare costs, and raises the health costs of a country with a high prevalence of obesity (US National Heart, Lung and Blood Institute, 1998). Obesity is caused by a variety of factors, including lifestyle, genetics, and the consumption of processed foods high in fat, sugar, or carbohydrate; however, BPA and analogues when ingested have been linked to obesity [47, 48, 49, 50, 51]. The causes of obesity are plenty, such as lifestyle, genetics, the eating of processed food rich in fat and sugar or carbohydrate; however, BPA and analogues when absorb into the human body play a role in promoting adipogenesis and cause weight gain resulting in obesity especially in adolescent [52, 53, 54, 55, 56, 57].

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9. Prevention measures

For developing safer replacement for the use of plastics, the following move can takes place against the use of BPA contained products. These steps may reduce the exposures,

  • Motivate the manufacturers are creating more and more BPA-free products. Look for products labelled as BPA-free products. If a product is not labelled, avoid to buy.

  • Avoid heating the plastic containers in oven and in the direct sunlight. It may cause breakdown the BPA molecule and leach to the food products.

  • Reduce the usage of canned foods.

  • Cut down the used cans

  • Instead of using these products, go with alternates such as glass, porcelain, stainless steel, copper containers and earthen pots for hot foods as well as cold foods.

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10. Conclusions

Many research studies suffer from design and analysis flaws, limiting their utility for this purpose. The biological significance of many of the more sensitive end-points is still debated, as is whether studies that only examined conventional end-points are adequate for detecting all potentially relevant effects. Few clear trends have emerged from studies of BPA’s effects on wildlife. Terrestrial wildlife is likely to be exposed to low levels of BPA, and few studies have looked at environmentally relevant doses. Although the majority of BPA regulation focuses on human exposure through food packaging, these applications account for only a small portion of BPA use. In the absence of new regulations, if current trends continue, BPA production and environmental release will increase. BPA would not necessarily result in a safer or more thoroughly researched chemical substitute. A more cautious approach to chemical regulation and use may reduce potential environmental impacts. Issues like these will continue to arise as humans become more reliant on chemical advances to meet global needs.

