30 ELR 10277 | Environmental Law Reporter | copyright © 2000 | All rights reserved

Genetic Susceptibility and Environmental Risk Assessment: An Emerging Link

A. Dan Tarlock

Mr. Tarlock is a Professor of law at Chicago-Kent College of Law. This Dialogue is adapted from a report prepared for the Illinois Institute of Technology Institute of Law Science and Technology (ISLAT) Working Group on the Environmental Genome Project. A full version of the report will be published as an ISLAT report under the names of the members of the working group. This Dialogue does not represent the position of ISLAT or any member of the working group. Professor Tarlock would like to thank Ms. Rebecca Levin, who received a B.S. from the University of Michigan in 1999 and is a member of the 2002 class at the Chicago-Kent College of Law, for her research and editorial assistance. Special thanks go to Professor Tarlock's colleague and ISLAT director, Professor Lori Andrews, for her patience, support, and willingness to share her vast knowledge of the social implications of genetic research.

[30 ELR 10277]

Since the 1970s, the federal government has imposed progressively stringent regulations on the discharge of hazardous and toxic substances into the air, water, and soil in order to protect the public from the presumed health risks of exposure to these pollutants.1 The acceptance of the precautionary principle by Congress and the courts in the 1970s has led the U.S. Environmental Protection Agency (EPA) and other agencies to base toxic pollutant standards on risk assessments. The use of risk assessments has been criticized from many perspectives. Opponents of stringent regulation have charged that these assessments represent bad or junk science because the data do not support the need for regulation. More moderate or rational critics question that economic benefits generated by standards compared to the costs of compliance. Environmentalists have argued that risk assessments use science to mask the hard policy and value choices involved in standard setting.2 Until recently, however, all participants in the debate have accepted two common assumptions. First, there is some need to protect the population at large and specific sub-populations of at-risk groups, such as children, from the adverse affects of involuntary exposures to specific pollutants. The regulatory focus has been on the prevention of cancer, neurological disorders, and the impairment of male and female reproductive capacity. Second, it would be unfair and inefficient to shift the burden of protection to individuals for a wide variety of pollution risks.3 These assumptions are open to question in light of advances in genetic research.

Toxic pollution and hazardous substance regulation is not yet based on advances in our understanding of the relationship between human genetics and exposure to a potentially dangerous substance, but this could change in the future. Put differently, pollution regulation is not based on individual susceptibility to risk; it is based on group susceptibility. We do not base environmental and occupational health regulation on the possibility that substantial variability in risk exists among individuals within the protected class. We do base some standards on worst-case scenarios; for example, many risk assessments are based on worst-case individual susceptibility. This practice, however, is different from explicitly assuming that each member of a protected class has a different cellular response to exposure or ingestion. The reason is that society normally assumes that all exposures are involuntary, but this is not always the case. Air pollutants are the clearest example of involuntary exposure, but even in this case, those at risk could move to less polluted areas.

Regulators have either had to assume that all persons subject to a specific exposure pathway are equally vulnerable to the same health risk or that exposure levels have been calculated for identifiable sub-populations for whom sufficient information exists that suggests that they are subject to higher exposure risks. These at-risk groups might include children, asthmatics, pregnant women, and members of particular ethnic groups.4 Our assumption that pollution and workplace regulation should be based on statistically observed population susceptibilities rather than the potentially more accurate individual genetic susceptibility to exposure to dangerous substances is at variance with advances in genetic research. For example, exposure to environmental agents at various stages of a child's life from gestation to young adulthood can cause severe damage to developing [30 ELR 10278] systems.5 Our understanding of the relationship between exposure to a toxic and harmful substance and the clinical appearance of cancer is still incomplete, but we now recognize that genetic sensitivity or susceptibility may kick in at any stage of carcinogenesis and may play a large role in explaining what risks actually materialize in specific individuals or sub-groups in the form of illness.6 The actual risk to which an individual is subject is ultimately a function of an individual response to a given dose of a hazardous substance, and this response is a function of individual genetic susceptibility.7 As a leading environmental geneticist has said, "Each person basically has his own fingerprint of drug-me-tabolizing enzymes and receptors, so we all handle drugs [and chemicals] differently."8

