HANDLING LUNG CANCER CLAIMS

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1 HANDLING LUNG CANCER CLAIMS JENNIFER S. KILPATRICK SWANSON, MARTIN & BELL, LLP 330 North Wabash Avenue Suite 3300 Chicago, Illinois (312) (312)

2 This paper sets forth some issues for practitioners to consider when handling asbestos-related lung cancer claims. I have not attempted to identify or explain every issue that may arise in lung cancer cases, as many of the issues have been exhaustively addressed in other publications. Rather, this paper is meant to provide an update on recent developments that may be of interest in lung cancer cases. I. Smoking Unquestionably, the single biggest issue in lung cancer cases is whether plaintiff s cancer was caused by asbestos exposure or by cigarette smoke. The majority of plaintiffs in lung cancer cases have smoked, sometimes heavily. It is critical to evaluate the extent of their smoking histories, and the role they played in the development of their lung cancer. The U.S. Surgeon General s reports conclude that cigarette smoking is the single leading cause of lung cancer incidence in the United States. Further, the consensus in the medical community is that cigarette smoking remains the leading preventable cause of premature disease and death in the United States. Given the profound effects smoking has had on human health, its potential causative role in the genesis of lung cancer and its effect on mortality rates cannot be overstated. The most significant development within the past year with respect to the literature on the effects of smoking is the publication of the Surgeon General s most recent report, The Health Consequences of Smoking 50 Years of Progress: A Report of the Surgeon General, U.S. Department of Health and Human Services (2014). The report provides updated data on the health consequences that are causally linked to smoking, statistics regarding death rates from smoking, and the risks posed by exposure to secondhand cigarette smoke. While the Surgeon General has issued reports on the effects of smoking since 1964, each version sets forth new information as the medical community evaluates new data that supports stronger associations between smoking and various ailments. The 2014 report causally links several diseases to smoking for the first time, including liver and colorectal cancers, and other chronic diseases such as tuberculosis, diabetes, and rheumatoid arthritis. Importantly, this 50-year retrospective analysis concludes that the risk of developing adenocarcinoma of the lung from cigarette smoke has increased since the 1960 s and that changes in the design and composition of cigarettes have contributed to this increased risk. 1 According to the report, the annual mortality from cigarette smoking is estimated to be around 480,000, and millions more Americans suffer from smokinginduced diseases. 2 The Surgeon General has issued over 28 reports on smoking over the years, and they can be found at The reports provide a treasure trove of data about the information that has been available regarding the health 1 Surgeon General s Report, chapter 6, page 8 (2014). 2 Surgeon General s report, Chapter 12, page 17 (2014). 2

3 risks attributable to smoking since the 1960 s. They identify the thousands of chemicals contained in cigarettes that are known carcinogens, and they explain the effects of those chemicals on the human body. When combined with the warnings on packages of cigarettes over the years 3, in addition to the admonitions most smokers receive from their physicians to quit smoking, it is difficult for plaintiffs to credibly argue that they were unaware of the hazards of smoking. While the Surgeon General s reports are an excellent source of information about the known risks attributable to smoking, they are not the only source. The Centers for Disease Control and Prevention has also amassed information regarding the health effects of smoking and tobacco use, including fact sheets and videos that explain the statistics. 4 The American Cancer Society is also a good source of information about the etiology of lung cancer, and their website provides information regarding the various sub-types of lung cancers, as well (including non-small cell lung cancers, such as squamous cell and adenocarcinomas, small-cell lung cancers, and lung carcinoid tumors). 5 Of course, all of the data in the world regarding the health effects of smoking won t make a difference in a lung cancer case without a clear understanding of plaintiff s smoking history. Plaintiffs depositions in any case are important, but are particularly so in lung cancer cases. The plaintiff must be questioned about the dates of his smoking, the extent of his smoking, and whether any of his health care providers (including nurses) advised him to quit. An even more fertile source of smoking information is plaintiff s medical records. All medical evaluations contain a section that sets forth the patient s social history, which typically includes notes regarding what the patient reported their smoking history to be. While patients generally tend to be poor historians (for a variety of reasons), it is worthwhile to carefully review all of the available medical records with an eye toward evaluating what the patient s smoking history was reported to be, how it changed over time, and any notes that indicate his health care providers advised him to quit smoking or offered to enroll him in a smoking cessation program. II. Asbestosis Another heavily debated and litigated issue in lung cancer cases is whether a plaintiff must have an underlying diagnosis of asbestosis for a physician to attribute the plaintiff s lung cancer to asbestos exposure. The literature that supports the contention that exposure to asbestos only raises lung cancer risk among individuals who have asbestosis 6 3 There are state and federal cases in different jurisdictions holding that individuals are deemed to have been adequately warned about the dangers of cigarette smoking as of See Cipollone v. Liggett Group, et al., 505 U.S. 504 (1992) See Churg, A, Asbestos, Asbestosis, and Lung Cancer, Mod. Pathol. 6: (1983); Churg, A., Neoplastic Asbestos-induced Disease, Ch. 10, Pathology of Occupational Lung Disease, 2d ed. Williams & Wilkins, Baltimore, 3

