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COPYRIGHT 2007 Stanford Law School
INTRODUCTION
I. THE DANCE OF LEGAL AND PHYSICAL INJURY A. The Latency Problem in Toxic Torts 1. Emergence of nontraditional tort theories 2. The asbestos controversy 3. Jurisprudence of ambivalence: Physical injury as a predicate to "risk-based" recovery 4. Requiring, injury to detect injury: The medical monitoring, paradox B. Genomics and Toxic Tort Law: Two Onrushing Freight Trains 1. Opening, the "black box": New intermediate biomarkers 2. Power, speed, and seale: Whole genome research 3. Emerging, fields: New molecular tapestries C. Implications: Challenging the Risk-Injury Divide II. EXPLORING THE RISK-INJURY DIVIDE A. "De Minimis Effects" or "Reversible Effects" Model B. "Significantly Enhanced Risk" or "Diseased State" Model C. Genomics and the Risk-Injury Divide 1. Genomics and "de minimis effects" 2. Genomics and the "diseased state" conception a. Objectivity and permanence b. Failure to repair c. "Early-stage disease" biomarkers D. Implications: The nebulous concept of physical injury III. TOWARD a NUANCED CONCEPTION OF INJURY AND REMEDY FOR THE GENOMIC AGE A. Reconsidering, Intermediate Remedies B. Physical Injury in the Context of Remedy: The Rainer Decision C. Medical Monitoring, in the Genomic Age: Recognizing, Risk or Redefining, Physical Injury? 1. Risk as legal injury: Returning to original conceptions of a nontraditional tort 2. Rethinking physical injury D. Future Convergence of Remedies E. Genomics and Toxic Tort Law: Unbridled Liability or Risks Without Remedies? CONCLUSION
INTRODUCTION
Advances in molecular biology and genomics are poised to transform current conceptions of "risk" and "injury" in the law of toxic torts. (1) The legal system has yet to anticipate or plan for this emerging reality. This Article argues that if the law remains wedded to conventional notions of injury, it will ignore the fruits of a scientific revolution and thus may forego new remedial opportunities that could benefit both plaintiffs and defendants in the end.
An elemental principle of personal injury law is that plaintiffs must demonstrate "harm" in the form of physical injury prior to recovery. The modern world of synthetic chemicals and toxic torts has challenged this bedrock principle. Unlike traditional accidents involving broken bones or other immediate and obvious injuries, toxic exposure may breed diseases whose symptoms take years to manifest. These delayed effects can create intractable barriers for tort plaintiffs, potentially undermining the law's deterrent and corrective justice functions. Thus, toxic torts pose the novel question of whether plaintiffs exposed to toxic hazards and placed at significant risk of disease--yet perhaps not physically "injured"--should nonetheless be entitled to some form of legal remedy.
In recent years, several nontraditional claims have evolved to help toxic tort plaintiffs overcome traditional barriers to recovery, including claims for "mental distress," "enhanced risk," and "medical monitoring." Courts are now struggling with these developments, some of which serve important fairness and deterrence goals, yet arguably may divert resources from the truly impaired and unsettle established tort doctrine. Fueled partly by recent asbestos litigation, in which claims by the allegedly "unimpaired" have overwhelmed court dockets, the "latency problem" has emerged as one of the most critical issues in modern tort law. The genomic revolution promises to make this problem even more salient and controversial in the future. (2)
Remarkably, the debate over the tort system's role in responding to risks of toxic hazards all but overlooks emerging science. While commentators engage in abstract normative discussions of whether the law should remedy for latent "risk" versus concrete "injury," I argue that science may no longer support this conceptual dichotomy. New genomic technologies will strike at the core of the current risk-injury divide.
This is happening because foundational developments in molecular biology, fueled by the application of new genomic technologies since the 1990s, are enabling progressively fine-tuned observation of the effects of toxic substances on the body and the role of genetic makeup in modifying those toxic effects. The identification of new biological markers or "biomarkers" at the genetic and molecular levels has allowed scientists to characterize a number of previously undetectable, intermediate events between chemical exposure and environmentally induced disease. New high-speed, high-volume technologies, such as DNA "microarrays," are generating new kinds of biomarkers at an unprecedented rate and level of resolution. And as observational techniques evolve, scientists can test for suites of biological changes, providing more information than the genome alone can reveal. As a result, science may detect evidence that bodily integrity has been compromised long before classic clinical symptoms emerge.
