Michigan Supreme Court

Lansing, Michigan

Stephen J. Markman,

 Chief Justice

Brian K. Zahra

Bridget M. McCormack

David F. Viviano 

Richard H. Bernstein

Joan L. Larsen

Kurtis T. Wilder,

Justices

Order 

July 25, 2017

151600

CHANCE LOWERY,

Plaintiff-Appellee,

v SC: 151600

COA: 319199

Calhoun CC: 2011-003414-NO

ENBRIDGE ENERGY LIMITED PARTNERSHIP

and ENBRIDGE ENERGY PARTNERS LP,

Defendants-Appellants.

_________________________________________/

On order of the Court, leave to appeal having been granted, and the briefs and oral 

arguments of the parties having been considered by the Court, we REVERSE the April 2, 

2015 judgment of the Court of Appeals and REINSTATE the November 8, 2013 order of 

the Calhoun Circuit Court granting the defendants’ motion for summary disposition. A 

plaintiff may show “cause in fact” through circumstantial evidence and “reasonable 

inferences” therefrom, but not through “mere speculation” or “conjecture,” Skinner v 

Square D Co, 445 Mich 153, 164 (1994), such as reasoning post hoc ergo propter hoc, 

see Genesee Merchants Bank & Trust Co v Payne, 381 Mich 234, 248 (1968) (opinion by 

KELLY, J.) (“But fact-finders, be they jury or court, may not indulge in conjecture. They 

are constrained to draw reasonable inferences from established facts. Reasoning ‘post 

hoc ergo propter hoc’ does not meet this test.”) (citation omitted). The plaintiff’s expert 

opined that the defendants’ oil spill was the cause in fact of the plaintiff’s injury, 

reasoning that the plaintiff “wasn’t having the problems before [the oil spill] and he was 

having the problems afterwards.” Contrary to the Court of Appeals conclusion that the 

plaintiff’s evidence reflects a “logical sequence of cause and effect,” we conclude that the 

plaintiff’s evidence reflects the logical fallacy of post hoc reasoning. Cf. West v Gen 

Motors Corp, 469 Mich 177, 186 n 12 (2003) (“Relying merely on a temporal 

relationship is a form of engaging in the logical fallacy of post hoc ergo propter hoc

(after this, therefore in consequence of this) reasoning.”) (quotation marks omitted). We, 

therefore, conclude that the plaintiff has failed to show a genuine dispute of material fact 

as to causation. 

We do not retain jurisdiction.

MARKMAN, C.J. (concurring). 

I concur in this Court’s decision to reverse the judgment of the Court of Appeals 

and write separately to provide counsel to the bench and bar concerning toxic tort 
2

litigation. This Court granted leave to appeal to consider: (a) the role of expert testimony 

in toxic tort cases; (b) the applicability of the general-and-specific-causation framework 

in toxic tort cases; and (c) the sufficiency of plaintiff’s evidence of causation in the 

instant toxic tort case. Lowery v Enbridge Energy Ltd Partnership, 499 Mich 886 (2016). 

The importance of these issues is evinced, in part, by the fact that of the 54 cases heard 

by this Court during the present term, only 13 involved, as did this case, full grants. 

Today, the Court does not address these issues but instead resolves this case in an order 

of reversal. Uncertainty continues to characterize our toxic tort jurisprudence despite the 

fact that the general-and-specific-causation framework has proven uncontroversial in 

contemporary toxic tort law outside Michigan. Bernstein, Getting to Causation in Toxic 

Tort Cases, 74 Brook L Rev 51, 52 (2008) (“American courts have reached a broad 

consensus on what a plaintiff must show to prove causation in a toxic tort case. First, a 

plaintiff must show that the substance in question is capable of causing the injury in 

question. This is known as ‘general causation.’ Second, a plaintiff must show that this 

substance caused his injury. This is known as ‘specific causation.’ ”) (citations omitted). 

I write separately only to provide some semblance of guidance to litigants in this and 

future cases-- to those pursuing and those defending toxic tort claims-- as well as similar 

guidance to the lower courts of our state in presiding over and in reviewing these claims. 

Such guidance is critical because in Michigan there is a paucity of law concerning toxic 

torts, much of what law exists is confusing and contradictory, and all this is occurring at a 

time when it appears that toxic tort litigation is on the upturn here as in other 

jurisdictions. I respectfully offer the following analysis to better clarify our toxic tort 

jurisprudence. 

* * *

First, I would clarify that Michigan’s long-held general rules regarding the 

necessity of expert testimony apply to toxic torts, i.e., expert testimony on causation is 

necessary in a toxic tort case when the legal proposition is beyond the common 

knowledge of an ordinary juror. Second, I agree with the vast majority of other 

jurisdictions that the general-and-specific-causation framework may be utilized to 

analyze the cause-in-fact element of a toxic tort claim. At a minimum, this framework 

should apply when a plaintiff seeks to prove factual causation employing group-based 

statistical evidence. In this case, plaintiff submitted such evidence to prove cause in fact. 

Accordingly, applying the framework, I would hold that plaintiff failed to present 

adequate evidence of cause in fact, specifically evidence establishing either general or 

specific causation. Therefore, I concur with the Court’s reversal of the judgment of the 

Court of Appeals and remand to the trial court for reinstatement of its order granting 

summary disposition in defendants’ favor. 

A review of the facts that led to this litigation is helpful to understanding my 

analysis that follows. This case concerns a large and severe oil spill into a Michigan 

woodland and river. On July 26, 2010, a pipeline belonging to defendants, Enbridge 
3

Energy Limited Partnership and Enbridge Energy Partners, LP, ruptured and released 

840,000 gallons of crude oil into a woodland area. The oil eventually migrated into 

Talmadge Creek and the Kalamazoo River and further spread nearly 40 miles throughout 

Calhoun and Kalamazoo counties. The federal Environmental Protection Agency (EPA) 

eventually intervened, ordering a cleanup and conducting air monitoring and sampling to 

measure the level of volatile organic compounds (VOCs) in the air.1 A voluntary 

evacuation was issued for the immediate geographic area of the spill. 

Plaintiff, Chance Lowery, lived roughly 250 feet from the banks of the Kalamazoo 

River and approximately 11 to 13 miles downstream from the spill’s source. He claimed 

to have smelled chemicals shortly after the spill and to have become sick as a result--

coughing and vomiting for several days, and then proceeding to the hospital.2 A scan 

performed at the hospital indicated that plaintiff had a stomach hemorrhage. Dr. John 

Koziarski, a general and vascular surgeon who is board certified in general surgery and 

vein diseases, performed a successful operation to repair the hemorrhage, which revealed 

that “a short gastric vessel midway down the stomach . . . had avulsed off of the spleen.” 

On the basis of these injuries and damage to his property, plaintiff filed a 

complaint alleging defendants’ negligence. Regarding causation, the complaint alleged 

that plaintiff was exposed to “hazardous substances” that constituted “a proximate cause” 

of plaintiff’s injuries. Those injuries included “nausea, a severe cough and violent 

vomiting, which caused a rupture of his short gastric artery, which required subsequent 

surgical repair and resulted in a disfiguring prominent surgical scar.” Expert testimony 

on the matter of causation3consisted of deposition testimony by the treating physician, 

Dr. Koziarski, and deposition testimony and a report from Dr. Jerry Nosanchuk, a general 

physician who is board certified in family medicine. The former testified that plaintiff 

stated that he had taken Vicodin for a migraine, began vomiting, and then developed 

severe abdominal pain. Dr. Koziarski testified that Vicodin could cause vomiting but that 

 

1 VOCs are an aggregation of chemicals that may be found in crude oil and can be 

harmful to humans at certain exposure levels. See generally Wallace, Personal 

Exposures, Indoor and Outdoor Air Concentrations, and Exhaled Breath Concentrations 

of Selected Volatile Organic Compounds Measured for 600 Residents of New Jersey, 

North Dakota, North Carolina and California, 12 Toxicological & Envtl Chemistry 215 

(1986). 

2 Despite the uncertain timeline to which plaintiff testified-- describing symptoms 

manifested over the course of approximately five to seven days immediately following 

the spill-- his medical records show that he was admitted to the hospital on August 18, 

2010, which was 23 days after the initial spill. 

