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6 Opportunities for Action to Reduce Environmental Risks for Breast Cancer T he committee was asked to consider the potential for evidence-based actions to reduce the risk of breast cancer. Individual women, health care providers, advocacy organizations, and many other stakeholders are all eager to know what concrete steps can be taken to reduce the risk of breast cancer for an individual or the population, and when during the life course those actions might be most effective. This chapter outlines several evidence-based actions that women can take. However, the scientific com- munity still has only limited understanding of which exposures might best be avoided and when, and which actions might have a long-term positive benefit in reducing risk for breast cancer. Even when research strongly supports classifying an exposure as a risk factor for breast cancer, that research does not necessarily provide the infor- mation needed to determine the appropriate response to reduce risk. Should exposure be avoided completely? Will reducing or eliminating exposure in adulthood reduce a risk that has accrued from exposure at younger ages? Will the presence or absence of other risk factors for breast cancer influ- ence the likely benefit or harm from a change in exposure to a given risk factor? Will changing one type of exposure lead to another that carries new and possibly as yet unrecognized risks for breast cancer, other diseases, or perhaps some other adverse economic or environmental outcome? Finding ways to reduce risk and avert cases of breast cancer is a high priority for everyone concerned about this disease. Although some definite actions can be taken to reduce risk, the committee found overall that evi- dence-based options are limited because few studies have been done to test the effectiveness of actions that may be hypothesized to reduce risk. In this 283
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284 BREAST CANCER AND THE ENVIRONMENT chapter, the committee discusses some specific areas where action appears warranted, but it first summarizes the significance of the uncertainty around preventive action. RECOGNIZING UNCERTAINTY OF BENEFITS AND RISKS Potential for Introducing New Hazards or Risks A key concept to remember when evaluating a particular risk associated with a particular factor is that an action that is aimed at eliminating the specific risk of concern may result in a substitution of one risk for another, or perhaps shifting risk from one group to another. Any risk of the alterna- tive action thus needs to be considered and weighed against the risk that the change is intended to reduce or eliminate. The complexity of trade-offs from substitutions can be illustrated with the case of contamination of potable ground water sources with pesticides or industrial chemicals shown to be carcinogenic in experimental animals or humans. Reducing exposures to potentially carcinogenic substances in drinking water from groundwater sources seems to be a logical, health- protective action, even if the actual or perceived risk from the contaminants is small. A typical action to reduce the potential cancer risk from using the contaminated ground water is to switch the consumer to an alternative source of potable water, such as a public water supply system. However, such systems require disinfection, usually by chlorination, and chlorination of surface water introduces trace levels of disinfection by-products (DBPs). Several DBPs have been found to be carcinogenic in animal bioassays (e.g., NTP, 2007a,b), and some epidemiologic studies have suggested that long- term exposure to DBPs is associated with an increase in bladder cancer (reviewed in Richardson et al., 2007), especially in a subset of the popula- tion with specific genetic polymorphisms (Cantor et al., 2010). In this scenario, one would have to consider many factors, including (1) the relative carcinogenic potency of the groundwater contaminant(s) versus that of the DBPs, (2) the concentrations of the groundwater contaminants or the DBPs in the drinking water and indoor air following use, and (3) the duration and frequency of likely exposure to a given drinking water source over a lifetime. Depending on these values, it is possible that a com- parative risk assessment would show that switching from the contaminated groundwater supply to the uncontaminated but disinfected surface water supply actually increased, rather than decreased, potential cancer risks to the exposed population. This example, however, also illustrates the challenges in assessing trade- offs in population- and individual-level risks and benefits. There are cer- tainly no clear benefits, at least to the individual consumer, of drinking
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285 OPPORTUNITIES FOR ACTION TO REDUCE ENVIRONMENTAL RISKS groundwater contaminated with low levels of pesticides. But the potential cancer risk associated with the presence of DBPs in a public water system must be assessed against the very real risks of widespread acute illness from microbial contamination that could result in the absence of disinfection (Gibbons and Laha, 1999; Schoeny, 2010). This pattern of trading one hazardous substance for another is not uncommon. Although federal agencies evaluate the toxicity and carcinoge- nicity of new pesticides and prescription drugs before they are approved for sale, the United States does not have a comprehensive program to evaluate the safety of chemicals before their widespread use in consumer products. In the face of consumer concern about bisphenol A (BPA), for example, BPA-free plastics are now available, but new research appears to show that BPA-free plastics may leach other chemicals with estrogenic activity comparable to that of BPA (Yang et al., 2011). As noted in Chapter 2, the European Union has adopted a program (Registration, Evaluation, Authori- sation and Restriction of Chemical Substances, or REACH) for broader safety testing by manufacturers of their products before they are approved for use. In the United States, the Government Accountability Office (GAO, 2009a,b) has recommended changes to improve the effectiveness of federal regulation of chemicals. Risk trade-offs may also be hard to judge because a given factor can have both positive and negative health effects. For example, there is fairly compelling evidence that moderate alcohol consumption is associated with a small but consistently observed increase in the risk of breast cancer.1 However, there is also compelling evidence that consumption of the same moderate amounts of alcohol is associated with a reduction in mortality from cardiovascular disease (Maskarinec et al., 1998; Gunzerath et al., 2004; Klatsky, 2009; Ronksley et al., 2011). The risks associated with any specific environmental exposure occur against the background of a woman’s genetic susceptibility, reproductive history, and lifestyle. Challenges in Public Health Policy Aimed at Risk Reduction A significant challenge—relevant to the discussion of environmental risk factors for breast cancer and frequently faced by regulators of envi- ronmental pollutants and public health officials—is a lack of information about the nature of the effects of many exposures on risks for breast cancer. Chapter 4 reviewed the diverse challenges in trying to generate and interpret relevant information. Noted here are a few specific areas where substantial uncertainty faces policy makers. Assessing the net effect of environmental exposures is one challenge. 1 The trade-offs associated with alcohol use are discussed further later in this chapter.