Yet despite these developments, I argue that the law clings tenaciously to an older scientific model. Although the case law addressing subcellular damage is limited and has not yet addressed the fruits of "whole genome" research, most courts have treated such damage as benign, de minimis, or otherwise legally inconsequential. (3) Courts greatly prefer to draw bright lines between risk and injury, and continue to place the boundary at proof of classic medical symptoms or overt impairment. And indeed, this was fitting in an earlier era, when research tools were insufficient to identify many intermediate effects or to establish their relationship to ultimate disease--giving birth to the metaphor of disease emerging from an impenetrable "black box." (4) But these traditional legal presumptions about when "risk" translates to "injury" or disease may become less appropriate or desirable in the future.
Challenging this conventional framework, I draw upon the scientific literature to illustrate a growing "middle ground" between de minimis effects and classic medical symptoms. It follows that certain asymptomatic conditions, though perhaps not qualifying as fully developed (and hence fully compensable) "illness" or "disease," may nevertheless constitute risks or injuries that merit some form of legal recognition. New technologies lend support to my claim through their ability to identify damage to the body's repair functions. And so-called "early-stage" disease biomarkers may represent not only risk but the presence of disease itself. Thus, I argue, newly identifiable subclinical events may themselves represent substantially enhanced risk of disease or even a "diseased state."
Not only is the law failing to anticipate emerging science, but it may also be moving at cross purposes. For example, a growing number of jurisdictions require plaintiffs to show separately compensable physical injuries in the form of overt disease prior to recovering for medical monitoring. (5) Yet a defining feature of this cause of action, as it evolved to address the perils of toxic hazards, (6) is that exposed plaintiffs need not prove physical injury prior to recovery. This principle is grounded in pragmatism, as the very purpose of monitoring is to detect the onset of disease and allow for preventive medical intervention. Indeed, preventing disease progression at earlier stages may reduce treatment costs, limit future personal injury claims, and ultimately reduce health care costs for the nation. By forcing plaintiffs to attain late-stage injury, toxic tort law may actually discourage medical interventions that could benefit defendants and plaintiffs alike. Hence, recent legal developments not only undermine monitoring's preventive and deterrent functions, but run counter to a primary goal of twenty-first century medicine, which is to detect, prevent, and treat disease at the molecular level. (7)
Therefore, I conclude that the judiciary's retreat from medical monitoring may be coming at precisely the time when increased attention to this remedy is necessary. As research opens up new possibilities for ever-earlier medical intervention, society will need to consider whether a legal system whose remedies depend on unclear and perhaps outmoded notions of "physical injury" reflects sound science or appropriate legal policy. Limited relief for monitoring, where plaintiffs can prove the necessary elements, may appropriately balance deterrence and legal restraint in an age of accelerating scientific change.
Part I of this Article provides a snapshot of the remarkably unsettled legal landscape that the molecular-genomic revolution is soon to confront. Illustrating judicial ambivalence toward nontraditional tort theories, I highlight the growing role of a "physical injury" requirement in claims based presumptively on exposure and risk. In particular, I note the irony of requiring separately compensable injuries as predicates to medical monitoring recovery. And while a frequent justification for the injury requirement is to create a principled standard for separating valid from speculative claims, there is no consistency in the courts as to how to define physical injury. This Part also introduces elements of the new science most relevant to the future of toxic tort law. In brief, I suggest that as new molecular biomarkers blur the boundaries between risk and injury, health and disease, the oft-stated presumption that tort law provides remedies for injury but not for risk may prove to be a distinction without a difference. The concept of physical injury, already a tenuous standard for assigning legal rights and remedies, will become even more opaque as science observes the mechanisms of toxicity at the subcellular level. Courts will need to rethink just where in the exposure-disease continuum remediable injury or harm has occurred.
