Environmental Health Perspectives 105, Supplement 3, March 1997
Sandra Steingraber
Women's Community Cancer Project, Cambridge, Massachusetts
Cancer activists who participate with cancer researchers in shapingpublic health policy provide a different perspective on the question ofbreast cancer etiology. We place a higher priority on reducing women'sexposure to suspected breast carcinogens than in debating the specificbiochemical mechanisms by which these agents may operate. As the fruitsof AIDS activism and antismoking campaigns illustrate, answers to mechanisticquestions have not been and should not be the driving force behind publichealth policy. As such, cancer activists embrace a form of conservatismthat advocates prudence in the face of exposure to estrogenic and otherendocrine-disrupting chemicals. This perspective stands in contrast toscientific conservatism, which directs its caution toward the issue ofproof. Unmet needs for cancer activists refer not so much to data gapsas to the failure to eliminate ongoing cancer hazards. For this authorand activist, unmet needs include ending women's continued exposure tosuch common estrogenic compounds as detergents, triazine herbicides, plastics,and polychlorinated biphenyls. -- Environ Health Perspect 105(Suppl3):685-687 (1997)
Key words: breast cancer etiology, cancer activism, public policy, breastcancer, breast carcinogens, endocrine disrupters, environmental estrogens,National Action Plan on Breast Cancer
This paper was presented in part at the Workshop on Hormones,Hormone Metabolism, Environment, and Breast Cancer held 28-29 September1995 in New Orleans, Louisiana. Manuscript received at EHP 6 June 1996;manuscript accepted 10 September 1996.
This work was supported by a fellowship in women's healthpolicy from the Center for Research on Women and Gender at the Universityof Illinois, Chicago, IL.
For information on PVC-free hospitals, contact MichaelLerner, Director, Commonweal, P.O. Box 316, Bolinas, CA 94924 or RobertMusil, Director, Physicians for Social Responsibility, 1101 14th StreetNW, Suite 700, Washington, DC 20005.
Address correspondence to Dr. S. Steingraber, Women'sCommunity Cancer Project, 46 Pleasant Street, Cambridge, MA 02139. Telephone:(617) 354-9888. Fax: (617) 666-4725.
Abbreviations used: APEOs, alkylphenol polyethoxylates;NAPBC, National Action Plan on Breast Cancer; PCBs, polychlorinated biphenyls;PVC, polyvinyl chloride.
When we in the cancer activist community look at breast cancer research,we are interested not only in results, sample size, elegance of experimentaldesign, or validity of the conclusions based on the data. We are also interestedin--and are most interested in--saving women's lives. Therefore, we areinterested in understanding how particular lines of scientific inquiryare chosen for funding and intellectual pursuit, and we are interestedin influencing those choices. We are interested in how public health policyis made in the face of scientific uncertainty. We are interested in researchthat identifies breast carcinogens, and we are interested in social changesthat could keep those agents out of women's breasts in the first place.In short, when researchers and activists meet (for example, as membersof the National Action Plan on Breast Cancer [NAPBC]), activists bringto the table a particular perspective on the role of science, the directionit travels, and its methodologies.
Consider the issue of unmet needs, which members of the NAPBC's etiologyworking group are requested to address. To a scientist, an unmet need mayrepresent a data gap within his or her area of expertise. To an activist,an unmet need may refer to life without a breast cancer diagnosis. In thecontext of estrogenic chemicals and their relationship to breast cancer,I have my own personal list of unmet needs.
Learning how to clean clothes without the use of estrogenic detergentsis an unmet need. Household detergents, as well as paints and pesticides,contain estrogenic alkylphenol polyethoxylates (APEOs). Since their introductionas chemical surfactants in the 1940s, APEOs have become widely disseminatedin rivers, lakes, and streams, and therefore in drinking water. In 1994,researchers in England discovered that APEOs, in trace amounts, can stimulatethe growth of breast cancer cells (1).
