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4 Challenges of Studying Environmental Risk Factors for Breast Cancer T he committee was asked to review the methodologic challenges involved in conducting research on breast cancer and the environ- ment. New insights into carcinogenesis are giving researchers new opportunities to explore both the biology and the epidemiology of breast cancer in relation to environmental exposures. Although progress has been made in investigating the role (whether adverse or not) of environmental factors in breast cancer, the scope of the potential research questions is vast and the questions to be answered are complex. This chapter reviews challenges facing researchers on a variety of fronts, including the nature of the various forms of breast cancer; the diversity and complexity of environ- mental factors; identifying and measuring exposures at appropriate times; genetic complexity that is still unfolding; and the inherent limitations of the laboratory and epidemiologic tools available to evaluate associations between environmental exposures and disease. COMPLEXITY OF BREAST CANCER As noted in Chapter 2, breast cancer is a term that captures what is likely to be several diseases. Tumor types have been categorized based on several different characteristics, including age or menopausal status of the woman at the time of diagnosis; the state of the tumor as in situ or invasive; the extent of spread from the initial tumor site; cell type (lobular, ductal); and molecular features of the cells, such as the presence or absence of hor- mone or growth factor receptors (e.g., estrogen or progesterone receptors [ER or PR], human epidermal growth factor receptor 2 [HER2]). Within 177
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178 BREAST CANCER AND THE ENVIRONMENT each of these broad categories is considerable variability in tumor charac- teristics and gene expression. A study examining the gene expression of 65 surgical samples of breast tumors from 42 individuals’ cancers found each tumor to have a distinctive molecular portrait. The tumors showed great variation in their patterns of gene expression, and the variation was multi- dimensional: different sets of genes showed largely independent patterns of variation (Perou et al., 2000). Further study of the molecular pathology of breast cancer has shed additional light on the possible divergent evolution- ary pathways of breast cancer progression, revealing still more complexity (Bombonati and Sgroi, 2011), as discussed in Chapter 5. While characterizations of tumor and cancer types, such as those noted above, are proving increasingly useful as guides to clinical care and prog- nosis, their relevance to etiology is not clear. Some associations have been observed between certain tumor types and risk factors (e.g., obesity and ER-positive [ER+]) tumors, but for the most part, the mechanistic basis for these relationships remains to be clarified, as described further in Chapter 5. Various schematics have been used to illustrate the complexity and interconnectedness of potential factors in breast cancer causation. Howell et al. (2005), for example, illustrate possible roles for genes, pathways, risk factors, modifiable variables, and life events (Figure 4-1). In this represen- tation of some of the known modifiable and unmodifiable risk factors for breast cancer, alcohol serves as an example of a factor that might alter risk for breast cancer in multiple ways. Through induction of aromatase activ- ity, it may foster conversion of androgens to estrogens that have a causal role in breast cancer (Etique et al., 2004). It has also been hypothesized to contribute to genomic instability (Benassi-Evans and Fenech, 2011). Fur- thermore, it may act indirectly in that its calories can contribute to obesity that itself is associated with breast cancer. Another illustration (Figure 4-2) of the numerous interrelated factors important in the etiology of breast cancer comes from a complex systems model developed by Robert Hiatt and colleagues as part of a project spon- sored by the California Breast Cancer Research Program.1 The developers of this model used expert opinion to select causal factors from four large domains (Societal/Cultural, Physical/Chemical, Behavioral, and Biologi- cal) to illustrate the multiple levels of causation that must be considered along with how the factors are integrated across levels and over time. Even though multiple key factors are present, all possible etiologic factors were not included for relative simplicity in interpretation. The model focuses solely on postmenopausal breast cancer because of the different etiologic factors and pathways for premenopausal disease. It takes into account both 1 Personal communication, R. A. Hiatt, University of California, San Francisco, May 21, 2011.
