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MS 06 - Regulation of Tobacco Products (ID 24)
- Event: WCLC 2015
- Type: Mini Symposium
- Track: Prevention and Tobacco Control
- Presentations: 4
- Moderators:E. Santos, N. Yamaguchi
- Coordinates: 9/07/2015, 14:15 - 15:45, 201+203
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MS06.01 - Global Effects of Smoking, of Quitting, and of Taxing Tobacco (ID 1868)
14:20 - 14:40 | Author(s): L. Joossens
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Evidence from countries of all income levels shows that price increases on cigarettes are highly effective in reducing demand. Higher prices induce cessation and prevent initiation of tobacco use. Article 6 of the WHO Framework Convention on Tobacco Control, "Price and Tax Measures to Reduce the Demand for Tobacco", recognizes the importance of this policy and calls on governments to implement tax and price policies to contribute to their national health objectives. Guidelines on Price and Tax Measures to reduce the demand for Tobacco, adopted by the 180 parties to the FCTC at the Sixth Conference of the Parties in October 2014, stipulate: “Any policy to increase tobacco taxes that effectively increases real prices reduces tobacco use. According to the studies referenced in the WHO technical manual on tobacco tax administration and IARC Handbooks of Cancer Prevention: Tobacco Control. Volume 14, the relationship between real prices and tobacco consumption is generally inelastic, meaning that the decline in consumption is less than proportional to the increase in real price. Most estimates of the price elasticity of demand lie between -0.2 and -0.8. In all settings, studies have shown that the price elasticity of demand is higher (in absolute terms) in the long term, meaning that consumption will fall even more in the long term. People with lower socioeconomic status are more responsive to tax and price changes because such changes have a greater impact on their disposable income. As regards the effect of higher taxes and prices on tobacco use by young people, it is estimated that young people are two to three times more responsive to tax and price changes than older people. Therefore, tobacco tax increases are likely to have a significant effect on reducing tobacco consumption, prevalence and initiation among young people, as well as on reducing the chances of young people moving from experimentation to addiction.”[1] [1] Conference of the Parties to the WHO Framework Convention on Tobacco Control, Sixth session, Guidelines for implementation of Article 6 of the WHO FCTC (Price and tax measures to reduce the demand for tobacco), Moscow, Russian Federation,13–18 October 2014.
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MS06.02 - The Framework Convention on Tobacco Control (ID 1869)
14:40 - 15:00 | Author(s): G. Fong
- Abstract
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Abstract not provided
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MS06.03 - FDA Regulation of Tobacco Products in the US (ID 1870)
15:00 - 15:20 | Author(s): M. Zeller
- Abstract
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Learning Objectives: • Describe FDA’s authority under the Family Smoking Prevention and Tobacco Control Act and the steps FDA has taken to regulate tobacco products in the 6 years since enactment of the law. • Understand FDA’s Center for Tobacco Products’ (CTP) strategic priorities and CTP’s vision for the regulation of tobacco products to help reduce the death and disease toll caused by tobacco use. • Describe how the CTP Office of Science supports and evaluates research to ensure that CTP has the science base to make regulatory decisions. • Discuss the ways the public health community can engage with FDA to participate in tobacco product regulation. • Identify opportunities to inform FDA action on tobacco to promote public health. Abstract: The landmark Family Smoking Prevention and Tobacco Control Act (TCA) gave the U.S. Food and Drug Administration (FDA) sweeping new authorities to create a healthier future for America’s families by regulating the manufacture, marketing, and distribution of tobacco products. The law, passed by Congress and signed by the President in 2009, gave FDA the authority to establish the Center for Tobacco Products (CTP), which drives powerful change to protect children and families from the dangers of tobacco products. The TCA takes a comprehensive approach—grounded in rigorous, timely science and the law—to improve public health, especially for the next generation. FDA uses its regulatory authority to take action to protect American families, charting a new course for comprehensive change. These actions include: • Developing science-based regulations to safeguard the nation’s health. • Publishing guidance to help the industry comply with regulations for tobacco products. • Conducting retailer inspections to ensure compliance with laws restricting sales of tobacco products to youth, and issuing warning letters and monetary penalties for violations. • Requiring tobacco manufacturers to report the ingredients in their products so FDA can evaluate the harm caused by the ingredients, take steps to reduce the harm, and educate the public about the toxic substances in tobacco products so public health can be improved. • Reviewing proposed modified risk tobacco products before they can be sold. • Restricting the access and attractiveness of cigarettes and smokeless tobacco to young people. • Enforcing the ban on the manufacture and sale of fruit- or candy-flavored