STATS at George Mason University
 
   
 

Do pcbs cause cancer in animals?

There is robust evidence that PCBs, when administered in sufficiently large doses, can inflict cancerous tumors upon rats. And as far as the EPA is concerned, if a substance can be shown to cause cancer in animals, it must be treated as a probable carcinogen in humans.

Yet such a cautionary principle does not take into account nature’s delight in inconsistency: to be human is to be more than merely a very large rat, at least in terms of extrapolating the effects of grave research across species. The problem is that while animal dose-response testing may show that something causes cancer, it cannot show what the actual causal mechanism is. Causal mechanisms may differ between species, between closely related members of a single species, or even between the sexes of the same species.

Thus, not all proven carcinogens in humans will produce cancers in mice or rats, even after chronic exposure; and likewise, not all carcinogens in rodents (or other animals) will turn out to cause cancer in humans. (See Hugh La Folette and Niall Shanks, “Brute Science: Dilemmas of Animal Experimentation,” Routledge, 1996).

Though it is hardly a revelation that physiology is not always and everywhere the same in nature, the failure to account for possible differences between sexes and across species can produce spectacularly misleading results. For instance, when animal testing showed that the artificial sweetener saccharine “produced” bladder cancer in male rats, the Food and Drug Administration announced that it was a “probable carcinogen” in humans, after dallying with an outright ban. Years passed before further research revealed that the mechanism which triggered the cancer in male rats was neither present in female rats or humans.

The other major problem with animal dose-response testing is that any substance will prove toxic if consumed in sufficiently large quantities. Yet because researchers are trying to find health effects that are hard or impossible to detect in the general population, they are forced to compensate by giving very high doses of a substance to a relatively small number of animals over a sustained period of time. The dosages and the effects are then scaled back down to establish the lifetime exposure risk for humans.

This method assumes that the relationship between dosage and damage is linear; in other words, if a large amount of a substance produces widespread illness in a short space of time among laboratory animals, a tiny amount will produce a much lower rate of illness in an average person across an average lifetime. While plausible (indeed, elegantly so), this method yields little to precision; for even the most benign substance can prove toxic if administered in a large enough measure or with sufficient frequency to overwhelm the body’s ability to repair damage.

In testing whether saccharine was carcinogenic, for example, rats were given dosages equivalent to a person drinking over 1000 cans of diet soda per day. Should anyone be foolish enough to attempt such a feat, he or she would die from overhydration somewhere between the fortieth and fiftieth can.

Turning sick rats into human risks
The daily PCB doses administered to rats in the studies cited by the EPA ranged from zero parts per million (the control group) to 200 ppm over periods of one to two years. Elevated rates of liver tumors first became noticeable at 25ppm, although the numbers of rats affected varied depending on the PCB mixture.

Similarly, some PCB mixtures in some of the studies produced high rates of liver tumors at 100ppm, while others didn’t. A dose of twenty-five parts per million is between 15,625 and 31,250 times greater than the EPA monthly fish consumption limits for eight ounces of fish (.024ppm – .048ppm).

The EPA’s method of translating rat tumors into a quantifiable risk for cancer for humans has drawn fire from other scientists. Again, STATS’ survey of 401 randomly chosen members of the American Association of Cancer Research in 1993 found that almost two-thirds (63 percent) rejected assessing human cancer risks by this method.

And during the media coverage of Hites et al., the practice drew fire from some leading scientists. Professor Emeritus André McLean, a consultant toxicologist in the department of clinical pharmacology at University College London complained in the Times of London that, “...the risk statements are based on variants of a technical procedure known to toxicologists as the linear-forced-through-zero extrapolation, where risk to humans who get minute doses of some chemical is calculated simply in proportion to the cancers that a few unfortunate mice may get when stuffed with large amounts of the chemical. If it worked like that, we would all be dead from the dangerous mutationproducing effects of oxygen.”

Britain’s Food Standards Authority (FSA) has also questioned the appropriateness of the EPA’s model for calculating the risk from PCBs in salmon. The FSA states that: “This process is not recognized by international organizations responsible for food safety and public health who consider it scientifically flawed... The World Health Organization set safety levels for dioxins and PCBs in 2001 based exclusively on public health detection. These form the basis of safety levels set for consumers who eat fish sold in shops.”

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