Defending Lung Cancer Claims

Defending Lung Cancer Claims David A. Speziali Speziali, Greenwald & Hawkins 1081 Winslow Road, Box 1086 Williamstown, NJ 08094 (856) 728-3600 dspeziali@comcast.net

David A. Speziali is a partner at Speziali, Greenwald & Hawkins PC in Williamstown, New Jersey. Since 1981, he has managed and tried asbestos related claims on behalf of dozens of corporate defendants in more than 40 states. Mr. Speziali has conducted numerous training programs and lectured across the country. He is the program vice-chair of this seminar. The opinions expressed here are solely the authors and have not been reviewed nor agreed to by any client of his firm.

Defending Lung Cancer Claims Table of Contents I. Introduction...19 II. Tobacco...19 III. Historic Literature Related to Asbestos and Lung Cancer...20 IV. Selikoff Studies...20 V. Critique of Hammond/Selikoff...21 VI. Asbestosis/Lung Cancer Debate...23 VII. Helsinki...23 VIII. Discovery in Ling Cancer Cases...25 IX. Medical Records...26 X. Conclusion...26 Defending Lung Cancer Claims Speziali 17

Defending Lung Cancer Claims I. Introduction If there is an association between asbestos and lung cancer it is weak at best and weakened further when underlying asbestosis is not present. When significant cigarette smoking is in the patient s history there is no reason to point at asbestos as the cause of that patient s lung cancer. Research regarding asbestos and lung cancer goes back to the 1930 s. Despite countless studies it is difficult to find any linking asbestos to lung cancer in the absence of smoking and/or underlying asbestosis. The studies of Dr. Irving Selikoff and his colleagues are often cited as the primary basis for proving causation. Yet, even Dr. Selikoff cautioned regarding the strength of an association and the impact of smoking. This paper will provide a brief overview of state of art literature, analyze the Mt. Sinai (Selikoff) and Helsinki research and take a look at some available arguments in defending these claims. There is absolutely no effort here to be comprehensive. Countless published and unpublished studies are not discussed, many authored by plaintiff or defense experts. The goal is simply to show that lung cancer claims are defensible and one should be aggressive in challenging medical and liability issues. II. Tobacco It is ironic that an individual who smoked and has lung cancer seeks compensation at any level that does not involve a claim against the tobacco industry. What possessed that individual to go to a lawyer and claim he/she is a victim based upon conduct having no relationship with the tobacco companies? Surely, the individual knew tobacco was/is deadly and regardless of addiction horrible consequences could and apparently did result. No asbestos defendant played a role in an individual s decision to smoke or addiction. The day the individual decided to smoke he/she shortened life expectancy. Consider the statistics related to smoking and secondhand smoke from the Center for Disease Control (CDC): Tobacco has over 7,000 chemicals, many of which are poisons. Tobacco smoking damages your pulmonary immune system. 9 out of 10 men that die from lung cancer smoked. About 3,000 nonsmokers die each year from lung cancer caused by secondhand smoke. Smoking causes cancer of the mouth, nose, throat, larynx, trachea, esophagus, lungs, stomach, pancreas, kidneys, ureters, bladder, cervix, bone marrow and blood. Smoking is a leading cause of heart disease and stroke. Smoking causes emphysema, chronic bronchitis, increased pneumonia and other respiratory problems including cough and mucus production. Smoking impacts fertility and unborn babies. Smoking makes diabetes harder to control. Smoking has such a significant role in causing a given lung cancer that it belies belief tobacco companies are not included among the defendants in an asbestos claim. Yet, tobacco companies escape liability based upon the protection of government legislation related to warnings or settlement of state attorney general claims. This should not detract from any argument that tobacco contributed to a given cancer or that plaintiff s own conduct increased his chances of disease. Defending Lung Cancer Claims Speziali 19

