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The Complexity of Litigating Toxic Risks

By Rebecca Lowy*

Environmental pollution is a major public health issue. Some 80,000 chemicals are currently registered under the Toxic Substances Control Act, yet only a few hundred have been tested for safety by governmental agencies[i]. Thousands of new chemicals are introduced each year[ii]. These “emerging contaminants” and known chemicals enter the environment through industrial emissions and products[iii], creating an ever-growing burden on individuals who bear the health repercussions of such pollution, and a serious incentive to level the playing field and protect people whose livelihoods are at risk from these consequences.

Medical monitoring is a form of relief often sought in toxic tort class action cases arising from exposure as the cause of action[iv]. It uses typical medical screening devices to identify early symptoms of illnesses associated with exposure to toxic chemicals, and can have life-saving implications for plaintiffs through timely treatment[v]. In order to be awarded medical monitoring as post-trial relief, plaintiffs generally must prove by a preponderance of the evidence 1) that significant exposure exists, 2) that exposure resulted from defendants’ conduct, and 3) that a manifest injury resulted or that there is an increased likelihood such injury will result. Recovery on future injury is an unusual and difficult claim to support. To meet the third requirement, courts generally look for proof of illness or high likelihood of future illness[vi]. Thus, plaintiffs are typically not entitled to medical monitoring simply by identifying the presence of toxic chemicals in their bodies through biomonitoring.

This creates an unique obstacle in arguing for medical monitoring on the basis of biomonitoring or other exposure results; chemical exposure, standing alone, does not constitute legal injury under current tort law[vii]. One proposed alternative has been “toxic trespass” of chemicals into the body as a theory for the basis of medical monitoring[viii]. This theory suggests that the act of causing a chemical to enter into a person’s body involuntarily (by such acts as polluting a drinking water source) is sufficient cause for medical monitoring relief[ix]. However, courts have rejected this theory, continuing to require that complainants demonstrate the high likelihood of adverse health effects; as an injury based remedy, there must be actual or expected injury, since trespass without intent cannot suffice[x]. In some jurisdictions, medical monitoring is controversial because it contradicts conventional tort theory that there must be existing harm, or uncontested likelihood of harm, for recovery[xi].

The additional burden of proving future injury (i.e., adverse health effects) relies on medical and toxicological studies that are constantly evolving, hotly contested, and prone to long delays and uncertain results. This puts plaintiffs at a significant disadvantage: they must wait, sometimes years, for results that will help prevent their own illness. In the meantime, many become seriously ill. Though plaintiffs may be able to prove exposure through biomonitoring data, and that exposure resulted from defendants’ conduct, they may still fail to prove a sufficiently high likelihood of illness to attain medical monitoring in time to make a difference and protect their livelihood. This structure is extraordinarily prejudicial to plaintiffs, and assumes that chemicals themselves are innocent until proven guilty.

However, there may be another way to utilize biomonitoring data as evidence for injury and help meet the third requirement for toxic tort claims. Biomonitoring can test for biomarkers that are indicative of chemical toxicity[xii]. When developing epidemiological toxicology studies, scientists often begin with animal models that are representative of human biology to understand how chemicals interact with human biological pathways before researching the associated illnesses. These early-stage studies can show injury on a molecular level, such as: DNA damage; interference with metabolization of energy sources; and inhibition of normal cellular receptor activity. Though disease may not yet manifest itself, such molecular damage should, on its own, be considered injury. An individual’s cells are part of his or her body; any external damage to the normal functioning of those cells is also harm to the body. Causation is also significantly easier to prove here: studies showing cellular damage have a much higher degree of scientific certainty than do studies on causation of illness from exposure.

Subcellular or other physiological damage has occasionally been found by courts to be proof of injury,[xiii] but typically fails for medical monitoring, because courts still look for proof of illness or future illness as the sufficient injury (since medical monitoring specifically tests for illnesses). Rather than arguing that cellular harm be viewed as a sufficient injury on its own, it should be considered an extenuating factor in how likely future illness is to develop. Courts often require high levels of certainty, or increased degrees of likelihood, before granting medical monitoring (for instance, some courts require a minimum two-fold increased chance)[xiv]. Using a combined 1) cellular harm as injury and 2) ordinary likelihood of future illness, courts may be satisfied with lower, albeit still significant, increased risk of future illness to meet the third requirement of proof of injury or future injury. Some cases have suggested that courts may be amenable to considering subcellular harm, particularly chromosomal damage, as a factor in medical monitoring, but this is not yet widely accepted[xv].