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286 BREAST CANCER AND THE ENVIRONMENT Individuals and populations are never exposed to only one risk or protec- tive factor at a time, but complex combinations of exposures are rarely the subject of laboratory or epidemiologic studies. The U.S. Environmental Protection Agency (EPA) and other environmental regulatory agency scien- tists often assume that cancer risks in a population are simply the sum of risks estimated for each individual chemical in the absence of data on risks of co-exposures. In practice, this means that one might be confident that a lifetime of exposure to a single chemical that causes a theoretical increase in cancer risk of 1 additional case per 1 million exposed people is essentially lost in the background and that the risk from that exposure may be consid- ered minimal. But what if a population is exposed to 1,000 of these types of “1 in 1 million” lifetime risks? Are the risks simply additive (e.g., the increase in lifetime risk becomes 1,000 per 1 million, or 1 in 1,000), or is it possible that the chemicals can interact to alter risk in some nonadditive manner, either by reducing each other’s effects (e.g., competition for recep- tor binding) or by mutually enhancing each other’s effects? For example, smoking and asbestos exposure are each well-recognized risk factors for lung cancer, but exposure to both multiplies the risk of lung cancer, making the risk far greater than the addition of the individual effects of these two exposures. A study of asbestos workers found that the lung cancer mortality rate was 122.6 per 100,000 among men with a history of smoking and no asbestos exposure; 58.4 per 100,000 among those with asbestos exposure but no history of smoking; and 601.6 per 100,000 with exposure to both smoking and asbestos (Hammond et al., 1979). As a qualitative example, cigarette smoke is a mixture of relatively low levels of numerous carcino- gens, and both direct and passive exposure to cigarette smoke are associ- ated with a variety of cancers, including breast cancer. On the other hand, some exposures may increase risks for breast cancer, but reduce them for other cancers. In the vast majority of instances, the scientific information is typically not sufficiently developed to calculate the joint effects of multiple exposures with confidence. Another area of uncertainty is whether risks occur at very low levels of exposures and whether those risks can be estimated from information on hazards and risks that are determined for high-dose exposures. The EPA and other regulatory agencies have made specific assumptions about the shape of the dose–response curve in relation to certain mechanisms of action. For example, a linear extrapolation of cancer risk from high doses to low doses is used for carcinogenic agents determined to be mutagenic. Although linear extrapolation may not apply in some circumstances, it is considered a protective approach in the absence of evidence to guide the selection of an alternative model (EPA, 2005). Directly detecting small differences in risk in human or animal studies may be difficult, if not impossible, because of challenges that include the need for very large study
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287 OPPORTUNITIES FOR ACTION TO REDUCE ENVIRONMENTAL RISKS populations, the potential for errors in measuring exposure, and the pos- sibility of unrecognized confounding. Finally, as highlighted in earlier chapters, the risk from a given expo- sure may depend on the age at which it occurs, although current knowledge about susceptible windows pertains to few exposures. Perhaps most salient is the difficulty in assessing whether reduction or elimination of an exposure will alter long-term risk of breast cancer, and if so, by how much. EVIDENCE-BASED OPPORTUNITIES FOR ACTION TO REDUCE RISK Identifying evidence-based opportunities for action to reduce risk of breast cancer depends, ideally, on a convergence of several elements, including • sufficient evidence to demonstrate that a specific factor is associated with increasing or decreasing breast cancer risk; • a means by which to modify exposure to the risk factor; • an understanding of whether effective changes can be made by an individual or would require instead, or in addition, changes at governmental, social, or cultural levels; • evidence that a specific action to modify exposure will result in the desired impact on breast cancer risk, the characteristics of women who could be expected to benefit, and when the intervention needs to occur; and • awareness of the trade-offs (potentially as yet unrecognized) that may occur in terms of other health outcomes, personal preferences, or economic consequences. As illustrated in the reviews in Chapter 3, the evidence on many of the environmental factors that have been investigated as potential risk factors for breast cancer remains inconclusive. But for a modest set, the evidence is relatively strong and points to likely opportunities for prevention when these factors are modifiable. What, then, is the distinction between “modi- fiable” and “nonmodifiable” risk factors? For example, the age at which women have a first full-term pregnancy is known to influence the risk of breast cancer, with later age at first birth generally associated with higher risk. At the individual level, women can make decisions as to when they will have their first pregnancy, but changes at the population level are influenced by a range of social, economic, educational, cultural, and personal forces, and any effort to influence personal choices could have unexpected conse- quences. Furthermore, opportunities for modification of some factors may
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288 BREAST CANCER AND THE ENVIRONMENT be limited to certain ages—a woman’s age at a first full-term pregnancy may be modifiable before menopause, but obviously it is not after menopause. Another question is whether particular actions to change a modifiable risk factor will actually translate into lowered risk. For example, although the evidence is relatively strong that greater body fatness is associated with increased risk of breast cancer for postmenopausal women (WCRF/AICR, 2007), it is less clear whether these women can reduce their risk if they lose weight during the postmenopausal period. It is possible that the adverse effects of being overweight are hard to reverse at older ages and can best be prevented by avoiding overweight and obesity throughout life. Overweight and weight reduction also illustrate the complexity of fram- ing guidance on action when the consequences of an exposure differ among groups in a population. Whereas evidence indicates that greater weight is associated with an increased risk for breast cancer for postmenopausal women, it also indicates that greater weight is associated with a lower risk of breast cancer for premenopausal women (WCRF/AICR, 2007). There- fore, avoiding overweight is not a reasonable strategy for reducing the low, but still present, risk of premenopausal breast cancer, although avoiding overweight has many other important health benefits for women of all ages. The association between shift work and increased risk of breast cancer concerns the committee, but it does not see a sound basis, at this time, for proposing action. More research is needed to understand the mechanisms underlying the association between shift work and breast cancer and to develop a clearer, more consistent characterization of the kind of work or work schedule that is associated with increased risk. This deeper under- standing is needed to guide any effort to frame and test interventions in a realm with significant socioeconomic ramifications. A specific call for research on shift work is included in the recommendations in Chapter 7. In some cases, the available evidence from animal or mechanistic stud- ies suggests that a chemical or other factor may be a hazard, but evidence to directly assess the breast cancer risk for women is lacking (or perhaps not possible to obtain). In such circumstances, policy makers may use formal risk assessments to gauge the magnitude of possible risk and the appropriateness of actions to mitigate it. The identification of hazards— factors that have the ability to cause adverse effects—is an essential element in risk assessment and is often based on laboratory studies of biological mechanisms and effects of exposures on laboratory animals. Estimates of risk represent the probability that a particular adverse outcome—breast cancer in this case—will occur in an individual person or a population as a result of defined exposures to a hazard. A risk assessment considers not only the hazard of the substance, but also its potency (roughly speaking, how strong its effect is for a given dose) and the magnitude, nature, and timing of expected human exposure. A highly potent carcinogen may pose
