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Cogliano, Vincent, Kurt Straif, Robert Baan, Yann Grosse, Béatrice Secretan, and Fatiha El Ghissassi. "Smokeless tobacco and tobacco-related nitrosamines." Lancet Oncology 5, no. 12 (December 2004): 708. http://dx.doi.org/10.1016/s1470-2045(04)01633-x.
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Myers, Steven R., and M. Yeakub Ali. "Haemoglobin adducts as biomarkers of exposure to tobacco-related nitrosamines." Biomarkers 13, no. 2 (January 2008): 145–59. http://dx.doi.org/10.1080/13547500701470561.
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Bošković, Maria, Blanka Roje, Felicia Fei-Lei Chung, Andrea Gelemanović, Vincent Cahais, Cyrille Cuenin, Rita Khoueiry, Katarina Vilović, Zdenko Herceg, and Janoš Terzić. "DNA Methylome Changes of Muscle- and Neuronal-Related Processes Precede Bladder Cancer Invasiveness." Cancers 14, no. 3 (January 19, 2022): 487. http://dx.doi.org/10.3390/cancers14030487.
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Bladder cancer (BC) is the ninth leading cause of cancer death with one of the highest recurrence rates among all cancers. One of the main risks for BC development is exposure to nitrosamines present in tobacco smoke or in other products. Aberrant epigenetic (DNA methylation) changes accompanied by deregulated gene expression are an important element of cancer pathogenesis. Therefore, we aimed to determine DNA methylation signatures and their impacts on gene expression in mice treated with N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN), a carcinogen similar to compounds found in tobacco smoke. Following BBN administration mice developed non-invasive or invasive bladder cancers. Surprisingly, muscle- and neuronal-related pathways emerged as the most affected in those tumors. Hypo- and hypermethylation changes were present within non-invasive BC, across CpGs mapping to the genes involved in muscle- and neuronal-related pathways, however, methylation differences were not sufficient to affect the expression of the majority of associated genes. Conversely, invasive tumors displayed hypermethylation changes that were linked with alterations in gene expression profiles. Together, these findings indicate that bladder cancer progression could be revealed through methylation profiling at the pre-invasive cancer stage that could assist monitoring of cancer patients and guide novel therapeutic approaches.
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Amin, Shantu, Dhimant Desai, Stephen S. Hecht, and Dietrich Hoffmann. "Synthesis of Tobacco-SpecificN-Nitrosamines and Their Metabolites and Results of Related Bioassays." Critical Reviews in Toxicology 26, no. 2 (January 1996): 139–47. http://dx.doi.org/10.3109/10408449609017927.
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Doukas, Sotirios G., Dimitra P. Vageli, Panagiotis G. Doukas, Dragana Nikitovic, Aristidis Tsatsakis, and Benjamin L. Judson. "The Effect of Tobacco Smoke N-Nitrosamines, NNK and NDEA, and Nicotine, on DNA Mismatch Repair Mechanism and miRNA Markers, in Hypopharyngeal Squamous Cell Carcinoma: An In Vivo Model and Clinical Evidence." Current Oncology 29, no. 8 (August 4, 2022): 5531–49. http://dx.doi.org/10.3390/curroncol29080437.
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Deregulation of the DNA mismatch repair (MMR) mechanism has been linked to poor prognosis of upper aerodigestive tract cancers. Our recent in vitro data have provided evidence of crosstalk between deregulated miRNAs and MMR genes, caused by tobacco smoke (TS) N-Nitrosamines, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), in hypopharyngeal cells. Here, we explored whether chronic exposure to TS components can affect MMR mechanism and miRNA profiles in hypopharyngeal mucosa. Using a mouse model (C57Bl/6J wild type) of in vivo 14-week exposure to NNK (0.2 mmol/L) and N-Nitrosodiethylamine (NDEA; 0.004 mmol/L), with or without nicotine (0.02 μmol/L), we provide direct evidence that TS components can promote dysplasia, significant downregulation of Msh2 and Mlh1 genes and deregulation of miR-21, miR-155, miR-34a, and miR-451a. By analyzing eight human specimens from tobacco smokers and eight controls, we provide clinical evidence of a significant reduction in hMSH2 and hMLH1 mRNAs in hypopharyngeal squamous cell carcinoma (HSCC). In summary, deregulation of the MMR mechanism and miRNAs is caused by chronic exposure to TS-related N-Nitrosamines, with or without nicotine, in the early stages of upper aerodigestive tract carcinogenesis, and can also be detected in human HSCC. Thus, we encourage future studies to further elucidate a possible in vivo dose-dependent effect of individual or combined N-Nitrosamines, NNK and/or NDEA, and nicotine, on the MMR mechanism and their clinical testing to elaborate prognosis and risk assessment.
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Ahijevych, Karen. "Biological Models for Studying and Assessing Tobacco Use." Annual Review of Nursing Research 27, no. 1 (December 2009): 145–68. http://dx.doi.org/10.1891/0739-6686.27.145.
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The purpose of this chapter on biological models for studying and assessing tobacco use is to provide an introduction to some of the common concepts and biomarkers in this arena to ultimately inform intervention research by nurse scientists. An overview of selected biomarkers of tobacco exposure in individuals includes exhaled carbon monoxide, cotinine (the proximate metabolite of nicotine), and measurement of an individual’s puffing pattern termed smoking topography. Common tobacco contents discussed include tobacco specific nitrosamines (TSNA) and polycyclic aromatic hydrocarbons (PAH) some of which increase disease risk including cancer. Exemplars of additives to cigarettes by the tobacco industry will be described including menthol, one additive marketed by the industry. Genetics and tobacco addiction has emerged as a rapidly expanding field. Illustrative of this area are twin studies, nicotinic receptors, CYP2A6 polymorphisms, and genes that impact dopamine receptors. The cadre of nurse scientists conducting research in this much needed area is small. The opportunity for nurse scientists educated in biological inquiry in tobacco-related research is great. Nurse scientists actively involved in multidisciplinary translational teams to address nicotine addition are needed.
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Kankanamage, Rumasha N. T., Abhisek Brata Ghosh, Di Jiang, Karmel Gkika, Tia Keyes, Laura A. Achola, Steven Suib, and James F. Rusling. "Metabolites of Tobacco- and E-Cigarette-Related Nitrosamines Can Drive Cu2+-Mediated DNA Oxidation." Chemical Research in Toxicology 33, no. 8 (July 16, 2020): 2072–86. http://dx.doi.org/10.1021/acs.chemrestox.0c00027.
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Rodgman, A. "Studies of Polycyclic Aromatic Hydrocarbons in Cigarette Mainstream Smoke: Identification, Tobacco Precursors, Control of Levels: A Review." Beiträge zur Tabakforschung International/Contributions to Tobacco Research 19, no. 7 (October 1, 2001): 361–79. http://dx.doi.org/10.2478/cttr-2013-0724.
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AbstractDuring the period of tobacco smoke research from the early 1950s to the mid-1960s it was repeatedly asserted that a) tobacco and many tobacco components were involved in the pyrogenesis of polycyclic aromatic hydrocarbons (PAHs), several of which were reported to initiate tumors on the skin of laboratory animals and b) tobacco additives (flavorants, casing materials, humectants) were highly likely to be similarly involved in PAH pyrogenesis. Extensive knowledge on PAHs was deemed highly necessary because of their claimed importance in the smoking-health issue. The numerous assertions about the generation of PAHs in cigarette mainstream smoke (MSS) triggered extensive and intensive research both within and outside the Tobacco Industry to define the nature of the PAHs, their per cigarette MSS delivery amounts, their precursors, etc. It was not until 1960 that VAN DUUREN et al. (1) reported three specific aza-arenes in cigarette MSS that were asserted to be involved in smokers’ respiratory tract cancer. As noted in a recent Letter to the Editors (2), the presence of these three aza-arenes in tobacco smoke has never been confirmed. Between 1960 and 1965, other MSS components (phenols as promoters, polonium-210, N-nitrosamines, ciliastatic compounds) were asserted to be responsible for smoking related diseases. However, no major assertions were made that phenols, polonium-210, or the N-nitrosamines were derived from flavorants, casing materials, or humectants. Some investigators did report that several ciliastats were derived from added sugars and glycerol. The ciliastat proposal was drastically diminished in importance by the findings in the 1960s that only a relatively small proportion of the ciliastats reached the smoker's cilia. During that time, pertinent skills and competencies in research on tobacco smoke composition, particularly the PAH fraction, have been developed. Such skills permitted the isolation in crystalline form of 14 PAHs and the quantitation of these and many other PAHs. They were also used to put in perspective the pyrogenesis of PAHs from a) specific tobacco components, b) additives, and c) processed tobaccos (reconstituted tobacco sheet [RTS], expanded tobacco). R.J. Reynolds Tobacco Company (RJRT) pioneered the use of RTS (1953) and expanded tobaccos (1969) in cigarette blends and generated much previously unpublished data on the effect of such processed tobaccos on MSS composition.
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Brown, Buddy G., August J. Borschke, and David J. Doolittle. "An Analysis of the Role of Tobacco-Specific Nitrosamines in the Carcinogenicity of Tobacco Smoke." Nonlinearity in Biology, Toxicology, Medicine 1, no. 2 (April 1, 2003): 154014203914343. http://dx.doi.org/10.1080/15401420391434324.
