Physics is Fun Memoires of Richard Wilson Version of September 25th 2009

Uses of Risk Analysis for Regulation
Some scientists involved in scientific policy argue that one should take no action, even preventative, unless there is rigorous scientific proof of the efficacy of the action. I think this is overly conservative. I believe that one must be cautious in new situations. This is often discussed as the “Precautionary Principle) which is important but badly defined. Often there is more evidence that a substance or procedure is safe than a person knows or is willing to admit. We have discussed this in a couple of papers (544, 571, 847). I differ with many persons demanding action in that I think that it is important at all times to be fully aware of what is scientifically proved and what is conjecture. If one regulates on the basis of a conjecture, or fails to regulate, one must always be willing to change one’s mind as new information becomes available. This “intermediate “ position has been hard to sustain.
Historically it seemed reasonable that cancer might appear in man in the same organ as it appears in animals (rodents). In 1973 Tomatis noticed that there is a greater correlation between animal carcinogenicity and human carcinogenicity if the sites were allowed to be different for the two species, than if they were forced to be the same. This was further confirmed by Crouch and Wilson (1979) and by Crouch (1983a,1983b) who studied the comparison of carcinogenic potency between rats and mice. In 1983 the Carcinogenic Assessment Group (CAG) of the EPA, made this assumption explicit for regulatory purposes. No explicit biological rationale was ever put forth to support this assumption. The Carcinogen Assessment Group (CAG) of EPA now assumes that if a chemical produces a statistically significant excess of tumors in a group of animals, usually rats or mice, at any one site, then it will be considered to pose a probable risk of cancer to humans at some unspecified site. There are several problems with this interpretation. Since carcinogenic potency and acute toxicity have been found to be correlated, and there is an inter-species correlation of acute toxicities, there is a strong empirical connection between toxicity and carcinogenicity as noted above. This could be explained simply if acute toxicity is the cause of tumors with most chemicals, as urged by Bruce Ames and Lois Gold, although other explanations are possible. There are problems with this simple explanation. In particular if the Ames and Gold explanation applies to most chemicals it is hard to understand why there appears to be little concordance across tumor sites.
EPA did not formally consider it to be relevant to the quantitative risk assessment whether the site in which tumors are found in rats differs from the site in which they are found in mice, and makes no implication that tumors will be found at the same site in humans. However, such considerations appear in discussing the general toxicological profile of the substance, for instance the appearance of tumors in the same site in both sexes or species tested is taken as stronger evidence for potential human carcinogenicity. In this sense, all carcinogens are considered the same. However, other uses of bioassay data by EPA, PBPK models for example, have the concordance of sites as an implicit assumption. Although EPA developed a fairly well defined method for risk assessment, the logical and scientific underpinning for this method remains weak. The EPA theory is "unified" in the sense that the risk is calculated for most chemicals in the same way, regardless of any mechanism for carcinogenisis that may have been proposed. The EPA assumes a linear dose-response at low doses, but allows data to suggest differences from linearity at high doses. Although often called a "linearized multistage" model, it is more accurately called a "truncated polynomial" procedure, (379) since it is a mathematical model whose relationship to the biological multistage model is not unique. This method generates a "plausible upper bound" estimate of carcinogenic potency that has been widely criticized in the scientific community. It has more recently been replaced by a default approach that gives a similar low dose risk - to draw a straight line from the lowest response at a low dose (LD10) to the origin.
