It is estimated that in the world today, there are at least 120,000 synthetic chemicals, or xenobiotics registered for commercial use and around 1,000 new chemicals are formulated each year. While many have been proven to be highly toxic and carcinogenic, little is known about the chronic effects particularly their potential to alter, or disrupt the function(s) of the endocrine system and our hormones. These synthetic chemicals are known as ‘environmental estrogens’, estrogen mimics, or xenoestrogens and have been found to affect hormonal functions by ‘mimicking’ the function of naturally occurring estrogen in the body.
Estrogens are a group of naturally occurring hormones present in both male testes and female ovaries, with females producing a considerably higher amount. They are particularly influential during puberty, menstruation and pregnancy; however they also assist in regulating the growth of bones, skin, liver and organs of the cardiovascular system. Estrogens, like all hormones, act as chemical signals and are important in helping cells in various organs to sense and respond to changing physiological conditions; therefore the right balance of hormones is critical in order to carry out the functions required of a healthy, strong body. Estrogen binds to a protein, or estrogen receptor, and the estrogen receptor complex can then bind to specific genes and by this, alter the way they are expressed, resulting in a change in cell programming 1.
Environmental estrogens, are now present in everyday products such as polycarbonate plastics, food packaging and cans. However the greatest source for many people is through cosmetics and personal care products and include chemicals such as triclosan, cyclosiloxanes, parabens and phthalates which are often left on the skin to absorb and accumulate 2. Women are disproportionately exposed to many environmental estrogens like paraben and phthalates because they use more personal care products on average than men 3 and teenage girls tend to use even more products than women, averaging 17 different products per day, compared with 12 for women 4.
Since the 1980’s, there has been a growing amount of research toward the potential interaction between these environmental estrogens and wild animals, with a number of reports detailing the emergence of ‘feminised wildlife’ around the world, and a range of adverse effects in humans including decreased sperm count, increased cases of testicular cancer and testicular abnormalities, increased breast cancer in men and women and premature or precocious puberty. Other adverse health include headache, migraine, depression, gastrointestinal disturbances, insomnia, mastopathia, changes in vaginal bleeding 5. More chronic symptoms affect the cardiovascular system, the skin (itching, rash, abnormal pigmentation), the gallbladder, and tumours, particularly of the breast but also uterus, cervix, vagina and liver 5.
One of the most troubling is their association with breast cancer 6,7,8. Breast cancer is the major cancer affecting women in the Western world 9 and one of the most disturbing and well documented current trends is the alarming increase in breast cancer incidence over the past few decades. Fifty years ago the risk rate was one woman in 20; today it is one in 8 and approximately two-thirds of breast tumors are estrogen receptive, and environmental estrogens like parabens are known to bind to estrogen receptors. Estrogen-dependent cancers, such as breast cancer, are known to be highly responsive to estrogens for growth. Even more disturbing is the increase in numbers of young girls developing breast cancer. Although many factors such as radiation, alcohol, smoking and diet, add to the risk of developing breast cancer, the predominant influencing factor has been identified as the exposure to estrogens throughout an individual’s lifetime 9.
The breast is under hormonal control and a fine balance of hormones is what allows the cell to cell communication. Interaction between these cells and the surrounding fluid of the breast tissue is what controls differentiation and growth of the breast 9. If there is a disruption of those hormones, i.e. through the use of synthetic chemicals, the balance of hormonal control is thrown and the cells do not function normally which may lead to breast cancer. In support of this clinical studies show that estrogen has the capacity to drive breast tumours to grow in laboratory studies. Animal experimental studies have also shown the role of estrogen on the growth of breast cancer cells 9. While chemicals which mimic estrogen have been shown to promote and stimulate the proliferation of breast cancer cells 2,10,11, and activate other processes involved in breast cancer 2,11,12. Recent studies have also shown other factors can dramatically increase the the toxicity of Xenoestrogens and studies of individual estrogens may seriously underestimate their growth and spreading effects in breast tissue cells and their potency to promote breast cancer, particularly at lower doses 13.
Although the vast majority of studies on breast cancer are aimed towards women, men can also suffer from the disease, indicating that they have similar risk factors, with one case in a hundred diagnosed breast cancers being a male 14. Although this number is relatively small, the rate of incidence has increased by 25% in 25 years.
Sperm count of the average male in the US or Europe has been found to be declining continuously over the past four decades, dierectly linked with environmental estrogen exposure, and today it is less than 50% of what it was forty years ago15,16. One result of this lower count is the increased rate of male infertility; which is also the single most common cause of infertility. The rate of infertility has quadrupled in the past forty years, from 4% in 1965 to at least 16% today 15.
