Environmental Estrogens:

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The Invisible Threat That Surrounds Us By Kimberly Pryor Daily, we eat and breathe substances shown to cause birth defects and cancer in animals. These environmental estrogens are everywhere. In the milk and water we drink, in the food we consume, in birth control pills, dental sealants, and plastics. Based on breast milk concentrations nationwide, it has been estimated that at least 5% and possibly more of the babies born in the United States are exposed to quantities of polychlorinated biphenyls (PCBs) sufficient to cause neurological defects.1

to approximately 50 environmental estrogens.2

Concern over environmental estrogens is so great that in 1999 the Environmental Protection Agency (EPA) initiated a screening and testing program to identify the potential endocrine-system impact of the 87,000 chemicals in commercial use. In addition, the Centers for Disease Control (CDC) and the National Institutes of Health (NIH) are examining blood and urine samples to quantify what risk Americans may face from exposure

Meanwhile, what can we do to protect ourselves from these prolific chemicals? Scientists are exploring certain nutrients in vivo and in vitro to determine if they can guard against environmental estrogens. Before addressing which nutrients may act as an ecoestrogen shield, however, we must examine how and why these chemicals threaten both our longevity and our children’s health. Widespread Contamination One particularly sobering example of the heart-breaking consequences of human interaction with environmental estrogens was illustrated in a 1984 study. The study involved 242 newborn infants whose mothers consumed, over six years, moderate quantities of PCB-contaminated Lake Michigan fish. The infants belonging to mothers who had consumed the fish weighed an average of 190 grams less at birth than controls. This level was comparable to the low birth weights of children whose mothers smoked during pregnancy. The PCB-exposed infants had smaller head circumferences and exhibited poorer neuromuscular maturity. Furthermore, the mothers who had consumed the most fish had the highest serum PCB concentrations, and their babies had the highest umbilical cord PCB levels. This was particularly disturbing considering the mothers ate as little as two salmon or lake trout meals per month.3 (1 of 8) [2008-03-25 21:17:37]

A follow-up study indicated that, at six to seven months of age, the contaminated infants experienced delays in psychomotor development and poorer visual recognition compared with controls. At four years of age, the children exhibited short-term memory problems. During the testing, 17 of the children whose mothers’ breast milk had the highest PCB concentrations became unmanageable and refused to cooperate. In another study comparing the same infants to children of mothers exposed to a PCB farming accident, both groups experienced growth retardation and neurological defects. These defects were directly dose- related to umbilical cord serum PCB concentrations and levels in fetal blood.1 Many drainage basins are just as contaminated in other parts of the country as the Great Lakes. In the Central Valley of California, wildlife drink from agricultural drain canals containing estrogenic chemicals. In the farm communities of Southeastern Spain, fat samples from local children contained a total of 14 pesticides.4-6 Banned in the U.S. since the early 1970s, synthetic estrogens such as DDT and PCBs continue to poison the environment, partially due to their ongoing use in developing countries and their ability to vaporize and drift across the globe.7 In addition, ecoestrogens keep a tenacious grip on the planet, as DDT has a half-life of 57.5 years in temperate soils. Despite the ban on these two destructive chemicals, other estrogenic pesticides, plasticizers and chemicals continue to be used in the United States. This widespread contamination is particularly alarming given that PCBs, dioxins, DDT and a number of other pesticides — often called organochloride compounds — are lipid-soluble and find a home in fatty tissue in the body. In particular, these organochloride compounds are found in breast milk, with its high lipid content. The concentrations in embryos and fetuses parallel those in mothers. Infants, therefore, are at an increased risk.1 Humans also are exposed to estrogenic compounds through the consumption of sex-steroidtreated meat and dairy products. The Joint Food and Agricultural Organization/World Health Organization Expert Committee on Food Additives (JECFA) and the FDA claimed in 1988 that the estrogenic residues found in meat from treated animals posed no risk for consumers. One group of scientists who re-evaluated the JECFA conclusions, however, were particularly concerned with meat concentrations of the natural estrogen, estradiol. These scientists believed that these estrogenic residues could jeopardize the health of prepubertal children. In the scientists’ opinion, JECFA’s conclusions concerning the safety of hormone residues in meat “seem to be based on uncertain assumptions and inadequate scientific data.”8 The Danger Begins In the early 1970s, scientists first realized that substances not intentionally made to act as hormones could unintentionally take on an estrogenic role. This realization came after a chemical spill of Kepone, a chemical used in manufacture of the pesticide Mirex™, resulted in lowered sperm counts in exposed men. Researchers confirmed that Kepone was a weak estrogen, although its chemical structure bore no resemblance to the natural hormone. (2 of 8) [2008-03-25 21:17:37]

