Medical Monitoring Class Action Rejected at Pleading Stage

A federal court recently rejected a proposed medical monitoring class action brought by alleged Pepsi drinkers.  The case reminds readers of the importance of the causation element of medical monitoring claims, even though plaintiffs don't need to allege traditional personal injury.  See Riva v. Pepsico, Inc., No. C-14-2929 EMC, 2015 WL 993350 (N.D. Cal.,  3/4/15).

Plaintiffs alleged that two of defendant's beverages contained levels of a chemical, 4–MeI, that caused them to experience an “increased risk of cancer,” specifically bronchioloalveolar cancer.  Plaintiffs sought  medical monitoring as a remedy; specifically, seeking an order requiring Pepsi to establish a “fund from which those individual class members can seek monetary recovery for the costs of actual or anticipated medical monitoring expenses incurred by them.”  Plaintiffs alleged that outcomes in bronchioloalveolar cancer show a clinically significant benefit from early evaluation, detection, and diagnosis. 

California is one of the few states that recognizes a claim for medical monitoring. “In the context of a toxic exposure action, a claim for medical monitoring seeks to recover the cost of future periodic medical examinations intended to facilitate early detection and treatment of disease caused by a plaintiff’s exposure to toxic substances.” Potter v. Firestone Tire & Rubber Co., 6 Cal.4th 965, 1004–05, 25 Cal.Rptr.2d 550, 863 P.2d 795 (1993). In Potter, the California Supreme Court identified five factors in determining the reasonableness and necessity of monitoring:
(1) the significance and extent of the plaintiff’s exposure to chemicals;
(2) the toxicity of the chemicals;
(3) the relative increase in the chance of onset of disease in the exposed plaintiff as a result of the exposure, when compared to
(a) the plaintiff’s chances of developing the disease had he or she not been exposed, and
(b) the chances of the members of the public at large of developing the disease;
(4) the seriousness of the disease for which the plaintiff is at risk; and
(5) the clinical value of early detection and diagnosis.

Based on such factors, the trier of fact decides, “on the basis of competent medical testimony, whether and to what extent the particular plaintiff’s exposure to toxic chemicals in a given situation justifies future periodic medical monitoring.” Id.

Defendant attacked the medical monitoring claim under Rule 12(b)(6), particularly as to the Potter factors related to whether medical monitoring is reasonable and necessary.  Accordingly, the Court examined the allegations related to these critical Potter factors: plaintiff’s exposure to chemicals; the toxicity of the chemicals; and the relative increase in the chance of onset of disease in the exposed plaintiff as a result of the exposure, when compared to (a) the plaintiff’s chances of developing the disease had he or she not been exposed, and (b) the chances of the members of the public at large of developing the disease.

To demonstrate the proximate causation element of the claim, a plaintiff seeking medical monitoring must. among other things, show the significance of her exposure to the toxic chemical. Potter, 6 Cal.4th at 1009, 25 Cal.Rptr.2d 550, 863 P.2d 795; see also Abuan v. Gen. Elec. Co., 3 F.3d 329, 335 (9th Cir.1993) (applying comparable Guam law on medical monitoring). The California Supreme Court has explained, “[e]vidence of exposure alone cannot support a finding that medical monitoring is ... necessary.” Lockheed Martin Corp., 29 Cal.4th at 1108–09, 131 Cal.Rptr.2d 1, 63 P.3d 913. A plaintiff must demonstrate sufficient severity of exposure (its significance and extent) and that “the need for future monitoring is a reasonably certain consequence of [the] toxic exposure” Id. at 1109, 131 Cal.Rptr.2d 1, 63 P.3d 913 (citation omitted).

In this case, Plaintiffs alleged that the chemical had been found to cause lung tumors in laboratory animals -- at a daily dose thousands of times higher than the amount in soda.  Plaintiffs sought to represent a class of all persons who purchased Diet Pepsi or Pepsi One within a four-year period, regardless of consumption amount. What was missing was any allegation of what the significance of this unspecified exposure to the chemical may be; they did not allege what threshold level of exposure allegedly created the increased risk.

Thus, there was insufficient information about the significance and extent of exposure of the class to make the necessary ultimate showing that “the need for future monitoring is a reasonably certain consequence of [the] toxic exposure” Lockheed Martin Corp., 29 Cal.4th at 1109, 131 Cal.Rptr.2d 1, 63 P.3d 913. They simply failed to demonstrate a credible risk of bronchioloalveolar cancer resulting from the human consumption of cola products at the levels alleged by the named plaintiffs. In fact, if anything, the specific scientific finding incorporated into the Complalnt from the mice study was that the amounts of 4–MeI ingested in cola products “may not be significant.”

The Court also found that Plaintiffs had not sufficiently pled their injury or shown the toxicity of 4–MeI. It was not enough thatt 4–MeI is on the Proposition 65 list of known carcinogens, that a toxicologist has stated that there is “no safe level of 4–MeI,” and that advocacy groups have called for the FDA to ban 4–MeI.  The full picture was that “caramel coloring” (the manufacturing of which allegedly produces 4–MEI as a byproduct) is “generally recognized as safe” when used in accordance with good manufacturing practice and as a food color additive. Under the FDCA, the inclusion of “caramel color” as a “color additive” means that the FDA has determined that caramel coloring has not been found “to induce cancer when ingested by man or animal.” 21 U.S.C. § 379e(b)(5)(B).

