Forwarded on by Milt Bowling:
Breast Cancer Fund has just released the new fourth edition of State of the Evidence 2006: What is the Connection Between Environment and Breast Cancer?
You can access the report online at
We hope this report will be useful to you in your work.
Health Science Consultant
State of the Evidence 2006 Executive Summary
Edited by Nancy Evans, Health Science Consultant,
Breast Cancer Fund
Published by Breast Cancer Fund and Breast Cancer Action
Breast cancer rates have been climbing steadily in the United States and other industrialized countries since the 1940s, amounting to more than one million cases per year worldwide.1 In the United States, a woman”šs lifetime risk of breast cancer has nearly tripled during the past four decades. In 2005, an estimated 211,240 U.S. women were diagnosed with invasive breast cancer and more than 58,000 women were expected to be diagnosed with one type of in situ breast cancer, meaning the tumor is confined to its original location in the breast. In 2005, breast cancer was expected to kill more than 40,000 American women2 and more than 410,000 women worldwide.3 The rate of new cases per year continues to inch upward in the United States even though billions of dollars have been spent on breast cancer research.
Less than one out of every 10 cases occurs in women born with a genetic predisposition for the disease, and as many as half of all breast cancers occur in women who have no known risk factors for the disease. Recent research has made it more and more clear that breast cancer arises from a complicated mix of multiple factors, which may include inherited or acquired genetic mutations, altered gene expression and/or exposures to external agents that affect genes or the production of estrogen or other hormones. More than one exposure or event is usually required before cancer will develop, but the same set of genetic and environmental circumstances will not produce cancer in every individual.
Two decades of research on laboratory animals, wildlife and cell behavior4 have shown the inadequacy of the long-held belief that ”žthe dose makes the poison.”° Scientists now know that the timing, duration and pattern of exposure are at least as important as the dose. Low-dose exposure to chemicals in the environmentËœparts per billion or even per trillionËœduring a critical window of an organism”šs development can cause permanent damage to organs and systems.
We are all exposed to radiation and to hundreds, if not thousands, of chemicals every day of our lives, yet we know very little about the likely synergistic effects of these multiple exposures.5 Testing one exposure at a time for its effects ignores this reality.
An estimated 100,000 synthetic chemicals are believed to be in use today in the United States. Another 1,000 or more are added each year.6 More than 90 percent have never been tested for their effects on human health.7 Many of these chemicals persist in the environment, accumulate in body fat and remain in breast tissue for decades. Studies by the U.S. Centers for Disease Control and Prevention (CDC) show that Americans of all ages carry a body burden of at least 148 chemicals that have been measured, some of them banned for more than two decades because of toxicity.8 These studies alone cannot establish cause but can reveal the internal contamination of our bodies by chemicals with known carcinogenic activity.
Patterns of breast cancer incidence indicate the importance of environmental exposures. Women who move from countries with low breast cancer rates to industrialized countries soon acquire the higher risk of their new country. The largest study ever conducted among twins found that environmental exposures unique to those with breast cancer made the most significant contribution to the development of the disease.
This State of the Evidence report demonstrates that a significant body of scientific evidence links exposure to radiation and synthetic chemicals to an increased risk of breast cancer. It summarizes the findings of more than 350 experimental, epidemiologic and ecological studies and describes some of the ongoing controversies in breast cancer research. The report recommends new directions for future research and includes a 10-point plan to act on the evidence and reduce human exposure to radiation and synthetic chemicals. This plan is based primarily on the precautionary principle, which in part states that indication of harm, not just proof of harm, is grounds for action.9
Evidence That Environmental Factors Cause Breast Cancer
Ionizing radiation is the longest-established environmental cause of human breast cancer. In 2005, the National Toxicology Program classified X-radiation and gamma radiation as known human carcinogens.10 Radiation is a mutagen as well as a carcinogen; the same is true of some chemicals. Radiation may even enhance the ability of hormones or other chemicals to cause cancer.11,12
Compelling scientific evidence points to some of the 100,000 synthetic chemicals13 in use today as contributing to the development of breast cancer, either by altering hormone function or gene expression.
ï£¿ There is broad agreement that exposure over time to natural estrogens in the body increases the risk of breast cancer. Hormone replacement therapy (HRT)14 and hormones in oral contraceptives15,16,17,18,19 and some other pharmaceuticals also increase this risk. The National Toxicology Program now lists steroidal estrogens (the natural chemical form of estrogen) as known human carcinogens.20 The International Agency for Research on Cancer (IARC) has listed both steroidal and nonsteroidal estrogens as known human carcinogens since 1987.