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Unavoidable LOW PENETRANCE GENES HIGH PENETRANCE GENES Aging (inherited) risk factors CHEK2/ATM Fibrosis genes BRCA1/BRCA2 RE-EXPRESSION OF FETAL GENES RADIOSENSITIVITY GENOMIC INSTABILITY Steroid hormone ‘Obesity genes’ ‘CAFs’ DENSITY TUMORIGENESIS pathway ESTROGEN Early menarche INFLAMMATION Late menopause OBESITY No or late 1st pregnancy Modifiable Healthy diet Alcohol Exercise SERMs & AIs Oophorectomy HRT risk factors/ management AGE FIGURE 4-1 Overview of risk factors associated with breast complexity.eps diagram summarizes the unavoidable (inherited) and Figure 4-1 cancer. “The modifiable risk factors that can ultimately lead to tumorigenesis. Genes/pathways/risk factors are shown in red; inherited or un- modifiable factors are shown in green; modifiable variables are shown in blue; life events are represented by gray boxes; increased/ positive effects are denoted by solid arrows; and reduced/negative effects are denoted by dashed arrows. AIs, aromatase inhibi- tors; ATM, ataxia telangiectasia mutated; BRCA1 and BRCA2 (genes in which deleterious germline mutations increase the risk of cancer); CAFs, cancer-associated fibroblasts; CHEK2, CHK2, checkpoint homolog; HRT, hormone replacement therapy; SERMs, selective estrogen receptor modulators.” SOURCE: Adapted from Howell et al. (2005, p. 638). Used with permission; Howell, A., A. H. Sims, K. R. Ong, M. N. Harvie, D. G. Evans, and R. B. Clarke. 2005. Mechanisms of disease: Prediction and prevention of breast cancer—cellular and molecular 179 interactions. Nat Clin Pract Oncol 2(12):635–646.
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SOCIETAL/ 180 CULTURAL PHYSICAL/ CHEMICAL Country of Birth Environmental tobacco Education Sleep disturbance Occupation Endocrine disruptors (e.g., BPA, organochlorines) Race/Ethnicity Latitude Radiation/ Income Medical imaging Breastfeeding Vitamin D HRT Post Menopausal Alcohol Breast Cancer Genotoxins Incidence Phytoestrogens (e.g., soy) Age at first birth, parity Age Physical Breast density quality of data activity Height High penetrance genes (1 = strongest) (e.g., BRCA1, BRCA2, TP53) 1 Tobacco use Age at 2 Endogenous hormones menopause 3 (e.g., IGF, estradiol) strength of assoc Low penetrance genes Obesity Immune function (1 = strongest) (e.g., CASP8, 2a35, (inflammation) FGFR2) 1 Age at menarche 2 3 4 Insulin resistance BEHAVIORAL Ancestry BIOLOGICAL • This model is specific to incidence, not survival • Factors may differ by tumor subtype FIGURE 4-2 Illustration of an evidence-based complex-systems model of postmenopausal breast cancer causation. This model dis- plays multiple factors associated with postmenopausal breast cancer causation in four broad domains and shows their interconnec- tions across levels (genes to society) by arrows that indicate variations in the strength of the associations and the quality of the data. SOURCE: Personal communication, R. A. Hiatt, University of California, San Francisco, May 21, 2011. Developed with support from the California Breast Cancer Figure 4-2 Hiatt Model for NAP 12-6-11.eps Research Program. type is small, landscape
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181 CHALLENGES OF STUDYING ENVIRONMENTAL RISK FACTORS the strength of the associations as well as the quality of the data in the size and hatching of the interconnecting arrows. Diagrams such as these, which attempt to depict the multiplicity of factors that seem to have a role in breast cancer, help underline the biologi- cal complexity of the pathways along which those factors may be acting, the difficulty of distinguishing truly causal effects from associations with intermediate factors, and the challenges of designing, conducting, and interpreting studies that try to evaluate risk factors for the various forms of this disease. Although these challenges share similarities across the spectrum of risk factors evaluated in this report, they may be particularly acute for evaluat- ing risk relationships from exposures to environmental chemicals. For stud- ies in humans, these include the issues inherent to estimating and assessing exposures, the study design and analytic challenges of environmental epi- demiology, and efforts to account for genetic differences in susceptibility to cancer and potential gene–environment interactions. The next portion of this chapter pays particular attention to the challenges in studying environ- mental chemicals. Studies in animals and in vitro systems pose their own technical obstacles and challenges of interpretation and extrapolation to humans, which are discussed in a subsequent portion of the chapter. STUDYING ENVIRONMENTAL CHEMICAL AND PHYSICAL EXPOSURES THROUGH HUMAN STUDIES As noted previously, the committee has adopted a broad approach to the definition of “environment.” A subset of environmental exposures that are of potential concern in the etiology of breast cancer is that of specific