Part II situates future scientific discoveries in the existing doctrinal landscape, examining case law dealing with subcellular damage and other subclinical effects of toxic exposure. I suggest that two competing conceptions undergird these decisions and offer these two models as heuristic devices for thinking about the implications of the genomic revolution for the future of toxic tort law. The first model, clearly the dominant view, treats subcellular damage as benign, de minimis, or, at best, legally inconsequential "risk." The alternative model, which I label the "diseased state" model, presumes that although disease may be undetectable using traditional techniques, it may nevertheless be present and ongoing, and thus the latency period may be shorter than classic medical symptoms would suggest. In applying the new science to both models, I argue that although the new data could be used to support either view, over time genomic tools may provide additional ammunition for the "diseased state" view. As a result, certain subcellular events may need to be treated as "injuries" rather than "risks," at least for certain types of claims. Viewed another way, society must decide when indicators of future harm are sufficiently predictive to qualify as harms in themselves--particularly where early intervention could thwart the ultimate disease. In sum, new molecular discoveries may represent risks or injuries that may justify certain measured remedies.
Part III discusses how the law should respond once this new generation of subclinical information inevitably finds its way into the courtroom. As can be expected, evidence of subclinical biological effects and susceptibilities may serve as ingredients for a new generation of tort claims based on exposure, risk, or the earmarks of developing disease. I argue that tailored relief for medical monitoring may be more worthwhile, and less speculative, than a new generation of claims for enhanced risk, mental distress, or "personal injury" based on subcellular damage. In essence, as technology continues to move toward earlier detection and treatment, the law may need to adapt by either: (1) recognizing the reality of "risk" while tailoring the remedy (e.g., monitoring funds), or (2) avoiding "risk" rhetoric altogether and redefining physical injury to include subcellular damage where the monitoring remedy is sought. More globally still, in the genomic age, society may need to rethink physical injury in the context of the requested remedy. For the present--until such time as science can determine just when bodily integrity has been compromised--I suggest that the law should maintain a risk-oriented framework for medical monitoring.
Next, anticipating justifiable concerns about opening the floodgates of litigation, I argue that monitoring claims will be limited by transaction costs, barriers to class certification, and other access barriers rarely discussed in this context. Moreover, while I present asbestos litigation as a useful metaphor for understanding the legal status of non-impairing conditions, I also argue that the asbestos problem is unique and must be distinguished from problems posed by genomics. (8) In this vein, I similarly distinguish the Supreme Court's holding in Metro-North Commuter Railroad v. Buckley, (9) which denied a monitoring claim for "lump-sum" damages in an asbestos case arising under the Federal Employers' Liability Act (FELA). (10) The Sixth Circuit's decision in Rainer v. Union Carbide Corp., (11) which denied a personal injury claim based on subcellular damage, provides hints of alternative litigation scenarios for the future.
Finally, I conclude that the blurring of risk and injury in the genomic era ultimately may lead to a convergence of remedies. Where science can not only diagnose but also treat disease at the molecular level, medical monitoring would be converted into the equivalent of a compensatory damage remedy--yet with damages greatly reduced from the damages of today. Indeed, monitoring may prove to be not just an intermediate legal remedy, but a transitional remedy in the law of torts. This future convergence of monitoring and personal injury claims will demand entirely new ways of thinking about tort law's treatment of "latent" harms.
I. THE DANCE OF LEGAL AND PHYSICAL INJURY
This Part sets the stage for thinking about the future of toxic tort law in the genomic age. In so doing, it examines the interplay of concepts of physical injury and legal injury in contemporary tort law. The concept of physical injury, the fulcrum upon which legal rights and remedies traditionally have been balanced, is an elusive one, and will become even more so in the future. This Part illustrates how an unsettled legal landscape is soon to confront a complex, increasingly controversial, yet enormously beneficial area of science, as new and powerful technologies move toward practical application. The genomic revolution will present the courts with formidable challenges, yet opportunities to fashion new remedies and create new efficiencies must not be overlooked in the process. The danger is that the coming inundation of highly complex information could prove so overwhelming and controversial that courts will retreat to the relative clarity and simplicity of traditional medical symptoms, hence reinforcing the conventional risk-injury divide.