Other conditions including undescended testes caused by prenatal estrogen exposure to environmental estrogens have also been found in studies on mice and it has been suggested undescended testes increases the rate of testicular cancer 17. The incidence of testicular cancer, namely affecting males between the ages of 20 to 30, has also seen an increase worldwide. Studies have found strong links with exposure to excessive levels of estrogen with hypospadias (abnormal congenital opening of male urethra upon under surface of the penis) 18,19, lower libido 19, congenital anomalies, cryptorchidism and testicular cancer 20,21,22.
Environmental estrogens have also been linked to early puberty in girls and increasing number of girls experiencing precocious puberty in recent years 15. A study in the United States of 17, 000 girls indicated that 7% of white and 27% of black girls exhibited physical signs of puberty by age seven, and for girls aged 10 the percentages increased to 68 and 95 respectively 16. This trend for earlier puberty has been found to be widespread, with similar cases found in the United Kingdom, Canada and New Zealand (Trankina, M. V L., 2001).
Environmental estrogens are also suspected of disrupting thyroid functioning, sexual differentiation of the brain in foetal development and cognitive motor function 23. It is also believed that high levels of environmental estrogen exposure results in lower birth weights, smaller head circumferences, poorer neuromuscular maturity and visual recognition, delays in psychomotor development, short term memory problems, and growth retardation in newborn babies 24.
Prenatal exposure to environmental estrogens also poses a serious health risks to developing fetus and children as evidence of adverse effect on birth outcomes, childhood obesity, and intellectual disability are increasing 25. The placental barrier has been shown to allow these chemicals to cross as many of them have been measured in human fetal cord blood and tissue. More importantly, because organogenesis begins at the time when the fetus is solely dependent on maternal supply, early life exposure to environmental estrogens may lead to adverse short or long term health outcomes due to fetal reprogramming 26.
From testing on animals it has further been proposed that excessive estrogen levels could cause anxious behaviour 27,28, altered fecundency 29, reduced penis size 30 and increased embryo mortality 24. Environmental estrogens are not only capable of binding to estrogen receptors on cell membranes but are also able to bind to neurotransmitters such as epinephrine, neuroepinophrine and dopamine enabling estrogens to influence the body’s central nervous system (CNS) 31. Environmental estrogens have also been shown to effect the body’s immune system 30. A large number of studies have also environmental estrogens to contributing to obesity and diabetes, independent of poor diet and physical inactivity; such chemicals including ingredients found in personal care products and cosmetics such as phthalates and phenols 32,33.
More recently studies have found effects of direct exposure to products instead of just individual chemicals. Extensive observational studies have indicated a relationship between certain hair product use and hormonally imbalances including early menache (puberty) 34,35 and uterine fibroids 36 as well as enlargement of breast tissue in boys and men 37.
However, estrogenic (or anti-estrogenic) effects of the personal care products as commercial mixtures have rarely ever been evaluated. In a study of eight commonly used hair and skin products four of the eight personal care products tested (Oil Hair Lotion, Extra-dry Skin Lotion, Intensive Skin Lotion and Petroleum Jelly demonstrated detectable estrogenic activity 38. The estrogenic activity of these products was not predictable by examining their listed ingredients. However, perhaps the most surprising finding about any one product was the estrogenic activity of SP4 (Petroleum Jelly). Petroleum jelly products are also often used on infants as low-cost therapies for common problems such as diaper rash and is manufactured by refinement of the crude petroleum product. While other studies have shown that hair oil use as a child was significantly associated with earlier menarche and hair relaxer use and uterine fibroids among participants in the 36. A third study found an elevated incidence of endometriosis and use of personal care products containing benzophenone-type UV filters 39.
Fortunately, studies have also shown it is relatively easy to reduce exposure by reducing personal care use or using safer products. In one study of around 100 girls they replaced their personal care products with safer alternatives for 3 days. The replacement products were chosen on the basis of whether their ingredient lists included triclosan, benzophenone-3, or parabens. Phthalates are not listed on ingredient lists, but they are often found in scented products. So the researchers avoided products that listed “fragrance” as an ingredient unless they were specifically labeled as phthalate free. More than 90% of the participants had detectible levels of phthalates, parabens, and benzophenone-3 before they started using the replacement products. After using the alternative products for 3 days urinary concentrations of methyl and propyl paraben decreased by 43.9% and 45.4%, respectively, mono-ethyl phthalate decreased by 27.4%, and triclosan decreased by 35.7%. However, there were increases in concentrations of butyl and ethyl paraben, which were detected in about half the girls. These chemicals might have been unintentional contaminants or unlabeled ingredients in replacement products, which they acknowledge they were unable to ensure were paraben free 40.
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