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Vol. 07 Issue 4, Early Winter 2002
by Suzanne M. Snedeker, PhD.
Cornell University
When I started my career as a senior staff fellow at the National Institute of Environmental Health Sciences (NIEHS) in the late 1980s, I often started my talks with the following quote from cancer researchers Irma and Jose Russo:
"The complexity of breast cancer and our failure to stop the 120,000 cases (1987 figures) that strike American women annually, or the fact that one out of four women will die as a consequence of it, is basically rooted our lack of knowledge of the disease."
Fifteen-years later, the Russo quote is still apt. We still do not have a complete picture of the biology of this disease nor of the many factors that affect breast cancer risk. The American Cancer Society predicts that in the year 2002 over 205,000 new cases of breast cancer will be diagnosed in Americans and 40,000 will die of the disease.
It is unfortunate that the media has given the impression that few environmental factors have been associated with human cancer. The World Health Organization's International Agency for Research on Cancer (IARC) has identified 80 natural and synthetic chemicals, occupational situations, pharmaceuticals and viruses that cause cancer in humans. For most cancers, we do not have exposure data or cancer risk data in humans. The National Toxicology Program has successfully used screening tests in rodents to identify potential human carcinogens. Of the 509 compounds evaluated, nearly 9% (42) have been identified as causing mammary (breast) tumors in laboratory rodents. The types of chemicals include industrial chemicals, dyes, flame retardants, solvents, pesticides, toxins from molds, and pharmaceuticals (See BCERF Fact Sheet no. 45, Environmental Chemicals and Breast Cancer Risk; Why is there Concern, http://www.cfe.cornell.edu/bcerf/FactSheet/General/fs45.chemical.cfm)
It is not possible for one study to provide all the data needed to fully identify causes of breast cancer or explain the rising incidence rates. We cannot paint the picture of breast cancer in a single stroke. Rather, each study contributes a small piece to the mosaic of breast cancer risk. Each piece starts as a question, a hypothesis, based on the best information available at that time.
During the early 1990s, the results of several studies suggested that a high blood level of DDE, the metabolite of the persistent pesticide DDT, was associated with a higher risk of breast cancer. DDT and other persistent organochlorines, such as chlordane and dieldrin, were known to cause other types of cancers. Therefore, it was logical to pick these chemicals as factors to study in relation to breast cancer risk. These chemicals are also stored in body fat and can be easily measured in blood or fat samples.
The hypothesis of whether blood or fat levels of organochlorine pesticides or industrial contaminants (such as polychlorinated biphenyls - PCBs) predict breast cancer risk was tested in over 30 other studies, and most recently in the Long Island Breast Cancer Project (LIBCP). Most studies of white Western adult women have not shown that blood levels of these compounds predict breast cancer risk. It is still unclear whether women of other ethnic backgrounds may have a higher breast cancer risk from past or current DDT exposure, or whether exposure during early periods of breast development affects later risk. (see BCERF Fact Sheet no. 2, DDT, DDE and the Risk of Breast Cancer, http://www.cfe.cornell.edu/bcerf/FactSheet/Pesticide/fs2.DDT.cfm). For other chemicals, including polyaromatic hydrocarbons, the LIBCP results suggested a modest increased breast cancer risk (about 50% higher) associated with exposure to these compounds which are found in burned fossil fuels, cigarette smoke, and charred foods
Dr. Mary Wolff, one of the co-authors of the organochlorine and PAH paper for the LIBCP recently discussed the results and the analyses still underway for the LIBCP at a Health Science Advisory Board meeting (HSRB). While the media has given the impression that all results have been published, this is not the case. Important analyses on interactions between genes that activate cancer causing chemicals and breast cancer risk are still being compiled. The LIBCP needs to be embraced as an evaluation of important hypotheses. Results of this study will ultimately add to our mosaic of breast cancer. Because several chemicals were not associated with breast cancer, we should not abandon all research on how environmental factors affect the risk of breast cancer. On the contrary, it should force us to refocus our thinking, our approach, and refine the tools and methods needed to test future hypotheses.
For example, the timing of exposure to environmental factors affects future breast cancer risk. Japanese infants and girls exposed to ionizing radiation at Nagasaki and Hiroshima subsequently had a very high breast cancer risk compared to women who were over 40 when exposed. Recent research suggests high exposure to the environmental contaminant dioxin in younger women may increase breast cancer risk later in life. Silent Spring Institute researchers are characterizing household exposures to environmental toxins in women with and without breast cancer on Cape Cod. The "Agricultural Health Study" is evaluating whether exposure to agricultural chemicals affects health, including cancer risk, in over 85,000 men and women in farm families from North Carolina and Iowa. The "Sister Study" will follow over 50,000 sisters of women with breast cancer in an attempt to identify causes, including possible environmental links, to the disease. The results from these studies will better inform regulatory agencies, and at risk populations of the environmental factors that do and do not pose a cancer risk in target populations.
Much media attention has focused on the role cancer activists and policy makers play in influencing funding for cancer research. In 1899, a doctor from western New York wrote a essay published in the Transactions of the Medical Society of New York on possible causes of the rapidly rising rates of cancer. Because of this concern, he mentioned how a modest laboratory had been established dedicated to investigating the causes and treatment of cancer. He wrote, "...as the result of persistent efforts on the part of a number of men, both professional and laymen, both in and out of the Legislature, the Legislature of New York appropriated a small sum for the purpose of equipping and maintaining a laboratory devoted to this kind of (cancer) research." This modest cancer laboratory located in Buffalo, New York has grown into the prestigious cancer research center named after the author of the essay, who was Dr. Roswell Park.
Over the last year I was invited to attend a series of workshops held at the National Institute of Environmental Health Sciences. Scientists, risk assessors and cancer activists engaged each other in a full discussion of approaches that could be used to better evaluate and understand the role of environmental factors in breast cancer risk. This November, I will be attending an international symposium in Oxford, England that will bring international scientists from many different disciplines together to discuss the role of pesticides in cancer risk. Such interaction and partnerships at the local and global level are not only necessary, they are instrumental in enabling us to foster research agendas that will ultimately lead to risk reduction strategies for ourselves and our children.