The LA Times exposes breast cancer's challenge to epidemiology.

Writing in the Los Angeles Times, Jill A. Adams explores what is known about what causes breast cancer, especially environmental exposures.  The headline gets it right: "Pollution link remains hazy."

In the text, Adams goes on to summarize "... so far, no clear relationship between exposure and disease [breast cancer] has been shown in people."

As Adams points out, laboratory data "have shown that the offspring of pregnant mice and rats exposed to dioxins or bisphenol A at levels comparable to those encountered by humans were more susceptible to experimentally induced mammary tumors as adults compared with control animals that weren't exposed."

Why, then, is it hard to find strong evidence in people? One possibility is that there is no link. Many scientists don't find this likely because of the fundamental similarity between the ways that hormones work in mammals, including people.  And thus the United States and other governments are investing heavily in research that looks for links. If one or more were found, it might provide an opportunity to prevent cases of breast cancer.

Adams touches on one of the key challenges to finding that signal using epidemiology: that there may be long delays – even decades – between the relevant exposure and manifestation of breast cancer.

Animal studies show that exposures during development, right in the womb, can cause cancers much later in the life of the individual. Linda Birnbaum, now Director of the National Institute of Environmental Health Sciences, and Suzanne Fenton, a researcher at the National Toxicology Program, wrote compellingly about this in 2003. Exposures at crucial times in life, not just the womb but also during other periods when tissues and organs are maturing, such as during puberty, appear to be windows of vulnerability.

But while animal studies highlight the role of developmental exposures, most epidemiological studies of people have been of adults after they were diagnosed with breast cancer. The further in time away from the critical exposure, the less likely a link will be found. If breast cancer's origin lies in fetal development, looking back in time from when a case is diagnosed is not likely to find anything, even if causation is strong.

The Long Island breast cancer study, which Adams cites as finding little evidence of a link, is impaired by this limitation. 

A recent study found a clever way around this challenge. Epidemiologist Barbara Cohn and colleagues reported that women exposed to DDT before puberty were up to five times more likely to develop breast cancer later in life than women who had not been so exposed. They found that exposure after adolescence did not increase the risk. They were able to do this study because they obtained blood samples that had been frozen long ago, when the patients were children, and analyzed exposure in the stored serum in relation to risk of breast cancer.

The National Children's Study, now under way, is addressing this challenge directly. The researchers are tracking kids through development, beginning with measurements of their parents prior to pregnancy and following them into adulthood. It is a vital and exciting study, but the results, by definition, will be a long time in coming.

Increasingly, research, mostly with animals, is suggesting that other diseases of adulthood, in addition to breast cancer, may have their origins in developmental exposures. These include prostate cancer, diabetes, obesity and heart disease. Hopefully epidemiologists will find more ways to work with this challenge, and the media will continue to cover and report on the steps forward. 

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