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Cigarette smoke is a complex mixture consisting of more than 4500 chemicals, including several tobacco-specific nitrosamines (TSNA). TSNA typically form in tobacco during the post-harvest period, with some fraction being transferred into mainstream smoke when a cigarette is burned during use. The most studied of the TSNA is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). NNK has been shown to be carcinogenic in laboratory animals. Studies examining the carcinogenicity of NNK frequently are conducted by injecting rodents with a single dose of 2.5 to 10 μmol of pure NNK; the amount of NNK contained in all of the mainstream smoke from about 3700 to 14,800 typical U.S. cigarettes. Extrapolated to a 70-kg smoker, the carcinogenic dose of pure NNK administered to rodents would be equivalent to the amount of NNK in all of the mainstream smoke of 22 to 87 million typical U.S. cigarettes. Furthermore, extrapolating results from rodent studies based on a single injection of pure NNK to establish a causative role for NNK in the carcinogenicity of chronic tobacco smoke exposure in humans is not consistent with basic pharmacological and toxicological principles. For example, such an approach fails to consider the effect of other smoke constituents upon the toxicity of NNK. In vitro studies demonstrate that nicotine, cotinine, and aqueous cigarette “tar” extract (ACTE) all inhibit the mutagenic activity of NNK. In vivo studies reveal that the formation of pulmonary DNA adducts in mice injected with NNK is inhibited by the administration of cotinine and mainstream cigarette smoke. Cigarette smoke has been shown to modulate the metabolism of NNK, providing a mechanism for the inhibitory effects of cigarette smoke and cigarette smoke constituents on NNK-induced tumorigenesis. NNK-related pulmonary DNA adducts have not been detected in rodents exposed to cigarette smoke, nor has the toxicity of tobacco smoke or tobacco smoke condensate containing marked reductions in TSNA concentrations been shown to be reduced in any biological assay. In summary, there is no experimental evidence to suggest that reduction of TSNA will reduce the mutagenic, cytotoxic, or carcinogenic potential of tobacco smoke.
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Smith, Danielle M., Richard J. O’connor, Binnian Wei, Mark Travers, Andrew Hyland, and Maciej L. Goniewicz. "Nicotine and Toxicant Exposure Among Concurrent Users (Co-Users) of Tobacco and Cannabis." Nicotine & Tobacco Research 22, no. 8 (August 7, 2019): 1354–63. http://dx.doi.org/10.1093/ntr/ntz122.
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Abstract Background Smoking cannabis may potentially increase exposure to numerous toxic chemicals that are commonly associated with tobacco use. There is a paucity of data related to toxicant exposures among concurrent users of tobacco and cannabis (co-users). Methods Data are from the Population Assessment of Tobacco and Health Study Wave 1 Biomarker Restricted-Use Files. Analyses focused on adults who provided urine samples (N = 5859). Urine samples were analyzed for biomarkers of exposure to nicotine, tobacco-specific nitrosamines, polycyclic aromatic hydrocarbons, and volatile organic compounds. Using weighted linear regression, we compared adjusted geometric mean concentrations of 15 biomarkers between user groups of various tobacco product types according to their self-reported past 30-day cannabis use. Results Past 30-day cannabis use was similar across various types of tobacco product use subgroups (range: 13%–23%) and significantly more common compared to non-tobacco users (1.0%; p < .001). Across all groups of tobacco users, those who co-used cannabis exhibited significantly higher concentrations of the biomarker of exposure to acrylonitrile (CYMA) compared to non-cannabis users (by 39%–464%). Tobacco–cannabis co-users also showed significantly elevated levels of the biomarker of exposure to acrylamide (AAMA) compared to exclusive tobacco users, and significantly higher exposure to many polycyclic aromatic hydrocarbons (including fluorene and pyrene). Conclusions Co-users exhibited higher concentrations for biomarkers of exposure to many combustion byproducts, compared to exclusive tobacco users. More robust measurements of cannabis use can address potential confounding in assessments of exposures to tobacco-related constituents, and potential health effects resulting from co-use. Implications With disproportionately greater rates of cannabis use occurring among tobacco users, it is critical to consider how concurrent cannabis use may influence health-related outcomes among smokers. Our findings suggest potential additive toxicant exposures among co-users of tobacco and cannabis. Lack of consideration and measurement of cannabis use in assessing tobacco-related exposures may confound estimates thought to be attributable to tobacco, particularly for non-specific biomarkers. Assessing tobacco and cannabis use in tandem will allow for more precise measurement of outcomes related to one or both substances, and can provide additional information on potential health effects related to co-use.
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Han, Jing, Yasser M. Sanad, Joanna Deck, John B. Sutherland, Zhong Li, Matthew J. Walters, Norma Duran, Matthew R. Holman, and Steven L. Foley. "Bacterial Populations Associated with Smokeless Tobacco Products." Applied and Environmental Microbiology 82, no. 20 (August 26, 2016): 6273–83. http://dx.doi.org/10.1128/aem.01612-16.
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ABSTRACTThere are an estimated 8 million users of smokeless tobacco products (STPs) in the United States, and yet limited data on microbial populations within these products exist. To better understand the potential microbiological risks associated with STP use, a study was conducted to provide a baseline microbiological profile of STPs. A total of 90 samples, representing 15 common STPs, were purchased in metropolitan areas in Little Rock, AR, and Washington, DC, in November 2012, March 2013, and July 2013. Bacterial populations were evaluated using culture, pyrosequencing, and denaturing gradient gel electrophoresis (DGGE). Moist-snuff products exhibited higher levels of bacteria (average of 1.05 × 106CFU/g STP) and diversity of bacterial populations than snus (average of 8.33 × 101CFU/g STP) and some chewing tobacco products (average of 2.54 × 105CFU/g STP). The most common species identified by culturing wereBacillus pumilus,B. licheniformis,B. safensis, andB. subtilis, followed by members of the generaOceanobacillus,Staphylococcus, andTetragenococcus.Pyrosequencing analyses of the 16S rRNA genes identified the generaTetragenococcus,Carnobacterium,Lactobacillus,Geobacillus,Bacillus, andStaphylococcusas the predominant taxa. Several species identified are of possible concern due to their potential to cause opportunistic infections and reported abilities to reduce nitrates to nitrites, which may be an important step in the formation of carcinogenic tobacco-specific N′-nitrosamines. This report provides a microbiological baseline to help fill knowledge gaps associated with microbiological risks of STPs and to inform potential regulations regarding manufacture and testing of STPs.IMPORTANCEIt is estimated that there 8 million users of smokeless tobacco products (STPs) in the United States; however, there are limited data on microbial populations that exist within these products. The current study was undertaken to better understand the potential microbiological risks associated with STP use and provide a baseline microbiological profile of STPs. Several bacterial species were identified that are of possible concern due to their potential to cause opportunistic infections. In addition, some species have abilities to reduce nitrates to nitrites, which may be an important step in the formation of carcinogenic tobacco-specific N′-nitrosamines. Overall, this report provides a microbiological baseline to help fill knowledge gaps related to the microbiological risks of STPs and to inform potential regulations regarding the manufacture and testing of STPs.
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Ma, Bin, Irina Stepanov, and Stephen Hecht. "Recent Studies on DNA Adducts Resulting from Human Exposure to Tobacco Smoke." Toxics 7, no. 1 (March 19, 2019): 16. http://dx.doi.org/10.3390/toxics7010016.
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DNA adducts are believed to play a central role in the induction of cancer in cigarette smokers and are proposed as being potential biomarkers of cancer risk. We have summarized research conducted since 2012 on DNA adduct formation in smokers. A variety of DNA adducts derived from various classes of carcinogens, including aromatic amines, polycyclic aromatic hydrocarbons, tobacco-specific nitrosamines, alkylating agents, aldehydes, volatile carcinogens, as well as oxidative damage have been reported. The results are discussed with particular attention to the analytical methods used in those studies. Mass spectrometry-based methods that have higher selectivity and specificity compared to 32P-postlabeling or immunochemical approaches are preferred. Multiple DNA adducts specific to tobacco constituents have also been characterized for the first time in vitro or detected in vivo since 2012, and descriptions of those adducts are included. We also discuss common issues related to measuring DNA adducts in humans, including the development and validation of analytical methods and prevention of artifact formation.
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Richmond, Mitchell D., Robert C. Pearce, Ben M. Goff, and William A. Bailey. "Analysis of Variability in Curing Conditions and Tobacco-Specific Nitrosamines Within Barns of Dark Air-Cured Tobacco." Tobacco Science 54, no. 1 (January 1, 2017): 6–14. http://dx.doi.org/10.3381/17-060.
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Significant variability in cured-leaf tobacco-specific nitrosamine (TSNA) content is commonly observed when sampling within dark air-curing barns. This variability may be due to inconsistency in the curing environment within different areas of the barn. A study was initiated in 2012, through support from a CORESTA Study Grant, to evaluate if cured-leaf TSNA content is related to microenvironmental conditions in the barn. Low-converter (TRsc) and high-converter (TRHC) selections of TR Madole dark tobacco were air cured in barns near Princeton and Lexington, KY. Temperature and relative humidity were measured with data loggers placed at 27 different locations within each barn for the duration of curing. There were no significant effects of individual data logger placement in either variety selection on hours above 24°C temperature, hours above 80% relative humidity, or TSNA; therefore, we investigated these data within the 3-dimensional aspects of tier, room, and bent within each barn. There were various effects of tier, room, and bent on temperature, relative humidity, and TSNA. Temperature data followed an understandable pattern across tiers in the barn within each year and location; however, relative humidity and TSNA were more difficult to characterize adequately. There was a significant relationship between hours above 24°C and TSNA, but not hours above 80% relative humidity. This study has shown that the effect of within-barn position on TSNA cannot be easily predicted.
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Hang, Bo. "Formation and Repair of Tobacco Carcinogen-Derived Bulky DNA Adducts." Journal of Nucleic Acids 2010 (2010): 1–29. http://dx.doi.org/10.4061/2010/709521.
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DNA adducts play a central role in chemical carcinogenesis. The analysis of formation and repair of smoking-related DNA adducts remains particularly challenging as both smokers and nonsmokers exposed to smoke are repetitively under attack from complex mixtures of carcinogens such as polycyclic aromatic hydrocarbons andN-nitrosamines. The bulky DNA adducts, which usually have complex structure, are particularly important because of their biological relevance. Several known cellular DNA repair pathways have been known to operate in human cells on specific types of bulky DNA adducts, for example, nucleotide excision repair, base excision repair, and direct reversal involvingO6-alkylguanine DNA alkyltransferase or AlkB homologs. Understanding the mechanisms of adduct formation and repair processes is critical for the assessment of cancer risk resulting from exposure to cigarette smoke, and ultimately for developing strategies of cancer prevention. This paper highlights the recent progress made in the areas concerning formation and repair of bulky DNA adducts in the context of tobacco carcinogen-associated genotoxic and carcinogenic effects.
