##article.abstract##
Introduction: Bisphenol-A, a constituent of plastic and an endocrine disrupting chemical has been
implicated in the aetiology of sexual dysfunction.This study was aimed at evaluating sexual function in
males occupationally exposed to Bisphenol-A in a plastic industry in Ibadan, Nigeria.
Methodology: Eighty apparently healthy males aged 18-62 years with normal renal function were enrolled
into this case-control study. They were forty male employees of a plastic industry (PIW) age matched
with forty males who were non-employees of any plastic industry (Controls). Sexual history, blood
pressure, socio-demographic and anthropometric indices were obtained by standard methods. Venous
blood (10mL) was obtained from participants for sex hormones analyses by enzyme linked
immunosorbent assay while nitric oxide and superoxide dismutase activities were estimated
spectrophotometrically. Bisphenol-A was estimated in spot urine samples using high performance liquid
chromatography-tandem mass spectrometry. Data analysed were statistically significant at p<0.05.
Result: Bisphenol-A was detected in both groups but was significantly raised in controls compared with
PIW (p<0.003). The controls also showed significantly raised diastolic blood pressure and adiposity
indices but lower nitric oxide compared with PIW (p<0.05). In controls, bisphenol-A had a direct
relationship with systolic BP and waist circumference but indirect relationship with diastolic blood
pressure and waist height ratio (p<0.05). Although bisphenol-A was not associated with physical sexual
function indices, it had a direct relationship with oestradiol in PIW (p<0.010).
Conclusion: Bisphenol-A was present in both exposed and unexposed groups but was not associated with
sexual function. However, its endocrine disrupting capacity especially in the exposed group is suggested.
Keywords: Bisphenol-A, Endocrine disrupting chemicals, Hormones, Industrialisation, Sexual
dysfunction.
Résumé
Introduction : Bisphénol-A, un constituant du plastique et un agent chimique perturbant le système
endocrinien, a été impliqué dans l’étiologie de la dysfonction sexuelle. Cette étude visait à évaluer la
fonction sexuelle chez les hommes exposés professionnellement au bisphénol- A dans une industrie du
plastique à Ibadan, au Nigéria.
Méthodologie:Quatre-vingtshommes apparemment enbonne santé âgés de 18-62ans avec la fonction rénale
normaleétaient enrôlés dans cette étude cas-témoins.Ils y’avaient quarante employés masculins d’une industrie
plastique(PIW) appariés pour l’âge avec quarante hommes qui étaient non-employés de toute l’industrie
plastique(Contrôle).Les antécédents sexuels, la pression artérielle,les indices socio-démographiques et anthropométriques ont
été obtenus par des méthodes standard.Le sang veineux (10 ml) a été prélevé chez les participants pour une analyse des
hormones sexuelles pardosage d’immunosorbantlié à une enzyme,tandis que les activités d’oxyde nitrique et de superoxyde
dismutase étaient estimées parspectrophotométrie.Le bisphénol-A a été estimé dans des échantillons ponctuels d’urine en
utilisant une spectrométrie de masse à haute performance par chromatographie en phase liquide et tandem.Les données
analysées étaientstatistiquement significatives à p <0,05.
Résultat : Lebisphénol-A a été détecté dans les deux groupes, mais il était significativement élevé chez lestémoinspar rapport
au PIW (p <0,003).Les témoins ont également montré une augmentation significative de lapression artérielle diastoliqueet des
indices d’adiposité, mais une réduction de l’oxyde nitrique par rapport à l’IPW (p <0,05).Chez lestémoins, lebisphénol-A
avait une relation directe avec la pression artérielle systolique et le tour de taille, mais une relation indirecte avec la pression
artérielle diastolique et le rapport hauteur / taille (p <0,05).Bien que lebisphénol-A n’ait pas été associé à des indices de
fonction sexuelle physique, il existait une relation directe avec l’œstradioldans IPW(p <0,010).
Conclusion : Le bisphénol- A était présent dans les groupes exposés et non exposés, mais n’était pas
associé à la fonction sexuelle. Cependant, sa capacité de perturbation endocrinienne, en particulier dans le
groupe exposé, est suggérée.
Mots - clés : Bisphénol-A, produits chimiques perturbateurs du système endocrinien, hormones,
industrialisation, dysfonctionnement sexuel.
Correspondence: Dr. Mabel A. Charles-Davies, Department of Chemical Pathology, College of
Medicine, University of Ibadan, Nigeria. Email: mcharlesdavies@yahoo.com
##submission.citations##
Hunt PA, Koehler KE, Susiarjo M et al. Bisphenol-A exposure causes meiotic an euploidy in the female mouse. Current Biology 2003; 13: 546–553.
Ajayi O, Charles-Davies M, Anetor J and Ademola A. Serum Polychlorinated Biphenyls and Bisphenol-A levels in Nigerian women with Breast Cancer. Archive of Basic Applied Medicine 2014; 2: 71-75.