III. Historic Literature Related to Asbestos and Lung Cancer In 1935 Lynch and Smith published a case report discussing the association of asbestosis and lung cancer in a cotton mill weaver. Lynch and Smith, Pulmonary Asbestosis III: Carcinoma of Lung in Asbestos-Silicosis, Am Journal of Cancer, Vol. XXIV, 56-64 (1935). There were no definitive conclusions other than to point to the occurrence of disease in these workers. Three years later Dr. Dreessen issued a report to the United States Public Health Service regarding asbestos and disease. Public Health Bulletin 241, A Study of Asbestosis in the Asbestos Textile Industry, USPHS August 1938; also Sayers and Dreessen, Asbestosis, Am. J. Pub. Health, Vol. 29, 205-214 (March 1939). He concluded asbestos is associated with high levels of exposure to asbestos in textile factories. In the index he reported three cases of lung cancer in association with asbestosis. Id. at 125. Through 1949 there were miscellaneous discussions and articles referencing asbestos and lung cancer. At that time an anonymous letter to the editor concluded the available evidence shows that the occurrence of cancer of the lung is related to pulmonary asbestosis and is not merely a possible sequel of exposure to asbestos dust. JAMA, Asbestosis and Cancer of the Lung, Volume 140, 1219-1220 (Aug. 1949). The article by Doll in 1955 is often cited as the study that finally established an association between lung cancer and asbestos. Richard Doll, Mortality From Lung Cancer in Asbestos Workers, Brit. J. Ind. Med, Vol. 12, 81-86 (1955). Doll looked at the cause of death of 105 people who had been employed at an asbestos factory. Among them were 18 cases of lung cancer, 15 with associated asbestosis. Doll concluded there is a casual relationship between lung cancer and asbestosis. He also noted they found no cases in workers exposed after enactment of British dust regulations in 1931. Those regulations reduced exposure to asbestos in factories. IV. Selikoff Studies In 1961 Dr. Irving Selikoff began his study of the Asbestos Workers Union. In his first peer reviewed paper arising out of this research Dr. Selikoff reported an increase risk of lung cancer in association with asbestos insulation work. Selikoff, Asbestos Exposure and Neoplasia, JAMA, April 6, 1964, 142-146. In doing so he stated he was unable to answer the question as to whether the high rate of lung cancer among these asbestos workers could possibly be attributed to an unusually large proportion of cigarette smokers among them. Id at 144. In 1967 Dr. Selikoff told representatives of the Asbestos Worker s Union Cancer of the lung can be wiped out in your trade if you people wouldn t smoke cigarettes, period. Dr. Irving Selikoff Address to the Delegates of the Twenty-First Convention of the International Association of Heat and Frost Insulators and Asbestos Workers, Chicago, Illinois (September 1967). By 1968 Dr. Selikoff had expanded his study of the Asbestos Worker s Union to all members in the United States and Canada; some 17,800 insulators. He opined further on the relationship of lung cancer and asbestos. Selikoff, Hammond and Churg, Asbestos Exposure, Smoking and Neoplasia, JAMA, Vol. 204, No. 2, 104-110 (April 8, 1968). He reported that to date there were 24 cases of lung cancer in the study group. All had a history of cigarette smoking. Of the subjects that never smoked regularly and those who smoked only pipes or cigars, none died of bronchogenic carcinoma whereas 0.18 of these men were expected to die of lung cancer. Id. at 108. Yet, because the number of lung cancer deaths so greatly exceeded the expected, even among the smokers, Dr. Selikoff concluded asbestos exposure increases the risk of lung cancer: However, considering the small number of such subjects in this study, we only conclude that exposure to asbestos dust does not greatly increase the risk of bronchogenic carcinoma among men who never smoked cigarettes regularly. Id. at 108. By 1978 Dr. Selikoff had yet to find an increased risk of lung cancer among asbestos insulation workers with no history of cigarette smoking. Selikoff and Lee, Asbestos and Disease, Academic Press Inc. (1978) at 20 Asbestos Medicine Seminar November 2012

page 327, Table 12-9. The authors concluded in the absence of smoking, there may be an increase in prevalence but it is not significant. Id at 336. On June 24-27 1978 scientists, researchers and even lawyers met in New York to exchange data regarding asbestos health hazards. The conference was sponsored by the NY Academy of Sciences and chaired by Drs. Irving Selikoff and E. Cuyler Hammond. The proceedings led to publication of a compilation of papers delivered at the conference. Selikoff and Hammond, Health Hazards of Asbestos Exposure, Annals of the NY Academy of Sciences, Vol. 330, December 14, 1979. At this conference Drs. Hammond and Selikoff presented the data they felt showed the relationship of asbestos with lung cancer. Id., Asbestos Exposure, Cigarette Smoking and Death Rates, 473-490. Many