References

  1. 1. Apau J, Acheampong A, Adua E. Exposure to bisphenol A, bisphenol F, and bisphenol S can result in obesity in human body. Medicinal Chemistry. 2018;4:1-8
  2. 2. Available from:https://www.healthandenvironment.org/environmental-health/environmental-risks/chemical-environment-overview/bpa
  3. 3. Baillie-Hamilton PF. Chemical toxins: A hypothesis to explain the global obesity epidemic. The Journal of Alternative & Complementary Medicine. 2002;8(2):185-192
  4. 4. Bonefeld-Jorgensen EC, Long M, Hofmeister MV, Vinggaard AM. Endocrine-disrupting potential of bisphenol A, bisphenol A dimethacrylate, 4-nnonylphenol, and 4-n-octylphenol in vitro: New data and a brief review. Environmental Health Perspectives. 2007;115:69. DOI: 10.1289/ehp.9021
  5. 5. Cabaton N, Zalko D, Rathahao E, Canlet C, Delous G, Chagnon MC, et al. Biotransformation of bisphenol F by human and rat liver subcellular fractions. Toxicology In Vitro. 2008;22(7):1697-1704. DOI: 10.1016/j.tiv.2008.07.004
  6. 6. Casals-Casas C, Desvergne B. Endocrine disruptors: From endocrine to metabolic disruption. Annual Review of Physiology. 2011;73:135-162. DOI: 10.1146/annurev-physiol-012110-142200
  7. 7. Clark E. Sulfolane and sulfones. Kirk-Othmer encyclopedia of chemical technology. Composition, H. B. (1987). In: Growth, Aging, Nutrition and Activity. New York: Springer-Verlag; 2012
  8. 8. Danzl E, Sei K, Soda S, Ike M, Fujita M. Biodegradation of bisphenol A, bisphenol F and bisphenol S in seawater. International Journal of Environmental Research and Public Health. 2009;6(4):1472-1484. DOI: 10.3390/ijerph6041472
  9. 9. Baillie-Hamilton PF. Chemical toxins: A hypothesis to explain the global obesity epidemic. The Journal of Alternative & Complementary Medicine. 2002;8(2):185-192
  10. 10. Inadera H. Neurological Effects of Bisphenol A and its Analogues. International Journal of Medical Sciences. 2015;12(12):926-936. DOI: 10.7150/ijms.13267
  11. 11. Bonefeld-Jorgensen EC, Long M, Hofmeister MV, Vinggaard AM. Endocrine-disrupting potential of bisphenol A, bisphenol A dimethacrylate, 4-nnonylphenol, and 4-n-octylphenol in vitro: New data and a brief review. Environmental Health Perspectives. 2007;115:69. DOI: 10.1289/ehp.9021
  12. 12. Cabaton N, Zalko D, Rathahao E, Canlet C, Delous G, Chagnon MC, et al. Biotransformation of bisphenol F by human and rat liver subcellular fractions. Toxicology In Vitro. 2008;22(7):1697-1704. DOI: 10.1016/j.tiv.2008.07.004
  13. 13. Casals-Casas C, Desvergne B. Endocrine disruptors: From endocrine to metabolic disruption. Annual Review of Physiology. 2011;73:135-162. DOI: 10.1146/annurev-physiol-012110-142200
  14. 14. Clark E. Sulfolane and sulfones. Kirk-Othmer encyclopedia of chemical technology. Composition, H. B. (1987). In: Growth, Aging, Nutrition and Activity. New York: Springer-Verlag; 2012
  15. 15. Danzl E, Sei K, Soda S, Ike M, Fujita M. Biodegradation of bisphenol A, bisphenol F and bisphenol S in seawater. International Journal of Environmental Research and Public Health. 2009;6(4):1472-1484. DOI: 10.3390/ijerph6041472
  16. 16. Williams EP, Mesidor M, Winters K, Dubbert PM, Wyatt SB. Overweight and obesity: Prevalence, consequences, and causes of a growing public health problem. Current Obesity Reports. 2015;4:363-370
  17. 17. Yamada H, Furuta I, Kato EH, Kataoka S, Usuki Y, Kobashi G, et al. Maternal serum and amniotic fluid bisphenol A concentrations in the early second trimester. Reproductive Toxicology. 2002;16(6):735-739
  18. 18. Yokota H, Iwano H, Mari E, Kobayashi T, Inoue H, Ikushiro S-I, et al. Glucuronidation of the environmental oestrogen bisphenol A by an isoform of UDP-glucuronosyltransferase, UGT2B1, in the rat liver. Biochemical Journal. 1999;340(2):405-409
  19. 19. Milosevic M et al. Immunoglobulins G from sera of amyotrophic lateral sclerosis patients induce oxidative stress and upregulation of antioxidative system in BV-2 microglial cell line. Frontiers in Immunology, Multiple Sclerosis and Neuroimmunology. 2017;2017(8):1619. DOI: 10.3389/fimmu.2017.016191-15