A. The Latency Problem in Toxic Torts
Toxic tort cases are widely recognized to have features that distinguish them from the traditional "accident" paradigm that the tort system is best equipped to address. Unlike traditional accidents, toxic exposure often results in diseases for which symptoms may not develop for significant periods of time. (12) Hence, among the many features that make toxic injuries problematic is that they are often latent, and such delayed effects aggravate the problem of proving causal relationships. (13) These and other features are widely recognized to create barriers for tort plaintiffs, (14) potentially undercutting the deterrent effect of civil liability.
1. Emergence of nontraditional tort theories
In recent decades, a variety of theories have evolved to help plaintiffs overcome traditional barriers to recovery in cases involving latent harm from toxic exposure. (15) Such theories support recovery for "mental distress," (16) "enhanced risk of disease," (17) and "medical monitoring." (18) These nontraditional (or newly adapted) (19) theories are significant because they redefine what constitutes a legally cognizable injury (20) and hence limit the amount of evidence needed to show causation. (21) For example, for a mental distress claim, the legally cognizable injury is characterized as the plaintiff's current suffering due to fear of developing disease in the future. (22) In the enhanced risk cause of action, the legally cognizable injury is the present risk of future disease. (23) In a medical monitoring claim, the legal injury is variously characterized as the imposition of costs of periodic checkups, (24) the exposure and the need for monitoring, (25) or "the invasion of [plaintiff's] interest in being free from the economic burden of extraordinary medical surveillance." (26) Under these alternative theories, the tradeoff for the reduced evidentiary burden of proving injury and causation is a nontraditional remedy or reduction in recoverable damages. (27)
This expansion of the universe of legally cognizable harms has piqued impassioned debate in the courtroom and the academy. Perhaps what makes these claims most intriguing is that the normative arguments for honoring them are as persuasive as the arguments for limiting or even eliminating them. Supporters of post-exposure, pre-symptom claims argue that the fundamental objectives of modern tort law, both moral (corrective justice and individual fairness) (28) and utilitarian (deterrence and loss spreading), (29) are better served if liability for toxic hazard is based on risk of injury rather than on actual occurrence of physical harm. (30) In the absence of alternative remedies, toxic torts would go seriously underdeterred. (31) Moreover, some have suggested that imposing a significant risk of disease is an affront to personal autonomy or dignitary interests, (32) making the absence of physical injury normatively irrelevant.
Critics counter that these alternative theories represent a major disruption of the longstanding intellectual framework. (33) Whether characterized as new tort theories or adaptations of earlier ones, these theories--at least in concept--may permit physically "uninjured" plaintiffs to recover. (34) To many, this represents a radical departure from common law tradition, where tort recovery generally required physical contact that caused bodily harm. (35) Moreover, expending judicial resources in the pre-symptom stage can result in awards of speculative damages that may over- or under-compensate for actual loss. (36) Such a program may bring about an inefficient and inequitable distribution of a finite asset pool, diverting judicial resources from plaintiffs with disabling diseases. (37) Beyond this, the expansive conception of legally cognizable injury arguably raises enormous practical challenges in limiting the universe of potential claimants, given that most people are exposed to potentially hazardous substances in their daily lives. (38)
2. The asbestos controversy
The asbestos problem, while unique on many dimensions, (39) has heightened the debate over post-exposure, pre-symptom claims. (40) A significant proportion of new asbestos claims are by plaintiffs who may have recognized markers of asbestos exposure but who are not currently considered impaired or diseased. (41) The vast majority are those experiencing non-impairing "pleural plaques," or calcified deposits on the lining of the lung that occur well before development of serious asbestos-related malignancies such as lung cancer or mesothelioma. (42) Indeed, many plaque cases never progress at all. (43) Other plaintiffs may have asbestosis, scarring of the lung tissue that is non-impairing in some forms but "debilitating and even fatal" in others. (44) Although plaques and asbestosis are clear markers of asbestos exposure, enormous controversy has surrounded the question of whether they are "injurious" in their own right or whether they are predictive of future disease. Underscored by the surge in asbestos filings, the problem of latent risk claims has emerged as one of the most nettlesome and critical problems in modern tort law. (45) Although problems posed by genomics are readily distinguishable from those posed by asbestos, (46) the genomic revolution promises to make the problem of latent risk claims even more nuanced and compelling in the future.