Finding ways to keep weeds out of corn fields without the use of triazineherbicides is an unmet need. Classified as a possible human carcinogen,the chloroplast-destroying triazines have been used since the 1950s. Theyhave been detected in raindrops in 23 states in the upper Midwest and northeastUnited States, including pristine areas such as Isle Royale National Parkin northern Minnesota, and they gain entry into our bodies as contaminantsof drinking water and as residues on food. At least one of the triazines,atrazine, is a known endocrine disrupter and is restricted for use in Germany,the Netherlands, and several Nordic countries. However, in the United States,atrazine is used on about 73% of all corn fields. Atrazine causes mammarygland cancer in at least one strain of laboratory rat (2). It also causeschromosomal breakage in the tissues of hamster ovaries at concentrationsbelow its maximum legal limit in drinking water (3). Case-control studiesin northern Italy show a connection between exposure to triazine herbicidesand ovarian cancer among women farmers (4,5). Triazine weed killers inthe Corn Belt states where I grew up can reach breathtaking levels in riversand streams, and in the finished drinking water drawn from these sources,during the spring months of planting and rain (6).
Discovering substitutes for polyvinyl chloride (PVC) plastic is an unmetneed. Vinyl chloride, the industrial feedstock of PVC, is considered aknown human carcinogen because of its link to a rare form of liver cancer(7). A 1977 study showed that women who breathe vinyl chloride vapors onthe job showed a 36% excess in breast cancer mortality (8). Inhalationof vinyl chloride as well as ingestion of PVC dust triggers breast cancerin female rats even at the lowest doses (9). Freshwater fish contain residuesof vinyl chloride as does drinking water, both because vinyl chloride isa frequent contaminant of groundwater and because PVC water pipes can shedvinyl chloride from their interior surfaces. Vinyl chloride vapors alsowaft from hazardous waste sites and are an important air pollutant (7,10).It is time to phase out vinyl chloride.
PVC also contains phthalate plasticizers, which demonstrate estrogenicproperties. Traces of phthalates can be found in food where, like vinylchloride monomers, they have migrated from their plastic packaging (11).Ironically, women cancer patients may have higher exposures to vinyl chlorideand phthalates than the general population; hospitals are full of PVC products,including the equipment used for blood transfusions and intravenous drips.Are cancer patients receiving breast carcinogens by direct entry into thebloodstream even as they are being treated for their disease? Recent interestin developing a healthy hospitals campaign that would address such issuesis circulating among cancer activists and progressive health care professionals.
A plan to recall, recapture, and contain polychlorinated biphenyls (PCBs)is an unmet need. Invented in 1929 and banned in 1978, PCBs are the eldersof the synthetic organochlorine family. Preliminary research has linkedthese electrical insulators to breast cancer, and wildlife research revealstheir potential for endocrine disruption (12). When painted on the eggsof certain turtle species, PCBs turn male embryos into females. Moreover,they have the power to do so at very low concentrations--levels that arecomparable to the average level of PCBs now found in the breast milk ofwomen living in industrialized countries (13). Of the 209 possible PCBconfigurations, some appear to be estrogenic and some not. We could decideto funnel resources toward deciphering which congeners belong in whichcategory, or we could decide to fund a campaign to recapture them, thuspreventing additional PCBs from entering our food chain. Only about one-thirdof the world's total production of PCBs is believed to have escaped intothe general environment. Like thousands of tiny bombs exploding in slowmotion, pieces of discarded equipment containing the oily fluid (electricaltransformers, television sets, old french fryers) leak their contents dropby drop into the soil and water. From there, PCB molecules rise into theatmosphere, circulate with the wind, and are redeposited all over the globe.They then enter the food chain (14,15). We could very well save more women'slives by allocating money to get PCBs out of landfills than we could bycontinuing to debate the specific pathways by which estrogenic chemicalssuch as PCBs are metabolized. The impossibility of quantifying the precisenumbers of breast cancer deaths due to PCBs, or any other suspected breastcarcinogen, should not deter us from the task. Recognizing that canceris a multicausal disease with interlocking risk factors, breast canceractivists follow ecologist Rachel Carson's lead in arguing that a substantialreduction in the total load of chemical carcinogens to which we are allexposed would prevent considerable numbers of cancer diagnoses and cancerdeaths (16).