 Because proof of future illness is so difficult to prove, and the epidemiological scientific studies are often influenced by the very companies who produce the toxic chemicals in question[xvi], it is reasonable to apply a factor that mitigates the “high” likelihood of future injury requirement for medical monitoring. This also acknowledges the scientific theory that where there is cellular damage, some form of illness is may follow or at least be exacerbated by that damage, even if a specific effect is not yet identified[xvii]. This would allow courts to, while not holding cellular harm as independently sufficient for injury, use it as a factor in evaluating the likelihood of future injury with slightly less weight placed on future illness where scientific evidence is uncertain. Requiring complainants to prove that their risk for future disease is elevated as more probable than not completely disregards the fact that for some chemicals, it simply is not yet known whether that risk is present.

Constraints on the use of this theory will be needed: any exposure at all to a chemical cannot be said to constitute injury and alone be sufficient for medical monitoring. Arguments against using animal models for illness as proof of injury suggest that epidemiological pathways of animal models are not always sufficiently similar to justify extrapolation to human biology[xviii]. Some may try to apply this same argument against proof of cellular damage. However, while model disease pathways may not always be predictive, models are more representative of human biology when it comes to cellular function[xix]. These animal models ought to pass muster on being predictive of chemical damage to human cellular function, regardless of illness pathology.

Medical monitoring is a valuable tool that can prevent and/or mitigate harm to individuals whose health is at risk from toxic exposure. Unfortunately, the current approach of relying only on epidemiological studies often fails to protect plaintiffs until it is too late.  Using biomonitoring data as evidence both of exposure and injury may alleviate some of the stricter requirements where illness resulting is uncertain. Cellular damage from exposure ought to be applied as proof of injury sufficient to lessen the strict requirements of “high” likelihood from studies of resulting illness. This may help address the gap in scientific understanding and technological advancements with the real world implications of toxic exposure and public health.

*Rebecca Lowy is a Junior Editor on MJEAL. They can be reached via email at

The views and opinions expressed in this blog are those of the authors only and do not reflect the official policy or position of the Michigan Journal of Environmental and Administrative Law or the University of Michigan.

[i] Laura Hall et. al., Litigating Toxic Risks Ahead of Regulation: Biomonitoring Science in the Courtroom, 31 Stan. Envtl. L.J. 3, 5 (2012)

[ii] “It Could Take Centuries for EPA to Test All the Unregulated Chemicals Under a New Landmark Bill”

[iii] Ott, W., & Roberts, J. (1998). Everyday Exposure to Toxic Pollutants. Scientific American, 278(2), 86-91. Retrieved from

[iv] Laura Hall et. al., Litigating Toxic Risks Ahead of Regulation: Biomonitoring Science in the Courtroom, 31 Stan. Envtl. L.J. 3, 25 (2012)

[v] Id.

[vi] § 15:4.How is increased risk of disease established?, 1 Toxic Torts Prac. Guide § 15:4 (2019)

[vii] Laura Hall et. al., Litigating Toxic Risks Ahead of Regulation: Biomonitoring Science in the Courtroom, 31 Stan. Envtl. L.J. 3, 10 (2012)

[viii] Id. at 47.

[ix] Id.

[x] Id.

[xi] § 15:4.How is increased risk of disease established?, 1 Toxic Torts Prac. Guide § 15:4 (2019)

[xii] See § 3:8.Biomarkers as evidence of injury and exposure to a toxic agent?, 1 Toxic Torts Prac. Guide § 3:8 (2019)

[xiii] Genereux v. Raytheon Co., Prod. Liab. Rep. (CCH) P 19405, 2014 WL 2579908, *3 (1st Cir. 2014).

[xiv] § 15:4.How is increased risk of disease established?, 1 Toxic Torts Prac. Guide § 15:4 (2019)

[xv] See Ayers v. Jackson Twp., 106 N.J. 557, 525 A.2d 287 (1987); Brafford v. Susquehanna Corp., 586 F. Supp. 14 (D. Colo. 1984).

[xvi] Sharon Lerner, The Intercept, EPA Used Monsanto’s Research to Give Roundup a Pass (2015)

[xvii] Yong Zhang, Cell toxicity mechanism and biomarker. 7 Clin. & Translational Med. 34 (2018)

[xviii] § 15:3.Issues in establishing proof of exposure, injury, and causation, 1 Toxic Torts Prac. Guide § 15:3 (2019)

[xix] Luca Chaible et al. Chapter 27 – Genetically Modified Animal Models, Animal Models for the Study of Human Disease (Second Edition) 703-726 (2017).

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