This guest post was written by J.C. McElveen of Jones Day. J.C. gets all the credit for this post; your dynamic blogging duo had nothing to do with it:
On September 11, 2008, the U. S. Court of Appeals for the Ninth Circuit held, in the context of a lawsuit brought under the Price-Anderson Act, that subcellular damage, including damage to DNA, does not amount to bodily injury, for purposes of recovery under that Act. Dumontier, et al. v. Schlumberger Technology Corp., 2008 WL 4166406 (9th Cir. 2008).
This decision is a pretty narrow one, because the Price-Anderson Act, as applicable here, is a federal statute designed to compensate only individuals who have been involved in a “nuclear incident,” and experienced “bodily injury, sickness, disease, or death,” (or loss of, loss of use of, or damage to property) arising out of or resulting from the “radioactive, toxic, explosive or other hazardous properties of source, special nuclear or byproduct material.” 42 U.S.C. § 2014(q). However, in affirming the granting of a motion for summary judgment against the plaintiffs, the Ninth Circuit was holding, as a matter of law, that there were no circumstances under which a plaintiff could prove that subcellular damage was a bodily injury, illness or disease.
This issue – whether subcellular and DNA damage can ever be a bodily injury for purposes of a lawsuit under Price-Anderson – has been decided by several courts, and each of them has held that, as a matter of law, bodily injury means something more than subcellular damage. See, Ranier, et al. v. Union Carbide Corp., 402 F.3d. 608 (6th Cir. 2004); In Re Berg Litigation, 293 F.3d. 127 (9th Cir. 2002). These decisions, and several other cases that have considered whether subcellular damage rises to the level of bodily injury, have held that such de minimis damage should not be compensable. See Caputo v. Boston Edison Co., 1990 WL 98694 (D. Mass. 1990) (unpublished). However, a couple of cases have gone the other way, holding that such a question should go to the jury. Brafford v. Susquehanna Corp., 586 F. Supp. 14 (D. Colo. 1984), and Werlein v. United States, 746 F. Supp. 887 (D. Minn. 1990).
These cases bring to mind the excellent article written by Jamie Grodsky, an Associate Professor of Law at George Washington University Law School, and published in the Stanford Law Review last year, Grodsky, J. A. “Genomics and Toxic Torts: Dismantling the Risk-Injury Divide,” 59 STAN. L. REV. 1671. That article argues that the decisions holding that subcellular damage cases shouldn’t go to the jury have been wrongly decided. The article is thought-provoking, but is, at the least, extremely premature.
Before I comment, let me see if I can paraphrase the gist of the article (NOTE TO AUTHOR: Feel free to use the comments to tell me how wrong I am). The argument, I think, goes something like this: If the plaintiff has an expert who, after looking at some cells or genes, is willing to say that genetic material has been damaged as a result of an exposure to a defendant’s chemical or agent, and the defendant’s conduct otherwise arguably satisfies the requirements of negligence, or strict product liability, or other viable legal theory, that plaintiff should be allowed to go to the jury on the issues (among others) of whether the damage was, in fact, caused by the exposure, the extent of injury resulting from the exposure, and the amount of damages, if any, recoverable on account of the injury. The argument to the jury would be either (1) that the damage is a significant personal injury, itself (As the author said, “So-called early disease biomarkers may represent not only the risk, but the presence of disease itself.”) or (2) that the damage increases the risk of future personal injury to such an extent that damages should be recoverable for increased risk of, or fear of, disease. At the least, medical monitoring of those individuals should be available as a remedy, so as to detect, at an early stage, the symptomatic disease that will surely spring from this cellular damage. (Said the author, “Therefore, I conclude that the judiciary’s retreat from medical monitoring may be coming at precisely the time when increased attention to this remedy is necessary.”)
Although the suggestion that contentions such as “whether there is cellular damage caused by an exposure,” and “whether that damage amounts to permanent injury to the person,” ought to be submitted to a jury is facially appealing, the idea that a jury ought to be presented matters of this sort has the potential for real mischief. There are at least three major problems.