4 has been thoroughly examined in other publications and by experts on both sides of the debate. The same can be said for the literature that takes the position that one does not need underlying asbestosis to have an increased risk of lung cancer following exposure to asbestos. 7 The most significant recent development that relates to this issue was the publication of Markowitz, SB, Levin, SM, Miller, A, Morabia, A, Asbestos, Asbestosis, Smoking, and Lung Cancer: New Findings From the North American Insulator Cohort, Am. J. Respir. Crit. Care. Med. Jul 1, 188(1): 90-6 (2013). The authors studied the lung cancer mortality rates for 2,377 North American male insulators whose information was culled from the National Death Index from The insulators surveyed had chest x-ray, spirometry, occupational, and smoking data. This data was compared with 54,243 nonasbestos exposed blue collar male workers from the Cancer Prevention Study II ( CPS2 ). Occupational and smoking data were collected from the individuals in CPS2 in The authors primary conclusions were that lung cancer mortality rates were higher in asbestos exposed non-smokers. Lung cancer rates were also increased among those with asbestosis who were non-smokers, and in smokers who were not exposed to asbestos. With respect to the contention that there is a synergistic effect between asbestos and cigarette smoking, the authors did not find a multiplicative effect. In asbestos exposed smokers, they found an additive effect; in smokers with asbestosis, the effect was supra-additive. Finally, ten years after smoking cessation, insulators risk for developing lung cancer was halved. Within 30 years of smoking cessation, their lung cancer risk converged with that of never-smokers. Two responses have been published to the article. In Ross, R, Asbestos, Asbestosis, Smoking, and Lung Cancer: Study Bias and Confounding Issues That Complicate the Interpretation of the Results, Am. J. of Respir. And Crit. Care Med., vol. 189, No. 1 (2014), the author noted that the study represents statistics from individuals who had high levels of amphibole exposures. Dr. Ross also pointed out that the study shows that those with asbestosis were at high risk for lung cancer, at a rate that is similar to what has been found pg (1998); Weill, H., Hughes, JM, Jones, RN, Asbestos: A Risk Too Far? (letter), Lancet, 346: 304 (1995); Browne, K., Is Asbestos or Asbestosis the Cause of the Increased Risk of Lung Cancer in Asbestos Workers? Br. J. Ind. Med. 43: (1986); Sluis-Kremer, GK, Bezuidenhout, BN, Relation Between Asbestosis and Bronchial Cancer in Amphibole Asbestos Miners, Br. J. Ind. Med. 46: (1989); Doll, R. Mortality From Lung Cancer in Asbestos Workers, Br. J. Ind. Med. 12:81-86 (1955); Liddell, FDK, McDonald, JC, Radiographic Findings As Predictors of Mortality in Quebec Asbestos Workers, Br. J. Ind. Med. 37: (1980). 7 See Cullen, MR, Controversies in Asbestos-Related Lung Cancer, Occup. Med. 2: (1987); Hillerdal, G, Pleural Plaques and Risk for Bronchial Carcinoma and Mesothelioma: A Prospective Study, Chest, 105: (1994); Becklake, MR, Asbestos-Related Diseases of the Lung and Other Organs: Their Epidemiology and Implications for Clinical Practice, Am. Rev. Respir. Dis. 114: (1976); Wilkinson, P, Hansell, DM, Janssens, J, et al., Is Lung Cancer Associated With Asbestos Exposure Without Small Opacities on the Chest Radiograph? Lancet 345: (1995); Reid, A, deklerk, N, Ambrosini, GL, Pang, SC, Berry, G, Musk, AW, The Effect of Asbestosis on Lung Cancer Risk Beyond the Dose Related Effect of Asbestos Alone, Occup. Environ. Med. 62: (2005); Jamrozik, E, deklerk, N, Musk, AW, Asbestos-Related Disease, Int. Med. J. 41: (2011). 4

