Mass Torts: State of the Art : Mass Torts Lawyer & Attorney : Vorys, Sater, Seymour & Pease Law Firm : Toxic Torts & Wrongful Death

One explanation for Genna v. Jackson (a new opinion out of the Michigan Court of Appeals) and Gass v. Marriott Hotel Services, Inc is that the courts thought about it and decided to shift the burden of proof regarding causation to the defendant any time a plaintiff suffers an injury that is consistent with the possible harm, as set out on a warning label or MSDS, associated with a potentially toxic material. In Genna the court reversed summary judgment in favor of the defendant in part because "[h]ere, like in Gass, defendant has not submitted any scientific evidence that the mold in her condominium could not have cause [sic] plaintiffs' injuries." In Gass the 6th Circuit noted "Defendants have offered no evidence to refute the MSDS's representation of Demand CS as a chemical which could have caused Plaintiffs' symptoms". The court later continued saying "[p]laintiffs are not required to produce expert testimony on causation where Defendants have failed to offer scientific evidence regarding the effects of Demand CS or Suspend SC."

The Genna court concluded, on the issue of causation, "[t]his is not a complicated case: the children were sick, the children were removed from the home, the mold was discovered, and the children recovered." Noting evidence that there was lots of mold and that mold in general had been reported to cause some of "the types of symptoms suffered by the children" the court concluded [i]t does not take an expert to conclude that, under these circumstances, defendant more likely than not is responsible for plaintiffs' injuries." (citing Gass). "Here, there was ample circumstantial evidence that would "facilitate reasonable inferences of causation, not mere speculation."

Under this view of an unannounced burden-shifting approach taken by these two courts it appears that in Michigan if a plaintiff develops ailments consistent with a those listed on a product's label or MSDS the jury is free to infer causation even in the absence of evidence of what dose produces those ailments and what dose plaintiff suffered and even in the absence of an expert to opine that the product in question caused the harm at issue.

Another explanation for these cases is that Michigan does not require toxic tort plaintiffs to show what some call specific causation - a concept common in cases in which causal inferences are derived from epidemiological evidence. The idea is that when dealing with an illness that has been associated with multiple causes, among which is the chemical at issue, the plaintiff must show that the putative cause was more likely than not the cause in fact of his illness.  Evidence for this view can be found in the following passage from Genna: "Defendant urges this Court to adopt the requirement that, in order to prove causation in a toxic tort case, a plaintiff must show both that the alleged toxin is capable of causing injuries like those suffered by the plaintiff in human beings subjected to the same exposure as the plaintiff, and that the toxin was the cause of the plaintiff's injury. They urge this Court to find that direct expert testimony be required to establish the causal link, not inferences. We decline to adopt this requirement. There is no published Michigan case law on the subject."

A final explanation is that more attention to Aristotle's Rhetoric is needed. As Chief Judge Boggs, dissenting in Gass wrote the problem here is the logical fallacy behind post hoc, ergo propter hoc causal inferences such as those suggested by the plaintiffs in Genna and Gass. "It is the fallacy of saying that because effect A happened at some point after alleged cause B, the alleged cause was the actual cause. Such logic has never been enough to survive summary judgment. See, e.g., Abbott v. Federal Forge, ("[P]ost hoc, ergo propter hoc is not a rule of legal causation.") 912 F.2d 867, 875 (6th Cir.1990).

Equally importantly Chief Judge Boggs understands that lay juries are in no position to judge whether there has been a breach of the duty of care without evidence of what levels are harmful and the levels to which plaintiffs were actually exposed. If you don't know the dose you can't know what risk, if any, the defendant imposed on the plaintiff. He wrote: "Thus presented, the question is whether the plaintiffs needed expert testimony in this case to prove how much chemical exposure is too much chemical exposure or to prove whether the amount of exposure actually caused the alleged harmful consequence. In my view, the majority pays too little attention to this issue, rushing from the fact of exposure and odd symptoms to the legal conclusion of fault." He continued: "As I understand it, these cases require expert testimony in complex, professional, or scientific-based negligence cases in order to limit the dangers associated with indulging the post hoc impulse: it is too easy to charge an uncommon harm to the presence of a mysterious substance. Properly credentialed expert testimony operates as a bulwark against such fallacious attribution of guilt. As in the Daubert context, our concern in applying these cases should be to "assure that the powerful engine of tort liability ... points towards the right substances and does not destroy the wrong ones." General Electric v. Joiner, 522 U.S. 136, 148-49, 118 S.Ct. 512, 139 L.Ed.2d 508 (1997) (Breyer, J. concurring).