This brings me to the issue of mechanisms and proof. The NAPBC, it seemsto me, spends a great deal of time and energy on the topic of genetic andbiochemical mechanisms of carcinogenesis. While I am as fascinated as anyother biologist at the exquisite nexus of interactions among chemical metabolites,cellular receptors, and DNA, I contend that public health policy has notand should not be driven by the answers to mechanistic questions. Whenwe become concerned about handgun violence in the cities in which we live,we do not need to understand everything about the ballistics of bulletsin order to take preventive action. When we become concerned about children'sexposure to lead, we do not need to describe every link in the biochemicalchain between blood levels and lowering of IQ in order to demand an endto lead additives in gasoline and a remediation of lead-based paint inhousing. When we need to protect ourselves against AIDS, we do not needto know everything about CD4 receptor molecules or cofactor fusin proteinsbefore learning how to use condoms. Indeed, safe sex education and needleexchange dramatically lowered HIV infection rates among certain key populationsyears before scientists identified the mechanisms by which the AIDS virusgains entry into human immune cells. Thousands more lives would have beenlost had we waited to take action until all the viral mechanisms of infectionwere elucidated. Breast cancer prevention efforts need to take a lessonfrom the successes of AIDS activism. (Ironically, the focus on AIDS preventionhas been facilitated in part by the incurable nature of the disease. Bycontrast, breast cancer prevention efforts have historically been overshadowedby the glamor of seeking a cure, and more recently, by the fatalistic focuson early detection.)
The issue of mechanisms is closely allied with the issue of proof. Here,scientists and activists bring two different types of conservatism to thetopic of cancer research. As argued brilliantly by science historian RobertProctor, scientists are conservative when they take care not to overestimatea hazard or when they speak cautiously when making statements of fact.What is being conserved here is the existing body of scientific knowledge,as well as the reputation of the speaker. Cancer activists, on the otherhand, tend to embrace the brand of conservatism practiced within the fieldof public health: prudence for us means acting to reduce cancer hazardseven in the face of incomplete scientific knowledge. In the words of Proctor,"to do otherwise, to wait and see, to delay in the face of good butpartial evidence, is tantamount to experimenting on humans" (17).
This second definition of conservatism was certainly the driving forcebehind the decision to criminalize secondhand smoke. Of the 30 studiesinvestigating its connection to lung cancer, only 9 showed statisticallysignificant risks; 6 showed no risk at all or negative risks. Despite thenegative studies and despite the fact that the mechanisms behind tobacco'sability to cause lung cancer are still not well understood, the U.S. EnvironmentalProtection Agency declared environmental tobacco smoke a known human carcinogen(18). Changes in public policy quickly followed. Tireless efforts by antismokingactivists played as much a role in codifying our right to smoke-free airplanes,restaurants, hospitals, and work places as the results of scientific study.
Many breast cancer activists have been inspired by this kind of weight-of-the-evidenceapproach to environmental health problems. In considering what kind ofcriteria should be used for regulating known and suspected breast carcinogens,we are additionally inspired by a key principle that has emerged from thefield of environmental ethics. This is the precautionary principle, whichdictates that indication of harm, rather than proof of harm, should bethe trigger for action (19). By contrast, our current system of regulationappears governed by what some of us have referred to as "the deadbody approach," which waits until damage is proven before action istaken.
"'We need more study' is the grandfather of all arguments for takingno action," warns Peter Infante, director of the Health StandardsProgram at the Occupational Safety and Health Administration (20). As wego forward, activists and scientists together, we must debate the questionof what constitutes sufficient evidence to advocate public health actioneven as we advocate for more research into the question of how exactlythe metabolism of endogenous estrogens and xenoestrogenic chemicals contributesto rising breast cancer incidence (21).
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