While lung cancer has been the leading cause of cancer-related deaths for many years in the United States, incidence and mortality statistics – among other measures – vary widely worldwide. The aim of this study was to review the evidence on lung cancer epidemiology, including data of international scope with comparisons of economically, socially, and biologically different patient groups. In industrialized nations, evolving social and cultural smoking patterns have led to rising or plateauing rates of lung cancer in women, lagging the long-declining smoking and cancer incidence rates in men. In contrast, emerging economies vary widely in smoking practices and cancer incidence but commonly also harbor risks from environmental exposures, particularly widespread air pollution. Recent research has also revealed clinical, radiologic, and pathologic correlates, leading to greater knowledge in molecular profiling and targeted therapeutics, as well as an emphasis on the rising incidence of adenocarcinoma histology. Furthermore, emergent evidence about the benefits of lung cancer screening has led to efforts to identify high-risk smokers and development of prediction tools. This review also includes a discussion on the epidemiologic characteristics of special groups including women and nonsmokers. Varying trends in smoking largely dictate international patterns in lung cancer incidence and mortality. With declining smoking rates in developed countries and knowledge gains made through molecular profiling of tumors, the emergence of new risk factors and disease features will lead to changes in the landscape of lung cancer epidemiology.

https://www.annalsofglobalhealth.org/articles/10.5334/aogh.2419/galley/2525/download/

Global Epidemiology of Lung Cancer

Electronic cigarettes (E-cigs) have experienced sharp increases in popularity over the past five years due to many factors, including aggressive marketing, increased restrictions on conventional cigarettes, and a perception that E-cigs are healthy alternatives to cigarettes. Despite this perception, studies on health effects in humans are extremely limited and in vivo animal models have not been generated. Presently, we determined that E-cig vapor contains 7x1011 free radicals per puff. To determine whether E-cig exposure impacts pulmonary responses in mice, we developed an inhalation chamber for E-cig exposure. Mice that were exposed to E-cig vapor contained serum cotinine concentrations that are comparable to human E-cig users. E-cig exposure for 2 weeks produced a significant increase in oxidative stress and moderate macrophage-mediated inflammation. Since, COPD patients are susceptible to bacterial and viral infections, we tested effects of E-cigs on immune response. Mice that were exposed to E-cig vapor showed significantly impaired pulmonary bacterial clearance, compared to air-exposed mice, following an intranasal infection with Streptococcus pneumonia. This defective bacterial clearance was partially due to reduced phagocytosis by alveolar macrophages from E-cig exposed mice. In response to Influenza A virus infection, E-cig exposed mice displayed increased lung viral titers and enhanced virus-induced illness and mortality. In summary, this study reports a murine model of E-cig exposure and demonstrates that E-cig exposure elicits impaired pulmonary anti-microbial defenses. Hence, E-cig exposure as an alternative to cigarette smoking must be rigorously tested in users for their effects on immune response and susceptibility to bacterial and viral infections.

/pdf/exposure-to-electronic-cigarettes-impairs-pulmonary-anti-4snrc0dr7h.pdf

Exposure to electronic cigarettes impairs pulmonary anti-bacterial and anti-viral defenses in a mouse model

The use of electronic cigarettes (e-cigs) is increasing rapidly, but their effects on lung toxicity are largely unknown. Smoking is a well-established cause of lung cancer and respiratory disease, in part through inflammation. It is plausible that e-cig use might affect similar inflammatory pathways. E-cigs are used by some smokers as an aid for quitting or smoking reduction, and by never smokers (e.g., adolescents and young adults). The relative effects for impacting disease risk may differ for these groups. Cell culture and experimental animal data indicate that e-cigs have the potential for inducing inflammation, albeit much less than smoking. Human studies show that e-cig use in smokers is associated with substantial reductions in blood or urinary biomarkers of tobacco toxicants when completely switching and somewhat for dual use. However, the extent to which these biomarkers are surrogates for potential lung toxicity remains unclear. The FDA now has regulatory authority over e-cigs and can regulate product and e-liquid design features, such as nicotine content and delivery, voltage, e-liquid formulations, and flavors. All of these factors may impact pulmonary toxicity. This review summarizes current data on pulmonary inflammation related to both smoking and e-cig use, with a focus on human lung biomarkers. Cancer Epidemiol Biomarkers Prev; 26(8); 1175-91. ©2017 AACR.