So while Plaintiffs adequately pled that 4–MeI is toxic and is, generally speaking, a carcinogen—i.e., that 4–MeI is capable of causing cancer, they had not adequately pled their specific theory of injury—an increased risk for bronchioloalveolar cancer sufficient to warrant medical monitoring—“above the speculative level.” Twombly, 550 U.S. at 555. Plaintiffs are not mice, and there was nothing in the Complaint, or the studies incorporated by reference, to suggest that 4–MeI causes this specific form of lung cancer in humans. The same mouse study found no increased cancer in rats and discussed a “species difference” identified in previous studies in terms of how various species absorb, distribute, metabolize, and excrete this very chemical. So this study did not lead to a plausible inference that these Plaintiffs are at increased risk of the specific lung cancer for which they request screening. 


In short, the  Plaintiffs failed to plead factual content to show they had been injured due to a “significant” increase in their risk of lung cancer sufficient to justify medical testing in the absence of any symptoms or present injury. See Potter, 6 Cal.4th at 1008–09, 25 Cal.Rptr.2d 550, 863 P.2d 795. The only factual content supporting the allegation of increased risk of lung cancer came from scientific studies, which had no demonstrable bearing on cancer toxicity for humans at the consumption levels alleged in the case at bar.

A plaintiff seeking medical monitoring must show a need for “specific monitoring beyond that which an individual should pursue as a matter of general good sense and foresight.” Potter, 6 Cal.4th at 1009, 25 Cal.Rptr.2d 550, 863 P.2d 795. In this case, Plaintiffs sought CT scans of their lungs and molecular screening for lung cancer. Lung scans are not needed to remedy injury absent a credible showing that 4–MeI causes this lung cancer in humans.

The Court took the Prop 65 argument head on.  Proposition 65 is broad; its listing embraces “ substances listed as human or animal carcinogens. In other words, “the Proposition 65 list includes chemicals that are known to cause cancer in animals, even though it has not been definitively established that the chemicals will cause cancer in humans.” Baxter Healthcare, 120 Cal.App.4th at 352, 15 Cal.Rptr.3d 430. Furthermore, listing under Proposition 65 only requires one excess case of cancer in an exposed population of 100,000, assuming lifetime exposure at the level in question. Because the burden on a defendant to fund medical screening for thousands, potentially millions, of people is so substantial, the Potter factors serve a critical gatekeeping function, regulating a potential flood of costly litigation; Potter requires a higher level of proof of health risk than that required for inclusion of a substance on the Proposition 65 list.

Finally, the Court addressed the increased risk above background, and other possible sources of exposure.  There can be many possible “causes,” indeed, an infinite number of circumstances which can produce an injury or disease. A possible cause only becomes “probable” when, in the absence of other reasonable causal explanations, it becomes more likely than not that the injury was a result of its action. This is the outer limit of inference upon which an issue may be submitted to the jury. As a result, under California personal injury law the mere possibility of causing cancer alone is insufficient to establish a prima facie case.

The Court said that this concept of causation inheres in the Potter test for the reasonableness of medical monitoring; the trier of fact considers, among other factors, “the relative increase in the chance of onset of disease in the exposed plaintiff as a result of the exposure, when compared to (a) the plaintiff’s chances of developing the disease had he or she not been exposed, and (b) the chances of the members of the public at large of developing the disease.” Potter, 6 Cal.4th at 1009, 25 Cal.Rptr.2d 550, 863 P.2d 795. Consistent with this approach, the Ninth Circuit has affirmed a grant of summary judgment where plaintiffs seeking medical monitoring failed to introduce facts regarding the “quantitative (or even qualitative) increased risk to individuals.” Abuan, 3 F.3d at 335.

The Complaint admitted that there are many sources of consumption of 4–MeI, including “baked goods, confectionary, extruded breakfast cereals, instantaneous soups, and dark beers” as well as “soy sauce and coffee.” The many alternative sources of 4–MeI was problematic to the establishment of any causation between the Pepsi products at issue and the Plaintiffs’ alleged consumption of 4–MeI “at or above certain threshold levels” (whatever those threshold levels, if any, may be). The many sources of 4–MeI prevented these Plaintiffs from satisfying the third Potter factor.

Where the pleadings reveal so many commonly consumed foods with similar levels of a chemicaI, it is implausible to conclude that any alleged increased risk of cancer is “more likely than not” caused by drinking/using one product, said the Court.  As a result, the Plaintiffs’ claims were dismissed. See Twombly, 550 U.S. at 557 (“something beyond the mere possibility of loss causation must be alleged”).

 

 

Cancer Study of 9/11 Responders

Your humble blogger was quoted in a recent article in a Product Liability Law 360 story on the recent JAMA stud, which found no significant increase in most cancers among first responders and others exposed to dust and debris from the 9/11 terrorist attacks.  The study included more than 55,000 people enrolled in a 9/11-related health registry and examined data from 2003 to 2008.

 

Defense Verdict in Chemical Case Affirmed

The Eleventh Circuit last week affirmed a jury verdict for chemical defendant E. I. DuPont de Nemours & Co. in a personal injury claim arising out of the use of the agricultural product Benlate. Ramirez v. E.I. DuPont de Nemours & Co., No. 11-10035 (11th Cir. 12/13/11).
 