cigarettes. • Prohibiting the use of misleading claims such as “low,” “light,” and “mild” that falsely imply that some tobacco products are safer. • Reviewing new tobacco products to determine whether they can be legally marketed. • Launching public information and education campaigns, particularly targeted to youth, about the dangers of regulated tobacco products. • Partnering with other public health agencies to conduct cutting-edge research on a range of topics such as smoking initiation and nicotine addiction. Currently, FDA regulates cigarettes, cigarette tobacco, roll-your-own tobacco, and smokeless tobacco. FDA has also published a proposed rule to bring other products that meet the definition of tobacco product under FDA’s regulatory authority, such e-cigarettes, waterpipes, some or all cigars, and pipe tobacco. Despite major progress over the past half-century tobacco use kills more than 480,000 Americans each year, making it the leading cause of preventable death and disease in the United States.[1] Every day in the United States, nearly 2,900 youth under the age of 18 smoke their first cigarette, and more than 700 youth under age 18 become daily smokers.[2] Nationwide, 5.5 percent of high school students currently use smokeless tobacco.[3] Nearly 9 out of 10 daily adult smokers used their first cigarette before the age of 18.1 On a global level, tobacco use causes nearly six million deaths a year and at current rates could kill up to one billion people this century.[4] Tobacco use is the most important risk factor for cancer causing around 20% of global cancer deaths and around 70% of global lung cancer deaths.[5] Tobacco regulators around the globe seek to protect present and future generations from the devastating health, social, environmental and economic consequences of tobacco consumption and exposure to tobacco smoke. We share common priorities and face common challenges in the fight to improve global public health. It is imperative that all global stakeholders, including the medical and scientific community, learn from one another’s successes and failures. In the United States, FDA's unique position as a regulatory agency allows for a framework of decisionmaking based on – and within the limits of – both the science and the law. CTP uses a comprehensive approach as the best way to end the negative health effects of tobacco use. This includes defining policy, issuing regulations, conducting research, educating Americans on regulated tobacco products, and making decisions on whether new products and claims can be marketed—including reviewing and evaluating applications and claims before the products are allowed on the market. CTP educates the public about the harms of tobacco products, working to reduce their appeal and keep them out of the hands of America’s youth. CTP is committed to protecting and improving public health by focusing on three top priorities: • Reduce initiation rates and prevent youth from starting to use tobacco • Encourage tobacco users to quit • Decrease the harms of tobacco product use This session will help the global medical, research, and public health communities understand the authority granted to the FDA to regulate tobacco and how science is used to make the most effective regulatory decisions. FDA staff will describe actions taken by the FDA in the first six years of regulating tobacco products and preview future regulatory priorities. Attendees will learn about specific ways in which they can collaborate with and inform FDA’s work. At the conclusion of this session, attendees will be able to describe the FDA's role, its activities to date and priorities for the future. References: 1. US Department of Health and Human Services. The Health Consequences of Smoking—50 Years of Progress. A Report of the Surgeon General. Atlanta, GA: US Dept of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2014. 2. Substance Abuse and Mental Health Services Administration (SAMHSA). Results from the 2012 National Survey on Drug Use and Health, NSDUH: Table 4.10A Past Year Initiation of Substance Use Among Persons Aged 12 or Older Who Initiated Use Prior to the Age of 18, by Gender: Numbers in Thousands, 2012 and 2013. Rockville (MD): US Dept of Health and Human Services, Substance Abuse and Mental Health Services Administration, Center for Behavioral Health Statistics and Quality, 2014. 3. Centers for Disease Control and Prevention. Tobacco Product Use Among Middle and High School Students - United States, 2011-2014. Morbidity and Mortality Weekly Report 2015; 64: 381-385. 4. http://www.who.int/mediacentre/factsheets/fs339/en/ 5. http://www.who.int/mediacentre/factsheets/fs297/en/ The U.S. Food and Drug Administration (FDA) Center for Tobacco Products (CTP) oversees the implementation of the Family Smoking Prevention and Tobacco Control Act (TCA). This session will help the medical, research, and public health communities understand the authority granted to FDA to regulate tobacco and how science is used to make the most effective regulatory decisions. Mr. Zeller will describe actions taken by the FDA in the first six years of regulating tobacco products and provide an overview of CTP’s strategic priorities. Attendees will learn about specific ways in which they can collaborate with and inform FDA’s work. At the conclusion of this session, attendees will be able to describe the FDA's role, its activities to date and priorities for the future and understand CTP's strategic priorities and vision for the regulation of tobacco products to help reduce the death and disease toll caused by tobacco use.