ï£¿ Synthetic agents that mimic the actions of estrogens are known as xenoestrogens and are one type of endocrine-(hormone-) disrupting compound. They are present in many pesticides, fuels, plastics, detergents and prescription drugs.21 Chronic exposure to widespread and persistent xenoestrogens may help explain the increase in breast cancer in industrialized countries around the world. Xenoestrogens known to increase the risk of breast cancer include:
Ë† Bisphenol-A (BPA), one of the most pervasive chemicals in modern life, used to make polycarbonate plastic;
Ë† Diethylstilbestrol (DES), prescribed for three decades to millions of women to prevent miscarriage, the drug was banned in 1971 because it caused cancer in their daughters;
Ë† Polyvinyl chloride (PVC), used extensively in plastics including food packaging, medical products, appliances, cars, toys, credit cards and rainwear;
Ë† Dieldrin, a pesticide banned from all uses in 1987; and
Ë† Ingredients in many household products, especially cleaning agents, solvents and pesticides.
ï£¿ Elevated rates of breast cancer have been found among workers exposed to a variety of solvents in the electronics, fabricated metal, lumber, furniture, printing, chemical, textile and clothing industries.
ï£¿ Aromatic amines are a class of chemicals found in the plastic and chemical industries, in air and water pollution, diesel exhaust, tobacco smoke and in grilled meats and fish.22 One type of aromatic amine, o-toluidine, is known to cause mammary tumors in rodents.23,24
ï£¿ The Environmental Protection Agency determined that 1,3-butadiene is carcinogenic to humans by inhalation and the National Toxicology Program classifies 1,3-butadiene as a known human carcinogen.25 1,3-butadiene is an air pollutant created by internal combustion engines and petroleum refineries. It is also used in some manufacturing processes and is found in tobacco smoke.
Evidence Indicating Probable Environmental Links To Breast Cancer
ï£¿ Various studies have shown that polycyclic aromatic hydrocarbons (PAHs) appear to play a role in the development of breast cancer. PAHs are compounds found in soot and fumes from combustion of diesel and other fuels, and from grilling meat.
ï£¿ Two types of chemicals known to disrupt hormone function are the organochlorine pesticide DDT and PCBs (polychlorinated biphenyls), which were used to manufacture electrical equipment and numerous other industrial and consumer products. Both DDT and PCBs have been banned in the United States for three decades, yet both are still found in the body fat of humans and animals, as well as in human breast milk.26,27
ï£¿ Of all toxic chemicals, dioxin may be the most ubiquitousËœand the most toxic. Dioxin is formed by the incineration or combustion of products containing chlorinated compounds, including PVC (polyvinyl chloride) and PCBs. The body fat of every human being, including every newborn, contains dioxin.
ï£¿ Ethylene oxide is a known human carcinogen; the National Toxicology Program identifies it as a mammary carcinogen in animals. Ethylene oxide is a fumigant used to sterilize surgical instruments and is also used in some cosmetics products.28
Evidence Indicating Possible Environmental Links To Breast Cancer
ï£¿ The insecticide heptachlor was used widely in the United States throughout the 1980s, especially for termite control. It still contaminates both soil and humans. Heptachlor”šs breakdown product (heptachlor epoxide) is known to accumulate in body fat, including breast tissue. It affects the way the liver processes estrogen, thus allowing levels of circulating estrogens to rise. Heptachlor epoxide may also increase breast cancer risk by disrupting cell growth regulation.29
ï£¿ Triazine herbicides are the most heavily used agricultural chemicals in the United States. Triazines include atrazine, simazine and cyanazine. All three have been shown to cause mammary cancer in animals.
ï£¿ Growing concern about exposure to ultraviolet (UV) radiation from the sun and the risk of skin cancer has led to widespread use of sunscreens. Research has found that some sunscreens contain chemicals (also used in other cosmetics) that are not only estrogenic but also lipophilic (fat-seeking).
ï£¿ Phthalates are a group of endocrine-disrupting compounds commonly used to render plastics soft and flexible. They are found in soft plastic ”žchew toys”° marketed for infants and also in some varieties of nail polish, perfumes, skin moisturizers, flavorings and solvents. Disruption of hormonal processes can increase breast cancer risk.
