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Journal articles on the topic '-(méthyl-nitrosamino)-1-(3-pyridyl)-1-butanone'

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Published: 4 June 2021

Last updated: 12 February 2022

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1

Murphy, Sharon E., Deborah A. Spina, Maria G. Nunes, and Dominic A. Pullo. "Glucuronidation of 4-[(Hydroxymethyl)nitrosamino]-1-(3-pyridyl)-1-butanone, a Metabolically Activated Form of 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone, by Phenobarbital-Treated Rats." Chemical Research in Toxicology 8, no. 5 (July 1995): 772–79. http://dx.doi.org/10.1021/tx00047a018.

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2

Anderson, L. M., S. S. Hecht, R. M. Kovatch, S. Amin, D. Hoffmann, and J. M. Rice. "Tumorigenicity of the tobacco-specific carcinogen 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone in infant mice." Cancer Letters 58, no. 3 (July 1991): 177–81. http://dx.doi.org/10.1016/0304-3835(91)90097-2.

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3

Liu, Xiao-Keng, Thomas E. Spratt, Sharon E. Murphy, and Lisa A. Peterson. "Pyridyloxobutylation of Guanine Residues by 4-[(Acetoxymethyl)nitrosamino]-1-(3-pyridyl)-1-butanone Generates Substrates ofO6-Alkylguanine−DNA Alkyltransferase." Chemical Research in Toxicology 9, no. 6 (January 1996): 949–53. http://dx.doi.org/10.1021/tx960067t.

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4

Vijayaraj, Panneerselvam, Jayaraja Sabarirajan, and Vasanthi Nachiappan. "Impaired phospholipid metabolism inSaccharomyces cerevisiaeby increased phospholipase B activity induced by 4-(methyl nitrosamino)-1-(3-pyridyl)-1-butanone." Toxicological & Environmental Chemistry 93, no. 4 (April 2011): 700–714. http://dx.doi.org/10.1080/02772248.2011.556638.

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5

Haglund, Johanna, Alistair P. Henderson, Bernard T. Golding, and Margareta Törnqvist. "Evidence for Phosphate Adducts in DNA from Mice Treated with 4-(N-Methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK)." Chemical Research in Toxicology 15, no. 6 (June 2002): 773–79. http://dx.doi.org/10.1021/tx015542o.

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6

Aizawa, Koichi, Chun Liu, Sudipta Veeramachaneni, Kang-Quan Hu, Donald E. Smith, and Xiang-Dong Wang. "Development of ferret as a human lung cancer model by injecting 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK)." Lung Cancer 82, no. 3 (December 2013): 390–96. http://dx.doi.org/10.1016/j.lungcan.2013.09.012.

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7

Lantry, L. E. "5-Aza-2'-deoxycytidine is chemopreventive in a 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone-induced primary mouse lung tumor model." Carcinogenesis 20, no. 2 (February 1, 1999): 343–46. http://dx.doi.org/10.1093/carcin/20.2.343.

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8

Kim, M. Y. "Combined treatment with 4-(N-methyl-N-nitrosamino)-1- (3-pyridyl)-1-butanone and dibutyl phthalate enhances ozone-induced genotoxicity in B6C3F1 mice." Mutagenesis 17, no. 4 (July 1, 2002): 331–36. http://dx.doi.org/10.1093/mutage/17.4.331.

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9

Kim, Min Young, and Myung Haing Cho. "Tumorigenesis in B6C3F1 mice exposed to ozone in combination with 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone and dietary dibutyl phthalate." Toxicology and Industrial Health 25, no. 3 (April 2009): 189–95. http://dx.doi.org/10.1177/0748233709106185.