Scientists soon realized that Kepone had plenty of company. They confirmed that DDT and other pesticides acted like endogenous estrogens or produced estrogenic breakdown products.9 Wildlife seemed to be particularly vulnerable to environmental estrogens. In fact, problems with wildlife provided the first hint that environmental estrogens might also be causing problems in humans. After examining two- and four-year-old salmon in the Great Lakes, researchers discovered enlarged thyroids in every specimen. Of the male salmon, 40 to 80% also experienced a high rate of precocious sexual maturation. In addition, many of the salmon eggs did not hatch. These disastrous effects traveled up the food chain. In bald eagle nests, egg shells thinned and cracked, an effect attributed to DDT.1 Further support for environmental estrogens’ destructive role arose when University of Florida researchers discovered reproductive abnormalities in females, and feminization of male alligators nesting at Florida’s Lake Apopka. Lake Apopka is located adjacent to an EPA Superfund site contaminated with dicofol and DDT. Both of these substances are known estrogen mimics. At six months of age, female alligators from Lake Apopka had plasma estrogen concentrations almost two times greater than normal females. In addition, the alligators suffered from abnormal ovaries, and an increased mortality rate. The plasma testosterone levels in male juvenile alligators from Lake Apopka were more than three times lower than control males in Lake Woodruff. Lake Apopka males also had poorly organized testes and abnormally small phalli. In two cases, Lake Apopka alligators without penises were identified as females, but were subsequently observed to have testes. Two animals with penis-like appendages were identified as males yet possessed ovarian tissue. The researchers concluded the reproductive abnormalities were likely due to the alligators’ exposure to an estrogenic substance.10 Reproductive Abnormalities Many synthetic chemicals serve as sex steroid imposters. They trick the body into believing they are natural, endogenous estrogens, which enables them to push the real hormone out of the way. As these imposters replace the endogenous estrogen, they are capable of sending the wrong signals to the chemical messenger pathways through which estrogens normally work. Although there is considerable debate over the extent of harm environmental estrogens cause, much evidence points toward a possible link between environmental estrogens and reproductive diseases and cancer. In 1948, doctors began prescribing the estrogenic Diethylstilbestrol (DES) to prevent miscarriages. Twenty-three years later, scientists discovered that some of the adolescent daughters whose mothers had taken DES developed adenocarcinoma, a rare form of vaginal cancer. The cells in the vagina or fallopian tubes of these female offspring were deformed and there were structural changes in the girls’ uteri. Some men exposed in utero to DES experienced increased incidences of cryptorchidism, where one or both testicles had not descended into the scrotum, an important risk factor for (3 of 8) [2008-03-25 21:17:37]

testicular cancer. Abnormal congenital openings of the male urethra upon the undersurface of the penis, called hypospadias, and decreased semen volume and sperm counts, were also found in the DES-exposed men.11 Breast cancer incidence has steadily climbed in the US, which has been attributed to the accumulation of estrogenic chemicals in the environment.12-13 Many of these chemicals have caused cancer in animals and are suspected human carcinogens. Both DDT and PCBs have been shown to be tumor promoters and demonstrate estrogenic activity. According to Merriam Webster’s Medical Dictionary, DDE is a persistent organochlorine produced by the metabolic breakdown of DDT. In 58 breast cancer patients, DDE levels were approximately 35% higher than in 171 matched, healthy controls.14 Increased incidences of male reproductive disorders have accompanied the breast cancer rise. Testicular cancer, cryptorchidism and urethral abnormalities (hypospadias) — all conditions that arise at the fetal development stage — have more than doubled in the past 30-50 years, while sperm counts have declined by about half. Furthermore, testicular cancer is now a leading cause of death in young men.15-20 Impact of Synthetic Estrogens The natural estrogen, estradiol, binds to extracellular proteins, and is less effective at entering the cells, whereas the synthetic estrogen DES, is attracted to the estrogen receptor, and more easily gains access to the cell. At equivalent concentrations in the blood, more DES enters the cell than does the natural estrogen estradiol. As one researcher describes, “DES is a functionally more efficient estrogen than is the natural hormone.”10 Studies in rats have shown that estrogenic environmental toxicants dramatically affect fertility. Estrogenic chemicals have altered the tissue structure of the male animals’ seminiferous tubules, with higher doses impairing testicular mass and sperm count. Estrogenic chemicals have also had toxic effects on both rat testes and epididymis. Researchers have speculated that the same effects might also occur in humans.21 Other researchers have suggested that small amounts of many estrogenic chemicals may have as disastrous an effect as large amounts of any one chemical. Scientists also have connected reproductive disorders to populations where exposure to estrogenic agents are high.22 Furthermore, another recent in vitro study determined that PCBs significantly increased MCF-7 human breast cancer cell proliferation, an estrogenic form of cancer. The addition of the drug hydroxytamoxifen, an estrogen antagonist, inhibited the increased cell proliferation associated with cancer.23 Clearly, protection against these harmful environmental invaders is needed. Scientists have investigated the following nutrients for the role they may play in protecting humans against ecoestrogens. Indole-3-Carbinol Indole-3-carbinol inhibits cell proliferation in human MCF-7 breast cancer cells even more (4 of 8) [2008-03-25 21:17:37]