Ehrlich S, Calafat AM, Humblet V, Smith T and Hauser R. Handling of thermal receipts as a source of exposure to bisphenol-A. Journal of the American Medical Association 2014; 8: 859-860.
Walsh B. The Perils of Plastic – Environmental Toxins –TIME”. 2010. Retrieved from April 30, 2015.
Maduka IC, Ezeonu F.C, Neboh EE, Shu EN and Ikekpeazu EJ. Urinary bisphenol-A output in plastic industry workers: A possible indicator of occupational exposure. Tropical Journal of Medical Research 2014; 17: 117-12.
Volkel W, Kiranoglu M and Fromme H. Determination of free and total bisphenol-A in human urine to assess daily uptake as a basis for a valid risk assessment. Toxicology Letters 2008; 30: 155-162.
Jarow JP. Endocrine causes of male infertility. Urologic clinics of North America 2003; 30: 83-90.
Newbold RR, Padilla- Banks E and Jefferson WN. Environmental estrogens and obesity. Molecular and Cellular Endocrinology 2009; 304: 84- 89.
VomSaal FS and Myers JP. Bisphenol-A and Risk of Metabolic Disorders. Journal of the American Medical Association 2008; 11: 1353–1355.
Hess RA, Bunick D and Bahr J. Oestrogen, its receptors and function in the male reproductive tract - a review. Molecular and Cellular Endocrinology 2001; 178: 29–38.
Li D, Zhou Z, Qing D et al. Occupational exposure to bisphenol-A (BPA) and the risk of self-reported male sexual dysfunction. Human Reproduction 2010; 252: 519-527.
Perez J, Vrooma L, Ricke WA and Hunt PA. Bisphenol-A and Reproductive Health: Update of Experimental and Human Evidence 2007-2013. Environmental Health Perspectives 2014; 122: 8.
Gronemeyer H, Gustafsson JA and Laudet V. Principle of modulation of the nuclear receptor super family. Nature Review. Drug Discovery 2004; 3: 950-964.
Lau TY, Wang, Y. and Chiu J. Reactive oxygen species: Current knowledge and applications in cancer research and therapeutic. Journal of cellular Biochemistry 2008; 2: 657-667.
Agarwal A, Nandipati KC, Sharma RK, Zippe CD and Raina R. Role of oxidative stress in the pathophysiological mechanism of Erectile Dysfunction.Journal of Andrology 2006; 27: 3.
Kabuto H. Effect of Bisphenol-A on the metabolism of active oxygen species in mouse tissues. Environmental Research 2003; 1: 31-35.
Anjum S, Rahman S, Kaur M, et al. Melatomin ameliorates Bisphenol-A induced biochemical toxicity in testicular mitochondria of mouse. Food and chemical Toxicology 2011; 49: 2849-2854.
Liu C, Duan W, Li R, et al. Esposure to Bisphenol-A disrupts meiotic progression during spermatogenesis in adult rats through estrogen-like activity. Cell Death and Diseases 2013; 4: 67-203.
Kabuto H, Amakawa M and Shishibor T. Exposure to Bisphenol-A during embryo/fetal life and enfancy increases oxidative injury and causes underdevelopment of the brain and testis in mice. Life Sciences 2004; 24: 2931-2940.
Heba S, Aboul E, Yasser A and Khadrawy M. The effect of Bisphenol-A on some oxidative stress parameters and acetyl cholinesterase activity in the heart of male albino rats. Cytotechnology 2015; 1: 145.
Burnett AL. Nitric oxide in the penis: physiology and pathology. Journal of Urology 1997; 157: 320–324.
Jones RW, Rees RW, Minhas S, et al. Oxygen free radicals and the penis. Expert Opinion Pharmacotherapy 2002; 3: 889-897.
Prieto D, Kaminski PM, Armed M and Wolin MS. Hypoxic relaxation of penile arteries: involvement of endothelial nitric oxide and modulation by reactive oxygen species. American Journal of Physiology. Heart and Circulatory Physiology 2010; 299: 915-924.
Zou M, Martin C and Ullrich V. Tyrosine nitration as a mechanism of selective inactivation of prostacyclin synthase by peroxynitrite. Biological Chemistry 1997; 378: 707–713.
Khan MA., Thompson CS, Mumtas FH et al. The effect of Nitric oxide and peroxynitrite on rabbit cavernosal smooth muslerelaxation.World Journal of Urology 2001; 19: 220-224.
Charles-Davies MA, Fasanmade AA, Olaniyi JA et al. Metabolic alterations in different stages of hypertension in an apparently healthy Nigerian population. International journal of hypertension 2013: 351-357.
Tsang VCW, Wilson BC and Majid KH. Kinetic studies of a quantitative single-tube enzyme-linked immunosorbent assay. Clinical Chemistry 1980; 26: 1255-1260.
Markham D, Waechter J, Budinsky R et al. Development of a method for the determination of Total Bisphenol-A at trace levels in human blood and urine and elucidation of factors influencing method Accuracy and Sensitivity. Journal of Analytical Toxicology 2014; 38: 194-203.