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MS06.04 - The Role of Litigation in Controlling Tobacco Use (ID 1871)
15:20 - 15:40 | Author(s): R. Daynard
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Product liability litigation has played a critical, if supporting, role in tobacco control. Most prominently, lawsuits brought by US state attorneys general in the mid-1990s seeking reimbursement for expenses incurred in treating residents for smoking-related diseases forced the industry to begin disgorging incriminating internal documents, with over 14 million now available on the internet, detailing industry misbehavior around the world (http://legacy.library.ucsf.edu). Public exposure of these misdeeds made the tobacco industry politically toxic, easing the way for subsequent regulatory legislation. Under the Master Settlement Agreement resolving these cases, the industry agreed to eliminate various marketing techniques and promotional stratagems and pay the states about $10 billion/year, resulting in dramatic cigarette price increases that greatly reduced teenage smoking. Some of that money went into effective tobacco control programs. Every stage of tobacco litigation (initial filings, motions, hearings, decisions, appeals) provides ‘teachable moments’ for public education about the underlying issues: the health consequences of smoking, addictiveness, and tobacco industry misbehavior. The cases dramatize the impact of smoking on real people, not just statistics. Even the industry's counter-spin, that smokers who contract lung cancer ‘assumed the risk’, implicitly acknowledges the reality of the causal link. Product liability litigation can take many forms. Most legal systems allow individuals, including smokers or their survivors, to seek compensation for their financial and emotional losses from product manufacturers that sell unreasonably dangerous products, fail to warn about the dangers of these products, and/or actually lie about these dangers. In the USA, multimillion-dollar punitive damages, designed to deter others from misbehaving like tobacco companies, are sometimes also available. Similar cases can be brought by victims of secondhand smoke, though establishing causation in cases against tobacco manufacturers has proven extremely difficult; obtaining workers compensation from employers, however, has become fairly routine. Injuries from cigarette-caused fires are compensable, since cigarettes with low ignition propensity can easily be manufactured. Injured smokers and non-smokers are not the only possible plaintiffs: as mentioned, many US states were permitted to sue tobacco companies in the 1990s for medical costs incurred in caring for smokers whose diseases could be attributed to tobacco industry misconduct. Similar cases are pending in Israel, and most Canadian provinces now have legislation facilitating such lawsuits. Finally, legal systems sometimes permit consumers with similar claims to proceed in a single class action, greatly reducing litigation costs. In May 2015 a judge in Quebec, Canada awarded more than US$100,000/smoker to a class of about 100,000 smokers with lung or throat cancer or emphysema, as well as about $100 million to another class of addicted smokers. U.S. courts have allowed class actions to go forward to fund medical monitoring programs for long-term smokers, and to compensate smokers who were fooled into thinking that “light” cigarettes were safer than regular cigarettes. Cases can be brought to stop tobacco industry misconduct brought by parties who were not themselves injured by that behavior. Thus, the US Department of Justice brought a successful case against the major tobacco companies to prevent their continued violations of the Racketeer Influenced and Corrupt Organizations Act. And cases can even be brought in some jurisdictions to force the government to protect the lives and health of their citizens. Thus, the Indian Supreme Court insisted upon legislation to protect nonsmokers from secondhand smoke. The efficacy of product liability litigation depends as much on procedural rules as on substantive legal doctrines (legal ‘rights’). In most countries other than the USA, the absence of contingency fees (where plaintiff's lawyers are compensated with a portion of the plaintiff's judgment or settlement, if any) means the lawyers must either provide their services for free or bill their ill, dying, or bereaved clients on an ongoing basis: hence, few such cases are brought. Worse, many legal systems require plaintiffs who lose their cases to pay the defendant's legal costs, thus putting the plaintiff's remaining assets at risk. These unfortunate procedural rules can, of course, be changed by court rule or statute. Going forward Article 4.5 of the WHO Framework Convention on Tobacco Control (FCTC) recognizes that ‘issues relating to liability… are an important part of comprehensive tobacco control’. Article 19, ‘Liability’, provides that ‘Parties shall consider taking legislative action… to deal with… civil liability, including compensation where appropriate’. Legislation correcting the procedural rules that prohibit contingency fees and shift litigation costs to the losing party, permitting consumer class actions, and facilitating healthcare cost recovery lawsuits, are examples of such highly desirable legislative action. Article 19 also encourages parties to assist each other in carrying out legal proceedings and to share relevant information with each other, and invites the Conference of the Parties (COP) to develop ‘appropriate international approaches to these issues’ as well as to support parties in their activities relating to liability. The COP has currently charged an expert group to design a mechanism for collecting, archiving and sharing litigation documents and for providing advice and assistance—electronically or in person—to attorneys bringing liability cases against the tobacco industry. For at least a decade tobacco company defendants in the US have admitted on their websites and ceased to deny in court that smoking is the major cause of lung cancer and chronic obstructive pulmonary disease (COPD), though they often contest the diagnosis or aetiology in particular cases. By contrast, and despite universal availability of the internet, tobacco defendants in Europe and Asia have been remarkably successful in confusing courts on the epidemiology of smoking and disease. The recent acceleration in the globalization of tobacco control efforts, inspired by the FCTC and supported by the Bloomberg and Gates Foundations, and the commitment of parties under Article 12 of the FCTC to conduct public education on tobacco control issues, can be expected to equalize around the world knowledge of basic tobacco epidemiology. Similarly, the presence of millions of easily accessible internal tobacco industry documents on the internet should simplify the process of establishing the liability of the major transnational tobacco companies and their affiliates.