3. Jurisprudence of ambivalence: Physical injury as a predicate to "risk-based" recovery
As a result of the tensions between traditional and emerging tort theories, courts have not reached consensus regarding the requisite elements or even the legitimacy of the newer claims. Perhaps ironically, escalating judicial discomfort with "risk-based" theories has led to renewed efforts to require "present physical injuries" as predicates to recovery. In some cases, as with claims for mental distress, evidence of impact or some physical consequence may help validate plaintiffs' claims. (47) Yet where late-stage injuries are required, such conditions challenge the very premise of these alternative theories by restoring the traditional injury-causation relationship and reconstructing traditional barriers to recovery. (48) Thus, inextricably bound up with the philosophical question of whether the tort system should redefine legal injury is the appropriate definition of physical injury. And while an oft-stated justification for the injury requirement is to create a principled standard for separating valid from speculative claims, (49) there is no consistency in the courts as to what constitutes physical injury. (50)
4. Requiring injury to detect injury: The medical monitoring paradox
Most emblematic of escalating judicial tensions are recent decisions requiring predicate injuries for medical monitoring recovery. (51) Importantly, the sine qua non of a cause of action for medical monitoring--arguably the most distinctive feature that sets it apart from a traditional tort claim--is that plaintiffs need not prove physical injury prior to recovery. (52) Instead, plaintiffs generally must prove significant exposure to known hazardous substances, significant risk of serious disease, and a demonstrated need for special testing. (53) This exclusion of a physical injury requirement is logical, given monitoring's inherently preventive function. (54) Indeed, requiring late-stage injury as a precondition to recovery (55) arguably eviscerates the monitoring claim. (56) Hence, the heightened focus on present physical injury is part of a deeper, foundational struggle over whether this alternative form of recovery should even be recognized. (57)
B. Genomics and Toxic Tort Law: Two Onrushing Freight Trains
As if the present legal muddle were not enough, it will soon be transformed by the genomic revolution. In the not-so-distant future, this unsettled and increasingly controversial area of the law will come face-to-face with an unsettled, enormously complex, and increasingly controversial area of science, as emerging molecular and genomic techniques push toward practical application.
1. Opening the "black box ": New intermediate biomarkers
First, developments emerging in the 1980s (58) and fueled by the application of new genomic technologies since the 1990s have enabled progressively more nuanced and fine-tuned observation of the effects of toxic substances on the body and the role of genetic makeup in modifying those toxic effects. (59) The identification of new biological markers, or "biomarkers," (60) at the genetic and molecular levels has allowed scientists to characterize a number of previously undetectable, intermediate events between chemical exposure and environmentally induced disease.
Traditionally, the science of toxic injury has focused on health effects toward the end of the exposure-disease continuum, such as tumor formation, major organ and tissue dysfunction, or other clinical symptoms. (61) Classical toxicological methods were insufficient to identify and characterize many intermediate events or to establish their relationship to ultimate disease, giving rise to the concept of a "black box." (62) The tools of molecular biology effectively opened this black box, (63) revealing a continuum of events between chemical exposure and clinical disease. (64) As a result, science may detect evidence of chemically induced changes long before clinical symptoms emerge. In addition, new genetic technologies are revealing gene sequence variations, or "polymorphisms," (65) that may confer differential human sensitivity to the effects of toxic substances. (66) These susceptibilities may influence an individual's rate of progression from one biomarker to the next along the exposure-disease continuum (67)--suggesting that, for a given exposure, certain individuals are at greater risk of future disease. The molecular-level biomarkers have been roughly divided into three categories signifying exposure, (68) effects of exposure, (69) and susceptibility. (70)
2. Power, speed, and scale: Whole genome research
Since the mid-1990s, "high-throughput" technologies, (71) including DNA "microarrays" or "gene chips," (72) have permitted thousands of genes to be monitored simultaneously to observe their responses to chemical exposures. (73) Whereas scientists traditionally focused on one or a few genes at a time, these high-speed, high-volume technologies can potentially be used to scan the entire human genome to search for chemically induced changes. (74) The fields of "toxicogenomics" (75) and "toxicogenetics" (76) are devoted exclusively to this research. The former focuses on general mechanisms of toxin-induced disease, while the latter studies how an individual's genetic makeup may affect the response to toxic substances.