The plaintiff/appellant alleged in his complaint that he used Benlate in conjunction with his farming
operations. Ramirez asserted that Benlate was a defective product because it contained an allegedly known carcinogen, atrazine. He also contended that the use of Benlate caused him to contract cancer. The case was tried to a jury which returned a verdict favorable to DuPont.  Specifically, although the jury found that Benlate was a defective product, it did not find that the Benlate was the cause of Ramirez’s cancer.
 
On appeal, Ramirez argued that the verdict in the case was inconsistent because the jury determined that the product was defective, but was not the cause of Ramirez’s injuries. The court agreed with DuPont's argument that defect and causation are separate elements of the strict liability cause of action, and a jury is free to go different directions on each.
 
The record showed that the jury was presented with numerous plausible reasons for determining that Benlate did not cause Ramirez’s cancer. For example, the jury heard that when Ramirez sprayed his crops, he rode inside an enclosed tractor cab, wore protective clothing, including goggles, a mask, a jumpsuit, gloves and boots, and thus had minimal exposure.  The jury also heard evidence demonstrating that Ramirez had numerous risk factors for cancer, including a family history of cancer and a history of smoking cigarettes.
 
Finally, plaintiff attacked DuPont’s expert, Dr. Cohen, contending that the testimony of Dr. Cohen should have been stricken pursuant to Daubert.  The court of appeals disagreed, finding Cohen was one of the world’s leading experts in cancer and chemical causation; clearly, he considered the type of scientific and factual information that experts in his field would reasonably rely upon in opining on causation.
 

NTP Proposes Changes to Process for Next Report on Carcinogens

The National Toxicology Program is accepting comments on a revised process for reviewing substances that may be added to its widely cited "Report on Carcinogens." NTP is accepting comments up to Nov. 30th.

The Report is required by Congress to be published every two years, and is designed to provide
information on substances that may pose a hazard to human health by virtue of their  carcinogenicity.  Substances are listed in the report as either known or reasonably anticipated human carcinogens. The 12th Report was published in June, 2011. But now, the NTP is proposing changes to the review process for listing substances in the 13th Report.

The NTP will hold a listening session on November 29, 2011, from 1–5 p.m. (EST), as well, to receive oral comments on the proposed review process.

Under the proposed process, NTP says it would make its substance review process more flexible, and more descriptive of the  reasoning it used to develop a proposed classification of an agent, and  thus would summarize the relevant science and also the agency's reasoning about how the agent should be classified.

Toxic tort practitioners among our readers may want to take a look (and have their experts do so).
 

State Supreme Court Holds Causation Evidence Insufficient

The Vermont Supreme Court recently held that a plaintiff's evidence that exposure to benzene allegedly caused his cancer was insufficient to get to the jury.  Blanchard v. Goodyear Tire & Rubber Co.,  No. 2010-250 (Vt. 8/5/11).

Plaintiff was diagnosed with non-Hodgkin's lymphoma, and he attributed the onset of the disease to benzene exposure that allegedly occurred between 1968 and 1973 while he was a teenager playing on a ball field on the grounds of the former Goodyear rubber manufacturing plant. That  plant operated in Windsor, Vermont from 1936 to 1986. He sued, alleging that the field itself was polluted and that there was a gully in the outfield that transported foul-smelling and oily stormwater discharge away from the manufacturing plant.

Defendants moved for summary judgment. The lower court concluded that plaintiff was not entitled to present his case to a jury because he had provided insufficient evidence to support an inference that he had been exposed to benzene in any amount, let alone an amount that could have caused his illness, nor sufficient expert testimony sufficient to eliminate other potential causes of his disease. On appeal, plaintiff argued that his circumstantial evidence of causation was sufficient to present his case to the jury.

The state Supreme Court noted that the plaintiff could not survive the motion for summary judgment on his toxic tort claim unless he was able to point to evidence suggesting a probability, rather than a mere possibility, that (1) he was exposed to the specified chemical at a level that could have caused his physical condition (general causation); and (2) the exposure to that chemical did in fact result in the condition (specific causation).  In a toxic tort case, general causation addresses whether a substance is capable of causing a particular injury or condition in a population, while specific causation addresses whether a substance caused a particular individual's alleged injury. E.g., King v. Burlington Northern Santa Fe Ry. Co., 762 N.W.2d 24, 34 (Neb. 2009). General causation is typically shown through epidemiological studies, and plaintiffs in toxic exposure cases in Vermont generally must demonstrate specific causation by submitting evidence concerning the amount, duration, intensity, and frequency of exposure. Citing  Henricksen v. ConocoPhillips Co., 605 F. Supp. 2d 1142, 1157 (E.D. Wash. 2009) (citing several appellate court cases holding that experts testifying as to specific causation must pay careful attention to amount, intensity, and duration of exposure).

The court recognized that in some toxic tort cases it is impossible to quantify exposure with hard proof, such as the presence of the alleged toxic substance in the plaintiff's blood or tissue and the precise amount of the toxic substance to which an individual plaintiff was exposed. Plourde v. Gladstone, 190 F. Supp. 2d 708, 721 (D. Vt. 2002).  Therefore, expert testimony on toxic injuries may be admissible where dosage or exposure levels have been established through sufficient reliable circumstantial evidence. While it is not always necessary for a plaintiff to quantify exposure levels precisely, the courts generally preclude experts from testifying as to specific causation without having any some measurement or reasonable estimate of a  plaintiff's exposure to the allegedly harmful substance. Finally, a defendant's concession that its product contains a carcinogen, say benzene, does not excuse a plaintiff from having to show the benzene contained in defendant's product is capable of causing the illness at issue.