ï£¿ Modern food production methods have created avenues for exposure to environmental carcinogens and endocrine-disrupting compounds in food and food additives. These exposures include pesticides sprayed on crops, antibiotics used on poultry and hormones injected into cattle, sheep and hogs. Consumption of animal products may present inherent risks because pesticides and other environmental toxicants can accumulate in fatty tissue of animals, just as they do in humans. Two examples of agricultural practices that may increase breast cancer risk include:
Ë† Monsanto”šs genetically engineered hormone product, recombinant bovine growth hormone (rBGH), which increases milk production in dairy cows and which was subsequently renamed recombinant bovine somatotrophin (rBST).
Ë† Zeranol (Ralgro), a nonsteroidal growth promoter with estrogenic activity and one of the most widely-used hormones in U.S. beef cattle.
ï£¿ A growing body of evidence implicates nonionizing radiation (electromagnetic fields and radio-frequency radiation [EMF]) as possible contributors to the development of breast cancer. The International Agency for Research on Cancer (IARC) has classified EMF as a possible human carcinogen. Microwaves, radio waves, radar and lights are examples of nonionizing radiation. Everyone in the industrialized world is exposed to electromagnetic fields every day.
New Research Included In This 2006 Edition
ï£¿ A major study by Tufts University scientists demonstrated the critical importance of early life exposure to chemicals and the profound effects that can occur from very low doses. The scientists found that exposing pregnant mice to extremely low levels of bisphenol-A altered the development of the mammary gland in their offspring at puberty.30
ï£¿ Re-analysis of a large study of Nordic twins published in 200031 concluded that ”žgenetic susceptibility makes only a small to moderate contribution”° to the incidence of breast cancer.32
ï£¿ The U.S. Centers for Disease Control and Prevention Third National Report on Human Exposure to Environmental Chemicals revealed that the bodies of Americans of all ages contain 148 synthetic chemicals, some of which are known or suspected carcinogens.33 Many of these chemicals were also found in the umbilical cord blood of newborn babies.34
ï£¿ Two new articles that reviewed evidence linking breast cancer with environmental factors found that environmental exposures, in combination with genetic predisposition, age at exposure and hormonal factors, have a cumulative impact on breast cancer risk.35,36
ï£¿ A new report from the National Research Council confirms there is no safe dose of ionizing radiationËœeven the smallest dose has the potential to cause an increased cancer risk in humans.37
ï£¿ A number of new studies implicate exposure to ionizing radiation, particularly before age 20 or during pregnancy, as increasing breast cancer risk.38,39,40,41,42,43 Additional studies implicate radiotherapy for breast cancer in increasing the risk of additional breast and other cancers.44,45
ï£¿ Research on the structure of genes shows that exposure to ionizing radiation can induce genomic instability and other neoplastic heritable changes, not only in directly-irradiated cells but also in cells not directly exposed to radiation.46,47,48,49
ï£¿ An interdisciplinary analysis of the history of hormone replacement therapy (HRT) revealed that scientists were aware of the cancer risk of HRT in the 1930s. The team of experts asked the question: Why, for four decades, since the mid-1960s, were millions of women prescribed powerful pharmacological agents already demonstrated, three decades earlier, to be carcinogenic? In answering this question, the experts identified five missing elements in the process: the invisible industrialist, regulatory agencies and public interest compared with private interests, beliefs regarding individual risk compared with collective risk, the growth of individualized ”žpreventive medicine”° and the gendering of hormones and regulation of women”šs sexuality. They stated that understanding HRT use in the 20th century demands engaging ”žwith core issues of accountability, complexity, fear of mortality and the conduct of socially responsible science.”°50
ï£¿ Progestin was linked to increased risk of breast cancer recurrence in two large trials: the Hormone Replacement Therapy After Breast CancerËœIs It Safe? (HABITS)51 and the Stockholm trial.52
ï£¿ Polychlorinated biphenyls (PCBs) were associated with increased breast cancer risk in a study from Belgium.53
ï£¿ Researchers found an increased breast cancer risk among Long Island, NY, women residing within one mile of hazardous waste sites containing organochlorine pesticides.54 A separate study measured levels of organochlorine pesticides and PCBs in the adipose tissue of 224 Long Island women with non-metastatic breast cancer and found that those with the highest level of PCBs had an increased risk of recurrence.55
ï£¿ Pesticide use and breast cancer risk among farmers”š wives was examined in a large prospective cohort study in Iowa and North Carolina. Researchers found an increased risk of breast cancer among the wives of farmers using certain chlorinated pesticides and among those living closest to areas of pesticide application.56
ï£¿ An ecological study in 82 Mississippi counties showed a significant association between breast cancer incidence and maximum emissions of environmental chemicals.57
ï£¿ Longer residence on Cape Cod, Mass., is associated with elevated breast cancer risk.58 Suspected environmental exposures include pesticides and drinking water contaminated by industrial, agricultural and residential land use.