https://cebp.aacrjournals.org/content/cebp/26/8/1175.full.pdf

A Review of Pulmonary Toxicity of Electronic Cigarettes In The Context of Smoking: A Focus On Inflammation

Combustible tobacco use remains the number one preventable cause of disease, disability, and death in the United States. Electronic nicotine delivery systems (ENDS), which include e-cigarettes, are devices capable of delivering nicotine in an aerosolized form. ENDS use by both adults and youth has increased rapidly, and some have advocated these products could serve as harm-reduction devices and smoking cessation aids. ENDS may be beneficial if they reduce smoking rates or prevent or reduce the known adverse health effects of smoking. However, ENDS may also be harmful, particularly to youth, if they increase the likelihood that nonsmokers or formers smokers will use combustible tobacco products or if they discourage smokers from quitting. The American Association for Cancer Research (AACR) and the American Society of Clinical Oncology (ASCO) recognize the potential ENDS have to alter patterns of tobacco use and affect the public9s health; however, definitive data are lacking. AACR and ASCO recommend additional research on these devices, including assessing the health impacts of ENDS, understanding patterns of ENDS use, and determining what role ENDS have in cessation. Key policy recommendations include supporting federal, state, and local regulation of ENDS; requiring manufacturers to register with the FDA and report all product ingredients, requiring childproof caps on ENDS liquids, and including warning labels on products and their advertisements; prohibiting youth-oriented marketing and sales; prohibiting child-friendly ENDS flavors; and prohibiting ENDS use in places where cigarette smoking is prohibited. Clin Cancer Res; 21(3); 514–25. ©2015 AACR. American Association for Cancer Research and American Society of Clinical Oncology .

https://clincancerres.aacrjournals.org/content/clincanres/21/3/514.full.pdf

Electronic nicotine delivery systems: a policy statement from the American Association for Cancer Research and the American Society of Clinical Oncology.

E-cigarettes, a relatively new product, storming the tobacco industry are causing a massive stir among public health advocates. While e-cigarettes have the potential to serve as an effective harm reduction tool for existing smokers, they also may present an equally tempting pathway to first time smoking, particularly among youth. Many fear that e-cigarettes will revive the popular smoking culture that has taken decades to dismantle. In April 2014, the FDA issued proposed rules to “deem” or extend its authority over tobacco products to regulate electronic cigarettes, cigars, pipe tobacco, nicotine gels, waterpipe (hookah) tobacco, and orally ingested dissolvable tobacco products. As proposed, FDA’s rules, among other things, would set a federal minimum age of 18 years to use e-cigarettes, require identification to purchase them (currently, just more than half of states impose age restrictions), prohibit most sales in vending machines, mandate warning labels on packaging, and prohibit manufacturers from providing free samples. Further, companies would be permitted to make claims for reduced risk only if the agency confirms the claim based on scientific evidence while also finding a benefit to the health of the public. While the proposed rules represent a watershed moment in tobacco control, they still leave major regulatory gaps affecting the most vulnerable population, youth. FDA’s silence when it comes to the use of flavored nicotine and marketing practices is certain to have negative consequences for youthful smokers. The agency should move boldly and rapidly to prevent companies from exploiting youth. By bolstering the proposed rules to limit advertising and prohibit flavored nicotine, the agency could prevent proliferation of e-cigarette use among adolescents, while not undermining its regulatory goal of reducing harm. The public health community must speak with a clear voice to urge meaningful and effective regulation to protect US youth against the reinvention of Big Tobacco.

/pdf/e-cigarettes-vaping-and-youth-3qkvx3qyte.pdf

E-cigarettes, vaping, and youth.

