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Tracking Our Environmental Health

We're championing legislation to create a national system that tracks environmental pollution and diseases like breast cancer.

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STRONG VOICES

Sarah Janseen, M.D., Ph.D., M.P.H.
Sarah Janssen

A physician, scientist, advocate and mother committed to protecting our health and our environment, Dr. Janssen is a 2010 Hero.

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Prenatal Exposures

Prenatal chemical exposure can have profound effects on subsequent breast cancer risk. Recent data indicates that increased exposure to endocrine disruptors and chemicals in air can lead to a higher incidence of breast cancer in adulthood.

Encouraged by health care providers and empowered by modern scientific understanding, pregnant women often change their habits to protect their developing babies. They may change the foods they eat, reduce their alcohol consumption and stop smoking. Unfortunately, we've not reached the same level of understanding and action when it comes to reducing exposures to environmental chemicals, which can have equally significant impacts on fetal development and long-term health.

A significant and growing body of research shows that pregnant women's exposure to chemicals—particularly endocrine disruptors—can increase their children's risk for breast and other cancers later in life. During fetal development, hormones orchestrate the development of the reproductive and endocrine systems. This includes the structures of breast tissue, hormone metabolism and other important factors in breast development.

One of the most striking examples is the legacy of diethylstilbestrol (DES), a synthetic estrogen that was prescribed to prevent miscarriage from 1947 to 1970. DES was not effective at preventing miscarriage. But it did affect the development of female babies' reproductive tracts, leading to increased infertility and vaginal and cervical cancer rates later in life.[1] There's also evidence that both the mothers who took the drug and their daughters who were exposed in the womb have higher than average rates of breast cancer.[2],[3],[4]

Fetal exposures to environmental chemicals from sources like car exhaust and tobacco smoke are also implicated in later-life breast cancer risk. A study in western New York linked higher exposure to polycyclic aromatic hydrocarbons (PAHs) to later-life breast cancer.[5] PAHs are chemicals from car exhaust, incineration, tobacco and grilled foods that alter how the body's cells deal with estrogen.[6]

Animal studies also point to concerns about fetal environmental exposures, even from the kinds of products we encounter daily. Research suggests that exposures to low doses of the endocrine disruptor bisphenol A (BPA)—found in polycarbonate plastics and the linings of canned foods—can alter fetal mammary gland development.[7],[8],[9],[10] These changes show up in puberty and can predispose female mice to later-life breast cancers. Additional exposures to carcinogens increase the likelihood of cancers,[11] illustrating that lifetime exposures that begin in the womb add up over time to increase breast cancer risk.

  1. Guisti RM, Iwamoto K, Hatch EE. (1995). Diethystilbestrol revisited: A review of the long-term health effects. Annals of Internal Medicine 122:778-788.
  2. Colton T, Greenberg ER, Noller K, Resseguie L, Van Bennekom C, Heeren T, Zhang Y (1993). Breast cancer in mothers prescribed diethylstilbestrol in pregnancy. Further follow-up. Journal of the American Medical Association. 269:2096-2100.
  3. Titus-Ernstoff L, Hatch EE, Hoover RN, Palmer J, Greenberg ER, Ricker W, Kaufman R, Noller K, Herbst AL, Colton T, Hartge P (2001). Long-term cancer risk in women given diethylstilbestrol (DES) during pregnancy.  British Journal of Cancer 84: 126-133.
  4. Troisi R, Hatch EE, Titus-Ernstoff L, Hyer M, Palmer JR, Robboy SJ, Strohsnitter WC, Kaufman R, Herbst AL, Hoover RN.  (2007).  Cancer risk in women prenatally exposed to diethylstilbestrol.  International Journal of Cancer 121: 356-360.
  5. Bonner MR, Han D, Nie J, Rogerson P, Vena JE, Muti P, Trevisan M, Edge SB, Freudenheim JL (2005). Breast cancer risk and exposure in early life to polycyclic aromatic hydrocarbons using total suspended particulates as a proxy measure. Cancer Epidemiology, Biomarkers & Prevention 14:5 3-60.
  6. Santodonato J (1997). Review of the estrogenic and antiestrogenic activity of polycyclic aromatic hydrocarbons: relationship to carcinogenicity.  Chemosphere 34: 835-848.
  7. Munoz de Toro M, Markey C, Perinaaz RW, Luque EH, Rubin BS, Sonnenschein C, Soto A (2005). Perinatal exposure to bisphenol A alters peripubertal mammary gland development in mice. Endocrinology 146: 4138-4147.
  8. Vandenberg LN, Maffini MV, Wadia PR, Sonnenschein C, Rubin BS, Soto AM (2007).  Exposure to environmentally relevant doses of the  xenoestrogen bisphenol-Aalters development of the fetal mouse mammary gland. Endocrinology 148: 116-127.
  9. Markey CM, Luque EH, Munoz de Toro MM, Sonnenschein C, Soto AM (2001). In utero exposure to bisphenol A alters the development and tissue organization of the mouse mammary gland. Biology of Reproduction 65:1215-1223.
  10. Soto AM, Vandenberg LN, Maffini MV, Sonnenschein C (2008).  Does breast cancer start in the womb?  Basic & Clinical Pharmacology & Toxicology 102:125-133.
  11. Murray TJ, Maffini MV, Ucci AA, Sonneschein C, Soto AM (2007). Induction of mammary gland ductal hyperplasias and carcinoma in situ following fetal bisphenol A exposure.  Reproductive Toxicology 23: 383-390.