Whatever the explanation these cases will be a boon for Michigan toxic tort plaintiffs.

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Have you been worrying that your water softener is significantly increasing your risk of dying from a heart attack? I didn't think so. But just because you haven't been feeling vulnerable around your water softener doesn't mean the WHO hasn't been fretting for you.

Thanks to epidemiological studies going back a decade or more (e.g. "Magnesium and Calcium in Drinking Water and Death from Acute Myocardial Infarction in Women") a worry arose that we were killing ourselves by eliminating the minerals naturally found in most drinking water. Yet subsequent studies have failed to confirm the finding including the just published "Effect of water hardness on cardiovascular mortality: an ecological time series approach". So what gives?

Well, what gives is that most of what gets published in peer reviewed journals is probably false; and when it comes to causal inferences drawn from epidemiological studies "the apparently indiscriminate indentification of particular aspects of daily life as dangerous to health" is, as witty programmers say, a feature, not a bug.

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The New York Times has published another report by Gina Kolata on the Forty Years' War against cancer. In it you'll find part of the answer to the question I've posed.

"Dr. Barnett Kramer, associate director for disease prevention at the National Institutes of Health, recently discovered a paper that startled him. It was published in the medical journal The Lancet in 1962, about a decade before the war on cancer was announced by President Richard M. Nixon. In it, Dr. D. W. Smithers, then at Royal Marsden Hospital in London, argued that cancer was not a disease caused by a rogue cell that divides and multiplies until it destroys its host. Instead, he said, cancer may be a disorder of cellular organization.

'Cancer is no more a disease of cells than a traffic jam is a disease of cars,' Dr. Smithers wrote. 'A lifetime of study of the internal-combustion engine would not help anyone understand our traffic problems.'

Dr. Kramer said: 'I only wish I had read this paper early in my career. Here we are, 46 years later, still struggling with issues this author predicted we’d be struggling with.'"

There may be lots of science going on these days but review any journal and you'll quickly see that there's often not a lot of deep thinking behind it. Most science is derivative and most of it is false.

What people think of as science nowadays is in fact a vast jobs program, the main purpose of which, after the employment of academics, is to maintain and expand the pardigms on which its various parts rest. Accordingly, research outside the prevailing paradigms is typically starved for cash and efforts to falsify dominant theories don't just go unrewarded, often they are punished. I suspect therefore that the prayer of many if not most scientists today is, to paraphrase St. Augustine, "Lord grant me critical thinking and skepticism, but not yet."  

Reading an old journal article is one way to step back from the minutiae of microarrays and data dredging and to consider big ideas from a time when no one had the ability to sequence the genes of a malignant cell or unleash sophisticated software to find never before noticed confirmatory associations among mountains of numbers. A time when ideas were, perhaps, more likely the spark of sudden insight rather than the product of of a self-replicating system.

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We live in strange times. Though whole genomes, of an individual as well as a malignant progenitor stem cell responsible for AML, have been sequenced and though modern medical diagnositic machinery and implantable devices increasingly look like things that Gene Roddenberry would have rejected as too futuristic, the fact is that scientists know very little about how our bodies work. Take C-reactive protein for example.

Let's say you decide to study heart attacks by measuring the levels of certain proteins in the blood and then later checking to see if there's been an association between the levels measured and an adverse event like a subsequent heart attack. Bingo! People with high levels of C-reactive protein have a high risk of heart attack. Wow!