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Dos Santos Costa, Gislaine Natiele, Bruna Gomes Vasconcelos, Tayná De Souza Vargas de Moura, Vivianne Galvão Martins, and Simone Carvalho Chiapetta. "Trends in Analytical Methods for Analysis of Tobacco Products: An Overview." Revista Eletrônica TECCEN 15, no. 1 (June 30, 2022): 2–20. http://dx.doi.org/10.21727/teccen.v15i1.3117.
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Abstract. Currently, due to the strong trends in policies to reduce smoking, several concerns related to quality control and regulation of tobacco products have been raised, as a great variety of products are available to consumers in the market. Considering that development of robust and selective analytical methods for tobacco and derivative products has been an important and necessary task over the years, however laborious, due to the complexity of the matrices. This work presents an overview of advances, innovation, and trends in analytical methods, focused on the chromatographic analysis of nicotine, tobacco-specific nitrosamines (TSNAs), humectants, pesticides, polycyclic aromatic hydrocarbons (PAHs) and sugars in different tobacco products. Gas chromatography (GC) coupled with different detectors is widely used to analyze nicotine, humectants and TSNAs in tobacco leaves and derivative products, while liquid chromatography-tandem mass spectrometry (LC-MS/MS) has been frequently used to analyze TSNAs in mainstream cigarette smoke and smokeless tobacco products. Pesticides were mainly analyzed in tobacco using GC or LC coupled with mass detector (MS), while PAHs and sugars were generally analyzed in tobacco and smoke using LC-MS and GC-MS techniques, respectively. In addition to already established methods and despite the lack of a worldwide standardization of methods, significant efforts have been made to develop analytical procedures for a wide variety of tobacco products, with a broad range of innovative chromatographic methods available. In this sense, a potential trend is the possibility of simultaneous determination of multiple components aiming to reduce the analysis time. The present study examined the main works that developed or improved analytical methods for identifying and quantifying priority compounds in different tobacco matrices and aims to contribute to future research with this objective, in addition, to promoting standardization of technical terms used in this analytical area. It is noteworthy that some of the methods mentioned here have not been validated and further studies are needed in order to obtain reproducible analytical methods for regulatory purposes.
Keywords: chromatography analyses; tobacco leaves; cigarette; cigarette smoke; smokeless tobacco products.
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Son, Yeongkwon, Daniel P. Giovenco, Cristine Delnevo, Andrey Khlystov, Vera Samburova, and Qingyu Meng. "Indoor Air Quality and Passive E-cigarette Aerosol Exposures in Vape-Shops." Nicotine & Tobacco Research 22, no. 10 (May 23, 2020): 1772–79. http://dx.doi.org/10.1093/ntr/ntaa094.
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Abstract Introduction Direct emissions of nicotine and harmful chemicals from electronic cigarettes (e-cigarettes) have been intensively studied, but secondhand and thirdhand e-cigarette aerosol (THA) exposures in indoor environments are understudied. Aims and Methods Indoor CO2, NO2, particulate matter (PM2.5), aldehydes, and airborne nicotine were measured in five vape-shops to assess secondhand exposures. Nicotine and tobacco-specific nitrosamines were measured on vape-shop surfaces and materials (glass, paper, clothing, rubber, and fur ball) placed in the vape-shops (14 days) to study thirdhand exposures. Results Airborne PM2.5, formaldehyde, acetaldehyde, and nicotine concentrations during shop opening hours were 21, 3.3, 4.0, and 3.8 times higher than the levels during shop closing hours, respectively. PM2.5 concentrations were correlated with the number of e-cigarette users present in vape-shops (ρ = 0.366–0.761, p < .001). Surface nicotine, 4-(N-methyl-N-nitrosamino)-4-(3-pyridyl)butanal (NNA), and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) were also detected at levels of 223.6 ± 313.2 µg/m2, 4.78 ± 11.8 ng/m2, and 44.8 ± 102.3 ng/m2, respectively. Substantial amounts of nicotine (up to 2073 µg/m2) deposited on the materials placed within the vape-shops, and NNA (up to 474.4 ng/m2) and NNK (up to 184.0 ng/m2) were also formed on these materials. The deposited nicotine concentrations were strongly correlated with the median number of active vapers present in a vape-shop per hour (ρ = 0.894–0.949, p = .04–.051). NNK levels on the material surfaces were significantly associated with surface nicotine levels (ρ=0.645, p = .037). Conclusions Indoor vaping leads to secondhand and THA exposures. Thirdhand exposures induced by e-cigarette vaping are comparable or higher than that induced by cigarette smoking. Long-term studies in various microenvironments are needed to improve our understanding of secondhand and THA exposures. Implications This study adds new convincing evidence that e-cigarette vaping can cause secondhand and THA exposures. Our findings can inform Occupational Safety and Health Administration, state authorities, and other government agencies regarding indoor air policies related to e-cigarette use, particularly in vape-shops. There is an urgent need to ensure that vape-shops maintain suitable ventilation systems and cleaning practices to protect customers, employees, and bystanders. Our study also demonstrates that nicotine can deposit or be adsorbed on baby’s clothes and toys, and that tobacco-specific nitrosamines can form and retain on baby’s clothes, highlighting children’s exposure to environmental e-cigarette aerosol and THA at home is of a particular concern.
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Moolky, A., N. Moolky, M. Ankush, K. Usha, and M. Nagabhushan. "Spices May Prevent Human Cancers." Journal of Global Oncology 4, Supplement 2 (October 1, 2018): 195s. http://dx.doi.org/10.1200/jgo.18.78602.
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Industrial and domestic use of fossil fuel (coal, gasoline, natural gas), wood burning (for heating, cooking, forest wild fire), and tobacco smoking releases harmful chemicals to human environment. Air pollutants include a mixture of noxious gases such as carbon monoxide, carbon dioxide, nitrous oxide, polycyclic aromatic hydrocarbons (PAHs). PAHs are cancer causing agents are highly toxic and mutagenic/genotoxic. Spices are widely used on a daily basis around the world. Some of the major spices/active principles used in large quantities are turmeric (curcumins), ginger (gingerol, shaogol, zingerone), betel leaf (hydroxy chavicol) and catechu (catechin).With short-term mutagenic assay, these spices extract and their active principles are nonmutagenic. We have tested these compounds against well-known mutagenic/carcinogenic PAHs, benzo(a)pyrene (BaP) and dimethyl(a)benzanthracene (DMBA). Nontoxic doses of extracts of spices/principles, turmeric/curcumins, ginger/gingerol, shaogol, zingerone, betel leaf/hydroxy chavicol and catechu/catechin dose dependently decreased the mutagenicity of BaP and DMBA. The protective activities of these compounds were also confirmed by animal tumor models. Nitrite is a water pollutant that is a precursor of mutagenic/carcinogenic nitrosamines and nitrosoamides. Amines/amides are present in vegetables and cured meat. Human stomach maintains acidic conditions, favors the chemical reaction of nitrite with amines/amides to form mutagenic/carcinogenic nitrosamines/amides. We mimic these conditions and have shown that turmeric and ginger their active principles dose dependently block the formation of nitrosamines/amides. Further the human efficacy of turmeric extract and its principle curcumin was confirmed in cigarette and bidi smokers. Consuming turmeric and curcumin reduced excretion of mutagens in human smokers. Large quantity of active principle are present in these spices, turmeric - curcumin 2%-2.5%, ginger - gingerol, shaogoal, zingerone - 2%-2.5%, betel leaf - hydroxychavicol 5%-10% and catechu - catechu 40%-50%. Human consumption of these spices may play an important role reducing the harmful effects of environmental toxicants, thus reducing cancer and other age related human chronic degenerative diseases.
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Aguayo, Francisco, Juan P. Muñoz, Francisco Perez-Dominguez, Diego Carrillo-Beltrán, Carolina Oliva, Gloria M. Calaf, Rances Blanco, and Daniela Nuñez-Acurio. "High-Risk Human Papillomavirus and Tobacco Smoke Interactions in Epithelial Carcinogenesis." Cancers 12, no. 8 (August 6, 2020): 2201. http://dx.doi.org/10.3390/cancers12082201.
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Cervical, anogenital, and some head and neck cancers (HNC) are etiologically associated with high-risk human papillomavirus (HR-HPV) infection, even though additional cofactors are necessary. Epidemiological studies have established that tobacco smoke (TS) is a cofactor for cervical carcinogenesis because women who smoke are more susceptible to cervical cancer when compared to non-smokers. Even though such a relationship has not been established in HPV-related HNC, a group of HPV positive patients with this malignancy are smokers. TS is a complex mixture of more than 4500 chemical compounds and approximately 60 of them show oncogenic properties such as benzo[α]pyrene (BaP) and nitrosamines, among others. Some of these compounds have been evaluated for carcinogenesis through experimental settings in collaboration with HR-HPV. Here, we conducted a comprehensive review of the suggested molecular mechanisms involved in cooperation with both HR-HPV and TS for epithelial carcinogenesis. Furthermore, we propose interaction models in which TS collaborates with HR-HPV to promote epithelial cancer initiation, promotion, and progression. More studies are warranted to clarify interactions between oncogenic viruses and chemical or physical environmental factors for epithelial carcinogenesis.
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Scherer, G., and E. Richter. "Biomonitoring exposure to environmental tobacco smoke (ETS): A critical reappraisal." Human & Experimental Toxicology 16, no. 8 (August 1997): 449–59. http://dx.doi.org/10.1177/096032719701600806.
