Toxic Tort Litigation Blog : Toxic Tort Lawyer & Attorney : Epstein Becker Green Law Firm : Product Liability, Contamination, Pollution

New York’s appellate courts continue to hold toxic tort plaintiffs and their experts to rigorous standards when it comes to proof of causation. To escape an adverse summary judgment ruling, it is not enough for a plaintiff to merely allege, with the support of an expert, that she was exposed to a toxic substance, and that this exposure resulted in the illness alleged. Rather, the plaintiff must raise a triable issue of fact as to her “exposure to a specific toxin or allergen; quantify the level of exposure to some degree; and posit that such level of exposure was sufficient to produce the alleged injuries.” Such was the holding of the Appellate Division, First Department, in Cleghorne v. City of New York, (2012 NY Slip Op 06648), decided on October 4, 2012.

Cleghorne was a school teacher employed by the New York City Board of Education. She claims that after her school was relocated to the Bronx in 2000, she developed respiratory problems while cleaning her classroom at the new location. Thereafter, she was diagnosed with asthma and bronchitis. After returning to work about a month later, she had an asthma attack at the school and was hospitalized. At her General Municipal Law § 50-h examination in September 2001, Cleghorne testified that she developed a persistent cough while cleaning her classroom and a storage area in the new building and that afterward her condition deteriorated. In October 2001, she commenced an action against the Board of Education and others.

 In 2010, both sides moved for summary judgment. Each side presented their own experts’ medical affidavits. The defendants’ physician, Jack J. Adler, a pulmonologist, determined that plaintiff had developed asthma prior to moving to the new school location. Adler opined that the environmental contaminants at the school did not cause the condition. He reported that plaintiff suffered from atopic or allergic asthma and that she was allergic to several common allergens, including tree and ragweed pollen, dust mites, dogs, cats, cockroaches, mold, spores and mouse and rat antigens, none of which were exclusive to her school. Because these environmental contaminants are extremely prevalent, Dr. Adler opined that she would have similar symptoms in any urban environment.

Cleghorne stated in her affidavit (which the court noted was executed more than nine years after the relevant events) that the school premises “were replete with rodents, rodent carcases, rodent droppings, cobwebs, cockroaches, cockroach and other bug carcasses, mildew, thick-black dust, and excessive dirt, and had numerous ceiling tiles that were water damaged and broken.” In addition, mold was in the ceiling tiles by the vents, on the walls, and in the closets. Her daily routine was to clean out all of this material before starting class.

Based upon Cleghorne’s affidavit, her expert, Dr. Hugh Cassiere, opined that Cleghorne was exposed to a “high level” of daily inhalation of these allergens, which caused her to develop “airway hyperresponsiveness.” Faced with two sets of dueling summary judgment motions, the trial court determined that questions of fact required the denial of both motions.

 In its opinion, the Appellate Division, First Department, unanimously reversed, holding that the trial court should have dismissed plaintiff’s case. Relying on the Court of Appeals landmark case, Parker v. Mobil Oil Corp., the First Department held that Cleghorne had failed to raise a triable issue of fact as to the specific toxin or allergen; that she had failed to quantify the level of exposure; and that she had failed to posit (through her expert) that such level of exposure was sufficient to produce the alleged injury.

In pertinent part, the Court held,

"While Parker recognizes that the level of exposure need not always be quantified “precisely,” it is still necessary that “whatever methods an expert uses to establish causation [they be] generally accepted in the [medical] community”… such methods include “mathematical modeling or comparing plaintiff’s exposure level to those of study subjects whose exposure levels were precisely determined."

In Cleghorne, the court found that the only so-called “method” plaintiff’s expert used to establish specific causation was to “accept, at face value, the anecdotal allegations of plaintiff’s uncorroborated affidavit that she was exposes to dust, bugs, rodent droppings and carcases in unspecified quantities and began experiencing asthma, purportedly for the first time, as a result.”
Although plaintiff’s expert characterized  Cleghorne’s exposure as “high level,” the Court found that this assessment was an insufficient basis for his causation theory and that plaintiff’s use of the term “replete” in her affidavit was a “meaningless and vague quantifying adjective.”