Ok, let's assume the association is strong and consistent so that the finding probably reveals something about how the body works. But what?

Too often these sorts of findings have precipitated a Whac-A-Mole reaction from the medical community whereby drugs are promptly designed and thereafter prescribed to begin whacking the protein back down to "normal" levels. Causes precede effects, right? So this must be a cause, right?

Well, what if C-reactive protein is actually part of the body's response to accumulating plaque and inflammation? What if its level correlates with risk because it's part of the body's attempt to fix whatever is broken? What if it's not a cause of heart disease but is really an effect of heart disease? Reuters is reporting on a new analysis published in Lancet indicating that at least in the case of C-reactive protein earlier assumptions had indeed confused cause and effect. The authors conclude that it is unlikely that C-reactive protein is a cause of heart disease.

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Reuters is reporting on the results of a new poll conducted by the Harvard School of Public Health into the attitudes of Americans towards getting their children vaccinated against swine flu. Slightly more than twenty percent of the parents surveyed had decided not to immunize their children and the main reason disclosed was fear about the safety of the vaccine.

The CDC has been monitoring those who have been vaccinated and has a web page up about the safety of the vaccine, the weekly updated Vaccine Adverse Event Reporting System report and just about anything else you'd want to know about vaccines in general or this one in particular. Nevertheless, and in spite of the fact that by all measurements the vaccine appears to be safe and effective, a sizeable number of Americans fear the vaccine more than they fear a virus that has sickened millions and killed over 10,000. Why?

Part of the answer can be found in a 2002 study in which researchers compared their subjects' reactions to scientific evidence from reliable scientists that debunked a health scare versus inaccurate non-scientific emotional appeals from activists that merely raised the possibility of an adverse health effect. "The surprising result is that when we presented both positive and negative information simultaneously, the negative information clearly dominated. This was true even though the source of the negative information was identified as being a consumer advocacy group and the information itself was written in a manner that was non-scientific." The authors concluded that "even though the scientific evidence is favorable, claims by opponents, even if they are inaccurate and only suggest potential risks, will tend to reduce consumer demand". Hat tip TheGoodTheBadTheSpin

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"Every age has its own outlook. It is specially good at seeing certain truths and specially liable to make certain mistakes. We all, therefore, need the books that will correct the characteristic mistakes of our own period. And that means the old books. ...

We may be sure that the characteristic blindness of the twentieth century—the blindness about which posterity will ask, "But how could they have thought that?"—lies where we have never suspected it, and concerns something about which there is untroubled agreement between Hitler and President Roosevelt... None of us can fully escape this blindness, but we shall certainly increase it, and weaken our guard against it, if we read only modern books. Where they are true they will give us truths which we half knew already. Where they are false they will aggravate the error with which we are already dangerously ill. The only palliative is to keep the clean sea breeze of the centuries blowing through our minds, and this can be done only by reading old books.  Not, of course, that there is any magic about the past. People were no cleverer then than they are now; they made as many mistakes as we. But not the same mistakes. They will not flatter us in the errors we are already committing; and their own errors, being now open and palpable, will not endanger us. Two heads are better than one, not because either is infallible, but because they are unlikely to go wrong in the same direction."

- C.S. Lewis, Introduction to "Athanasius: On the Incarnation"

The question of whether we should read old books is the subject of a spirited debate over at Overcoming Bias.

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Suggested as an accurate and convenient alternative to the PCM method of estimating airborne concentrations of asbestos fibers, Japanese researchers have devised a method of using different E. coli proteins  to selectively bind to either amphiboles or chrysotile. The resulting mix of amphiboles and chrysotile fibers can then be more precisely counted and differentiated.

The number of methods available to estimate asbestos exposure, each generating a different answer, continues to grow; further muddying the already murky waters of extrapolating past exposures from modern methods.

