From the Director’s Desk — “Breast Cancer and the Environment… Case Closed?”
—Marion Kavanaugh-Lynch, M.D., M.P.H.
Since the release of the long-awaited results from the Long Island Breast Cancer Study Project, there has been a flurry of articles, editorials, and private debate concerning further study of the role of environmental toxins in the causation of breast cancer.
The Long Island study, created by the political efforts of Long Island breast cancer activists and funded by the National Institutes of Health, looked at blood levels of the organochlorine pesticides DDT, chlordane, and dieldrin and electrical insulators known as PCBs, as well as evidence of DNA changes that are caused by polycyclic aromatic hydrocarbons (PAHs), a ubiquitous toxin created by cigarette smoke, motor vehicle exhaust, and smoking or burning meat. The results? … Researchers found no association between breast cancer and exposure to these pesticides or PCBs. They identified a 50 percent elevated risk of breast cancer with higher levels of PAH-associated DNA changes, but this did not correlate with exposure to PAHs. The conclusion of many: there is no solid environmental link to breast cancer.
We feel that the environmental debate around breast cancer is far from being settled by the Long Island study.
The real conclusion to be made from the Long Island study comes from a quote that appeared several years ago in Science (“Epidemiology Faces its Limits”). Sander Greenland, a noted epidemiologist said, “There is nothing sinful about going out and getting evidence… the sin comes in believing a causal hypothesis is true because your study came up with a positive result, or believing the opposite because your study was negative.”
Anything short of this conclusion is a disservice to the 4,200 California women who will die of breast cancer this year, and to the thousands of women who are survivors.
As further explanation:
-
No definitive conclusion can be made from Dr. Marilie Gammon's comment that, “Whether environmental contaminants increase breast cancer risk among women on Long Island, NY, is unknown.” The study addressed only five compounds—a small portion of the spectrum. In fact, one of the compounds, PAHs, was associated positively with breast cancer in Long Island. (Dr. Gammon has served CBCRP as a research application reviewer and speaker at our bi-annual symposium.)
-
The Long Island study was severely compromised from the outset by conflicting political, scientific, and emotional needs. The study couldn't hope to address activists' concerns or even a significant portion of the underlying scientific questions (see the recent in-depth Newsweek feature, “Tattered Hopes.”)
-
The Long Island study demonstrates that traditional epidemiologic approaches have limits when dealing with diseases that are likely multi-causal. Why? It takes many years for breast cancer to develop, and causal factors probably act decades before a woman is diagnosed with breast cancer. The relevant dose, timing of exposures, effects of exposures to multiple mixed compounds, and interactions between exposures and an individual's genetic make-up are still largely unknown. True comparison groups (groups of people who have not been exposed) may not even be possible.
It's true that there is no “smoking gun” for breast cancer as there is for cigarettes and lung cancer. However, as women continually witness the devastating toll of breast cancer, they hear bewildering shots in the night and smell gun smoke. Both come from a tantalizing volume of observations that point to environmental exposures as likely suspects in the breast cancer mystery.
It is for this reason the CBCRP is calling for innovative research that focuses on environmental exposures and breast cancer. If the methods we have used until now have not brought us definitive answers (and they have not), then we must push for new methods and new approaches.