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289 OPPORTUNITIES FOR ACTION TO REDUCE ENVIRONMENTAL RISKS substantial risk to an exposed individual, but if exposure to the general public is very low or extremely uncommon, the population risk will tend to be low. Alternatively, a low-potency carcinogen may pose risks that are low, but if exposures are common, it may be associated with a measureable effect in the population as a whole. The committee did not undertake formal risk assessments for the envi- ronmental chemicals it found to be biologically plausible or possible con- tributors to breast cancer. Critical pieces of information were lacking, particularly robust data for estimating the magnitude of human breast cancer risk for a given dose (potency) at different life stages, and the preva- lence and magnitude of the exposures across the population at different life stages. These data gaps were an obstacle to proposing evidence-based action that women could take to reduce risks from exposure to any par- ticular chemical. LIKELY OPPORTUNITIES TO ACT TO REDUCE RISK OF BREAST CANCER With these limitations to the evidence in mind, the committee high- lights here the areas where it sees the clearest indications of opportuni- ties for actions to reduce breast cancer risk. These actions are reviewed in this section and summarized in Table 6-1. It is important to recognize that the evidence is generally more extensive and therefore stronger for postmenopausal women than for premenopausal women, and for white, non-Hispanic women than for women of other races and ethnicities. In addition, some of the prevention opportunities that the committee points to appear more likely to apply to the prevention of the more common estro- gen receptor–positive (ER+) tumors than estrogen receptor–negative (ER–) tumors. Younger women, however, tend to have ER– forms of breast cancer, as do women who have strong inherited susceptibility to breast cancer, such as carrying a mutation in BRCA1. All women should know their personal risk factors for breast cancer and seek clinical guidance from their health care providers regarding their breast cancer risk and how to modify it. Medical Radiation Among the strongest evidence reviewed by the committee regarding environmental exposures that have been causally linked to breast cancer was the evidence on ionizing radiation. Based on standard models developed from the radiation exposures of the Japanese atomic bomb survivors, it is commonly assumed that the breasts are most sensitive to carcinogenic effects of radiation at early ages (e.g., below ages 20–30). Nevertheless, models also predict elevated risks after exposure, even in middle age (Berrington
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290 BREAST CANCER AND THE ENVIRONMENT TABLE 6-1 Summary of Committee Assessment of Opportunities for Actions by Women That May Reduce Risk of Breast Cancer Modification of Exposure Strength of Evidence That Personal Requires Opportunity for Exposure Is Associated Action Action with Breast Cancer Riska Action Possible by Others Avoid +++ Yes Yes inappropriate medical radiation exposured Avoid combination +++ Yes Confer with physician menopausal hormone therapy, unless medically appropriatee Avoid or end active + Yes Others can facilitate smoking Avoid passive (no committee consensus) Varies Yes smoking Limit or ++ Yes Others can facilitate eliminate alcohol consumption – –f Maintain or Yes Others can facilitate increase physical activity Maintain healthy +++ Yes Others can facilitate weight or reduce overweight or obesity to reduce postmenopausal risk
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291 OPPORTUNITIES FOR ACTION TO REDUCE ENVIRONMENTAL RISKS Action Other Prominent Effective Form Known Risks or Target Population and Timing Affects Risk for Benefits from Taking Establishedb Actionc Defined Specific Subtype All ages Yes, especially at ? May result in loss younger ages of clinically useful information in some instances Likely to decrease risk for other cancers Postmenopausal Yes ER+ May experience women moderate to severe menopausal symptoms, continued menopausal associated bone loss All ages, especially Yes (form) ? Likely to reduce risk before first pregnancy No (timing) for other cancers, heart disease, stroke All ages Yes ? Likely to reduce risk for other cancers, heart disease All women Yes (form) ER? May increase risk for No (timing) cardiovascular disease No known benefit of high alcohol consumption All ages No ? Likely to reduce risk for cardiovascular disease, diabetes May increase risk for injury Unclear No ER+? Likely to reduce risk for cardiovascular disease, diabetes, other cancers continued
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292 BREAST CANCER AND THE ENVIRONMENT TABLE 6-1 Continued Modification of Exposure Strength of Evidence That Personal Requires Opportunity for Exposure Is Associated Action Action with Breast Cancer Riska Action Possible by Others Limit or eliminate Varies by chemical Varies Yes workplace, consumer, and environmental exposure to chemicals that are plausible contributors to breast cancer risk while considering risks of substitutesg – – –h If at high risk Yes Confer with physician for breast cancer, consider use of chemoprevention aThe assessments of the evidence of an association between an exposure and risk of breast cancer are qualitative representations of the committee’s conclusions from its review of avail- able evidence: strong conclusion of increased risk, +++; moderately strong conclusion of increased risk, ++; conclusion of increased risk, +; unclear, ?; conclusion of reduced risk, –; moderately strong conclusion of reduced risk, – –; strong conclusion of reduced risk, – – –. bActions to address risk factors can take various forms, some of which may be more effec- tive than others. For example, increasing physical activity might be based on amount of time spent in any one exercise opportunity, on increasing specific types of exercise, or increasing the frequency of exercise, or perhaps some combination of any of these. Studies have not been done that provide evidence that a specific form of physical activity is optimal for reducing breast cancer risk. cThe committee’s comments on other benefits or risks highlight major considerations, but are not intended to be exhaustive. de Gonzalez et al., 2009; Shuryak et al., 2010). Recent models suggest the possibility that exposures to ionizing radiation across the age range of 10 to 50 years may result in excess relative risks of tumors in breast tissue that are more similar than previously estimated (Preston et al., 2007). For the U.S. population, about half of the exposure to ionizing radia- tion comes from medical radiation, primarily in the diagnostic setting and
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293 OPPORTUNITIES FOR ACTION TO REDUCE ENVIRONMENTAL RISKS Action Other Prominent Effective Form Known Risks or Target Population and Timing Affects Risk for Benefits from Taking Establishedb Actionc Defined Specific Subtype Varies No ? May reduce risk for other forms of cancer May result in replacement with products that have health or other risks not yet identified High-risk women Yes ER+ Depending on the agent, increased risk of endometrial cancer, stroke, deep-vein thrombosis among others dWhile recognizing the risks of ionizing radiation exposure, particularly for certain higher dose methods (e.g., CT scans), it was not the committee’s intent to dissuade women from routine mammography screening, which aids in detecting early-stage tumors. eCombination hormone therapy with estrogen and progestin increases the risk of breast cancer and the associated risk is reduced upon stopping therapy. Oral contraceptives are also associated with an increased risk of breast cancer while they are being used. This risk is superimposed on a low background risk for younger women, who are most likely to use oral contraceptives. These contraceptives are associated with long-term risk reduction for ovarian and endometrial cancer. fReflects reduced risk of breast cancer associated with greater physical activity. gPlausibility may be indicated by epidemiologic evidence, animal bioassays, or mechanistic studies. hReflects reduced risk of breast cancer associated with use of chemopreventive agents. especially from computed tomography (CT) scans and myocardial perfu- sion imaging (Fazel et al., 2009). As outlined in a paper commissioned by the committee (see Appendix F), the average annual dose of radiation from medical diagnostic sources in the U.S. population approximately doubled from 1985 to 2006 (Smith-Bindman, 2011). As further elaborated in that paper, there is evidence that exposure doses for the same imaging tests vary