Tumor sites are said to be concordant across species if the tumors appear at the same anatomical site in different species when they are exposed to the same carcinogenic agent. Although usually ignored in risk assessment, concordance plays a very large implicit role in the process. In the hazard identification portion of risk assessment the underlying assumption of perfect concordance plays a role in both epidemiology and the interpretation of the relevance of animal bioassay results to humans. Tumor site concordance often guides the design of epidemiology studies. The results of an animal bioassays may lead to case/control epidemiologic studies examining the risk of cancer in humans in the same site in which it was found in animals. If carcinogenic agents frequently affect humans and animals at the same site this strategy can help to focus the efforts of epidemiologist. On the other hand, if tumor site concordance is not to be expected, this approach may hinder attempts to identify human carcinogens by focusing the attention of epidemiologist on single tumor sites. In addition to its influence on epidemiology, in hazard identification tumor site concordance is frequently invoked by those who wish to ignore or downgrade the relevance to humans of tumors in rodent tissues with no human equivalent (e.g. zymbal gland) or when concordance is lacking.
In dose-response evaluation tumor site concordance is important both as the basic assumption of dose-response modeling and in the determination of "dose." The standard models of dose response used in risk assessment, such as the "linearized multistage (LMS) model" (more accurately called a truncated polynomial model) that used to be favored by the U.S. Environmental Protection Agency (EPA), actually calculate a site specific cancer potency from animal data which theoretically is only applicable to the same site in humans. The use of this model to estimate risk to humans at any site is out of necessity rather than theory. Tumor site concordance is also an important but usually unacknowledged assumption in the use of physiologically-based pharmacokinetic (PBPK) models in risk assessment. In order to improve the cross-species and high dose to low dose evaluation of risk it is often advocated that PBPK models be used to calculate the dose to the target organ rather than the dose administered to animals or humans for purposes of dose-response evaluation. If, however, target organs are not concordant across species, then target organ dose may be an inappropriate dose metric. Examining the issue of tumor site concordance, and perhaps identifying cases when it is an appropriate assumption, and when it is not, should increase our knowledge in these issues of cross-species extrapolation. In addition, study of concordance should generate biologically based hypotheses about factors known to influence tumor site concordance - such as similarities or differences in pharmacokinetics, metabolism, or gene expression, in different species.
Most of the examination of cross-species extrapolation of carcinogenic response has focused on the fact of carcinogenicity itself, rather than the site of response. In addition to the purported 100% correlation between humans and animals it has been demonstrated that rats and mice have a fairly high, about 75% concordance of carcinogenic response when challenged with the same chemical Others have shown, however, that cross species prediction is somewhat better for mutagens that nonmutagens and for chemicals with high acute toxicity again indicating that scientific research may be able to demonstrate qualitative and quantitative differences between chemical carcinogens.
Twenty years ago, in the 1970s, it seemed natural to search for evidence of carcinogenicity after chronic administration of a substance at the same site where the substance had been shown to cause toxicity. Many historical examples exist. Benzene at high doses produces pancytopenia (it kills blood cells), and it also produces leukemia. Exposure to asbestos results in asbestosis (of the lung) and later was shown to cause lung cancer. Vinyl chloride is toxic to both human and rat liver, and also causes angiosarcoma in both humans and rats. Aflatoxin B1 is both toxic to the liver and is an established risk factor for liver cancer. In two of these cases (benzene and asbestos) it is still an open question whether it is the substance that causes the cancer directly or whether the cancer is caused by the toxicity. In spite of the regulatory assumption that all carcinogens are alike, scientists have endeavored to find distinctions between different types of carcinogens. Following the seminal work of Meyerson and Russell in 1977 that suggested that animal carcinogenicity is quantitatively related to mutagenicity Parodi et al. in Italy began to study possible correlations between mutagenic and carcinogenic potencies. Parodi et al. discovered, to most scientists' surprise, that carcinogenic potency is more strongly correlated with acute toxicity, than with mutagenicity. As noted above this was confirmed and expanded by our group, using a larger database. Associated with this correlation, and a possible cause of it, is the fact that many substances only produce statistically significant tumor responses at the highest dose tested. This Maximum Tolerated Dose (MTD) is related to the acute toxic effects of the substance. This led to concern that this correlation might be merely a statistical artifact of the bioassay experimental design. But our extensive Monte Carlo simulation of the bioassays (461, 479)) showed that while the correlation could in principle be a statistical artifact of the bioassay itself, it would be so only if many substances cause tumors in 100% of the animals in a bioassay. The actual values of the various parameters preclude such an explanation. Only 2% or less of chemicals produce tumors in 100% of the animals in long-term bioassays.