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MS 23 - Risk Factors: Beyond the Cigarette (ID 41)
- Event: WCLC 2015
- Type: Mini Symposium
- Track: Prevention and Tobacco Control
- Presentations: 5
- Moderators:N. Yamaguchi
- Coordinates: 9/09/2015, 14:15 - 15:45, 605+607
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MS23.01 - Radon and Lung Cancer (ID 1949)
14:20 - 14:35 | Author(s): B. Melloni
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Radon exposure is recognized as the second cause of lung cancer, after active cigarette smoking (1,2). Each year, 15 000 to 21 000 lung cancer deaths are estimated for the consequence of radon exposure in USA. In Europe, 18 000 deaths are attributable to radon, around 9 % of deaths from lung cancer. Atmospheric concentrations of natural radon gas vary importantly due to concentration of [226]Ra and [232]Th, present in soil of some geographic areas. Most of the radon in indoor spaces of houses and other dwellings is derived from the inert gas transfer from the soil or rock. Short-lived radioactive progeny from inhaled radon, polonium-214 and polonium-218 induce emission of alpha particles (2 protons and 2 neutrons) that directly damage DNA and can induce lung cancer. Radon progenies are inhaled either as free particles, or attached to airborne particles, as dust. The adverse effect of radon has been described since the fifteenth century in the Ore Mountains of Eastern Europe. As early as the 20[th] century, radon was identified a cause of lung cancer in miners in Eastern Europe. Large epidemiological studies on miners showed a link between lung cancer risk and radon exposure at high concentration. In 1988, International Agency for Research on Cancer (IARC) recognized radon, as a group 1 carcinogen, based on the results of epidemiological studies in uranium miners. The risk was correlated to radon exposure in eleven cohort studies in non-smoker and smoker miners, with a sub-multiplicative interaction between smoking and radon (3). In 1970s, it was recognized that the population could be exposed to radon in indoor environments, including home and dwellings. An association between the risk of lung cancer and residential radon concentration during the previous 30 years was outlined. Epidemiological case-control studies have reported clear evidence of a relation between lung cancer incidences in the general population and radon indoor exposure, at an average annual concentration above 200 Bq/m[3] (4,5,6). A dose-response model is used without a threshold value, but this concept is matter of controversy for low dose To improve the statistical power, pooled case-control studies have been made in the USA, Europe and China, after variable adjustment for sex, smoking habits (Table 1). The combined estimation from the pooling studies showed an increase of 10% per 100 Bq/m[3 ](7). In the European pooled case-control studies, the estimated lung cancer risk, at 0, 100, and 400 Bq/m[3], was 25.8, 29.9, 42.3 for current smokers (15-24 cigarettes per day) versus 1.0, 1.2, 1.6 for lifelong non-smokers (6). The relationship between active smoking and radon exposure seems to be synergic. The same relation is observed in patients with lung cancer exposed both to radon and environmental tobacco smoke (ETS). In Spain, a case control-study demonstrates that ETS exposure at home upgrades significantly the risk in individuals with radon exposure than 200 Bq/m[3 ](7). Concerning histological types of lung cancers observed, an excessive relative risk for small-cell lung cancer was first reported among the underground miners. In fact, all the histological types are present, most common being adenocarcinoma and squamous cell carcinomas. A recent study in Spain, in never-smoker cases exposed to radon, finds that the most frequent histology is adenocarcinoma, as now observed in non-smoker patients (8). The exact mechanism of lung cancer induced by alpha particles is not known. Alpha particles can cause DNA damage, chromosome aberrations, and generate reactive oxygen species. The results are a cell cycle modification, an up- and down-regulation of cytokines, and an increased potential for carcinogenesis. Despite these promising investigations on a mutation hotspot in one codon of the TP53 gene and in other regions, any molecular fingerprint of alpha particles has been identified in specific genes involved in lung cancer carcinogenesis. Reducing and controlling this natural radiation, the second cause of lung cancer, is paramount in the general population, especially in radon prone area. The WHO guideline has proposed a reference level of 100 Bq/m[3] (2.7 pCi/L) to reduce the risk of lung cancer in the population (9). In the USA, the Environmental Protection Agency action level is 148 Bq/m[3] (4 pCi/L) for the home. In Sweden, 35-40 % of lung cancer attributable to radon could be prevented if in all homes or dwellings radon concentrations over 100 Bq/m[3] were lowered to 100 Bq/m[3] (10). Buildings or houses with high radon concentration must be identified. New constructions should be “radon-proof”. Many strategies have been proposed to reduce indoor radon levels in the home. In conclusion, radon is the second leading cause of lung cancer among smokers and a major cause in non-smokers. Radon exposure must be identified in the population to reduce the level of exposure to individuals. Preventive measures are necessary for new homes in a high radon area. Smoking cessation is also important to reduce the risk of lung cancer from radon exposure. Bibliography 1. Samet JM, Avila-Tang E, Boffetta P, et al. Lung cancer in never smokers: clinical epidemiology and environmental risk factors. Clin Cancer Res 2009;15(18):5626-45. 