3. Emerging fields: New molecular tapestries
As new observational techniques evolve, scientists are testing for suites of interrelated biological changes rather than changes to the genome alone. (77) Beyond genomics, developments in "proteomics" (study of proteins), (78) "metabonomics" (metabolism), (79) "epigenetics" (non-genetic processes that activate genes), (80) and molecular imaging (81) seek to provide holistic portraits of the molecular mechanisms of disease. Studied in combination, these multidimensional suites of biomarkers may reveal new clues as to when inchoate risks transform into disease. (82)
Indeed, we are entering an age of "molecular epidemiology," (83) in which individual biological evidence of exposure, risk, and developing disease (84) increasingly will supplement traditional, population-based estimates of exposure and disease risk. (85) The science of epidemiology, historically the study of health effects in populations, (86) must now evaluate and incorporate new kinds of direct biological evidence--and hence individualized evidence--of toxic risk and harm. A crucial step in developing this new evidence is biomarker "validation," (87) an extensive and rigorous process whereby each biomarker must be evaluated for its accuracy and reliability as a measure of exposure, risk, or harm. (88)
C. Implications: Challenging the Risk-Injury Divide
Over time, new genomic technologies will permit us to identify an expanding progression of biological effects between chemical exposure and fully developed disease. For those effects that can be validated, we may expect new legal claims by plaintiffs who are classified as unimpaired yet show signs of exposure, enhanced risk, or nascent disease.
The concept of physical injury, already a tenuous standard for assigning legal rights and remedies, will become even more unsettled as science gazes into cells to observe the mechanisms of toxicity at the subcellular level. Although there will be scores of molecular signs that do not portend illness, new technologies will expand considerably the number of signs of disease beyond those detectable using traditional diagnostic techniques. Technological advancements will prompt us to reconsider exactly where in the exposure-disease continuum remediable harm has occurred.
At the same time, as new molecular biomarkers supplant the conventional "black box" model, one must ask whether there is any principled way to distinguish those who are "injured" from those who are merely "at risk." Although courts struggle to apply these labels, science will challenge this longstanding legal dichotomy. In the future, as science opens up new possibilities for earlier medical intervention, society will need to reconsider whether a legal system whose remedies depend on unclear and perhaps outmoded notions of "physical injury"--late-stage symptoms and "actual loss" (89) or damage--continues to reflect sound science or appropriate legal policy.