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314 BREAST CANCER AND THE ENVIRONMENT of overweight and obesity to breast cancer cases in the population as a whole. An uncommon exposure will usually have a small PAR because the percentage of all cases that is attributable to the exposure will be small. However, for a woman who has that exposure, reducing or eliminating it could substantially lower her risk and be very important to her individually. That is, a rare, high-risk exposure may have little impact on population rates of cancer, but it may be a quite important determinant of an exposed woman’s personal risk. Recent efforts have tried to further clarify risks for both individual women and populations by developing models that estimate the absolute risk of breast cancer from relative risks and estimates of attributable risk. In a study by Petracci et al. (2011), the authors used data on Italian women to develop a model to predict breast cancer risk, making use of both nonmodi- fiable risk factors and the modifiable risk factors of BMI, alcohol consump- tion, and physical activity. Data from a cohort study were used to assess the potential impact on absolute breast cancer risk of reducing exposures to the modifiable risk factors. The projected 20-year absolute risk of breast cancer for 65-year-old women, for example, ranged from 6.5 to 18.6 per- cent, depending on their risk profiles. If these women optimized their BMI, alcohol consumption, and physical activity, the estimated 20-year absolute risks would be reduced to 4.9 and 14.1 percent, respectively (Petracci et al., 2011). Presentation of the absolute risk reductions along with estimates of relative risk and the PAR reduction that could maximally be achieved may be a useful approach to both individual counseling and public health deci- sion making (Schwartz et al., 2006; Akl et al., 2011; Helzlsouer, 2011). It illustrates the well-known concept that small changes at the individual level can have a large impact at the population level (Rose, 1992). SUMMARY Many of the established risk factors for breast cancer—age, sex, age at menarche and menopause, age at first full-term pregnancy—offer little or no opportunity to intervene. For a limited set of other risk factors, evi- dence suggests that action can be taken in ways that that have the potential to reduce risk for breast cancer for many women: eliminating unneces- sary medical radiation throughout life, avoiding use of postmenopausal hormone therapy, avoiding active and passive smoking, reducing alcohol consumption, increasing physical activity, and minimizing weight gain. Chemoprevention may be an appropriate choice for some women. For the many chemicals that are manufactured or generated as by- products of other processes, the committee found little basis in the human evidence it examined to point to avoiding or eliminating exposure as a specific strategy for reducing breast cancer risk. Exceptions were benzene,
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315 OPPORTUNITIES FOR ACTION TO REDUCE ENVIRONMENTAL RISKS 1,3-butadiene, ethylene oxide, for which certain measures to control occu- pational exposures are already be in place. However, these chemicals can also be encountered by the general public (although likely at much lower exposure levels) through exposure to facilities emissions, tobacco smoke, and gasoline vapors and vehicular exhaust (benzene and 1,3-butadiene). While for other compounds that were reviewed, such as BPA, animal and mechanistic evidence may indicate breast cancer hazard is biologically plausible, given sufficient dosing, information to assess the magnitude of risk in humans is lacking or inadequate in human studies, posing a sub- stantial challenge for gauging the extent to which an individual’s actions may reduce risk. Even when action appears possible, most approaches to risk reduction come with potentially complex trade-offs. These trade-offs may be social or economic (e.g., the potential influence of earlier age at first birth on a woman’s education or employment), or they may be health related (e.g., moderate alcohol consumption increases breast cancer risk, but it may reduce risk of heart disease; tamoxifen reduces risk for breast cancer but increases risk for stroke and endometrial cancer). It is also important to keep in mind that what the committee has outlined in this chapter are areas where the evidence indicates that action is likely to reduce risk in an average population. The actual change in risk for any individual woman who takes such actions might range from very small to moderate. Chapter 7 outlines the committee’s recommendations for further research to strengthen the knowledge base on breast cancer and, hopefully, to point to more and better opportunities to reduce risk for this disease. REFERENCES Ahn, J., A. Schatzkin, J. V. Lacey, Jr., D. Albanes, R. Ballard-Barbash, K. F. Adams, V. Kipnis, T. Mouw, et al. 2007. Adiposity, adult weight change, and postmenopausal breast cancer risk. Arch Intern Med 167(19):2091–2102. Akl, E. A., A. D. Oxman, J. Herrin, G. E. Vist, I. Terrenato, F. Sperati, C. Costiniuk, D. Blank, et al. 2011. Using alternative statistical formats for presenting risks and risk reductions. Cochrane Database Syst Rev (3):CD006776. Alliance for Radiation Safety in Pediatric Imaging. 2008. Image gently. http://www.pedrad. org/associations/5364/ig/ (accessed June 23, 2011). Ashar, B. H., T. N. Rice, and S. D. Sisson. 2007. Physicians’ understanding of the regulation of dietary supplements. Arch Intern Med 167(9):966–969. Bakken, K., E. Alsaker, A. E. Eggen, and E. Lund. 2004. Hormone replacement therapy and incidence of hormone-dependent cancers in the Norwegian Women and Cancer study. Int J Cancer 112(1):130–134. Baumann, B. M., E. H. Chen, A. M. Mills, L. Glaspey, N. M. Thompson, M. K. Jones, and M. C. Farner. 2011. Patient perceptions of computed tomographic imaging and their understanding of radiation risk and exposure. Ann Emerg Med 58(1):1–7. Beral, V., G. Reeves, D. Bull, and J. Green. 2011. Breast cancer risk in relation to the interval between menopause and starting hormone therapy. J Natl Cancer Inst 103(4):296–305.
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316 BREAST CANCER AND THE ENVIRONMENT Berrington de Gonzalez, A., M. Mahesh, K. P. Kim, M. Bhargavan, R. Lewis, F. Mettler, and C. Land. 2009. Projected cancer risks from computed tomographic scans performed in the United States in 2007. Arch Intern Med 169(22):2071–2077. Bogdanich, W. 2011. West Virginia hospital overradiated brain scan patients, records show. New York Times, March 5. Bogdanich, W., and K. Rebelo. 2010. A pinpoint beam strays invisibly, harming instead of healing. New York Times, December 28. Boyd, N. F., L. J. Martin, M. Yaffe, and S. Minkin. 2009. Mammographic density. Breast Cancer Res 11(Suppl 3):S4. Boyd, N. F., L. J. Martin, M. Bronskill, M. J. Yaffe, N. Duric, and S. Minkin. 2010. Breast tissue composition and susceptibility to breast cancer. J Natl Cancer Inst 102(16): 1224–1237. Brinton, L. A., D. Richesson, M. F. Leitzmann, G. L. Gierach, A. Schatzkin, T. Mouw, A. R. Hollenbeck, and J. V. Lacey, Jr. 2008. Menopausal hormone therapy and breast cancer risk in the NIH–AARP Diet and Health Study Cohort. Cancer Epidemiol Biomarkers Prev 17(11):3150–3160. Brody, J. G., K. B. Moysich, O. Humblet, K. R. Attfield, G. P. Beehler, and R. A. Rudel. 2007. Environmental pollutants and breast cancer: Epidemiologic studies. Cancer 109(12 Suppl):2667–2711. CalEPA (California Environmental Protection Agency). 2005. Proposed identification of en- vironmental tobacco smoke as a toxic air contaminant. http://www.arb.ca.gov/regact/ ets2006/ets2006.htm (accessed November 9, 2011). California Breast Cancer Research Program. 2007. Identifying gaps in breast cancer research: Addressing disparities and the roles of the physical and social environment. http://cbcrp. org/sri/reports/identifyingGaps/index.php (accessed October 25, 2011). Cantor, K. P., C. M. Villanueva, D. T. Silverman, J. D. Figueroa, F. X. Real, M. Garcia-Closas, N. Malats, S. Chanock, et al. 2010. Polymorphisms in GSTT1, GSTZ1, and CYP2E1, disinfection by-products, and risk of bladder cancer in Spain. Environ Health Perspect 118(11):1545–1550. CDC (Centers for Disease Control and Prevention). 2011. Alcohol and public health– frequently asked questions. http://www.cdc.gov/alcohol/faqs.htm#heavyDrinking (ac- cessed November 9, 2011). Chen, W. Y., G. A. Colditz, B. Rosner, S. E. Hankinson, D. J. Hunter, J. E. Manson, M. J. Stampfer, W. C. Willett, et al. 2002. Use of postmenopausal hormones, alcohol, and risk for invasive breast cancer. Ann Intern Med 137(10):798–804. Chlebowski, R. T., L. H. Kuller, R. L. Prentice, M. L. Stefanick, J. E. Manson, M. Gass, A. K. Aragaki, J. K. Ockene, et al. 2009. Breast cancer after use of estrogen plus progestin in postmenopausal women. N Engl J Med 360(6):573–587. Chuang, S. C., V. Gallo, D. Michaud, K. Overvad, A. Tjonneland, F. Clavel-Chapelon, I. Romieu, K. Straif, et al. 2011. Exposure to environmental tobacco smoke in childhood and incidence of cancer in adulthood in never smokers in the european prospective inves- tigation into cancer and nutrition. Cancer Causes Control 22(3):487–494. Cirigliano, M. 2007. Bioidentical hormone therapy: A review of the evidence. J Womens Health (Larchmt) 16(5):600–631. Clarke, C. A., D. M. Purdie, and S. L. Glaser. 2006. Population attributable risk of breast cancer in white women associated with immediately modifiable risk factors. BMC Cancer 6:170. Cohen, P. A. 2009. American roulette—contaminated dietary supplements. N Engl J Med 361(16):1523–1525.