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Although ozone exposure has been suspected as a risk factor for the development of lung cancer, data are still inconclusive. Studies in the literature infrequently recognize that the potential toxicity of ozone could be influenced by the combined exposure with other environmental carcinogens. To evaluate the carcinogenic potential of ozone alone or in combination with other toxicants, male and female B6C3F1 mice were exposed through inhalation and diet, to 0.5 ppm of ozone, 1.0 mg/kg of 4-( N-methyl- N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), 5000 ppm of dibutyl phthalate (DBP), individually and in combination for 1 year. No treatment-related death was seen, but significant differences in body and organ weights between control and treated mice were observed during the study. No tumor incidence was found in mice of either gender exposed to ozone alone. Pulmonary neoplasms were found in both, male and female mice exposed to NNK alone and in combination, ozone with NNK only or NNK plus DBP. Oviductal carcinomas were observed in females exposed to DBP alone and together with ozone plus NNK. These results indicate that ozone alone is not a lung carcinogen and in conjunction with NNK and/or DBP have no effect on tumor development in B6C3F1 mice under our experimental conditions.

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10

Jorquera, Rossana, Andre Castonguay, and Hildegard M. Schuller. "DNA single-strand breaks and toxicity induced by 4–(methyl-nitrosamino)–1–(3-pyridyl)-1-butanone or N-nitrosodimethylamine in hamster and rat liver." Carcinogenesis 15, no. 2 (1994): 389–94. http://dx.doi.org/10.1093/carcin/15.2.389.

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11

Karamanakos, Petros Nikolaos, D. T. P. Trafalis, G. D. Geromichalos, P. Pappas, P. Harkitis, M. Konstandi, and M. Marselos. "Inhibition of rat hepatic CYP2E1 by quinacrine: molecular modeling investigation and effects on 4-(methyl nitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced mutagenicity." Archives of Toxicology 83, no. 6 (August 27, 2008): 571–80. http://dx.doi.org/10.1007/s00204-008-0350-6.

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12

Chuang, Cheng-Hung, and Miao-Lin Hu. "Synergistic DNA damage and lipid peroxidation in cultured human white blood cells exposed to 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone and ultraviolet A." Environmental and Molecular Mutagenesis 47, no. 2 (2006): 73–81. http://dx.doi.org/10.1002/em.20168.

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13

Haneef, Mohd, Mohtashim Lohani, Anupam Dhasmana, Qazi M. S. Jamal, S. M. A. Shahid, and Sumbul Firdaus. "Molecular Docking of Known Carcinogen 4-(Methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) with Cyclin Dependent Kinases towards Its Potential Role in Cell Cycle Perturbation." Bioinformation 10, no. 8 (August 30, 2014): 526–32. http://dx.doi.org/10.6026/97320630010526.

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14

Kawano, Ryoji, Yukio Takeshima, and Kouki Inai. "Effects of K-rasGene Mutations in the Development of Lung Lesions Induced by 4-(N-Methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone in A/J Mice." Japanese Journal of Cancer Research 87, no. 1 (January 1996): 44–50. http://dx.doi.org/10.1111/j.1349-7006.1996.tb00198.x.

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15

KIM, Min Young, and M. Yung CHO. "Toxicity and Carcinogenicity of Ozone in Combination with 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone and Dibutyl Phthalate in B6C3F1 Mice for 16 and 32 Weeks." Biomedical and Environmental Sciences 22, no. 3 (June 2009): 216–22. http://dx.doi.org/10.1016/s0895-3988(09)60048-9.

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16

Kim, Min Young, Kyung Suk Song, Gun Ho Park, Seung Hee Chang, Hyun Woo Kim, Jin Hong Park, Hwa Jin, et al. "B6C3F1 mice exposed to ozone with 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone and/or dibutyl phthalate showed toxicities through alterations of NF-kappaB, AP-1, Nrf2, and osteopontin." Journal of Veterinary Science 5, no. 2 (2004): 131. http://dx.doi.org/10.4142/jvs.2004.5.2.131.

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17

Bhagwat, Shripad V., C. Vijayasarathy, Haider Raza, Jayati Mullick, and Narayan G. Avadhani. "Preferential effects of nicotine and 4-(N-methyl- N-nitrosamino)-1-(3-pyridyl)-1-butanone on mitochondrial glutathione S-transferase a4-4 induction and increased oxidative stress in the rat brain." Biochemical Pharmacology 56, no. 7 (October 1998): 831–39. http://dx.doi.org/10.1016/s0006-2952(98)00228-7.