When direct evidence of the precise amount of exposure to a toxic substance is limited, some courts have allowed expert witnesses to use a differential diagnosis process as a method of proving specific causation. We have posted before about the mis-use and mischaracterization of this process.  Differential diagnosis is a scientific analysis entailing the weighing of relevant evidence, listing all likely explanations of the patient's observed symptoms or injury, then eliminating all but one.  Some courts have made the leap from allowing the process designed to arrive at a diagnosis (what disease caused the symptoms) to arrive at a cause (what substance caused the disease). However, said the state court, even the courts that do recognize differential diagnosis are reluctant to admit causation testimony based on a differential diagnosis where the proffered expert possesses only weak circumstantial evidence that some exposure occurred and makes insufficient effort to scientifically evaluate or estimate the degree of exposure or dosage. Also, and significantly, standing alone, the presence of a known risk factor is not a sufficient basis for ruling out idiopathic origin in a particular case, particularly where most cases of the disease have no known cause. In such cases, analysis beyond a differential diagnosis is required.

Here, plaintiff pointed to three bits of circumstantial evidence. First, he offered statements made by himself and boyhood friends concerning their alleged exposure to chemicals from the Goodyear plant when they were teenagers playing ball on a field adjoining the plant.  Second, plaintiff relied on the testimony of the project manager for an environmental firm hired by Goodyear in 2007 to conduct a site investigation in response to a clean-up agreement reached by Goodyear and the State of Vermont. The 2009 report stemming from the investigation listed contaminants of concern, including petroleum products containing benzene, that could have been released into the environment. Third, plaintiff relies upon the testimony of his two experts, who testified that occupational exposure to benzene is generally associated with a risk of non-Hodgkin's lymphoma, and that plaintiff's cancer was not caused by an immunodeficiency disorder, one of the known causes of that form of cancer.

That evidence "falls well short" of what plaintiff would be required to show in order to prevail in a jury trial. Indeed, if a jury were to find in favor of plaintiff on the evidence relied upon by plaintiff, said the court, "we would have to overturn the verdict." In the end, plaintiff's suspicion that his cancer was caused by exposure to benzene on the Goodyear ball field when he was a teenager was purely speculative. There was no way to know whether any benzene-containing product actually contaminated the ball field.  And there was no evidence indicating the amount or concentration of benzene that was present, even assuming some was. Nor was there any evidence indicating plaintiff's level of exposure to any benzene that may have been present on the field. Nor was plaintiff able to point to studies indicating a risk of cancer posed by exposure to limited amounts of benzene from petroleum products in an outside environment.  

Further, plaintiff could not rely upon differential diagnosis to overcome the complete lack of evidence as to the level of any exposure to benzene. A large percentage of cases of plaintiff's type of lymphoma are of unknown origin. Thus plaintiff's experts could not rule out all other causes, an essential part of the differential diagnosis.  E.g., Whiting v. Boston Edison Co., 891 F. Supp. 12, 21 n.41 (D. Mass. 1995) (concluding that differential diagnosis cannot be used to explain disease where 90% of cases of disease are of unknown origin).
 

Appeals Court Upholds Summary Judgment Based on Daubert in Benzene Case

The Sixth Circuit last week upheld the dismissal of a plaintiff''s claim that benzene exposure caused her cancer. Pluck v. BP Oil Pipeline Co., No. 09-4572 (6th Cir.,  5/12/11).  The central issue was the exclusion of plaintiff's causation expert's opinion based on a "differential diagnosis" that failed to reliably rule in benzene exposure as a potential cause of plaintiff's cancer, and to rule out some other potential exposures.

This case arose from benzene contamination allegedly caused by gas-pipeline releases allegedly resulting in the seepage of gasoline into the surrounding soil and groundwater. Benzene, a component of gasoline, is a known carcinogen in sufficient doses under certain exposure circumstances, and is also ubiquitous in the ambient air and is a component or constituent of vehicle exhaust and cigarette smoke, said the court. Plaintiffs purchased a home in the area,  and used well water to drink, wash, shower, and irrigate their yard and garden. In October,  1996, plaintiffs say they noticed a gasoline odor in their home and water, and benzene was first detected in the well on their property in the amount of 3.6 parts per billion (“ppb”).  They began drinking bottled water in lieu of tap water, although they claim to have resumed drinking tap water upon the drilling of a new, deeper well. Between 1997 and May 2002, the new well tested negative for benzene twenty-two times.

Mrs. Pluck was diagnosed with Non-Hodgkins lymphoma (“NHL”) in 2002 at age forty-eight. She filed suit, alleging claims of strict liability for hazardous activity, negligence, and loss of consortium. To support their claims, plaintiff and spouse retained Drs. Joseph Landolph and James Dahlgren as experts on causation to demonstrate that benzene is generally capable of causing NHL and specifically caused Mrs. Pluck’s NHL. Defendant filed motions in limine to exclude the testimony of Dahlgren and Landolph on the grounds that their testimony failed to satisfy the standard for reliability set forth in Daubert. In particular, BP argued that Dr. Dahlgren’s testimony on specific causation was unreliable because he formulated a specific causation opinion without evidence of dose, and subsequently performed an unreliable dose reconstruction in an attempt to support his opinion.  Dahlgren then submitted a supplemental declaration in which he evaluated Mrs. Pluck’s illness under a "differential-diagnosis" methodology. The district court granted the motions, and plaintiff appealed.