arguments can be made about how the data reported at the conference somehow changed from the data published in the earlier publication by Selikoff and Lee, supra. For purposes of this discussion we will ignore the inconsistencies in the data. The Hammond/Selikoff paper is typically cited in support of the conclusion that there is an association between asbestos and lung cancer in the absence of cigarette smoking and that there is a synergistic effect between asbestos and smoking. Most government agencies and researchers rely upon Hammond/Selikoff for this proposition. Not only are these conclusions unwarranted but also Drs. Hammond and Selikoff cautioned against such conclusions. One cannot properly defend a lung cancer claim unless there is a thorough understanding of the Hammond/Selikoff study. V. Critique of Hammond/Selikoff The goal of the study was to determine what impact cigarette smoking has on the high incidence of lung cancer among asbestos insulation workers. The cohort consisted of 12,051 asbestos workers who had passed the 20-year point of first exposure as of January 1, 1977. Id. At 481. Each was sent a questionnaire asking for smoking, exposure and medical history. 8,220 responded. Of this group 891 said they never smoked regularly; 488 had a history of pipe or cigar smoking but never smoked cigarettes regularly and 6,841 were either current or ex-cigarette smokers. The control groups for determining expected death rates were obtained from American Cancer Society Cancer Prevention Study I (CPS I). Id at 474. Selection was based upon the socio-economic background of the asbestos workers. For this reason a control group was selected of all male subjects who met the following specifications: white, not a farmer, no more than a high school education, a history of occupational exposure to dust, fumes, vapors, gases, chemical or radiation and alive as of January 1, 1967. Id. at 475. The idea was simple; with the support of the data from CPS I the researchers could predict the expected number of lung cancer deaths had the cohort never been exposed to asbestos. To the extent lung cancer deaths exceeded the expected rates asbestos was considered the cause. Of the insulators that never smoked regularly the researchers expected 0.7 lung cancer deaths but 4 were identified. Id, Table 7A at 486. Of those with a history of cigarette smoking 4.7 deaths were expected and 268 observed. The data also included death rates addressing cessation of smoking as well as pipe/cigar smokers. In Table 8 Drs. Hammond and Selikoff provide morality ratios based upon comparison of death rates with the control group. It is Table 8 that most government agencies and plaintiff experts rely upon for the conclusion there is a synergistic relationship between asbestos and smoking. Such a conclusion is simply unwarranted. The Hammond/Selikoff data suggest bias for many reasons. They fail to consider bystander-smoking risk, impact of other carcinogens or the intensity of smoking. It is not clear how the comparison group was selected or what was meant by never smoked regularly. One only need consider what the authors said in Defending Lung Cancer Claims Speziali 21

order to understand it is wrong to argue the Hammond/Selikoff data supports the concept of synergy or that asbestos causes lung cancer in the absence of smoking: Taken at face value it would appear that the risk of dying of lung cancer is about five times as great for a nonsmoker occupationally exposed to asbestos dust as for a nonsmoker without such exposure. However, because of small numbers the ratio is subject to considerable statistical sampling variation. By chance, the observed number might have been as low as one or two or as high as about nine. Therefore, all we can say is that the actual mortality ratio is probably >1 but could be as high as 12.00 or even a little higher. In any event, the mortality ratio for men who never smoked regularly was very small as compared with the mortality ratios of the cigarette smokers. Id. at 485. The data was limited to intense exposures experienced by insulators, not low dose exposures outside insulation work (ie, auto, household, electrical etc). The data only applied to men. Bystanders were not included and there was no information regarding exposures limited to chrysotile products (ie, gaskets, brakes, plastics). Regardless of how you view Hammond/Selikoff, one fact cannot be refuted: Despite countless publications and presentations, to this day, 34 years later, the researchers have not reported another lung cancer death in an asbestos worker who never smoked regularly. Consider the comments of