Possible biochemical reasons for the existence of this correlation (in which it could be described as a biological artifact of the experimental design of the NTP bioassays) have recently been discussed. In particular, substances at high doses, approaching the maximum tolerated dose, kill cells. Ames et al. propose that this results in cell proliferation, and subsequent tumor development by a mitotic effect. If this is the case, such substances would be expected to show a very non-linear dose response relationship at these doses. However, at lower doses, a linear dose response might still be appropriate, especially for initiators.
More recently several examples have emerged of situations in which carcinogenisis indeed appears to be secondary to direct organ toxicity, and there is a clear biological explanation. For example, sodium saccharin causes microcrystals to form in the bladder at high doses, and it is probable that these crystals cause the bladder cancers that are observed, presumably by an irritant effect . As calls to de-emphasize the results of animal bioassays have intensified , so has the need to empirically investigate this relationship in as many ways as possible.
Long-term rodent bioassays are conducted with the intention of identifying chemicals with the potential to increase cancer rates. It has long been known, but often dismissed, that statistically significant dose-related decreases for certain tumor sites and types are also found in many long-term rodent bioassays. A well known example is the work of Kociba et al, in 1978 on dioxin. Anti-carcinogenicity has recently come to be taken more seriously. My colleague Igor Linkov, (542, 650) demonstrated that anti-carcinogenic effects in animal bioassays apparently have a biological basis. In addition, Clark, in a human study in 1996 demonstrated convincing anti-carcinogenicity for selenium administered at low doses to humans, whereas it is carcinogenic at high doses,.. The fact that rodent bioassays also shows anti-carcinogenicity for selenium indicates the potential generality of protective effects.
In spite of the findings of anti-carcinogenicity, it has been regulatory practice to consider only tumor increases when classifying and regulating a substance as a carcinogen. Factors contributing to the view that anti-carcinogenic effects are not important included the inability to account for biases due to experimental conditions, inadequate attention to random responses, and the presence of significant weight loss and other effects of exposing animals at the maximum tolerated dose.
We, Linkov et al, (542, 550) maintain that anti-carcinogenic tumor decreases are as common in the bioassays as increases and are not a single isolated phenomenon. This contention continues even after some corrigenda and addenda are made to the analysis.   I have discussed in an unpublished lecture that in the same animal one can often have both anti-carcinogenic at one tumor site and carcinogenic effects at another tumor site.  No one has discussed the implication of this for regulation. The Carcinogenisis Bioassay Data System (CBDS) database of the National Toxicology Program (NTP) is the primary tool for these studies. Not only are sites of all tumors listed, but also toxic lesions are listed. The weights of the animals are listed at the end of life and of the groups of animals at other times.
The results so far indicate that any attempt to a priori predict the target organ for human carcinogenicity from experience of an individual chemical would be fraught with uncertainty. When the goal of testing a chemical for carcinogenicity in animals is to identify potential human carcinogens it appears that the rodent tests can qualitatively confirm whether a compound has carcinogenic potential but rodent tests in general appear to have little ability to predict the target tissue for human carcinogenicity.
The regulatory expression of these observation is confused but the scientific community already has discussed an important implication, namely that all carcinogens are not the same. Therefore, a unified regulatory method to identify carcinogens and estimate carcinogenic potency may no longer be appropriate. In principle this is already recognized in the EPA carcinogen policy; the three key assumptions discussed above are stated to be only default assumptions to be replaced when better data or more generally accepted theories are available. Then risk assessors can adopt a case-by-case approach that utilizes more biological information such as a nonlinear dose response relationship rather than the default linear relationship. But while it seems to be now accepted that there are examples of this, such as saccharin and the case of dioxin is being seriously discussed, this has not been generally accepted for other non-genotoxic compounds.
