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Janet Gray, Ph.D.
Janet Gray, Ph.D.

As author of our 2008 and 2010 State of the Evidence reports, Dr. Gray drives the science behind all our work.

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Prenatal Exposures

Prenatal chemical exposure can have profound effects on later breast cancer risk. Data indicate that increased fetal exposure to endocrine disruptors (substances that can alter the body’s hormonal responses) and other chemicals 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 have not reached the same level of understanding and action when it comes to reducing environmental exposures, which can also have significant impacts on fetal development and long-term health. Researchers from the Program on Reproductive Health and the Environment recently found that most obstetricians do not ask pregnant women about their exposures to chemicals (Trowbridge, 2012).

A significant and growing body of research shows that pregnant women’s exposure to chemicals — particularly endocrine-disrupting compounds — can increase their children’s risk for breast and other cancers later in life. During the fetal stage, hormones orchestrate the development of the reproductive and endocrine systems. These systems include breast tissue structure, 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 as well as vaginal and cervical cancer rates later in life (Giusti, 1995).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 (Colton, 1993; Titus-Ernstoff, 2001; Troisi, 2007). 

Fetal exposures to environmental chemicals from sources such as 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 (Bonner, 2007). PAHs—chemicals from car exhaust, incineration, tobacco and grilled foods—can alter the way the body’s cells deal with estrogen (Sandodonato, 1997). 

Animal studies also raise concerns about fetal environmental exposures to chemicals found in products we encounter daily. Research suggests that maternal exposures to low doses of the endocrine disruptor bisphenol A (BPA) — found in the linings of canned foods — can alter fetal mammary gland development (Muñoz-de-Toro, 2005; Vandenberg, 2007; Markey, 2001; Soto, 2008; Ayyanan, 2011). These changes continue through puberty and can predispose female mice to later-life breast cancers (Murray, 2007). Additional exposures to carcinogens increase the likelihood of cancers (Lozada, 2011; Betancourt, 2011; Jenkins, 2009), illustrating that lifetime exposures beginning in the womb add up over time to increase breast cancer risk.