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Journal articles on the topic 'Tobacco-related nitrosamines'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

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 (2004): 708. http://dx.doi.org/10.1016/s1470-2045(04)01633-x.

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2

Myers, Steven R., and M. Yeakub Ali. "Haemoglobin adducts as biomarkers of exposure to tobacco-related nitrosamines." Biomarkers 13, no. 2 (2008): 145–59. http://dx.doi.org/10.1080/13547500701470561.

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3

Bošković, Maria, Blanka Roje, Felicia Fei-Lei Chung, et al. "DNA Methylome Changes of Muscle- and Neuronal-Related Processes Precede Bladder Cancer Invasiveness." Cancers 14, no. 3 (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. F

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4

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 (1996): 139–47. http://dx.doi.org/10.3109/10408449609017927.

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5

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 (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

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Ahijevych, Karen. "Biological Models for Studying and Assessing Tobacco Use." Annual Review of Nursing Research 27, no. 1 (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

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7

Kankanamage, Rumasha N. T., Abhisek Brata Ghosh, Di Jiang, et al. "Metabolites of Tobacco- and E-Cigarette-Related Nitrosamines Can Drive Cu2+-Mediated DNA Oxidation." Chemical Research in Toxicology 33, no. 8 (2020): 2072–86. http://dx.doi.org/10.1021/acs.chemrestox.0c00027.

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8

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 (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 a

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9

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 (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

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10

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 (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 com

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11

Han, Jing, Yasser M. Sanad, Joanna Deck, et al. "Bacterial Populations Associated with Smokeless Tobacco Products." Applied and Environmental Microbiology 82, no. 20 (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 gra

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12

Ma, Bin, Irina Stepanov, and Stephen Hecht. "Recent Studies on DNA Adducts Resulting from Human Exposure to Tobacco Smoke." Toxics 7, no. 1 (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 st

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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 (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

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14

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,

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15

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 (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

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16

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 (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 thir

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17

Moolky, A., N. Moolky, M. Ankush, K. Usha, and M. Nagabhushan. "Spices May Prevent Human Cancers." Journal of Global Oncology 4, Supplement 2 (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, zin

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18

Aguayo, Francisco, Juan P. Muñoz, Francisco Perez-Dominguez, et al. "High-Risk Human Papillomavirus and Tobacco Smoke Interactions in Epithelial Carcinogenesis." Cancers 12, no. 8 (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 an

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19

Scherer, G., and E. Richter. "Biomonitoring exposure to environmental tobacco smoke (ETS): A critical reappraisal." Human & Experimental Toxicology 16, no. 8 (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 benzen

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20

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 (1989): 3439–42. http://dx.doi.org/10.1016/0006-2952(89)90112-3.

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21

Bendik, Patrick B., Sharyn M. Rutt, Brittany N. Pine, et al. "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 (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

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22

Lin, Che-Yi, Tien-Szu Pan, Chun-Chan Ting, et al. "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 meta

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23

Putri, Andi Anggun Mauliana, and Gus Permana Subita. "APAKAH SHISHA BERBAHAYA BAGI KESEHATAN RONGGA MULUT ?" ODONTO : Dental Journal 4, no. 2 (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 Aromat

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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 (1989): 37–43. http://dx.doi.org/10.1016/0887-2333(89)90022-2.

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26

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 (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

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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 se

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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 (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 w

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29

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 (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 biolo

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Fix, Brian V., Sarah E. Adkison, Richard J. O’Connor, et al. "Evaluation of modified risk claim advertising formats for Camel Snus." Health Education Journal 76, no. 8 (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 format

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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 (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 har

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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 (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 l

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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 wh

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Saad, Mohamed I., Louise McLeod, Liang Yu, et al. "The ADAM17 protease promotes tobacco smoke carcinogen-induced lung tumorigenesis." Carcinogenesis 41, no. 4 (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

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Azzopardi, David, Linsey Ellen Haswell, Justin Frosina, et al. "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 (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 Participant

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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 (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

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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 та ін. "TIPE2 Induced the Proliferation, Survival, and Migration of Lung Cancer Cells Through Modulation of Akt/mTOR/NF-κB Signaling Cascade". Biomolecules 9, № 12 (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

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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 (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

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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 (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 estima

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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 (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

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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, 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 o

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Brusco, Simone, Paola Ambrosi, Simone Meneghini та Andrea Becchetti. "Agonist and antagonist effects of tobacco-related nitrosamines on human α4β2 nicotinic acetylcholine receptors". Frontiers in Pharmacology 6 (22 вересня 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, 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 usi

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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 (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 (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 Sw

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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 (1990): 120. http://dx.doi.org/10.1016/0169-5002(90)90124-5.

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