effectively than the drug tamoxifen. If tamoxifen can halt the activity of estrogenic chemicals such as PCBs, then I3C may do the same.24 An antiestrogen, I3C is found in cruciferous vegetables (broccoli, cauliflower, brussels sprouts). It alters the way estrogen is metabolized in the body, from the “bad” pathway to the “good” pathway, as reported in the October 1999 issue of Vitamin Research News. The “tumor enhancer” metabolic pathway, 16 alphahydroxylation, is elevated in patients with breast and endometrial cancer and in those at increased risk of such estrogen-dependent cancers. When estrogen veers away from the 16alpha pathway and instead takes the “tumor suppressor” metabolic pathway — called 2hydroxylation — the incidence of cancer decreases. Healthy individuals not at risk for estrogendominant breast or endometrial cancer bypass the 16-alpha route and metabolize estrogen through the 2-hydroxylation pathway. Research has indicated that some organochlorine-based pesticides elevate estrogen excretion through the “tumor promoter” pathway in MCF-7 breast cancer cells, while phytochemicals like indole-3-carbinol (I3C) switch the elimination route to the “tumor suppressor” pathway.25-26 In studying the effects of I3C and ICZ (an acid-derived condensation product of I3C) on the effects of estrogen metabolism, researchers concluded that I3C’s antiestrogenic properties may help expel estrogenic contaminants from the body.27 Sperm Counts and Nutrients Carnitine, arginine, zinc, selenium, vitamin B-12, and the antioxidants vitamin C, vitamin E, glutathione, and coenzyme Q10 have all been shown to improve sperm counts, sperm motility and male infertility. In one study of mice fed one of three different pesticides, 20 to 40 mg/kg body weight per day of vitamin C offered protection against the decreased sperm count and deformed sperm that developed in the animals treated with only the chemicals. 28-29 Antioxidants and Ecoestrogens Research indicates that oxidative damage may account for some of the toxicity of environmental estrogens. In mice, vitamins C and E have protected the liver against some of the damaging effects exerted by the estrogenic chemical dieldrin. It also has been shown that estrogenic chemicals such as PCBs increase the rate at which the body excretes ascorbic acid. Administering ascorbic acid to environmental-estrogen-exposed fish considerably neutralized the toxic effect of the chemical with a 10-fold decrease in the number of fish killed. Furthermore, ascorbic-acid-deficient guinea pigs have a harder time biodegrading pesticide residue and experience a greater accumulation of pesticide in tissue. 30-32 In rats and guinea pigs exposed to the potent environmental estrogen, PCB, the administration of 1000 mg/kg dietary vitamin E significantly reduced the amount of ascorbic acid excreted and the amount of thiobarbituric acid-reactive substances (TBARS), a significant marker of oxidation. In PCB-contaminated guinea pigs, feeding high levels of both ascorbic acid and vitamin E was more effective in reversing the PCB-induced severe growth retardation and in lowering the TBARS level than feeding the vitamins separately. 33-34 Furthermore, scientists have discovered that carotenes and carotenoids, including beta (5 of 8) [2008-03-25 21:17:37]