3

The trial court granted summary judgment in plaintiff’s favor regarding defendants’

breach of duty-- i.e., that defendants acted negligently. That order has not been 

challenged here.
4

he had no medical opinion whether Vicodin was what specifically caused plaintiff’s 

vomiting. He also had no opinion concerning whether plaintiff’s anti-depression 

medication, Lamictal, could also cause migraines. Plaintiff never indicated to Dr. 

Koziarski that fumes wafting from the Kalamazoo River had caused or contributed to his 

vomiting or his headaches. Dr. Koziarski concluded that he could not opine as to 

whether plaintiff had exposure to the fumes or whether that exposure accounted for the 

“rupture or avulsion of the gastric artery[.]” He also could not determine the avulsion’s 

medical cause. 

Given that Dr. Koziarski did not opine as to whether the fumes caused plaintiff’s 

condition, expert testimony on causation before the trial court was limited to Dr. 

Nosanchuk’s testimony. He reviewed plaintiff’s hospital records, a Michigan 

Department of Community Health document about the spill, a newspaper report 

concerning the spill, plaintiff’s deposition testimony as well as his interrogatory answers, 

and photographs of plaintiff’s backyard displaying its proximity to the river. He did not 

physically examine plaintiff. Dr. Nosanchuk was “of the opinion that the fumes from the 

oil spill caused [plaintiff] to have the migraine headaches, extreme coughing and nausea 

as well as vomiting. Ultimately, these problems caused a tear of the short gastric artery 

resulting in hemorrhage within the [stomach].” 

Plaintiff also presented deposition testimony from his roommate, a neighbor, and a 

friend regarding the noticeable smell4near and within his apartment as well as 

information regarding VOCs exposure from the Centers for Disease Control and 

Prevention (CDC).5 After discovery, defendants moved for partial summary disposition 

under MCR 2.116(C)(10). Following arguments, the trial court granted defendants’ 

motion for summary disposition, limited only to plaintiff’s ailments beyond vomiting and 

headaches. The court determined that there was nothing to link the cause of the ruptured 

artery to the oil spill. In response, plaintiff’s counsel stated that he would rather the court 

grant summary disposition in its entirety because this “whole case is all about the 

surgery” and plaintiff would prefer to appeal the ruling immediately. The trial court 

concurred, and an order was entered by the court affirming its ruling on the record. 

In a split opinion, the Court of Appeals reversed the grant of summary disposition 

and remanded for further proceedings. Lowery v Enbridge Energy Ltd Partnership, 

 

4

Plaintiff’s roommate compared the smell to “asphalt . . . like burning, rubber, tar . . . .” 

Plaintiff’s friend explained, “[I]t smelled like you tipped over fuel oil in your driveway.” 

Plaintiff’s neighbor testified that the smell was “like rubber burning.” 

5

Plaintiff attached the CDC documents to his response to defendants’ motion for 

summary disposition. I make no determination as to whether these documents were 

properly in the record or would have been deemed admissible absent expert testimony; I 

assume they are properly part of plaintiff’s proofs for purposes of my analysis. 
5

unpublished per curiam opinion of the Court of Appeals, issued April 2, 2015 (Docket 

No. 319199), p 1. The majority held that expert testimony showing that the toxin, VOCs, 

was capable of causing the injuries alleged and that it actually did cause such injuries was 

not required in light of the Court’s earlier decision in Genna v Jackson, 286 Mich App 

413 (2009). Lowery, unpub op at 2-3. The Court found it sufficient that the 

circumstantial evidence plaintiff had presented established “a strong enough logical 

sequence of cause and effect for a jury to reasonably conclude that plaintiff’s exposure to 

oil fumes caused his vomiting, which ultimately caused his short gastric artery to 

rupture.” Id. at 3. In dissent, Judge JANSEN would have affirmed the trial court’s grant of 

summary disposition. She reasoned that “[p]laintiff’s theory of causation was attenuated” 

and that a jury comprised of lay people would be unable to determine whether the oil 

fumes could have caused vomiting and the resulting arterial tear absent the aid of expert 

testimony. Id. at 1 (JANSEN, J., dissenting). She further noted that Dr. Nosanchuk was 

unqualified to give such testimony and therefore that the jury was left on its own to 

speculate concerning the issue of causation. Id. 

Defendants subsequently filed an application seeking leave to appeal in this Court, 

and we granted its application, requesting that the parties address “(1) whether the 

plaintiff in this toxic tort case sufficiently established causation to avoid summary 

disposition under MCR 2.116(C)(10); and (2) whether the plaintiff was required to 

present expert witness testimony regarding general and specific causation.” Lowery, 499 

Mich 886. 

I. ANALYSIS

In a typical tort claim grounded in negligence, plaintiffs “must prove (1) that 

defendant owed them a duty of care, (2) that defendant breached that duty, (3) that 

plaintiffs were injured, and (4) that defendant’s breach caused plaintiffs’ injuries.” Henry 

v Dow Chemical Co, 473 Mich 63, 71-72 (2005). “Proof of causation requires both cause 

in fact and legal, or proximate, cause.” Haliw v Sterling Heights, 464 Mich 297, 310 

(2001). “[L]egal cause or ‘proximate cause’ normally involves examining the 

foreseeability of consequences, and whether a defendant should be held legally 

responsible for such consequences.” Skinner v Square D Co, 445 Mich 153, 163 (1994). 

“The cause in fact element generally requires showing that ‘but for’ the defendant’s 

actions, the plaintiff’s injury would not have occurred.” Id. A plaintiff must demonstrate 

as a threshold matter that there is “more than a mere possibility” that the defendant 

caused the injury, id. at 166 (citation and quotation marks omitted), and must then present 

“substantial evidence” from which a jury could conclude that, more likely than not, “but 

for the defendant’s conduct, the plaintiff’s injuries would not have occurred,” Weymers v 

Khera, 454 Mich 639, 647-648 (1997) (citation and quotation marks omitted). That 

substantial evidence “must exclude other reasonable hypotheses with a fair amount of 

certainty,” Skinner, 445 Mich at 166 (citation and quotation marks omitted), because a 

jury cannot be permitted to merely guess about causation, id. at 174. 
6

This Court has defined “an ordinary ‘toxic tort’ cause of action” as one in which 

“a plaintiff alleges he has developed a disease [or other injury] because of exposure to a 

toxic substance negligently released by the defendant.” Henry, 473 Mich at 67. Toxic 

torts are thus a specific type of negligence claim. In order to establish a claim under a 

toxic tort theory, a plaintiff must prove an injury arising from exposure to a toxic 

substance. Id. at 72-73 (holding that plaintiffs could not maintain a toxic tort claim to 

recover damages for the cost of medical monitoring for potential future injuries), citing 

Larson v Johns-Manville Sales Corp, 427 Mich 301 (1986). This Court has not yet 

addressed whether the causation element of a toxic tort claim differs in any meaningful 

way from that of a traditional negligence claim. Indeed this case implicates several 

issues regarding causation in toxic tort cases in Michigan: namely, whether the cause-infact element of a toxic tort claim includes separate analyses of general and specific 

causation; if so, what evidence a plaintiff must provide on those issues to survive a 

summary disposition motion; and whether such evidence must include expert testimony. 

To address these questions, I begin with an analysis of the unique challenges posed by the 

cause-in-fact element of a toxic tort claim, i.e., those challenges that arise in addressing 

the general-and-specific-causation inquiries subsumed within.