On the other hand we have been emphasizing the generality of linear dose-response relations They apply whenever the mechanism of the medical ailment being discussed is similar for the carcinogen and for whatever causes the background. In all of this I emphasize proper attention to uncertainty (305, 327). In 2000-2008 this program has changed to a detailed study of the multistage theory of cancer and how it must be modified to address cancer at old age. Our latest work on a very careful study of cancer incidence at old age (882) came out the prestigous journal “Cancer Research.” . My work on chemical carcinogens has been funded personally as a by product of my consulting work for industries facing regulation or lawsuits. Alas, while I have been able to obtain occasional funding for this work it has become sporadic and I have had none at all since 1995.

Arsenic
As noted earlier, bioassays in mice and rats did not show that arsenic causes cancer. Whether for this or other reasons, the world was not looking out for problems of chronic, continuous, low level exposure. Although Edmund Crouch and I had noted the skin cancers, and lung cancers, I was surprised when in 1990 I was helping Dr Steven Lamm evaluate risks of mining tailings, and found in our review of the data on arsenic that C.J.Chen and collaborators,. found high cancer rates NE of Tainan in Taiwan some 4 years before. The death rate from internal cancers was 100 times that from skin cancers which had formed the basis of the EPA risk assessment at the time. Although it was, and is, only an “ecological study”, and therefore limited in its ability to inform us about dose response, a simple graph showed one of the best linear dose-response curve I have ever seen. The data should not be ignored, yet the EPA and much of the world was ignoring them. We looked at the literature, which we had just searched, and found that the direct interpretation, that the risk of arsenic repeated cancer was indeed that high, was not contradicted by any other study. On the contrary there were hints of the large risk in many places. Even so might the problem be due to some aspect of the Taiwan exposure? Thus began an aspect of my work which has continued for 20 years. A brief history of arsenic in water and food is being published (905), and I have for 10 years maintained a website with more than most people ever want to know about the subject. I rent a specific simple web address, http://arsenic.ws which at the moment leads to the page on my website http://physics.harvard.edu/~wilson/arsenic/arsenic_project_introduction.html.
The work on trying to help the people in Bangladesh is extraordinarily rewarding for me personally. It is all too easy for an American “do-gooder” to propose some action or another that people in a developing country “must do” to gain prosperity. In 1998 I thought somewhat along these lines. At the suggestion of Peter Rogers, a professor of Environmental Engineering at Harvard, I went to a conference in February 1998 run jointly by Dhaka Community Hospital (DCH) and the School of Environmental Studies in Jadvapur University in Kolkata. We were taken to a village, Chandripur, in the SE part of the country with 900 residents. There we were shown several victims. I saw over 120 cases of arsenic poisoning - more than an American dermatologist sees in a lifetime. I was hooked. On my return I gave an emotional talk at the School of Public Health and I gave a talk, which was well received, that if HASP were truly interested in global public health, then they must be involved with Bangladesh. I had given a talk at the 1998 conference outlining 3 actions that must take place simultaneously.

- studying the geochemistry of how the arsenic gets into the water with a hope of being able to have arsenic free supplies in the future

- studying by epidemiology (comparing a cohort now exposed and later less exposed) what arsenic actually does to people

- and I noted that neither the geochemist nor the epidemiologist could go back to a village a second time (either pragmatically or honorably) unless they did something to provide pure water for the villagers.

We had a false start in trying to get major funds from the World Bank, but then Professor Charles Harvey who was just moving from Harvard to MIT got NSF funding for the first task, and Professor David Christiani, HMS and HSPH found funds from NIH for the second. I got funds, alas, still in much smaller amounts, from 3 wealthy Arab friends, from the OPEC fund, from some friends and acquaintance, and some money of our own, to work on the third task. To help in this I started the “Arsenic Foundation” which is a 501(c)3 foundation to enable tax exempt donations to be made.