In a toxic tort case, as here, the plaintiff must establish both general and specific causation through proof that the toxic substance is capable of causing, and did cause, the plaintiff’s alleged injury.  As to specific causation, the plaintiff must show that she was exposed to the toxic substance and that the level of exposure was sufficient to induce the complained-of medical condition (based on a dose-response relationship). Both causation inquiries involve scientific assessments that must be established through the testimony of a medical expert. Without this testimony, a plaintiff’s toxic tort claim will fail.

The Plucks had to concede that the expert Dr. Dahlgren did not establish dose; they instead argued that Dahlgren used differential diagnosis to determine specific causation. Defendant argued that Dr. Dahlgren did not apply differential diagnosis in either his expert opinion or his deposition, but did so only in an untimely supplemental declaration filed five months after the deadline for expert reports. And in any event, his approach was flawed. The Sixth Circuit has recognized differential diagnosis, properly done, as an appropriate method for making a determination of causation for an individual instance of disease. Differential diagnosis -- originally a standard technique for determining what disease caused a patient's symptoms -- has been adapted in some courts as an acceptable scientific technique for identifying the cause of a medical problem by eliminating the likely causes until the most probable one is isolated. A physician who applies differential diagnosis to determine causation considers all ("rules in") relevant potential causes of the symptoms and then eliminates ("rules out") alternative causes based on a physical examination, clinical tests, and a thorough case history.

Even in courts that accept this adapted method, not every opinion that is reached via a differential-diagnosis method will meet the standard of reliability required by Daubert.  Calling something a “differential diagnosis” or “differential etiology” does not by itself answer the reliability question but prompts at least three more:

(1) Did the expert make an accurate diagnosis of the nature of the disease?

(2) Did the expert reliably rule in the possible causes of it?

(3) Did the expert reliably rule out the rejected causes?

If the court answers “no” to any of these questions, the court must exclude the ultimate conclusion reached.

Here the court agreed that Dahlgren could not reliably “rule in” benzene exposure as the cause of Mrs. Pluck’s NHL. In recognition of the fact that benzene poses a health concern at certain levels of exposure, the EPA has stated that the maximum permissible contaminant level for benzene in
drinking water is 5 ppb. 40 C.F.R. § 141.61(a)(2). Dahlgren, however, did not ascertain Mrs. Pluck’s level of benzene exposure, nor did he determine even whether she was exposed to quantities of benzene exceeding the EPA’s safety regulations. The levels of benzene in the Plucks’ wells never exceeded the maximum permissible contaminant level of 5 ppb designated by the EPA.

Dahlgren’s opinion that Mrs. Pluck’s “low-level exposure” to benzene caused her NHL was thus not grounded in “sufficient facts or data,”  nor did it reflect the “reliable principles and methods” required by Rule 702. It was, instead, pure conjecture.  Although the Plucks argued that the district court required too much specificity regarding Mrs. Pluck’s dose, this argument was also without merit. The mere existence of a toxin in the environment is insufficient to establish causation without proof that the level of exposure incurred could cause the plaintiff’s symptoms. See also McClain v. Metabolife Int’l, Inc., 401 F.3d 1233, 1242 (11th Cir. 2005) (causation “requires not simply proof of exposure to the substance, but proof of enough exposure to cause the plaintiff’s specific illness”).

Finally, even if Dr. Dahlgren had properly “ruled in” benzene exposure as the cause plaintiff's NHL, he failed to “rule out” alternative causes of her illness, as is required under the differential-diagnosis methodology. See also Wills v. Amerada Hess Corp., 379 F.3d 32, 50 (2d Cir. 2004) (expert’s opinion suffered from a “fatal flaw” when he acknowledged that cigarettes and alcohol were risk factors for developing squamous-cell carcinoma but failed to account for these variables in concluding that decedent’s cancer was caused by exposure to toxic chemicals such as benzene and PAHs).  In this case, Dahlgren acknowledged in his deposition that Mrs. Pluck was
exposed to other sources of benzene, from her extensive smoking habit and from other organic solvents.  Yet, Dr. Dahlgren neither identified these other solvents nor determined Mrs. Pluck’s potential level of exposure to these other possible sources of benzene.Thus, Dahlgren failed to “rule out” alternative causes of Mrs. Pluck’s NHL.

The court of appeals determined that the district court did not abuse its discretion in concluding that the expert did not perform a reliable differential diagnosis.  And summary judgment properly followed.

 

Science vs. Politics on Cell Phones Safety

The contrast is striking.  Recently, the San Francisco Board of Supervisors voted 10-1 vote in favor of an ordinance requiring cell phone retailers in that city disclose cell phones' specific absorption rate, or SAR, to customers.

The same day, a study was published that further substantiates the safety of cell phone use.  Mobile phone base stations and early childhood cancers: case-control study, BMJ 2010;340:c3077.  The study, in the British Medical Journal, showed no link between proximity to cell phone towers and increased cancer risk to children whose mothers were pregnant while living near such towers.

The study looked at almost 7,000 children and incidence of early childhood cancers across Great Britain.  This was compared with data from Britain's four national mobile phone operators -- Vodafone, O2, France Telecom's Orange, and Deutsche Telekom's T-Mobile -- on more than 80,000 mobile phone towers used from 1996 to 2001.   The researchers found that those who developed cancer before the age of five were not more likely to have been born close to a tower than their peers. The scientists found no association between risk of cancer in young children and estimated exposures to radiofrequency from mobile phone base stations during pregnancy.