  20. 20. Song Y, Hauser R, Hu F, Franke A, Liu S, Sun Q. Urinary concentrations of bisphenol A and phthalate metabolites and weight change: A prospective investigation in US women. International Journal of Obesity. 2014;38(12):1532-1537. DOI: 10.1038/ ijo.2014.63
  21. 21. Suiko M, Sakakibara Y, Liu M-C. Sulfation of environmental estrogen-like chemicals by human cytosolic sulfotransferases. Biochemical and Biophysical Research Communications. 2000;267(1):80-84
  22. 22. US Food and Drug Administration (FDA). CFR part 177. Indirect Additives Polymers Final Rule Federal Register. 2012;77:41899-41902
  23. 23. Food US, Administration D. Bisphenol A (BPA): Use in Food Contact Application. U.S. Department of Health and Human Services, Food and Drug Administration; 2012 Retrieved June 26, 2012 fromhttp://www.fda.gov/NewsEvents/PublicHealthFocus/ucm064437.htm
  24. 24. U.S. Food and Drug Administration. Summary of Bisphenol A Biomonitoring Studies. Washington, DC: U.S. Department of Health and Human Services, Food and Drug Administration; 2009. Memorandum from V. Komolprasert, dated November 16, 2009.http://www.regulations.gov/#!documentDetail;D=FDA-2010-N0100-0010
  25. 25. US National Heart, Lung and Blood Institute. (1998). Clinical guidelines on the identification, evaluation and treatment of overweight and obesity in adults. The Evidence Report. United States. Retrieved May 13, 2010 from http://www. nhlbi. nih. gov/guidelines/ obesity/prctgd_c. pdf
  26. 26. National Toxicology Program. NTP-CERHR Monograph on the Potential Human Reproductive and Developmental Effects of Bisphenol A. Research Triangle Park, NC: National Institute of Environmental Health Sciences, National Toxicology Program; 2008http://ntp.niehs.nih.gov/ntp/ohat/bisphenol/bisphenol.pdf
  27. 27. Palanza PL, Howdeshell KL, Parmigiani S, vom Saal FS. Exposure to a low dose of bisphenol A during fetal life or in adulthood alters maternal behavior in mice. Environmental Health Perspectives. 2002;110(Suppl 3):415-422
  28. 28. Rochester JR, Bolden AL. Bisphenol S and F: A systematic review and comparison of the hormonal activity of bisphenol A substitutes. Environmental Health Perspectives (Online). 2015;123(7):643-650. DOI: 10.1289/ehp.1408989
  29. 29. Rosenmai AK, Dybdahl M, Pedersen M, Alice van VugtLussenburg BM, Wedebye EB, Taxvig C, et al. Are structural analogues to bisphenol a safe alternatives? Toxicological Sciences. 2014;139(1):35-47
  30. 30. Hoepner A et al. The Effects of Corporate and Country Sustainability Characteristics on The Cost of Debt: An International Investigation.Journal of Business Finance & Accounting. 2016;43(1):n/a-n/a. DOI: 10.1111/jbfa.12183
  31. 31. Li J, Carlson BE, Lacis AA. A study on the temporal and spatial variability of absorbing aerosols using total ozone mapping spectrometer and ozone monitoring instrument aerosol index data. Journal of Geophysical Research. 2009;114:D09213. DOI: 10.1029/2008JD011278
  32. 32. Flint S, Markle T, Thompson S, Wallace E. Bisphenol A exposure, effects, and policy: A wildlife perspective. Journal of Environmental Management. 2012;104(19):14
  33. 33. Ying G-G, Kookana RS. Sorption and degradation of estrogen-like endocrine disrupting chemicals in soil. Environmental Toxicology and Chemistry. 2005;24:2640e2645
  34. 34. Yoon Y, Westerhoff P, Snyder SA, Esparza M. HPLC-fluorescence detection and adsorption of bisphenol A, 17b-estradiol, and 17a-ethynyl estradiol on powdered activated carbon. Water Research. 2003;37:3530e3537
  35. 35. Yu C-P, Chu K-H. Occurrence of pharmaceuticals and personal care products along the West Prong Little Pigeon River in east Tennessee, USA. Chemosphere. 2009;75:1281e1286
  36. 36. Zeng G, Zhang C, Huang G, Yu J, Wang Q, Li J, et al. Adsorption behavior of bisphenol-A on sediments in Xiangjiang River, Central-south China. Chemosphere. 2006;65:1490e1499
  37. 37. Zhang S, Zhang Q, Darisaw S, Ehie O, Wang G. Simultaneous quantification of polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and pharmaceuticals and personal care products (PPCPs) in Mississippi river water, in New Orleans, Louisiana, USA. Chemosphere. 2007;66:1057e1069
