Abstract

Bisphenol A (BPA), an endocrine disruptor involved in synthesizing numerous types of plastics, is detected in almost the entire population’s urine. The present work aims to estimate daily exposure to BPA by systematically reviewing all articles with original data related to urinary BPA concentration. This approach is based on human pharmacokinetic models, which have shown that 100% of BPA (free and metabolized form) is eliminated only in a few hours through urine. Several extensive population studies and experimental data have recently proven a significant association between urinary excretion of BPA and albuminuria, associated with renal damage. Our team’s previous work has shown that low-dose BPA can promote a cytotoxic effect on renal mouse podocytes. Moreover, BPA administration in mice promotes kidney damage and hypertension. Furthermore, preliminary studies in human renal cells in culture (podocytes) strongly suggest that BPA might also promote kidney damage. Overall, the present review analyzed BPA exposure data from mammalian cell studies, experimental animal models, and several human populations. Studying principal cohorts calculated the exposures to BPA globally, showing a high BPA exposure suggesting the need to decrease BPA exposure more effectively, emphasizing groups with higher sensitivity as kidney disease patients.

Highlights

  • Bisphenol A (BPA) is a phenolic compound widely distributed due to its multiple uses as an additive and plasticizer in plastic polymers’ manufacture [1]

  • In the kidney’s case, BPA concentration has been positively correlated with a greater predisposition to kidney pathologies [15–17] or clinical signs associated with kidney diseases, such as increased albuminuria or decreased glomerular filtration rate [18–21]

  • The administration of 10 and 100 nM doses for nine days exerted loss of cell viability and increased apoptosis. These effects were accompanied by an increase in the synthesis of molecules classically involved in the pathogenesis of glomerulosclerosis, such as the cyclin-dependent kinase inhibitor p27kip1, the TGF-β system, and collagen IV. In these cells, BPA reduced the synthesis of nephrin and podocin, proteins of the filtration slits involved in proteinuria and podocyte survival mechanisms

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Summary

Introduction: brief historical overview

Bisphenol A is the perfect example of the double edge of industrial development. On the one hand, thanks to BPA, we have countless plastic objects with excellent physical properties at low prices; on the other hand, increasing exposure to this kind of xenobiotic compounds could be a severe health risk to the general population. The discoverer’s idea was to commercialize a compound that could treat female pathologies They succeeded with Diethylstilbestrol, a substance with much greater potency than BPA, and was introduced in the 1940s [8]. It took about 50 years since the Russian chemist Dianin synthesized it in 1891 [9, 10] until the BPA began to be used in the industrial manufacturing of epoxy resins. Due to its unique combination of physical properties, this type of compound has had a significant impact on the world industry, as have epoxy resins. Today they are still used in numerous applications, such as in the automotive or LED sector [12]. Novel role of BPA in renal, cardiovascular and hypertensive diseases; latest discoveries

BPA in the renal system
BPA in the cardiovascular system
Pharmacokinetics of BPA
Calculation of BPA exposure in the general population
Systematic review of BPA exposure in hemodialysis patients
Systematic review of occupational exposure to BPA
G1: extremely high BPA concentrations
G2: elevated BPA concentrations
G3: “normal” range but with significant differences
Discussion
Findings
Conclusions
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