I have learned that one must listen to the villagers who are being affected, and also listen to the local NGOs who work with them. The constraints and restrictions that each of these face are not easily discernible from abroad and vary from place to place and time to time. This became even clearer to me when I heard a talk by an American NGO, at the Second International Risk Analysis conference in Guadalajara, who was helping villagers in the desert regions on NW India in Rajastan. He also emphasized the importance of talking to the villagers. While I understood his list of constraints, each seemed very different from the ones I had heard in the Bangladesh villages. In discussions with Dr Meera Hira-Smith of West Bengal and UC Berkeley, California, the problems in the West Bengal villages are different again. While in Bangladesh it seems that agreement within a village is possible, to have a single large, “Indira” well servicing the whole village by pumping to a water tank with simple PVC pipe to a number of distributed taps, the remaining Moslem-Hindu differences in West Bengal add additional constraints that make this solution, which seems both technically sensible and politically possible in Bangladesh less palatable for West Bengal.
However, the way of ensuring that the water remaains free of bacteria, even during the rainy season, is still a problem (906).
Electromagnetic Fields
In the late 1980s and early 1990s there was a large public concern about electromagnetic fields from electric power lines. Associated with this public concern has been ignorance, misunderstandings, lake of attention to public concern by industry, modification of data to fit a preconceived notation, and some downright fakery. It is interesting as a fine example of how society can go crazy, and how careful scientists can be swept aside.
As noted at the start of these reminiscences, I became aware of dangers of electricity at an early age. When I was 15 I was sent by my father to look at the X ray machine of our local physician, Dr Kelly, which was giving electric shocks to her patients. She had dutifully asked the electrician to install 3 pin sockets in her surgery for the X ray machine, but when I checked, I found that the ground socket was unconnected! I was angry with the electrician for such incompetence. As noted earlier I was a little perturbed in 1942 when bicycling back from Winchester to Crowthorne in the rain by looking at the blue discharges around the insulators of the 300 kV transmission lines. The undergraduate laboratory in the Clarendon Laboratory had a vacuum system on the 4th floor doing some experiment. As usual for the time, it was all glass, and the valves were sealed with vacuum grease which sometimes had to be warmed to allow them to operate. One morning a student came in early at 8.30 and started working. He picked up a hair dryer to warm the valves. The metal case of the hair dryer was properly connected to the ground pin of a three pin plug. BUT someone had noticed that the fuse kept on blowing so he put a piece of paper as an insulator between one part of the case and the next. The student holding the hair dryer found himself connected to the live 230 volt connection in one hand while he was holding onto the grounded metal framework supporting the vacuum system with the other hand.. The current went from left hand to right through his chest. His fists automatically clenched and he could not let go. He screamed and a porter came up. By the time he got there the student had kicked the glass system apart and finally managed to pull the hair dryer out of the power socket. He was badly burned but otherwise he was OK. It was a lesson I never forgot. A year later Geoffrey and I rewired the building which was rented by the Oxford University Scout Club for our meetings, following in detail all the IEE requirements as well as some local ones of the Oxford building inspector. As a risk analyst I noted that 500 people in the US die every year from electrocution and some tens per year by lightning strikes. But we can also cure, or at least prevent deaths from electrocution. In 1960 or so, defibrillators became available to get a heart started after a heart attack or electric shock. Tom Collins at the CEA noticed this, and we became the first group after the Philadelphia fire department to het some and be trained in their use. They were never a need for treatment after a shock but twice we had heart attacks at the cyclotron. Firstly our engineer, Mike Wanagel, fell off his stool and his heart stopped. We brought him around, but alas he was never fit for work again. Then the janitor fell with a heart attack. We had just started this on him, when Dr Ray Kjellberg, who had been treating a patient with the proton beam came up. We explained, and he said “carry on.” When blood came out of the janitor’s ears we proposed to stop and Ray agreed and signed the death certificate.