Significantly, the court held that an expert’s calculation of the level of exposure may not be based upon assumptions not supported by the record and faulted the plaintiff’s expert for not providing any scientific measurement or employing any accepted method of extrapolating such a measurement. Moreover, plaintiff offered no other evidence concerning the “level of allergens or toxins present in the school.” Although Dr. Cassiere did cite six studies in support of his theory of causation, he failed to compare plaintiff’s exposure level to those of any of the study subjects.

What lessons does Cleghorne provide?

1. Although New York state trial courts are generally reluctant to dismiss the personal injury claim of a sympathetic plaintiff, there is strong precedent in the appellate courts that favors dismissal of toxic tort lawsuits without appropriate scientific support. Therefore, making a strong appellate record below, either on summary judgment or at trial, is essential for achieving a successful outcome;

2. Although some commentators are critical of the Frye rule in New York state court (preferring instead the federal Daubert rule), New York has developed some rigorous Frye jurisprudence. Therefore, all is not lost if you are in New York state court and seek to exclude plaintiff’s expert;

 3. A rigorous analysis of plaintiff’s expert’s opinions, expressed either in his affidavit or CPLR 3101(d) expert witness disclosure, is essential. As reflected in Cleghorne, plaintiff’s expert must be able to quantify the level of exposure albeit not “precisely.” However, plaintiff’s methodology must include “mathematical modeling” or, alternatively, a comparison of plaintiff’s exposure level to the exposure level of study subjects in the scientific studies cited by the expert in support of his theory of causation. It is not sufficient to use words like “replete” or “daily” in quantifying an exposure to a toxin or allergen; and

4. The trial court should be cautioned that, in opposing a motion for summary judgment, it is not sufficient for plaintiff’s expert to rely solely on plaintiff’s "anecdotal" remarks seeking to link cause and injury.

Asbestos defendants are frequently faced with medical causation testimony from the plaintiff that asserts that, because there is no “safe” level of asbestos exposure, any exposure above some ill-defined “background” level is a substantial contributing factor to the plaintiff’s asbestos-related injury. This theory has become the centerpiece of modern asbestos litigation and discourages minimal exposure cases from going to the jury. However, a strong defense can be mounted to a minimal exposure case, particularly if plaintiff alleges exposure to chrysotile asbestos fibers.

For the toxic tort defense lawyer, an understanding of the two major families of asbestos is critical. From a toxicity standpoint, amphibole asbestos fibers are more potentially toxic than fibers of the serpentine family. Amphiboles tend to: (1) be acid resistant; (2) be persistent in the body; (3) be straight fibers; and (4) contain iron. By comparison,chrysotile asbestos, a member of the serpentine family, has a much more lower toxicity profile, particularly in low exposure settings. Chrysotile: (1) breaks down in the body; (2) is acid soluble; (3) has a soft pliable curly shape; and (4) contains dissolvable magnesium. Because the body handles chrysotile fibers differently, chrysotile is much less potent than amphibole asbestos. An examination of the toxicological literature demonstrates that the mesothelioma mortality risk is much greater from amphibole exposure as compared to chrysotile exposure.

At a meeting of the IADC in February 2012, William G. Hughson, M.D., D.Phil., expressed criticism of the expert opinions commonly expressed by plaintiff experts in asbestos cases concerning chrysotile. Dr. Hughson is the Director of the University of California at San Diego Center for Occupational & Environmental Medicine. Dr. Hughson rejects the view that any exposure above background is a substantial contributing factor to disease and that dose has no bearing on causation. At the same meeting, Bob Manlowe, a lawyer with Seattle-based Williams Kastner, delivered a paper titled, “Literature Refuting Single-Fiber Theory and Zero-No-Threshold/Linear-Dose-Model.” For the asbestos practitioner, the two papers provide a valuable road map to cross-examining plaintiff experts and defending mesiothelioma cases involving chrysotile asbestos.
 

