Over the past 30 years, breast cancer rates have increased by nearly 20 percent in the United States (though more recent years have begun to see small declines). During this time, the number of synthetic chemicals in the environment has also increased. These trends have caused many to question whether the increasingly polluted environment is contributing to increased breast cancer rates. Although research in this area is growing and scientists are beginning to learn more about the role of environmental chemicals and breast cancer, there are few studies confirming the effects of chemicals in the environment on breast cancer risk. Understanding the links between environmental pollutants and breast cancer is critical, as it may help prevent the disease in some people.
Figure 1. Female Breast Cancer Rates, 1975-2011Cancer sites include invasive cases only. Rates are per 100,000 and are age-adjusted to the 2000 US Std PopulationSource: National Cancer Institute’s Surveillance, Epidemiology, and End Results Program
According to the Centers for Disease Control and Prevention (CDC), an environmental chemical is a chemical compound present in air, water, food, soil, dust or other items such as consumer products. Individuals are exposed to thousands of naturally occurring and synthetic chemicals over a lifetime—in the home, the workplace and the natural environment. Human exposure to some chemicals may occur through the ingestion of contaminated food and water, inhalation of contaminated air and absorption through the skin. Fetuses can be exposed to chemicals that cross the placenta during pregnancy, and some environmental contaminants can pass from mother to infant through breast milk .
Exposure to environmental chemicals is assessed by measuring the levels of chemicals in a person’s blood and urine, a process called biomonitoring. Blood and urine levels reflect the amount of the chemical that actually gets into the body from the environment. The presence of a chemical in the blood or urine does not mean it will cause cancer or disease. The toxicity of a chemical is related to its dose or concentration, as well as a person’s individual susceptibility to that chemical. Small amounts or low exposure to environmental chemicals may have no health consequence. The CDC conducts biomonitoring measurements in collaboration with other research institutions and government agencies like the National Toxicology Program to determine the levels of a chemical that may cause health affects and the levels that are not a significant health concern.
There have been many debates over the past decades whether chemicals in our environment have a connection to breast cancer. Cancer risk and chemicals such as pesticides (e.g. dichlorodiphenyltrichloroethane (DDT)) have been the focus of considerable research in the past 30 years. However, concern is now growing about non-pesticides and synthetic chemicals. Exposure levels and cancer risk for these chemicals are unclear and more research is needed to determine if they have any effect on breast cancer risk. Chemicals that may be associated with breast cancer include, among others [2, 3, 4]:
The scientific evidence on environmental exposures and breast cancer risk can be confusing. “There has been considerable public health concern regarding the role of many environmental exposures and risk of breast cancer, but adequately studying this risk has been a challenge for researchers,” says Komen Scholar Dr. Melissa Bondy, Professor of Hematology/Oncology at Baylor College of Medicine and The University of Texas M.D. Anderson Cancer Center. Researchers often lack the tools to adequately assess risk of chemicals and as a result, many studies are inconclusive or conflicting. As a result, many researchers, as well as government agencies like the CDC, are actively working to collect information about exposure to these and other chemicals, perform biomonitoring measurements and determine the effects of these environmental chemicals, if any, on breast cancer risk.
It has been well accepted that our body’s own hormones, especially estrogen, play an important role in breast cancer risk. However, research has found that numerous environmental chemicals can act like estrogen. These chemicals are often referred to as endocrine disrupting compounds (EDCs) and some researchers believe they may contribute to breast cancer risk by mimicking or disrupting the effects of the body’s natural estrogen [5, 6]. Some commonly recognized EDCs are DDT, BPA, PAHs, dioxin, PCBs, phtlalates and heavy metals (e.g., arsenic, cadmium, lead, mercury) .
Currently, there is no firm evidence that low-level EDC exposure causes breast cancer and neither the U.S. National Toxicology Program, nor the World Health Organization International Agency for Research on Cancer (WHO/IARC), has classified most EDCs as carcinogens (causing cancer). However, studies from the CDC have found widespread evidence of low-level exposure to several EDCs ; and there are some animal and epidemiological (population studies in humans) studies that link EDCs to increased breast cancer risk [8, 3, 2]. Although environmental estrogens are less potent than the body’s own estrogen, researchers think that routine exposure to these chemicals can add up and may work with the body’s own estrogen to increase the risk of breast cancer. More research is needed to determine which EDCs, if any, contribute to breast cancer risk.