Drs. Doll and Peto: The more important question is whether the large estimates of risk, which the OSHA paper carries over from Selikoff s studies of people who have been occupationally exposed as shipyard insulation workers for decades, really are applicable to about 10 percent of the men in the whole United States (half of whom are less than 40 years of age). Richard Doll and Richard Peto, The Causes of Cancer, Oxford University Press (1981) at page 1307. In other words, there is at least a tenfold exaggeration in the OSHA estimates of the number of mesotheliomas due to asbestos and, consequently, in their estimates of the other cancer hazards of asbestos. Id. at 1308. At the 1981 Cold Spring Harbor Laboratory meeting on the Quantification of Occupational Cancer, the speakers in the session devoted to asbestos came from a range of backgrounds (including Dr. Selikoff s department at New York, the National Cancer Institute and various industries and universities). Using some quite different epidemiological approaches, several of these speakers devised numerical estimates of the proportion of U.S. cancer deaths currently due to asbestos, all of which were around 1 or 2 percent (rather than 13-18 percent!), and no speaker or participant dissented from this consensus. Id. at 1308, FN 5. Cancer Prevention Study II (CPS II) The Hammond/Selikoff study relied on CPS I for the control group data. With only four cases of lung cancer among the non-smoking asbestos insulators any change in the expected rates would have a dramatic impact on the results. This is exactly the result of CPS II. CPS II began in September 1982 and consisted of 1.2 million persons. By 1991 the data indicated death rates from cigarette smoking were double what had previously been reported in CPS I. Shopland, Smoking-Attributable Cancer Mortality in 1991: Is Lung Cancer Now the Leading Cause of Death Among Smokers in the United States?, J. of the Nat. Cancer Inst. Vol. 83, No. 16, 1142-1148 (August 21, 1991). Male lung cancer death rates for current smokers had gone from 11.35 (CPS I and relied upon by Selikoff) to 22.36 (CPS II). Id. page 1143 Table 1. For former male cigarette smokers lung cancer death rates went from 4.96 to 9.36. The results for woman showed even more dramatic changes. 22 Asbestos Medicine Seminar November 2012

So, where does this leave the Hammond/Selikoff conclusions regarding lung cancer risk in nonsmokers and synergy? Based on CPS I the risk is exactly where Hammond/Selikoff and Doll/Peto said; anywhere from 1 or 2 percent to 12. Based on CPS II, if there is a risk it is significantly less. Simply stated Hammond/Selikoff conclusions regarding synergy and degree of risk of lung cancer from asbestos are no longer valid and will remain invalid until the research is update utilizing data from CPS II. VI. Asbestosis/Lung Cancer Debate The issue of whether a given lung cancer is associated with cigarette smoking as opposed to asbestos does not stop with the smoking debate. If asbestos does cause lung cancer must there first be underlying asbestosis before causation can be established in a given case? In 1955 the Chief of the Environmental Cancer Section for the NIH wrote Epidemiologic data available at present indicate that an increased liability to cancer of the lung is limited to the presence of asbestosis of the lung and does not extend to exposure to asbestos without the existence of a pneumoconiosis resulting therefrom. Heuper, Editorial, Silicosis, Asbestosis, and Cancer of the Lung, Am. J of Cl. Path., Vol. 25, No. 7-12, 1388-1390 (1955). Heuper noted all the cases of lung cancer associated with asbestos had co-existent asbestosis. This included the cases reported by Doll (1955), Dreessen (1938) and Lynch (1935). By 1966 Dr. Selikoff had already held an international health conference regarding asbestos and was 5 years into his research of the asbestos workers union. Still there were no reported cases of lung cancer associated with asbestos in the absence of underlying asbestosis. Since the presence of asbestosis has usually been considered the prerequisite for the subsequent development of a carcinoma of the lung or of a mesothelioma of the pleura or of the peritoneum, these deficiencies in the available information tend to impair a clear demonstration of the real scope of the existing associations between the two conditions. Hueper, Occupational and Environmental Cancers of the Respiratory System (1966) p. 42. It was not until 1987 that Dr. Selikoff and his fellow researchers provided any guidance on the debate regarding lung cancer and asbestosis. Kipen, Lilis, et al., Pulmonary Fibrosis in