A. CAUSE IN FACT

The great majority of jurisdictions have bifurcated the cause-in-fact element in 

toxic tort cases into separate and distinctive analyses of “general causation” and “specific 

causation.”6 This analytical approach for determining causation in toxic tort cases also 

 

6

See, e.g., CW ex rel Wood v Textron, Inc, 807 F3d 827, 831 (CA 7, 2015) (applying 

Indiana substantive law, which required “evidence of general and specific causation”); 

Knight v Kirby Inland Marine Inc, 482 F3d 347, 351 (CA 5, 2007) (“General causation is 

whether a substance is capable of causing a particular injury or condition in the general 

population, while specific causation is whether a substance caused a particular 

individual’s injury.”) (citation and quotation marks omitted); Mattis v Carlon Electrical 

Prod, 295 F3d 856, 860 (CA 8, 2002) (“To prove causation in a toxic tort case, a plaintiff 

must show both that the alleged toxin is capable of causing injuries like that suffered by 

the plaintiff in human beings subjected to the same level of exposure as the plaintiff, and 

that the toxin was the cause of the plaintiff’s injury.”) (citation and quotation marks 

omitted); Mitchell v Gencorp Inc, 165 F3d 778, 781 (CA 10, 1999) (“[A] plaintiff must 

demonstrate the levels of exposure that are hazardous to human beings generally as well 

as the plaintiff’s actual level of exposure to the defendant’s toxic substance before he or 

she may recover.”) (citation and quotation marks omitted); Ranes v Adams Laboratories, 

Inc, 778 NW2d 677, 687-688 (Iowa, 2010) (“Courts have commonly bifurcated toxictort-causation analysis into two separate but related parts: general causation and specific 

causation. . . . The Third Restatement of Torts has recognized this relatively recent 

common practice as a device to organize a court’s analysis and not as additional elements 
7

finds support in the secondary literature.7 Therefore, application of the general-andspecific-causation framework in toxic tort cases has been far from untested. The 

Restatement (Third) of Torts provides a lengthy discussion of the bifurcated general-andspecific-causation framework in its comments, noting in particular that 

[c]ases involving toxic substances often pose difficult problems of proof of 

factual causation. . . . Sometimes it is difficult to prove which defendant 

was connected to the toxic agent or whether an adequate warning would 

have prevented the plaintiff’s harm. The special problem in these cases, 

however, is proving the connection between a substance and development 

of a specific disease. [Restatement Torts, 3d, Liability for Physical and 

Emotional Harm, § 28, comment c, p 402 (citations omitted).]

After noting that most causation issues in this context are resolved under the “but 

for” standard of factual causation, the Restatement provides that when a plaintiff presents 

“group-based statistical evidence” concerning a toxin, a plaintiff must prove that “the 

substance must be capable of causing the disease (‘general causation’) and that the 

substance must have caused the plaintiff’s disease (‘specific causation’).” Id. at 404. 

This is not a novel concept. General causation is implicit in all negligence claims, 

but in negligence claims that do not involve toxic torts, the plaintiff typically does not 

need to present separate proof of each type of causation because the relationship between 

general and specific causation is sufficiently direct and straightforward such that both 

types of causation are effectively proven together. By analogy, imagine a simple 

negligence claim in which the defendant drove his car over the plaintiff’s foot, breaking 

it. Evidence proving that the car broke the plaintiff’s foot practically proves both the 

“general” causation requirement of proof (that the car was capable of causing the injury) 

and the “specific” causation requirement (that the car did in fact break the foot). In other 

words, in a typical negligence claim, the same evidence will often prove that exposure to 

 

of the tort. The Restatement authors supplement their explanation by asserting factual 

causation is a necessary element in every tort case; the general and specific language has 

simply become more prevalent in toxic-tort cases. . . . This bifurcated analysis has not 

been explicitly used as the standard in Iowa. However, due to its general acceptance 

among scholars and courts of other jurisdictions, as well as the relative ease of 

application the analysis offers to courts examining complex issues of causation, we 

believe it is appropriate for courts to use the bifurcated causation language in toxic-tort 

cases.”) (citations, quotation marks, and brackets omitted). 

7

See, e.g., Note, Causation in Environmental Law: Lessons from Toxic Torts, 128 Harv

L Rev 2256, 2261-2262 (2015); Sanders, The Controversial Comment C: Factual 

Causation in Toxic-Substance and Disease Cases, 44 Wake Forest L Rev 1029, 1031 

(2009); Stout & Valberg, Bayes’ Law, Sequential Uncertainties, and Evidence of 

Causation in Toxic Tort Cases, 38 U Mich J L Reform 781, 784 (2005). 
8

the harm produced by the defendant’s negligence could and did cause the injury in 

dispute. See Restatement, § 28, comment c, p 402 (“In most traumatic-injury cases, the 

plaintiff can prove the causal role of the defendant’s tortious conduct by observation, 

based upon reasonable inferences drawn from everyday experience and a close temporal 

and spatial connection between that conduct and the harm. Often, no other potential 

causes of injury exist. When a passenger in an automobile collision suffers a broken 

limb, potential causal explanations other than the collision are easily ruled out; common 

experience reveals that the forces generated in a serious automobile collision are capable 

of causing a fracture.”).

But in a toxic tort claim, this relationship may be considerably less clear. See 

Landrigan v Celotex Corp, 127 NJ 404, 413 (1992) (noting that in the toxic tort context, 

“proof that a defendant’s conduct caused decedent’s injuries is more subtle and 

sophisticated than proof in cases concerned with more traditional torts”). For example, 

an injury such as cancer has many suspected causes, including exposure to various toxins 

in various quantities and durations. See Farber, Toxic Causation, 71 Minn L Rev 1219, 

1227 (1987) (“One [issue] is the problem of establishing that the chemical involved is 

capable of causing the type of harm from which the plaintiff suffers. This is often 

difficult because the causation of diseases like cancer is so poorly understood.”). In such 

cases, proof of cause in fact may need to take the form of separate proofs that the toxin 

can cause the harm and that it did. See, e.g., Mattis v Carlon Electrical Prod, 295 F3d 

856, 860 (CA 8, 2002) (“To prove causation in a toxic tort case, a plaintiff must show 

both that the alleged toxin is capable of causing injuries like that suffered by the plaintiff 

in human beings subjected to the same level of exposure as the plaintiff, and that the 

toxin was the cause of the plaintiff’s injury.”) (citation and quotation marks omitted). 

Absent evidence regarding each inquiry, a jury could be left improperly to speculate as to 

the nature of the relationship between the toxin and the plaintiff’s injury. Skinner, 445 

Mich at 164 (“To be adequate, a plaintiff’s circumstantial proof must facilitate reasonable 

inferences of causation, not mere speculation.”). For these reasons, the general-andspecific-causation framework is helpful in toxic tort cases to ensure that the cause-in-fact 

element is properly proven; at a minimum, this is true when the plaintiff avails himself or 

herself of the framework by presenting group-based statistical evidence or similar 

scientific evidence8because such evidence9by its nature can only speak to whether the 

 

8

The application of the general-and-specific-causation framework should not be limited

to instances in which the plaintiff presents group-based statistical evidence. As the 

Restatement further asserts: “In toxic-substances cases, the causal inquiry is modified by 

the limits of and available forms of scientific evidence. That inquiry often must address 

whether the [toxic] agent for which the actor is responsible is capable of causing the 

disease from which another suffers (known as general causation). In addition, the 

question whether the [toxic] agent caused the specific plaintiff’s disease (known as 

specific causation) is confronted.” Restatement, § 26, comment g, p 351 (emphasis 

added).
9

substance is capable of causing the alleged injury (general causation) and does not 

address whether the substance, in fact, caused the plaintiff’s injury (specific causation). 

In other instances, the general-and-specific-causation framework may be 

unnecessary to establish cause in fact, such as those instances in which the causal link 

between an injury and a toxin is as direct and apparent as it is in the case in which the car 

breaks the plaintiff’s foot. Sometimes the “mechanism of causation is well 

understood . . . [or] the causal relationship is well established,” such as when the resulting 

injury is immediate and traumatic rather than gradual and disease-based. Green et al, 

Reference Guide on Epidemiology, in Reference Manual on Scientific Evidence (3d ed), 

p 609 n 180. In such cases, the general-and-specific-causation framework might be 

unnecessary. Consider, for example, a plaintiff who suffers a severe chemical burn 

immediately after toxic acid has been spilled onto his skin. There might well be no need 

for the application of this analytical framework when the causal link is so clear and 

straightforward.10 

Michigan has little authority on this topic, and this Court has yet to provide 

significant guidance. I take this opportunity to begin to rectify this. 

B. GENERAL CAUSATION

General causation pertains to whether a toxin is capable of causing the harm 

alleged. A necessary predicate to this inquiry is identifying the asserted exposure level of 

the toxin. “A number of courts have required plaintiffs to prove the level of exposure 

(dose) in order to establish causation.” Goeb v Tharaldson, 615 NW2d 800, 815 (Minn, 

 

9

This less-direct evidence might not always consist of group-based statistical studies. 