2. Tirmarche M, Harrison JD, Laurier D et al. ICPR, 2010. Lung cancer risk from radon and progeny and statement on radon. ICPR publications 115, Ann. ICPR 40(1). 3. Lubin JH, Boice JD, Edling JC et al. 1994. Radon and lung cancer risk: A joint analysis of 11 underground miner studies. Publication No. 96-3644. US National Institutes of Health, Bethesda, MD, USA. 4. Krewski D, Lubin JH, Zielenski JM at al. Radon and risk of lung cancer: a combined analysis of 7 North-American case-control studies. Epidemiology 2005;16:137-45. 5. Lubin JH, Wang ZY, Boice JD Jr et al. Risk of lung cancer and residential radon in China: pooled results of two studies. Int J Cancer 2004;109:132-7. 6. Darby S, Hill D, Deo H et al. Residential radon and lung cancer-detailed results of a collaborative analysis of individual data on 7,148 persons with lung cancer and 14,208 persons without lung cancer from 13 epidemiological studies in Europe. Scand J Work Environ Health 2006;32(suppl 1):1-83. 7. Torres-Duràn M, Ruano-Ravina A, Parente-Lamelas I et al. Lung cancer in never smokers. A case-control study in a radon prone area (Galicia, Spain). Eur Respir J 2014;44(4):994-1001. 8. Torres-Duràn M, Ruano-Ravina A, Parente-Lamelas I et al. Residential radon and lung cancer characteristics in never smokers. Int J Radiat Biol. 2015 May 13:1-24. 9.World Health Organization. Handbook on indoor radon. A public health perspective. WHO Geneva, Switzerland, 2009. 10. Axelsson G, Anderssson EM, Barregard L. Lung cancer risk from radon exposure in dwellings in Sweden: how many cases can be prevented if radon levels are lowered? Cancer Causes Control 2015; 26 (4): 541-7.
Table 1: Pooled analysis of case-control studies of indoor radon exposure, based on measured concentration radon (4-6).Geographic area Population Controls Cases Relative risk per 100 Bq/m[3 ](95% CI) USA, Canada 7 studies 4 966 3 662 1.10 (0.99-1.26) China 2 studies 1 995 1 050 1.13 (1.01-1.26) Europe 13 studies 14 208 7 148 1.08 (1.03-1.16)
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MS23.02 - Air Pollution-Outdoor; Biomass Smoke; Cooking Fuels (ID 1950)
14:35 - 14:50 | Author(s): P. Boffetta
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Indoor air pollution. Indoor air pollution is thought to be the main determinant of the elevated risk of lung cancer experienced by nonsmoking women living in several regions of China and other Asian countries. The evidence is stronger for coal burning in poorly ventilated houses, but also burning of wood and other solid fuels, as well as fumes from high-temperature cooking using unrefined vegetable oils such as rapeseed oil. A positive association between various indicators of indoor air pollution and lung cancer risk has also been reported in populations exposed to less extreme conditions than those encountered by some Chinese women, for example populations in Central and Eastern Europe and other regions. Overall, the evidence is stronger for studies of indoor pollution in population which used coal as main fuel. IARC has classified indoor emissions from household combustion of coal as established human carcinogen, and indoor emissions from household combustion of biomass fuel (primarily wood) as probable human carcinogen. Outdoor air pollution. There is abundant evidence that lung cancer rates are higher in cities than in rural settings.This pattern, however, might result from confounding by other factors, notably tobacco smoking, and occupational exposures, rather than from air pollution. Cohort and case-control studies are limited by difficulties in assessing past exposure to the relevant air pollutants. The exposure to air pollution has been assessed either on the basis of proxy indicators—for example, the number of inhabitants in the community of residence, residence near a major pollution source—or on the basis of actual data on pollutant levels. These data, however, reflect mainly present levels or levels in the recent past and refer to total suspended particulates, sulfur oxides, and nitrogen oxides, which are not likely to be the agents responsible for the carcinogenic effect, if any, of air pollution. Furthermore, the sources of data might cover quite a wide area, masking small-scale differences in exposure levels. The combined evidence suggests that urban air pollution might entail a small excess risk of lung cancer on the order of 50%, but residual confounding cannot be excluded. In four cohort studies, assessment of exposure to fine particles was based on environmental measurements. The results of these studies are suggestive of a small increase in risk among people classified as most highly exposed to air pollution. IARC recently classified outdoor air pollution as an established lung carcinogen in humans.