Asbestos Insulation Workers with Lung Cancer: a Radiological and Histopathological Evaluation, BJ Ind. Med. Vol. 44; 96-100 (1987). They reviewed 138 lung cancer cases where they had both pathology and radiology from the 17,800 insulators union study. Of the 138 cases 82 percent or 8 out of 10 had radiological detectable asbestosis. In all 138 (100 percent) cases there were histopathological signs of interstitial fibrosis. Id. at 98. Despite finding underlying asbestosis in 100 percent of the cases the researchers, several of whom participate regularly as plaintiff experts in asbestos personal injury litigation, stated the following: The question of whether or not asbestosis always precedes lung cancer in subjects exposed to asbestos is unresolved, and our present data do not permit conclusions regarding the etiological relation between lung cancer and pulmonary asbestosis per se, as distinct from that of concurrence between lung cancer and exposure to asbestos. Id. at 100. In their report they also said they are investigating the relationship between underlying asbestosis and deaths other than from lung cancer. To this date, some 25 years later, the Mt. Sinai group has not been reported a single lung cancer death without co-existent asbestosis VII. Helsinki On January 20-22, 1997 a group of researchers met at an international meeting on asbestos in Helsinki. From that conference came a consensus report. Consensus Report; Asbestos, Asbestosis, and cancer: The Helsinki Criteria for Diagnosis and Attribution, Scand. J. Work Environ. Health, 23:311-6 (1997). The consen- Defending Lung Cancer Claims Speziali 23

sus committee, chaired by Professor Douglas Henderson, essentially concludes that any identifiable asbestos exposure is sufficient to attribute a lung cancer with asbestos. The only exception was when there is a tissue analysis demonstrating a fiber count at background levels. Id. at 313. The consensus report provides no research, data, citations to authoritative sources or other information in support of the conclusions. Rather, they state this document is based on a more comprehensive report providing scientific evidence for the conclusions and recommendations (People and Work Research Reports, No. 14, Finnish Institute of Occupational Health, Helsinki, 1997). Id. at 311. The comprehensive report is a compilation of papers presented at the conference. Of interest to the present discussion are the papers that looked at the relationship of lung cancer and asbestosis for attribution purposes: There is universal agreement regarding the increased risk of lung cancer in patients with asbestosis. Less certain is the association between an elevated pulmonary fibre burden and lung cancer risk in the absence of asbestosis. Id. Roggli, Criteria for Clinical Diagnosis; Histological Criteria at p. 52. Dr. Roggli notes that in the absence of underlying asbestosis an analysis should be done of pulmonary fibre burden with respect to subsequent lung cancer risk. Id. Professor Henderson, who served as Chairmen of the Helsinki Conference and Consensus Report committee, also opined regarding lung cancer and asbestos: In my experience, two propositions are often adduced in asbestos litigation: (1) asbestosis constitutes a clear and reproducible marker for the attribution of lung cancer to asbestos; and (2) scientific data point to asbestosis as an obligate precursor of asbestos-induced lung cancer. Id at 58. In relation to attribution of lung cancer to asbestos, the prevailing scientific evidence indicates that the asbestos fibre burden in lung tissue is the primary determinator for the development of lung cancer; within this context, asbestosis has significance primarily as a marker of high fibre burden. Id. Henderson, Asbestosis as a marker or precursor for asbestos-related lung cancer: Are the criteria for pathological diagnosis consistent or reproducible? at p. 63. Both Dr. Roggli and Professor Henderson made clear that in the absence of a clinical diagnosis of underlying asbestosis an asbestos fibre burden analysis is necessary before a given lung cancer can be attributed to asbestos. The only other presentation at the conference to analyze the issue of attribution of lung cancer to asbestos exposure considered it from the perspective of compensation organizations of various countries. Dr. Paul De Vuyst, Guidelines for the Attribution of Lung Cancer to Asbestos. Id. at 92-96. Dr. De Vuyst notes that compensation organizations of most countries will accept a lung cancer claim in the absence of radiological signs of fibrosis. Id. at 93. With litigation it is different: The attribution, in