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1 The most frequently used biomarkers for exposure to environmental tobacco smoke (ETS) are cotinine and thiocyanate in body fluids, carboxyhaemoglobin in red blood cells (COHb) and carbon monoxide in the expired air. Although not ideal, cotinine in blood, saliva or urine is an established biomarker for ETS exposure within the past 1-3 days. Comparison with cotinine concentrations in cigarette smokers reveals that passive smokers take up less than 1/100 of the nicotine dose of smokers. 2 Biomonitoring data available for the ETS-related exposure to genotoxic substances comprise uptake of benzene, polycyclic aromatic hydrocarbons (PAH), aromatic amines, tobacco-specific nitrosamines (TSNA), electrophilic compounds giving rise to ur inary thioethers, mutagens causing urinary mutagenic activity and the formation of various DNA adducts. With the exception of TSNA, these biomarkers are related to chemicals occurring ubiquitously in the environment and in the food. As a consequence, the background levels in unexposed nonsmokers are high compared to the observed increases (if any) associated with ETS exposure. 3 Some markers of biological effects, which, by defini tion, are non-specific with regard to the underlying exposure, have also been investigated in relation to ETS exposure. These markers comprise cytogenetic effects, aryl hydrocarbon hydroxylase (AHH) induc tion, urinary hydroxyproline excretion and various factors indicative of cardiovascular risks. The avail able data suggest that passive smoking is associated with a small induction of placental AHH and also with effects on cardiovascular risk markers. The latter findings in particular may be confounded by other risk factors, which have been observed to be more frequent in passive smokers than in unexposed nonsmokers.
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Schuller, Hildegard M. "Cell type specific, receptor-mediated modulation of growth kinetics in human lung cancer cell lines by nicotine and tobacco-related nitrosamines." Biochemical Pharmacology 38, no. 20 (October 1989): 3439–42. http://dx.doi.org/10.1016/0006-2952(89)90112-3.
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Bendik, Patrick B., Sharyn M. Rutt, Brittany N. Pine, Connie S. Sosnoff, Benjamin C. Blount, Wanzhe Zhu, June Feng, and Lanqing Wang. "Anabasine and Anatabine Exposure Attributable to Cigarette Smoking: National Health and Nutrition Examination Survey (NHANES) 2013–2014." International Journal of Environmental Research and Public Health 19, no. 15 (August 8, 2022): 9744. http://dx.doi.org/10.3390/ijerph19159744.
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Anabasine and anatabine are minor alkaloids in tobacco products and are precursors for tobacco-specific nitrosamines (TSNAs). The levels of these two compounds have been used to differentiate tobacco product sources, monitor compliance with smoking cessation programs, and for biomonitoring in TSNA-related studies. The concentrations of urinary anabasine and anatabine were measured in a representative sample of U.S. adults who smoked cigarettes (N = 770) during the 2013–2014 National Health and Nutrition Examination Survey (NHANES) study cycle, which was the first cycle where urinary anabasine and anatabine data became available. Weighted geometric means (GM) and geometric least squares means (LSM) with 95% confidence intervals were calculated for urinary anabasine and anatabine categorized by tobacco-use status [cigarettes per day (CPD) and smoking frequency] and demographic characteristics. Smoking ≥20 CPD was associated with 3.6× higher anabasine GM and 4.8× higher anatabine GM compared with smoking <10 CPD. Compared with non-daily smoking, daily smoking was associated with higher GMs for urinary anabasine (1.41 ng/mL vs. 6.28 ng/mL) and anatabine (1.62 ng/mL vs. 9.24 ng/mL). Urinary anabasine and anatabine concentrations exceeded the 2 ng/mL cut point in 86% and 91% of urine samples from people who smoke (PWS) daily, respectively; in comparison, 100% of them had serum cotinine concentrations greater than the established 10 ng/mL cut point. We compared these minor tobacco alkaloid levels to those of serum cotinine to assess their suitability as indicators of recent tobacco use at established cut points and found that their optimal cut point values would be lower than the established values. This is the first time that anabasine and anatabine are reported for urine collected from a U.S. population-representative sample of NHANES study participants, providing a snapshot of exposure levels for adults who smoked during 2013–2014. The results of this study serve as an initial reference point for future analysis of NHANES cycles, where changes in the national level of urinary anabasine and anatabine can be monitored among people who smoke to show the effect of changes in tobacco policy.
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Lin, Che-Yi, Tien-Szu Pan, Chun-Chan Ting, Shih-Shin Liang, Shu-Hung Huang, Hsiu-Yueh Liu, Edward Cheng-Chuan Ko, Chung-Wei Wu, Jen-Yang Tang, and Ping-Ho Chen. "Cytochrome P450 Metabolism of Betel Quid-Derived Compounds: Implications for the Development of Prevention Strategies for Oral and Pharyngeal Cancers." Scientific World Journal 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/618032.
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Betel quid (BQ) products, with or without tobacco, have been classified by the International Agency for Research on Cancer (IARC) as group I human carcinogens that are associated with an elevated risk of oral potentially malignant disorders (OPMDs) and cancers of the oral cavity and pharynx. There are estimated 600 million BQ users worldwide. In Taiwan alone there are 2 million habitual users (approximately 10% of the population). Oral and pharyngeal cancers result from interactions between genes and environmental factors (BQ exposure). Cytochrome p450 (CYP) families are implicated in the metabolic activation of BQ- and areca nut-specific nitrosamines. In this review, we summarize the current knowledge base regardingCYPgenetic variants and related oral disorders. In clinical applications, we focus on cancers of the oral cavity and pharynx and OPMDs associated withCYPgene polymorphisms, includingCYP1A1,CYP2A6,CYP2E1, andCYP26B1. Our discussion ofCYPpolymorphisms provides insight into the importance of screening tests in OPMDs patients for the prevention of oral and pharyngeal cancers. Future studies will establish a strong foundation for the development of chemoprevention strategies, polymorphism-based clinical diagnostic tools (e.g., specific single-nucleotide polymorphism (SNP) “barcodes”), and effective treatments for BQ-related oral disorders.
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Putri, Andi Anggun Mauliana, and Gus Permana Subita. "APAKAH SHISHA BERBAHAYA BAGI KESEHATAN RONGGA MULUT ?" ODONTO : Dental Journal 4, no. 2 (December 1, 2017): 129. http://dx.doi.org/10.30659/odj.4.2.129-135.
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Background: In recent years, the use of tobacco in Indonesia increasingly varied in the forms and methods of consumption, one of which is shisha. Smoking shisha is increasingly popular due to a misperception that smoking shisha is harmless and lack of knowledge about the effects of shisha smoking in oral health.Literature analysis: “PubMed” used as a search tool to identify all empirical studies related to the effects of shisha smoking on health, especially in oral cavity.Discussion: Shisha smoke contained various toxic substances such as Nicotine, Tobacco Specifc Nitrosamines, Polycyclic Aromatic Hydrocarbons, Volatile Organic Compounds, Carbon Monoxide, Tar, and high-temperature metal heating causing shisha smoke contained toxic heavy metals such as arsenic, nickel, cobalt, chromium, lead, and cadmium. The content of these toxic substances showed that smoked shisha is associated with dependence, acute and long-term negative health effects similar to cigarette smoking. Toxic substances may cause various infections of microorganism such as Candida sp, Herpes Simplex Virus (HSV-1), Epstein Barr Virus, Mycobacterium tuberculosis, Human Immunodefciency Virus; Oral mucosal changes such as Hairy Tongue, Smoker’s Melanosis, Nicotine Stomatitis, Frictional Keratosis, Fissured Tongues, gingival or periodontal inflammation, and leukodema; and lead to malignant lesions such as Keratosis, Leukoplakia, Erythroplakia, Oral Submucous Fibrosis and Lichenoid Lesions.Conclusion: Smoking shisha gives bad impact for human health especiallyoral health. Shisha smoking can lead to the development of various infectious diseases and potentially lead to malignancy in the oral mucosa. These foundings breaks the belief that shisha smoking is safe for health.
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Yamazaki, Hiroshi, Yukiharu Inui, Chul-Ho Yun, F. Peter Guengerich, and Tsutomu Shimada. "Cytochrome P450 2E1 and 2A6 enzymes as major catalysts for metabolic activation of N-nitrosodialkylamines and tobacco-related nitrosamines in human liver microsomes." Carcinogenesis 13, no. 10 (1992): 1789–94. http://dx.doi.org/10.1093/carcin/13.10.1789.
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Schuller, H. M., and T. J. Hegedus. "Effects of endogenous and tobacco-related amines and nitrosamines on cell growth and morphology of a cell line derived from a human neuroendocrine lung cancer." Toxicology in Vitro 3, no. 1 (January 1989): 37–43. http://dx.doi.org/10.1016/0887-2333(89)90022-2.
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Stevens, T. P., J. T. McBride, J. L. Peake, K. E. Pinkerton, and B. R. Stripp. "Cell proliferation contributes to PNEC hyperplasia after acute airway injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 3 (March 1, 1997): L486—L493. http://dx.doi.org/10.1152/ajplung.1997.272.3.l486.
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Pulmonary neuroendocrine cells (PNECs) are airway epithelial cells that are capable of secreting a variety of neuropeptides. PNECs are scattered throughout the bronchial tree either as individual cells or clusters of cells termed neuroepithelial bodies (NEBs). PNECs and their secretory peptides have been considered to play a role in fetal lung development. Although the normal physiological function of PNECs and neuropeptides in normal adult lungs and in repair from lung injury is not known, PNEC hyperplasia has been associated with chronic lung diseases, such as bronchopulmonary dysplasia, and with chronic exposures, such as hypoxia, tobacco smoke, nitrosamines, and ozone. To evaluate changes in PNEC number and distribution after acute airway injury, FVB/n mice were treated with either naphthalene or vehicle. Naphthalene is an aromatic hydrocarbon that, at the dose used in this study, selectively destroys nonciliated bronchial epithelial cells (Clara cells) through cytochrome P-450-mediated metabolic activation into cytotoxic epoxides. PNECs were identified by immunohistochemical analysis of calcitonin gene-related peptide-like immunoreactivity (CGRP-IR). Proliferating cells were marked with [(3)H]thymidine incorporation. Acute naphthalene toxicity results in PNEC hyperplasia that is detectable after 5 days of recovery. PNEC hyperplasia is characterized by increased numbers of NEBs without significant changes in the number of isolated PNECs and by increased [(3)H]thymidine labeling of CGRP-IR cells. These data show that cell proliferation contributes to PNEC hyperplasia after acute airway injury and suggest that PNECs may be capable of more rapidly increasing their number in response to injury than previously recognized.