These advances in genetic research may now be applied to bear on environmental and workplace safety policy through the National Institute of Environmental Health Sciences' (NIEHS') Environmental Genome Project. The Environmental Genome Project builds on the Human Genome Project. The goal of the new project is to attempt to identify the genes that determine individual susceptibility to environmentally induced diseases. One plan is to select a group of candidate genes "on the basis of their hypothesized ability to influence vulnerability to noxious environmental agents."9 There are over 200 genes known to control susceptibility to environmental diseases. Having identified a number of potentially important genes, subsequent functional and epidemiological studies could then be used to infer individual associations between those genes and environmental response,10 and these links can be made at relatively low cost. Many differences among individuals exist that affect a person's sensitivity to or ability to resist environmentally induced diseases. Preexisting inherited genetic mutations can increase a person's risk of contracting cancer. The genes that we inherit affect the balance of enzymes that can either detoxify or enhance the toxicity of chemicals, causing different sensitivities to an exposure. Substantial differences exist among individuals with respect to the ability of their cells to repair deoxyribonucleic acid (DNA) damage caused by environmental exposure.11 Biological markers may improve the science of risk and open up new risk prevention strategies. This latter possibility has potentially profound implications for regulation designed to minimize public health risks. These risks include the presumed cellular responses to the effects of genotoxins,12 but there are many other potential uses of genetic information. When the information is combined with external factors such as occupational exposure or lifestyle, scientists can give more informed answers to questions such as why do some smokers get cancer and others do not, why certain groups have higher incidents of cancer after exposure to a toxicant and others do not, and why certain women are more prone to breast cancer.

Our current regulatory strategy for toxic pollutants is second-best. Ideally, regulation would be based on deterministic causal relationships between exposure and illness or genetic mutation, but this level of certainty is not possible13 through the use of either epidemiology or medical genetics. Epidemiology is the most reliable science to help understand these connections,14 but it remains difficult to substantiate [30 ELR 10279] the chain of media discharge, exposure, and the resulting human illness or death with the desired level of confidence. We do not know the role that genetic susceptibility places in cancer rates with the necessary confidence level15 to set discharge standards. Science can suggest but not conclusively establish links between exposure and illness. Due to the many practical and ethical difficulties of planning epidemiological studies of high-risk populations, regulators have been forced to aggregate presumed at-risk populations and draw inferences from biological processes and theories about the statistical probability of disease, death, or other health problems.16 The result has been "conservative" discharge standards designed to protect the public from assumed but not yet substantiated risks. Environmental law is based on scientifically "conservative" risk assessments.17 This practice forms the basis of the precautionary principle, which is the legal basis of all risk assessment, and its policy application, risk management. The principle bridges the gap between present and future states of knowledge.

During the 1970s, when the environmental theory of cancer became the basis of federal cancer policy, the scientific issue centered on the proper dose-response curve. The primary regulatory issue was whether there was a safe threshold of exposure or not. Federal agencies used the linear, no-threshold model, which presumed "that the dose-response curve extends linearly to the origin (at least for low-level exposures), that there are no thresholds, and that a single hit is sufficient to induce cancer."18 This model was generally based on extrapolations from animal experiments to humans. Environmental and occupational health and safety regulation is still based on scientific inference and mathematical models. As long as we are convinced that we have begun to reduce a risk, "conservative" risk reduction strategies are legitimate.19 Ultimately, we do not care how many people actually die or suffer serious consequences from exposure to pollutants and hazardous substances. We do not care because we do not know, and we have made a societal decision that can be traced to the decision to cancel the registration of dichlorodiphenyltrichloroethane (DDT) in 1970 and that we cannot wait for precise scientific information before we act to prevent health risks, especially those likely to cause cancer and genetic mutation. We have based environmental regulation on risk assessment and management. Risk assessment tries to calculate exposure levels and possible dose-response curves. These are often based on extrapolation from laboratory animal studies or scattered epidemiological studies. Risk management seeks to calculate the costs and benefits of protection from different levels of exposure and to choose the appropriate protection level. These are mixed scientific inferences and value judgments.