a particular case, between the occupational exposure and the disease should be established or presumed with a reasonable certainty Influenced by recent epidemiological studies showing an increased risk for lung cancer in the absence of radiological signs of fibrosis, compensation organizations of many countries accept to compensate lung cancer with associated lesions. It should be underlined that these studies show a RR lower than 2, and that a RR of 2 corresponds to a doubling of the expected cases. Id. at 93. According to epidemiological studies, there is an increased lung cancer risk when there are no radiological signs of asbestosis. Nevertheless, the RR appears lower than with asbestosis (RR <2). 24 Asbestos Medicine Seminar November 2012

If we accept the principle that a substantial exposure is necessary to increase significantly the RR of lung cancer, any exposure or any increase lung burden should not be accepted. This is an important difference with mesothelioma. Id. at 96. Simply stated a RR <2 does not allow for a conclusion in terms of reasonable probability that a given lung cancer is associated with asbestos. All that can be said is that it may or may not have been associated. Although this may be sufficient for government compensation purposes it is inadequate in the courtroom. Since 1997 the plaintiff bar and their experts have pointed to the Helsinki Consensus Report as the gold standard for attribution of lung cancer to asbestos. On its face the report suggests that almost any history of exposure is sufficient to include asbestos as a cause. This position is contrary to the conclusions of Drs. Roggli and De Vuyst and Professor Henderson, the only presentations that addressed this issue directly. On the other hand, maybe we read far too much into the Consensus Report and fail to heed its own qualification: Estimates of the relative risk for asbestos-associated lung cancer are based on different-sized populations. Because of the high incidence of lung cancer in the general population, it is not possible to prove in precise deterministic terms that asbestos is the causative factor for an individual patient, even when asbestosis is present. However, attribution of causation requires reasonable medical certainty on a probability basis that the agent (asbestos) has caused or contributed materially to the disease. Helsinki Consensus Report at p. 314. Plaintiff and defense experts will continue to debate the significance of the statements arising out of the Helsinki Conference. From a defense perspective the presentations at the conference support the proposition that it is not probable asbestos is the cause in an individual lung cancer case with no underlying asbestosis. VIII. Discovery in Ling Cancer Cases Cigarette smoking is the single biggest issue in a lung cancer case. Ironically plaintiff s claim against the asbestos defendant contradicts his/her experience with tobacco. Whereas plaintiff will be adamant the asbestos company s failure to warn caused unprotected exposure to asbestos no such claim can be made as to tobacco. Warnings came from the packages, mass media, doctors, workplace rules and so many other places that it is undeniable a plaintiff appreciated the cancer risk. In fact, there is a whole body of State and Federal law that deems a person was adequately warned as of 1969. See for example Cipollone v Liggett Group Inc. et al, 505 U.S. 504 (1992); Spain v Brown & Williamson, 363 F.3d. 1183, 1196-1197 (11 th Cir. 2004); Allgood v RJ Reynolds Tobacco Company, 80 F. 3d 168, 171 (5 th Cir. 1996); Aldana v RJ Reynolds Tobacco Co., 2007 U.S. Dist. LEXIS 76050 (D. S.C. 2007); Waterhouse v RJ Reynolds Tobacco Co., 270 F. Supp. 2d 678 (D. Md. 2003); Small v Philip Morris, Inc. 252 A.D. 2d 1, 14-15 (NY App. Div. 1 st 1998); Cantley v Lorillard Tobacco Co., 681 So. 2d 1057, 1060-1061 (Ala. 1996). A motion finding plaintiff was adequately warned, as a matter of law, should be made in any case where smoking post dates 1969. Addiction is often given as the reason an individual continued to smoke in the face of known cancer risk. Clearly tobacco addiction claims are not frivolous. Yet, addiction does not reduce the health consequences of smoking and in many instances addiction is not an excuse for smoking. Smokers who began the habit after 1966, when warnings were first placed on cigarette packages, cannot claim addiction as an excuse. If you assume an individual starts smoking at age 17 it means someone born after 1949 was warned about the dangers of smoking before he/she took the first puff. That individual would be 63 years old today. Another undeniable fact is that people can and do stop smoking. Dr. Selikoff reported that among the insulator cohort a third were able to quit smoking (2,201 stopped and 4,472 were still smoking). Selikoff and Hammond, Asbestos and Smoking, Editorials, JAMA, Vol. 242, No. 5 at 458 (Aug. 3, 1979). According to the Defending Lung Cancer Claims Speziali 25