II. EXPLORING THE RISK-INJURY DIVIDE
The tenuous distinction between risk and injury is evident in case law dealing with DNA damage and other presumptively non-impairing conditions, such as pleural plaques resulting from asbestos exposure. (90) Although the law addressing subcellular damage is scant--and has not yet dealt with the discoveries of "whole genome" research (91)--jurisdictions differ as to whether such damage is injurious. While many courts exclude subcellular evidence as a matter of law, (92) others have ruled otherwise or have left the matter for juries to decide. (93) The U.S. District Court for the District of Minnesota, for example, refused to bar such evidence from the jury:
Based on the record before it, this Court cannot rule as a matter of law that plaintiffs' alleged injuries are not "real" simply because they are subcellular. The effect of volatile organic compounds on the human body is a subtle, complex matter. It is for the trier of fact, aided by expert testimony, to determine whether plaintiffs have suffered present harm. (94)
The status of subcellular damage will gain new urgency as high-throughput technologies identify molecular-level biomarkers at a speed and scale unimaginable in the past. This Part examines principles emerging from case law dealing with DNA and other subclinical damage, providing examples from asbestos cases where relevant. I suggest that two competing paradigms undergird these decisions, and offer these models as alternate conceptual frameworks for thinking about the implications of the genomic revolution for the future of tort law. The first I will call the "de minimis effects" or "reversible effects" model; and the second, the "significantly enhanced risk" or "diseased state" model. These models overlap, in that they both may acknowledge the predictive capacity of certain subclinical markers. But the former would treat risk (or early injury) as legally inconsequential, while the latter would--at the very least--preserve the question for expert debate. (95)
A. "De Minimis Effects" or "Reversible Effects" Model
The "de minimis effects" model treats subclinical damage as legally inconsequential. This model presumes that overt clinical symptoms--such as tumor formation or major organ dysfunction--provide an appropriate line of demarcation between risk and injury, health and disease. It follows that the law should not recognize toxic effects as "injurious" or harmful prior to the manifestation of medical symptoms. In cases where subcellular changes or other asymptomatic conditions are recognized as damaging to some degree, such changes are considered insufficiently serious, harmful, or detrimental to trigger legal remedies. (96) Moreover, subclinical damage may be invisible to the naked eye and thus considered subjective and speculative. (97) This model emphasizes the myriad possibilities for adaptation and repair following subclinical insults to the body. (98) Accordingly, subclinical effects may be of limited predictive value. (99) As the First Circuit has noted:
Every disease is presumably preceded by the onset of sub-clinical changes in the body. To state that the disease occurs when these sub-clinical alterations take place, where, as here, the disease does not inevitably or even usually result from the sub-clinical changes, is to subvert the plain meaning of "disease." (100)
Not surprisingly, courts embracing this paradigm often treat plaintiffs alleging subclinical damage as "healthy." The Sixth Circuit's decision in Rainer v. Union Carbide Corp. (101) is illustrative. Although plaintiffs suffered permanent and extensive chromosomal damage from radiation exposure, the court underscored the district court's observation that plaintiffs were not "sick." (102) As a matter of policy, subscribing to a contrary view could mean that most human beings are "diseased" in some manner, (103) potentially unleashing a torrent of litigation. (104) Hence, this model clearly distinguishes the domains of latent risk and patent injury, drawing the Maginot Line at classic medical symptoms or overt impairment.
B. "Significantly Enhanced Risk" or "Diseased State" Model
The alternative model, which I label the "significantly enhanced risk" or "diseased state" model, presumes that although disease may be invisible to the naked eye or undetectable using traditional techniques, it may nevertheless be present and ongoing. (105) The latency period, viewed as an incubator of developing disease, may be shorter than classic medical symptoms would suggest. (106) It follows that legally relevant injury or harm may occur well prior to manifestation of classic symptoms. Certain subclinical changes may represent disease itself, or a substantial probability that full-fledged disease or impairment will develop.
Reflecting this conception, plaintiffs' expert in Rainer argued that "[r]adiation damage to chromosomes is the quintessential determinant of altered physiologic function because our chromosomes control each and every bodily function.... As such this premorbid state is disease." (107) That expert analogized such damage to infection with HIV: "[P]atients who test positive for the HIV virus may not have any signs or symptoms of clinical disease for many years.... [But] even though a person with HIV does not have 'clinical disease' they are clearly in a diseased state." (108)
The diseased state conception would treat as artificial any a priori distinction between cellular and gross harm. Hints of this thinking emerged in Anderson v. W.R. Grace & Co., (109) the well-known toxic tort case chronicled in the best-selling book and movie, A Civil Action. (110) Among other claims, residents of Woburn, Massachusetts alleged subcellular damage from ingesting heavily contaminated drinking water. (111) Rejecting defendants' contentions that such damage was insufficient to support a claim for emotional distress, (112) the court emphasized that the law did not distinguish between gross and subcellular harm. (113) Rather, the law distinguished between "harm which is merely speculative or based solely on a plaintiff's unsupported assertions" and harm that could be "objectively evidenced" through expert medical testimony. (114) As plaintiffs could support their allegation of subcellular damage through expert medical testimony, there was sufficient evidence to preclude summary judgment....
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