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If you've dealt with the Chemical Safety Board or the National Transportation Safety Board or any similar organization following an explosion or accident you know about their emphasis on systems and their reluctance to blame individuals for the events being investigated. Obviously, the working assumption that most errors are committed by good people trying to do the right thing has been a sound one and an emphasis on improving systems so those people can in fact do the right thing has yielded some impressive results. But you've likely asked yourself "does there ever come a point when everyone has been trained enough; when safety systems are redundant enough; when an individual needs to be held accountable rather than some unaccountable 'system'"? Apparently, at least in the case of medical errors, there does.

The New York Times is reporting on the growing concern that "a blame-free culture carries its own safety risks." When hand sanitizers are ubiquitous and training about hand sanitation is incessant, yet some doctors and nurses still fail to wash their hands something's wrong. And it's something, according to the researcher interviewed, that can't be fixed by tweaking the system. Someone has to be held accountable.

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As my mentor used to say, "most people like to help others; and they really like to help when they can do it with someone else's money." 

$100 million is a lot of help.

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As part of its REACH effort the European Chemicals Agency (ECHA) has today launched what it describes as the "pilot form" of a webpage which, it is hoped, will ultimately "allow EU citizens to make informed decisions about the use of chemicals to which they may be exposed."

Today's press release has a link to the new database. When using the database search function be sure to check the "I accept the Terms and Conditions" box or it won't work. Gotta love lawyers. Anyway, when looking for something like benzene be sure to look in the "Pre-Registered Substances" directory because it won't be found in the "Registered Substances" directory and the search engine apparently doesn't look outside of whatever directory you're in.

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The New York Times has run an extensive article about the nation's drinking water claiming that our public water is contaminated with thousands of chemicals, hundreds of which are "associated with a risk of cancer". It even has a link to the articles on which the claims are based. Unfortunately, or fortunately depending on your point of view, the evidence cited for the proposition that tap water is putting the citizenry at risk of cancer is pretty thin if that's all there is.

For example, under "Studies Regarding Illnesses and Drinking Water" (of which there are only eight) the only one to make a broad claim of tap water carcinogenesis is a 28 year old study titled "Cancer and Drinking Water in Louisiana: Colon and Rectum" which used the 1970 census to compare 692 rectal cancer deaths from 1969-1975 by where along the Mississippi River they and controls got their drinking water. The authors noted a small increase in risk as the source got closer to the Gulf of Mexico and suggested that the finding may have something to do with an increasing concentration of industries along the river as it approaches the Gulf. More importantly they wondered whether by-products of chlorination might have something to do with the finding.

The link suggests just four other papers that have cited the study and of those only two studied drinking water. Of the two, the first is a Canadian paper from 2000 (the first true Y2K victim I've ever run across - note: "Received 1999 Accepted 1900") which found no association with rectal cancer but a small one for colon cancer among males who drank "chlorinated surface water for 35-40 years".

Following the papers that cited the Canadian paper you quickly find another drinking water paper that finds a small protective effect for all leukemias combined, a large protective effect for chronic lymphocytic leukemia and a small but significant association with chronic myeloid leukemia.

The other papers are similarly all over the place and there appears to be no consensus that U.S. drinking water is a cause for concern about cancer from the perspective of chemical contaminants.

On the other hand, there's a growing body of literature associating drinking water contaminated by microorganisms with cancer. There's a new one discussing the waterborne transmission of helicobacter pylori to be published in next month's Journal of Water and Health and then there's this alarmingly titled paper in the same journal: "Free-living amoebae, Legionella and Mycobacterium in tap water supplied by a municipal drinking water utility in the USA" 

It's unclear why the NYTimes focused on trace levels of chemicals as a cause for concern when there does appear to be something to be worried about when it comes to bugs in our water.

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There was more good news last week about Americans' incidence and rates of death due to cancer. The rates of new cases and the rates of death from all cancers combined are dropping and dropping steadily. For example, cancer deaths for all forms of cancer collectively dropped 1.6% per year for each of the last six years for which data is available (2001 - 2006). The progress being made against colorectal cancer was highlighted in the report.

