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Genetic Polymorphisms as Key Modulators of Cardiovascular Risk from Endocrine-Disrupting Chemicals.

Mariangela Palazzo1, Francesca Gorini1, Ludovica Simonini1

  • 1Institute of Clinical Physiology, National Research Council, 56124 Pisa, Italy.

Genes
|June 26, 2026
PubMed
Summary
This summary is machine-generated.

Environmental pollutants like PFAS and phthalates increase cardiovascular disease risk. Genetic variations influence susceptibility, highlighting the need for gene-environment interaction studies in preventive cardiology.

Keywords:
PAHsPBDEsPCBsPFASbisphenolscardiovascular riskdioxinsendocrine-disrupting chemicalsgenetic polymorphismsphthalates

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Area of Science:

  • Environmental Health
  • Cardiovascular Science
  • Toxicology

Background:

  • Environmental exposure to endocrine-disrupting chemicals (EDCs) is linked to increased cardiovascular disease (CVD) risk.
  • Persistent and non-persistent EDCs include PFAS, PCBs, PBDEs, PAHs, dioxins, phthalates, and bisphenols.
  • Gene-environment interactions are crucial in determining individual susceptibility to EDC-induced cardiovascular effects.

Purpose of the Study:

  • To review current knowledge on EDCs and their association with cardiovascular outcomes.
  • To evaluate the role of genetic variability in modulating EDC-induced cardiovascular risk.
  • To synthesize evidence on gene-environment interactions in EDC-related CVD.

Main Methods:

  • Literature review and synthesis of studies on EDCs and cardiovascular health.
  • Analysis of genetic polymorphisms involved in oxidative stress, xenobiotic metabolism, hormone signaling, and lipid homeostasis.
  • Examination of specific gene variants (e.g., CAT, eNOS, PON1, GSTP1, CYP2C19, ABCB1, MTHFR, ESR2, FTO, LEPR, INSIG2) and their association with EDC exposure and cardiovascular outcomes.

Main Results:

  • Genetic variants in antioxidant defense genes (CAT, eNOS, PON1) are linked to hypertension and vascular dysfunction from bisphenol and PAH exposure.
  • Polymorphisms in GSTP1, CYP2C19, CYP1A2, CYP2E1, ABCB1, and MTHFR may affect susceptibility to cardiometabolic issues and congenital heart defects.
  • Variants in ESR2, FTO, LEPR, and INSIG2 are associated with obesity, dyslipidemia, and hypertension linked to PFAS, PBDEs, and bisphenols.

Conclusions:

  • Gene-environment interactions significantly modulate cardiovascular risk associated with EDC exposure.
  • Understanding these interactions is vital for advancing preventive cardiology.
  • Targeted strategies considering genetic predispositions are needed to mitigate the cardiovascular impact of environmental pollutants.