See, e.g., King v Burlington N Santa Fe R Co, 277 Neb 203, 215-221 (2009) (explaining 

the value of epidemiological studies in evidencing general causation and providing that in 

the absence of epidemiological studies, an expert may refer alternatively to the United 

States Surgeon General’s “Bradford Hill” factors for evidence of general causation).

10 Because I recognize that not every toxic tort claim requires separate proof of general 

and specific causation in order to establish cause in fact, I also recognize that the absence 

of separate proofs regarding general and specific causation does not prevent a plaintiff 

from establishing a prima facie case of negligence in every toxic tort case. See Christian 

v Gray, 65 P3d 591, 604 (Okla, 2003) (“[G]eneral causation should be shown unless the 

particular controversy is inappropriate for general causation. We decline to list 

hypothetical controversies where general causation need not be shown.”). It should be 

emphasized that these concepts “are not ‘elements’ of a plaintiff’s cause of action” but 

rather “function as devices to organize a court’s analysis . . . . So long as the plaintiff 

introduces admissible and sufficient evidence of factual causation, the burden of 

production is satisfied.” Restatement, § 28, comment c, p 405 (emphasis added). 
10

2000). “[T]he mere existence of a toxin in the environment is insufficient to establish 

causation without proof that the [particular] level of exposure could cause the plaintiff’s 

symptoms.” Pluck v BP Oil Pipeline Co, 640 F3d 671, 679 (CA 6, 2011). Put another 

way, causation “requires not simply proof of exposure to the substance, but proof of 

enough exposure to cause the plaintiff’s specific illness.” McClain v Metabolife Int’l, 

Inc, 401 F3d 1233, 1242 (CA 11, 2005). 

Knowledge of the exposure level is crucial to determining whether the toxin can 

cause the harm because many substances are harmful in certain quantities but are safe at 

lower levels; carbon monoxide, for instance, is constantly in the air, but it only causes 

adverse health symptoms in certain higher concentrations. See Zuchowicz v United 

States, 140 F3d 381, 391 (CA 2, 1998) (“[A]ll drugs involve risks of untoward side

effects. . . . At the approved dosages, the benefits of the particular drug have presumably 

been deemed worth the risks it entails. At greater than approved dosages, . . . the risks of 

tragic side effects (known and unknown) increase . . . .”); Eaton, Scientific Judgment and 

Toxic Torts-- A Primer in Toxicology for Judges and Lawyers, 12 J L & Pol’y 5, 11 

(2003) (“ ‘All substances are poisonous—there is none which is not; the dose 

differentiates a poison from a remedy.’ ”) (citation and emphasis omitted). Moreover, a 

substance may cause different harmful effects in different doses. See Goldstein, Toxic 

Torts: The Devil is in the Dose, 16 J L & Pol’y 551, 554 (2008) (“Dose is defined as 

concentration multiplied by frequency or duration—it is not just the exposure level at any 

one point in time.”). As a result, a substance may be harmful at a certain level of 

exposure but may not be sufficient to cause a particular adverse health effect. In re Agent 

Orange, 570 F Supp 693, 695 (ED NY, 1983) (stating that general causation “is 

addressed to the common question of whether exposure to [the toxin] in the manner that 

it was used in [plaintiff’s location] could cause the kinds of injuries that plaintiffs claim 

to have suffered”) (emphasis added). Accordingly, a plaintiff’s evidence of general 

causation should be tailored to the estimated amount and duration of exposure at issue to 

enable the fact-finder to reasonably conclude that exposure to the defendant’s toxin in the 

amount and duration alleged is capable of causing the alleged injury. See Wright v 

Willamette Indus, Inc, 91 F3d 1105, 1107 (CA 8, 1996) (“[T]here must be evidence from 

which the factfinder can conclude that the plaintiff was exposed to levels of that agent 

that are known to cause the kind of harm that the plaintiff claims to have suffered.”).

C. SPECIFIC CAUSATION

Evidence of specific causation consists of proof that exposure to the toxin more 

likely than not caused the plaintiff’s injury. Specific causation requires at minimum an 

approximate estimate of the plaintiff’s exposure level as well as an evaluation and 

elimination of other reasonable potential causes. It is well accepted that “a plaintiff in a 

toxic tort case must prove . . . the plaintiff’s actual level of exposure to the defendant’s 

toxic substance before he or she may recover.” Id. at 1106. I recognize that “it is 

often . . . particularly difficult . . . to establish [exposure levels] in a [toxic] tort suit” 
11

given “the adventitious, often accidental, and even unknown (at the time) exposures 

typical of toxic tort cases . . . .” Cranor, Toxic Torts: Science, Law, and the Possibility of 

Justice (New York: Cambridge University Press, 2d ed, 2016), at 252. Therefore, as in 

ordinary negligence claims, circumstantial evidence of causation may be sufficient to 

establish exposure adequate to prove specific causation. See Skinner, 445 Mich at 164 

(stating that a plaintiff can satisfy his or her burden to prove causation in a negligence 

claim by providing circumstantial proof that facilitates reasonable inferences of 

causation). This position is also in accordance with that of other jurisdictions that have 

held that exposure levels in a toxic tort case can be “roughly established through reliable 

circumstantial evidence.” See, e.g., Blanchard v Goodyear Tire & Rubber Co, 190 Vt 

577, 578-579 (2011) (citation and quotation marks omitted). Federal courts likewise 

have concluded that “exact details pertaining to the plaintiff’s exposure are beneficial” 

but “not always available, or necessary,” Westberry v Gislaved Gummi AB, 178 F3d 257, 

264 (CA 4, 1999), and that “precise data on the exact degree of exposure to each 

chemical” is not always required, see Harper v Illinois Cent Gulf R, 808 F2d 1139, 1141 

(CA 5, 1987).

Nevertheless, to avoid leaving the jury to speculate, a plaintiff should set forth at 

least some evidence that he or she was exposed to the toxin at issue, including the 

estimated amount and duration of exposure. Skinner, 445 Mich at 164 (“To be adequate, 

a plaintiff’s circumstantial proof must facilitate reasonable inferences of causation, not 

mere speculation.”). While toxic tort plaintiffs are not required to provide “a 

mathematically precise table equating levels of exposure with levels of harm, . . . there 

must [nonetheless] be evidence from which a reasonable person could conclude that a 

defendant’s emission has probably caused a particular plaintiff the kind of harm of which 

he or she complains before there can be a recovery.” Wright, 91 F3d at 1107. A plaintiff 

should not rely “merely on a temporal relationship [to establish causation because this] is 

a form of engaging in ‘the logical fallacy of post hoc ergo propter hoc (after this, 

therefore in consequence of this)’ reasoning.” See West v Gen Motors Corp, 469 Mich 

177, 186 n 12 (2003) (citation omitted); McClain, 401 F3d at 1243 (“[S]imply because a 

person takes drugs and then suffers an injury does not show causation. Drawing such a 

conclusion from temporal relationships leads to the blunder of the post hoc ergo propter 

hoc fallacy.”). 

Instead, the plaintiff’s exposure level should be shown, at minimum, by 

circumstantial evidence that facilitates reasonable inferences.11 See Mitchell v Gencorp 

 

11 For instance, in Curtis, the Fifth Circuit held that the plaintiff’s expert gave rise to a 

genuine issue of fact regarding specific causation when he opined that the plaintiff had 

been exposed to a toxin at levels of at least 200 to 300 parts per million based on results 

of lower level exposure tests, work practices at the exposure site, and the nature of his 

symptoms. Curtis v M&S Petroleum, Inc, 174 F3d 661, 671 (CA 5, 1999).
12

Inc, 165 F3d 778, 781 (CA 10, 1999) (“Guesses, even if educated, are insufficient to 

prove the level of exposure in a toxic tort case.”). “In cases claiming personal injury 

from exposure to toxic substances, it is essential that the plaintiff demonstrate that she 

was, in fact, exposed to harmful levels of such substances.” Abuan v Gen Electric Co, 3 

F3d 329, 333 (CA 9, 1993) (citation, quotation marks, and emphasis omitted). Evidence 

of the plaintiff’s exposure level should encompass proof that the plaintiff was actually

exposed to the defendant’s toxin as well as the estimated amount and duration of 

exposure. See Allen v Pennsylvania Engineering Corp, 102 F3d 194, 199 (CA 5, 1996) 

(stating that a toxic tort plaintiff must show that he or she was exposed to harmful 

quantities of a chemical to sustain his or her burden); Wintz ex rel Wintz v Northrop 

Corp, 110 F3d 508, 513 (CA 7, 1997) (holding that the plaintiff’s expert testimony failed 

to establish exposure to a chemical when the expert did not address “how frequently, in 

what quantity, or in what form” the plaintiff was exposed to the chemical or the 

plaintiff’s “specific dose”). 