Regulators still rely on scientific extrapolations from laboratory animals to humans, because we cannot set up human control groups on which to test exposure levels. We are, of course, in fact running experiments by exposing society to different substances and then collecting the epidemiological evidence about the results, but we cannot formally subject different groups to different dose levels. The evidence is inferential and abstract and thus relies on possible average dose-response curves and aggregate damage estimates, e.g., risks per million and lives saved or deaths postponed per million. We have had to assume that all individuals within a defined population have the same biological response to equal doses of a carcinogen. Much conservative standard setting is driven by societal fear of exposure to cancer causing agents.20 This practice was recently validated by the Presidential/Congressional Commission on Risk Assessment and Risk Management, which noted that "the policy of presuming that a chemical causes cancer when tested in laboratory rodents is potentially carcinogenic in humans is justified by considerable evidence and by the precautionary principle of being protectivewhen uncertain."21

Cancer theories have changed substantially since the 1970s, but the law has not yet responded to these changes. Environmental law is still premised on the one-hit theory of cancer that posits that there are no safe exposure thresholds. As cancer researchers increasingly focus on genetic explanations of cancer, these theories are being replaced by theories that examine how environmental factors may act in conjunction with genetic and acquired susceptibility. The scientific validity of the one-hit theory has now been questioned by one of the originators of the theory,22 and modern genetic theory suggests that cancer is caused in part by the genetic susceptibility of individuals. In short, cancer is more likely to be the result of multiple hits rather than a single hit as previously assumed.23 But, the one-hit hypothesis may still be valid in some circumstances.

[30 ELR 10280]

The First-Order Implications for Environmental Regulation

The first-order implication is that genetic information is now a relevant source of scientific information in the assessment of the risks of toxic and hazardous substances and other pollutants. Science-based regulation must adapt to new information. Advances in genetic understanding may influence the way in which regulators conduct risk assessments. At this time, it is not clear if risk management strategies will change, but this possibility cannot be discounted. We do not know if genetic research will provide us with a clearer understanding of the link between environmental exposure and illness at the level generality necessary to make changes in our environmental and workplace regulatory strategies. Specifically, we do not presently know whether a particular individual's genetic makeup can increase cancer and other health risks after exposure to an environmental agent even if, in the aggregate, people with that susceptibility present a higher risk.24

The first step in understanding the potential implications of the Environmental Genome Project for environmental regulation is to compare the objectives of genetic research and risk assessment. Genetic research proceeds from the opposite assumption from conventional environmental risk assessment. Genetic research seeks to isolate the information encoded in DNA molecules to yield information about human predisposition to disease and other adverse human health impacts. As the forensic use of DNA evaluation has taught us, the sequence of nucleotides is unique for each individual. An individual's genetic background—genetic polymorphism—determines his or her sensitivity todisease-causing agents. Modern cancer research is focused on the relationship between an individual's genetic makeup and environmental exposure to carcinogens. Much of the research of genetic predisposition will have no direct relevance to environmental regulation because some people will incur cancer regardless of any environmental exposure.

Second-Order Effects: From Societal to Individual Responsibility

Environmental and to a lesser extent occupational health regulation assumes that exposure is involuntary and thus the focus is always on the group level. The major legal and moral ramification of this is either that the individual has no responsibility for self-protection because there are no reasonable, effective steps that an individual can take to avoid the risk or that the producers of the waste product or toxic substance are the cheapest cost avoiders. We do not think of individuals voluntarily increasing their risk exposure because they think that the government will bail them out. Another important ramification is the recognition, well recognized among those who work in the area of clinical genetics, that the disclosure of susceptibility information to target groups may stigmatize individuals in the group. The trauma may be the wholly internal fear of the disclosed risk materializing. It may also reflect real lost employment and personal relationship opportunities. Involuntary risk exposure is the opposite of the moral hazard problem. One of the central criticisms of current risk assessment practices is that the psychological costs of being at risk are underestimated. The major policy long-run implication of the Environmental Genome Project is that it could shift the responsibility for risk minimization from society to the individual.