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Filippov, S. V., A. A. Yarushkin, A. K. Yakovleva, V. V. Kozlov, and L. F. Gulyaeva. "Effect of benzo(a)pyrene on the expression of AhR-regulated microRNA in female and male rat lungs." Biomeditsinskaya Khimiya 66, no. 3 (2020): 224–32. http://dx.doi.org/10.18097/pbmc20206603224.
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Smoking is the main risk factor for lung cancer, mainly due to presence of nitrosamines and polycyclic aromatic hydrocarbons, including benzo[a]pyrene (BP) in tobacco smoke composition. The genotoxic effect of BP is based on the high DNA-binding ability of its metabolites, while the epigenetic effects are mediated by a change in the expression of cancer related genes or regulatory RNAs. It has been shown that women have a higher risk to develop lung cancer upon smoking rather than men. We hypothesized that crosstalk between signaling pathways activated by BP and estrogens could underlie the sex-dependent differences in miRNAs expression. To test this hypothesis, male and female rats were subjected to short-term or long-term BP exposure. Using in silico analysis, miRNAs containing the ER- and AhR-binding sites in the promoters of the genes (or host genes) were selected. During chronic exposure of BP the expression of miR-22-3p, -29a-3p, -126a-3p, -193b-5p in the lungs of male rats were significantly increased, while the level of miRNA-483-3p were decreased. Expression of miRNA-483-3p was up-regulated during chronic BP exposure in the lungs of female rats and the levels of other studied miRNAs were unchanged. In turn, changes in the expression of miRNAs were followed by changes in the expression of their target genes, including PTEN, EMP2, IGF1, ITGA6, SLC34A2, and the observed changes in female and male rat lungs were varied. Thus, our results suggest that sex-dependent epigenetic effects of BP may be based on different expression of AhR- and ER- regulated miRNAs.
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Intorp, M., SW Purkis, and W. Wagstaff. "Determination of Selected Volatiles in Cigarette Mainstream Smoke. The CORESTA 2009 Collaborative Study and Recommended Method." Beiträge zur Tabakforschung International/Contributions to Tobacco Research 24, no. 5 (May 1, 2011): 243–51. http://dx.doi.org/10.2478/cttr-2013-0904.
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AbstractA recommended method has been developed and published by CORESTA, applicable to the quantification of selected volatiles (1,3-butadiene, isoprene, acrylonitrile, benzene, and toluene) in the gas phase of cigarette mainstream smoke. The method involved smoke collection in impinger traps and detection and measurement using gas chromatography/mass spectrometry techniques.This report describes the final collaborative study applying the recommended method. It provides additional notes to inform other laboratories that might wish to adopt it, about some of the main features that need to be well controlled to provide data as robust and consistent as the data presented herein.Data was provided by 15 industry-related and 4 independent laboratories and one governmental laboratory. Overall, 6 linear and 14 rotary smoking machines were used.The joint experiments and collaborative work between the large number of participating laboratories has provided solutions to several methodological problems and reduced the high data variability that had initially been found particularly for 1,3-butadiene and acrylonitrile smoke yields.Even so, the levels of reproducibility among laboratories are much greater than the levels found for ‘tar’, nicotine and carbon monoxide and given in the equivalent ISO standards. When expressing the reproducibility (R) value as a percentage of the mean yield among-laboratories and across all of the studied products, values ranged from 63-93% for 1,3-butadiene; from 36-62% for isoprene; from 41-110% for acrylonitrile; from 35-70% for benzene, and from 27-116% for toluene. For the higher ‘tar’ yielding products, the lower levels of variability were in line with those previously evaluated during Task Force work on standard methods for benzo[a]pyrene and tobacco specific nitrosamines. As expected, the lowest ‘tar’ yielding product gave the most variable data.
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Torres, Sònia, Carla Merino, Beatrix Paton, Xavier Correig, and Noelia Ramírez. "Biomarkers of Exposure to Secondhand and Thirdhand Tobacco Smoke: Recent Advances and Future Perspectives." International Journal of Environmental Research and Public Health 15, no. 12 (November 29, 2018): 2693. http://dx.doi.org/10.3390/ijerph15122693.
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Smoking is the leading preventable disease worldwide and passive smoking is estimated to be the cause of about 1.0% of worldwide mortality. The determination of tobacco smoke biomarkers in human biological matrices is key to assess the health effects related to the exposure to environmental tobacco smoke. The biomonitoring of cotinine, the main nicotine metabolite, in human biofluids—including urine, serum or saliva—has been extensively used to assess this exposure. However, the simultaneous determination of cotinine together with other tobacco biomarkers and the selection of alternative biological matrices, such as hair, skin or exhaled breath, would enable a better characterization of the kind and extent of tobacco exposure. This review aims to perform a critical analysis of the up-to-date literature focused on the simultaneous determination of multiple tobacco smoke biomarkers studied in different biological matrices, due to the exposure to secondhand smoke (SHS) and thirdhand smoke (THS). Target biomarkers included both tobacco-specific biomarkers—nicotine and tobacco specific nitrosamine biomarkers—and tobacco-related biomarkers, such as those from polycyclic aromatic hydrocarbons, volatile organic compounds, metals and carbon monoxide. To conclude, we discuss the suitability of determining multiple biomarkers through several relevant examples of SHS and THS exposure.
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Fix, Brian V., Sarah E. Adkison, Richard J. O’Connor, Maansi Bansal-Travers, K. Michael Cummings, Vaughan W. Rees, and Dorothy K. Hatsukami. "Evaluation of modified risk claim advertising formats for Camel Snus." Health Education Journal 76, no. 8 (September 20, 2017): 971–85. http://dx.doi.org/10.1177/0017896917729723.
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Objectives: The US Food and Drug Administration (FDA) has regulatory authority for modified risk tobacco product advertising claims. To guide future regulatory efforts, we investigated how variations in modified risk claim advertisements influence consumer perceptions of product risk claims for Camel Snus. Methods: Young people and adults (15–65), including current, never, and former smokers, were randomised to view one of five Camel Snus print advertisements as part of a web-based survey. Four of the advertisements presented information related to nitrosamine content of snus using four formats: (1) text, (2) a bar chart, (3) a text/testimonial and (4) a bar chart/testimonial. The fifth format, used as a control, was a current advertisement for Camel Snus without the explicit claims made about nitrosamine content. After viewing advertisements for all products, participants were asked which product they would be most interested in trying. Results: Participants exposed to advertisements that contained an explicit reduced risk message agreed the advertising claim for that product posed fewer health risks than cigarettes. However, advertisements containing the reduced risk messages were also viewed as containing less truthful information and respondents were more sceptical of the information presented. Advertisement claim format was not associated with selecting snus over the other tobacco products, nor was it associated with purchase intentions. Conclusion: The results of this research indicate that consumers respond to reduced risk messages, though perhaps not in the direct way anticipated. We found no significant differences by advertisement format (numerical, graphical, testimonial).
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Dai, Hongying, and Ali S. Khan. "A Longitudinal Study of Exposure to Tobacco-Related Toxicants and Subsequent Respiratory Symptoms Among U.S. Adults with Varying E-cigarette Use Status." Nicotine & Tobacco Research 22, Supplement_1 (December 1, 2020): S61—S69. http://dx.doi.org/10.1093/ntr/ntaa180.
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Abstract Background The link between e-cigarette use and subsequent development of respiratory diseases remains an open question. Aims and Methods A subset of a probability sample of U.S. adults from the Population Assessment of Tobacco and Health Study Waves 1 and 2 were selected for biospecimen analysis (n = 4614). Subjects were divided into three mutually exclusive groups at baseline: nonusers (n = 2849), exclusive e-cigarette users (n = 222), and poly e-cigarette/tobacco users (n = 1,543). Geometric mean concentrations of baseline biomarkers from five classes of harmful and potentially harmful constituents were reported. Multivariable linear regressions were conducted to examine the relationship between baseline biomarkers and subsequent respiratory symptoms among user groups. Results Baseline exclusive e-cigarette users (33.6%[confidence interval, CI: 26.7% to 41.4%]) and poly e-cigarette/tobacco users (50.8%[CI: 47.4% to 54.2%]) had higher prevalence of subsequent respiratory symptoms than nonusers (21.7%[19.2% to 24.4%]). As compared with nonusers, poly e-cigarette/tobacco users had higher concentrations in clinically relevant biomarkers at baseline than exclusive e-cigarette users. Among poly e-cigarette/tobacco users, baseline nicotine metabolites (TNE2, cotinine), tobacco-specific nitrosamine (NNAL), PAH (1-NAP, 3-FLU), and volatile organic compound (N-Acetyl-S-(2-carboxyethyl)-l-cysteine, N-acetyl-S-(2-cyanoethyl)-l-cysteine) were significantly higher among those reporting subsequent respiratory symptoms than those who did not. Among exclusive e-cigarette users, baseline NNAL was significantly higher among those reporting subsequent respiratory symptoms than those who did not. Within subjects with subsequent respiratory symptoms, NNAL was 2.5 times higher in exclusive e-cigarette users (10.7[6.5 to 17.5]) and 63.4 times higher in poly e-cigarette/tobacco users (199.6[176.7 to 225.4]) than nonusers (3.1[2.4 to 3.9]). Conclusions E-cigarette use is associated with higher concentrations of known tobacco-related toxicants and risks of subsequent respiratory symptoms than nonusers. Poly e-cigarette/tobacco users exhibit higher risk than exclusive e-cigarette users. Implications This longitudinal study identified positive associations between baseline urinary biomarkers of exposure to tobacco-related toxicants and increased risks of subsequent respiratory symptoms across varying e-cigarette use groups. E-cigarette use is associated with increased exposure to known tobacco-related toxicants, and certain toxicant exposure increases the risk of respiratory symptoms.
