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Environmental Estrogens: Close this window

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

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
to approximately 50 environmental estrogens.2

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

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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-steroid-
treated 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.

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Scientists soon realized that Kepone had plenty of company. They confirmed that DDT and
other pesticides acted like endogenous estrogens or produced estrogenic breakdown

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

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

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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 inhibits cell proliferation in human MCF-7 breast cancer cells even more

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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 alpha-
hydroxylation, 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 16-
alpha pathway and instead takes the “tumor suppressor” metabolic pathway — called 2-
hydroxylation — the incidence of cancer decreases. Healthy individuals not at risk for estrogen-
dominant 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-

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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 beta-
carotene 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

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.

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):315-

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.

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9. McLachlan JA, Arnold SF. Environmental Estrogens. American Scientist. 1996. Available over
the Internet at www.sigmaxi.org/amsci/articles.

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;

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.

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;

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.

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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

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