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Estrogens in Plastic and Breast Cancer: BPA and DES

Breast cancer incidence rates in the United States increased by more than 40 percent between 1973 and 1998. In 2008, a woman's lifetime risk of breast cancer is one in eight. These two chemicals could have much to do with this.

 

Bisphenol A (BPA) is one of the most universal chemicals in modern life, found in baby bottles, other food and beverage containers, linings of metal food cans, dental sealants and countless other products. It’s also found in air, dust, rivers and estuaries — and in Americans of all ages, including newborns. More than 2 billion pounds of BPA are produced in the United States each year; globally, more than 6 billion pounds are produced. Worldwide, BPA generates an estimated $1 million a day in revenue for corporations such as Bayer, Dow, GE Plastics and Sunoco.

BPA is a result of the 1930s search for cheap synthetic estrogens, compounds designed to keep post-menopausal women “feminine forever” and to promote the rapid growth of cattle and poultry industry profits. Synthesized in 1936, BPA was shunted aside two years later by a more potent synthetic estrogen: diethylstilbestrol (DES), now known to cause cancer and reproductive abnormalities in both males and females.

Though they differ in potency, DES and BPA share striking similarities in their structures, functions and histories. Both chemicals:

  • Were developed when the health effects of estrogen were poorly understood. Early animal studies linked both chemicals with increased risk of mammary and other cancers and reproductive abnormalities;
  • Entered the food chain: DES as an intentional additive and BPA through food containers and packaging. DES was prescribed for pregnant women to prevent miscarriage (which it failed to do) and BPA is associated with recurrent miscarriage as seen in a recent study from Japan; and
  • Were aggressively marketed, despite scientific evidence suggesting the need for caution. BPA is still marketed globally. The Food and Drug Administration (FDA) ignored the animal evidence of DES reproductive toxicity and approved the drug for medical use in humans in 1941, then for use during pregnancy and for use in livestock and chickens in 1947. When male agricultural workers exposed to DES suffered sterility and breast cancer, FDA banned the use of DES in poultry, but not in cattle or in women. Between 1938 and 1971, an estimated 5 to 10 million women in the U.S. were prescribed DES. Use of DES in cattle continued into the 1980s.

In 1970, doctors noted an unprecedented number of rare vaginal cancers in young women whose mothers had taken DES during their pregnancy. Ultimately, DES proved to be a transgenerational carcinogen and a reproductive toxicant, resulting in an FDA alert on the drug. Subsequent research showed an indisputable cause-effect relationship between maternal use of DES and clear cell vaginal carcinoma in daughters. DES also increased the risk of breast cancer in the mothers, and studies now show that increased breast cancer risk extends to DES daughters. Decades of research on DES daughters and sons have shown that animal studies can be useful in predicting effects in people. More information on DES is available from the CDC.

Discarded as an estrogen replacement therapy pharmaceutical, BPA was rediscovered by polymer scientists in the late 1940s and quickly became a mainstay of the plastics industry. It is the building block of polycarbonate plastic and is also used in the manufacture of epoxy resins and other plastics, such as polyester and styrene.

Although never prescribed as a drug or deliberately added to foods, BPA enters the food chain by leaching from plastic packaging or containers as the plastic ages or is heated. Once in food, BPA moves quickly into people, including placental tissue and umbilical cord blood, where it can disrupt normal prenatal development, even at low levels—parts per billion or parts per trillion.

BPA exposure during critical windows of development has been linked with increased risk of breast, prostate and testicular cancer. It’s also linked to birth defects, including neurobehavioral disorders, increased risk of miscarriage, decreased sperm production, early puberty in females, obesity and insulin-resistant diabetes.

One recent study showed that neonatal exposure to low levels of BPA causes uterine fibroids, cystic ovaries and precancerous lesions in female middle-aged mice. These results closely parallel the effects of comparable DES exposure. In women, such effects are major contributors to infertility and the most common reasons for hysterectomy. For evidence connecting BPA and breast cancer see page 46.