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18

Qi, Haolong, Shanshan Wang, Juekun Wu, Shucai Yang, Steven Gray, Calvin S. H. Ng, Jing Du, Malcolm J. Underwood, Ming-Yue Li, and George G. Chen. "EGFR-AS1/HIF2A regulates the expression of FOXP3 to impact the cancer stemness of smoking-related non-small cell lung cancer." Therapeutic Advances in Medical Oncology 11 (January 2019): 175883591985522. http://dx.doi.org/10.1177/1758835919855228.

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Background: Early data showed that FOXP3 could induce epithelial-mesenchymal transition by stimulating the Wnt/β-catenin signaling pathway in non-small cell lung cancer (NSCLC). However, how the expression of FOXP3 is regulated in NSCLC remains unknown. We thus explored the impacts of the long noncoding RNA EGFR antisense RNA 1 (EGFR-AS1) and hypoxia-inducible factor-2A (HIF2A) on FOXP3 expression and the cancer stemness of NSCLC. Methods: Lung tissues samples from 87 patients with NSCLC and two NSCLC cell lines were used in this study. The regulation of FOXP3 and lung cancer cell stemness by EGFR-AS1 and HIF2A was determined at molecular levels in NSCLC tissue samples and cultured cells in the presence/absence of the smoking carcinogen, 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (also known as nicotine-derived nitrosamine ketone). The results were confirmed in tumor xenograft models. Results: We found that NNK decreased the expression of EGFR-AS1 in the long term, but increased the expression of HIF2A and FOXP3 to stimulate lung cancer cell stemness. EGFR-AS1 significantly inhibited FOXP3 expression and NSCLC cell stemness, whereas HIF2A obviously promoted both. The enhancement of lung cancer stemness by FOXP3 was, at least partially, via stimulating Notch1, as the inhibition of Notch1 could markedly diminish the effect of FOXP3. Conclusions: FOXP3, the expression of which is under the fine control of EGFR-AS1, is a critical molecule that promotes NSCLC cancer cell stemness through stimulating the Notch1 pathway.

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19

Li, M. Y., Johnson Yip, T. W. Lee, A. P. Yim, and George G. Chen. "THE PROLIFERATION OF NON-SMALL LUNG CANCER INDUCED 4-(N-METHYL-N-NITROSAMINO)-1-(3-PYRIDYL)-1-BUTANONE (NNK) CAN BE OFFSET BY TROGLITAZONE, A LIGAND OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR GAMMA." Chest 130, no. 4 (October 2006): 234S. http://dx.doi.org/10.1378/chest.130.4_meetingabstracts.234s-c.

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20

Rehan, Virender K., Reiko Sakurai, and John S. Torday. "Thirdhand smoke: a new dimension to the effects of cigarette smoke on the developing lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 301, no. 1 (July 2011): L1—L8. http://dx.doi.org/10.1152/ajplung.00393.2010.

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The underlying mechanisms and effector molecules involved in mediating in utero smoke exposure-induced effects on the developing lung are only beginning to be understood. However, the effects of a newly discovered category of smoke, i.e., thirdhand smoke (THS), on the developing lung are completely unknown. We hypothesized that, in addition to nicotine, other components of THS would also affect lung development adversely. Fetal rat lung explants were exposed to nicotine, 1-( N-methyl- N-nitrosamino)-1-(3-pyridinyl)-4-butanal (NNA), or 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), the two main tobacco-specific N-nitrosamine constituents of THS, for 24 h. We then determined key markers for alveolar paracrine signaling [epithelial differentiation markers surfactant phospholipid and protein synthesis; mesenchymal differentiation markers peroxisome proliferator-activated receptor γ (PPAR-γ), fibronectin and calponin], the BCL-2-to-Bax ratio (BCL-2/Bax), a marker of apoptosis and the involvement of nicotinic acetylcholine receptors (nAChR)-α3 and -α7 in mediating NNA's and NNK's effects on the developing lung. Similar to the effects of nicotine, exposure of the developing lung to either NNK or NNA resulted in disrupted homeostatic signaling, indicated by the downregulation of PPAR-γ, upregulation of fibronectin and calponin protein levels, decreased BCL-2/Bax, and the accompanying compensatory stimulation of surfactant phospholipid and protein synthesis. Furthermore, nAChR-α3 and -α7 had differential complex roles in mediating these effects. NNK and NNA exposure resulted in breakdown of alveolar epithelial-mesenchymal cross-talk, reflecting lipofibroblast-to-myofibroblast transdifferentiation, suggesting THS constituents as possible novel contributors to in utero smoke exposure-induced pulmonary damage. These data are particularly relevant for designing specific therapeutic strategies, and for formulating public health policies to minimize THS exposure.