OCR for page 317
317 OPPORTUNITIES FOR ACTION TO REDUCE ENVIRONMENTAL RISKS Collaborative Group on Hormonal Factors in Breast Cancer. 1996. Breast cancer and hor- monal contraceptives: Collaborative reanalysis of individual data on 53,297 women with breast cancer and 100,239 women without breast cancer from 54 epidemiological studies. Lancet 347(9017):1713–1727. Collaborative Group on Hormonal Factors in Breast Cancer. 1997. Breast cancer and hormone replacement therapy: Collaborative reanalysis of data from 51 epidemiological studies of 52,705 women with breast cancer and 108,411 women without breast cancer. Lancet 350(9084):1047–1059. Collaborative Group on Hormonal Factors in Breast Cancer. 2002. Alcohol, tobacco and breast cancer—collaborative reanalysis of individual data from 53 epidemiological stud- ies, including 58,515 women with breast cancer and 95,067 women without the disease. Br J Cancer 87(11):1234–1245. Collishaw, N. C., N. F. Boyd, K. P. Cantor, S. K. Hammond, K. C. Johnson, J. Millar, A. B. Miller, M. Miller, J. R. Palmer, A. G. Salmon, and F. Turcotte. 2009. Canadian expert panel on tobacco smoke and breast cancer risk. OTRU Special Report Series. Toronto, Canada: Ontario Tobacco Research Unit. http://www.otru.org/pdf/special/expert_panel_ tobacco_breast_cancer.pdf (accessed October 29, 2011). Cummings, S. R., J. A. Tice, S. Bauer, W. S. Browner, J. Cuzick, E. Ziv, V. Vogel, J. Shepherd, et al. 2009. Prevention of breast cancer in postmenopausal women: Approaches to esti- mating and reducing risk. J Natl Cancer Inst 101(6):384–398. Cuzick, J. 2008. Assessing risk for breast cancer. Breast Cancer Res 10(Suppl 4):S13. Cuzick, J., A. DeCensi, B. Arun, P. H. Brown, M. Castiglione, B. Dunn, J. F. Forbes, A. Glaus, et al. 2011. Preventive therapy for breast cancer: A consensus statement. Lancet Oncol 12(5):496–503. Davidson, N. E., and K. J. Helzlsouer. 2002. Good news about oral contraceptives. N Engl J Med 346(26):2078–2079. DeRoo, L. A., P. Cummings, and B. A. Mueller. 2011. Smoking before the first pregnancy and the risk of breast cancer: A meta-analysis. Am J Epidemiol 174(4):390-402. Don, S. 2011. Pediatric digital radiography summit overview: State of confusion. Pediatr Radiol 41(5):567–572. Eliassen, A. H., G. A. Colditz, B. Rosner, W. C. Willett, and S. E. Hankinson. 2006. Adult weight change and risk of postmenopausal breast cancer. JAMA 296(2):193–201. Endocrine Society. 2006. Position statement: Bioidentical hormones. http://www.endo-society. org/advocacy/policy/upload/BH_Position_Statement_final_10_25_06_w_Header.pdf (ac- cessed November 8, 2011). EPA (Environmental Protection Agency). 2005. Guidelines for carcinogen risk assessment. EPA/630/P-03/001F. http://www.epa.gov/raf/publications/pdfs/CANCER_GUIDELINES_ FINAL_3-25-05.PDF (accessed November 17, 2011). EPA. 2011. Integrated risk information system (IRIS). http://www.epa.gov/ncea/iris/index.html (accessed October 28, 2011). Fazel, R., H. M. Krumholz, Y. Wang, J. S. Ross, J. Chen, H. H. Ting, N. D. Shah, K. Nasir, et al. 2009. Exposure to low-dose ionizing radiation from medical imaging procedures. N Engl J Med 361(9):849–857. FDA (Food and Drug Administration). 2005. FDA authority over cosmetics. http://www.fda. gov/Cosmetics/GuidanceComplianceRegulatoryInformation/ucm074162.htm (accessed November 17, 2011). FDA. 2009. Consumer information: Overview of dietary supplements. http://www.fda.gov/ Food/DietarySupplements/ConsumerInformation/ucm110417.htm (accessed November 9, 2011).
OCR for page 318
318 BREAST CANCER AND THE ENVIRONMENT FDA. 2010. Initiative to reduce unnecessary radiation exposure from medical imaging. http://www.fda.gov/radiation-emittingproducts/radiationsafety/radiationdosereduction/ ucm199904.htm (accessed November 17, 2011). Fennell, T. R., J. P. MacNeela, R. W. Morris, M. Watson, C. L. Thompson, and D. A. Bell. 2000. Hemoglobin adducts from acrylonitrile and ethylene oxide in cigarette smokers: Effects of glutathione S-transferase T1-null and M1-null genotypes. Cancer Epidemiol Biomarkers Prev 9(7):705–712. Fisher, B., J. P. Costantino, D. L. Wickerham, R. S. Cecchini, W. M. Cronin, A. Robidoux, T. B. Bevers, M. T. Kavanah, et al. 2005. Tamoxifen for the prevention of breast cancer: Current status of the National Surgical Adjuvant Breast and Bowel Project P-1 study. J Natl Cancer Inst 97(22):1652–1662. Flegal, K. M., M. D. Carroll, C. L. Ogden, and L. R. Curtin. 2010. Prevalence and trends in obesity among US adults, 1999–2008. JAMA 303(3):235–241. Freedman, A. N., B. Yu, M. H. Gail, J. P. Costantino, B. I. Graubard, V. G. Vogel, G. L. Anderson, and W. McCaskill-Stevens. 2011. Benefit/risk assessment for breast cancer chemoprevention with raloxifene or tamoxifen for women age 50 years or older. J Clin Oncol 29(17):2327–2333. Friedenreich, C. M. 2010. The role of physical activity in breast cancer etiology. Semin Oncol 37(3):297–302. Friedenreich, C. M., C. G. Woolcott, A. McTiernan, R. Ballard-Barbash, R. F. Brant, F. Z. Stanczyk, T. Terry, N. F. Boyd, et al. 2010. Alberta physical activity and breast cancer prevention trial: Sex hormone changes in a year-long exercise intervention among post- menopausal women. J Clin Oncol 28(9):1458–1466. Friedenreich, C. M., C. G. Woolcott, A. McTiernan, T. Terry, R. Brant, R. Ballard-Barbash, M. L. Irwin, C. A. Jones, et al. 2011. Adiposity changes after a 1-year aerobic exercise intervention among postmenopausal women: A randomized controlled trial. Int J Obes (Lond) 35(3):427-435. Gail, M. H., L. A. Brinton, D. P. Byar, D. K. Corle, S. B. Green, C. Schairer, and J. J. Mulvihill. 1989. Projecting individualized probabilities of developing breast cancer for white fe- males who are being examined annually. J Natl Cancer Inst 81(24):1879–1886. GAO (Government Accountability Office). 2005. Options exist to improve EPA’s ability to assess health risks and manage its Chemical Review Program. GAO-05-458. Washington, DC: GAO. http://www.gao.gov/new.items/d05458.pdf (accessed November 9, 2011). GAO. 2006. Actions are needed to improve the effectiveness of EPA’s Chemical Review Program. GAO-06-1032T. Washington, DC: GAO. http://www.gao.gov/new.items/ d061032t.pdf (accessed November 9, 2011). GAO. 2007. Comparison of U.S. and recently enacted European Union approaches to protect against the risks of toxic chemicals. GAO-07-825. Washington, DC: GAO. http://www. gao.gov/new.items/d07825.pdf (accessed November 9, 2011). GAO. 2009a. Options for enhancing the effectiveness of the Toxic Substances Control Act. GAO-09-428T. Washington, DC: GAO. http://www.gao.gov/new.items/d09428t.pdf (ac- cessed November 9, 2011). GAO. 2009b. Biomonitoring: EPA needs to coordinate its research strategy and clarify its authority to obtain biomonitoring data. GAO-09-353. Washington, DC: GAO. http:// www.gao.gov/new.items/d09353.pdf (accessed October 29, 2011). Gapstur, S. M., J. D. Potter, T. A. Sellers, and A. R. Folsom. 1992. Increased risk of breast cancer with alcohol consumption in postmenopausal women. Am J Epidemiol 136(10):1221–1231. Gibbons, J., and S. Laha. 1999. Water purification systems: A comparative analysis based on the occurrence of disinfection by-products. Environ Pollut 106(3):425–428.
