The HPV-Lung Cancer Link: A New Issue for the Asbestos Bar?

011516_hpv_THUMB_LARGELong known for its link to cervical cancer, recent medical research suggests a potential link between the Human Papilloma Virus (“HPV”) and lung cancer. While the science in this field is still developing, it is trending towards a conclusion that HPV may independently cause lung cancer in non-smokersincluding those that have never smoked —  and may also contribute to the causation of lung cancer in smokers and former smokers.

Two recent papers have addressed this hypothesis. The earlier is HPV and lung cancer risk: A meta-analysis from Zhai et al in the Journal of Clinical Virology 63 (2015) 84 – 90.  These authors looked at nine published studies spanning 1995 to 2013 and covering 1094 cases of lung cancer.  They set the context by commenting that “Lung cancer (LC) is the most common cause of morbidity and mortality worldwide”  and “approximately 25% of those with LC are never smokers.”

The authors broke out their results for HPV in general, and for subtypes such as HPV 16 and HPV 18.  For HPV in general they reported:  “A statistically significant association was observed  between HPV and LC patients” and recorded an Odds Ratio (OR) of 5.67 with a 95% confidence interval.  Compare that odds ratio for the similar calculations that are discussed in asbestos disease cases involving auto mechanics for example. They then looked at specific subtypes of LC and noted:

We also evaluated the cancer risk of HPV16/18 in different LC histological types. In SCC (squamous cell cancer), HPV 16/18 was significantly associated with cancer risk (OR=9.78, 95% confidence interval: 6.28 – 15.22, P<0.001, l2=44.9%); however, OR was not significant in AC (adenocarcinoma) (OR=3.69, 95% confidence interval: 0.99 – 13.71, P= 0.052; l2 + 75.5%).  [Author’s note:  this OR is not “significant” because the 95% CI includes 1, but just barely so.]

In discussing their findings, these authors note that “Most people are infected with HPV at some point in their lives, but only persistent infections cause pathological changes.” They reiterate their conclusion that HPV plays a distinct role in the pathogenesis of different LCs.  They ultimately address the elephant in the room by stating “Whether smoking interacts with HPV to promote the development of LC is unclear.”

A second recent paper is Human papillomarivirus infection and risk of lung cancer in never-smokers and women: an “adaptive” meta-analysis; Bae et al, Epidemiology and Health 37 (2015).  One of their initial observations is: “The increasing incidences of lung cancer among women never-smokers is a global trend {citations omitted} and it has been suggested that lung cancer in never-smokers should be considered separately, a disease different from lung cancer in smokers {citations omitted}.”  These researchers note the work of Zhai discussed above and comment that they are expanding on it by analyzing women and never-smokers.

These researchers ultimately focused on four case control studies and calculated a “summary odds ratio” (SOR).  They found a SOR for women of 5.32 and for never-smokers of 4.78.  The authors conclude that the risk of HPV caused lung cancers for women never-smokers was expected to be even higher.

Given the substantial increase in asbestos-related lung cancer civil case filings over the past five years, the hypothesis, if ultimately proven, could result in novel new claims by both plaintiffs and defendants in the litigation. This issue has already arisen in a recent California case, in which a core needle biopsy of the lung tumor of the plaintiff was obtained and reviewed by two defense pathologists.  Administering an accepted immuno-histochemical test to that tumor tissue, the pathologists found it to be positive for P16, signifying the presence of the HPV  in the tumor.  From that, both experts were prepared to opine that the presence of the HPV in this plaintiff more probably than not caused or contributed to her cancer. The literature discussed above was part of the scientific basis they were prepared to point to in support of their conclusion.    Therefore, while more research may be indicated, in lung cancer cases for which tumor tissue is available, defense counsel may want to consider if testing for the presence of HPV is indicated.

Whodunit? Plaintiffs set up showdown between tobacco and asbestos defendants

On June 10, 2015, two well-known “asbestos” plaintiff firms, The Shepard Law Firm and Levy Konigsberg, LLP, together filed a complaint in the Superior Court of the Commonwealth of Massachusetts on behalf of plaintiffs Louis and Joanna Summerlin. Mr. Summerlin’s claimed injury is lung cancer, while Mrs. Summerlin’s claim is for loss of consortium. However, this is not a run-of-the-mill asbestos lawsuit. Rather, the plaintiffs have named more typical asbestos and big tobacco defendants Philip Morris USA and RJ Reynolds Tobacco Company in a clear effort to potentially pit asbestos against tobacco in a “whodunit” battle over what caused Mr. Summerlin’s cancer. Time will tell if this tactic will be successful.

cigaretteAsbestos cases generally fall into three categories: 1) mesothelioma claims; 2) non-malignant asbestosis claims/pleural disease; and 3) lung cancer claims. While categories (1) and (2) involve injuries commonly associated with asbestos exposure, lung cancers claims are not generally associated with asbestos, especially when the person with lung cancer smoked cigarettes for decades. That is, lung cancer claims are generally attributed to smoking and, absent very specific underlying diagnoses and smoking histories, are heavily contested by defendants in the asbestos litigation.