When governmental or quasi-governmental agencies formulate a chemical risk assessment, it is part of their legitimate exercise of public health, policy-oriented regulation.  Regulators often develop risk assessments due to scientific uncertainty concerning the toxicity of a particular compound and utilize conservative risk models in the interest of protecting public health and the environment.  Thus, when a substance is labeled “possibly carcinogenic” or even “probably carcinogenic” by an agency, it may have little or no bearing on general and specific causation issues.

For this reason, risk assessments, and the assumptions that go into making them, have no legitimate place in toxic tort litigation.  Agency classifications and risk assessment certainly cannot legitimately be used by a toxic tort plaintiff to help establish his case-in-chief.  Agency classification and risk assessments are based upon standards that very significantly from the burdens of proof in a courtroom.  Thus, they are not legally relevant and pose a significant risk of confusion to jurors and prejudice to defendants. 

In a compelling article appearing in the Bloomberg BNA Toxics Law Reporter (February 3, 2012) titled, “When ‘Likely’ Does Not Mean ‘More Likely Than Not’: The Dangers of Allowing Government Chemical Classifications and Numeric Risk Assessments at Trial,” Mark P. Fitzsimmons and Leah M. Quadrino at Steptoe and Johnson, and Sneha Desai at BASF, describe how governmental agencies perform risk assessments and how the assumptions employed in reaching these risk assessments can easily mislead lay persons serving on juries in assuming that particular chemicals are carcinogenic to humans when, in fact, they may not be. 

Frequently, plaintiffs seek to introduce as evidence general and specific causation and increased risk.  The authors observe that the critical distinction between a regulatory classification of a chemical and the burden of proof required in court has been widely litigated.  Thus, in Gates v. Rohm and Haas Co., No. 10-108, 2011 U.S. App. LEXIS 17756, *33 (3d Cir. Aug. 25, 2011), the Third Circuit held that, “plaintiffs could not carry their burden of proof for a class of specific persons simply by citing regulatory standards for the population as a whole.” 

Similarly, other courts have excluded expert testimony for relying on regulatory ratings or standards in determining whether a plaintiff’s exposure to a substance above regulatory limits was sufficient to establish causation.  Baker v. Chevron USA Inc., 680 F.Supp. 2d. 865, 880 (S.D. Ohio 2010).  Defense counsel also must be vigilant against a court’s use of numeric risk assessment as a benchmark for determining increased risk.  The takeaway is that “probably” in a regulatory context does not mean “more probable than not” in a tort context.

A Sixth Circuit case, Moeller v. Garlock Sealing Technologies, LLC, 2011 U.S.App.Lexis 19987 (6^th Cir. Sept. 28, 2011), is the most recent in a series of judicial decisions that have rejected the opinions of plaintiffs’ experts in asbestos cases who espouse the “any exposure” or “any fiber” or “single fiber” theory of causation.  Pursuant to this specious line of reasoning, asbestos disease is a cumulative dose response process. Each and every exposure to asbestos during a person’s lifetime, no matter how small or trivial – even a single fiber – substantially contributes to the disease, whether it be asbestosis, lung cancer or mesothelioma. Using this theory of causation, plaintiffs have initiated a wave of new lawsuits against defendants far removed from the production of asbestos containing products.  As defense practitioners are well aware, successfully challenging weak causation expert opinions is key to winning any toxic exposure case, whether it involves asbestos or some other substance.

