Twenty Suspected Carcinogens

The American Cancer Society is calling for new research to settle the issue of whether or not twenty different agents do indeed cause the types of cancer in which they've been implicated. The twenty are:

(1) Lead and lead compounds; (2) indium phosphide (used in many flat screen TVs); (3) cobalt with tungsten carbide; titanium dioxide; (4) welding fumes; (5) refractory ceramic fibers; (6) diesel exhaust; (7) carbon black; (8) styrene oxide and styrene; (9) propylene oxide; (10) formaldehyde (does it cause leukemia?); (11) acetaldehyde; (12) formaldehyde; (13) methylene chloride; (14) trichloroethylene; (15) tetrachloroethylene; (16) chloroform; (17) PCBs; (18) DEHP (a phthalate); (19) atrazine (a herbicide and the subject of a coordinated attack by various activists groups resulting in a new EPA review); and, (20) shift work (the presumed exposure being "light at night" leading to a disruption of circadian rhythms and the most commonly associated malignancy being breast cancer).

You can find the press release here: Report Outlines Knowledge Gaps for 20 Suspected Carcinogens; and you can find the IARC report summarizing past rationale for assigning these suspected carcinogens to groups 2A - 3, the new evidence forming the basis for the recommendation that the status be updated and the sorts of epidemiological and mechanistic studies necessary to answer the question of whether they ought to be added to the list of 107 Group 1 agents known to be carcinogenic to humans, here: Identification of Research Needs to Resolve the Carcinogenicity of High-Priority IARC Carcinogens.

Clostridium Difficile in the News

Can C. difficile be spread through the air? What does C. difficile have to do with COPD? How should physicians treat the new and especially virulent strain of C. difficile? At what temperature should you cook ground meat to kill C. difficile and its spores? Do alcohol-based gels kill it? Why do antacids administered in hospital increase the risk of infection? Are there new antibiotics that work against C. difficile?

Click on the links for a sense of current thinking on these issues.

An Unusual Benzene/MDS Opinion

In Quillen v. Safety-Kleen Systems, Inc., 2010 WL 2044508 (E.D.Ky.) the court determined that plaintiff's expert, Dr. George Rogers, could properly attribute a case of myelodysplastic syndrome (MDS) to benzene by doing a differential diagnosis. That some courts have taken to using differential diagnosis to identify the root cause of say splenomegaly rather than to distinguish histoplasmosis induced splenomegaly from Hodgkin's disease induced splenomegaly would likely set many physicians' eyes rolling.  Yet, that's apparently what the 6th Circuit said in Hardyman v. Norfolk & Western Railway Co., 243 F.3d255 (6th Cir. 2001) and thus the thinking by the Quillen court.

The point of doing a differential diagnosis, of course, is to rule out possible causes until just one is left - it's a process of elimination. But just because every other cause of splenomegaly has been ruled out in the case of a male patient that doesn't mean that it makes sense to conclude that the cause must be the remaining possibility - a metastatic ovarian cancer. To be considered for elimination in the first place the putative cause has to be one that makes sense. In Quillen though there was no effort to demonstrate that plaintiff's experience with benzene was the sort that would make benzene a reasonably plausible cause of his MDS.

Finally, please ponder the following. In response to the defendant's objection that plaintiff's expert had not ruled out ionizing radiation  the court wrote: "Defendant points to nothing in the record demonstrating that Quillen was ever exposed to a statistically significant amount of such radiation." Somewhere an epidemiologist just fell out of her chair.

Occupational Exposure to Endotoxins: A Good Thing?

In the newest edition of the journal Cancer Causes and Control you'll find a paper titled "Endotoxin Exposure and Lung Cancer Risk: A Systematic Review and Meta-Analysis of the Published Literature on Agriculture and Cotton Textile Workers". The authors examined 28 studies of workers occupationally exposed to high levels of endotoxins and their risk of developing lung cancer. Previous studies had suggested acute and chronic lung conditions could be caused by endotoxins.

Interestingly, endotoxin exposure was consistently associated with a large and statistically significant decrease in lung cancer. Furthermore, the protective effect was strengthened as dose was increased.

Also this month, in Cancer Epidemiology, Biomarkers & Prevention, you'll find "Lower Risk of Lung Cancer After Multiple Pneumonia Diagnoses". It turns out that getting pneumonia three or more times is even better than high exposure to endotoxins if you want to avoid lung cancer.

What is it about these biological challenges to the lung that leads to significant anti-lung cancer protective effect? It's anyone's guess but perhaps keeping your immune system tuned up is part of the answer.

No Association Between Industrial-Grade Talc and Mesothelioma

A new review of available toxicological, mineralogical and epidemiological data pertaining to talc mined in northern New York by R T Vanderbilt shows no support for the claim that exposure to it causes mesothelioma. See: "Industrial-Grade Talc Exposure and the Risk of Mesothelioma" just published in Critical Reviews in Toxicology.

Chemical Safety Board Issues Hot Work Safety Bulletin

The Chemical Safety Board (CSB) has developed recommendations following its investigation of a triple fatality accident that occurred when welding on a tank containing hydrogen, due to bacteria digesting organic matter within, sparked an explosion. The seven key lessons learned from CSB's recent hot work accidents are:

1. Use alternatives when possible

2. Analyze the hazards

3. Monitor the atmosphere even in areas where a flammable atmosphere is not anticipated

4. Test the area whenever work is done near other tanks containing flammable liquids or gases.

5. Use written permits (Editorial comment: there are places where Hot Work permits aren't used? In 2010?

6. Train thoroughly

7. Supervise contractors - Provide safety supervision for outside contractors conducting hot work. Inform contractors about site-specific hazards including the presence of flammable materials.