5 in other studies regarding asbestosis. He took issue with the authors position that it was unlikely that any of the insulators who did not have asbestosis did not develop it after the 1980 s, when their radiographs were performed. Using Dr. Ross interpretation of the data, about 12% of insulators who did not have asbestosis when they were initially evaluated later developed asbestosis. As a result, the ratio of those without asbestosis was a high estimate, as many of those individuals likely developed asbestosis later. Dr. Ross concluded that among individuals with heavy exposures to asbestos, if there is an increased risk of lung cancer among smokers who do not have asbestosis, it is quite small. In a second response, Geyer, S., Asbestos, Asbestosis, Smoking, and Lung Cancer: Study Bias and Confounding Issues That Complicate the Interpretation of the Results (letter), Am. J. Respir. And Crit. Care Med., Vol. 189, No. 1 (2014), Dr. Geyer also criticized the study, but on different grounds. Dr. Geyer pointed out that the study s authors did not take into account bias and other confounding factors that could have caused or contributed to the individuals lung cancers, including radon, secondhand smoke, and diesel exhaust emissions exposures. He notes that the authors did not consider the method of selection of the individuals whose data was included in the study, nor potential bias that could have been introduced by differences in qualifications of the B-readers who examined the radiographs at issue. Ultimately, Dr. Geyer concluded that asbestosis remains an unambiguous marker of a fiber burden sufficient to raise one s risk of developing lung cancer. The authors of the study published a reply to both responses. They contended that Dr. Ross misquoted them in stating that it was unlikely that some of the insulators later developed asbestosis, when their article stated that it was unlikely that many insulators would have developed asbestosis. They disagreed with Dr. Ross contention that 12% of insulators without asbestosis later developed it. They responded that they did not have sufficient information regarding the quality of the diagnoses of asbestosis on death certificates to support such a conclusion. They disagreed with Dr. Ross contention that the insulators studied were heavily exposed to amphibole asbestos, when the insulators were actually exposed to a variety of fiber types, and the study s authors made no attempt to study the fiber types at issue. In response to Dr. Geyer s response letter, the authors noted that they did state the method of selection of the individuals in the Methods section of the article. Further, the spirometric results were associated with anticipated findings, which supports the validity of the B-readings. With respect to confounding factors, the authors noted that their use of the CPS2 data was a strength of their study, as it minimized the differences in risk factors of the studies participants due the similarities in their occupations, socioeconomic statuses, residences, and smoking habits. They further noted that any excess lung cancer risk attributed to confounding factors was modest compared to those of asbestos and asbestosis. 5

6 Ultimately, the study has some limitations, including those mentioned by Drs. Ross and Geyer. In addition to Dr. Ross point that the study only evaluated the participants asbestosis once and did not fully account for the possibility that some insulators without asbestosis later developed it, the study also only evaluated their smoking status on one occasion. In addition to focusing on insulators who presumably had high exposures to asbestos, the article didn t address the length of exposures, and could include data from insulators who only had brief exposures. The disparities in the numbers of the groups studied (2,733 as opposed to 54,243) could also have affected the outcome, as well. While this study is an important development in the literature with respect to lung cancer and asbestosis, it does not appear to have effected a profound change in how the parties view the literature. Those who had previously reached opinions regarding this issue are unlikely to change those views solely based on this study. 8 III. Dose In addition to considerations of causation and underlying asbestosis, it is also important in lung cancer cases to evaluate dose. As noted in section II above, the inhaled dose of asbestos that the individual receives is critical when determining whether the plaintiff would have developed lung cancer from the exposure they received. Not all workers are at the same risk of developing cancer from asbestos exposure. Additionally, the dose-response relationship applies equally to the relationship of cigarette smoking and the development of lung cancer. The more an individual smokes, the higher their risk of developing lung cancer. The Surgeon General s reports offer ample support for the dose-response relationship between smoking and lung cancer. 8 The book Pathology of Asbestos-Associated Diseases, Third Edition, Oury, T, Sporn, T, and Roggli, V had a third edition published in The third edition presents the same position on this issue as was presented in the second edition: to attribute an individual s lung cancer to asbestos exposure, one must either have underlying asbestosis or there should be a tissue asbestos burden within the range of values observed in patients with asbestosis. 6

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