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Kovi, Ramesh C., Charles S. Johnson, Silvia Balbo, Stephen S. Hecht, and M. Gerard O’Sullivan. "Metastasis to the F344 Rat Pancreas from Lung Cancer Induced by 4-(Methylnitrosamino)- 1-(3-pyridyl)-1-butanone and Enantiomers of Its Metabolite 4-(Methylnitrosamino)-1-(3-pyridyl)- 1-butanol, Constituents of Tobacco Products." Toxicologic Pathology 46, no. 2 (February 2018): 184–92. http://dx.doi.org/10.1177/0192623317751573.
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Lung cancer is the most common cause of cancer-related deaths in humans worldwide. There is strong evidence that the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and its metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) play an important role in carcinogenesis caused by tobacco products. NNK and racemic NNAL are reported to induce lung and pancreatic tumors in rats. The carcinogenicity in Fischer 344 rats of NNK, NNAL, and its enantiomers ( R)-NNAL and ( S)-NNAL has been studied recently, and all test compounds induced significant numbers of lung tumors. We report here the detailed histopathological and immunohistochemical characterization of these tumors and their aggressive nature as shown by their metastasis locally and to the pancreas. The spectrum of treatment-related histopathological findings comprised pulmonary alveolar/bronchiolar (A/B) epithelial hyperplasia, A/B adenomas, and A/B carcinomas. A/B carcinomas frequently exhibited local invasion/metastasis within the mediastinum and thoracic cavity and distant metastasis to the pancreas that was confirmed by immunohistochemistry using the lung-specific markers prosurfactant protein-C and club (Clara) cell-10. Our observation regarding metastasis to the pancreas was an important, and unexpected, finding in this study both for the experimental animal model and potential human relevance.
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Mahabee-Gittens, E. Melinda, Georg E. Matt, and Ashley L. Merianos. "High Levels of the Carcinogenic Tobacco-Specific Nitrosamine NNAL and Associated Findings in Children of Smokers: A Case Series." Biomarker Insights 17 (January 2022): 117727192211188. http://dx.doi.org/10.1177/11772719221118868.
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High levels of NNAL, the tobacco smoke exposure (TSE) biomarker of the carcinogen 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), indicate future cancer risk. A prior study of smokers’ children revealed NNAL levels as high as active smokers. Therefore, we conducted a case series to examine the sociodemographics, TSE and clinical patterns, and other TSE biomarker levels in 9 children with extreme NNAL levels of >200 pg/ml to generate hypotheses and explore potential causes and implications. We identified 0 to 4-year-olds who presented to an emergency setting and lived with ⩾1 smoker who were part of a parental tobacco cessation trial (n = 461). Of these children, 52 had urinary NNAL, cotinine, and N-oxides results (n = 52). Nine children (17.3%) had NNAL levels >200 pg/ml, ranging from 206.4 to 1399.0 pg/ml (Median (Mdn) = 489.2 pg/ml; Interquartile Range (IQR) = 222.7-1289.3 pg/ml). The cotinine Mdn (IQR) was 38.5 (10.3-102.2) ng/ml and the N-oxides Mdn (IQR) = 93.8 (24.7-109.6) pg/ml. While all biomarker levels were alarmingly high, these young children would not have been flagged for very high cancer risk based on urinary cotinine levels alone. This underscores the critical role of comprehensive TSE biomarker measurement in capturing different TSE exposure patterns and assessing children’s future risk for cancer and other TSE-related morbidities.
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Saad, Mohamed I., Louise McLeod, Liang Yu, Hiromichi Ebi, Saleela Ruwanpura, Irit Sagi, Stefan Rose-John, and Brendan J. Jenkins. "The ADAM17 protease promotes tobacco smoke carcinogen-induced lung tumorigenesis." Carcinogenesis 41, no. 4 (June 27, 2019): 527–38. http://dx.doi.org/10.1093/carcin/bgz123.
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Abstract Lung cancer is the leading cause of cancer-related mortality, with most cases attributed to tobacco smoking, in which nicotine-derived nitrosamine ketone (NNK) is the most potent lung carcinogen. The ADAM17 protease is responsible for the ectodomain shedding of many pro-tumorigenic cytokines, growth factors and receptors, and therefore is an attractive target in cancer. However, the role of ADAM17 in promoting tobacco smoke carcinogen-induced lung carcinogenesis is unknown. The hypomorphic Adam17ex/ex mice—characterized by reduced global ADAM17 expression—were backcrossed onto the NNK-sensitive pseudo-A/J background. CRISPR-driven and inhibitor-based (GW280264X, and ADAM17 prodomain) ADAM17 targeting was employed in the human lung adenocarcinoma cell lines A549 and NCI-H23. Human lung cancer biopsies were also used for analyses. The Adam17ex/ex mice displayed marked protection against NNK-induced lung adenocarcinoma. Specifically, the number and size of lung lesions in NNK-treated pseudo-A/J Adam17ex/ex mice were significantly reduced compared with wild-type littermate controls. This was associated with lower proliferative index throughout the lung epithelium. ADAM17 targeting in A549 and NCI-H23 cells led to reduced proliferative and colony-forming capacities. Notably, among select ADAM17 substrates, ADAM17 deficiency abrogated shedding of the soluble IL-6 receptor (sIL-6R), which coincided with the blockade of sIL-6R-mediated trans-signaling via ERK MAPK cascade. Furthermore, NNK upregulated phosphorylation of p38 MAPK, whose pharmacological inhibition suppressed ADAM17 threonine phosphorylation. Importantly, ADAM17 threonine phosphorylation was significantly upregulated in human lung adenocarcinoma with smoking history compared with their cancer-free controls. Our study identifies the ADAM17/sIL-6R/ERK MAPK axis as a candidate therapeutic strategy against tobacco smoke-associated lung carcinogenesis.
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Azzopardi, David, Linsey Ellen Haswell, Justin Frosina, Michael McEwan, Nathan Gale, Jesse Thissen, Filimon Meichanetzidis, and George Hardie. "Biomarkers of Exposure and Potential Harm in Exclusive Users of Nicotine Pouches and Current, Former, and Never Smokers: Protocol for a Cross-sectional Clinical Study." JMIR Research Protocols 11, no. 10 (October 6, 2022): e39785. http://dx.doi.org/10.2196/39785.
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Background Tobacco harm reduction (THR) aims to reduce the health burden of cigarettes by encouraging smokers to switch to using alternative tobacco or nicotine products. Nicotine pouches (NPs) are smokeless, tobacco-free, oral products that may be beneficial as part of a THR strategy. Objective This 2-center, cross-sectional confinement study conducted in Denmark and Sweden aimed to determine whether biomarkers of exposure (BoEs) to tobacco toxicants and biomarkers of potential harm (BoPHs) in exclusive users of NPs show favorable differences compared with current smokers. Methods Participants were healthy NP users (target n=100) and current, former, or never smokers (target n=40 each), as confirmed by urinary cotinine and exhaled carbon monoxide concentrations. During a 24-hour confinement period, participants were asked to use their usual product (NP or cigarette) as normal, and BoEs and BoPHs were measured in blood and 24-hour urine samples, with compliance determined using anabasine, anatabine, and N-(2-cyanoethyl)valine. BoEs and BoPHs were compared between NP users and current, former, and never smokers. Urinary total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (BoE to nicotine-derived nitrosamine ketone) and urinary 8-epi-prostaglandin F2α type III, exhaled nitric oxide, blood carboxyhemoglobin, white blood cell count, soluble intercellular adhesion molecule-1, and high-density lipoprotein cholesterol (BoPHs) were evaluated as primary outcomes. Other measures included urinary 11-dehydrothromboxane B2, forced expiratory volume, carotid intima-media thickness, self-reported quality of life, and oral health. Results The results of this study were received in mid-2022 and will be published in late 2022 to early 2023. Conclusions The results of this study will provide information on toxicant exposure and biomarkers associated with the development of smoking-related diseases among users of NPs compared with smokers, as well as on the potential role of NPs in THR. Trial Registration International Standard Randomised Controlled Trial Number (ISRCTN) ISRCTN16988167; https://www.isrctn.com/ISRCTN16988167 International Registered Report Identifier (IRRID) DERR1-10.2196/39785
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Strauss, G. M., A. Jemal, M. B. McKenna, J. A. Strauss, and K. M. Cummings. "Creation of an epidemic: The tobacco industry (TI) and smoking-related adenocarcinoma (AD) of the lung." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 7583. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.7583.