ï£¿ Researchers in Spain studied the combined effects of environmental estrogens, measured as the total effective xenoestrogen (estrogenmimicking) burden, and found increased risk among postmenopausal women with the highest levels. The pesticides aldrin and lindane were also individually associated with elevated risk.59
ï£¿ Clustering patterns of breast cancer cases among premenopausal women in western New York state were found to be more related to residence at birth and menarche than residence in any time period of adult life.60
ï£¿ Prenatal and early life exposure to genistein (a phytoestrogenËœfound in plants) and a mixture of organochlorine chemicals induced marked changes in mammary glands of adult female rats, indicating that phytoestrogens influence the toxicologic effects of mixtures.61
ï£¿ Early life exposure to high levels of polycyclic aromatic hydrocarbons (PAHs), present in tobacco smoke and other air pollution, increased the risk of premenopausal breast cancer in a case-control study of more than 3,200 women.62
ï£¿ A study of 21,000 Japanese women concluded that smoking, both active and passive, increases the risk of developing breast cancer in premenopausal women.63
ï£¿ Methyl mercury can significantly alter growth-related signaling in human breast cancer cells and, therefore, should be considered a potential endocrine-disrupting compound.64
ï£¿ Phthalates, which are ingredients ubiquitous in cosmetics and personal care products, were shown to significantly increase cell proliferation in human breast cancer cells. Scientists also found that certain phthalates inhibited the cell-killing capacity of tamoxifen (a drug with antiestrogen activity) in MCF-7 breast cancer cells.65
ï£¿ German scientists reported that Eusolex 6300, a sunscreen, showed estrogenic effects similar to 17-beta-estradiol (the most common form of natural estrogen) on mammalian and amphibian cells.66
ï£¿ Studies showed that zeranol, the nonsteroidal growth promoter used in beef cattle, and 17-beta-estradiol have a similar potential to induce neoplastic changes in human breast epithelial cells.67
ï£¿ Three new studies link insulin-like growth factors with increased breast cancer risk. This suggests that rBST, the genetically engineered hormone product found in many dairy products, which stimulates production of IGF-1, may be associated with increased risk of breast cancer.68,69,70
ï£¿ Three pesticidesËœchlordane, malathion and 2,4-DËœwere associated with increased risk of breast cancer in Latina agricultural workers in California.71
ï£¿ A study of female autoworkers linked exposure to metalworking fluids with increased risk of breast cancer, particularly when the exposure occurred within 10 years of diagnosis.72
ï£¿ Occupational exposure to extremely low-frequency electromagnetic fields was shown to increase breast cancer risk among postmenopausal women, especially when exposure occurred before age 35.73
ï£¿ A cluster of male breast cancers was reported among a small group of men occupationally exposed to high electromagnetic fields.74
ï£¿ An Italian study found that truck driving was the most frequent occupation of male breast cancer patients with BRCA1/BRCA2 mutations, possibly implicating exposure to PAHs.75 A review of the epidemiologic literature on male breast cancer also identifies exposure to EMFs and PAHs as risk factors.76
Advance The Research Agenda
To reduce the burden of breast cancer in our society, public officials and the scientific and corporate communities must act based on what is already known about agents that increase the risk of this disease. At the same time, major gaps exist in our current knowledge and we need more studies asking tough questions about the underlying causes of breast cancer. While we need further research on screening, diagnosis and treatment, decades of paying little attention to true prevention of breast cancer have resulted in needless sickness and death. Research efforts should seek information that will compel public policies aimed to prevent breast cancer. The types of research most likely to support such policies are those examining:
ï£¿ The interplay between timing of exposures, multiple exposures, low-dose exposures, chronic exposures (including occupational exposures) and cumulative exposures;
ï£¿ Exposures of women at home and in the paid workplace;
ï£¿ Disparities in health outcomes and environmental exposures; and
ï£¿ Development of less invasive, more effective breast cancer screening methods.
Implement Policy Changes
While research proceeds, fundamental changes are needed in both the public and private sectors regarding exposure to radiation and the production, use and disposal of chemicals found to increase the risk of breast cancer or suspected of doing so. Considerable resources continue to be spent to encourage women to make changes in their personal lives that might reduce their risk of breast cancer. But many factors that contribute to the disease lie far beyond an individual”šs personal control and can only be addressed by government policy and private sector changes. Breast cancer is not just a personal tragedy; it is a public health crisis that requires political will to change the status quo.
