The Association of Carotid Intima-Media Thickness with Endocrine Disrupting Chemicals

The Association of Carotid Intima-Media Thickness with Endocrine Disrupting Chemicals

Mini Review
Endocrine Disrupting Chemicals
Endocrine disrupting chemicals (EDCs) are chemicals that have the capacity to modulate endocrine systems. They are mostly man-made, found in various materials such as phytochemicals, pesticides, consumer products, and plastics [1]. Given the terrible burden of type 2 diabetes mellitus (DM) and macrovascular disease in modern society, understanding the links between environmental pollutants and these disease states is critical for formulating effective prevention strategies and identifying novel therapeutic interventions. Phthalates are a class of industrial chemicals that consist of mono-benzyl phthalate (MBzP) and mono-2-ethylhexyl phthalate (MEHP) widely applied in the increase of flexibility and resilience in consumer products such as plasticizers [2]. MBzP and MEHP, phthalate metabolites, potentially affect traditional cardiovascular risk predictors including carotid intima-media thickness (CIMT) and the echogenicity of intima-media and plaques in the Prospective Investigation of the Vasculature in Uppsala Seniors study [3-4]. As a weak EDC, plenty of animal studies have shown low-dose effects of Bisphenol A (BPA).

Those investigations have addressed complications of BPA on neurologic development, reproductive function and metabolic process [5]. It is now known that BPA exposure is likely to increase cardiovascular risk factors. BPA exposure is positively correlated with obesity, insulin resistance, metabolic syndrome, and DM [6]. In addition, these findings of changes in heart rate variability and higher blood pressure are typically caused by higher urinary BPA [7]. Those studies have well discussed the association between BPA exposure and the risk predictions of cardiovascular diseases or atherosclerosis. According to toxicological studies in animal experiments, perfluorooctanoic acid (PFOA) and perfluorooctane sulfate (PFOS) lead to thyroid dysfunction [8], immune suppression [9], dyslipidemia [10], carcinogenesis [11], and oxidative stress [12]. Given the importance in our understanding of the activation of the PPARα, a physiology-based clinical approach is a crucial component to make the trigger of tumorigenesis, hepatitis, immunosuppression, developmental defects in the association with exposure to perfluorinated compounds (PFCs) [13].

Counteracting Carotid Intima-Media Thickness with Endocrine Disrupting Chemicals
A cross-sectional research to demonstrate a significant linkage between CIMT, phthalate metabolites, BPA and PFOS is to indicate the atherogenic effects of EDS exposure in adolescents and young adults. Younger participants exposed to higher levels of BPA in the study of U.S. National Health and Nutrition Examination Survey (NHANES) [14]. Soft drinks, food prepared outside the home, and school lunches which have been correlated with urinary BPA levels are more consumed by younger populations [15]. Depending on assessment of CIMT and the echogenicity of the intimae-media complex, BPA may obtain interrelation with the echogenicity of the plaques but no correlation with CIMT in the Swedish study [16]. The different findings may attribute to the confounding factors such as the race between Caucasian and Asian and the age between older and younger participants. The environmental exposure to PFCs may cause long-term health complications in in adolescents and young adults. An appealing alternative theory described by Qian et al has been suggested by exposure of human microvascular endothelial cells to PFOS, in which subsequent detrimental effects of ROS was induced by PFOS in cells [17]. As a result of this increase in ROS combined with oxidative stress, the situation gave rise to reorganize actin filaments and ameliorate endothelial permeability. The increase in atherosclerosis exposed to phthalate esters demonstrate the cardiovascular risks among high exposures, mostly coming from the first phase metabolite MEHP in young population. In the presence of prenatal phthalate exposure, a Spanish birth cohort literature revealed postnatal growth and blood pressure in a gender-specific factor associated with girls particularly [18].

Conclusion
EDCs including phthalates, BPA, and PFOS may aggravate subclinical atherosclerosis in adolescents and young adults. MEHP metabolite is the major component of phthalates-induced atherogenic pathogenesis. We discuss the important circumstantial evidence to find the relationship between EDCs and subclinical atherosclerosis in primary prevention of environmental cardiology. Moreover, the potential influence of exposure to EDCs on the major atherosclerotic cardiovascular events warrants more extensive and prospective cohort researches in the future.

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