chemical and physical agents that might influence breast cancer develop- ment. Although information on exposure and the toxicology of many chemicals may be incomplete, for many other chemicals, knowledge of some their properties indicates that they are unlikely to be mutagenic or carcinogenic. Whether other agents in the environment are able to causally contribute to breast cancer is highly dependent upon both the duration and magni- tude (dose) of exposure. One of the most difficult problems in conducting epidemiologic studies on environmental exposures and health effects is to obtain reasonably accurate measurements or estimates of exposures rel- evant to the disease process. These exposures may occur at low or varying levels or both, for which the relevant time period—the window when the exposure might influence the development of a tumor—is unknown, or they may have occurred years or decades previously. The sections that follow address some of the specific challenges associated with assessing exposures to environmental and physical agents and illustrate the need for additional
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182 BREAST CANCER AND THE ENVIRONMENT or more refined tools to aid in disentangling the possible contributions of these environmental factors to breast cancer. Assessing Exposures to Chemical and Physical Agents in the Environment Both the nature of the exposures to chemical and physical agents and the limited means for measuring or assessing them pose challenges for observational research. Human exposures to substances in the environ- ment take place throughout the life course, and in all settings. People are exposed to myriad substances in air, water, and food encountered in homes, schools, workplaces, and even before birth via in utero exposures. A per- son is exposed not only to individual chemicals, but to mixtures of many different substances, at varying doses simultaneously or at different times. Sometimes it is possible to identify individuals or groups, such as workers in particular occupations, whose typical exposures are considerably higher than those of the average person. Epidemiologic studies assess whether groups with higher exposures are more likely to experience the outcome of interest, cancer for example, than groups with lower exposures. Determining who is exposed and the degree of their exposures are critical to accurately assessing the association with the health outcome. However, errors in classifying who is more and who is less exposed (exposure misclassification) could limit the ability of a study to show an association with the risk factor where there is one. Thus, accurate exposure assessment is a critical component of human studies to evaluate risk factors for breast cancer or any health outcome. Historically, studies in occupational settings have been an important means for identifying most chemical carcinogens because in occupational settings, chemical use is often documented and exposure levels tend to be higher than elsewhere. Assessment of exposures in occupational studies are facilitated by extensive sources of data, such as job histories, understanding of production processes and chemicals used, and data from personal or area sampling to measure exposures, as required by the Occupational Safety and Health Administration (OSHA) and standard industrial hygiene practices. Exposure of certain workers to some chemicals may be thousands (or more) times greater than that experienced by the general public, while other work- ers with different job tasks might experience a wide range of exposures. This variability makes it easier to distinguish people who are exposed to very high levels from those with lesser exposure. The greater the contrast, the firmer the conclusions that can be drawn about differences in risk of disease. When exposure levels are low, contrasts are smaller and exposure misclassification is likely to be relatively greater. Determining exposures can be more difficult in environmental settings, particularly for chemicals that are not regularly monitored in air or food, or for chemicals for which
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183 CHALLENGES OF STUDYING ENVIRONMENTAL RISK FACTORS exposure occurs indoors as a result of specific behaviors or products used. For these reasons, environmental epidemiologic studies are a less effective or efficient approach than occupational epidemiologic studies for demon- strating associations between chemicals and increased rates of disease. Few of the chemicals identified by the International Agency for Research on Cancer (IARC) or the U.S. Environmental Protection Agency (EPA) as human carcinogens have been classified as such on the basis of studies showing breast cancer in humans. One cannot conclude, however, that these chemicals do not contribute to breast cancer. For virtually all carcinogens identified by IARC and EPA, the evidence base has primarily been