MassTortDefense notes some strengths in the study: its size and national coverage, avoiding selection and reporting bias in the choice of cases and areas for study. Also, because it focused on early childhood cancers, it avoided issues of long latency that can affect interpretation of some mobile phone studies in adults.

The study adds to a growing body of scientific research which has found no links between cell phones and cancer. Use of mobile phones has increased markedly in recent years. In the United Kingdom, the number of mobile connections has risen from just under nine million in 1997 to almost 74 million in 2007.

In light of the real science, we wonder if the ordinance will actually mislead consumers with point of sale requirements implicitly suggesting that some phones are "safer" than others based on radiofrequency (RF) emissions. In fact, all phones sold in the U.S. must comply with the Federal Communications Commission's safety standards for RF emissions.  

ACS Head Offers Different View of Medical Monitoring

Readers of MassTortDefense involved in the defense of medical monitoring cases will want to follow the ongoing debate occasioned by the New York Times story this week, quoting Dr. Otis Brawley, chief medical officer of the American Cancer Society, admitting that American medicine has over-promised when it comes to medical screening and that the advantages of screening have been “exaggerated.”

Medical monitoring, whether a remedy or cause of action, is a claim for the cost of medical screening for a plaintiff exposed to a toxic substance allegedly because of the defendant’s wrongful conduct and who is accordingly at risk of future disease. Medical monitoring is designed to early detect the disease and thus maximize the chances of a cure or beneficial treatment.

As a an advocacy matter, medical monitoring is presented by plaintiffs with the seemingly unchallengeable notion that early detection saves lives. Plaintiff attorneys rely heavily on juror pre-loads about the importance and benefits of screening; virtually every juror has had a Pap smear, or mammogram, or prostrate test, and they have all been inundated with messages from the American Cancer Society that screening is highly efficacious-- messages that ignore the risks of screening. Defendants fight an uphill battle when they try to get the jury to keep an open mind about the risks and benefits of plaintiffs’ experts' proposed screening program.

Reportedly, the ACS is now working on a message, to put on its Web site early next year, to emphasize that screening for breast, prostate, and other cancers can come with a real risk. Those risks include not only the risks of the screening procedures themselves (such as radiation), but the risks of false positives, and the follow-on risks of over-treating a nodule that would never have developed into life-threatening disease. On the flip side, many researchers point out that the prostate cancer screening test has not been shown to prevent prostate cancer deaths. Similar lack of benefit has been noted with chest x-rays and CT scans for lung cancer. If cancer screening was really as effective as plaintiffs assert, the cancers that once were found late, when they were untreatable or incurable, would now be found earlier, when they could be treated and cured. Thus, a large increase in early cancers found would be accompanied by a decline in late-stage cancers, and an improvement in mortality. That just hasn’t happened for many types of screening.

Whether the issue is the screening tool or the screening itself, plaintiffs should no longer be allowed to base their medical monitoring claims on a widely accepted misconception that all screening is good, and all early detection saves lives.  Defense attorneys may have a juror pool more receptive to the evidence-based argument that plaintiffs must be held to their burden of proof to show that a monitoring procedure exists that makes early detection of the disease possible; the prescribed monitoring regime is different from that normally recommended in the absence of the exposure; and the prescribed monitoring regime is reasonably necessary according to contemporary scientific principles.
 

 

FDA Considering Rules on Acrylamide in Food

The FDA is considering issuing guidelines on acrylamide content in food.  The agency has published a notice seeking comments from industry on the issue.

Acrylamide is a chemical formed primarily in baked and fried foods by a reaction between sugars and the amino acid asparagine. The reaction is partly responsible for the golden color and tasty flavor of baked, fried, and toasted foods. In 2002, some Swedish scientists reported unexpectedly high levels of acrylamide in carbohydrate-rich foods and also published a study associating the chemical to cancer in laboratory rats. Further research subsequently determined that acrylamide can form in some foods during certain types of high-temperature cooking.

FDA has not yet issued guidance for manufacturers on reducing acrylamide in food. However, it is anticipated by the agency that new information will soon be available about the toxicology of acrylamide, which may shed light on acrylamide's potential carcinogenicity in laboratory animals. Readers of MassTortDefense know how difficult it is to leap from animal studies to causation conclusions in human beings, because of the physiological and metabolism differences between species, the excessive dosages that are (and typically must be) given to experimental animals, and the varying biological defense mechanisms that species have to environmental insults.

International efforts to develop approaches to acrylamide mitigation are also beginning to prove successful. Moreover, FDA is aware that at least some manufacturers in the United States are seeking ways to reduce acrylamide in their products. In this context, FDA is considering issuing guidance for industry on reduction of acrylamide levels in food products.

Health Canada recently added acrylamide to that nation’s toxic substances list, as part of its ongoing review of over 200 chemical substances in commercial use. It stated that current consumption levels “may constitute a danger in Canada to human life or health,” but it also acknowledged that research into a possible carcinogenic link for humans has so far been inconclusive.