CSB notes that while OSHA does not explicitly require the use of a combustible gas detector it is good practice to do so. The American Petroleum Institute and FM Global both have long stressed the need for combustible gas detectors to prevent fires and explosions.

As an aside, your writer learned, shortly after being admitted to the practice of law in 1986, that the oil and chemical companies here in Southeast Texas were using such gas detectors by the 1960s. In fact, in the case of one of my clients, a major refiner, its very first recorded fatality occurred in the 1930s when a man was killed by a manhole cover thrown through the air as the result of an explosion caused by hot work near a sewer. After its investigation the company paid to have someone develop a gas detector and it instituted a hot work permitting system more than 60 years ago.

An Explanation for the Quebec/South Carolina Chrysotile Conundrum?

Why is there such a disparity between health outcomes of the workers who mined chrysotile and the textile workers who used it? In "Comparing Milled Fiber, Quebec Ore, and Textile Factory Dust: Has Another Piece of the Asbestos Puzzle Fallen into Place?" Berman reports that the dusts encountered at the facilities vary in two important ways. First, whether assessed by PCM or TEM, samples revealed that mine and mill dusts contain only 67% asbestos. On the other hand, typical feedstock for the textile facility was 100% asbestos. Second, the feedstock asbestos fibers were significantly longer than those typically encountered by workers exposed to mined or even refined asbestos.

Thus, for a given quantity of dust textile workers would have an approximately 50% greater exposure to asbestos and that exposure, on a fiber per fiber basis, would be significantly riskier. The author also suggests a method for reconstructing past exposures which would more accurately estimate the risk posed by each of those exposures.

To How Much Manganese Are Welders Exposed?

In "Manganese, Iron, and Total Particulate Exposures to Welders" the authors analyzed multiple sets of data in an attempt to characterize exposures generated by welding. They conclude that manganese exposures are likely often above the current TLV of 0.2 mg/cubic meter.

Significantly, they also report strong and consistent correlations between levels of manganese, iron and total particulate that, they suggest, would allow the extrapolation of manganese exposure where only data on say iron exposure is available. Expect to see this approach used to demonstrate high exposures where none were seen before.

Are Michigan Courts Shifting the Burden of Proof to Defendants?

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.

Using Proteins to Count and Differentiate Asbestos Fibers

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.

DTSC: Green Chemistry Initiative

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.
 

Improving the Consistency and Effectiveness of Hazard Communication

The United Nations Globally Harmonized System (GHS) of Classification and Labelling of Chemicals was developed by a number of countries, including the United States, to address inconsistencies in hazard classification and communications. 

OSHA is adopting the GHS approach and believes it will increase workplace safety, facilitate international trade in chemicals, and generate cost savings from production efficiencies for firms that manufacture and use hazardous chemicals.

Forsterite: Less DNA Damage Than Chrysotile

If a chronic inflammatory process is behind asbestos' mayhem, then forsterite, the product of asbestos heated to very high temperatures, is likely to be far less harmful than even chrysotile.

See article.
 

How Safe is Your Drinking Water?

Helicobacter pylori has been identified as a causative agent in cancers that are often the subject of mass tort cases such as lymphoma, stomach and colon cancer.  Though the route of transmission of helicobacter pylori is unknown it's believed that the infection is acquired early in life through drinking water.   

Here's a paper that will be presented at a conference on water and public health to be held in Philadelphia, Pennsylvania this November by the American Public Health Association that discusses how helicobacter pylori might catch a ride on amoebas to infect our water supply.  Or if you want to worry about bladder cancer from exposure to arsenic in the water supply then you might find this link of interest.  The full program can be found here.

Two other papers you might find of interest on this cancer-causing agent via the public water supply can be found here and here.

Chrysotile Mining Worldwide Is Back Up To 1960 Levels

According to this rather expensive article published in The Lancet, despite a ban in 40 countries and dramatically reduced consumption levels in other industrialized countries like the U.S., 2.2 million metric tonnes of chrysotile is still being mined and used annually with much of it going into projects in China and India. For good or ill a laboratory for studying the effects of white asbestos exposure in humans has been established.

Lead Take-Home Poisonings

The CDC has reported on six cases of children exposed to lead while in their car seats who developed lead poisoning.  The lead was not in the car seats but rather tracked into the vehicles by the husbands or boyfriends of the children's' mothers.  The contamination had come from metal recycling or paint removal job sites.  Hat tip:  Dr. Buttery's Public Health BLOG.

Childhood Lead Poisoning Associated with Lead Dust Contamination of Family Vehicles and Child Safety Seats.

Lung disease including deaths among Chinese paint workers

Reuters is reporting on an outbreak of lung disease among workers at a Chinese paint factory potentially due to exposure to nanoparticles.

Industrial Hygiene Survey, Navy Yard, New York, NY 1943

Dr. Leonard J. Goldwater, whom I was fortunate to get to know and with whom I corresponded for several years after finding him alive and well after an expert witness in one of my cases testified that "Dr. Goldwater, if he were alive today, would tell you that by 1939 it was known that benzene caused leukemia", gave me this document out of his trove of articles and letters that he'd collected over a long and especially distinguished career. 

In subsequent posts I'll relate some of his stories ranging from his testimony at the 1936 Gauley Bridge Disaster hearings before the U.S. Congress, to his work on benzene and blood dyscrasias in the late 1930's and early 1940's, through his extensive work on mercury and to his deposition testimony in the 1980's about the history of the knowledge of asbestos all gleaned from his work with the New York Department of Health, as Industrial Health Officer responsible for Navy shipyards during World War II and as a researcher and academic.