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Critical Analysis of Human Exposure to Bisphenol A and Its Novel Implications on Renal, Cardiovascular and Hypertensive Diseases
Summary
This critical review analyzed urinary BPA concentration data across major population studies and found widespread human exposure to bisphenol A, with mounting evidence linking chronic low-level BPA exposure to renal, cardiovascular, and hypertensive diseases through its endocrine-disrupting mechanisms.
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.
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