Another significant component of specific causation in a toxic tort case pertains to 

the evaluation and elimination of other reasonably relevant potential causes of a 

plaintiff’s symptoms.12 In order to demonstrate specific causation, a plaintiff’s 

“ ‘evidence must exclude other reasonable hypotheses with a fair amount of certainty.’ ” 

Skinner, 445 Mich at 166, quoting 57A Am Jur 2d, Negligence, § 461, p 442. One 

common method for excluding reasonably relevant potential causes of a plaintiff’s injury 

may be a “differential etiology,” sometimes characterized as a “differential diagnosis.” 

Myers v Illinois Cent R Co, 629 F3d 639, 644 (CA 7, 2010) (explaining that the former 

term is the more accurate in referring to causation because it focuses on identifying the 

cause of the ailment from which plaintiff suffers, whereas the latter term focuses on the 

identification of that ailment). Differential etiology is “a method by which all 

[reasonably relevant] possible causes of a condition are listed and then the various causes 

are ruled out so as to leave the most likely cause or causes of a particular patient’s 

problem.” Dengler v State Farm Mut Ins Co, 135 Mich App 645, 649 (1984); see also 

Attorney General v Beno, 422 Mich 293, 312-313 (1985) (differential diagnosis describes 

“the process of elimination of other possible maladies” as the cause of a plaintiff’s 

symptoms); Westberry, 178 F3d at 262 (“[D]ifferential etiology is a standard scientific 

technique of identifying the cause of a medical problem by eliminating the likely causes 

until the most probable one is isolated.”) (emphasis added; punctuation omitted). 

 

12 Plaintiff’s evidence need not address every remote possible cause in the universe. See 

Skinner, 445 Mich at 166, quoting 57A Am Jur 2d, Negligence, § 461, p 442 (“ ‘The

evidence need not negate all other possible causes . . . .’ ”); Viterbo v Dow Chem Co, 826 

F2d 420, 424 (CA 5, 1987) (holding in a toxic tort case that the plaintiff’s expert need not 

disprove or discredit every possible cause of the plaintiff’s injury other than the one 

espoused by him, but must do more than simply pick the cause that is most advantageous 

to the plaintiff’s claim).
13

Without the performance of a differential etiology,13 “ ‘[t]here may be 2 or more 

plausible explanations as to how an event happened or what produced it; yet, if the 

evidence is without selective application to any 1 of them, they remain conjectures only 

[and are insufficient to establish causation].’ ” Skinner, 445 Mich at 164, quoting 

Kaminski v Grand Trunk W R Co, 347 Mich 417, 422; 79 NW2d 899 (1956). As 

explained earlier, specific causation is subsumed within the cause-in-fact inquiry. In 

order to prove cause in fact, a plaintiff must demonstrate that there is more than an 

“evenly balanced” probability that the conduct of the defendant was, rather than was not, 

the cause in fact of the harm suffered. Mulholland v DEC Int’l Corp, 432 Mich 395, 416 

n 18 (1989) (citation and quotation marks omitted); see also Skinner, 445 Mich at 164 

(“Nor is it sufficient to submit a causation theory that, while factually supported, is, at 

best, just as possible as another theory.”). A differential etiology is included in the 

specific-causation inquiry under this burden because a plaintiff that fails to perform a 

differential etiology or some equivalent will not be able to meet his or her overall burden 

as described in Mulholland, i.e., when various possible causes of an injury exist, and 

when the plaintiff has not identified the most probable of these, the probability that the 

defendant’s conduct-- as opposed to some other potential cause-- constituted the cause in 

fact of the plaintiff’s harm remains “evenly balanced.” In such instances, the jury is left 

to infer causation from correlation, which it cannot do because “[i]t is axiomatic in logic 

and in science that correlation is not causation. This adage counsels that it is error to 

infer that A causes B from the mere fact that A and B occur together.” See, e.g., Craig v 

Oakwood Hosp, 471 Mich 67, 93 (2004). As a result, specific causation includes the 

need by some reasonable means to evaluate and eliminate other reasonably relevant 

potential causes of the plaintiff’s injury. 

D. EXPERT TESTIMONY

Because of the complexity of the general-and-specific-causation inquiry in toxic 

tort cases, it may also be necessary for a plaintiff to present expert testimony.14 Many 

 

13 While a differential etiology is not specifically or necessarily required in every toxic 

tort case, a plaintiff should utilize some reliable method, or introduce some evidence, 

designed to exclude other reasonably relevant potential causes of his or her injury. For 

example, some courts rely on studies comparing the incidence of the disease in groups 

exposed to the toxin and groups not exposed. See Green et al, pp 611-612.

14 I am cognizant that plaintiff in this case has presented expert testimony and thus 

whether he was required to do so is largely irrelevant to the resolution of his claim. I 

address this issue nonetheless because questions concerning the need for expert testimony 

will often be integral in cases of the instant sort-- toxic tort cases. It is altogether 

appropriate that this Court-- as the court of last resort of this state, as the court ultimately 

responsible for the fair and orderly development of our common law-- in reasonable 
14

jurisdictions have held that expert testimony is generally necessary or else even suggest 

that it is always required in a toxic tort case.15 That conclusion is reiterated in the 

secondary literature as well.16 Michigan has yet to address this matter in a toxic tort case 

 

ways, set forth the law more clearly so that litigants can reasonably apprehend their 

respective legal obligations in initiating and defending against claims of the instant sort. 

As members of this Court have stated on innumerable occasions during oral argument in 

our courtroom, it is the Court’s responsibility not only to address the case immediately 

before us in accordance with the law but also to afford guidance in the “next onehundred” similar cases. The question whether expert testimony is required is critical in 

identifying the proofs that must be provided by a plaintiff to satisfy his or her evidentiary 

burden when the general-and-specific-causation framework applies. My analysis would 

afford little guidance to litigants concerning the application of the general-and-specificcausation framework were I to fail to address the logically related and recurrent question 

of the need for expert testimony in such cases. Future litigants are entitled to at least 

minimal guidance concerning what is required to survive summary disposition in toxic 

tort cases. 

15 See, e.g., Milward v Rust-Oleum Corp, 820 F3d 469, 476 (CA 1, 2016) (requiring 

expert testimony in a toxic tort case and stating that “[a]s is well-established under 

Massachusetts law, ‘expert testimony is required to establish medical causation’ ”) 

(citation omitted); Junk v Terminix Int’l Co, 628 F3d 439, 450 (CA 8, 2010) (“In proving 

both types of causation, ‘expert medical and toxicological testimony is unquestionably 

required to assist the jury.’ ”) (citation omitted); Seaman v Seacor Marine LLC, 326 F 

Appx 721, 723 (CA 5, 2009) (“A plaintiff in such a case [i.e., a case involving injuries 

from exposure to toxins] cannot expect lay fact-finders to understand medical causation;

expert testimony is thus required to establish causation.”); Wills v Amerada Hess Corp, 

379 F3d 32, 46 (CA 2, 2004) (“In a case such as this [concerning exposure to a toxin], 

where an injury has multiple potential etiologies, expert testimony is necessary to 

establish causation . . . .”); Redland Soccer Club, Inc v Dep’t of Army of US, 55 F3d 827, 

852 (CA 3, 1995) (applying Pennsylvania law in a toxic tort case and stating that “[w]hen 

the complexities of the human body place questions as to the cause of pain or injury 

beyond the knowledge of the average layperson . . . the law requires that expert medical 

testimony be employed”) (brackets, quotation marks, and citation omitted); Harris v CSX 

Transp, Inc, 232 W Va 617, 653 (2013) (“[T]he need for expert testimony to supply [the] 

critical causal connection is often the key to a plaintiff’s toxic tort case . . . .”). 