In a “must read” column in the New York Law Journal, dated October 19, 2011 titled "Courts Shoot Down Asbestos Causation Theory", Michael Hoenig, whose law firm defends asbestos case litigation, describes how plaintiff experts are promoting the “any fiber” or “any exposure” theory in courtrooms across the country and how a series of notable judicial decisions have begun to reject these theories as the underlying scientific methodology is subjected to scrutiny. In a recent amicus curiae brief filed by eleven distinguished scientists in a Pennsylvania asbestos case, none of whom received funding from or testified as experts for any of the parties in the case, the scientists attacked the methodological errors of the “any exposure” expert for:  (1) failing to consider the dose level of exposure and minimum threshold of asbestos fiber levels; (2) failing to consider the physical chemical and toxicological differences between various types of asbestos; (3) failing to distinguish between general causation and specific causation (and not even establishing general causation for chrysotile asbestos); (4) for suggesting that “every exposure” and “cumulative risk” theories are generally accepted when they are not; and (5) ignoring the large body of toxicological studies demonstrating that chrysotile asbestos is not potent as a cancer-causing agent. 

The Pennsylvania Supreme Court observed in Gregg v. V-J Auto Parts Co., 943 A.2d, 216, 223 (Pa. Sup. Ct. 2007), that although it was “common for plaintiffs to submit expert affidavits attesting that any exposure to asbestos, no matter how minimal, is a substantial contributing factor in asbestos disease,” such opinions are not “not couched within accepted scientific methodology.”  The court called the “willingness on the part of some experts” to offer such opinions “one of the difficulties” courts face in the mass tort cases.

As the plaintiff bar continues to look further and further afield in its “endless search for a solvent bystander,” as one well-known plaintiff’s lawyer described the litigation, successful challenges under Daubert and Frye should only increase.  The author thanks Mr. Hoenig for his thoughtful treatment of this important topic.

From a risk management perspective, peripheral toxic tort defendants often decline to mount  Daubert challenges due to the cost and time involved and the uncertainty of the result, particularly when the plaintiff presents them with seemingly  reasonable settlement demands.  As a result, hundreds of peripheral defendants continue to be named in these cases and often pay their "penny in tribute" just to get out of the case.  Unfortunately, in many jurisdictions, judges responsible for large asbestos dockets are unwilling to give appropriate consideration to motions by "shade tree" defendants who might otherwise challenge plaintiffs' experts'  theories of causation.  Cynically, these judges know that the cases will most likely settle out if this type of motion is given short shrift.  There is little incentive for a peripheral defendant to risk an adverse  judgment at trial merely to earn the right to bring an appeal, no matter how strong the grounds may be.  Hopefully, cases like Moeller will have a trickle down effect and motivate the trial judges responsible for the asbestos dockets to re-think their approach. 

Guest Blogger M.C. Sungaila, one of California's most best known appellate advocates,  briefed and successfully argued the Molina appeal discussed here on behalf of Shell and Chevron. 

A California appeals court rejected the lenient increased risk causation standard used to establish causation in asbestos cases in a toxic tort case not involving asbestos.  The Second Appellate District of the California Court of Appeal in Los Angeles upheld a defense verdict last month, in  Molina v. Shell Oil Company et al, determining that the trial court correctly refused to charge the Rutherford “increased risk” instruction applicable in asbestos cases because the ability of a product to cause the type of harm suffered by the plaintiff was hotly contested.

After a five-week trial and four days of deliberations in the trial court, a jury concluded that William Molina – who suffered from a variety of cancers and other ailments -- was not entitled to damages for his alleged exposure to defendants’ solvents during his 17-year career at a Firestone tire plant. The jury found that neither the solvents’ design nor any warning associated with them was a substantial factor in causing Molina’s non-Hodgkins lymphoma (NHL). Molina appealed, claiming among other things that the causation instruction used in California's asbestos litigation should have been given to the jury.

The appeals court court stopped short, however, of holding that the more liberal  Rutherford causation standard can never apply outside the asbestos context. Nevertheless, the Court of Appeal addressed a question repeatedly posed to trial courts throughout the state over the last five years: should a more lenient causation standard adopted by the California Supreme Court in the asbestos context be extended to other types of toxic tort cases like benzene? The appellate court’s answer was a qualified "no".