OCR for page 319
319 OPPORTUNITIES FOR ACTION TO REDUCE ENVIRONMENTAL RISKS Goss, P. E., J. N. Ingle, J. E. Ales-Martinez, A. M. Cheung, R. T. Chlebowski, J. Wactawski- Wende, A. McTiernan, J. Robbins, et al. 2011. Exemestane for breast-cancer prevention in postmenopausal women. N Engl J Med 364(25):2381–2391. Gray, J. 2010. State of the evidence: The connection between breast cancer and the environ- ment, 6th ed. San Francisco, CA: Breast Cancer Fund. Gronbaek, M. 2009. The positive and negative health effects of alcohol—and the public health implications. J Intern Med 265(4):407–420. Gunzerath, L., V. Faden, S. Zakhari, and K. Warren. 2004. National Institute on Alcohol Abuse and Alcoholism report on moderate drinking. Alcohol Clin Exp Res 28(6): 829–847. Ha, M., K. Mabuchi, A. J. Sigurdson, D. M. Freedman, M. S. Linet, M. M. Doody, and M. Hauptmann. 2007. Smoking cigarettes before first childbirth and risk of breast cancer. Am J Epidemiol 166(1):55–61. Hammond, E. C., I. J. Selikoff, and H. Seidman. 1979. Asbestos exposure, cigarette smoking and death rates. Ann N Y Acad Sci 330:473–490. Hankinson, S. E. 2005–2006. Endogenous hormones and risk of breast cancer in postmeno- pausal women. Breast Dis 24:3–15. Harvie, M., A. Howell, R. A. Vierkant, N. Kumar, J. R. Cerhan, L. E. Kelemen, A. R. Folsom, and T. A. Sellers. 2005. Association of gain and loss of weight before and after meno- pause with risk of postmenopausal breast cancer in the Iowa Women’s Health Study. Cancer Epidemiol Biomarkers Prev 14(3):656–661. Helzlsouer, K. J. 2011. The numbers game: The risky business of projecting risk. J Natl Cancer Inst 103(13):992–993. HHS (Department of Health and Human Services). 2006. The health consequences of in- voluntary exposure to tobacco smoke: A report of the Surgeon General. Atlanta, GA: Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Preven- tion and Health Promotion, Office on Smoking and Health. HHS. 2008. 2008 Physical activity guidelines for Americans. http://www.health.gov/ paguidelines/guidelines/default.aspx (accessed August 9, 2011). Horn-Ross, P. L., A. J. Canchola, D. W. West, S. L. Stewart, L. Bernstein, D. Deapen, R. Pinder, R. K. Ross, et al. 2004. Patterns of alcohol consumption and breast cancer risk in the California Teachers Study cohort. Cancer Epidemiol Biomarkers Prev 13(3):405–411. Huang, Z., S. E. Hankinson, G. A. Colditz, M. J. Stampfer, D. J. Hunter, J. E. Manson, C. H. Hennekens, B. Rosner, et al. 1997. Dual effects of weight and weight gain on breast cancer risk. JAMA 278(17):1407–1411. Hunter, D. J., G. A. Colditz, S. E. Hankinson, S. Malspeis, D. Spiegelman, W. Chen, M. J. Stampfer, and W. C. Willett. 2010. Oral contraceptive use and breast cancer: A prospec- tive study of young women. Cancer Epidemiol Biomarkers Prev 19(10):2496–2502. IARC (International Agency for Research on Cancer). 2010. Alcohol consumption and ethyl carbamate. IARC monographs on the evaluation of carcinogenic risks to humans. Vol. 96. Lyon, France: IARC. IARC. 2011. IARC monographs on the evaluation of carcinogenic risks to humans. http:// monographs.iarc.fr/ (accessed October 28, 2011). Key, T., P. Appleby, I. Barnes, and G. Reeves. 2002. Endogenous sex hormones and breast cancer in postmenopausal women: Reanalysis of nine prospective studies. J Natl Cancer Inst 94(8):606–616. Klatsky, A. L. 2009. Alcohol and cardiovascular diseases. Expert Rev Cardiovasc Ther 7(5): 499–506. La Vecchia, C. 2001. Epidemiology of ovarian cancer: A summary review. Eur J Cancer Prev 10(2):125–129.