The normal defense in a case like this is the obvious one: the plaintiff’s lung cancer was caused by smoking cigarettes. Here, Mr. Summerlin was a two pack per day smoker of six decades (1950’s – 2009). Given the lengthy, heavy, and recent smoking history of Mr. Summerlin, the expected and obvious defense of the defendants sued for asbestos exposure would be that Mr. Summerlin’s lung cancer was caused by smoking cigarettes. While it is unclear from his complaint as to whether Mr. Summerlin alleges any markers of asbestos exposure, the assertion that Mr. Summerlin’s lung cancer was caused by smoking cigarettes would likely be accepted by any medical professional, thereby calling into question plaintiff’s claim that asbestos exposure is a contributing cause of Mr. Summerlin’s cancer. This is especially true given Mr. Summerlin’s work as an automotive mechanic, which the defense has successfully argued on many occasions that the epidemiological evidence does not support a conclusion that an individual in the trade is at any increased risk of developing an asbestos-related disease.

This is where the plaintiffs’ firms in Mr. Summerlin’s case appear to have taken a unique approach in New England in the pursuit of a lung cancer claim: they have sued both asbestos and tobacco defendants and alleged that exposure to both carcinogens acted as “concurrent” causes of Mr. Summerlin’s lung cancer. Specifically, the plaintiffs allege that “[c]igarette smoking and asbestos exposure act ‘synergistically’ and in combination to cause lung cancer in persons, such as Mr. Summerlin, who regularly smoked cigarettes and were regularly exposed to asbestos.” For years, plaintiffs in the asbestos litigation have made this claim in the face of the smoking defense. Here, they make the claim with big tobacco in the room. Regardless of the outcome, it is guaranteed that counsel on both sides will closely monitor the success – or failure – of this strategy.

Courts Reject “Single Fiber” Theory Of Asbestos Causation

A Sixth Circuit case, Moeller v. Garlock Sealing Technologies, LLC, 2011 U.S.App.Lexis 19987 (6th Cir. Sept. 28, 2011), is the most recent in a series of judicial decisions that have rejected the opinions of plaintiffs’ experts in asbestos cases who espouse the “any exposure” or “any fiber” or “single fiber” theory of causation.  Pursuant to this specious line of reasoning, asbestos disease is a cumulative dose response process. Each and every exposure to asbestos during a person’s lifetime, no matter how small or trivial – even a single fiber – substantially contributes to the disease, whether it be asbestosis, lung cancer or mesothelioma. Using this theory of causation, plaintiffs have initiated a wave of new lawsuits against defendants far removed from the production of asbestos containing products.  As defense practitioners are well aware, successfully challenging weak causation expert opinions is key to winning any toxic exposure case, whether it involves asbestos or some other substance.

In a “must read” column in the New York Law Journal, dated October 19, 2011 titled "Courts Shoot Down Asbestos Causation Theory", Michael Hoenig, whose law firm defends asbestos case litigation, describes how plaintiff experts are promoting the “any fiber” or “any exposure” theory in courtrooms across the country and how a series of notable judicial decisions have begun to reject these theories as the underlying scientific methodology is subjected to scrutiny. In a recent amicus curiae brief filed by eleven distinguished scientists in a Pennsylvania asbestos case, none of whom received funding from or testified as experts for any of the parties in the case, the scientists attacked the methodological errors of the “any exposure” expert for:  (1) failing to consider the dose level of exposure and minimum threshold of asbestos fiber levels; (2) failing to consider the physical chemical and toxicological differences between various types of asbestos; (3) failing to distinguish between general causation and specific causation (and not even establishing general causation for chrysotile asbestos); (4) for suggesting that “every exposure” and “cumulative risk” theories are generally accepted when they are not; and (5) ignoring the large body of toxicological studies demonstrating that chrysotile asbestos is not potent as a cancer-causing agent. 

The Pennsylvania Supreme Court observed in Gregg v. V-J Auto Parts Co., 943 A.2d, 216, 223 (Pa. Sup. Ct. 2007), that although it was “common for plaintiffs to submit expert affidavits attesting that any exposure to asbestos, no matter how minimal, is a substantial contributing factor in asbestos disease,” such opinions are not “not couched within accepted scientific methodology.”  The court called the “willingness on the part of some experts” to offer such opinions “one of the difficulties” courts face in the mass tort cases.

As the plaintiff bar continues to look further and further afield in its “endless search for a solvent bystander,” as one well-known plaintiff’s lawyer described the litigation, successful challenges under Daubert and Frye should only increase.  The author thanks Mr. Hoenig for his thoughtful treatment of this important topic.

From a risk management perspective, peripheral toxic tort defendants often decline to mount  Daubert challenges due to the cost and time involved and the uncertainty of the result, particularly when the plaintiff presents them with seemingly  reasonable settlement demands.  As a result, hundreds of peripheral defendants continue to be named in these cases and often pay their "penny in tribute" just to get out of the case.  Unfortunately, in many jurisdictions, judges responsible for large asbestos dockets are unwilling to give appropriate consideration to motions by "shade tree" defendants who might otherwise challenge plaintiffs’ experts’  theories of causation.  Cynically, these judges know that the cases will most likely settle out if this type of motion is given short shrift.  There is little incentive for a peripheral defendant to risk an adverse  judgment at trial merely to earn the right to bring an appeal, no matter how strong the grounds may be.  Hopefully, cases like Moeller will have a trickle down effect and motivate the trial judges responsible for the asbestos dockets to re-think their approach.