Developmental Exposure to Endocrine Disrupting Chemicals and Its Impact on Cardio-Metabolic-Renal Health.

Radha Dutt Singh,Ratnakar Tiwari,Hafizurrahman Khan,Vineeta Sharma,Vikas Srivastava,Kavita Koshta

doi:10.3389/ftox.2021.663372

Abstract

Developmental origin of health and disease postulates that the footprints of early life exposure are followed as an endowment of risk for adult diseases. Epidemiological and experimental evidence suggest that an adverse fetal environment can affect the health of offspring throughout their lifetime. Exposure to endocrine disrupting chemicals (EDCs) during fetal development can affect the hormone system homeostasis, resulting in a broad spectrum of adverse health outcomes. In the present review, we have described the effect of prenatal EDCs exposure on cardio-metabolic-renal health, using the available epidemiological and experimental evidence. We also discuss the potential mechanisms of their action, which include epigenetic changes, hormonal imprinting, loss of energy homeostasis, and metabolic perturbations. The effect of prenatal EDCs exposure on cardio-metabolic-renal health, which is a complex condition of an altered biological landscape, can be further examined in the case of other environmental stressors with a similar mode of action.

Highlights

Environmental toxicants comprise a wide range of chemical agents released through natural or anthropogenic sources
Early-life exposure to Endocrine disrupting chemicals (EDCs) was associated with elevated levels of kidney toxicity markers such as albumin-to-creatinine ratio (ACR), estimated glomerular filtration rate, and urinary protein-to-creatinine ratio (UPCR) in some human population studies (Li et al, 2012; Trasande et al, 2013a, 2014; Malits et al, 2018)
A combined cohort study demonstrated that women prenatally exposed to DES are at higher risk of coronary artery disease (CAD), myocardial infarction (MI), high cholesterol levels, hypertension, and elevated blood pressure (Troisi et al, 2013, 2018)

Summary

Introduction

Environmental toxicants comprise a wide range of chemical agents released through natural or anthropogenic sources. Multiple studies have reported metabolic disruption after gestational arsenic exposure, including increased glucose intolerance, adiposity, and insulin resistance (Rodriguez et al, 2016; Huang et al, 2018). Early-life exposure to EDCs was associated with elevated levels of kidney toxicity markers such as albumin-to-creatinine ratio (ACR), estimated glomerular filtration rate (eGFR), and urinary protein-to-creatinine ratio (UPCR) in some human population studies (Li et al, 2012; Trasande et al, 2013a, 2014; Malits et al, 2018).

Results

Conclusion