16 Gold, The “Reshapement” of The False Negative Asymmetry in Toxic Tort Causation, 

37 Wm Mitchell L Rev 1507, 1536 (2011) (“[D]eciding a toxic causation dispute is 

inherently beyond the ken of lay people and therefore demands expert scientific 

testimony.”); see also Comment, Causation in Toxic Tort Litigation: “Which Way Do We 

Go, Judge?”, 12 Vill Envtl LJ 33, 34-35 (2001) (“The existence of . . . unique causation 

problems that confront plaintiffs in toxic torts makes it necessary for parties to offer 

expert testimony.”).
15

specifically, but the generally applicable rule in Michigan is that expert testimony is 

required when highly technical and scientific questions are at issue. Elher v Misra, 499 

Mich 11, 21-22 (2016) (requiring expert testimony on negligence in a medical 

malpractice action unless the matter “is within the common knowledge and experience” 

of the average juror); Teal v Prasad, 283 Mich App 384, 394 (2009) (generally requiring 

expert testimony on causation in a medical malpractice action); see also Amorello v 

Monsanto Corp, 186 Mich App 324, 331 (1990) (affirming summary disposition when 

the plaintiffs’ expert failed to establish the causation element of the plaintiffs’ productsliability claim). This rule originates in our common law and is grounded in the notion 

that scientific questions should be addressed by those with the relevant professional skill 

and knowledge so as not to leave jurors to speculate regarding matters beyond their 

knowledge. See, e.g., Miller v Toles, 183 Mich 252, 258 (1914); Spaulding v Bliss, 83 

Mich 311, 315 (1890); Mayo v Wright, 63 Mich 32, 40 (1886); Wood v Barker, 49 Mich 

295, 298 (1882). Put another way, the generally applicable rule is not a separate or a 

distinctive rule at all, but rather is a part of the plaintiff’s evidentiary burden to establish 

cause in fact. When the jury is able only to speculate concerning causation-- which is all 

jurors can do when a matter is scientific in character such that it is beyond their common 

knowledge-- the plaintiff has not satisfied his or her burden. Because the causation 

inquiry in toxic tort cases is often scientific in nature, a plaintiff will often be hardpressed to satisfy that evidentiary burden absent expert testimony; absent such testimony, 

the jury will only be left to speculate. For this reason, I would apply our general rule and 

conclude that the need for expert testimony regarding causation in a toxic tort case is 

determined on the basis of whether the matter “is so obvious that it is within the common 

knowledge and experience of an ordinary layperson.” Elher, 499 Mich at 21-22. If “the 

untrained layman would be qualified to determine intelligently and to the best possible 

degree [the elements of the claim] without enlightenment from those having a specialized 

understanding of the subject involved in the dispute,” then expert testimony is 

unnecessary and indeed is inadmissible.17 People v Kowalski, 492 Mich 106, 123 (2012) 

(opinion by MARY BETH KELLY, J.) (citation and quotation marks omitted); Gilbert v 

DaimlerChrysler Corp, 470 Mich 749, 790 (2004) (expert testimony is admissible to 

assist the trier of fact to understand a proposition that is “ ‘beyond the ken of common 

knowledge’ ”) (emphasis omitted), quoting Zuzula v ABB Power T & D Co, Inc, 267 F 

Supp 2d 703, 711 (ED Mich, 2003). Conversely, expert testimony may be required when 

 

17 Under MRE 702, expert testimony cannot be introduced at trial unless it assists the jury 

with a proposition beyond their common knowledge. As established by even our earliest 

medical malpractice jurisprudence, a party must introduce expert testimony at trial if the 

proposition is not within the common knowledge of the average juror. See, e.g., Miller,

183 Mich at 258. Both standards are helpful to the current inquiry due to their 

complementary character. Seemingly, when considered together, these rules suggest that 

expert testimony that is admissible is most often required, and expert testimony that is not 

required is most often inadmissible.
16

the causation inquiry “is scientific in nature,” Nelson v American Sterilizer Co (On 

Remand), 223 Mich App 485, 489 (1997), such that it is beyond “the common knowledge 

and experience of the jury,” see Bryant v Oakpointe Villa Nursing Ctr, Inc, 471 Mich 

411, 426 (2004) (holding that a claim sounds in medical malpractice and thus requires 

expert testimony when the questions at issue are not “within the common knowledge and 

experience of the jury”).18

II. APPLICATION

As explained earlier, in raising a toxic tort claim, a plaintiff is required to provide

proof of cause in fact. In the present case, plaintiff has relied on group-based statistical 

evidence or similar scientific proof. Therefore, the general-and-specific-causation 

framework would apply. Accordingly, the Court should examine plaintiff’s evidence to 

determine whether he has sufficiently shown general and specific causation, that is, 

whether the pertinent toxin (VOCs) is capable of causing the alleged injury and whether 

plaintiff here was actually exposed to that toxin at a level sufficient to cause the severe 

coughing and vomiting that, in turn, would cause his gastric artery to avulse. Given that 

the final step of this inquiry is clearly beyond “the common knowledge and experience of 

a jury,” Dorris v Detroit Osteopathic Hosp Corp, 460 Mich 26, 47 (1999), plaintiff was 

required to present expert testimony to that effect. Plaintiff also needed to reasonably 

evaluate and eliminate other reasonable potential causes of his injuries. 

A. GENERAL CAUSATION

Plaintiff here failed to establish that a causal link generally exists between the 

toxin released by the negligent act (VOCs) and the asserted harm (coughing, vomiting, 

and avulsion). Judge JANSEN correctly recognized that the harm suffered was 

“attenuated” from the negligent act, meaning that it required two findings to establish 

general causation: (1) VOCs in the level and duration at issue are capable of causing the 

degree and duration of coughing and vomiting at issue; and (2) coughing and vomiting in 

the degree and duration caused by the VOCs are capable of causing a gastric artery to 

avulse. Plaintiff’s proofs-- that is, the CDC documents-- contain the generally 

recommended exposure limits and the permissible exposure limits for three of the main 

chemicals found in VOCs-- Toluene, Benzene, and m-Xylene-- as well as state that 

overexposure to these chemicals can cause some amount of nausea or headaches. Indeed, 

plaintiff’s toxic tort claim did not fail with respect to damages for his coughing and 

nausea; the trial court denied defendants’ summary disposition motion regarding those 

injuries. Plaintiff also presented some evidence indicating that coughing and vomiting 

 

18 To the extent that the Court of Appeals’ opinion in Genna, 286 Mich App 413, has 

been understood never to require expert testimony in toxic tort cases, I believe that this is 

in error, and therefore I would explicitly reject this understanding. 
17

can cause a gastric artery to avulse, albeit only rarely.

Nevertheless, plaintiff’s general-causation evidence falls short because it fails to 

show what level and duration of exposure to VOCs can cause the severity and duration of 

coughing and vomiting that is necessary to cause a gastric artery to avulse. After all, not 

every person suffering stomach flu also suffers an avulsion of a gastric artery. When 

plaintiff’s expert was asked if he knew “what specific levels of exposure are required to 

cause any of [the] symptoms [plaintiff suffered],” he declined to provide an opinion: he 

did not “think that’s a question that could be answered unless you are speaking of a 

specific person and you would have to -- you would have to gauge that in retrospect 

because everybody is different, I think. I believe that to be true.” The remainder of 

plaintiff’s proofs also fail to address this critical point-- i.e., whether plaintiff’s level of 

VOCs exposure was capable of causing the level of vomiting necessary to cause a gastric 

artery to avulse. While plaintiff was not required to reference specific data and could 

have established general causation by alternative methods,19 plaintiff presented no

evidence regarding the exposure level necessary to cause his particular injuries and has 

failed to sustain his burden to prove general causation as a result. 

