What are Endocrine-Disrupting Chemicals?
Endocrine-disrupting chemicals (EDCs) are exogenous chemicals that interfere with hormone action, thereby increasing the risk of adverse health outcomes, including cancer, reproductive impairment, cognitive deficits, and obesity.
The endocrine system is composed of glands that secrete chemical messengers (hormones) that interact with specific targets (receptors). These interactions lead to the regulation of a vast set of functions, including growth, development, reproduction, energy balance, metabolism, and body weight regulation
EDCs come from many different sources, people are exposed in several ways, including the air we breathe, the food we eat, and the water we drink. EDCs can also enter the body through the skin. Common examples of EDCs are Industrial chemicals and pesticides, some processed foods, Soy-based products, and even household dust.
The group of molecules identified as endocrine disruptors is highly heterogeneous and includes synthetic chemicals used as industrial solvents/lubricants and their byproducts [polychlorinated biphenyls (PCBs), polybrominated biphenyls (PBBs), dioxins], plastics [bisphenol A (BPA)], plasticizers (phthalates), pesticides [methoxychlor, chlorpyrifos, dichlorodiphenyltrichloroethane (DDT)], fungicides (vinclozolin), and pharmaceutical agents [diethylstilbestrol (DES)].
Various researches have shown that EDCs could be very harmful to the system. For instance, EDC can interact with or activate hormone receptors, antagonize it and further alter the hormone receptor expression. It has also been shown EDC has the ability to alter signal transduction (including changes in protein or RNA expression, post-translational modifications, and/or ion flux) in hormone-responsive cells and induce epigenetic modifications in hormone-producing or hormone-responsive cells. It can also alter hormone transport across cell membranes and change the hormone distribution or circulating hormone levels. Moreover, it can also alter hormone metabolism or clearance and alter the fate of hormone-producing or hormone-responsive cells.
Thus, after coming across threats pose by EDCs, it would be a great move to go for 100% pure, non-toxic, and EDC-free products for healthy well-being.
EDC has the ability to affect different persons differently. For example, the effect that it incurs on females is quite different from her male counterpart.
Development and function of the female reproductive tract depend on coordinated biological processes that, if altered by endogenous or exogenous factors during critical periods of development or during different life stages, could have significant adverse effects on women’s health and reproductive function and outcomes.
A key question arises as to whether EDCs contribute to the development of female reproductive disorders, particularly those occurring during a critical window of susceptibility: in utero, neonatally, in childhood, during puberty, and during adulthood. There are increasing data from wildlife studies and laboratory studies with rodents, ungulates, and nonhuman primates that support the role of EDCs in the pathogenesis of several female reproductive disorders, including polycystic ovarian syndrome, aneuploidy, POF, reproductive tract anomalies, uterine fibroids, endometriosis, and ectopic gestation.
PCOS is a heterogeneous syndrome characterized by persistent anovulation, oligo- or amenorrhea, and hyperandrogenism in the absence of thyroid, pituitary, and/or adrenal disease. It is plausible that in utero exposure of human female fetuses to androgen-like EDCs could result in PCOS in adulthood, along with associated metabolic disorders. Very recent evidence for androgenic properties of personal-care products such as triclocarban adds to the possibility of environmental androgens, although a connection to PCOS has not yet been drawn.
Some studies have indicated that organochlorine pesticides (synthetic EDCs) adversely affect the ovary by reducing ovarian weight, follicle growth, and oocyte viability and/or increasing atresia. Several studies show that pesticide exposure is associated with reduced fertility in women and animal models. Organochlorine pesticide exposure was associated with an increased time to pregnancy in women.
Epidemiological data show that the selected EDCs are associated with adverse fertility outcomes such as reduced gestational age, weight, pregnancy gain, increased risk for miscarriage, and time to pregnancy in women. Experimental data show that EDC exposure during adulthood caused a range of effects such as estrous cyclicity abnormalities, decreased pregnancy rates, decreased pup survival, and the increased onset of reproductive senescence. Some studies report that EDCs exert toxicity through estrogen receptors, aryl hydrocarbon receptors, and peroxisome proliferator-activated receptor activation mechanisms, but they have not examined other potential pathways.
The male reproductive system may be susceptible to the effects of environmental toxicants. The general population continues to be exposed to EDCs through ingestion of contaminated food, inhalation of contaminated air and dust, and skin contact, while some areas are subjected to greater risk due to geographical and cultural reasons. Due to temporal downward trends in semen quality and testosterone levels and increased rates of testicular cancers among adult male populations. Scientific researchers and the general public have become increasingly concerned regarding the potential risk of EDCs to men’s reproductive health. Cellular models and animal toxicological studies have demonstrated that EDCs can exert adverse effects on the male reproductive system. In humans, there are a growing number of epidemiological studies about EDCs and detrimental reproductive function. However, a potential decline in human male reproductive health and a link to exposure to endocrine active chemicals in the environment has been controversial for almost two decades.
There is current scientific, public, and governmental interest in the potential health risks of exposure to EDCs, the human evidence on associations of EDCs with altered male reproductive health endpoints remains limited and, in certain instances, inconsistent across studies. There is a need for further epidemiological research on various classes of EDCs.
The exposure may occur early in life as every pregnant woman has EDs in her body and may transfer them through the placenta to the fetus and through milk to the infant. Inhalation, oral and dermal exposures are the main routes of adult exposure to environmental chemicals. EDs may act via classical nuclear receptors, nonnuclear steroid hormone receptors, nonsteroid receptors, orphan receptors, enzymatic pathways involved in steroid biosynthesis and/or metabolism, and other mechanisms involved in endocrine and reproductive system function.
The environmental toxins have been found in our air, water, and soil as well as in a range of household products, including children’s toys. Bisphenol A (BPA) is used in certain children’s toys, plastic bottles, and food containers, food can linings, and cash register receipts. The concern has grown since even a low level of exposure to EDCs can affect body functions, particularly in the most vulnerable populations including infants and children. Some EDCs may be stored in fat cells for years after exposure and may be passed on to children during pregnancy or when breastfeeding.
Although scientists are still working to understand how endocrine disruptors are accumulated and excreted. They do know that significant levels of these compounds can be detected in a vast majority of people today. Although tests that measure the presence of the metabolites made by endocrine disruptors can give you an idea of your overall exposure to these insidious chemicals, detoxification treatment protocols aren’t yet well-defined.
What experts do know, however, is that certain endocrine disruptors tend to accumulate in body fat. In such cases, simply losing a few extra pounds may be enough to decrease chemical concentration and restore optimal fertility. In most cases, the best way to protect your fertility from the harmful effects of endocrine disruptors is by taking steps to minimize your exposure to EDCs in the first place.