While men continue to have higher rates than women their decline in rates was also higher. Decreases in deaths and incidence for lung, prostate and colorectal cancer drove the decline for men.

Among women, breast and colorectal rates declines lead the overall improvement.

The news was not uniformly good. In men, rates increased for myeloma, kidney, liver and esophageal cancer as well as multiple myeloma and leukemia. In women the expected increase in lung cancer rates was found along with increases for thyroid, pancreatic, bladder, melanoma and kidney cancers as well as for non-Hodgkin's lymphoma and leukemia.

The NIH press release can be found here.

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In the recently decided Pennsylvania case of Hicks v. Dana Companies, LLC  the appellate court considered whether the trial court had committed error in its handling of the following question posed by the jury after two-and-a-half hours of deliberations:

"Judge Lynn, can we please have verification as to what a 'factual cause' is? To determine such, do we consider each company's product individually or all collectively?"

Rather than answer the question, which actually got right to heart of the matter, the trial court read the following instruction:

"If you find that a defendant's asbestos-containing product was defective, the defendant is liable for all harm to the plaintiff caused by such defective condition. A defective condition is [sic] the defendant's asbestos-containing product is the factual cause of the mesothelioma suffered by the plaintiff if the mesothelioma would not have occurred without exposure to the defendant's defective product. That's factual cause."

Is it any wonder that jury questions are invariably found to be confusing and often result in jurors rendering verdicts they didn't mean or want to render?

Anyway, the jury's question was a profound one. In this age of peripheral defendants, typically none of whose products alone could have produced mesothelioma, is it fair to lay at any one defendant's feet "all harm to the plaintiff" when alone its product could have produced no harm at all?

The opinion is significant in at least two other respects. First it embraces the logical fallacy of conflating risk and causation by approving of causation testimony founded only on the observation that in a dose response disease each quantum of dose increases risk. Second it appears to support the contention that a defendant's application of a warning label to its product is a tacit admission that the product causes the harm warned of.

While the court goes out of its way to distinguish this case from the Pennsylvania Supreme Court's ruling in Gregg v. V-J Auto Parts Company it is difficult to see how it has in fact done anything other than accept the one fiber theory so long as plaintiff has an expert willing to swear to it.

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The Texas Supreme Court released its opinion today in the Whirlpool v. Camacho case. Joab Camacho, a minor, burned to death in a trailer fire allegedly caused by a defectively designed Whirlpool dryer. The plaintiffs’ expert, who had never examined the dryer as it had been discarded, nevertheless opined that lint from the dryer somehow collected in a corrugated exhaust shoot, backed up through the mechanical systems of the dryer, caught fire in the tumbler, smoldered when the dryer shut off, was reignited by oxygen when the door was opened and then ignited the clothes in the dryer. Plaintiffs claimed a safer alternative design would have utilized a smooth exhaust shoot. The sole support for the opinion of plaintiffs’ expert was a review of an allegedly similar dryer and Consumer Product Safety Commission (CPSC) reports of various dryer tests. The jury accepted the assessment and awarded $14 million in damages against Whirlpool.

The Texas Supreme Court conducted a full review of the expert evidence and found Plaintiff’s expert ultimately unreliable under Robinson v. Merrill-Dow. For example, plaintiffs’ expert had not conducted any tests on the dryer in question nor on any similar dryer and could not explain why tests to see if the model in question posed such a risk wasn’t feasible. Further, his opinions were made solely for litigation. Finally, the only data he did rely upon was not sufficiently similar to that for the dryer and circumstances in Camacho’s case to make it reliable.

With this opinion the Texas Supreme Court has again confirmed that the mere ipse dixit of an expert witness is not sufficient to establish the reliability of the Robinson relevance/reliability analysis.
 

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California, the state in which a jury recently awarded $16.5 million for a woman’s toxic exposure to H2O (water), plans to force all manufacturers to use only “non-toxic” chemicals in their products. The so-called Green Chemistry program is to be run by the California Department of Toxic Substance Control (DTSC). The department’s director is quoted by ABCNews as saying that the plan will “save the environment and increase our economy”.