First, there is no “normal” against which to measure cellular damage. Suppose an expert sees something “unusual” about the genetic material – a deletion of part of a chromosome, a portion of one chromosome on another chromosome, or even at the more molecular level, a deletion of a part of a gene. How is that person to know whether that change was present from birth, was the result of the inevitable mistakes that occur by virtue of the aging process, or was caused by an environmental insult?
Nowadays, most people have been to see a doctor frequently enough to have some sort of baseline information about themselves. Many people have baseline electrocardiograms, liver function tests, blood tests, and some even have chest x-rays and hearing tests. Almost no-one has a baseline pre-exposure chromosome map, and no-one has a baseline gene map. [Although you can apparently now get your very own gene map. See “Risks of Direct-to-Consumer Genetic Testing Remain Unclear.” JAMA 300 (13): 1503 (Oct. 1, 2008)] Even if some people don’t have baseline information about themselves, as to some parameters, enough people do have such information that “normal” values can be established. But, what does a “normal” gene sequence in, for example, Chromosome 23, look like? No one knows. Does this or that person’s genome fall “within normal limits?” No one knows.
The second problem is: “If something is abnormal, how do you prove what caused it to be abnormal?” In the Three Mile Island personal injury litigation, discussed in my earlier guest post, the court believed that there were certain kinds of chromosomal changes, called dicentrics, that could be caused by radiation. However, in that case, the court held that counting dicentrics in the blood cells of people exposed to the radiation 15 years earlier is not a reliable methodology for determining radiation dose.
The interesting implication in that discussion is that there are other things, besides radiation, that can cause dicentric chromosomes. (And it is extremely unlikely that any genetic abnormality can only be caused by just one agent). So, how, with the present state of science, can you say a particular exposure caused a particular chromosomal change? Multiply that difficulty many-fold when you are talking about trying to pinpoint the cause of a gene segment deletion.
Finally, the third problem is: “What does it all mean?” What a lot of folks articulate is “I’m afraid of getting cancer.” But that is a straw man. That assumes, first of all, that cancer is one disease and is mediated through a common pathway. But no scientist believes that anymore. Viruses, some environmental agents, and other factors we don’t begin to understand may play some role, somewhere in the genome, and almost none is a sufficient cause, itself. But a more fundamental issue is that hundreds, if not thousands, of diseases are probably genetically mediated.
In an article in the May 6, 2008, New York Times, Andrew Pollack has a great map, called the Diseasome, of some of the diseases believed to be genetically mediated, and the probable number of genes in which changes have to occur, in order to produce the disease. Based on that chart, why would a person not say “I’m afraid of getting diabetes, or Parkinson’s, or Alzheimer’s”? And even at that, our genes replicate so frequently, and, as a result, mistakes in replication occur so frequently, that many scientists think the vast bulk of genetic mistakes don’t result in anything – either because cell death occurs, or because the mistake is at some part of the very large percentage of the genome that is either redundant or has no function, or for some other reasons nobody presently understands.
As the JAMA editorial, discussed above, pointed out: “There are also many basic scientific questions that remain to be answered about the genetic markers the tests identify and their connection with the development of disease. Lawrence C. Brody, Ph.D., head of the molecular pathogenesis section at the National Human Genome Research Institute in Bethesda, Maryland, explained that the companies are using data from case-control genome-wide association studies. Such studies attempt to identify some of the genetic factors that are more common among individuals with a disorder than among controls. These studies cannot demonstrate causation, and many of the markers being used by the testing companies have not been validated by other groups or by studies that explain the molecular mechanism by which these genes might lead to disease . . . Additionally, because these genetic factors are only weakly associated with disease, it is likely that to cause illness, they must interact with other genetic or environmental factors that have not yet been recognized, said Kathy Hudson, Ph.D., director of Johns Hopkins University’s Genetics and Public Policy Center in Washington, DC.”
That is why these cases shouldn’t go to juries.