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7583 Background: When epidemiologic research first demonstrated an association between cigarette smoking (CS) and lung cancer (LC) in the 1950s, AD comprised about 5% of LCs and was only weakly related to CS. In the 1960s and 1970s, AD increased sharply, and became strongly related to CS. Methods: We conducted an epidemiological and ecological analysis correlating time trends in LC histology with changes in cigarette design and TI actions over the past 30 yrs. We utilized SEER data on 307,797 LCs diagnosed from 1975 to 2003 to analyze time trends of age-standardized incidence rates of each LC subtype: AD, squamous (SQ), small cell, and large cell. Comparisons were drawn based on sex, race, and age. Because SEER contains no data on CS, other sources were utilized to correlate changing histology to time trends in smoking prevalence, the changing cigarette, and TI actions. Results: Among all pts, AD surpassed SQ by 1980–84 to become the most common histology. AD increased 62% from 1975–79 to 1995–99, but fell 8% in 2000–03. SQ peaked in 1980–84 and dropped 35% by 2000–03. AD surpassed SQ in 1985–89 in men, while AD was already most common in women by 1975–79. AD rose 38% in men from 1975–79 to 1995–99, while it doubled in women during this interval. Among whites, AD surpassed SQ by 1980–84, although this did not occur among blacks for another decade. Nonetheless, AD incidence has consistently been higher in black men than in other subgroups. AD was already most common in pts <50 yrs by 1975–79, while AD rapidly increased and surpassed SQ in all other age groups by 1990–94. By 2000–03, AD comprised 47% of all LCs (42% in men; 52% in women; 59% in pts <50 yrs). Currently, AD is the most common histology in both sexes, races, and in all age groups. Trends in AD correlate with the wide-scale adoption by smokers of filtered and low tar cigarettes, and with increasing nitrosamine levels in cigarettes. Conclusions: The rise of AD, particularly in women and younger persons, is consistent with the hypothesis that changes in cigarette design and composition was responsible for this rise. These changes were introduced by the TI in response to mounting evidence that CS caused other forms of LC. While low tar cigarettes do not reduce LC risk, their adoption appears to be responsible for creating an epidemic of smoking-related lung AD. No significant financial relationships to disclose.
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Eggert, Heike, Christopher Heppel, Oliver Peschel, Sebastian Kunz, and Elmar Richter. "Method for the determination of tobacco specific nitrosamine related DNA adducts as their pentafluorobenzoyl ester in pancreatic tissue of sudden death victims." Toxicology Letters 189 (September 2009): S158. http://dx.doi.org/10.1016/j.toxlet.2009.06.766.
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Bordoloi, Devivasha, Kishore Banik, Ganesan Padmavathi, Rajesh Vikkurthi, Choudhary Harsha, Nand Kishor Roy, Anuj Kumar Singh, et al. "TIPE2 Induced the Proliferation, Survival, and Migration of Lung Cancer Cells Through Modulation of Akt/mTOR/NF-κB Signaling Cascade." Biomolecules 9, no. 12 (December 6, 2019): 836. http://dx.doi.org/10.3390/biom9120836.
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Lung cancer represents the most common cause of cancer deaths in the world, constituting around 11.6% of all new cancer cases and 18.4% of cancer-related deaths. The propensity for early spread, lack of suitable biomarkers for early diagnosis, as well as prognosis and ineffective existing therapies, contribute to the poor survival rate of lung cancer. Therefore, there is an urgent need to develop novel biomarkers for early diagnosis and prognosis which in turn can facilitate newer therapeutic avenues for the management of this aggressive neoplasm. TIPE2 (tumor necrosis factor-α-induced protein 8-like 2), a recently identified cytoplasmic protein, possesses enormous potential in this regard. Immunohistochemical analysis showed that TIPE2 was significantly upregulated in different stages and grades of lung cancer tissues compared to normal lung tissues, implying its involvement in the positive regulation of lung cancer. Further, knockout of TIPE2 resulted in significantly reduced proliferation, survival, and migration of human lung cancer cells through modulation of the Akt/mTOR/NF-κB signaling axis. In addition, knockout of TIPE2 also caused arrest in the S phase of the cell cycle of lung cancer cells. As tobacco is the most predominant risk factor for lung cancer, we therefore evaluated the effect of TIPE2 in tobacco-mediated lung carcinogenesis as well. Our results showed that TIPE2 was involved in nicotine-, nicotine-derived nitrosamine ketone (NNK)-, N-nitrosonornicotine (NNN)-, and benzo[a]pyrene (BaP)-mediated lung cancer through inhibited proliferation, survival, and migration via modulation of nuclear factor kappa B (NF-κB)- and NF-κB-regulated gene products, which are involved in the regulation of diverse processes in lung cancer cells. Taken together, TIPE2 possesses an important role in the development and progression of lung cancer, particularly in tobacco-promoted lung cancer, and hence, specific targeting of it holds an enormous prospect in newer therapeutic interventions in lung cancer. However, these findings need to be validated in the in vivo and clinical settings to fully establish the diagnostic and prognostic importance of TIPE2 against lung cancer.
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Ginwala, Rashida, Laura Bukavina, Jodie Franklin, Mohit Sindhani, and Philip Abbosh. "Abstract 3060: Changes in mouse gut microbiome upon exposure to N-butyl-N-(4-hydroxybutyl) nitrosamine." Cancer Research 82, no. 12_Supplement (June 15, 2022): 3060. http://dx.doi.org/10.1158/1538-7445.am2022-3060.
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Abstract Background: BBN (N-butyl-N-(4-hydroxybuytl) nitrosamine), a closely related compound to the carcinogens found in tobacco smoke is an attractive and most commonly used agent to model bladder cancer in mice. BBN closely recapitulates the morphological characteristics of human bladder cancer and conceptually simulates tobacco exposure as the leading risk factor for bladder cancer. We employ the BBN model in mice to decipher the microbial changes that occur in the gut of the mice during the chemical carcinogenesis induced by BBN exposure. Methods: Starting at 8-12 weeks of age, male (N=30) and female (N=21) C57BL/6 mice were administered 0.05% BBN in drinking water for 12 weeks then switched to regular water. Control mice drank regular water. Stool was collected pre-exposure, after 6 and 12 weeks of exposure, and at the time of tumor identification (tumors typically detectable between 14-22 weeks from start of treatment using this model). DNA extracted from stool was subjected to PCR amplification using primers for the V3-V4 regions of the bacterial 16S rRNA. Results: Gender-based differences in the microbial composition were noted in response to BBN treatment. While gut microbial diversity in the female mice was markedly reduced (Shannon, Simpson, Inverse Simpson, and Richness) upon BBN treatment, that of male mice remained unchanged from baseline. Additionally, there was a distinct clustering of microbes based on sex (p=0.024) but not BBN exposure (p=0.86) as evidenced by principal coordinate analysis. Differences in the microbial composition were seen upon BBN exposure, with BBN mice showing an increase in Bacteroidales (53%), Lactobacillales (17.5%), Coriobacteriales (19.87%) in females and male mice exhibited an increase in Erysipelotrichales (14.76%) at the order level. On the other hand while male mice showed no significant decreases, female mice exhibited reduction in abundance of Clostridiales (log change -7.79, padj <0.004), Veeruccomicrobiales (log change -2.21, padj<0.005), and Bacillales (log -17.60, padj =0.005). Conclusions: Pronounced gut microbial changes are induced by BBN in the murine model, with microbiome of the female mice exhibiting more significant variations compared to baseline, suggesting gender-based disparities in the effect of BBN exposure. Citation Format: Rashida Ginwala, Laura Bukavina, Jodie Franklin, Mohit Sindhani, Philip Abbosh. Changes in mouse gut microbiome upon exposure to N-butyl-N-(4-hydroxybutyl) nitrosamine [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3060.
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Watson, Clifford H., Jane Yan, Stephen Stanfill, Liza Valentin-Blasini, Roberto Bravo Cardenas, and Benjamin C. Blount. "A Low-Cost, High-Throughput Digital Image Analysis of Stain Patterns on Smoked Cigarette Filter Butts to Estimate Mainstream Smoke Exposure." International Journal of Environmental Research and Public Health 18, no. 19 (October 8, 2021): 10546. http://dx.doi.org/10.3390/ijerph181910546.
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Standard machine smoking protocols provide useful information for examining the impact of design parameters, such as filter ventilation, on mainstream smoke delivery. Unfortunately, their results do not accurately reflect human smoke exposure. Clinical research and topography devices in human studies yield insights into how products are used, but a clinical setting or smoking a cigarette attached to such a device may alter smoking behavior. To better understand smokers’ use of filtered cigarette products in a more natural environment, we developed a low-cost, high-throughput approach to estimate mainstream cigarette smoke exposure on a per-cigarette basis. This approach uses an inexpensive flatbed scanner to scan smoked cigarette filter butts and custom software to analyze tar-staining patterns. Total luminosity, or optical staining density, of the scanned images provides quantitative information proportional to mainstream smoke-constituent deliveries on a cigarette-by-cigarette basis. Duplicate sample analysis using this new approach and our laboratory’s gold-standard liquid chromatography/tandem mass spectrometry (LC/MS/MS) solanesol method yielded comparable results (+7% bias) from the analysis of 20 commercial cigarettes brands (menthol and nonmentholated). The brands varied in design parameters such as length, filter ventilation, and diameter. Plots correlating the luminosity to mainstream smoked-nicotine deliveries on a per-cigarette basis for these cigarette brands were linear (average R2 > 0.91 for nicotine and R2 > 0.83 for the tobacco-specific nitrosamine NNK), on a per-brand basis, with linearity ranging from 0.15 to 3.00 mg nicotine/cigarette. Analysis of spent cigarette filters allows exposures to be characterized on a per-cigarette basis or a “daily dose” via summing across results from all filter butts collected over a 24 h period. This scanner method has a 100-fold lower initial capital cost for equipment than the LC/MS/MS solanesol method and provides high-throughput results (~200 samples per day). Thus, this new method is useful for characterizing exposure related to filtered tobacco-product use.
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Prasad, G. L., Bobbette A. Jones, Peter Chen, and Evan O. Gregg. "A cross-sectional study of biomarkers of exposure and effect in smokers and moist snuff consumers." Clinical Chemistry and Laboratory Medicine (CCLM) 54, no. 4 (January 1, 2016). http://dx.doi.org/10.1515/cclm-2015-0594.