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MS23.03 - Legalization of Marijuana: Implication for Lung Health (ID 1951)
14:50 - 15:05 | Author(s): J.R. Jett
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Marijuana is a mixture of dried, shredded leaves, flowers, stems, and seeds from the hemp plant, Cannabis Sativa. Cannabis is a genus of flowering plants that has psychoactive properties. The main active chemical is THC (delta-9-tetrahydrocannabinol). The psychoactive effects are primarily a state of relaxation and euphoria to some degree. Record of cannabis use dates back to the Chinese Emperor Shen Nung in 2727 BC. In the 1500s, Spaniards imported it into the Americas. The amount of THC in marijuana has been steadily increasing and is much stronger now than 30 years ago. The average THC levels have risen from less than 1% in the 1970s to 12% in 2012. (1,2) Uruguay is the first and only country to fully legalize marijuana, but a number of other countries are considering doing so. The Netherlands, especially Amsterdam, is well-known for its tolerance of marijuana use. Medical marijuana use is legal in 23 of the 50 states in the USA. The states of Colorado, Washington, Oregon, Alaska, and District of Columbia have legalized recreational marijuana use. A number of other states have decriminalized the use of marijuana and others are considering approval for recreational use. Most users smoke marijuana in hand-rolled cigarettes called joints, but it can also be smoked in blunts (cigars), bowls, pipes, bongs, or vaporizers. It is also available in oral forms for ingestion. This lecture will be limited to the health effects on the lungs of smoking marijuana. (2,3) Lung Effects: Marijuana smoke contains many of the same toxins and carcinogens as tobacco smoke. (4) In a systematic comparison of smoke from marijuana and tobacco cigarettes consumed under two sets of smoking conditions, there were qualitative similarities and some quantitative differences. Ammonia was 20-fold greater in marijuana. Nitric oxide, hydrogen cyanide, and some aromatic amines were three to five times more than those in tobacco smoke. Selected polycyclic aromatic hydrocarbons were in lower concentration in marijuana. (4) Accurate studies on the health effects of marijuana use are difficult due to the illegal status of its use, variation in its use, and concomitant use of tobacco. (3,5) Bronchoscopic biopsies from subjects who smoke marijuana alone or marijuana and tobacco have been evaluated for histopathologic changes and molecular alterations. Smokers of marijuana alone reported symptoms of cough, sputum, wheeze, and acute episodes of bronchitis. (6) Histologic abnormalities were most frequent in smokers of both marijuana and tobacco. However, smokers of marijuana along did show changes of basal cell hyperplasia, inflammation, and squamous cell metaplasia in a large percentage of the 40 subjects examined. (6) Immunohistochemical analysis of bronchial biopsies from smokers of marijuana only demonstrated increased Ki-67 expression (cell proliferation marker) in 92% and increased EGFR expression in 57%. (7) Marijuana smoking does not appear to cause airflow obstruction. A study with 20 years of follow-up did not observe any significant change in pulmonary function. In a large cross section of US adults, cumulative life-time marijuana use up to 20 joint-years was not associated with airway obstruction. (8) There have been conflicting reports on the association of marijuana smoking and lung cancer. A 40-year cohort study from Sweden evaluated the baseline use of cannabis and cigarette smoking and the risk of lung cancer. They observed a strong dose-response relationship between tobacco use and lung cancer. They also reported a two-fold risk of lung cancer [HR 2.12 (95% CI 1.08-4.14)] in heavy cannabis smokers, even after adjustment for baseline tobacco use. (9) A major weakness of the study was reliance on only baseline self reporting of tobacco and cannabis use. No other data on use of these two agents was obtained throughout the 40 years of the study. A pooled analysis of six case-control studies from the US, Canada, United Kingdom, and New Zealand was performed to study the specific association between cannabis smoking and lung cancer. This included data on 2,159 lung cancers and 2,985 controls. (10) The odds ratio was 0.88 (95% CI 0.63-1.24) for individuals who smoked one or more joint-equivalents of cannabis per day and odds ratio of 0.94 for those who consumed at least 10 joint-years. The results from the pooled analysis provide little evidence for an increased risk of lung cancer among habitual long-term cannabis smokers. In summary, smoking marijuana causes airway inflammation and bronchitis, but to date there is no convincing data that it causes COPD or lung cancer. The level of the evidence is limited by the suboptimal quality of past studies. The current use and dose of inhaled marijuana is changing and therefore measurement of the pulmonary health effects are a moving target. References: http://www.deamuseum.org/ccp/cannabis/history/html (last accessed June 30, 2015) Volkow ND, et al. NEJM 2014; 370:2219-27 Tashkin DP. Annals ATS 2013; 10:239-47 Moir D, et al. Chem Res Toxicol 2008; 21:494-502 Howden ML, et al. Expert Rev Resp Med 2011; 5:87-92 Fligiel SH, et al. Chest 1997; 112:319-26 Barsky SH, et al. J Natl Cancer Inst 1998; 90:1198-1205 Kempker JA, et al. Annals ATS 2015; 12:135-41 Callaghan RC, et al. Cancer Causes Control 2013; 24:1811-1820 Zhang LR, et al. Int J Cancer 2015; 136:894-903
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MS23.04 - Other Tobacco Products Electronic Devices/Water Pipes/Hookas (ID 1952)
15:05 - 15:20 | Author(s): E.L. Durmowicz
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Abstract:
The landscape of tobacco product use in the US is changing. Although cigarette smoking rates have declined in recent years, use of other tobacco products such as little cigars, waterpipe and electronic nicotine delivery systems (ENDS) is increasing. Background information about these “alternative” tobacco products, use trends, smoke or aerosol constituents and potential toxicities, especially those that may increase risk for lung cancer in users or bystanders, will be presented. Cigar consumption in the US increased from 6.2 billion cigars in 2000 to 13.3 billion in 2010 and is most common among young adults aged 18-24 years. This increased use has been attributed to use of little cigars and cigarillos, products that are less expensive alternatives to cigarettes in the US. “Small cigars” may be more likely to be smoked in similar fashion to cigarettes, especially by former cigarette smokers and dual users of cigarettes and cigars. Given that cigar smoke compared to cigarette smoke has higher concentrations of toxic and carcinogenic constituents (e.g., tobacco specific N-nitrosamines (TSNAs), carbon monoxide (CO), benzene), cigar users that inhale the smoke into the lungs may have greater risks for adverse health effects compared to cigarette smokers. Analysis of 25,000 participants from the US National Health and Nutrition Examination Survey (NHANES, 1999–2012) identified that current cigar/former cigarette smokers had significantly higher cotinine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) concentrations compared to cigar smokers with limited cigarette use, and NNAL concentrations were comparable between daily cigar and daily cigarettes smokers. Waterpipe (WP), also known as hookah, shisha and narghile, heat a mixture of tobacco, honey or molasses, and flavorings using charcoal. A centuries old style of smoking tobacco popular in Middle Eastern countries, waterpipe use has markedly increased in Europe and the US, and is especially popular among young people who frequently misperceive that the water filters out the harmful chemicals in the smoke. WP smoke contains many of the known toxicants and carcinogens found in cigarette smoke, including polycyclic aromatic hydrocarbons (PAHs), nicotine, TSNAs, volatile aldehydes and CO. Due to the burning charcoal, WP users are exposed to higher levels of CO, benzene and PAHs compared to cigarettes smokers. E-cigarettes, the most popular types of electronic nicotine delivery systems (ENDS), were developed in China in approximately 2003 and are increasingly popular in the US and Europe. ENDS heat an “e-liquid”, typically composed of nicotine, propylene glycol or glycerin, and flavorings into an aerosol that is inhaled by the user. The chemical constituents in ENDS aerosols are impacted by the device design, the e-liquid composition and user behaviors, and have not been adequately characterized. Carcinogenic and toxic compounds that have been detected in e-cigarette liquids and aerosols include TSNAs, formaldehyde, acetaldehyde, acrolein, PAHs and metals. However, in general, the amounts identified have been less than in cigarette smoke. The potential cytotoxicity and carcinogenicity of e-cigarette flavorings are being investigated.
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MS23.05 - Cost Efficacy of Tobacco Cessation Versus Treatment of Lung Cancer (ID 1953)
15:20 - 15:35 | Author(s): W.K. Evans, W. Isaranuwatchai, J. Hoch
- Abstract
- Presentation
Abstract:
The global burden of lung cancer is significant and growing. In 2015, WHO reported that there were almost 1.7 million deaths from lung cancer and this number could increase 1.5 times by 2030 (1).The cost associated with the management of lung cancer is significant and can be expected to increase dramatically. It has been estimated that the costs to manage lung cancer will increase in Canada by 80% from 2010 to 2030 but this may prove to be a gross underestimate because of new targeted and immuno-therapies (2). As smoking is the main cause of lung cancer, smoking cessation programs could improve not only the health of nations but also help to contain rising health care costs. In the face of the increasing global burden of lung cancer, it is instructive to consider the cost-effectiveness of lung cancer treatment in relation to smoking cessation programs. Cost effectiveness of lung cancer treatment options Treatment options for lung cancer depend on the stage and type of cancer. Recent advances in the treatment of metastatic non-small-cell lung cancer (NSCLC) have markedly increased the cost to health care systems and to patients themselves. When considering the implementation of new health care technologies, decision-makers consider the incremental cost of the new therapy (∆C) compared to the current standard in relation to the incremental benefit (∆E), usually expressed in life-years gained, to determine the incremental cost-effectiveness ratio or ICER. The life-years gained may be adjusted for the quality of the life lived with the disease and its treatment producing an estimate of cost per quality-adjusted life year or QALY. The ICER is influenced by many factors including the choice of comparator (best supportive care vs a chemotherapy regimen), the time horizon of the analysis, the inclusion of the cost of managing early and late adverse events, amongst other factors. Not surprisingly, the major determinant of the ICER for most new drugs is the price of the drug and the magnitude of the clinical benefit. A review of economic evaluations of drugs used for advanced non-squamous NSCLC suggests that ICERs are progressively rising: the ICER for erlotinib as a 3[rd] line therapy was only $39,000/LY when compared to BSC (3). However, the ICER for pemetrexed used as a 1[st ]line treatment in tumours with no known mutations was $142,500 