B. SPECIFIC CAUSATION

Plaintiff failed to establish specific causation. Again, plaintiff’s harm was 

attenuated from defendants’ action and required two findings to establish specific

causation-- plaintiff’s exposure to VOCs more likely than not caused him to cough and 

vomit, and such coughing and vomiting more likely than not caused his gastric artery to 

avulse. Plaintiff lacked evidence of specific causation on numerous grounds. First, he 

did not show that he was exposed to any VOCs, let alone exposure of the magnitude 

necessary to cause his particular symptoms. Second, he failed to reasonably consider and 

eliminate other potential causes of his symptoms. Third and last, he failed to provide 

adequate evidence concerning the causal link between his coughing and vomiting and the 

avulsion of his gastric artery-- a determination that is certainly beyond the common 

knowledge of the average juror and thus that required sufficient evidence in the form of 

expert testimony.20

 

19 See, e.g., King, 277 Neb at 215-221 (discussing the “Bradford Hill” factors for 

evidence of general causation in the absence of epidemiological studies).

20 I would presume for the purposes of my analysis that plaintiff’s expert testimony was 

admissible, but I would find that it was nevertheless insufficient. See Conde v Velsicol 

Chem Corp, 24 F3d 809, 813 (CA 6, 1994) (“Accordingly, we turn to the question of 

whether the [plaintiffs’] expert testimony, assuming that it is admissible, is sufficient to 

withstand summary judgment for [the defendant] on the issue of medical causation.”); 

Elkins v Richardson-Merrell, Inc, 8 F3d 1068, 1071 (CA 6, 1993) (affirming summary 

judgment in the defendant’s favor and concluding that precedent establishes that the court 
18

I examine each of these shortcomings in turn. Plaintiff’s first failure was to 

overlook the matter of personal exposure. When plaintiff’s expert, Dr. Nosanchuk, was 

questioned regarding his conclusion that plaintiff was exposed to VOCs that made him 

cough and vomit, Dr. Nosanchuk admitted that he did not know where the oil spill started 

or how far the release site was located from plaintiff’s home. When asked what 

chemicals were in the oil, he responded: “I think it was benzyl, toluylene, xylene. Maybe 

there was something else too.” He obtained this knowledge online and admitted that he 

lacked specific knowledge of which chemical constituents were present or in what 

quantities. Nor did he have any information concerning the emission or dispersion rates 

of VOCs. “[O]n a personal level” his understanding of VOCs effects was based on 

pumping gasoline into his own car: “[T]hey’re an irritant. I don’t really understand the 

toxicology. I know that they’re irritants and I know that they’re capable of causing 

cough, nausea, vomiting, irritation of the eyes and any other mucous membranes.” All 

that this testimony would reasonably demonstrate to the fact-finder is that VOCs 

contained in gasoline pumped into a car can, under some circumstances, act as an irritant. 

By itself, however, this fact neither evidences that plaintiff inhaled or was otherwise 

exposed to the VOCs contained in defendant’s oil nor that such VOCs acted as an irritant 

under these circumstances. 

Plaintiff himself only alleged that he smelled oil fumes “really strong” for several 

days. But, “[i]t is important to understand that these VOCs can be smelled at levels well 

below those that would cause health problems.” EPA, Enbridge Oil Spill: How is Air 

Quality Affected?, p 1 (emphasis omitted), available at <https://www.epa.gov/sites/ 

production/files/2016-06/documents/enbridge_fs_airquality_20100802.pdf> (accessed 

May 31, 2017) [https://perma.cc/5FU8-DKGD]. Despite knowledge here of the oil 

release site’s location, the amount spilled, and the duration of the incident, plaintiff did 

not provide any scientific information regarding VOCs, such as the conditions under 

which VOCs evaporate into the air, how quickly they do so and in what concentrations, 

the amount of surface oil necessary to produce a toxic level of VOCs in the air, how 

VOCs disperse in the air, and how long VOCs remain in the air.21 This list is only 

 

“treat[s] the plaintiff’s expert opinion indicating a basis of support for the plaintiffs’ [sic] 

theories . . . to be admissible but ‘simply inadequate . . . [to] permit a jury to conclude 

that [the toxin] more probably than not causes [the type of injury the plaintiff 

suffered]’ ”) (citation omitted; second alteration in original). 

21 Plaintiff did not even use the EPA air monitoring sampling data results, which 

provided the amounts of various VOCs in parts per billion by volume of the highest peak 

readings in locations near the oil spill. See, e.g., EPA, Enbridge Oil Spill: Human Health 

Air Screening Levels, available at 

<https://archive.epa.gov/region5/enbridgespill/data/web/pdf/

enbridge_voc_screening_levels_20100813.pdf> (accessed May 31, 2017) 
19

illustrative because plaintiff was not necessarily required to provide evidence on all these 

issues or to provide detailed chemical testing, modeling, and case studies to prove his 

claim. But he had to, at least approximately, establish his own level of exposure. 

Blanchard, 190 Vt at 579 (“[W]hile ‘it is not always necessary for a plaintiff to quantify 

exposure levels precisely,’ courts generally preclude experts from testifying ‘as to 

specific causation without having any measurements of a plaintiff’s exposure to the 

allegedly harmful substance.’ ”), quoting Henricksen v ConocoPhillips Co, 605 F Supp 

2d 1142, 1157 (ED Wash, 2009). Plaintiff here provided no information whatsoever 

regarding his potential exposure to VOCs. Absent evidence of his exposure level, 

plaintiff could not establish specific causation and therefore failed to show the cause-infact element of his toxic tort claim. See Henry, 473 Mich at 67 (“In an ordinary ‘toxic 

tort’ cause of action, a plaintiff alleges he has developed a disease because of exposure to 

a toxic substance negligently released by the defendant.”) (emphasis added).22 

Second, plaintiff failed to adequately consider and eliminate other factors that 

reasonably could have caused his injuries. Two days after his surgery, plaintiff was still 

in the hospital and informed Dr. Koziarski that another migraine headache was forming. 

Plaintiff reported to Dr. Koziarski that he was “reluctant to take Norco or Vicodin as this 

is what made him throw up the first time” and that he also thought Lamictal, the 

medication used to treat his depression, “may be causing his migraines.” Plaintiff’s 

medical history indicated that he “[g]ets migraines when stressed” and “has nausea and 

dry heaves[;] however it only occurs if he smokes or is around smoke.” The same record 

stated that plaintiff smokes. Further, plaintiff had visited the hospital in January 2008, 

complaining of headaches and nausea, which he then attributed to his recently increased 

dosage of Lamictal. Plaintiff was required to exclude these reasonably relevant potential 

causes of his injuries with a reasonable amount of certainty, but as shown in the record, 

his evidence to this effect was insufficient. 

 

[https://perma.cc/MF78-3UQU]. Plaintiff argues that defendants relied on information 

outside the record in providing the EPA’s sampling data to this Court, but defendants 

correctly argue that they were allowed to observe that such data existed and was publicly 

available in making the argument that plaintiff failed to demonstrate his exposure to 

harmful levels of VOCs. Such information is judicially noticeable. See MRE 201(b). 

22 Even assuming arguendo that plaintiff’s exposure could be garnered from reasonable 

inferences given the high number of other individuals in plaintiff’s area that developed 

symptoms consistent with VOCs exposure and plaintiff’s evidence to this effect, see 

Curtis, 174 F3d at 671-672 (holding that it was acceptable that the plaintiffs’ expert 

established exposure in part by considering the fact that several refinery workers 

developed the same cluster of symptoms consistent with benzene exposure shortly after 

the chemical was introduced to the refinery), plaintiff failed to establish specific 

causation for the additional reasons that follow.
20

Initially when plaintiff’s expert, Dr. Nosanchuk, was asked whether he had ruled 

out other relevant potential causes of plaintiff’s injuries, he essentially denied having 

performed a differential etiology of any kind, believing “that other potential causes were 

very unlikely.” But he later recalled not having been asked to consider alternative causes 

and stated: “I’m sure I considered a lot of them. I don’t remember any one that sticks in 

my mind.” When asked how he was able to rule out these other causes, his full response 

was, “Thought about it.” Then when he was pressed on his evaluation and elimination of 

alternative causes of plaintiff’s symptoms, Dr. Nosanchuk several times resorted to a 

well-known and insufficient manner of causal reasoning-- mistaking correlation for 

causation. See, e.g., Craig, 471 Mich at 93 (“It is axiomatic in logic and in science that 

correlation is not causation.”). 