At the present time, we lack the information to "force" greater individual responsibility for most harms that result from general environmental exposure. Groups can vary in size from the entire nation to a small ethnic sub-population. However, once a person is a member of the protected group, all members of the group are assumed to be equally at risk. We are presumed to be "victims" of environmental pollution with little or limited capacity to mitigate the harm of exposure. For example, asthmatics and other at-risk populations are not expected to move from ozone nonattainment areas designated by the Clean Air Act. At most, they are expected to refrain from strenuous activities on ozone alert days.

There are many possible outcomes of the Human and Environmental Genome Projects that could influence future risk assessment and management. It is possible that the projects will not produce sufficient information about individual genetic variability to warrant a change from the existing risk reduction strategy. Three other outcomes seem more likely. First, the study could produce information to identify new at-risk classes. This would support the growing environmental justice movement and provide more credible scientific support for existing regulations or more stringent regulations. One strand of the movement posits that existing environmental regulations under-protect minority populations; for example, minority groups who consume higher levels of contaminated fish. The Presidential/Congressional Commission on Risk Assessment and Risk Management assumed that standards would only go up not down.25 Second, the strategy could both identify those individuals who are susceptible to adverse consequences from exposure and could identify individual mitigation strategies. This is more likely in the workplace, but one cannot exclude the use of genetic information to alter human behavior to lessen the risks of pollutant and toxic substance exposure. Identified "at-risk" individuals can be medically monitored and subjected to preventive strategies, including, perhaps, prophylactic surgery to remove susceptible tissues.26 To date, medical monitoring has been a victim's remedy in toxic tort and Superfund suits. Some-times it is the primary remedy, and in other cases, it is a consolation prize for the general denial of recovery for the tort of increased cancer risk.27 However, genetic information would be welcomed by those who argue that current regulations over-protect and are economically inefficient. Third, the research could undermine the scientific basis of existing health-based regulation by demonstrating that assumed dose-response curves are grossly inaccurate.

[30 ELR 10281]

The results of scientific research cannot be predicted or ultimately channeled in an open society. As long as there is widespread access to the information—as there will be—groups are free to interpret the information in their self-interest and to convince legislators and regulators to do the same. The head of the Environmental Genome Project, Kenneth Olden, has recognized this and stated that the results of the project may be to provide evidence for both under and over regulation of human health risks. This said, it must be recognized that genetic research has positive and negative consequences for society and is as much a social as it is a scientific problem. For better or for worse, the environmental movement shattered the idea that all advances in science were progress. Instead, it established the idea that the societal consequences of new applications of science and technology must be carefully assessed before they are applied.

The Two Cultures of Environmental/Workplace Protection, Genetic Research, and an Interim Strategy

There is a well-established community of legal scholars and ethicists who have been studying the legal and ethical impacts of the use of genetic information. The environmental and occupational health community has much to learn from the genetics community, but environmentalists and those who study the use of genetic information to treat or to stigmatize specific individuals have divergent cultures. The two cultures, to borrow from C.P. Snow's famous explanation of the differences between science and the humanities, can roughly be described as the science of hope or optimism versus the science of concern or fear.28 Science has served the environmental movement by providing the basis for stringent regulation, and more often than not advances in science have reinforced the argument that substantial health and ecosystem risks need to be addressed. Thus, environmental protection advocates express science optimistically, although they are prepared to regulate beyond the levels justified by epidemiological science on ethical grounds. The enemy, as it were, is usually not science but benefit-cost analysis. Students of the use of genetics are much more concerned about the use of science because the impact on an individual can be drastic. A person may lose benefits, suffer the psychological trauma of an increased or unanticipated stigma. The genetic community has expressed great concern, grounded in earlier abuses of theories of eugenics, of the risks that the disclosure of genetic information will be used to put humans in a worse position than they were before the disclosure.29

These two cultures exist, and the second—the culture of concern—has defined the ethical terms of the genetics policy debate. The first step is to integrate the two cultures. Professor Wendy Wagner of Case Western University has usefully identified two concerns about genetic information: (1) overuse, and (2) under use. The concern with overuse is that genetic information will be used to disadvantage genetically susceptible individuals. Genetic screening could deny work opportunities, insurance coverage, and other societal benefits and cause profound and disturbing changes in a person's self-image. The specter of the earlier fascination with eugenics to build an ideal society that culminated in Nazi Germany looms over this debate. The ethical and legal issues associated with an individual's right not to have his or her genetic makeup disclosed when it is against the individual's interest are developing rapidly. The use of information to change the victim status of those exposed to pollution by forcing them to take individual avoidance steps must be added to this list.