In fact, dietary intakes of acrylamide are not related to increased risks of brain cancer, according to a recently released study of 58,279 men and 62,573 women, published by Maastricht University in the Netherlands. J.G.F. Hogervorst, et al., “Dietary Acrylamide Intake and Brain Cancer Risk,” 18 Cancer Epidemiology, Biomarkers & Prevention (2009).  Researchers have also reported in the Journal of the National Cancer Institute that dietary acrylamide was not linked to lung cancer risk, and that the compounds may even reduce the risk in women. "Lung Cancer Risk in Relation to Dietary Acrylamide Intake," 101(9) JNCI 651-662 (2009).

 

 

In seeking comments, the FDA has asked food manufacturers to respond with details of any manufacturing changes they have made, the success and cost-effectiveness of those changes, methods for acrylamide reduction that could be appropriate for smaller manufacturers, and changes to on-pack instructions for consumers to mitigate acrylamide formation.

 

 

Third Circuit Rejects Vaccine Plaintiffs' General Causation Expert Opinion

The Third Circuit recently upheld a judgment for the U.S. following a bench trial, in a suit by a couple who alleged that contaminated polio vaccine caused the husband's brain cancer. Gannon v. United States, 2008 WL 4151665 (3d Cir. 2008).

Plaintiffs alleged that an oral polio vaccine (OPV) received between 1973 and 1976 was contaminated with SV40, a simian virus found in both monkeys and humans. The Gannons claimed that the government was negligent in failing to prevent the manufacturer from making the OPV available to the public, and as a result, the contaminated vaccine caused Mr. Gannon to develop a form of brain cancer. Gannon and his wife filed an administrative claim against the government under the Federal Tort Claims Act and, later, a suit in the Eastern District of Pennsylvania.

The Court, for the convenience of the witnesses and to prevent recalling the experts later in the trial, decided to combine a Daubert hearing with the expert bench trial testimony on the issue of causation. Thus, the trial began with the Daubert examination of plaintiffs' expert, Dr. Adi Gazdar, who presented his full testimony on the issue of causation. He testified that SV40 plays a causal role in this type of cancer.

The district court denied the Daubert motion, but rejected the testimony as insufficient on the issue of general causation.  Safe approach in a bench trial, here it and then decide. The ruling came pursuant to Rule 52(c), which states that a trial court can enter judgment after hearing evidence on only one issue, provided the party against whom judgment has been entered is fully heard. (The appeals court rejected the plaintiffs' argument that they were not fully heard on causation: The plaintiffs asserted they would have called two other witnesses to testify, but those witnesses were not relevant to causation because their testimony would principally address the issue of contamination.) Interestingly, the United States did not offer an alternate source of causation but merely asserted that SV40 did not cause brain tumors and offered expert testimony to that effect.

Although Dr. Gazdar testified that it was his opinion that to a reasonable degree of medical certainty SV40 plays a causal role in the formation of medulloblastomas, the Court decided that the plaintiffs had not met their burden of proof on causation. Specifically, the Court found that Dr. Gazdar's testimony failed to satisfy the “Bradford Hill” criteria. The Bradford Hill criteria are broadly accepted criteria for evaluating general causation based on epidemiology;  they are: (1) Strength of Association, (2) Consistency, (3) Specificity, (4) Temporality, (5) Biologic Gradient, (6) Plausibility, (7) Coherence, (8) Experimental Evidence, and (9) Analogy.

On appeal, the Third Circuit observed that causation is an essential part of the plaintiffs' negligence claim. Based upon its thorough consideration of the record evidence, the Third Circuit could not say that the district court clearly erred in its findings of fact or that it erred in concluding that the Gannons had not met their burden of proof on the issue of causation.
 

  • The Court relied upon the fact that all three defense experts used established scientific frameworks and cited both biological and epidemiological evidence. Each of those experts opined that the evidence did not support the conclusion that SV40 causes human cancer.
  • The Court relied upon a 2003 Institute of Medicine report, which concluded that “ ‘the evidence is inadequate to accept or reject a causal relationship’ “ between SV40 and cancer.
  • Dr. Gazdar, the plaintiffs' expert, testified that he agreed that current epidemiological evidence does not support the conclusion that SV40 causes brain cancer.
  • He relied upon testing on rodents, which defense experts stated were not a good brain model for humans; even Dr. Gazdar admitted the results could not necessarily be extrapolated to humans.

Most importantly, the court considered each of the nine Bradford Hill criteria for causation and found that Dr. Gazdar's opinion did not meet the criteria.  The general causation opinion was thus rejected on the merits.
 

ATSDR Report on Benzene Impacting Litigation

The Agency for Toxic Substances and Disease Registry (ATSDR) issued a report on benzene a few months ago, and it has already begun to have an effect on the litigation.

ATSDR is an agency of HHS and is directed by congressional mandate to perform specific functions concerning the potential effect on public health of hazardous substances in the environment. These functions include public health assessments of waste sites, health consultations concerning specific hazardous substances, health surveillance and registries, response to emergency releases of hazardous substances, applied research in support of public health assessments, information development and dissemination, and education and training concerning hazardous substances.


A Toxicological Profile for Benzene, Draft for Public Comment was released in August 2005, and finalized in August, 2007. An ATSDR toxicological profile characterizes the toxicological and adverse health effects information for the hazardous substance at issue. They are peer-reviewed profiles, and each identifies and reviews the key literature that describes a hazardous substance's toxicological properties. Each profile is supposed to include the following:

(A) summary and interpretation of available toxicological information and epidemiological evaluations on a hazardous substance to ascertain the levels of significant human exposure for the substance and the associated acute and chronic health effects;

(B) determination whether adequate information on the health effects of each substance is available or in the process of development to determine levels of exposure that present a significant risk to human health; and

(C) identification of testing needed to identify the types or levels of exposure that may present significant risk of adverse health effects in humans.