As expected, a reading of the actual transcript of the “Green Ribbon Science Panel” proceedings reveals that the benefits of the effort are likely to be neither as overstated (as by the director) nor as absurd (going “chemical free”) as much of the media would have you believe. For example, “Now, I want to be clear about alternatives. You could have no alternatives…You could have an alternative that may not be safer” said DTSC staff member Evelia Rodriguez. There’s also a fair amount of effort to explain the risk/benefit concept; but, that’s about as far as things have really gone. The panel plans on doing something about 10,000 substances in the next two years but appears to be at least partially paralyzed at present as the only sensible approach, starting with the riskiest and working their way down is, not surprisingly, is rejected by those “stakeholders” whose chemical they love to hate would appear distressingly far down on such a list. How the Green Ribbon Science Panel intends to deal with the maxim “the dose makes the poison” also remains to be seen though there is some brief though ultimately fruitless discussion of what’s to be made of “de minimis” exposures.
 

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The initiative to make products with safer chemicals is gaining momentum and media attention. DTSC Acting Director Maziar Movassaghi explains in the linked article and video that green chemistry is a new type of environmental protection, which results in everyday products that contain less toxic chemicals. Movassaghi goes on to explain that the rules are currently being drafted; however, some companies are already embracing the change, as the wave of the future.
 

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In a recent published opinion the California Court of Appeal, Second Appellate District opined that for a wife to pursue a claim against her husband’s employer for so-called take home exposures, her complaint should specify the chemicals involved and injuries alleged. (Oddone v. The Superior Court of Los Angeles County, Cal. Ct. App., No. B213784, Nov. 24, 2009).

The plaintiff had alleged that she was secondarily exposed to chemicals from her husband and his work clothes. She also asserted claims on behalf of her husband for his personal injuries which remain pending. Her husband had worked for 33 years processing motion picture film for Technicolor Inc. She specified in her complaint her husband’s injuries (glioblastoma multiforme and skin rashes) and specific chemicals that allegedly harmed him (formaldehyde and perchloroethylene), but she made vague allegations regarding her own personal injury claims against Technicolor. She alleged that she was injured from chemical substances that her husband brought home with him either on his body or clothes but failed to identify her specific injures or chemicals that caused her harm.

The defendant moved to dismiss her secondary exposure claim on the basis that it owed no duty to its employee’s wife. The trial court agreed and this appeal ensued.

The appellate court acknowledged that “[t]here appears to be no reported California decision addressing the scope of the defendant’s duty in a case where the plaintiff claims to have been injured as a result of secondary exposure to chemicals.” However, the court continued that “[g]iven appropriately specific allegations, this may be quite possible.”

The court explained that in this case “petitioner’s allegations simply do not establish any connection, much less a close connection, between the defendant’s conduct and her alleged (and unspecified) injuries.”

According to the court, a “close connection” is required because under Rowland v. Christian, 69 Cal.2d 108 (1968), it is one of several significant factors to consider when determining whether a duty exists to an injured party in this circumstance. Although the Rowland factors are to be balanced against one another, the court stated the “close connection” factor is especially important in a secondary exposure suit.

“That connection is only shown by setting forth specifically which chemicals cause which specified injuries,” said the court. “In a secondary exposure case, the allegation that as a result of the exposure the specified chemical entered the plaintiff's body is of particular importance. Central issues in such a case are whether secondary exposure to a specified chemical is even possible and, if it is, whether the exposure will result in the ingestion of the chemical into the plaintiff's body.”

As the plaintiff failed to identify a specific chemical or to specify any one of her alleged injuries she could not “connect any specified chemical or chemicals to a specific injury or injuries” and so, in this case, her take home claim failed.

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The new jobless data show that for every educational category of worker (college graduates, those with some college, high school grads and dropouts) the unemployment rate today is higher than it was at the peak of the 1982 recession. The same data show that the overall unemployment rate today is lower than it was in 1982. How can this be?