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21

Onami, Saeko, Chigusa Okubo, Asuka Iwanaga, Hiroaki Suzuki, Hajime Iida, Yurie Motohashi, Yuki Tomonari, Seiji Otake, Hiroyuki Tsuji, and Hiroyuki Yoshimura. "Dosimetry for lung tumorigenesis induced by urethane, 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), and benzo[a]pyrene (B[a]P) in A/JJmsSlc mice." Journal of Toxicologic Pathology 30, no. 3 (2017): 209–16. http://dx.doi.org/10.1293/tox.2017-0005.

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22

Harpreet Kaur Gandhoke, Dr, Dr Vasanti Lagali Jirge, and Dr Anjana Bagewadi. "Assessment and comparison of the levels of N-nitrosonornicotine and 4-(n-methyl-n –nitrosamino) -1-(3-pyridyl)-1-butanone in the saliva of tobacco chewers and non- chewers -a hospital based study." International Journal of Dental Research 6, no. 2 (September 10, 2018): 66. http://dx.doi.org/10.14419/ijdr.v6i2.11943.

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Background: Studies estimating the Tobacco- specific nitrosamines, (TSNA’s) which are the strongest carcinogens in the saliva oftobacco users and tobacco quitters, are limited.Objectives: To assess and compare the levels of N- nitrosamines (NNN, NNK) in the saliva of tobacco chewers and non -chewers including those who have quit the habit of tobacco use.Methods: The study included 120 patients who were divided into three groups of 40 each: Group I- Smokeless tobacco chewersGroup II- Tobacco chewers who have completely stopped the habit at least 2 weeks prior to sample collection andGroup III- non-chewers. The salivary levels of two tobacco specific nitrosamines; NNN & NNK levels were estimated in the three study groups. Statistical analysis was done by Kruskal– Wallis, one-way analysis of variance (ANOVA) test, Mann-Whitney U test. (p-value < 0.05 was considered to be statistically significant)Results: In Group I, the mean level of NNN was 651.84 ± 359.78 and mean level of NNK was 168.32 ± 131.83. In Group II, the mean level of NNN was 119.52 ± 95.05 and mean level of NNK was 42.78 ± 43.19. In Group III, the mean level of NNN was 3.44 ±6.55 and mean level of NNK was 1.98 ± 3.68. There was a statistical difference in the 3 groups with respect to mean levels of NNN and NNK.Conclusion: The study indicated that salivary tobacco-specific nitrosamines are elevated in tobacco chewers. Saliva can be used to detect TSNA’s and screen for TSNA’s during each patient’s de-addiction process.

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23

Elisia, Ingrid, Mariah Hay, Michael Li, Brandon Cho, Vivian Lam, William Mohn, Hilary Leung, and Gerald Krystal. "The Effect of Diet on the Microbiome Composition and Incidence of NNK-Induced Lung Cancer." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 1557. http://dx.doi.org/10.1093/cdn/nzaa062_014.