Causation, of course, is an essential element of a tort action. California has definitively adopted the substantial factor test of the Restatement Second of Torts for cause-in-fact determinations. Implicit in the substantial factor causation standard in a toxic tort case is the requirement of proving both that a chemical can cause a particular adverse health effect and that it did cause that effect in the plaintiff.  In other words, proof of causation necessarily includes a threshold determination whether, in reasonable medical probability, a particular chemical is capable of causing in humans the type of harm suffered by the plaintiff (i.e., “general causation”).　 If the chemical does not possess that capacity, the chemical cannot have caused the particular plaintiff’s claimed harm.　 But if the chemical does have that capacity, then the causation inquiry shifts to whether the plaintiff’s exposure to the chemical in question was, in reasonable medical probability, a substantial factor in causing this particular plaintiff’s harm (i.e., “specific causation”).　Toxic tort causation also involves a threshold element of exposure. In order to determine whether an exposure is a possible contributing factor to a plaintiff’s injury, ‘[f]requency of exposure, regularity of exposure, and proximity of the . . . product to [the] plaintiff are certainly relevant.” (Lineaweaver v. Plant Insulation Co. (1995) 31 Cal.App.4th 1409, 1416.)

Molina contended that California Civil Jury Instruction (CACI) No. 435, a relaxed “increased risk” causation instruction, should have been given because of the difficulties of proving cancer causation. The defendants successfully urged that the increased risk instruction under Rutherford should not apply where, as in Molina’s case, the ability of a chemical to cause a particular type of cancer is hotly disputed and far from well-established.

In Rutherford v. Owens-Illinois, Inc. (1997) 16 Cal.4th 953, 960, at the end of the first phase of trial, the jury concluded that exposure to asbestos fibers proximately caused the decedent’s lung cancer and awarded damages. After this phase, several defendants settled. In a second phase of trial, the jury was asked to apportion damages and allocate fault to the remaining defendant, Owens-Illinois. Owens-Illinois objected to the use of an instruction in the second phase of trial which stated that, once the plaintiff had established both that he was exposed to defendants’ asbestos and that his injuries were legally caused by asbestos exposure generally, the burden then shifted to the defendant to establish that its product was not a legal cause of the plaintiff’s harm.

The California Supreme Court rejected the use of the burden-shifting instruction as too “fundamental” a departure from traditional substantial factor causation. However, the Court concluded that, rather than be required to “trace the unknowable path of a given asbestos fiber,” a “plaintiff[] may prove causation in [an] asbestos-related cancer case[] by demonstrating that the plaintiff’s exposure to defendant’s asbestos-containing product in reasonable medical probability [fn. omitted] was a substantial factor in contributing to the aggregate dose of asbestos the plaintiff or decedent inhaled or ingested, and hence to the risk of developing asbestos-related cancer, without the need to demonstrate that fibers from the defendant’s particular product were the ones, or among the ones, that actually produced the malignant growth.”

Thus, in Rutherford, “it was already determined what caused the plaintiff’s illness—asbestos. The only remaining issue before the Court was the proper standard for determining who manufactured or supplied the asbestos that caused the plaintiff’s illness.” (Loewen, Causation in Toxic Tort Cases: Has the Bar Been Lowered? (Spring 2003) 17 Nat. Res. & Env’t 228, 229 (hereafter Loewen).) As one commentator observed: “This is undoubtedly the reason that the Rutherford court consistently and repeatedly limited its holding to ‘asbestos-related cancer cases’: its language linking risk to cause was expressly limited to cases where it has been determined that the cancer was ‘asbestos-related.’” (Ibid.) Accordingly, Rutherford does not apply in a case like this, where the ability of the defendants’ products to cause the plaintiff’s type of cancer is hotly disputed.

In Molina’s case, defendants’ toxicology expert testified that solvents do not cause NHL.  While one plaintiffs’ expert asserted that solvents could cause NHL, another plaintiffs’ expert testified that the evidence of a causal link between benzene and NHL was “weak” and therefore he could not state to a reasonable degree of medical probability that benzene could cause NHL.  Moreover, one of plaintiffs’ experts admitted that NHL is frequently idiopathic or of unknown origin.