Of course electricity can kill. But can electromagnetic fields kill without causing a current to flow in the body? That is a far more difficult question. One learns that there is an electric field of about 300 volts per metre in much of the world, which reverses when a storm is approaching and then the insulation of the air breaks down and lightning strikes. Just before breakdown, the high reverse electric field is easily observable as one’s hair stands on end , but with no other known adverse consequence. No one has claimed that these magnetic fields cause cancer. But there is also a magnetic field; normally about 0.2 Gauss vertical component and about 0.3 Gauss overall. This changes near iron out croppings. Of course since 1800 people have made magnets with fields of 20,000 Gauss or more, and scientists have been exposed to them. In the period 1950 to 1965 I often put my head inside the magnetic field of a cyclotron. One could see occasional flashes of light in the retina, known since about 1900 as magnetophosphenes, and if I moved my head around I could taste the electric current induced between the mercury amalgam fillings in my teeth. Soon after he had discovered nuclear magnetic resonance, Ed Purcell put his head inside the Harvard Cyclotron magnet to see whether he could induce the spin transitions in his head - but nothing was observable. The number of atoms moving, although observable nowadays in (Nuclear) Magnetic Resonance Imaging, were too few to be felt. They seem and seemed to cause no adverse effects.
But about 1978 Wertheimer and Leeper made a big fuss with a claim that overhead electric power lines were causing cancer. They observed a doubling of leukemia rates among those in proximity to power lines in a particular area of Colorado. They attributed the increase to the magnetic fields, about 10 milliGauss, caused by the power lines. This set off a flurry of activity. Should I have taken notice at the time and started research on the subject? Ten milliGauss seemed small. I suggested it to a young research fellow but he agreed with me that there was almost certainly an alternative explanation and did not want to waste his time on a useless project.. Another epidemiologist suggested that the power lines went along main roads, and people living thereon had smaller incomes than those living elsewhere, and this was a “confounding” effect (alternative explanation). But this did not stop the flurry of activity.
The was, and is, no plausible explanation of how electromagnetic fields might cause cancer. So Dr Ross Adey, a medial scientist at the University of Loma Linda set out to find one. He believed he had it, when he exposed chicken embryos to a magnetic field. He found that he efflux of calcium ions peaked at 60 Hz. Here was, he became convinced, was the explanation. He became an activist, and , alas, stopped thinking. Other scientists, more careful and with better equipment failed to reproduce his results. Moreover, European activists quoted his results not, apparently realizing that a peak at 60 Hz was irrelevant to the European situation where the power line frequency is 50 Hz.! Another scientist produced data on experimental animals as a function of field on and off, but his data did not have the statistical scatter that was appropriate, and could not have been taken in the way he described. This was done with a government contract to the University of California. If it had been an industry spending government funds, there would perhaps have been an outcry demanding that the government money be returned, but few scientists wanted to challenge the University of California.
There are a number of situations where good safety practice will lead to a comparatively small magnetic field. For power lines, the load should be balanced among the phases and the individual fields will then cancel. Electric heating blankets should be wound with twisted pair wires rather than a single wire. Houses with old fashioned knob and tube wiring will have higher magnetic fields. Presumably it was these that led Grainger Morgan of Carnegie Mellon to propose a policy of “No Regrets” and encourage people to do those mitigation steps which are cheap. This is fine for personal behavior and even for a company which would spend money for good public relations, but to make it a public policy demands a definition. Grainger was insistent that the policy was not the same as “As Low As Reasonably Achievable” recommended for radiation protection. ALARA nowadays has a reasonable definition based on an assumption of low dose linearity for radiation induced cancers. Grainger’s policy had no such definition and that inevitably caused trouble. Lawsuits began to arise. A weekly journal was being published on how to prosecute cases of excessive (whatever that was) electromagnetic field exposure. I realized, somewhat late, that I had to get into the act.