Genetic information has many positive uses for society, but the costs and benefits of this information will be borne by different groups in society and, thus, could lead to under use. These benefits, in the aggregate, include reduced medical costs and early intervention to prevent disease or death. Greater occupation screening could avoid susceptible worker exposure and reduce a company's medical costs. Any gains would, of course, have to be compared to the monetized and unmonetized costs to screened workers. Genetic information could result in additional levels of environmental protection if it reveals under-protected groups. More generally, it could be part of a comprehensive comparative risk assessment effort that would better target regulatory resources to the highest probability for public health and ecological risks. For example, if certain at-risk groups can mitigate their exposure and risk through individual and group exposure avoidance, it might even be cheaper to subsidize these efforts than to require across the board pollutant reductions which create very low probability risks for the vast majority of a nongenetically susceptible population. For example, occasionally a Superfund remedy has removed populations from contaminated areas because removal was cheaper than cleaning up the contaminated soil, of which Times Beach, Missouri, is the most notable example.30

Economists have identified the problem of moral hazard as a substantial barrier to the efficient allocation of resources. That is, people assume risks with the knowledge that society will bail them out in whole or in part when the risk materializes and injures the individual or causes property damage. For example, people build in floodplains because we subsidize flood protection and post-flood relief even though we know that the more we spend on flood control, the more flood damages increase. The larger lesson is that in general, we as a society have been reluctant to make individuals responsible for avoiding most risks. However, if the links among individual risk, avoidance methods, and the costs to society become clearer, the case for new avoidance strategies becomes stronger.

One important lesson for environmental and occupational regulation that the genetic research community teaches is that the most immediate problems may come from the information byproducts of the project. Environmental standards are unlikely to change because the genetic information will be too uncertain to support a completely new approach to environmental and workplace health protection. However, the information generated by the project could be used to stigmatize groups, to deny insurance and medical [30 ELR 10282] benefits to certain groups, or to raise the costs of health care for these groups.

As this project moves forward, the environmental community must monitor it closely. The precautionary principle is ultimately based on advances in science and implicit in it is the idea that new information can confirm or modify the need for initial conservative standards. The best interim policy guidelines to follow are: (1) that no existing standard should be changed without extensive peer review of the science, opportunity for public comment (including lay comment), and full compliance with the notice-and-comment procedures of the Administrative Procedure Act (APA) because of the present difficulties of establishing clear associations between genetic variants and environmental exposures; (2) if research is used to lower standards for any currently protected group, the regulatory agency must fully comply with the APA, include a monitoring and mid-course correction process in any regulation, as was attempted with the 1992 Clean Water Act, and provide a credible, peer-reviewed, scientific justification for the new standard; and (3) the incorporation of possible genetic information scenarios in the EPA's comparative risk evaluations should be done with full disclosure of the uncertainties surrounding the use of this information.

1. Recently, concern has been expressed about chemicals that function as "endocrine disrupters," but the scientific jury is still out on the level of risk. Noah Sachs, Blocked Pathways: Potential Legal Responses to Endocrine Disrupting Chemicals, 24 COLUM. J. ENVTL. L. 289 (1999); NATIONAL RESEARCH COUNCIL, HORMONALLY ACTIVE AGENTS IN THE ENVIRONMENT 411-14 (1999).

2. E.g., Mark Elliot Shere, The Myth of Meaningful Environmental Risk Assessment, 19 HARV. ENVTL. L. REV. 409 (1995); Wendy E. Wagner, The Science Charade in Toxic Risk Regulation, 95 COLUM. L. REV. 1613 (1995).

3. William Rodgers, Legal Aspects of Genetic Susceptibility to Environmental Exposures, ISLAT workshop paper (on file with author), cites a counter example. To deter people from swimming in a polluted slough near Portland, Oregon, warning signs have been posted in six languages.