from occupational epidemiologic studies for reasons described. For the vast majority of these chemicals, the cohorts were assembled and followed during the 1940s through the 1970s, periods when most industrial firms employed only men. Historically, therefore, most epidemiologic studies of cancer in the workplace omitted women from the analysis because there were too few present to observe an effect. Because breast cancer is rare in men, such stud- ies lacked the power to detect breast carcinogens. (Power is a function of the expected number of cases of disease in the studies, the level and variabil- ity of exposure, the validity of the exposure assessment, and the strength of the true underlying association.) Not only are studies of breast cancer in men underpowered, but also, extrapolation of cancer findings from men to women, which may be justified for other forms of cancer, might not be appropriate for breast cancer. Beyond the Workplace: Environmental Chemical Exposures Outside the workplace, exposures to chemicals arise in multiple loca- tions (home, car, ambient air pollution); from multiple activities, including commuting, cleaning, gardening, and smoking; and through different routes of exposure (ingestion, inhalation, dermal absorption). The home, where people typically spend most of their time2 (Klepeis et al., 1995), provides opportunities for exposure to many chemicals, includ- ing naturally occurring chemicals in the diet as well as chemicals from food packaging, processing, or cooking; the release of volatile chemicals from carpets, furniture, clothing treatments, and cleaning products; home use of pesticides; use of cosmetics and personal care products; tobacco smoke; and infiltration of ambient air pollution. Typically, thousands of synthetic and naturally occurring chemicals are present in people’s homes and diet, most at relatively low concentrations. 2 Surveydata indicate that on average people spend 69 percent of their time in a residence and 87 percent of their time in enclosed buildings (Klepeis et al., 1995).
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184 BREAST CANCER AND THE ENVIRONMENT The 20th century saw a substantial increase in the synthesis of new chemicals. Tens of thousands of chemicals are used in commerce, and more than 3,000 industrial chemicals (excluding polymers), mostly organic com- pounds, are produced or imported into the United States at rates exceed- ing 1 million pounds per year (EPA, 1998b). These are known as high production volume chemicals. A 1998 EPA report found that insufficient testing had been done to evaluate the health effects of all but a few of these chemicals. Of 2,800 chemicals investigated, 93 percent lacked one or more of the six basic toxicity tests,3 and 43 percent of the chemicals had under- gone none of these tests, which are considered necessary for a minimum understanding of a chemical’s toxicity. The percentage of chemicals with complete or at least some toxicity information was considerably higher for chemicals with potential for greater exposure through industrial releases or for those in consumer or children’s products. In addition, not all of these 3,000 chemicals are of high priority for testing, because they belong to chemical classes or structural groups for which there is less concern regard- ing mutagenicity, carcinogencity, or endocrine effects. The High Production Volume Chemicals Program (HPV Program) is an international program to assess the potential hazard of chemicals produced in high volumes. Produc- tion levels of specific chemicals can change over time as demand for them increases or declines. Other chemicals of potential concern are by-products of industrial processes (e.g., dioxins), and the amounts produced cannot be measured as directly as those of deliberately produced chemicals. Opportunities for exposure may change in line with changes in production volumes, but they also may vary independently if industrial processes become more effective in reducing environmental release of a chemical during production. Among the substances reviewed in this report as potential risk factors for breast cancer, environmental releases from different sources have varied, and some have declined over recent years (e.g., dioxin, Figure 4-3 [EPA, 2006]; or perfluorooctanoic acid, Figure 4-4 [Paul et al., 2009]). Hazard Versus Risk In the assessment of the impact of environmental chemicals on humans, there is an important distinction between hazard and risk. A chemical may be identified as harmful or a hazard, but the risk it poses to people depends on both its toxic potency and the nature of the exposure, especially the amount to which people are exposed but also potentially the timing of the exposure. While thousands of chemicals are produced in or imported into 3 The tests evaluate acute toxicity, chronic toxicity, developmental and reproductive toxicity, mutagenicity, ecotoxicity, and environmental fate.