The report notes that benzene, a colorless liquid with a sweet odor, evaporates into air very quickly and dissolves slightly in water. Benzene is found in air, water, and soil. Benzene comes from both industrial and natural sources. Benzene was first discovered and isolated from coal tar in the 1800’s. Today, benzene is made mostly from petroleum. Because of its wide use, benzene ranks in the top 20 in production volume for chemicals produced in the United States. Various industries use benzene to make other chemicals, used in plastics, resins, synthetic fibers. Benzene is also used in the manufacturing of some types of rubbers, lubricants, dyes, detergents, drugs, and pesticides. Natural sources of benzene include gas emissions from volcanoes and forest fires. Benzene is also present in crude oil and gasoline and cigarette smoke.


Everyone is exposed to a small amount of benzene every day, in the outdoor environment, in the workplace, and in the home. Exposure of the general population to benzene mainly occurs through breathing air that contains benzene. The major sources of benzene exposure are tobacco smoke, automobile service stations, exhaust from motor vehicles, and industrial emissions. Vapors (or gases) from products that contain benzene, such as glues, paints, furniture wax, and detergents, can also be a potential source of exposure. Auto exhaust and industrial emissions account for about 20% of the total national exposure to benzene. About half of the exposure to benzene in the United States results from smoking tobacco, according to the report. People living in cities or industrial areas are generally exposed to higher levels of benzene in air than those living in rural areas. Benzene levels in the home are usually higher than outdoor levels. For most people, the level of exposure to benzene through food, beverages, or drinking water is not as high as through air. Drinking water typically contains less than 0.1 ppb benzene. Benzene has been detected in some bottled water, liquor, and food.

Individuals employed in industries that make or use benzene may be exposed to higher levels of benzene. These industries include benzene production (petrochemicals, petroleum refining, and coke and coal chemical manufacturing), rubber tire manufacturing, and storage or transport of benzene and petroleum products containing benzene.

In an unpublished decision, the 5th Circuit relied on the ATSDR report to reverse the dismissal of a toxic tort case involving benzene. See Leblanc v. Chevron USA Inc., 2008 WL 1805448 (5th Cir. April 22, 2008).

Plaintiff alleged that after working as a tanker truck driver for over 30 years transporting products containing benzene, he was diagnosed with myelofibrosis with myeloid metaplasia-MMM, a rare disease. They tendered an expert who supported their claim that the exposure to benzene caused plaintiff's disease. Defendants challenged the expert testimony as unreliable under Daubert. The trial court excluded the testimony and, as is typically the case, because plaintiff had no other evidence on the critical causation issue, the case was dismissed.


At the time the district court issued its order, the ATSDR had issued the draft report on benzene. Because the report was still in draft form and the time for notice and comment had not expired when the district court issued its ruling, the trial court declined to consider it. During the pendency of the appeal, however, the draft received final approval. The Fifth Circuit noted that the ATSDR report on benzene was authored by a number of experts, was reviewed internally by the ATSDR, and peer reviewed by additional experts who collectively have knowledge of benzene's physical and chemical properties, toxicokinetics, key health end points, mechanisms of action, human and animal exposure, and quantification of risk to humans.


Moreover, in the report, the ATSDR concluded that benzene causes a life-threatening disorder called aplastic anemia in humans and animals. In describing a case report of a gasoline station attendant who had been exposed to benzene by inhalation, and probably also through dermal contact, the report calls myelofibrosis a form of aplastic anemia.

Because of this, and the “number and quality of the experts” who participated in the production of the final version of the ATSDR report, the 5th Circuit concluded that this report deserved the careful consideration of the district court before reaching a final conclusion on the reliability of plaintiffs’ expert testimony.

As readers of MassTortDefense interested in toxic torts will know, there is significant litigation surrounding benzene exposures. Some jurisdictions have consolidated cases for pre-trial coordination. E.g., In re: Benzene Litigation, No. 06C-BEN-1 (Del. Super. Ct., New Castle Cty.).

A week ago, a San Francisco jury reportedly awarded $8 million to a benzene plaintiff who claimed that his 17-year employment at SeaRiver Maritime Inc. exposed him to benzene, causing his kidney cancer. See Shelby v. Seariver Maritime Inc., f/k/a Exxon Shipping Co., No. CJC-06-449350 (Calif. Super. Ct., San Francisco Cty.). SeaRiver was the lone remaining defendant at the time of the trial.

Last month, several plaintiffs filed suit contending that they were wrongfully exposed to benzene while working at a Goodyear Tire Plant. Hauptmeier, et al., v. Barton Solvents Inc., et al., No. 08-187 (D. Neb.).

The litigation raises multiple important issues, including product identification, general and specific causation, and important procedural issues as well. In Anderson, et al. v. Crown Central LLC, et al., No. 08-0033 (Texas), plaintiffs are appealing the intermediate appellate court’s severance of their claims, Crown Central LLC v. Anderson, 239 S.W.3d 385 (Tex.App.-Beaumont,2007). Plaintiffs, as is common, prefer consolidated trials in their hand picked venue, with trial plans in which the best case (strongest plaintiff case) elevates the weaker plaintiff claims, despite the fact that often they cannot show their claims arose from the same transactions or occurrences.