4. Id. (discussing the case approving dioxin levels for the Columbia River, Dioxin/Organochlorine Ctr. v. Clarke, 57 F.3d 1517, 25 ELR 21258 (9th Cir. 1995), which pointed out the difficulty that extra-risk subpopulations have in being counted in risk assessments).

5. William A. Suk & Gwen W. Coleman, Genes and the Environment: Their Impact on Children's Health, 106 ENVTL. HEALTH PERSP. 817-20 (1998).

6. Harri Vanio, Biomarkers in Metabolic Subtyping—Relevance for Environmental Cancer Control, 20 ARCHIVES OF TOXICOLOGY SUPPLEMENT 303-10 (1998).

7. Christopher J. Portier & Douglas A. Bell, Genetic Susceptibility: Significance in Risk Assessment, 102-103 TOXICOLOGY LETTER 185 (1998).

8. Environmental Institute Lays Plans for Gene Hunt, 278 SCIENCE 569 (1997).

9. Patrick O. Brown & Leland Hartwell, Genomics and Human Disease—Variations on Variation, 18 NATURE GENETICS 91 (1998).

10. Much of the research may not be directly relevant to pollution regulation, but it will be more directly relevant to workplace regulation and policies on lifestyle choices. Ideally, environmental and work-place regulation would target those most at risk from specific exposures. It was not possible to do this in the 1970s when environmental and workplace regulation was put in place. Epidemiological research could not provide this level of precision and regulators have been forced either to assume that the normal variability among responses to environmental exposure is small throughout the population or that if society protects the sub-population assumed to be subject to the highest level of risk from the presumed risks of exposure, all people are adequately protected.

11. Focus, Biomarkers: The Clues to Genetic Susceptibility, 102 ENVTL. HEALTH PERSP. 50 (1994).

12. Paul W. Brandt & Sherry I. Brandt-Rauf, Biomarkers—Scientific Advances and Societal Implications, in GENETIC SECRETS: PROTECTING PRIVACY AND THE CONFIDENTIALITY IN THE GENETIC ERA 184 (Mark A. Rothstein ed., 1997).

13. See SANDRA STEINGRUBER, LIVING DOWNSTREAM: AN ECOLOGIST LOOKS AT CANCER AND THE ENVIRONMENT (1997), for a very lucid effort to survey the relationship between environmental agents and cancer that comes to the reluctant conclusion that we still do not adequately understand the relationship between exposure and the disease.

14. The common-law requirement that a plaintiff prove that the defendant in fact caused an injury is based on a mechanistic theory of cause. Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579, 23 ELR 20979 (1993), enshrined this theory of cause in the Federal Rules of Evidence. The net result is that it is increasingly difficult to recover damages for risk exposure. Daubert has been read to require the rejection of asserted causal links if it is not supported by epidemiological studies. E.g., In re Paoli R.R. Yard PCB Litig., 35 F.3d 717, 743, 25 ELR 20989, 20997 (3d Cir. 1994). The high standard for cause in fact is based on a corrective justice model of liability. Judge Weinstein stated in In re Agent Orange Prod. Liab. Litig., 597 F. Supp. 740, 751 (E.D.N.Y. 1984), aff'd, 818 F.2d 145 (2d Cir. 1987), that in a tort action as opposed to an action to review a risk-based regulation, "a far higher probability (greater than 50 percent) is required since the law believes it unfair to require an individual to pay for another tragedy unless it is shown that it is more likely than not that he caused it." See also Guido Calabresi, Concerning Cause and the Law of Torts: An Essay for Harry Kalvin Jr., 73 U. CHI. L. REV. 69 (1975). The corrective justice model does not apply to risk prevention regulation. A lesser standard of proof is appropriate for public health-based regulation. Liability can be justified as a form of tax imposed on those who directly profit from harmful activities and which is fairly spread over larger segments of the population. Fortunately for the sustainability of governments, we never require a close causal relationship between revenue intake and government performance. However, the U.S. Supreme Court's increasing reliance on common-law baselines to judge the constitutionality of government regulation may require a higher standard of cause in fact for risk prevention regulation than the current precautionary one. The Supreme Court's treatment of liability "tax schemes" is mixed. Usrey v. Turner-Elkhorn Mining Co., 428 U.S. 1 (1976), upheld the Black Lung Benefits Act of 1972, which required coal operators to compensate miners who were no longer employed in the industry because the Act was "a rational measure to spread the costs of the . . . disabilities to those who have profited" by them. Id. at 18. Concrete Pipe & Prods. of Cal. v. Construction Laborers Pension Trust for S. Cal., 508 U.S. 602 (1993), held that Congress could impose with-drawal liability from a pension fund although such liability was not in the contract. But the plurality opinion in Eastern Enterprises v. Apfel, 118 S. Ct. 2131 (1998), held that the application of the Coal Industry Retiree Health Benefit Act of 1992 was a taking as applied to a mining company that had ceased operations and did not participate in a series benefit plan established under a National Bituminous Coal Wage Agreement that required operators to contribute to retiree health plans so long as they remained in the coal business. The opinion acknowledged that the case was not a classic taking case because there was no appropriation of a property interest and that Congress can impose retroactive liability in national legislation that adjusts the benefits and burden of national economic life. However, it found that the Act interfered with the company's investment-backed expectations. "Our decisions . . . have left open the possibility that legislation might be unconstitutional if it imposes severe retroactive liability on a limited class of parties that could not have anticipated the liability, and the extent of that liability is substantially disproportionate to the parties' experience." Id. at 2149. Justice Kennedy concurred in the result but not in the Court's taking analysis because the Act under the Due Process Clause did not affect an obligation relating to a specific property interest. Id. at 2156.

