At first glance, this study might appear to support Safe's argument, but in reality it does not. The study is the best to date available on association between breast cancer risk and adult exposure to PCBs and DDE. In and of itself, that is very important, but it does not warrant Safe's sweeping conclusion.

Why?

• First, Safe's conclusions extrapolate the data from two contaminants to all 'weakly estrogenic' compounds. This argument is illogical to begin with, to use data from two compounds to conclude no others are involved. Not only is it logically incorrect, and a classic ploy used by industry interests defending their products, the argument has been proven startlingly wrong by later studies showing that another weakly estrogenic compound, dieldrin, is associated with an increase in risk of breast cancer and higher mortality rates of breast cancer victims. If Safe's argument were correct, this result would have been impossible.
  
  
• It is also illogical because DDE and the most common forms of PCB found in human tissue are not weakly estrogenic. DDE is an anti-androgen, while the common, persistent forms of PCBs are anti-estrogens. Thus concluding that studies from just two compounds, neither of which are weakly estrogenic, disprove the hypothesis that weak estrogens are involved in breast cancer is logically ludicrous. More....
  
  Safe's got his toxicology wrong here, which is surprising given his long experience in toxicology. It's akin to concluding on the basis of toxicology experiments with water that oil isn't toxic. The hypothesis that weakly estrogenic compounds increase risk of breast cancer rest on well-established observations that life-time exposure to estrogen increases breast cancer risk. On that basis, one would not expect DDE or PCBs to be involved in breast cancer [although there might be other mechanisms through which they could be involved.]
  
  
• Third, this study looks at exposure measured in adulthood in relation to risk of breast cancer. It says nothing about developmental exposure, either during fetal development or during puberty (when human breast tissue is undergoing rapid development). While it is possible that the origins of breast cancer lie in exposure during adulthood, it is equally plausible that the antecedents occur much earlier in life. To argue that a study finding no relationship between adult exposures and adult risk rules out developmental effects is obviously wrong.
  
  
• And fourth, Safe argues that the time trends of breast cancer vs. DDT and PCBs argue against a role of these compounds in causing breast cancer. Breast cancer has been increasing in the US just as DDT and PCBs have been declining because of restrictions on their use. Superficially this sounds plausible. But if the chemical's impact is through disruption of development, then this argument must be rejected, at least at this time. Women entering into the prime years of risk for breast cancer today, in the year 2000, were exposed in the womb and during childhood development to the highest levels of DDT and PCBs ever experienced by any generation in history. The rise in breast cancer rates, if associated with developmental exposures to these compounds, should continue to rise for at least two more decades, until women born to women whose earlier experience was long after the peak periods of use.

Safe ends this editorial with rhetorical flourish: "However, it is incumbent on scientists, the media, legislators, and regulators to distinguish between scientific evidence and hypothesis, and not to allow a "paparazzi science" approach to these problems." It would seem even more important to avoid science conflicted by vested interests.

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