The Court of Appeal agreed that the trial court correctly refused the Rutherford “increased risk” instruction applicable in asbestos cases. Rutherford involved a very different situation: in that case, a jury had already determined that the asbestos had caused the plaintiff’s lung cancer. The only remaining question was which manufacturers were responsible. The cause of Mr. Molina’s NHL, however, was not established.  In fact, the capability of defendants’ products to cause Mr. Molina’s injury was one of the most critical and hotly disputed issues in the case.

Guest Blogger M.C. Sungaila  is a partner in the appellate law firm of Horvitz & Levy in Los Angeles. Her appellate work has helped shape toxic tort law in California, including the scope of the duty to warn sophisticated users of product hazards and the guidelines for admitting expert testimony at trial.

Toxic Tort Litigation Blog’s post earlier this year about a Michigan appellate court’s affirmance of an award to residents of a home overrun with mold – without any expert testimony to prove causation – raises the question: what would happen to such a claim in a more famously liberal state like California? In this instance at least, California seems more likely to come to a more ‘conservative’ conclusion than Michigan.

Expert Testimony

California not only requires expert testimony for complex causation questions; it tests the foundation for that testimony and requires trial courts to exclude expert opinions that are unsupported. See an early article describing the development of these standards by M.C. Sungaila and David M. Axelrad published in California Lawyer. The California courts of appeal have specifically considered the admissibility of expert testimony in mold cases and ruled in favor of the defendants. Most recently, in Dee v. PCS Property Management, one of the appellate divisions in Los Angeles confirmed the trial court’s ability to exclude unfounded expert testimony in a residential mold case. Darcee Dee lived in an apartment for slightly over four months. She sued her landlord and property management company for alleged physical injuries, as well as fear of cancer, from living in an apartment that purportedly had toxic mold in it. After hearing the plaintiff’s experts testify over several days concerning their opinions and the foundation for them, the trial court granted the defendants’ motions in limine to exclude most of the experts’ testimony based on a lack of foundation. The remaining portions of Dee’s claims were tried to a jury, and the jury rejected her claims. The appellate court affirmed the judgment in Dee, concluding that the trial court did not abuse its discretion by excluding plaintiff’s experts for lack of an adequate foundation.  Each of Dee’s experts sought to testify that her exposure to mold mycotoxins caused her symptoms and her susceptibility to cancer, without any evidence that she was exposed to potentially harmful mycotoxins at her residence. The court relied on the decision in another mold case, Geffcken v. D’Andrea,  and distinguished its own prior decision in Roberti v. Andy’s Termite, the only published opinion to have rejected the trial court’s authority under the California Evidence Code to thoroughly analyze the foundation for expert testimony in order to determine its admissibility.  For another take on the Geffcken and Dee mold decisions, see an article on the Kring & Chung LLP website.

Toxic Tort Causation Standards

While California appellate courts would be certain to require expert testimony on causation, it is not as clear how they would analyze causation in a toxic tort case.  In toxic tort cases, a plaintiff must generally prove not only that a chemical or substance can cause a particular adverse health effect but also that it did cause the harm to the plaintiff.  Proof of causation therefore necessarily includes a threshold determination whether, as a matter of reasonable medical probability, a particular chemical is capable of causing in humans the type of harm suffered by the plaintiff (i.e., “general causation”). If the answer is that the chemical does not possess that capacity, then the chemical cannot have been a cause of plaintiff’s harm. But if the chemical does have that capacity, then the causation inquiry (in jurisdictions like California which apply a substantial factor causation standard) becomes whether the plaintiff’s exposure to the chemical in question was as a matter of reasonable medical probability a substantial factor in causing the particular plaintiff’s harm (i.e., “specific causation”).   For a helpful analysis of causation in toxic tort cases, see the excellent discussion by David E. Bernstein, a Professor at the George Mason University School of Law, in an article  titled "Getting to Causation in Toxic Tort Cases".  This two-step general and specific causation framework is almost universally accepted by federal courts analyzing toxic tort causation (including the Ninth Circuit, see, e.g., Golden v. CH2M Hill Hanford Group, Inc. (9th Cir. 2008) 528 F.3d 681, 683).  Trial courts in California have analyzed proof of causation in toxic tort cases along general and specific causation lines as well. California appellate courts have not, however, expressly adopted the general and specific causation distinction in a published decision. This has led to some confusion, as plaintiffs have attempted to convince courts that such a “two-part”causation test is incompatible with California’s prevailing causation standards.  In Dee v. PCS Property Management, the plaintiff raised this argument on appeal, but the Court of Appeal declined to reach it because the jury had found no negligence, which made an argument about causation standards “irrelevant.” An opportunity to address the general and specific causation distinctions head-on may come later this year, however, when the Court of Appeal in Los Angeles is likely to hear argument in and decide the plaintiffs’ appeal of summary judgment in a high-profile benzene exposure case brought by former students at Beverly Hills High. The appellate docket for the case, Lee v. Venoco, is attached here. The original summary judgment decision ruled on the admissibility of expert opinion on both general causation and specific causation.