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AbstractCigarette smoking is a major risk factor for several chronic diseases. Epidemiological data indicate the use of smokeless tobacco (ST) is associated with significantly lower risk for smoking-related diseases compared to cigarettes. Several biomarkers of exposure (BioExp) and effect (BioEff) associated with smoking and use of moist snuff (ST) were evaluated.A single site, cross-sectional clinical study enrolled three groups of generally healthy male smokers (SMK), moist snuff consumers (MSC), and non-tobacco consumers (NTC), and several BioExp and BioEff were evaluated.Blood and urinary BioExp, including total nicotine equivalents and tobacco-specific nitrosamines, were higher in MSC compared to SMK. Biomarkers of combustion-related toxicants and cadmium were elevated in SMK. Elevated levels of some BioEff associated with oxidative stress (urinary isoprostanes and leukotriene E4), inflammation (white blood cell count), platelet activation (thromboxane metabolites), and lipid metabolism (apolipoprotein B100 and oxidized low-density lipoprotein) were observed in SMK relative to NTC and MSC (all p<0.05). The non-smoking groups (MSC and NTC) showed similar levels of combustion-related BioExp and BioEff.Higher levels of exposure to nicotine and some N′-nitrosamines may be observed in MSC, and SMK are exposed to higher levels of combustion-related toxicants. Changes in BioEff consistent with some aspects of inflammation, oxidative stress, and altered lipid metabolism were detected in SMK compared to the non-smoking groups. The biomarker data further improve our understanding of pathophysiological changes and the risk continuum associated with various tobacco products, and could be useful components of future assessments of tobacco products.
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Li, Yong, Tao Pang, Junli Shi, Xiuping Lu, Jianhua Deng, and Qian Lin. "Simultaneous Determination of Alkaloids and Their Related Tobacco-Specific Nitrosamines in Tobacco Leaves Using LC–MS-MS." Journal of Chromatographic Science, June 26, 2015, bmv082. http://dx.doi.org/10.1093/chromsci/bmv082.
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Quintana, Penelope J. E., Nicolas Lopez-Galvez, Nathan G. Dodder, Eunha Hoh, Georg E. Matt, Joy M. Zakarian, Mansi Vyas, et al. "Nicotine, Cotinine, and Tobacco-Specific Nitrosamines Measured in Children’s Silicone Wristbands in Relation to Secondhand Smoke and E-cigarette Vapor Exposure." Nicotine & Tobacco Research, October 3, 2020. http://dx.doi.org/10.1093/ntr/ntaa140.
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Abstract Introduction Simple silicone wristbands (WB) hold promise for exposure assessment in children. We previously reported strong correlations between nicotine in WB worn by children and urinary cotinine (UC). Here, we investigated differences in WB chemical concentrations among children exposed to secondhand smoke from conventional cigarettes (CC) or secondhand vapor from electronic cigarettes (EC), and children living with nonusers of either product (NS). Methods Children (n = 53) wore three WB and a passive nicotine air sampler for 7 days and one WB for 2 days, and gave a urine sample on day 7. Caregivers reported daily exposures during the 7-day period. We determined nicotine, cotinine, and tobacco–specific nitrosamines (TSNAs) concentrations in WB, nicotine in air samplers, and UC through isotope-dilution liquid chromatography with triple-quadrupole mass spectrometry. Results Nicotine and cotinine levels in WB in children differentiated between groups of children recruited into NS, EC exposed, and CC exposed groups in a similar manner to UC. WB levels were significantly higher in the CC group (WB nicotine median 233.8 ng/g silicone, UC median 3.6 ng/mL, n = 15) than the EC group (WB nicotine median: 28.9 ng/g, UC 0.5 ng/mL, n = 19), and both CC and EC group levels were higher than the NS group (WB nicotine median: 3.7 ng/g, UC 0.1 ng/mL, n = 19). TSNAs, including the known carcinogen NNK, were detected in 39% of WB. Conclusions Silicone WB show promise for sensitive detection of exposure to tobacco-related contaminants from traditional and electronic cigarettes and have potential for tobacco control efforts. Implications Silicone WB worn by children can absorb nicotine, cotinine, and tobacco-specific nitrosamines, and amounts of these compounds are closely related to the child’s urinary cotinine. Levels of tobacco-specific compounds in the silicone WB can distinguish patterns of children’s exposure to secondhand smoke and e-cigarette vapor. Silicone WB are simple to use and acceptable to children and, therefore, may be useful for tobacco control activities such as parental awareness and behavior change, and effects of smoke-free policy implementation.
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Brusco, Simone, Paola Ambrosi, Simone Meneghini, and Andrea Becchetti. "Agonist and antagonist effects of tobacco-related nitrosamines on human α4β2 nicotinic acetylcholine receptors." Frontiers in Pharmacology 6 (September 22, 2015). http://dx.doi.org/10.3389/fphar.2015.00201.
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"LIPID PEROXIDATION AND ETHANOL-RELATED TUMOR PROMOTION IN FISCHER-344 RATS TREATED WITH TOBACCO-SPECIFIC NITROSAMINES." Alcohol and Alcoholism, September 1994. http://dx.doi.org/10.1093/oxfordjournals.alcalc.a045585.
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Pool-Zobel, B. L., R. G. Klein, U. M. Liegibel, F. Kuchenmeister, S. Weber, and P. Schmezer. "Systemic genotoxic effects of tobacco-related nitrosamines following oral and inhalational administration to Sprague-Dawley rats." Clinical Investigator 70-70, no. 3-4 (1992). http://dx.doi.org/10.1007/bf00184666.
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Xia, Baoyun, Benjamin C. Blount, Tonya Guillot, Christina Brosius, Yao Li, Dana M. Van Bemmel, Heather L. Kimmel, et al. "Tobacco-Specific Nitrosamines (NNAL, NNN, NAT, and NAB) Exposures in the US Population Assessment of Tobacco and Health (PATH) Study Wave 1 (2013–2014)." Nicotine & Tobacco Research, July 27, 2020. http://dx.doi.org/10.1093/ntr/ntaa110.
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Abstract Introduction The tobacco-specific nitrosamines (TSNAs) are an important group of carcinogens found in tobacco and tobacco smoke. To describe and characterize the levels of TSNAs in the Population Assessment of Tobacco and Health (PATH) Study Wave 1 (2013–2014), we present four biomarkers of TSNA exposure: N′-nitrosonornicotine, N′-nitrosoanabasine, N′-nitrosoanatabine, and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) which is the primary urinary metabolite of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. Methods We measured total TSNAs in 11 522 adults who provided urine using automated solid-phase extraction coupled to isotope dilution liquid chromatography–tandem mass spectrometry. After exclusions in this current analysis, we selected 11 004 NNAL results, 10 753 N′-nitrosonornicotine results, 10 919 N′-nitrosoanatabine results, and 10 996 N′-nitrosoanabasine results for data analysis. Geometric means and correlations were calculated using SAS and SUDAAN. Results TSNA concentrations were associated with choice of tobacco product and frequency of use. Among established, every day, exclusive tobacco product users, the geometric mean urinary NNAL concentration was highest for smokeless tobacco users (993.3; 95% confidence interval [CI: 839.2, 1147.3] ng/g creatinine), followed by all types of combustible tobacco product users (285.4; 95% CI: [267.9, 303.0] ng/g creatinine), poly tobacco users (278.6; 95% CI: [254.9, 302.2] ng/g creatinine), and e-cigarette product users (6.3; 95% CI: [4.7, 7.9] ng/g creatinine). TSNA concentrations were higher in every day users than in intermittent users for all the tobacco product groups. Among single product users, exposure to TSNAs differed by sex, age, race/ethnicity, and education. Urinary TSNAs and nicotine metabolite biomarkers were also highly correlated. Conclusions We have provided PATH Study estimates of TSNA exposure among US adult users of a variety of tobacco products. These data can inform future tobacco product and human exposure evaluations and related regulatory activities.
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Perez‐Paramo, Yadira X., Christy J. W. Watson, Zuping Xia, Gang Chen, and Philip Lazarus. "Cytochrome P450 Enzyme Contributions to the N ‐oxide Detoxification Pathway of Tobacco‐Specific Nitrosamines; a Possible Role in Tobacco‐Related Cancer Risk." FASEB Journal 33, S1 (April 2019). http://dx.doi.org/10.1096/fasebj.2019.33.1_supplement.508.8.
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Hemminki, Kari, Asta Försti, Akseli Hemminki, Börje Ljungberg, and Otto Hemminki. "Incidence trends in bladder and lung cancers between Denmark, Finland and Sweden may implicate oral tobacco (snuff/snus) as a possible risk factor." BMC Cancer 21, no. 1 (May 25, 2021). http://dx.doi.org/10.1186/s12885-021-08371-w.
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Abstract Background The dominant risk factor for urinary bladder cancer has been cigarette smoking, but, as smoking prevalence is decreasing in many populations, other risk factors may become uncovered. Such new risk factors could be responsible for halting the declining incidence of bladder cancer. We hypothesize that snuff use by Swedish men may increase the rate for bladder cancer, as snuff contains carcinogenic nitrosamines. Methods We carried out an ecological study by comparing incidence trends in lung and bladder cancers between Danish, Finnish and Swedish men in order to test if the Swedish bladder cancer rate deviates from the Danish and Finnish ones. We used the NORDCAN database for cancer data from 1960 through 2016 to test the hypothesis. Results In the three countries, the incidence of lung cancer started to decrease after a peak incidence, and this was later followed by declining incidence in bladder cancer in Denmark from 1990 to 2016 by 14.3%, in Finland by 8.3% but not in Sweden (the decline of 1.4% was not significant). The difference in trends can be partly explained by the increasing incidence in Swedish men aged 70 or more years. Sweden differs from the two other countries by low male smoking prevalence but increasing use of snuff recorded by various surveys. Conclusion The stable bladder cancer trend for Swedish men was opposite to the declining trends in Denmark, Finland and globally. We suggest that this unusual finding may be related to the increasing use of snuff by Swedish men. Average users of snuff are exposed to at least 3 times higher levels of carcinogenic tobacco-specific nitrosamines than a smoker of one daily pack of cigarettes.
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"Cell type specific, receptor-mediated modulation of growth kinetics in human lung cancer cell lines by nicotine and tobacco-related nitrosamines." Lung Cancer 6, no. 3-4 (October 1990): 120. http://dx.doi.org/10.1016/0169-5002(90)90124-5.
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