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Abstract Objectives Since lowering carbohydrate (CHO) intake has been hypothesized to reduce cancer risk, we investigated whether low-CHO diets could prevent lung cancer in A/J mice, induced by the tobacco-specific carcinogen, 4-(N-methyl-N-nitrosamino)-1-(3- pyridyl)-1-butanone (NNK), and, if so if this corresponded to changes in gut microbiome composition. Methods We compared the effect of different quantities and types of CHO (easily digestible vs resistant), protein (casein vs. soy) and fat (fish vs. coconut vs. a mixture of oils) in modulating lung nodule formation and gut microbiome composition in A/J mice. Mice were fed either the Western diet or the low CHO diets, composed of different types of CHO, protein and fat for two weeks before injections with NNK to initiate lung formation. After 20 weeks, their feces were collected for amplification and sequencing of the bacterial 16S RNA gene V4 regions and the lung nodules were counted. Results Diets low in easily digestible starch, high in fish oil and soy protein were the most effective at preventing the formation of NNK-induced lung nodules. Changing protein, CHO and fat type in the diets all resulted in significant differences in the fecal microbiome composition of the NNK-injected mice. We also found a reduced abundance of the Streptococacceae and Clostridiaceae families in mice with low lung nodule numbers. Conclusions We suggest that it is possible that the diets reduced lung nodule formation, at least in part, via alterations in the microbiomes of the mice. Funding Sources Lotte & John Hecht Memorial Foundation.

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Kim, Min Young, Hyun Woo Kim, Jin Hong Park, Jun Sung Kim, Hwa Jin, Seo Hyun Moon, Kook Jong Eu, et al. "Molecular analysis of hprt mutation in B6C3F1 mice exposed to ozone alone and combined treatment of 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone and/or dibutyl phthalate for 32 and 52 weeks." Journal of Veterinary Science 5, no. 4 (2004): 379. http://dx.doi.org/10.4142/jvs.2004.5.4.379.

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25

Ye, Yi N., Edgar S. L. Liu, Vivian Y. Shin, William K. K. Wu, and Chi H. Cho. "The Modulating Role of Nuclear Factor-κB in the Action of α7-Nicotinic Acetylcholine Receptor and Cross-Talk between 5-Lipoxygenase and Cyclooxygenase-2 in Colon Cancer Growth Induced by 4-(N-Methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone." Journal of Pharmacology and Experimental Therapeutics 311, no. 1 (May 25, 2004): 123–30. http://dx.doi.org/10.1124/jpet.104.068031.

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26

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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Elisia, Ingrid, Brandon Cho, Mariah Hay, Michelle Yeung, Sara Kowalski, Jennifer Wong, Vivian Lam, and Gerald Krystal. "The Effect of Low Carbohydrate Diets on Preventing and Treating Carcinogen-Induced Lung Cancer in Mice." Current Developments in Nutrition 4, Supplement_2 (May 29, 2020): 323. http://dx.doi.org/10.1093/cdn/nzaa044_022.

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Abstract Objectives Since cancer cells typically rely more on glycolysis than normal cells, we hypothesized that lowering carbohydrate intake may reduce cancer risk. We aimed to investigate the efficacy of low-carbohydrate (CHO) diets in preventing and treating a tobacco-specific carcinogen-induced lung cancer in female A/J mice. Methods We evaluated the role of different types of CHO (easily digestible vs resistant), protein (casein vs. soy) and fat (fish vs. coconut vs. a mixture of oils) in modulating 4-(N-methyl-N-nitrosamino)-1-(3- pyridyl)-1-butanone (NNK)-induced lung nodule formation in these mice. To assess the efficacy of these diets in preventing NNK-induced lung nodule formation, we put these mice in the different diets for 2 weeks, intraperitoneally-injected NNK once a week for two weeks to initiate lung nodule formation. After 5 months, the lung nodules in these mice were counted. Results The lowering of easily digestible CHO significantly reduced constitutive blood glucose levels and lung nodule formation in the mice. Interestingly, diets low in easily digestible starch, high in fish oil (FO) and soy protein (15%Amylose/Soy/FO) were the most effective at preventing the formation of NNK-induced lung nodules. To determine if this 15%Amylose/Soy/FO is also effective at slowing tumor progression, we fed NNK-injected A/J mice a Western diet until tumors were established (5 months post NNK) and then either switched them to the 15%Amylose/Soy/FO or kept them on the Western diet for 5 additional months. The 15%Amylose/Soy/FO diet prevented the formation of additional lung tumor nodules and reduced the size of the tumors, although no significant difference was observed in tumor stage. The reduction in size of the lung tumors on the 15%Amylose/Soy/FO diet was not due to a lower tumor proliferation (Ki67 index) but an increase in apoptosis, as determined by TUNEL assays. Conclusions We conclude that a diet change that lowers glucose intake, incorporates FO and soy protein may be effective not only in preventing lung cancer formation but also in slowing the growth of established lung tumors. Funding Sources Lotte & John Hecht Memorial Foundation.