Center for Disease Control the number of former smokers exceeds the number of current smokers. Centers for Disease Control and Prevention. Quitting Smoking Among Adults United States, 2001 2010. Morbidity and Mortality Weekly Report [serial online] 2011;60 (44):1513 19 [accessed 2011 Nov 10]. Nobody should argue that it is easy to quit smoking or that one will be successful if he/she tries. The issue is did the individual try? Over the counter medications, counseling and intervention programs are just some of the available resources. Jurors will not fault an individual for failing at efforts to quit; they may find fault in failing to try to quit. You must challenge a plaintiff who smoked with hard questions as to when he/ she started and why he/she did not quit. Even if you believe the plaintiff was a victim of addiction it does not change the fact tobacco caused the lung cancer. IX. Medical Records In a lung cancer case the plaintiff s medical records are the best independent source for addressing key issues. Usually there is detailed information regarding the exact smoking history. They often note medical advice to quit, efforts toward the same and show tobacco related medical conditions ranging from heart disease to COPD to emphysema. Medical records assist the experts in determining whether there is underlying asbestosis. The history in medical exams (noting symptomatology, breadth sounds, clubbing and benefits of bronchodilators) provides invaluable information in support of a diagnosis. Pulmonary function tests, blood gas studies and pathology and radiology reports can prove the presence or absence of medical conditions related to asbestos or smoking. The manner of reading these medical records and determining the disease process is outside the scope of this paper. Suffice it to say there is an art to deciphering the records. Do they show obstructive or restrictive lung disease, does the medical history explain the symptoms and results, are negative results related to an ongoing disease process or reader/laboratory variability, did the individual or laboratory fail to properly perform the tests and are radiology or pulmonary function tests supported by serial comparison of the results? Non-malignant diseases related to smoking cause obstructive lung problems; emphysema being the most significant, COPD the most common. Non-malignant asbestos diseases cause restrictive lung problems; asbestosis being the most significant. Restrictive lung problems can rarely be treated by medication and, if asbestos related, do not get better. Obstructive lung problems can get better and bronchodilators often provide relief. Record entries regarding inhalers, radiology or pulmonary function test results showing improvement or symptoms that go away are valuable evidence that the plaintiff does not have underlying asbestosis. Your goal should always be to obtain as much of the historic medical information that is available and have someone with experience do a detailed review. X. Conclusion One need only watch the onslaught of commercials from asbestos plaintiff attorneys trolling for cases to appreciate that lung cancer claims are the wave of the future in asbestos personal injury litigation. Do not be fooled by media coverage or intensity with which plaintiff experts argue asbestos causes lung cancer and point to studies and government pronouncements supporting the same. Although there are instances where asbestos will have played some role or it will be difficult to disprove the same, in the overwhelming majority of cases tobacco is the sole proximate cause of plaintiff s lung cancer. Smoking impacts every aspect of medical causation and places in question liability issues related to failure to warn. It is unfortunate that anyone suffers from lung cancer whether they smoked or not. Yet, if the person smoked and suffers from lung cancer but it 26 Asbestos Medicine Seminar November 2012

makes no sense asbestos personal injury litigation becomes the battleground for compensation. In defending these claims you must do everything possible to assure that the full impact of smoking is considered and, where appropriate, plaintiff be held accountable for the consequences arising from the personal decision to smoke. GOOD LUCK! DAS Defending Lung Cancer Claims Speziali 27