For instance, when Dr. Nosanchuk was questioned on his claim that the oil leak 

was the sole cause of plaintiff’s symptoms, he stated that he meant “as far as I was 

concerned that is what was causing it. He wasn’t having the problems before and he was 

having the problems afterwards. The oil spill and the problems associated with the oil 

spill are capable of doing that and I think they did do that and that is my clinical 

judgment based on what I knew.” As the majority’s order correctly notes, Dr. 

Nosanchuk’s reasoning is also an example of the post hoc ergo propter hoc fallacy. See 

State of Ohio v US Dep’t of the Interior, 279 US App DC 109, 150 (1989) (explaining the 

fallacy in an oil spill case and stating that it is “the fallacy of assuming that, simply 

because a biological injury occurred after a spill, it must have been caused by the spill”). 

Dr. Nosanchuk’s report, in which he opined that Lamictal was not related to plaintiff’s 

health problems, contained the same flawed analysis. In explaining the basis for his 

opinion, Dr. Nosanchuk cited the Michigan Department of Community Health report that 

stated that the chemicals released in the spill could cause headaches and nausea. Because 

plaintiff was “squarely within the parameters [i.e., the location of the affected area] as 

outlined in the report,” Dr. Nosanchuk believed the spill had to have caused plaintiff’s 

symptoms and that Lamictal had nothing to do with these symptoms. Demonstrating that 

the VOCs could have caused headaches and nausea fails to establish that Lamictal-- or 

any other potential cause-- did not cause plaintiff’s headaches and vomiting. The factfinder thus is left with no evidence ruling out other causes or even tending to show that 

other causes are less likely the cause of the injury than are the VOCs.

Additionally, when Dr. Nosanchuk was asked if smoking could have been related 

to the nausea and vomiting, his response was simply that it could not have been. Later, 

however, he acknowledged that Vicodin could cause nausea and that smoking could 

cause coughing, but he did not believe that smoking was related to plaintiff’s problems: 

“Now, whether or not the smoking played any part at all [in plaintiff’s symptoms], I don’t 

know. All I know is my understanding is . . . he didn’t complain of significant cough 

before the fumes.” This type of correlative reasoning is not enough to reasonably 

eliminate an alternative cause. It does not provide a fact-finder any rationale for 

concluding that the VOCs are more likely the cause of plaintiff’s maladies than smoking. 
21

In sum, plaintiff’s expert only provided conclusory conjecture based on correlative 

reasoning, and therefore his testimony was insufficient to reasonably eliminate other 

reasonably relevant potential causes of plaintiff’s injuries as is required to establish 

specific causation. Skinner, 445 Mich at 164 (holding that impermissible conjectures do 

not amount to reasonable causal inferences).

Third and finally, plaintiff did not provide adequate evidence concerning the 

causal link between his coughing and vomiting and the avulsion of his gastric artery. The 

average juror cannot be expected to know the internal bodily reactions necessary to cause 

a gastric artery to avulse off of the spleen, and plaintiff did not provide adequate medical 

expert testimony on this topic. Plaintiff’s expert provided “ ‘an explanation consistent 

with [the] known facts or conditions, but not deducible from them as a reasonable 

inference,’ ” otherwise known as a conjecture, which explanation is insufficient to 

establish causation. Skinner, 445 Mich at 164, quoting Kaminski, 347 Mich at 422.

When questioned about the duration of VOCs exposure necessary to trigger an 

avulsion, Dr. Nosanchuk speculated that the injury could have occurred suddenly or 

“[m]aybe” “minor micro injuries” occurred over time, but he acknowledged, “I don’t 

know what happened,” followed by: “I can’t really comment on the-- I felt this is what 

did it and it happened. As far as why it took that long, I don’t know.” When asked if 

anything in the medical literature supported his testimony, he stated, “Not as much as my 

experience and my clinical judgment.” Even if Dr. Nosanchuk’s experience was 

relevant, he still failed to offer the fact-finder any rationale for his conclusions and, in 

fact, likely undercut those conclusions by repeatedly saying that he did not “know” why 

he reached them.

Regarding what may have caused the avulsion of plaintiff’s gastric artery, Dr. 

Nosanchuk had to “look this up” because he was “not an anatomist”-- an expert in the 

structure or internal workings of the human body. He reviewed the abstracts of three 

articles that he considered to be relevant. The abstracts list several potential causes of 

gastric artery tears and note that “rarely [is] vomiting” a predisposing condition. 

(Emphasis added.) Dr. Nosanchuk made no attempt to explain why plaintiff’s avulsion 

was among those rare cases in which coughing or vomiting caused the injury as opposed 

to other possibilities. 

In explaining what he relied on to form his ultimate opinion concerning the cause 

of plaintiff’s avulsion, he testified: “[T]here was an oil spill. That’s a known fact. There 

[were] fumes. That was a known fact. People got sick and some of them coughed, had 

nausea, and vomiting. It was the-- without anything specific, the total of that is what I 

based my opinion on. . . . I’m a very simple guy. Spill, fumes, sick people, to me they’re 

related based on 40 years doing this for a living.” In other words, the oil spill caused the 

injuries because it occurred before the injuries. A fact-finder could not rely on this 

rationale to reach a verdict favoring plaintiff. See West, 469 Mich at 186 n 12.
22

Overall, Dr. Nosanchuk provided only correlative reasoning based on his “clinical 

judgment.” For purposes of this Court’s review, the problems associated with his 

testimony are not ones of reliability or soundness of methodology, but rather speak to 

whether he produced any evidence tending to show that defendants’ oil fumes more 

likely than not caused the avulsion of plaintiff’s gastric artery.23 I, in agreement with the 

majority, conclude that he did not. Wright, 91 F3d at 1107 (stating that it is “not enough 

for a plaintiff to show that a certain chemical agent sometimes causes the kind of harm 

that he or she is complaining of”). Plaintiff’s expert did not show that a causal 

relationship between defendants’ VOCs and plaintiff’s arterial tear was more probable 

than not, and plaintiff thereby failed to create a genuine issue of fact as to specific 

causation. Skinner, 445 Mich at 174 (“Because the experts’ conclusions regarding 

causation are premised on mere suppositions, they did not establish an authentic issue of 

causation.”). Therefore, the trial court properly granted summary disposition in 

defendants’ favor. 

III. CONCLUSION

A toxic tort is no different than any other negligence claim in that a plaintiff must 

present evidence establishing factual or “but for” causation. Where, as here, a plaintiff 

presents evidence in the form of group-based statistical studies or similar proof, the 

general-and-specific-causation framework would apply. Evidence of general causation 

must include proof that the toxin in the alleged exposure level can cause the alleged 

harm. Evidence of specific causation must include proof that the plaintiff was actually 

exposed to the relevant toxin as well as a rough estimation of his or her exposure level. 

Specific causation additionally requires a plaintiff to evaluate and eliminate to a

reasonable extent other reasonably relevant potential causes of his or her injuries. 

Furthermore, if the issue or proposition in a toxic tort case is beyond the common

 

23 When considering scientific evidence of specific causation in a toxic tort case at the 

summary disposition stage, “the question is not whether there is some dispute about the 

validity or force of a given study, but rather, whether it would be unreasonable for a 

rational jury to rely on that study to find causation by a preponderance of the evidence.” 

In re Joint Eastern & Southern Dist Asbestos Litigation, 52 F3d 1124, 1133 (CA 2, 

1995).
I, Larry S. Royster, Clerk of the Michigan Supreme Court, certify that the

foregoing is a true and complete copy of the order entered at the direction of the Court.

 

July 25, 2017

t0724

23

Clerk

knowledge of an ordinary juror, expert witness testimony is required. Because plaintiff 

here failed to present evidence establishing either general or specific causation, I concur 

in the Court’s reversal of the judgment of the Court of Appeals and remand to the trial 

court for reinstatement of its order granting summary disposition in defendants’ favor. 

ZAHRA, J., and WILDER, J., join the statement of MARKMAN, C.J.