Hazards: Technology and Fairness (1986)

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SCIENCE AND ITS LIMITS: THE REGULATOR'S DILEMMA 15 original typesetting files. Page breaks are true to the original; line lengths, word breaks, heading styles, and other typesetting-specific formatting, however, cannot be About this PDF file: This new digital representation of the original work has been recomposed from XML files created from the original paper book, not from the retained, and some typographic errors may have been accidentally inserted. Please use the print version of this publication as the authoritative version for attribution. Natural Carcinogens Is cancer "environmental" in the sense of being caused by technology's effluents, or is cancer a natural consequence of aging? In the past few years we have seen a remarkable shift in viewpoint: whereas 15 years ago most cancer experts would have accepted a primarily environmental etiology for cancer, today the view that natural carcinogens are far more important than man-made ones has gained many converts. In his famous Science article illustrated by Robert Indiana's modern painting Eat-Die, Bruce N. Ames (1983) marshaled powerful evidence that many of our most common foods contain carcinogens. Indeed, John R. Totter (1980), supported by the late Philip Handler, has offered epidemiological evidence for the oxygen radical theory of carcinogenesis: that we grow older and eventually get cancer because we metabolize oxygen, and oxygen radicals can play havoc with our DNA. As such views of the etiology of cancer acquire scientific support, the trans-scientific question of how much cancer is caused by a tiny chemical or physical insult likely will be recognized as irrelevant. One does not swat gnats in the face of a stampeding elephant. Ambiguous Carcinogens To further complicate the cancer pic ture, certain agents, such as dioxin, various dyes, and even moderate levels of radiation, seem to diminish the incidence of some cancers at the same time that they increase the incidence of others; the lifespan of animals treated with such substances on average exceeds that of untreated animals (Weinberg and Storer, 1985). A most striking example, given by Haseman (1983), is that of yellow dye #14: given to leukemia-prone female F344 rats, the dye completely suppresses leukemia, which is always fatal, but causes liver tumors, most of which are benign. These two findings—or, perhaps, points of view—illustrate an underlying point: with regard to low-level insult to human beings, we can say very little about the cancer dose-response curve. Saying that so many cancers will be caused by so much low-level exposure to so many people, a practice that terrifies many people, goes far beyond what science actually can say. How Science Reacts to Intrinsic Uncertainty Does the scientific community accept the notion that there are intrinsic limits to what it can say about rare events? That as events become rarer, the uncertainty in the probability of occurrence of a rare event is bound to grow? Perhaps a better way of framing the question is this: To what use can we put 

SCIENCE AND ITS LIMITS: THE REGULATOR'S DILEMMA 16 original typesetting files. Page breaks are true to the original; line lengths, word breaks, heading styles, and other typesetting-specific formatting, however, cannot be About this PDF file: This new digital representation of the original work has been recomposed from XML files created from the original paper book, not from the retained, and some typographic errors may have been accidentally inserted. Please use the print version of this publication as the authoritative version for attribution. the tools of scientific investigation of rare events—say, probabilistic risk assessment and large-scale animal experimentation as surrogate for epidemiological inquiry—if we concede that we can never get definitive answers? An uncertainty as high as a factor of 10 is often useful in probabilistic risk assessment, especially if one uses the PRA for comparing risks. For example, the 1,500 reactor-years already experienced since the TMI-2 accident suggest that a reactor core-melt probability is likely to be less than 10-3/yr and may well be as low as the PRA predicts, less than 10-4/yr. This is to be compared with dam failures, whose probability, based on many hundreds of thousands of dam years (and where time has annihilated uncertainty), is around 10-4/yr. Even with this uncertainty, we can judge roughly how safe reactors are compared to dams. When one compares the relative intrinsic safety of two very similar devices —e.g., two water-moderated reactors—probabilistic risk assessment is on much more solid ground. Here one is not asking for absolute estimates of risk, but rather for estimates of relative safety. If the reactors, A and B, differ in only a few details—say that reactor A has two auxiliary feed water (AFW) trains whereas B has only one—the ratio of core-melt probabilities should be much more reliable than their absolute values, since the ratio requires an estimate of failure of a single subsystem, in this case, the extra AFW on reactor A. Not only can one say with reasonable assurance how much safer reactor A is than reactor B, but one can, as a result of the detailed analysis, identify the subsystems that contribute most to the estimated failure rate. Even if PRA is inaccurate, it is very useful in unearthing deficiencies: one can hardly deny that a reactor in which deficiencies revealed by PRA have been corrected is safer than one in which they have not been corrected, even if one is unwilling to say how much safer. Somewhat the same considerations apply to low-level insult. An agent that does not shorten lifespan at higher dose will not shorten lifespan at lower dose. An agent that is a very powerful carcinogen at high dose is more likely to be a carcinogen at low dose than is an agent that is a less powerful high-dose carcinogen. Thus, animal experiments surely are useful in deciding which agents to worry about and which not to worry about. And of course the Ames test has made at least some preliminary screening of carcinogens more feasible. The difficulty today seems to be not so much identifying agents that at high dose may be carcinogens as it is prohibiting exposures far below levels at which no effect can be, or ever will be, demonstrated. The regulator and the concerned citizen are inclined to go so far as to approve the Delaney Clause [21 U.S. C. 348(c)], which forbids in interstate commerce any carcinogenic agent in food, without ever saying anything about allowable levels or relative risks of, say, cancer induction by nitrosoamines and digestive disorders caused by meat untreated with nitrites!