Try this example of an unnervingly common flaw that can arise when you reason from percentages alone. There are two treatments for kidney stones, Treatment A and Treatment B. Each treatment is tried out on two different types of kidney stones - small stones and large stones. Here are the results:

Treatment A   small stones - 93% effective    large stones - 73% effective

Treatment B   small stones - 87% effective   large stones - 69% effective

Which treatment do you think would be most effective overall among small and large stones? As it turns out:

Treatment B was effective 83% of the time for  either small or large stones

Treatment A was effective 78% of the time for either small or large stones

Huh? Here are the actual numbers:

Treatment A   small stones - 81 out of 87 effective       large stones 192 out of 263 effective

Treatment B   small stones - 234 out of 270 effective   large stones - 55 out of 80 effective

Thus the overall success rate for Treatment A is (81 + 192) / 350 = 78% whereas the overall success rate for Treatment B is (234 = 55) / 350 = 83%

This effect, where the results seem to switch between subcategories and overall rates is known as Simpson's Paradox. I don't think it's as much a paradox as it is a problem that arises out of an all too common problem people, including lots of expert witnesses, have with percentages - specifically, thinking of percentages as something independent of the data from which they were generated. The result of this flawed thinking is often a classic, but sometimes hard to perceive, apples to oranges comparison failure.

Here's a good discussion of the issue as it relates to the unemployment conundrum at The Wall Street Journal. For further discussion, including a take on why comparing unemployment among education categories over time is even dicier than comparing different treatments for different types of kidney stones there's another good write up at Andrew Gelman's Statistical Modeling, Causal Inference, and Social Science blog.

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According to an excellent write up of this Galinsky paper at Mind Hacks the short answer is: The side that wants to get the best deal.

The first number offered acts as an anchor. Individuals then reflexively tend to look for information that is consistent with, and so to them confirms, that the number is indeed legitimate. People tend to take the first number as a working hypothesis and so, as with any hypothesis that does not produce an immediate rejection, this first number too often induces people to recall and magnify supporting data while failing to recall or underestimating contradictory data. Is there a way to protect against this effect?

The author suggests that 1) despite the advice of many books on negotiation that recommend waiting for the other side to go first, several studies demonstrate that the buyer, or defendant, will do better by going first with a low offer; 2) when faced with a high demand the buyer (defendant) should focus on information inconsistent with the first offer; and, 3) the initial focus should be on the buyer's / defendant's ideal price by recapitulating the basis for the buyer's / defendant's valuation.

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IARC has determined that there is strong evidence that formaldehyde is the cause of nasopharyngeal cancer and moderate evidence that it causes leukemia, especially of the myeloid variety. Here's the ungated table from "A review of human carcinogens - Part F: Chemical agents and related occupations".

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The LATimes is reporting on a new study finding that neuroticism and extraversion in patients suffering from major depressive disorder are respectively alleviated and enhanced in patients taking Paxil. As compared to those taking placebos, Paxil patients not only experienced longer lasting relief from depression they also saw significant positive personality changes becoming less neurotic and more outgoing. "That is a dramatic change," said Robert McCrae, a leading researcher on personality, now retired. "If you were these patients or someone in their family, you'd notice a difference."
 

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In a new article in the Journal of the National Cancer Institute an association between embalming, as a proxy for exposure to formaldehyde, and myeloid leukemia was found to be strong, significant and dose dependent. In coming days we'll be discussing the controversial claim of a causal link between leukemia and formaldehyde and IARC's recent musings about it.

The article is Mortality From Lymphohematopoietic Malignancies and Brain Cancer Among Embalmers Exposed to Formaldehyde .

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This afternoon the EPA announced that “greenhouse gases (GHG) threaten the public health and welfare of the American people.”