This crisis must be addressed by adopting the precautionary principle as a public policy. Under this principle, indication of harm, rather than definitive proof of harm, triggers policy actions. In addition, the precautionary principle obligates producers of chemicals and radiological products to assess the health, safety and environmental impacts of their products before introducing or releasing them. It also requires industry to make the results of their assessments publicly available. Industry is further obliged to examine a full range of alternatives to toxic ingredients and to select the alternative with the least potential impact on human health and the environment, including the possibility of not introducing a questionable product at all. The precautionary principle rests on the democratic principle that government officials are obligated to serve the public interest by protecting human health and the environment. Decision-making under the precautionary principle must be transparent, participatory and informed by the best available data.
We ignore at our peril evidence that radiation and chemicals are contributing to the growing human and economic cost of breast cancer. Halting the scourge of this disease requires that we take action based on existing evidence to protect the health of people and the planet. Waiting for absolute proof brings more needless suffering and loss of lives. It is in our power to change the course we are on. It is time to act on the evidence.
A 10-Point Plan For Reducing The Risk Of Breast Cancer And Ultimately Ending The Epidemic:
1. Establish environmental health tracking (EHT) programs at state and federal levels.
2. Practice ”žhealthy purchasing”° by adopting precautionary purchasing laws at the local, state and federal levels.
3. Protect workers from hazardous exposures.
4. Educate the public about the health effects of radiation and how to reduce exposure to both ionizing and non-ionizing radiation.
5. Hold corporations accountable for hazardous practices.
6. Offer local, state and federal incentives for clean, green practices.
7. Strengthen right-to-know legislation and public participation in decisions about toxic exposures.
8. Enforce existing environmental protection laws.
9. Require greater transparency in funding of scientific and medical training, research and publications.
10. Create a comprehensive chemicals policy based on the precautionary principle.
1 Parkin DM, Bray F, Ferlay J, Pisani P (2005). Global cancer statistics, 2002. CA: A Cancer Journal for Clinicians 55:74-108.
2 American Cancer Society (2005). Cancer Facts and Figures 2005.
3 Parkin DM, Bray F, Ferlay J, Pisani P (2005). Global cancer statistics, 2002. CA: A Cancer Journal for Clinicians 55:74-108.
4 Calabrese EJ, Baldwin LA (2003). Toxicology rethinks its central belief: Hormesis demands a reappraisal of the way risks are assessed. Nature 421:691-692.
5 Carpenter DO, Arcaro K Bush B, Niemi WD, Pang S, Vakharia DD (1998). Human health and chemical mixtures: An overview. Environmental Health Perspectives 106(S6):1263-1270.
6 National Cancer Institute (2003). Cancer and the Environment: What you need to know, what you can do. National Institutes of Health.
7 Bennett M, Davis BJ (2002). The identification of mammary carcinogens in rodent bioassays. Environmental and Molecular Mutagenesis. 39(2-3): 150-157.
8 CDC (2005). Third National Report on Human Exposure to Environmental Chemicals. Atlanta: Centers for Disease Control and Prevention.
9 Horton R (1998). The new public health of risk and radical engagement. Lancet 352:251-252.
10 National Toxicology Program (2005). Eleventh Report on Carcinogens. National Institute of Environmental Health Sciences. National Institutes of Health.
11 Calaf GM, Hei TK (2000). Establishment of a radiation and estrogen-induced breast cancer model. Carcinogenesis 21:769-776.
12 Segaloff A, Maxfield WS (1971). The synergism between radiation and estrogen in the production of mammary cancer in the rat. Cancer Research 31:166-168.
13 National Cancer Institute (2003). Cancer and the Environment: What you need to know, what you can do. National Institutes of Health.
14 Krieger N, LÃ¶wy I, Aronowitz, Bigby J, Dickersin K, Garner E, et al (2005). Hormone replacement therapy, cancer, controversies, and women”šs health: historical, epidemiological, biological, clinical, and advocacy perspectives. Journal of Epidemiology and Community Health 59:740-748.
15 Kumle M, Weiderpass E, Braaten T, Persson I, Adami HO, Lund E (2002). Use of oral contraceptives and breast cancer risk: The Norwegian-Swedish Women”šs Lifestyle and Health Cohort Study. Cancer Epidemiology, Biomarkers and Prevention 11:1375-1381.