15. Susceptibility is more important in occupational settings where exposure is presumed to be restricted to acceptable risk. Stanley Venitt, Mechanisms of Carcinogenesis and Individual Susceptibility Cancer, 40 CLINICAL CHEMISTRY 1421 (1994).

16. David P. Herrington & Alice S. Whittemore, Defining, Identifying and Studying High Risk Families: Developing Cohorts for Epidemiological Study, 17 J. NAT'L CANCER INST. MONOGRAPHS 91 (1995).

17. This Dialogue adopts the dichotomy between risk assessment and risk management. Risk assessment attempts to quantify risks and risk management uses assessment information to set the level of risk protection and to chose the policy instruments to achieve this level.


19. Lisa Heinzerling, Regulatory Costs of Mythic Proportions, 107 YALE L.J. 1981 (1998); Lisa Heinzerling, Environmental Law and the Present Future, 87 GEO. L.J. 2025 (1999).

20. PROCTOR, supra note 18.


22. Bruce N. Ames, Six Common Errors Relating to Environmental Pollution, 7 REG. TOXICOLOGY & PHARMACOLOGY 281 (1987).

23. The shift in thinking and its possible regulatory consequences is summarized by the Presidential/Congressional Commission on Risk Assessment and Risk Management, created by the 1990 Clean Air Act Amendments. PRESIDENTIAL/CONGRESSIONAL COMMISSION ON RISK ASSESSMENT AND RISK MANAGEMENT, supra note 21, at 63-78.

24. Portier & Bell, supra note 7.


26. Frederick P. Li, Cancer Control in Susceptible Groups: Opportunities and Challenges, 17 J. CLINICAL ONCOLOGY 719 (1999).

27. The tort of increased risk of cancer has been recognized. See Buckley v. Metro N. Commuter R.R., 957 F.2d 1337 (2d Cir. 1996). However, most courts have rejected such a tort because it would require compensation for speculative damages. The courts that recognize it make it very difficult to recover. The Supreme Court of California recognized the tort in Potter v. Firestone Tire & Rubber Co., 863 P.2d 795 (Cal. 1993), but the plaintiff must prove that it is more likely than not that the cancer will occur.


29. Colin L. Soskoine, Ethical, Social, and Legal Issues Surrounding Studies of Susceptible Populations and Individuals, 105 ENVTL. HEALTH PERSP. 837 (1997).

30. The community of Times Beach, Missouri, was contaminated with large amounts of dioxin as a result of the improper disposal of waste oils. So substantial was the contamination that EPA purchased numerous homes and moved families from the area, thereby making that area the object of considerable investigation of dioxin soil contamination.

30 ELR 10277 | Environmental Law Reporter | copyright © 2000 | All rights reserved