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  • Writer's pictureKirk Hartley

Implications of New Molecular Research on the Inflammasome, Interleukin and Asbestos as a “Cau

An online article published April 10, 2008 in ScienceNOW provides an overview of detailed research published in Science indicating that asbestos fibers stimulate production of a form of interleukin (IL-1β), which promotes inflammation. I’ve not yet read the article and so cannot say whether the article addresses asbestos fibers in the generic sense or if it distingushes between fiber types.

The article and commenters quoted in it suggest there will be future efforts to determine whether anti-inflammatory drugs can limit the biologic processes (disease, one might say), and that it may in the future become possible to test for increased levels of the implicated form of interleukin. (Wikipedia offers a nice article on interleukin, including striking color illustrations.)

So, how is this article relevant to asbestos litgation in particular and tort litigation in general? For asbestos litigation, the relevance is that scientific discoveries of this sort may lead to new tests that asbestos claimants could use to try to recover for increased future risk of contracting “disease,” or for the defense side to try to use to show that a particular person person is not at “meaningful” risk of suffering from a “disease” deemed appropriate for compensation.

The research also may make its way into the factual proofs that have historically been part of the legal rationales for the “triple trigger” rationale for defining the “injuries” that courts decide are sufficient to “trigger” traditional CGL insurance coverage that was often but not always purchased by manufacturing firms prior to the advent of the so-called “asbestos exclusion” that became fairly common around 1985. The U.S. law on insurance coverage for asbestos claims is quite developed, but insurance coverage remains a wide open topic in many countries where asbestos litigation is just starting to take shape. And, depending on the scope and results of this and future research, it may add new grist for arguments about the “chrysotile defense” and/or whether a “low dose” exposure actually plays a legally meaningful role in the onset of what we define as “disease.”

For tort litigation in general, this is an illustration of the type of issues that courts and lawyers will have to confront as science pushes forward at ever increasing speed. Over the coming years, it seems inevitable that courts and lawyers will spend increasing amounts of time thinking about how “disease” occurs on a biologic basis, and what can be done to prevent a biologic process from resulting in a tumor that actually causes “physical impairment.” The answers may have a profound impact on the scope of new and old legal rationales for tort law claims (e.g. fear of cancer claims), and on the scope of recoverable damages.

Legislative and regulatory bodies also will have opportunties to consider and apply new science, and might even come to sensible conclusions to avoid the “wastes” inherent in litigation. But we’ve gone for decades without much sensible action from federal U.S. legislators, and the states have taken various approaches, mainly but not always after the federal legislators failed to act. It remains to be seen how legislators and regulators will respond in other nations. Legislative and regulatory actions related to asbestos are picking up speed outside the US, but that topic must wait for another day.

____________________________ Set out below is an excerpt from the ScienceNOW article as to the biologic process investigated:

“Tschopp and colleagues exposed to asbestos human and mouse immune cells that lurk in the lungs. They found that the material stimulated an inflammasome called Nalp3 to release interleukin-1β (IL-1β), a chemical that incites inflammation. But the real proof came from mice that were bred to lack Nalp3. When these mice were exposed to asbestos for 9 days, they produced lower levels of IL-1β and less lung inflammation than did mice with Nalp3, confirming that the inflammasome is key to triggering at least some of the negative effects of the fiber, the researchers report online today in Science. Tschopp speculates that because asbestos fibers lodge in the body, prolonged exposure causes chronic inflammation that over time could result in lung scarring and cancer. The details still need to be worked out, but the researchers note that IL-1β has been linked to other cancers.”

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