OCR for page 320
320 BREAST CANCER AND THE ENVIRONMENT LaCroix, A. Z., R. T. Chlebowski, J. E. Manson, A. K. Aragaki, K. C. Johnson, L. Martin, K. L. Margolis, M. L. Stefanick, et al. 2011. Health outcomes after stopping conjugated equine estrogens among postmenopausal women with prior hysterectomy: A randomized controlled trial. JAMA 305(13):1305–1314. Lee, C. I., A. H. Haims, E. P. Monico, J. A. Brink, and H. P. Forman. 2004. Diagnostic CT scans: Assessment of patient, physician, and radiologist awareness of radiation dose and possible risks. Radiology 231(2):393–398. Luo, J., K. L. Margolis, J. Wactawski-Wende, K. Horn, C. Messina, M. L. Stefanick, H. A. Tindle, E. Tong, et al. 2011. Association of active and passive smoking with risk of breast cancer among postmenopausal women: A prospective cohort study. BMJ 342:d1016. Marchbanks, P. A., J. A. McDonald, H. G. Wilson, S. G. Folger, M. G. Mandel, J. R. Daling, L. Bernstein, K. E. Malone, et al. 2002. Oral contraceptives and the risk of breast cancer. N Engl J Med 346(26):2025–2032. Maskarinec, G., L. Meng, and L. N. Kolonel. 1998. Alcohol intake, body weight, and mortal- ity in a multiethnic prospective cohort. Epidemiology 9(6):654–661. McTiernan, A., S. S. Tworoger, K. B. Rajan, Y. Yasui, B. Sorenson, C. M. Ulrich, J. Chubak, F. Z. Stanczyk, et al. 2004a. Effect of exercise on serum androgens in postmenopausal women: A 12-month randomized clinical trial. Cancer Epidemiol Biomarkers Prev 13(7): 1099–1105. McTiernan, A., S. S. Tworoger, C. M. Ulrich, Y. Yasui, M. L. Irwin, K. B. Rajan, B. Sorensen, R. E. Rudolph, et al. 2004b. Effect of exercise on serum estrogens in postmenopausal women: A 12-month randomized clinical trial. Cancer Res 64(8):2923–2928. Mezzetti, M., C. La Vecchia, A. Decarli, P. Boyle, R. Talamini, and S. Franceschi. 1998. Popu- lation attributable risk for breast cancer: Diet, nutrition, and physical exercise. J Natl Cancer Inst 90(5):389–394. Million Women Study Collaborators. 2003. Breast cancer and hormone-replacement therapy in the Million Women Study. Lancet 362(9382):419–427. Monninkhof, E. M., S. G. Elias, F. A. Vlems, I. van der Tweel, A. J. Schuit, D. W. Voskuil, and F. E. van Leeuwen. 2007. Physical activity and breast cancer: A systematic review. Epidemiology 18(1):137–157. Monninkhof, E. M., M. J. Velthuis, P. H. Peeters, J. W. Twisk, and A. J. Schuit. 2009. Effect of exercise on postmenopausal sex hormone levels and role of body fat: A randomized controlled trial. J Clin Oncol 27(27):4492–4499. Moreno, M. A. 2011. Advice for patients: Decreasing unnecessary radiation exposure for children. Arch Pediatr Adolesc Med 165(5):480. NCI (National Cancer Institute). 2010. SEER cancer statistics review, 1975–2007. Edited by S. F. Altekruse, C. L. Kosary, M. Krapcho, N. Neyman, R. Aminou, W. Waldron, J. Ruhl, N. Howlader, Z. Tatalovich, H. Cho, A. Mariotto, M. P. Eisner, D. R. Lewis, K. Cronin, H. S. Chen, E. J. Feuer, D. G. Stinchcomb, and B. K. Edwards. Bethesda, MD: NCI. http://seer.cancer.gov/csr/1975_2007/ (accessed January 6, 2011). NCI. 2011a. Breast cancer risk assessment tool. http://www.cancer.gov/bcrisktool/ (accessed December 21, 2011). NCI. 2011b. Breast cancer risk assessment tool: About the tool. http://www.cancer.gov/ bcrisktool/about-tool.aspx (accessed December 21, 2011). Nelson, H. D., R. Fu, J. C. Griffin, P. Nygren, M. E. Smith, and L. Humphrey. 2009. System- atic review: Comparative effectiveness of medications to reduce risk for primary breast cancer. Ann Intern Med 151(10):703–715, W-226–W-735. Neutel, C. I., and H. Morrison. 2010. Could recent decreases in breast cancer incidence really be due to lower HRT use? Trends in attributable risk for modifiable breast cancer risk factors in Canadian women. Can J Public Health 101(5):405–409.
OCR for page 321
321 OPPORTUNITIES FOR ACTION TO REDUCE ENVIRONMENTAL RISKS NTP (National Toxicology Program). 2007a. Toxicology and carcinogenesis studies of dibromoacetic acid (CAS No. 631-64-1) in F344/N rats and B6C3F1 mice (drinking water studies). NTP TR 537. Research Triangle Park, NC: NTP. http://ntp.niehs.nih.gov/ files/537_FINAL_web.pdf (accessed December 21, 2011). NTP. 2007b. Toxicology studies of dichloroacetic acid (CAS No. 79-43-6) in genetically modi- fied mice. NTP GMM 11. Research Triangle Park, NC: NTP. http://www.epa.gov/iris/ toxreviews/0654tr.pdf (accessed November 8, 2011). NTP. 2011. 12th report on carcinogens (RoC). http://ntp.niehs.nih.gov/index.cfm? objectid=03C9AF75-E1BF-FF40-DBA9EC0928DF8B15 (accessed November 9, 2011). Palmer, J. R., L. L. Adams-Campbell, D. A. Boggs, L. A. Wise, and L. Rosenberg. 2007. A prospective study of body size and breast cancer in black women. Cancer Epidemiol Biomarkers Prev 16(9):1795–1802. Petracci, E., A. Decarli, C. Schairer, R. M. Pfeiffer, D. Pee, G. Masala, D. Palli, and M. H. Gail. 2011. Risk factor modification and projections of absolute breast cancer risk. J Natl Cancer Inst 103(13):1037–1048. Physical Activity Guidelines Advisory Committee. 2008. Physical activity guidelines advisory committee report, 2008. Washington, DC: HHS. http://www.health.gov/paguidelines/ committeereport.aspx (accessed August 9, 2011). Preston, D. L., E. Ron, S. Tokuoka, S. Funamoto, N. Nishi, M. Soda, K. Mabuchi, and K. Kodama. 2007. Solid cancer incidence in atomic bomb survivors: 1958–1998. Radiat Res 168(1):1–64. Ravdin, P. M., K. A. Cronin, N. Howlader, C. D. Berg, R. T. Chlebowski, E. J. Feuer, B. K. Edwards, and D. A. Berry. 2007. The decrease in breast-cancer incidence in 2003 in the United States. N Engl J Med 356(16):1670–1674. Reeves, G. K., V. Beral, J. Green, T. Gathani, and D. Bull. 2006. Hormonal therapy for menopause and breast-cancer risk by histological type: A cohort study and meta-analysis. Lancet Oncol 7(11):910–918. Reynolds, P., S. Hurley, D. E. Goldberg, H. Anton-Culver, L. Bernstein, D. Deapen, P. L. Horn-Ross, D. Peel, et al. 2004. Active smoking, household passive smoking, and breast cancer: Evidence from the California Teachers Study. J Natl Cancer Inst 96(1):29–37. Reynolds, P., D. Goldberg, S. Hurley, D. O. Nelson, J. Largent, K. D. Henderson, and L. Bernstein. 2009. Passive smoking and risk of breast cancer in the California Teachers Study. Cancer Epidemiol Biomarkers Prev 18(12):3389–3398. Richardson, S. D., M. J. Plewa, E. D. Wagner, R. Schoeny, and D. M. Demarini. 2007. Occurrence, genotoxicity, and carcinogenicity of regulated and emerging disinfec- tion by-products in drinking water: A review and roadmap for research. Mutat Res 636(1–3):178–242. Ronksley, P. E., S. E. Brien, B. J. Turner, K. J. Mukamal, and W. A. Ghali. 2011. Association of alcohol consumption with selected cardiovascular disease outcomes: A systematic review and meta-analysis. BMJ 342:d671. Rose, G. 1992. Strategies of prevention: The individual and the population. In Coronary heart disease epidemiology: From aetiology to public health. Edited by M. Marmot and P. Elliott. Oxford, UK: Oxford University Press. Pp. 311–324. Rothman, K. J., and S. Greenland, eds. 1998. Modern epidemiology, 2nd ed. Philadelphia, PA: Lippincott–Raven. Rudel, R. A., K. R. Attfield, J. N. Schifano, and J. G. Brody. 2007. Chemicals causing mam- mary gland tumors in animals signal new directions for epidemiology, chemicals testing, and risk assessment for breast cancer prevention. Cancer 109(12 Suppl):2635–2666.