The use and production of DDT and PCBs were banned by the Environmental Protection Agency in the 1970s; but, because they remain in products that were manufactured before the ban, they continue to be detected in the environment and remain a focus of attention in breast cancer research [9, 10] . DDT and PCBs have both been shown to cause cancer, but studies linking them to breast cancer in particular have not found an association [11, 12, 13]. Reviews of several studies in humans concluded there was no association with DDT or PCB exposure and increased breast cancer risk in the general population [4, 14].
However, there are some shortcomings to these studies. Few studies analyzed specific population groups (e.g. younger, older, childless, mothers, menopausal, etc.) to see if certain groups of women are more vulnerable to the effects of these chemicals compared to the population as a whole. New evidence suggests that these compounds may have their greatest impact on women with particular susceptibilities, and looking broadly at large populations will not tell the full story of cancer risk [15, 16]. In addition, the methods used in most studies do not account for exposures during early breast development when mammary tissue may be particularly sensitive to the toxic effects of many environmental chemicals [17, 18]. For example, many studies measured the levels of these chemicals after cancer was diagnosed or in older subjects, which are not a good index of what was experienced earlier in life.
These shortcomings are leading to more carefully designed studies, particularly for PCBs, which can be stored in fat tissue, having consequences long after exposure . For example, although DDT and PCB were both banned in the 1970s, many of the women heavily exposed to them in childhood have not yet reached the age of 50; thus, the consequences of this exposure have yet to be fully revealed and remain an active area of breast cancer research.
BPA is a chemical that is commonly found in in many household products, such as plastics, paints, adhesives, protective coatings that line metal food cans and until recently, baby bottles. It is of rising concern because it appears to disrupt the normal functioning of estrogen and is considered an EDC. BPA is also of concern because early-life exposure may affect breast cancer risk later in life [17, 18]. Animal studies have linked BPA to a variety of health problems such as infertility, prostate cancer and breast cancer [5, 20, 21]. However, there is no concrete evidence that exposure to low levels of BPA causes breast cancer in humans , and an FDA assessment released in March 2013 said that BPA is safe at the very low levels that occur in some foods .
The possible effects of BPA on breast cancer are an active area of research. The FDA is currently taking steps to reduce human exposure to BPA in the food supply, including efforts to replace BPA in plastics and other food can linings, and has banned BPA from baby bottles and infant formula packaging. The FDA is also supporting more robust regulations for oversight of BPA, including biomonitoring studies in humans [24, 25].
Parabens are preservatives found in antiperspirants, cosmetics and skin care products. Parabens have been linked to breast cancer because a small study in 2004 found parabens in breast cancer cells. However, the study did not consider other factors that could have led to the presence of parabens in the cells. Since this study, there have been many discoveries about parabens and breast cancer. Although parabens have some weak estrogen-like activity and may be considered a weak EDC, they do not appear to build up in the tissue from cosmetic use and they have not been found to cause cancer in animals [26, 27]. Further study is needed to prove or rule out parabens as a possible risk factor or cause of breast cancer, and parabens are not considered a health risk at this time.
PAH’s are produced by combustion and can be found in household sources such as car and other vehicle exhaust; cigarette smoke; and barbequed, smoked or charred foods. They are also found in industrial sources from petroleum production, waste incineration and coal or oil-fired power plants. Inhalation is the major means of PAH exposure because it can become suspended in the air. Like other chemicals associated with breast cancer risk, PAHs are stored in fat tissue and are considered EDCs because they can interact with the estrogen receptor [28, 29]. They can also act directly on DNA to cause mutations .
Although PAH’s are well documented to cause certain cancers in laboratory animals, only a few studies have demonstrated a link between PAHs and breast cancer risk, and this remains an active area of research . Some studies suggest that specific mutations or genetic differences may be involved in the development of PAH-related breast cancer, and that PAHs may not broadly contribute to increased breast cancer risk. .
Researchers believe the time in a person’s life in which they are exposed to environmental chemicals may affect how these chemicals impact breast cancer risk. The development of the breast begins in the womb and continues after birth through puberty, and even goes through many developmental changes during pregnancy, lactation and menopause. Some studies suggest that developing breasts are more susceptible than mature breasts to damage by some chemicals, including BPA, PAHs and others [33, 34, 35]. Therefore, early-life exposure to some chemicals may affect breast cancer risk later in life [17, 18]. This is an active area of research.