BNA Toxics Law Reporter reported on December 31, 2009, that a Michigan Appeals Court affirmed a mold exposure verdict for $303,260, finding that expert testimony was not necessary under Michigan State law to prove either general causation or specific causation.  In Genna v. Jackson, Mich. Ct. App., No. 285746, the Michigan Court Of Appeals (Oakland Circuit Court) affirmed the trial court's denial of defendant's post-judgment motion for judgment notwithstanding the verdict (JNOV) and for a new trial. Based upon a review of the decision, it is not disputed ( at least by this writer) that defendant's negligent conduct resulted in substantial  flooding in the plaintiffs' home and the gross mold contamination that resulted. Plaintiff's microbial expert identified two molds in the home--penicillum and aspergillus--which he testified at trial could affect human health and pose safety issues.  Plaintiffs' children began to experience what the court described as "flu-like symptoms including: diarrhea, vomiting, congestion and nosebleeds".  Over a period of months, these symptoms worsened and the symptoms did not respond to aggressive treatment.  Plaintiffs did not call an expert to testify that these symptoms were the result of the mold contamination. Nonetheless, the appeals court held that plaintiff did not have to demonstrate that the alleged toxin is "capable" of causing injuries like those suffered by the children, let alone requiring the plaintiffs to prove that these children's symptoms were caused by mold exposure. The court reasoned as follows: "This is not a complicated case: the children were removed from the home, the mold was discovered, and the children recovered".  Thus, the court based its decision on "circumstantial evidence that would 'facilitate reasonable inferences of causation, not mere speculation'."  With due respect to the appellate panel, which was obviously impressed with the graphic description of "patches of mold of all different colors all over the walls and ceilings in her kitchen, family room and dining area", this is a really bad decision and a potentially dangerous precedent in Michigan!  It is a mistake to base toxic tort causation on a temporal relationship,i.e., the "children were removed from the home, the mold was discovered, and children recovered."  Flu-like symptoms can be caused by......well, the flu.  That the children's symptoms went away could signify that they had recovered from a prolonged bout of the  flu. Based upon this court's reasoning, the children's illness could have been caused just as easily by lead paint poisoning, contamination of their drinking water, VOC's emanating from their carpeting,  formaldehyde in the walls....or just a really bad allergic reaction to the family's cats.  Did anyone check the family furnace for carbon monoxide gas?  It is not as if the symptoms that the children suffered from were unique to mold "poisoning". Moreover, no one appears to have apprised the trial court that it is not unusual that the antibiotics the children were administered did not cure a viral infection! We also suffer from flu-like symptoms all the time. It is not unusual, particularly in the frigid month of February in Royal Oak, Michigan, when this incident occurred, for these symptoms to occur and to persist in the absence of an exposure to toxic mold. The court faults the defendant for not submitting "any scientific evidence that the mold in her condominium could not have caused plaintiffs' injuries." (emphasis theirs).  And since when does the burden in a negligence case shift to the defendant, and to prove a negative no less?