OCR for page 322
322 BREAST CANCER AND THE ENVIRONMENT Rudel, R. A., J. M. Gray, C. L. Engel, T. W. Rawsthorne, R. E. Dodson, J. M. Ackerman, J. Rizzo, J. L. Nudelman, et al. 2011. Food packaging and bisphenol A and bis(2- ethyhexyl) phthalate exposure: Findings from a dietary intervention. Environ Health Perspect 119(7):914–920. Santen, R. J., D. C. Allred, S. P. Ardoin, D. F. Archer, N. Boyd, G. D. Braunstein, H. G. Burger, G. A. Colditz, et al. 2010. Postmenopausal hormone therapy: An Endocrine Society scientific statement. J Clin Endocrinol Metab 95(7 Suppl 1):s1–s66. Schoeny, R. 2010. Disinfection by-products: A question of balance. Environ Health Perspect 118(11):A466–A467. Schwartz, L. M., S. Woloshin, E. L. Dvorin, and H. G. Welch. 2006. Ratio measures in lead- ing medical journals: Structured review of accessibility of underlying absolute risks. BMJ 333(7581):1248. Secretan, B., K. Straif, R. Baan, Y. Grosse, F. El Ghissassi, V. Bouvard, L. Benbrahim-Tallaa, N. Guha, et al. 2009. A review of human carcinogens—Part E: Tobacco, areca nut, alcohol, coal smoke, and salted fish. Lancet Oncol 10(11):1033–1034. Shuryak, I., R. K. Sachs, and D. J. Brenner. 2010. Cancer risks after radiation exposure in middle age. J Natl Cancer Inst 102(21):1628–1636. Smith-Bindman, R. 2010. Is computed tomography safe? N Engl J Med 363(1):1–4. Smith-Bindman, R. 2011. Ionizing radiation exposure to the U.S. population, with a focus on radiation from medical imaging. Paper commissioned by the Committee on Breast Cancer and the Environment (see Appendix F; available at http://www.nap.edu/catalog. php?record_id=13263). Smith-Warner, S. A., D. Spiegelman, S. S. Yaun, P. A. van den Brandt, A. R. Folsom, R. A. Goldbohm, S. Graham, L. Holmberg, et al. 1998. Alcohol and breast cancer in women: A pooled analysis of cohort studies. JAMA 279(7):535–540. Sovak, M., A. L. Seligson, M. Konas, M. Hajduch, M. Dolezal, M. Machala, and R. Nagourney. 2002. Herbal composition PC-SPES for management of prostate cancer: Identification of active principles. J Natl Cancer Inst 94(17):1275–1281. Taylor, H., and R. Leftman, eds. 2002. Widespread ignorance of regulation and labeling of vitamins, minerals, and food supplements. Health Care News 2(23):1–5. http://www. harrisinteractive.com/news/newsletters/healthnews/HI_HealthCareNews2002Vol2_Iss23. pdf (accessed August 9, 2011). Teras, L. R., M. Goodman, A. V. Patel, W. R. Diver, W. D. Flanders, and H. S. Feigelson. 2011. Weight loss and postmenopausal breast cancer in a prospective cohort of overweight and obese U.S. women. Cancer Causes Control 22(4):573–579. Tseng, M., C. R. Weinberg, D. M. Umbach, and M. P. Longnecker. 1999. Calculation of population attributable risk for alcohol and breast cancer (United States). Cancer Causes Control 10(2):119–123. Tyrer, J., S. W. Duffy, and J. Cuzick. 2004. A breast cancer prediction model incorporating familial and personal risk factors. Stat Med 23:1111–1130. USPSTF (U.S. Preventive Services Task Force). 2002. Chemoprevention of breast cancer: Recommendations and rationale. http://www.uspreventiveservicestaskforce.org/uspstf/ uspsbrpv.htm (accessed August 9, 2011). USPSTF. 2005. Hormone therapy for the prevention of chronic conditions in postmeno- pausal women: Recommendation statement. http://www.uspreventiveservicestaskforce. org/uspstf/uspspmho.htm (accessed August 9, 2011). Vogel, V. G., J. P. Costantino, D. L. Wickerham, W. M. Cronin, R. S. Cecchini, J. N. Atkins, T. B. Bevers, L. Fehrenbacher, et al. 2010. Update of the National Surgical Adjuvant Breast and Bowel Project Study of Tamoxifen and Raloxifene (STAR) P-2 Trial: Prevent- ing breast cancer. Cancer Prev Res (Phila) 3(6):696–706.
OCR for page 323
323 OPPORTUNITIES FOR ACTION TO REDUCE ENVIRONMENTAL RISKS WCRF/AICR (World Cancer Research Fund/American Institute for Cancer Research). 2007. Food, nutrition, physical activity, and the prevention of cancer: A global perspective. Washington DC: AICR. WCRF/AICR. 2008. The associations between food, nutrition and physical activity and the risk of breast cancer. WCRF/AICR systematic literature review continuous update report. http://dietandcancerreport.org/downloads/cu/cu_breast_cancer_report_2008.pdf (accessed October 29, 2011). WCRF/AICR. 2010. Food, nutrition and physical activity and the prevention of breast cancer. WCRF/AICR continuous update report summary. http://dietandcancerreport.org/down- loads/cu/cu_breast_cancer_summary_2008.pdf (accessed October 29, 2011). White, J. 2002. PC-SPES—a lesson for future dietary supplement research. J Natl Cancer Inst 94(17):1261–1263. Winzer, B. M., D. C. Whiteman, M. M. Reeves, and J. D. Paratz. 2011. Physical activity and cancer prevention: A systematic review of clinical trials. Cancer Causes Control 22(6):811–826. Writing Group for the Women’s Health Initiative Investigators. 2002. Risks and benefits of estrogen plus progestin in healthy postmenopausal women: Principal results from the Women’s Health Initiative randomized controlled trial. JAMA 288(3):321–333. Xue, F., W. C. Willett, B. A. Rosner, S. E. Hankinson, and K. B. Michels. 2011. Cigarette smoking and the incidence of breast cancer. Arch Intern Med 171(2):125–133. Yang, C. Z., S. I. Yaniger, V. C. Jordan, D. J. Klein, and G. D. Bittner. 2011. Most plastic products release estrogenic chemicals: A potential health problem that can be solved. Environ Health Perspect 119(7):989–996.
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