In addition, some chemicals can be stored in the body’s tissue for long periods of time. Therefore, the long-term effects of some chemicals, like those banned in the 1970s such as DDT, are of concern because they continue to be detected in the environment and in the food supply, breast milk and fat tissue of animals and humans . Even more, because there is a long period of time between chemical exposure and diagnosis of breast cancer, the link between chemical exposure and breast cancer may take many decades to show up.
Determining how breast cancer risk is affected by exposure to environmental chemicals is challenging. Many existing studies are inconclusive or offer contradictory findings. This is partly because the current models and methods for measuring and assessing chemical exposures have many limitations. The result is that numerous institutes, agencies and advocacy groups publish conflicting or vague information that can be confusing.
Many of the studies on chemicals linked to breast cancer have been done in animals. Animal models are an important tool that allows researchers to study complicated questions in human biology that cannot be done in humans. However, it is often difficult to translate the results of animal studies to humans. For example, chemicals that cause cancer in animals may or may not cause cancer in humans, or the cancer site may be different. In addition, the animal’s age at which it is exposed to the chemical and the time it’s examined for tumors, can affect the outcome. In most animal studies, chemical exposure occurs after puberty and tumor assessment is only two years later. This method does not consider early-life exposures or the long time period between exposure and potential cancer development that occurs in humans [4, 37, 38].
Human studies are the gold standard for evaluating cancer risk. However, certain studies are not ethical to do in humans. For example, it would not be ethical to expose a group of people to a chemical to determine whether it affects breast cancer risk. When studies can be done in humans, they are usually done as epidemiological studies – studies where a population of people are followed over time, information about exposure to chemicals is collected, and breast cancer risk is assessed. However, these types of studies are considerably more expensive than animal studies because they require a large number of women and a long period of time to complete the study.
In addition, measuring the amount and types of chemical exposures in humans is challenging. Detailed measurements of exposure over long time periods are rarely available, and current methods do not consider that exposure may involve more than one chemical or a mixture of chemicals. It is difficult to measure chemical exposures that occurred 10, 20 or even 30 years before a breast tumor is detected. It is also hard to determine how individual chemicals may affect breast cancer risk when people are exposed to low levels of thousands of chemicals over a lifetime. More importantly, there are few studies that take into account the impact of other environmental factors such as obesity or diet, or the differences in environmental chemical risks among population subsets such as minorities, menopausal women or those with genetic mutations [3, 4, 1].
Policies and Community Action
A number of government-funded programs provide access to environmental pollution data and support basic research related to environmental chemicals and cancer risk. For example, the CDC biomonitoring and tracking programs have generated data on the U.S. population's exposure to hundreds of environmental chemicals. The National Institute of Environmental Health Sciences (NIEHS) and the National Cancer Institute (NCI), among others, support studies on how chemical factors in the environment interact with genetic factors to contribute to breast cancer risk. Several nonprofit organizations advocate for increased research into environmental links to breast cancer, including Susan G. Komen.
There are enormous challenges in establishing whether exposure to individual chemicals or to chemical mixtures causes cancer. More studies are needed to explore the wide variety of chemicals that may affect breast cancer risk. There is also need for better tools to identify potential cancer-causing chemicals and better methods to measure exposures to chemicals. Studies are ongoing to screen for and identify chemicals that cause breast cancer in animals, and human studies continue to search for gene-environment interactions that could help identify groups of women who may be at higher risk when exposed to certain chemicals. In addition, more research is needed not only to define the types of exposures encountered in the workplace and the home, but also to evaluate how exposure during critical periods of breast development may affect cancer risk later in life.
It is our goal to improve our understanding of the environmental piece of the breast cancer risk puzzle. If we can understand the early events that set the stage for genetic changes that increase breast cancer in later life, we will have a better chance to modify those risks to prevent breast cancer in the future. We must work in multidisciplinary teams to understand how environmental exposures may interact to cause susceptibility to breast cancer later in life,” says Dr. Bondy. Better understanding of the environmental factors that affect breast cancer risk could greatly impact the numbers of preventable cases. Even a small population-level change in risk factors has the potential to considerably impact breast cancer burden.
Since 1982, Komen has invested more than $21 million in 50 research grants focused on environmental factors and breast cancer. These grants not only include research on environmental chemicals, but also on other environmental factors that may affect breast cancer risk and survival such as radiation, hormone use, obesity/weight and other lifestyle factors such as alcohol consumption, vitamin use and shift work.
In addition to research, Komen has provided nearly $1.5 million in support of Special Program grants, including support of the 2011 Institute of Medicine report on the current evidence on breast cancer and the environment.
Read more about the IOM report.
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