[1][2] Xenoestrogens are clinically significant because they can mimic the effects of endogenous estrogen and thus have been implicated in precocious puberty and other disorders of the reproductive system.
Most scientists that study xenoestrogens, including The Endocrine Society, regard them as serious environmental hazards that have hormone disruptive effects on both wildlife and humans.
[15] Xenoestrogens in plastics, packaged food, drink trays and containers, (more so, when they've been heated in the Sun, or an oven), may interfere with pubertal development by actions at different levels – hypothalamic-pituitary axis, gonads, peripheral target organs such as the breast, hair follicles and genitals.
[21] Xenoestrogens have been implicated in a variety of medical problems, and during the last 10 years many scientific studies have found hard evidence of adverse effects on human and animal health.
For example, discharge from human settlement including runoff and water flowing out of wastewater treatment plants release a large amount of xenoestrogens into streams, which lead to immense alterations in aquatic life.
[35] Furthermore, xenoestrogens expose fish to CYP1A inducers through inhibiting a putative labile protein and enhancing the Ah receptor, which has been linked to epizootics of cancer and the initiation of tumors.
In addition, xenoestrogens stimulate vitellogenin (Vtg), which acts as a nutrient reserve, and Zona readiata proteins (Zrp), which forms eggshells.
[37] However, there is substantial evidence in a variety of recent studies to indicate that xenoestrogens can increase breast cancer growth in tissue culture.
Life relies on the transmission of biochemical information to the next generation, and the presence of xenoestrogens may interfere with this transgenerational information process through "chemical confusion" (Vidaeff and Sever),[47] who state: "The results do not support with certainty the view that environmental estrogens contribute to an increase in male reproductive disorders, neither do they provide sufficient grounds to reject such a hypothesis."
A 2008 report demonstrates further evidence of widespread effects of feminizing chemicals on male development in each class of vertebrate species as a worldwide phenomenon.
[citation needed] Puberty is a complex developmental process defined as the transition from childhood to adolescence and adult reproductive function.
Although the sequence may be reversed, androgen dependent changes such as growth of axillary and pubic hair, body odor and acne (adrenarche) usually appears 2 years later.
[54] A leading hypothesis for this change toward early puberty is improved nutrition resulting in rapid body growth, increased weight and fat deposition.
[3][4][60] American, European and Asian studies suggest breast development in girls occurs at a much younger age than a few decades ago, irrespective of race and socioeconomic conditions.
[63] The presence of phthalates were measured in the blood of 41 girls experiencing early onset breast development and matched set of controls.
[64] Not all cases of premature thelarche in the study sample contained elevated levels of phthalate esters and there was concern whether artificial contamination from vinyl lab equipment and tubing invalidated the results, hence weakening the link between exposure and causation.
This region of Italy is represented by a high density of navy yards and greenhouses where exposures to pesticides and mycoestrogens (estrogens produced by fungi) are common.
Although unable to identify a definitive cause of the high rates of precocious puberty, the authors concluded environmental pesticides and herbicides may be implicated.
[67][71] The current literature is inadequate to provide the information we need to assess the extent to which environmental chemicals contribute to precocious puberty.
[17] The ability to detect the possible role of chemicals in altering pubertal development is confounded by many nutritional, genetic and lifestyle factors capable of affecting puberty and the complex nature of the reproductive endocrine system.
Non-human animal studies have shown that exposure to environmental contaminants with estrogenic activity can accelerate the onset of puberty.
[18][77][78][79] Atrazine is widely used as an herbicide to control broad-leaf weed species that grow in crops such as corn, sugarcane, hay and winter wheat.
The damage that results in these dysfunctions is via the mechanisms of enzyme interference, cellular oxidation, epigenetic changes, and the breaking of DNA strands.
[84][85] One study demonstrated that when cultured rat pituitary cells were exposed to low levels of BPS, it altered the estrogen-estradiol signaling pathway and led to the inappropriate release of prolactin.
DDT's hazardous effects on the environment include being linked to the production of fragile eggshells in birds and showed a 90% decline in the birth rates of alligators.
[86] Though it is banned in the United States, DDT continues to be used in many parts of the world for agricultural use, insect control, and to fight the spread of malaria.
[86] Dioxin, a group of highly toxic chemicals are released during combustion processes, pesticide manufacturing and chlorine bleaching of wood pulp.
Upon significant exposure and accumulation in the system, toxicity of the major organs such as the heart, liver and kidneys has been reported and can lead to death within hours.
Low molecular weight phthalates are found in perfumes, lotions, cosmetics, varnishes, lacquers and coatings including timed releases in pharmaceuticals.
In children, exposure to phthalates has a marked difference when compared to adults, having been associated with disrupted reproductive hormone levels and thyroid function.