Breast cancer is cancer originating from breast tissue, most commonly from the inner lining of milk ducts or the lobules that supply the ducts with milk. Factors across the woman life cycle, beginning before birth, influence breast cancer risk. This is known from epidemiologic studies of characteristics self-reported by older women or gleaned from medical records. For example, larger babies have a higher breast cancer risk decades later, while preeclampsia (pregnancy hypertension) is associated with a lower risk in daughters. Earlier puberty increases the risk, and women with fewer or no pregnancies have a higher risk later on. These factors span sensitive periods of breast development, prenatally and during puberty and pregnancy. If environmental chemicals have comparable effects during sensitive developmental periods, identifying these risks could lead to prevention. But epidemiologic data to assess the effects of chemicals in early life are rarely attainable. The primary risk factors for breast cancer are sex, age, lack of childbearing or breastfeeding, higher hormone levels, race, economic status and dietary iodine deficiency. If environmental chemicals have comparable effects during sensitive developmental periods, identifying these risks could lead to prevention. But epidemiologic data to assess the effects of chemicals in early life are rarely attainable. Recent studies are attempting to narrow the environmental effect uncertainties with improved test methods and protocols. Some studies are indicating that effects on mammary gland development and cancer risk factors are not limited to estrogenic endocrine disruptors, but are induced by diverse chemicals including perfluorinated compounds and the herbicide atrazine, in addition to the soy phytoestrogen genistein and synthetic estrogens such as bisphenol A.
Breast cancer is cancer originating from breast tissue, most commonly from the inner lining of milk ducts or the lobules that supply the ducts with milk. Factors across the woman life cycle, beginning before birth, influence breast cancer risk. This is known from epidemiologic studies of characteristics self-reported by older women or gleaned from medical records. For example, larger babies have a higher breast cancer risk decades later, while preeclampsia (pregnancy hypertension) is associated with a lower risk in daughters. Earlier puberty increases the risk, and women with fewer or no pregnancies have a higher risk later on. These factors span sensitive periods of breast development, prenatally and during puberty and pregnancy. If environmental chemicals have comparable effects during sensitive developmental periods, identifying these risks could lead to prevention. But epidemiologic data to assess the effects of chemicals in early life are rarely attainable. The primary risk factors for breast cancer are sex, age, lack of childbearing or breastfeeding, higher hormone levels, race, economic status and dietary iodine deficiency. If environmental chemicals have comparable effects during sensitive developmental periods, identifying these risks could lead to prevention. But epidemiologic data to assess the effects of chemicals in early life are rarely attainable. Recent studies are attempting to narrow the environmental effect uncertainties with improved test methods and protocols. Some studies are indicating that effects on mammary gland development and cancer risk factors are not limited to estrogenic endocrine disruptors, but are induced by diverse chemicals including perfluorinated compounds and the herbicide atrazine, in addition to the soy phytoestrogen genistein and synthetic estrogens such as bisphenol A.
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Exceptional events or decades-long studies can provide some information. For example, studies of atom bomb survivors revealed breast cancer risk was highest from radiation exposure to young girls.
A unique study using blood collected in the 1960s and stored for over 40 years found higher breast cancer risk in women who were under age 14 when DDT was first put into use.
Improving test methods in animals and cells is essential to identify chemicals that may interfere with breast development and contribute to cancer, so we can use this knowledge for primary prevention. These methods will expand on recent changes in toxicity testing, which were designed to respond to research on endocrine disrupting compounds by evaluating how exposures in utero and during other windows of development set the stage for later life chronic diseases. New procedures include dosing in utero and throughout development, adding morphological and functional assessments of reproductive organs, and longer-term follow-up.
Mammary gland development has usually not been assessed in the protocols. Mounting evidence supports the importance of testing for breast effects during development for several reasons. The breast develops over a long period, with vulnerability beginning in utero and extending through the first pregnancy. For some chemicals tested to date, mammary gland development in males and females is altered at lower doses than the levels that cause changes in other tissues. The effects that have been observed following disrupted mammary gland development include impaired lactation and increased susceptibility to cancer, so they are of potentially great public health significance.
Rudel et al. have presented a review of hormone and chemical effects on mammary gland development, lactation, and cancer. Emerging from a meeting of 60 international experts, this article reports the majority opinion of this group that normal mammary gland development and carcinogenesis are similar in rodents and humans, that chemical and hormone exposure in utero or early in life leads to altered mammary gland development, and that these changes may be risk factors for impaired lactation and cancer.
The elevated incidence of breast cancer in women has been potentially associated with prolonged exposure to high levels of estrogens. Xenoestrogens, such as bisphenol A have the capacity to perturb normal hormonal actions.
For further information: http://ehp03.niehs.nih.gov/article/info%3Adoi%2F10.1289%2Fehp.1104077