16 Althuis MD, Brogan DD, Coates RJ, Daling JR, Gammon MD, Malone KE, Schoenberg JB, Brinton LA (2003). Breast cancers among very young premenopausal women (United States). Cancer Causes and Control 14:151-160.
17 Deligeroroglou E, Michailidis E, Creatsas G (2003). Oral contraceptives and reproductive system cancer. Annals of the New York Academy of Science 997:199-208.
18 Newcomer LM, Newcomb PA, Trentham-Dietz A, Longnecker MP, Greenberg ER (2003). Oral contraceptive use and risk of breast cancer by histologic type. International Journal of Cancer 106:961-964.
19 Grabrick DM, Hartmann LC, Cerhan RJ, et al (2000). Risk of breast cancer with oral contraceptive use in women with a family history of breast cancer. Journal of the American Medical Association 284:1791-1798.
20 National Toxicology Program (2005). Eleventh Report on Carcinogens. National Institute of Environmental Health Sciences. National Institutes of Health.
21 National Academy Press (1999). Hormonally active agents in the environment. ISBN-0309-06419-8.
22 DeBruin LS, Josephy PD (2002). Perspectives on the chemical etiology of breast cancer. Environmental Health Perspectives 110:S1:119-128.
23 National Toxicology Program (2003). Chemicals associated with site-specific tumor induction in mammary gland.
24 Layton DW, Bogen KT, Knize MG, Hatch FT, Johnson VM, Felton JS (1995). Cancer risk of heterocyclic amines in cooked foods: An analysis and implications for research. Carcinogenesis 16:39-52.
25 National Toxicology Program (2005). Eleventh Report on Carcinogens. National Institute of Environmental Health Sciences. National Institutes of Health.
26 Zheng T, Holford T, Mayne S, Ward B, Carter D, Owens P, Dubrow R, Zahm S, Boyle P, Archibeque S, Tessari J (1999). DDE and DDT in breast adipose tissue and risk of female breast cancer. American Journal of Epidemiology 150:453-458.
27 Rogan WJ (1996). Pollutants in breast milk. Archives of Pediatric and Adolescent Medicine 150:81-90.
28 Agency for Toxic Substances and Disease Registry (ATSDR) 1990. Toxicological Profile for Ethylene Oxide. U.S. Public Health Service, U.S. Department of Health and Human Services, Atlanta, GA. 1990.
29 Dich J, Zahm SH, Hanberg A, Adami HO (1997). Pesticides (heptachlor) and cancer. Cancer Causes and Control 8, 420-443.
30 Munoz de Toro M, Markey C, Perinaaz R W, Luque EH, Rubin BS, Sonnenschein C, Soto A (2005). Perinatal exposure to bisphenol A alters peripubertal mammary gland development in mice. Endocrinology online doi:10.1210/en.2005-0340.
31 Lichtenstein P, Niels V, Pia K (2000). Environmental and heritable factors in the causation of cancer-Analyses of cohorts of twins from Sweden, Denmark and Finland. New England Journal of Medicine 343(2):78-85.
32 Baker SG, Lichtenstein P, Kaprio J, Holm N (2005). Genetic susceptibility to prostate, breast, and colorectal cancer among Nordic twins. Biometrics 61: 55-63.
33 CDC (2005). Third National Report on Human Exposure to Environmental Chemicals. Atlanta: Centers for Disease Control and Prevention.
34 Environmental Working Group (2005). Body Burden: The Pollution in Newborns.
35 Coyle YM (2004). The effect of environment on breast cancer risk. Breast Cancer Research and Treatment 84:273-288.
36 Mitra AK, Faruque FS, Avis AL (2004). Breast cancer and environmental risks: Where is the link? Journal of Environmental Health 66:24-32.
37 National Research Council (2005). Biologic effects of ionizing radiation VII: Health risks from exposure to low levels of ionizing radiation. National Academy of Science, Washington DC.
38 Ronckers CM, Erdmann CA, Land CE (2005). Radiation and breast cancer: A review of current evidence. Breast Cancer Research 7:21-32.
39 Guibout C, Adjadj E, Rubino C, Shamsaldin A, Grimaud E, Hawkins M, Mathieu MC, Oberlin O, Zucker JM, Panis X, Lagrange JL, Daly-Schveitzer N, Chavaudra J, deVathaire F (2005). Malignant breast tumors after radiotherapy for a first cancer during childhood. Journal of Clinical Oncology 23:197-204.
40 Wahner-Roedler DL, Petersen IA (2004). Risk of breast cancer and breast cancer characteristics in women after treatment for Hodgkin lymphoma. Drugs Today 40:865-79.