In 1991 a draft document was prepared by Dr Robert Gaughy I believe, for the EPA

suggesting that Electromagnetic fields be considered a “Class C carcinogen”, probably carcinogenic to humans. A review committee was being formed composed mainly of epidemiologist and toxicologists. Robert Park, on behalf of the American Physical Society, and Alan Bromley, President Bush’s Science advisor, pointed out that there should be on the committee someone who understood electromagnetic fields. As I understand it, each was asked to submit a dozen names, and I was on each list and the least objectionable to the EPA! So I was called by the secretary of the Science Advisory Board. His critical question was:“Have you ever taken a public position on electromagnetic fields?” I began my usual nit picking. “Yes. Every Tuesday and Thursday from 9.30 to 11 am before 40 students.” “I did not mean that.” “What did you mean?” “Have you publicly taken a position on whether electromagnetic fields cause cancer?” With a more precise question I could take give a more precise and simple answer. “No”. Interestingly, I found, when I attended my first committee meeting, that I was one of the few who had not taken a public position - most of the committee members had said that they thought that electromagnetic fields can cause cancer!

My involvement with that committee confirmed the importance of adjectives and adverbs. The nouns had been decided in advance. But adverbs could alter the sense. I cannot remember the exact words in the documents, but they were something like the following with my corrections in italics: yes, electromagnetic fields could cause effects on a biological system at some field level. Not necessarily adverse. They might cause cancer. The might cure cancer. And so on. I tried, but failed, to get the committee to recognize three simple facts. The “proponents “ of the hypothesis that power line fields cause cancer used terms that showed they had little understanding of electromagnetic fields. Elementary physics history tells us that EMF stands for “Electro Motive Force”. To use EMF for Electromagnetic Fields” displays ignorance. Also, the energy in a magnet field varies as B2 not as B, and measurements on chemical effects, such the measurements by Jeenicke and myself on modification of scintillation light by magnetic fields show a low field behavior as B2 not as B (168). Yet the proponent epidemiologists were plotting their data versus B, as if B is a scalar not a vector, without saying what B was. Since the AC fields from power lines alternate the average value of B is strictly zero! Presumably they were using a meter produced for the power industry which measures average B2 and plots it as if it were a measurement of B. But the papers never state this. . Moreover none of them seem to have realized that B is a vector. If an adverse effect increases linearly with B and the field is reversed, the effect would become beneficial! More fundamentally, symmetry principles tell us that at low fields, any effect cannot vary as B but can vary as B2. Worse still, there is an old fashioned principle about pollutants: “more is worse, less is better.” The proponent epidemiologists struggle to find a “dose response” relationship with a positive slope, but fail to look at the whole mass of data. Drivers of electric trains are exposed to AC fields of 1 or more Gauss as the electricity is picked up from the overhead wire and deposited in the ground with the train in between. Yet studies of railroad engineers fail to find excess leukemia.
Although I was not able to get the committee to include any words such as these in the report, I did manage to persuade them that the EPA, or the International Agency for Research on Cancer (IARC), classification that is suitable for substances, is inappropriate for electromagnetic fields , and a deeper understanding must prevail.