carotene, were significantly lower in cancer patients compared to healthy controls. In postmenopausal women with breast cancer, serum xanthophyll (e.g. lutein) levels were significantly lower than among healthy controls. In premenopausal women, serum betacarotene levels tended to be lower among breast cancer cases than among controls.35 These results suggest that combination antioxidant nutritional formulas may offer significant protection against environmental estrogens. Other Potential Protectors High fiber intake may lower blood estrogen concentrations, particularly in premenopausal women. Also, selenium deficiency may be an indicator of environmental estrogens. Feeding PCBs to chicks has decreased the animal’s ability to utilize selenium, leaving cell membranes vulnerable to the harmful effects of pesticide-induced peroxidation.36-37 This selenium deficiency in PCB-treated animals suggests a possible need for additional selenium supplementation. Conclusion Environmental estrogen contamination is widespread. It is almost impossible to escape encounters with these chemicals. However, antioxidants, I3C and other nutrients can play a significant role in protecting us from such ecoestrogens. References: 1. Colborn Theo, vom Saal Frederick, Soto Ana. Developmental effects of endocrine-disrupting chemicals in wildlife and humans. Environmental Health Perspectives. 1993; 101(5):378-84. 2. CNN, report posted on the Internet. Rochelle Jones. January 3, 2000. Copyright 1999. 3. Fein G, Jacobson J, Jacobson S, Schwartz P, Dowler J. Prenatal exposure to polychlorinated biphenyls: effects on birth size an gestational age. The Journal of Pediatrics. 1984; 2(105):31520. 4. Johnson ML, Salveson A, Holmes L, Denison MS, Fry DM. Environmental Estrogens in agricultural drain water from the Central Valley of California. Bull Environ Contam Toxicol. 1998; 60:609-14. 5. Olea N, Olea-Serrano F, Lardelli-Claret P, Rivas A, Barba-Navarro A. Inadvertent exposure to xenoestrogens in children. Toxicol Ind Health. 1999; 15(1-2):151-8. 6. Purdom CE, Hardiman PA, Bye VJ, Eno NC, Tyler CR, Sumpter JP. Estrogenic effects of effluent from sewage treatment works. Chem Ecol. 1994; 8:275-85. 7. Colborn T, Davidson A, Green SN, Hodge RA, Jackson CI, Liroff RA. Great Lakes, great legacy? Washington, DC: The Conservation Foundation, 1990. 8. Andersson AM, Skakkebaek NE. Exposure to exogenous estrogens in food: possible impact on human development and health. Eur J Endocrinol. 1999;140(6):477-85. (6 of 8) [2008-03-25 21:17:37]

9. McLachlan JA, Arnold SF. Environmental Estrogens. American Scientist. 1996. Available over the Internet at 10. Guillette LJ Jr., Gross TS, Masson GR, Matter JM, Percival HF, Woodward AR. Developmental abnormalities of the gonad and abnormal sex hormone concentrations in juvenile alligators from contaminated and control lakes in Florida. Environ Health Perspect. 1994; 102(8):680-8. 11. Sharpe RM, Skakkebaek NE. Are oestrogens involved in falling sperm counts and disorders of the male reproductive tract? The Lancet. 1993; 341:1392-95. 12. Harris JR, Lippman ME, Veronesi U, et al. Breast cancer (part 1). N Engl J Med. 1992; 327:319-28. 13. Ries LAG, Hankey BF, Miler BA, et al. Cancer Statistics Review. 1973-88. DHEW Publ No. (NIH)91-2789. Washington DC: US Govt Print Ofc. 1991. 14. Wolff MS, Toniolo PG, Lee EW, Rivera M, Dubin N. Blood Levels of Organochlorine Residues and Risk of Breast Cancer. J Nat Can Inst. 1993;85(8):648-52. 15. Giwercman A, Skakkebaek NE. The human testis -- an organ at risk? Int J Androl. 1992;15:373-75 16. Osterlind A. Diverging trends in incidence and mortality of testicular cancer in Denmark, 1943-1982. Br J Cancer. 1986; 53:501-05. 17. Carlsen E, Giwercman A, Keiding N, Skakkebaek NE. Evidence for decreasing quality of semen during past 50 years. BMJ. 1992;305:609-13. 18. Hutson JM, Williams MPL, Fallat ME, Attah A. Testicular descent: new insights into its hormonal control. In: Milligan SR, ed. Oxford reviews of reproductive biology. Oxford: Oxford University Press, 1990:1-56. 19. Skakkebaek NE. Carcinoma-in-situ and cancer of the testis. Int J Androl. 1987;10:1-40. 20. Swan SH, Elkin EP. Declining semen quality: Can the past inform the present? BioEssays. 1999; 21:614-21. 21. de Jager C, Bornman MS, van der Horst G. The effect of p-nonylphenol, an environmental toxicant with oestrogenic properties, on fertility potential in adult male rats. Andrologia. 1999; 31(2):99-106. 22. Olea N, Olea-Serrano F, Lardelli-Claret P, Rivas A, Barba-Navarro A. Inadvertent exposure to xenoestrogens in children. Toxicol Ind Health. 1999; 15(1-2):151-8. (7 of 8) [2008-03-25 21:17:37]

23. Andersson PL, Blom A, Johannisson A, Pesonen M, Tysklind M, Berg AH, Olsson PE, Norrgren L. Assessment of PCBs and hydroxylated PCBs as potential xenoestrogens: In vitro studies based on MCF-7 cell proliferation and induction of vitellogenin in primary culture of rainbow trout hepatocytes. Arch E © 2008 Vitamin Research Products (888) 303-6151 · 4610 Arrowhead Drive, Carson City, NV 89706 · (8 of 8) [2008-03-25 21:17:37]