41 Horwich A, Swerdlow AJ (2004). Secondary primary breast cancer after Hodgkin”šs disease. British Journal of Cancer 90:294-298.
42 Kenny LB, Yasui Y, Inskip PD, Hammond S, Neglia JP, Mertens AC, Meadows AT, Friedman D, Robison LL, Diller L (2004). Breast cancer after childhood cancer: A report from the Childhood Cancer Survivor Study. Annals of Internal Medicine 141:590-597.
43 Patlas M, McCready D, Kullkarni S, Dill-Macky MJ (2004). Synchronous development of breast cancer and chest wall fibrosarcoma after previous mantle radiation for Hodgkin”šs disease. European Radiology E-Pub: DOI:10.1007/s00330-004-2437-7 Online First.
44 Roychoudhuri R, Evans H, Robinson D, Moller H (2004). Radiation-induced malignancies following radiotherapy for breast cancer. British Journal of Cancer 91:868-872.
45 West JG, Qureshi A, West JE, Chacon M, Sutherland ML, Haghighi B, Harrison J (2005). Risk of angiosarcoma following breast conservation: A clinical alert. The Breast Journal 11:115-123.
46 Little JB (2003). Genomic instability and radiation. Journal of Radiological Protection 23:173-181.
47 Goldberg Z, Lehnert BE (2003). Radiation-induced effects in unirradiated cells: A review and implications in cancer. International Journal of Oncology 21:337-349.
48 Morgan WF (2003). Non-targeted and delayed effects of exposure to ionizing radiation: II. Radiation-induced genomic instability and bystander effects in vivo, clastogenic factors and transgenerational effects. Radiation Research 159:581-596.
49 Wright EG (2004). Radiation-induced genomic instability: Manifestations and mechanisms. International Journal of Low Radiation 1:231-241.
50 Krieger N, LÃ¶wy I, Aronowitz, Bigby J, Dickersin K, Garner E, et al (2005). Hormone replacement therapy, cancer, controversies, and women”šs health: historical, epidemiological, biological, clinical, and advocacy perspectives. Journal of Epidemiology and Community Health 59:740-748.
51 Holmberg L, Anderson H (2004) HABITS (hormonal replacement therapy after breast cancer-is it safe?), a randomized comparison stopped. Lancet 363:453-455.
52 Von Schoultz E, Rutqvist LE (2005). Menopausal hormone therapy after breast cancer: The Stockholm Randomized Trial. Journal of the National Cancer Institute 97:533-555.
53 Charlier CJ, Albert AI, Zhang L, Dubois NG, Plomteux GJ (2004). Polychlorinated biphenyls contamination in women with breast cancer. Clinica Chimica Acta 347:177-181.
54 O”šLeary ES, Vena JE, Freudenheim JL, Brasure J (2004). Pesticide exposure and risk of breast cancer: A nested case-control study of residentially stable women living on Long Island. Environmental Research 94:134-144.
55 Muscat JE, Britton JA, Djordjevic MV, Citron ML, Kemeny M, Busch-Devereau E, Pittman B, Stellman SD (2003). Adipose concentrations of organochlorine compounds and breast cancer recurrence in Long Island, New York. Cancer Epidemiology, Biomarkers & Prevention 12:1474-1478.
56 Engel LS, Hill DA, Hoppin JA, Lubin JH, Lynch CF, Pierce J, Samanic C, Sandler DP, Blair A, Alavanja MC (2005). Pesticide use and breast cancer risk among farmers”š wives in the Agricultural Health Study. American Journal of Epidemiology 161:121-135.
57 Mitra AK, Faruque FS (2004). Breast cancer incidence and exposure to environmental chemicals in 82 counties in Mississippi. Southern Medical Journal 97:259-263.
58 McKelvy W, Brody JG, Aschengrau A, Swartz CH (2004). Association between residence on Cape Cod, Massachusetts, and breast cancer. Annals of Epidemiology 14:89-94.
59 Ibarluzea Jm J, Fernandez MF, Santa-Marina L, Olea-Serrano MF, Rivas AM, Aurrekoetxea JJ, Exposito J, Lorenzo M, Torne P, Villalobos M, Pedraza V, Sasco AJ, Olea N (2004). Breast cancer risk and the combined effect of environmental estrogens. Cancer Causes and Control 16:591-600.
60 Han D, Rogerson PA, Nie J, Bonner MR, Vena JE, Vito D, Muti P, Trevisan M, Edge SB, Freudenheim JL (2004). Geographic clustering of residence in early life and subsequent risk of breast cancer (United States). Cancer Causes and Control 15:921-929.