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185 CHALLENGES OF STUDYING ENVIRONMENTAL RISK FACTORS Grams 15,000 13,965 Other sources Bleached wood pulp and paper mills 12,000 Cement kilns Medical waste incineration Municipal waste combustion 9,000 6,000 3,442 3,000 1,422 0 1987 1995 2000 FIGURE 4-3 Sources and amounts (g/yr) of dioxin-like compounds released in the United States in 1987, 1995,4-3 2000. Figure and Dioxin releases.eps SOURCE: EPA (2006). the United States, not all of them pose risks to the general population. Some are used only in specific industrial processes, where potential exposure is limited to those in the workplace. Some chemicals have low potency, gen- erally causing health effects only at very high exposures. Thus, a chemical known to be a hazard on the basis of toxicologic studies, but with low potency and to which people are exposed at low concentrations, may pres- ent little risk of cancer or other adverse health effects. Route of Exposure In occupational settings, inhalation and dermal contact are frequently the primary routes of exposure (Eaton and Klaason, 1996), although inci- dental ingestion pathways can occur. In the home, opportunities exist for
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186 BREAST CANCER AND THE ENVIRONMENT Temporal trends (normalized percentage) FIGURE 4-4 Estimated releases of perfluorooctane sulfonyl fluoride (POSF) from Figure 4-4.eps 1970 to 2012 and exponential temporal trends in biota. POSF breaks down into bitmap, landscape perfluorooctanesulfonic acid (PFOS). Note: 2012 is when aqueous fire-fighting foams (AFFFs) are scheduled to be restricted and treated carpets end their natural life. The projection to zero is based on 3M’s production only, therefore some emis- sions will continue from remaining producers. Temporal trends in biota have been normalized to 100 percent for each species/dataset. Usage is depicted as follows: carpets (—), paper and packaging (- • -), apparel (- - -), performance chemicals (– • •), AFFFs (• • •). Biota trend lines are as follows: ringed seals from Arctic lo- cations, Qeqertarsuaq (purple) and Ittoqqortoormiit (yellow); Baltic guillemot eggs (pooled: light green; and mean: dark green); polar bears from western (light blue) and eastern Canadian Arctic (dark blue); herring gulls from Norway (orange); and lake trout from Lake Ontario (red). SOURCE: Paul et al. (2009, p. 390). Published in: Alexander G. Paul; Kevin C. Jones; Andrew J. Sweetman; Environ Sci Technol 2009, 43, 386–392. Copyright © 2008 American Chemical Society. exposure via ingestion, inhalation, and dermal contact. Pesticide exposures, for example, can occur through consumption of food (from agricultural applications), inhalation (directly from exposure to sprays and foggers or subsequently from volatilization of residues of past use or resuspension of contaminated dust), and dermal absorption (from contact with residues on the surfaces of tables, countertops, or household objects). Various assess- ments have found that concentrations of some volatile and semivolatile
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187 CHALLENGES OF STUDYING ENVIRONMENTAL RISK FACTORS chemicals are much higher in indoor spaces, such as homes and schools, than in outdoor areas around the home (Sax et al., 2006; Turpin et al., 2007; Ward et al., 2009; Rudel et al., 2010). Dermal exposure may be the predominant exposure pathway for chemicals in some cleaning or personal care products. Each chemical must be examined for how it is used as well as its vola- tility and ability to pass through the skin. Sometimes potential routes of exposure can be overlooked—for example, in taking showers, people may experience both dermal and inhalational exposure to some volatile organic compounds (VOCs) in the water supply. Typically, however, this exposure to VOCs is primarily via inhalation and may equal the exposure from drinking water (Jo et al., 1990). Measurement of Exposure In occupational studies, job titles and records from industrial hygiene measurements (individual air monitoring, or air sampling from work areas) are frequently used to estimate exposures. For population studies, research- ers may use location of residence or distance from a source of concern (transmission wires, freeways, factories); structured questionnaires