According to the press release the EPA’s final findings responded to the 2007 U.S. Supreme Court decision (Commonwealth of Massachusetts et al. v. Environmental Protection Agency, decided Apr. 2, 2007) that GHGs fit within the Clean Air Act definition of air pollutants. The findings allow EPA to finalize the GHG standards proposed earlier this year for new light-duty vehicles as part of the joint rulemaking with the Department of Transportation.

The EPA’s endangerment finding covers emissions of six gases – carbon dioxide, methane, nitrous oxide, hydrofluorocarbons, perfluorocarbons and sulfur hexafluoride.

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The American Cancer Society has published "The Global Burden of Cancer: Priorities for Prevention" this month in the journal Carcinogenesis. While tobacco use is discussed first and diet, obesity and lack of physical activity second, it's cancers related to chronic infections that gets the most coverage. "Persistent infection with various microbial organisms accounts for about 18 percent of cancers worldwide." Preventive approaches including the development of vaccines and lifestyle modifications are discussed in detail.

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Despite decades of emphasis on putative man-made carcinogens, and a corresponding tendency to dismiss nature's brutish side as a possible cause of cancer, the case for viruses in causing human cancers has only gotten stronger. In "Human tumor-associated viruses and new insights into the molecular mechanisms of cancer" the roll of Epstein-Barr virus (EBV), human papillomavirus (HPV), hepatitis B and C (HBV and HCV respectively), human T-cell lymphotropic virus (HTLV-1) and Kaposi's associated sarcoma virus (KSHV) in a significant percentage of human cancers is discussed along with insights into molecular biological mechanisms and some very interesting thoughts about how these insights might reveal other heretofore unsuspected viral-induced cancers, novel treatments and public health strategies to reduce cancer by preventing viral infections.

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A series of lungs from California farm workers who died in accidents or from illness were examined for evidence of pneumoconiosis.   Despite being young these Hispanic farm workers had significantly more evidence of interstitial fibrosis than did non-farm workers.  A variety of analytical techniques demonstrated that those with pneumoconiosis had significant exposure to crystalline silica and aluminum silicate.

The article is "Pneumoconiosis from agricultural dust exposure among young California farmworkers".  As for the source of mineral dust exposure the authors note "most agricultural soils are composed largely of silicate materials (e.g., feldspars, mica, clay minerals) and crystalline silica (CSi) (quartz)".

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An important new study was recently released indicating that there is no causal association between ambient exposure to either solvents or benzene and the development of non-Hodgkin’s lymphoma (NHL). The report adds to a growing body of literature demonstrating no discernable risk for typical community benzene exposures.

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Researchers from Mayo Clinic have published "An outbreak of neurological autoimmunity with polyradiculoneuropathy in workers exposed to aerosolised porcine neural tissue: a descriptive study" in The Lancet Neurology. Workers exposed to aerosolised pig brains (ugh) developed polyradiculoneuropathy - a painful and disabling autoimmune illness. Of the 24 workers affected 17 required immunomodulatory therapies, six improved after exposure ceased and one was lost to follow up.

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In the on-going debate over when to start getting mammograms and how often to have them the assumption by many of those supporting an "early and often" policy has been that false positives lead to little more than worry and maybe a needle biopsy. Now The New York Times is reporting on a study that appears to demonstrate that young women already at heightened risk of breast cancer double that risk if they start getting mammograms early.

Five prior studies of women carrying a mutation that is thought to put them at increased risk of breast cancer were examined to determine whether low dose radiation exposures from mammograms further increased that risk. The results, which were statistically significant at a 95% confidence interval, showed that women carrying the breast cancer gene who started mammography early in life or who had five or more mammograms were more than twice as likely to develop breast cancer as women with the breast cancer gene who started getting mammogramps later and had fewer of them.

The working hypothesis is that mammography actually causes many cases of breast cancer in susceptible women. An alternate explanation, I suppose, is that about half of all breast cancers detected by mammography either aren't cancerous or were never going to develop into a malignancy.

Hopefully doctors are finally beginning to discuss the large and unsettling uncertainties associated with the diagnosis, treatment and causal attribution of poorly understood diseases like cancer.

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