61 Foster WG, Younglai EV, Boutross-Tadross O, Hughes CL, Wade MG (2004). Mammary gland morphology in Sprague-Dawley rats following treatment with an organochlorine mixture in utero and neonatal genestein. Toxicological Science 77:91-100.
62 Bonner MR, Han D, Nie J, Rogerson P, Vena JE, Muti P, Trevisan M, Edge SB, Freudenheim JL (2005). Breast cancer risk and exposure in early life to polycyclic aromatic hydrocarbons using total suspended particulates as a proxy measure. Cancer Epidemiology, Biomarkers & Prevention 14:53-60.
63 Hanaoka T, Yamamoto S, Sobue T, Sasaki S, Tsugane S (2005) Japan Public Health Center-Based Prospective Study on Cancer and Cardiovascular Disease Study Group. Active and passive smoking and breast cancer risk in middle-aged Japanese women. International Journal of Cancer 114:317-322.
64 Sukocheva OA, Yang Y, Gierthy JF, Seegal RF (2005). Methyl mercury influences growth-related signaling in MCF-7 breast cancer cells. Environmental Toxicology 20:32-44.
65 Kim IY, Han SY, Moon A (2004). Phthalates inhibit tamoxifen-induced apoptosis in MCF-7 human breast cancer cells. Journal of Toxicology and Environmental Health 67:2025-2035.
66 Klann A Levy G, Lutz I, Muller C, Kloas W, Hildebrandt JP (2005). Estrogen-like effects of ultraviolet screen 3-(4methylbenzylidene)-camphor (Eusolex 6300) on cell proliferation and gene induction in mammalian and amphibian cells. Environmental Research 97:274-281.
67 Liu S, Lin YC (2004). Transformation of MCF-10A human breast epithelial cells by zeranol and estradiol-17beta. The Breast Journal 10:514-521.
68 Allen NE, Roddam AW, Allen DS, Fentiman IS, Dos Santos Silva I, Peto J, Holly JM, Key TJ (2005). A prospective study of serum insulin-like growth factor-I (IGF-1), IIBF-II, IBG-binding protein-3 and breast cancer risk. British Journal of Cancer 92:1283-1287.
69 Schernhammer ES, Holly JM, Pollak MN, Hankinson SE (2005). Circulating levels of insulin-like growth factors, their binding proteins, and breast cancer risk. Cancer Epidemiology, Biomarkers and Prevention 14:699-704.
70 Jernstrom H, Sandberg T, Bageman E, Borg A, Olsson H (2005). Insulin-like growth factor-I (IGF-1) genotype predicts breast volume after pregnancy and hormonal contraception and is associated with circulating IGF-1 levels: implications for risk of early-onset breast cancer in young women from hereditary breast cancer families. British Journal of Cancer 92:857-866.
71 Mills PK, Yang R (2005). Breast cancer risk in Hispanic agricultural workers in California. International Journal of Occupational and Environmental Health 11:123-131.
72 Thompson D, Kriebel D, Quinn MM, Wegman DH, Eisen EA (2005). Occupational exposure to metalworking fluids and risk of breast cancer among female autoworkers. American Journal of Industrial Medicine 47:153-160.
73 Labreche F, Goldberg MS, Valois M, Nadon L, Richardson L, Lakhani R, Latreille B (2003). Occupational exposures to extremely low frequency magnetic fields and postmenopausal breast cancer. American Journal of Industrial Medicine 44:643-652.
74 Milham S (2004). A cluster of male breast cancer in office workers. American Journal of Industrial Medicine 46:86-87.
75 Palli D, Masala G, Mariani-Constantini R, Zanna I, Saieva C, Sera F, Decarli A, Ottini L (2004). A gene-environment interaction between occupation and BRCA1/BRCA2 mutations in male breast cancer? European Journal of Cancer 40:2474-2479.
76 Weiss JR, Moysich KB, Swede H (2005). Epidemiology of male breast cancer. Cancer Epidemiology, Biomarkers and Prevention 14:20-26.
BREAST CANCER FUND
1388 Sutter St., Suite 400
San Francisco, CA 94109
BREAST CANCER ACTION
55 New Montgomery St., Suite 323
San Francisco, CA 94105
Breast Cancer Fund
1388 Sutter Street, Suite 400
San Francisco, CA 94109-5400
Clean Energy Foundation
Phone: 1 888 436 2152
or 604 436 2152 in Vancouver
Fax: 604 436 2154