  38. 38. Zoeller RT, Bansal R, Parris C. Bisphenol-A, an environmental contaminant that acts as a thyroid hormone receptor antagonist in vitro, increases serum thyroxine, and alters RC3/neurogranin expression in the developing rat brain. Endocrinology. 2005;146:607e612
  39. 39. Flint S, Markle T, Thompson S, Wallace E. Bisphenol A exposure, effects, and policy: A wildlife perspective. Journal of Environmental Management. 2012;104:19-34
  40. 40. Yamamoto TA, Yasuhara A, Shiraishi H, Nakasugi O. Bisphenol-A in hazardous landfill leachates. Chemosphere. 2001;42:415e418
  41. 41. Yang FX, Xu Y, Wen S. Endocrine-disrupting effects of nonphenol, bisphenol A and p, p0-DDE on Rana nigromaculata tadpoles. Bulletin of Environmental Contamination and Toxicology. 2005;75:1168e1175
  42. 42. Wilson MP, Schwarzman MR. Health policy: Toward a new US chemicals policy: Rebuilding the foundation to advance new science, green chemistry, and environmental health. Environmental Health Perspectives. 2009;117(8):1202e1209
  43. 43. Crain et al. Chapel Hill bisphenol A expert panel consensus statement: Integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure. HHS Publications. 2007;24(2):131-138
  44. 44. Wright-Walters M, Volz C, Talbott E, Davis D. An updated weight of evidence approach to the aquatic hazard assessment of Bisphenol A and the derivation a new predicted no effect concentration (Pnec) using a nonparametric methodology. Science of the Total Environment. 2011;409:676e685
  45. 45. Witorsch RJ. Endocrine disruptors: Can biological effects and environmental risks be predicted? Regulatory Toxicology and Pharmacology. 2002;36:118e130
  46. 46. Searcey D, Richtel M. Obesity was Rising as Ghana Embraced Fast Food. Then Came KFC. Manhattan, NY: The New York Times Company; 2017
  47. 47. Nishikawa Y. Endocrine Disruptors Effects of Bisphenol A on Human Health. JMAJ. 2003;46(3):103-107
  48. 48. Pellegrini M, Bulzomi P, Lecis M, Leone S, Campesi I, Franconi F, et al. Endocrine disruptors differently influence estrogen receptor beta and androgen receptor in male and female rat vsmc. Journal of Cellular Physiology. 2013;229(8):1061-1068. DOI: 10.1002/jcp.24530
  49. 49. Ottawa, Canada. Toxicological and Health Aspects of Bisphenol A Report of Joint FAO/WHO Expert Meeting 2-5 November 2010 and Report of Stakeholder Meeting on Bisphenol. 2010
  50. 50. Apau J, Acheampong A, Adua E. Exposure to bisphenol A, bisphenol F, and bisphenol S can result in obesity in human body Cogent. Chemistry. 2005;4(1):1506601. DOI: 10.1080/23312009.2018.1506601
  51. 51. Hoepner LA, Whyatt RM, Widen EM, Hassoun A, Oberfield SE, Mueller NT, et al. Bisphenol A and adiposity in an inner-city birth cohort. Environmental Health Perspectives. 2016;124(10):1644. DOI: 10.1289/ehp.1409567
  52. 52. Gerona RR, Woodruff TJ, Dickenson CA, et al. Bisphenol-A (BPA), BPA glucuronide, and BPA sulfate in midgestation umbilical cord serum in northern and central California population. Environmental Science & Technology. 2013;47:12477-12485
  53. 53. Mahalingaiah S, Meeker JD, Pearson KR, et al. Temporal variability and predictors of urinary bisphenol A concentrations in men and women. Environmental Health Perspectives. 2008;116:173-178
  54. 54. Huang H, Leung LK. Bisphenol a downregulates CYP19 transcription in JEG-3 cells. Toxicology Letters. 2009;189(3):248-252
  55. 55. Vandenberg LN, Hauser R, Marcus M, Olea N, Welshons WV. Human exposure to bisphenol A (BPA). Reproductive Toxicology. 2007;24(2):139-177. DOI: 10.1016/j.reprotox.2007.07.010
  56. 56. Vinas, Watson. Bisphenol S disrupts extradiolinduced nongenomic signalling in a rat pituitary cell line: Effect on cell functions. Environmental Health Perspectives. 2013a;121:352-358. DOI: 10.1289/ehp.1205826
  57. 57. WHO. Technical Report Series 894. In: 2000 World Health Organization (WHO) “Obesity Situation and Trends” “http://www.who.org” int. Geneva: World Health Organization; 2014

Written By

Geethamani Palanisamy and Divya Palanisamy

Submitted: May 21st, 2021 Reviewed: October 7th, 2021 Published: March 23rd, 2022