After “Roundup” of Evidence, EPA finds Glyphosphate “Not Likely to be Carcinogenic to Humans”

croppyEarlier this month, the EPA issued a position paper regarding the risks of glyphosate.  Notably, in classifying glyphosate’s cancer risk to humans, the EPA states, “The strongest support is for ‘not likely to be carcinogenic to humans’ at doses relevant to human health risk assessment.”

Although the EPA report is not dispositive on the issue and will be followed by with a “final assessment” in early 2017, it is a positive development.  The FIFRA Scientific Advisory Panel of the EPA, much like the European Food Safety Authority, is not accepting the recent IARC position that glyphosate is “probably” carcinogenic to humans.  Consequently, causation in litigation involving glyphosate will remain a challenge for plaintiffs’ firms to establish.

Since the IARC position was issued in 2015, plaintiff’s firms have filed a number of lawsuits in California, Illinois, and New York against Monsanto.  In late July, one plaintiffs’ firm filed a motion requesting that the multidistrict panel be in the U.S. District Court for the Southern District of Illinois, where three lawsuits are pending. In total, 21 lawsuits have been filed in 14 district courts nationwide naming Monsanto only.  The parties expect a ruling this fall on whether the matters against Monsanto will be consolidated.

Formaldehyde Exposures and Leukemia Links Tenuous or Absent, New Study Finds

A new study cases doubt on the longstanding, generally accepted link between formaldehyde exposure and certain disease end points, including Acute Myeloid Leukemia.   Within the past few months, Dr. Harvey Checkoway of the University of California at San Diego and six other occupational medicine specialists published an article entitled “Formaldehyde Exposure and Mortality Risks From Acute Myeloid Leukemia and Other Lymphohematopoietic Malignancies in the US National Cancer Institute Cohort Study of Workers in Formaldehyde Industries.”   (Harvey Checkoway, PhD, Linda D. Dell, MS, Paolo Boffetta, MD, MPH, Alexa E. Gallagher, PhD, Lori Crawford, MS,Peter SJ. Lees, PhD, CIH, and Kenneth A. Mundt, PhD , J Occup Environ Med. 2015 Jul; 57(7): 785–794.)  This article will have a significant impact on those defending chemical exposure matters involving claimed exposure to formaldehyde and other related chemicals.  Should other epidemiologists accept the findings of this article, there may be a shift away from claiming formaldehyde at any dose can cause AML and certain other blood-related cancers.  The end result will likely put the spotlight back on alleging trace benzene as the potential culprit.

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The stated goal of the review in this article was ambitious.  The authors of the review considered all available literature addressing the issue of the potential link between exposure to formaldehyde and various hematopoietic disease end points.  The article focused on whether formaldehyde is in fact a recognized risk factor in the development of lymphohematopoietic malignancies, including Acute Myelogenous Leukemia (“AML”), Non-Hodgkins Lymphoma (“NHL”), and other related disease end points.  The article’s authors concluded, “Insofar as there is no prior epidemiologic evidence supporting associations between formaldehyde and either Hodgkin leukemia or chronic myeloid leukemia, any causal interpretations of the observed risk patterns are at most tentative. Findings from this re-analysis do not support the hypothesis that formaldehyde is a cause of AML.”

These conclusions are significant in matters alleging exposure causing AML, NHL, and other leukemias as disease end points.  We have seen a recent uptick in matters alleging lower exposures to formaldehyde in the mortuary and laboratory settings as a cause of AML and NHL.  This article questions the very suggestion that AML can be caused by exposure to formaldehyde.  It is also suggests that NHL and chronic myeloid leukemia may not be caused by formaldehyde exposure.  We expect that there will be increased motion practice challenging general causation in these cases.

Should the focus shift away from alleging formaldehyde as the agent of causation, another likely effect of this study, if accepted, is a return to the use of the argument that trace benzene may cause the disease end points in these cases.  In most instances, cases involving formaldehyde exposure often involve exposure to trace levels of benzene in chemicals used simultaneously in various industrial settings.  We expect there to be more to come in terms of scientific literature addressing this topic given the potential significant paradigm shift this article promotes.

Recent SCIENCE Article a Potential Game Changer for Arguing Medical Causation in Cancer Cases: Stem Cell Division and “Bad Luck”

This month’s Science Magazine features a paper by two Johns Hopkins scientists that provides support for a more refined theory of causation in a number of types of cancer.  The article by Drs. Christian Tomasetti and Bert Vogelstein entitled “Variation in Cancer Risk Among Tissues Can Be Explained By The Number of Stem Cell Divisions” includes the following abstract:

Some tissue types give rise to human cancers millions of times more often than other tissue types. Although this has been recognized for more than a century, it has never been explained. Here, we show that the lifetime risk of cancers of many different types is strongly correlated (0.81) with the total number of divisions of the normal self-renewing cells maintaining that tissue’s homeostasis. These results suggest that only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to “bad luck,” that is, random mutations arising during DNA replication in normal, noncancerous stem cells. This is important not only for understanding the disease but also for designing strategies to limit the mortality it causes.

This finding may have broad implications in determining what may cause the cancer at issue in a particular case.  This article concludes that the incidence or lifetime risk of many cancers directly correlates to the number of stem cell divisions in the tissue involved in the cancer.  This correlation appears to be, in many cases, independent of any environmental or external factors.  Because the article provides a potential explanation for the cause of many types of cancer, this may allow experts to use rate of stem cell division as a causation argument in lieu of saying the cause is “idiopathic.”

Interestingly, among the cancers that have a higher rate of stem cell divisions are acute myelogenous leukemia and chronic lymphocytic leukemia, two types of cancer that are prevalent in matters involving allegations of exposure to trace benzene. This fact will certainly be the source of future argument regarding general causation.  We expect there to be future scientific inquiry into the findings in this article, but the findings alone do raise important issues.  Further studies in this area may provide further support for arguing against an environmental correlation between cancer risk and exposure in cases where the cancer involved has a high rate of stem cell division.  We expect that this study and future studies will have a significant effect in matters involving allegations of toxic exposure.