Alex Shlaykhter and I started collecting data on all studies, by that time about 110 of them, which addressed the issue. The next summer I hired a young Freshman student, Loh, from Malaysia to collect and categorize them Within 6 weeks he and Alex had a fine compilation. I started going to a summer conference of the Bioelectromagnetic Society, which had split into two on this issue. I persuaded them to invite Loh. He gave a fine straightforward description now published (619). Not one study had a Risk Ratio exceeding 2 and the average was below 1.5. One man from the Air Force Research Center in Texas was highly impressed. “I paid $150,000 for a conference of epidemiologists to discuss this issue, and they never came up with anything. Now you have done it all!” He gave us a small contract to continue this work which, inter alia, supported Daniel Kammen for 2 years. At that meeting I pointed out that it was vital that not a single legal case where plaintiffs claimed damages from electromagnetic fields should ever be decided for the plaintiff. If it was, the legal onus of proof would switch from the plaintiff to the defendant. Professor Robert (Bob) Adair, from the Yale University physics department said that here was a case before the California Supreme Court (COVALT vs San Diego Power and Light) right now, and that amicus briefs might be considered if they were submitted within 10 days. It only took me a minute to decide. “I will draft a brief of amicus curiae for the California court, and the counsel will be the Atlantic Legal Foundation. I invite any and all of you to join me as amici”. For various reasons of conflict, only one, Bob Adair, did so. The next day I flew to Washington for a meeting of a committee on Plutonium Management of the American Nuclear Society, chaired jointly hy Glenn Seaborg, and Bill Kennedy. Glenn agreed to join me. I drafted the brief on AMTRAK on my way back to New York, handed it to Martin Kaufman, General Counsel of ALF. Then I went back to Boston and telephoned my friends to sign on as amici. It took little persuasion. Already there were lawsuits totaling in the billions of dollars. Power companies were spending over a billion dollars to put power lines underground. It was likely to consume the entire research budget of DOE. I lined up 6 Nobel Laureates. 2 each in Physics, Chemistry and Medicine I was pleased with the brief. That and two similar briefs in lower courts stopped the legal cases cold. An amusing mistake was made by the plaintiff’s lawyer. He complained to the newspapers that we were just a bunch of physicists who knew nothing about public health. The matter should be left to epidemiologist! But the only reason that I had not persuaded an epidemiologist to join us was that all the epidemiologists I knew were on vacation! But the complaint of the plaintiff’s lawyer gave us an opportunity. Using his public statements as a reason, we successfully petitioned the court to allow the names of three distinguished epidemiologist to join the brief.
But there was more detail to attend to. The National Institute for Environmental Health Sciences had $30 million a year in research money and scientists, even level headed scientists who did not believe in the effect, wanted to keep it. California politicians, as often politically active in environmental affairs, wanted to continue. Neither report paid attention to my concerns and in each case, I put in a very detailed and strong rebuttal to each of their points. The National Center for Radiation Protection and Measurements (NCRPM) had a committee to study the matter, chaired by Dr Ross Adey, a medical scientists who had claimed a peak at 6o Hz of calcium efflux from chicken embryos, a study which has failed to be replicated in more careful subsequent work. Adey was a strong proponent of the idea that magnetic fields are dangerous and must be reduced without further thought. Strong representations was made to NCRPM and the review committee quashed the report. A study committee of the National Academy of Sciences was originally going to be a weak committee. But Dick Garwin got on the committee and ensured that truth and reason would prevail.
Since about 2000 I have heard little more on the subject. I have stated my views in public and on the web but taken no action. But silliness has a habit of re-raising its ugly head and I am wary. There were many others working to bring scientific sense into the system, but I feel that our action in submitting the brief of amicus curiae to the California Supreme Court was crucial. Too few good scientists are willing to enter the legal arena, but so often that is where the action is. I am proud that this is a field where I have spent some of my energies.
Looking back, I realize that epidemiologists were not wrong in expressing their original thoughts. Epidemiologists correctly look for problems and speculate on possible reasons for adverse effects on public health. It becomes natural to postulate a mechanism that they do not understand and may well be outside their expertise. But the critical epidemiologists were completely wrong in not searching for colleagues who had that expertise in electromagnetism to enlighten them. They should have used their notation. When flaws were discovered in their speculative arguments, and the critical epidemiologists became obstinate they ceased to be scientists. This raises the important issues of interdisciplinary research. The problem is when to use data when rigorous scientific proof is lacking. Also how to express an uncertainty in such situations and of how to address that uncertainty in recommendations on public policy and how to be appropriately cautious.