Lung cancer is the leading cause of cancer-related mortality in the United States. Despite a strong correlation between cigarette smoking and the onset of lung cancer, the prevalence of smoking still remains high. Strategies to eliminate cigarette smoking have led to the emergence of new tobacco-related products as alternatives for cigarette smoking or tools for smoking cessation. The electronic cigarette (ECIG) is a battery-powered electronic nicotine delivery system (ENDS) designed to deliver nicotine without combusting tobacco. Since nicotine is widely considered the addictive component in tobacco with limited ability to initiate cancer, ECIGs have been advertised to be a safer alternative to tobacco cigarettes (TCIGs). However, the toxicity and potential carcinogenicity of ECIGs have not previously been evaluated. In this study, we assess the impact of ECIG exposure on the carcinogenic potential of immortalized human bronchial epithelial cells on a background of silenced p53 and activated KRAS (H3mut-P53/KRAS). This model is utilized because p53 and KRAS mutations are often observed in the airway of current and former smokers at risk for lung cancer. The epithelial cells were exposed to both a low and high concentration of nicotine in the ECIG vapor- or TCIG smoke-conditioned media. The lower nicotine concentration was selected to mimic the average plasma nicotine levels in ENDS users and did not demonstrate toxic or anti-proliferative effects on the cells. The higher concentration was chosen to represent the anticipated nicotine levels to which the epithelial cells of smokers are actually exposed. In anchorage independent growth assays, the in vitro correlate of malignant transformation, we found enhanced colony growth in the H3mut-P53/KRAS cells following a 10-day treatment with the high nicotine ECIG- and TCIG-conditioned media compared to the untreated and low nicotine treatment groups. We next assessed the effect of ECIG and TCIG exposure on cell invasion using a three-dimensional air-liquid interface (ALI) model. At baseline, H3mut-P53/KRAS cells exhibit invasive behavior in the ALI model, due to the downstream effects of P53 silencing and KRAS activation. Treatment of H3mut-P53/KRAS cells with low nicotine ECIG- and TCIG-conditioned media did not further enhance the degree of invasion observed in the untreated group. We will next examine the effects of high nicotine conditioned media on cell invasion. Finally, gene expression studies show 263 differentially expressed genes following in vitro exposure to ECIG-conditioned media for 96hrs. The high nicotine ECIG-conditioned media induced a gene expression pattern similar to TCIG- conditioned media and whole cigarette smoke exposure in the H3mut-P53/KRAS cells. Preliminary analyses indicate the observed ECIG-specific gene expression changes were concordantly changed following TCIG-conditioned media exposure. We will next compare the ECIG-induced gene expression signature to carcinogenicity-related gene signatures established in previous and ongoing clinical investigations and test ECIG-altered candidate genes for their ability to drive the malignant transformation of airway epithelial cells. These studies will determine the impact of ECIG exposure on lung carcinogenicity and provide needed scientific guidance to the FDA regarding the physiologic effects of ECIGs.

These studies were supported by funding from the following: NIH/NCI #U01CA152751 (SMD, TCW), NCI #U01CA152751-S1 (SMD, TCW, SJP), NCI #U01CA152751-AS (SMD, KK), NCI #T32-CA009120-36 (SMD, SJP, PCP), NIH/NHLBI #T32HL072752 (SMD, EL), University of California Tobacco-Related Disease Research Program (TRDRP) #18FT-0060 (TCW), TRDRP #20KT-0055 (TCW), Lung Cancer SPORE P50CA70907 (JDM, JEL)

Citation Format: Stacy J. Park, Tonya C. Walser, Catalina Perdomo, Teresa Wang, Paul C. Pagano, Elvira L. Liclican, Kostyantyn Krysan, Jill E. Larsen, John D. Minna, Marc E. Lenburg, Avrum Spira, Steven M. Dubinett. The effect of e-cigarette exposure on airway epithelial cell gene expression and transformation. [abstract]. In: Proceedings of the AACR-IASLC Joint Conference on Molecular Origins of Lung Cancer; 2014 Jan 6-9; San Diego, CA. Philadelphia (PA): AACR; Clin Cancer Res 2014;20(2Suppl):Abstract nr B16.

Abstract B16: The effect of e-cigarette exposure on airway epithelial cell gene expression and transformation.

gene expression in nasal and bronchial epithelium Similarities and differences between smoking-related

Diagnostic des troubles pulmonaires à l'aide d'une prédiction de classe

Diagnose- und Prognoseverfahren für Lungenerkrankungen mittels Genexpressionsprofilen aus Nasenepithelzellen

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