Many scientists and the public are increasingly concerned about BPA because of (1) high production volume, (2) widespread human exposure and (3) evidence of reproductive toxicity in laboratory animals. Much of the research indicating health risks of early life exposure to BPA has occurred since 1995 and the accumulated evidence is compelling. However, the chemical is regulated based on research findings prior to 1984. The U.S. Environmental Protection Agency standard for BPA safety, called a reference dose, is 50 micrograms per kilogram of body weight, per day. Government studies indicate that human exposure may be 10 times that high.

Manufacturing Doubt

Manufacturers of BPA responded to concern about health risks by criticizing the evidence as controversial, limited and overblown. They called for more research. This all-too-familiar tactic has enabled many industries to continue profiting from tobacco, lead, asbestos, DES and other toxic products while damaging public health. When media reported early studies of BPA’s estrogenic effects on the male reproductive system, the chemical industry attacked, saying their scientists could not replicate the studies. Laboratories hired by chemical companies quickly produced studies that found no harmful effects.

A 2005 analysis of the BPA literature revealed a clear pattern of bias in reporting results: the funding source often determined the findings. Of 115 studies on health effects of BPA, 94 government-funded studies conducted in academic laboratories in Japan, Europe and the United States found adverse effects at low dose exposure. None of the studies funded by industry reported adverse effects.

Leading scientists called for a new assessment of BPA based on mounting evidence of its DES-like effects. The National Toxicology Program (NTP) responded by appointing an advisory committee to assess the evidence and prepare a report. In March 2007, it was revealed that the advisory committee’s report had been drafted by a private consulting firm with ties to the chemical industry. NTP fired the firm but accepted the report as unbiased.

When the advisory committee reconvened in August 2007 to review the report, leading BPA researchers testified about errors in the report, failure to consider the full range of evidence and reliance on flawed data from industry. The committee remained largely unconvinced, noting in their summary statement “some concern” only for pregnant women, fetuses, infants and children “that exposure to BPA causes neural and behavioral effects.”

Neural and behavioral effects are a significant concern—particularly for women of childbearing age who are the first environment for babies. Four million babies are born each year in the United States exposed to BPA in their mother’s wombs. One in every six children in the U.S. suffers from some type of learning or neurobehavioral disorder, ranging from attention-deficit hyperactivity disorder to autism. This amounts to as many as 640,000 children who are harmed each year—an enormous public health issue and a lifelong problem for children and families.

In a parallel process, a collaboration of 38 internationally recognized scientific experts on BPA and other endocrine disruptors published a more exhaustive analysis of the research on BPA, which included a consensus statement plus five peer-reviewed articles. Unlike the NTP committee, the international collaboration concluded: “The wide range of adverse effects of low doses of BPA in laboratory animals exposed both during development and in adulthood is a great cause for concern with regard to the potential for similar adverse effects in humans. Recent trends in human diseases relate to adverse effects observed in experimental animals exposed to low doses of BPA.”

Among the examples of trends they cited:

  • Increase in breast and prostate cancer
  • Uro-genital abnormalities in male babies
  • Decline in semen quality in men
  • Early onset of puberty in girls
  • Metabolic disorders including insulin-resistant (type 2) diabetes
  • Obesity in children and adults
  • Neurobehavioral problems such as ADHD

The next step for NTP is to compile the data from the two reports, draft its own report and solicit public comment. Meanwhile, California may seek a Proposition 65 listing of BPA as a reproductive toxicant.

One other country has taken action on BPA. Norway has advised the World Trade Organization of its intention to prohibit BPA and 17 other substances from consumer goods in that country. This prohibition will include clothing, bags and toys but will not apply to food products or food packaging. While this legislation applies only to Norway, it could become the new de facto standard for companies exporting to Europe since few companies will vary a product for one small market.

Regulation of the manufacture and use of BPA in the United States may be years away. Meanwhile, consumers can limit exposure to this chemical through the following measures recommended by the Environmental Working Group:

  • Minimize the use of plastics, especially plastic wraps and containers, with the recycling label No. 7, which may contain BPA.
  • Use glass baby bottles and dishes.
  • Discard old, scratched plastic dishes and containers. Don’t wash plastic dishes in the dishwasher using strong detergents, which can speed up wear and tear.
  • Avoid canned foods and drinks.

Data Source:

See full story at:

http://www.breastcancerfund.org/site/pp.asp?c=kwKXLdPaE&b=3959141