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28

Moldoveanu, SC, and M. Borgerding. "Formation of Tobacco Specific Nitrosamines in Mainstream Cigarette Smoke; Part 1, FTC Smoking." Beiträge zur Tabakforschung International/Contributions to Tobacco Research 23, no. 1 (April 1, 2008): 19–31. http://dx.doi.org/10.2478/cttr-2013-0845.

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AbstractThis report evaluates the formation of nitrosonornicotine (NNN) and of 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) from nicotine, and of NNN from nornicotine in the mainstream smoke of a burning cigarette. The cigarettes analyzed in the study were Kentucky reference cigarettes 1R4F and 2R4F, and five other cigarettes, three of them having tobaccos with low levels of tobacco specific nitrosamines (TSNAs). All cigarettes had ‘tar’ levels around 10 mg [where ‘tar’ is defined as the weight of total wet particulate matter (TPM) minus the weight of nicotine and water]. Cigarettes were smoked according to the U.S. Federal Trade Commission (FTC) puffing regimen, using a 35 mL puff volume, 2 sec puff duration and 60 sec puff intervals. Three separate experiments were performed in this study to evaluate the proportion of TSNAs transferred from preexistent tobacco TSNAs and the proportion formed during smoking (pyrosynthesized). In one experiment, the results were obtained by GC/MS analysis of 13C3-TSNAs formed in smoke when 13C3-nicotine was intentionally added to cigarettes. Another experiment used GC analysis with chemiluminescence detection of TSNAs from smoke before and after an excess of nornicotine was intentionally added to cigarettes, and another experiment consisted of LC/MS/MS analysis of 2H4-TSNAs formed in the smoke when 2H4-nicotine and when 2H4-nornicotine were intentionally added to cigarettes. The use of different analytical methods for the study of TSNA formation conveyed an additional level of confidence regarding the reliability of the results obtained. It was found that NNK was generated during smoking from nicotine with 3 × 10-5% to 8 × 10-5% conversion (0.3 ppm to 0.8 ppm conversion of the nicotine) while the result for NNN generation was not conclusive. One experiment demonstrated the formation of NNN from nicotine between 4 × 10-5% and 1.5 × 10-4% (0.4 ppm to 1.5 ppm reported to nicotine), but another experiment did not provide proof of NNN formation, with a limit of quantitation LOQ for NNN corresponding to 5 × 10-5% (or 0.5 ppm). Nornicotine was proven to generate NNN, and the results for the 2R4F cigarette showed 3.3 × 10-3% yield (33 ppm reported to nornicotine) in one experiment and 4.6 × 10-3% (46 ppm reported to nornicotine) in a different experiment, the agreement being very good. Using the results from this study, it was concluded that pyrosynthesis may account for about 5% to 10% of the NNK in mainstream smoke for a filter cigarette with the FTC ‘tar’ level around 10 mg. Pyrosynthesis may account for higher proportions of smoke TSNAs when the cigarette tobacco is low in TSNAs, since the mainstream smoke TSNAs yield from direct transfer from tobacco is small in this case. The contribution of pyrosynthesis may account for 5% to 25% of NNN in mainstream cigarette smoke, or potentially an even higher proportion when the tobacco blend is both low in TSNAs and high in nornicotine. Anabasine is typically present at low levels in tobacco and therefore the formation of nitrosoanabasine(NAB) is of less interest. Anatabine is present in different tobaccos in a range similar to that of nornicotine and being a secondary amine has the potential to act similarly to nornicotine. However, the pyrosynthesis of nitrosoanatabine (NAT) from anatabine was not evaluated in the present study. The study indicated that complete elimination of TSNAs from tobacco is unlikely to completely eliminate the TSNAs from cigarette smoke, and that high nornicotine tobaccos should be avoided in order to minimize the levels of NNN in cigarette smoke.

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