US dollars (2013) per QALY when compare to best supportive care (BSC) and $164,000 per life year (LY) gained when compared to erlotinib (4).Estimates of the ICER for afatinib based on the pan-Canadian Oncology Drug Review (pCODR) ranged from $39,000 to 211,000/QALY when compared to gefitinb reflecting the uncertainty in the clinical benefit in the absence of a head-to-head comparative trial (5). The ICER for crizotinib as first-line therapy in ALK +ve patients ranged from $173,570 (CDN) to $285,299, reflecting uncertainty in economic model assumptions related to the incremental benefit and the time horizon selected (5). ICERs above $100,000 per QALY are generally not considered “cost-effective” in Canada. The trend to higher ICERs could reverse with immune check point inhibitors given the potential for long term survival (much greater ∆E) in some patients, although the incremental cost may be unacceptably high (6). However, it must be remembered that dollars spent on lung cancer treatments cannot be spent on something else and represent a lost opportunity cost no matter how cost-effective the treatment appears. Value of smoking cessation programs Although some countries and American states have invested in public health programs to reduce smoking, globally there has been a low level of investment suggesting that there is resistance to investing in smoking cessation. This may be due to the perception that cessation interventions are ineffective, that smokers do not want to quit or that smoking cessation interventions are not cost effective (7). These commonly held perceptions are wrong. Smoking cessation (e.g., telephone counseling and pharmacological interventions) has been shown to improve health outcomes and survival. Most smokers in the general population, at least in North America, have made multiple quit attempts and express the desire to quit and cost-effectiveness estimates range from about $330 to $1500 US per life-year gained (7). A review of economic evaluations of smoking cessations programs shows that these programs are economically attractive and can even be cost-saving. For example, the American Cancer Society’s telephone counseling service nearly doubled a smoker’s odds of quitting and staying stopped for one year at a cost of approximately $1,500 per smoker (8).Nicotine Replacement Therapies (NRT) compared to self-help have an ICER of $1,500/QALY while varenicline was a dominant option compared to NRT. Also generally unrecognized are the health benefits to cancer patients, although these benefits have been well outlined in the 2014 U.S. Surgeon General’s Report on Smoking (9). Nonetheless, smoking cessation programs are rare in the oncology setting and information on the cost-effectiveness of smoking cessation in the oncology setting is limited. One study examined the cost-effectiveness of a pre-operative smoking cessation program for patients with early-stage NSCLC in the United States (10), and reported an ICER of $2,609/QALY and $2,703/LY at 5-years post-surgery. The cost-effectiveness of smoking cessation programs could be more dramatic over longer time horizons. Even though the benefits of smoking cessation programs on clinical outcomes have been reported, including the value for money of these programs, more evidence on the impact of smoking on outcomes for lung cancer patients receiving radiotherapy and systemic therapy is clearly needed. Discussion Faced with a global epidemic of lung cancer and a growing number of new but expensive drugs, recognition that smoking cessation programs are both effective and cost-effective should drive public policy. References 1. World Health Organization. Projections of mortality and burden of disease, 2002-2030. World Health Organization,; 2002 [cited 2015]; Available at:http:www.who.int/healthinfo/global_burden_disease/projections2002/en/. 2. Hermus G, Stonebridge C, Goldfarb D, et al. Cost risk analysis for chronic lung disease in Canada: The Conference Board of Canada 3. Cromwell I, van der Hoek K, Taylor SCM, et al. Erlotinib or best supportive care for third-line treatment of advanced non-small-cell lung cancer: a real-world cost-effectiveness analysis. Lung Cancer 2012;76(3):472-7 4. Matter-Walstra K, Joerger M, Kuhnel U, et al. Cost-effectiveness of maintenance pemetrexed in patients with advanced nonsquamous-cell lung cancer from the perspective of the Swiss health care system. Value in health. 2012;15165-71 5. Available at pcodr website . 6. Available at am.asco.org/aso-plenary-nivolumab-ipilimumab-combination-effective-advanced-melanoma. 7. Parrott S, Godfrey C, Raw M, et al. Guidance for Commissioners on the cost-effectiveness of smoking cessation interventions. Thorax 1998; 53 (Suppl 5, Part 2): S2-S3 8. McAlister A, Rabius V, Geiger A, et al. Telephone assistance for smoking cessation: one year cost effectiveness estimations. Tobacco control. 2004;13(1):85-6. 9. The Health Consequences of Smoking - 50 Years of Progress. A report of the Surgeon General, 2014. U.S Department of Health and Human Services, Office of the Surgeon General, Rockville, MD 10. Slatore CG, Au DH, Hollingworth W. Cost-effectiveness of a smoking cessation program implemented at the time of surgery for lung cancer. Journal of Thoracic Oncology. 2009;4(4):499-504.
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PLEN 04 - Presidential Symposium Including Top 4 Abstracts (ID 86)
- Event: WCLC 2015
- Type: Plenary
- Track: Plenary
- Presentations: 1
- Moderators:T. Mok, F.R. Hirsch
- Coordinates: 9/09/2015, 10:45 - 12:15, Plenary Hall (Bellco Theatre)
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PLEN04.08 - Discussant for PLEN04.07 (ID 3483)
12:03 - 12:11 | Author(s): N. Yamaguchi
- Abstract
- Presentation
Abstract not provided
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