relying on participants to report product use; measurements taken in air, water, soil, or other environmental media; and measurements in biological speci- mens (e.g., blood lead, urinary metabolites of pesticides, cotinine from the breakdown of nicotine to indicate tobacco smoke exposure). The utility of these chemical measurements in both environmental and biological samples depends on when the samples are taken relative to the disease in question; the half-life in the environment or human body, respectively; and the vari- ability in actual exposures over time. In the 1990s, researchers began to develop biomarkers as a means not only to improve estimation of exposure, but also to document intermediate steps along the pathway between expo- sure and effect. For example, markers of oxidative stress, DNA adducts, and epigenetic marks such as methyl groups can provide evidence that tis- sues have been affected. Such markers may suggest a mechanism by which an exposure may increase or decrease the risk of breast cancer; however, it can be difficult to demonstrate a direct relationship between the exposure and the marker, and between the marker and subsequent disease. Importance of Timing of Exposure Understanding the link between chemical exposure and disease is espe- cially challenging when studying chronic diseases that develop gradually over many years, such as cancer. Because the first steps in carcinogenesis may begin decades before the diagnosis of a cancer, relevant exposures
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228 BREAST CANCER AND THE ENVIRONMENT fish, worms), and high-throughput whole-genome analytical methods to evaluate mechanisms of toxicity. The ultimate end is to generate data with the new tools for use in the protection of human health and the environment. An important consideration in the development of tests that have adequate coverage will be the degree to which they cover the pathways involved in the general mechanisms underlying breast cancer—mutagenesis, estrogen receptor signaling, epigenetic programming, growth promotion via mitogenic cell signaling, microenvironmental change, and modulation of immune functioning. This will require attention in selection of cell types and environments relevant to breast cancer. SUMMARY Better understanding of the contribution of environmental factors to breast cancer entails understanding the multiple challenges in carrying out and interpreting studies in humans, animals, and in vitro systems. For stud- ies in humans, these include the issues inherent in estimating and assessing exposures, the study design and analytic challenges of environmental epi- demiology, and efforts to account for genetic differences in susceptibility to cancer and potential gene–environment interactions. Studies in animals and in vitro systems bring with them their own technical obstacles and challenges of interpretation and extrapolation to humans. An understand- ing of these challenges informs understanding of the existing data and their implications for next steps for action and research. REFERENCES Allred, D. C. 2010. Ductal carcinoma in situ: Terminology, classification, and natural history. J Natl Cancer Inst Monogr 41:134–138. Axelson, O., and L. Sundell. 1978. Mining, lung cancer and smoking. Scand J Work Environ Health 4(1):46–52. Bellocq, J. P., and G. Magro. 2003. Fibroepithelial tumours. In Pathlogy and genetics of tu- mours of the breast and female genital organs. Edited by F. A. Tavassoli and P. Devilee. Lyon, France: IARC Press. Benassi-Evans, B., and M. Fenech. 2011. Chronic alcohol exposure induces genome damage measured using the cytokinesis-block micronucleus cytome assay and aneuploidy in hu- man B lymphoblastoid cell lines. Mutagenesis 26(3):421–429. Benichou, J. 2001. A review of adjusted estimators of attributable risk. Stat Methods Med Res 10(3):195–216. Bennett, L. M., and B. J. Davis. 2002. Identification of mammary carcinogens in rodent bioas- says. Environ Mol Mutagen 39(2–3):150–157. Bernstein, J. L., B. Langholz, R. W. Haile, L. Bernstein, D. C. Thomas, M. Stovall, K. E. Malone, C. F. Lynch, et al. 2004. Study design: Evaluating gene–environment interactions in the etiology of breast cancer—the WECARE study. Breast Cancer Res 6(3):R199–R214.
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