Mistra HP and Fridovich I. The role of Suproxide anion in the antioxidation of epinephrine and a simple assay for superoxide dismutase. Journal of Biological Chemistry 1972; 247: 3170-3171.
Chaea SY, Lee M, Kim SW and Bae YH. Protection of Insulin secreting cells from Nitric oxide induced cellular damage by cross linked haemoglobin. Biomaterials 2004; 5: 843-850.
Beronius A, Ruden C, Hakansson H and Hanberg A. A comparative analysis of controversies in the the health risk assessment of Bisphenol-A. ReproductiveToxicology 2010; 29: 132-46.
Lassen TH, Frederiksen H, Jensen TK et al. Urinary bisphenol-A levels in young men: association with reproductive hormones and semen quality. Environmental Health Perspectives 2014; 122: 478–484
Geens T, Goeyens L and Covaci A. Are potential sources for human exposure to bisphenol-A overlooked? International Journal of Hygiene and Environmental Health 2011; 5: 339-347.
Cooper JE, Kendig EL and Belcher SM. Assessment of bisphenol-A released from reusable plastic, aluminium and stainless steel water bottles. Chemosphere 2011; 6: 943-947.
Genuis SJ, Beesoo and S, Birkholz D. Human excretion of bisphenol A: blood, urine, and sweat (BUS) study. Journal of Environmental and Public Health, 2012. Article ID 185731.
Landis WG and Yu MH. Introduction to environmental toxicology, 3rd ed. Levis Boca Raton. FL.142. 2004.
Grønbaek M and Sørensen TI. Prospective associations between sedentary lifestyle and BMI in midlife. Obesity (Silver Spring)2006; 8: 1462-71.
Charles-Davies MA, Fasanmade AA, Olaniyi JA et al. Prevalent components of metabolic syndrome and their correlates in apparently healthy individuals in sub-saharan Africa. International journal of tropical Disease and Health 2014; 7: 740-752.
Fernandez F, Arrebola JP, Taoufki J et al. Bisphenol-A and chlorinated derivatives in adipose tissue of women. Reproductive Toxicology 2007; 24: 259-264.
Miyawaki J, Sakayama K, Kato H, Yamamoto H an Masuno H. Perinatal and Postnatal exposure to BPA increases adipose tissue mass and serum cholesterol level in mice. Journal of Atherosclerosis and Thombosis 2007; 14: 245-252.
Hugo ER, Brandebourg TD, Woo JG, et al. Bisphenol-A at environmentally relevant doses inhibits adiponectin release from human adipose tissue explants and adipocytes. Environmental Health Perspectives 2008; 12: 116
Meeker JD, Ehrlich S, Toth TL et al. Semen quality and sperm DNA damage in relation to urinary bisphenol-A among men from an infertility clinic. Reprodive Toxicology 2010b; 30: 532–539.
Galloway T, Cipelli R, Guralnik J et al. Daily bisphenol-A excretion and associations with sex hormone concentrations: results from the InCHIANTI adult population study. Environmental Health Perspectives 2010; 118: 1603–1608.
Knez J. Endocrine disrupting chemicals and male reproductive health. Reproductive Bio Medicine 2013; 26: 440-448.
Casals-Casas C and Desvergne B Endocrine Disruptors: From Endocrine to Metabolic Disruption. Annual Review of Physiology 2011; 73:135–162.
Eagleson CA, Gingrich MB, Pastor CL et al. Polycystic ovarian syndrome: evidence that flutamide restores sensitivity of the gonadotropin-releasing hormone pulse generator to inhibition by estradiol and progesterone. Journal of Clinical Endocrinology and Metabolism 2010; 11: 4047-4052.
Carreau S and Hess RA. Oestrogens and spermatogenesis. Philosophical Transactionsofthe Royal Society B 2010; 365: 1517–1535.
Carreau S, Wolczynski S and Galeraud-Denis. Aromatase, oestrogens and human male reproduction. Philosophical Transactions of the Royal Society B 2010; 365:1571–1579.
Furuya M, Adachi K, Kuwahara S, Ogawa K, Tsukamoto Y. Inhibition of male chick phenotypes and spermatogenesis by Bisphenol-A. Life Sciences 2006; 78: 1767–1776.
Kim JY, Han EH, Kim HG et al. Bisphenol-A-inducedaromatase activation is mediated by cyclooxygenase-2 up-regulation in rat testicular Leydigcells. Toxicology Letters 2010; 193: 200–208.
Déchaud H, Ravard C, Claustrat F, De la Perrière AB and Pugeat M. Xenoestrogen interaction with human sex hormone-binding globulin (hSHBG). Steroids 1999; 5: 328–334.
Kellogg DL, Zhao JL, Coey U and Green JV. Acetylcholine-induced vasodilation is mediated by nitric oxide and prostaglandins in human skin. Journal of Applied Physiology 2005; 2: 629–632.