Relation between chemical constituents of tobacco and mutagenic activity of cigarette smoke condensate

Mizusaki, Shigenobu; Okamoto, Hitoshi; Akiyama, Alan; Fukuhara, Yoko

doi:10.1016/0027-5107(77)90175-0

Cited by 83 publications

(17 citation statements)

References 7 publications

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“…This study also showed that nicotine alone had no mutagenic activity and did not affect the slope of CSC-F-induced mutation in the Ames test when added back to mirror the levels found in CSC-L. This is in agreement with prior reports (Mizusaki et al 1977).…”

Section: Discussionsupporting

confidence: 82%

Toxicological analysis of low-nicotine and nicotine-free cigarettes

et al. 2008

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Section: Discussionsupporting

confidence: 82%

Toxicological analysis of low-nicotine and nicotine-free cigarettes

et al. 2008

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“…There also is evidence that nicotine may promote metastasis because of stimulation of cell motility and migration (13,18). Although nicotine may be able to form DNA adducts, it generally is not genotoxic (27)(28)(29)(30)(31)(32)(33). Taken together, these studies support the hypothesis that nicotine could enhance carcinogenesis and raise a concern that nicotine could promote carcinogenesis in former smokers, who have a background of initiated cells with genetic damage left over from the earlier smoking days.…”

supporting

confidence: 73%

Long-term Nicotine Replacement Therapy: Cancer Risk in Context

Shields

2011

Cancer Prevention Research

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Nicotine replacement therapy (NRT) for up to 12 weeks is well established, safe and efficacious for fostering smoking cessation. Some smokers at a high risk of relapse may benefit from long-term use, and so long-term NRT safety and efficacy have become a paramount question for the FDA and others. Laboratory studies have indicated a carcinogenic potential of nicotine. Animal model studies reported in this issue of the journal by Maier and colleagues (beginning on page 1743) and Murphy and colleagues (beginning on page 1752), however, provide additional reassurance that NRT does not promote lung cancer. Very long-term studies of NRT effects do not yet exist and would be needed to definitively answer the question about NRT efficacy and cancer risk and some decision making will need to be made based on limited human data and experimental studies. The overall NRT safety question is complex and requires consideration of three contexts and comparator groups (long-term NRT/abstinence vs. smoking, long-term intermittent NRT/ reduced smoking vs. smoking, and long-term NRT/abstinence vs. abstinence without long-term NRT). Although the data on these issues are insufficient, the first comparison seems intuitive and may be compelling enough to allow the FDA to approve a long-term indication for NRT. An important public health goal is to help smokers and their health care providers understand the implications of potential long-term NRT risks in the context of its potential benefits and the far greater risks of continued smoking. Cancer Prev Res; 4(11); 1719-23. Ó2011 AACR.The efficacy and safety of short-term nicotine replacement therapy (NRT) for fostering long-term smoking cessation is well established, and up to 12 weeks of therapy is approved by the U.S. Food and Drug Administration (FDA; refs. 1-4). A meta-analysis indicates that there are measurable benefits in studies of 12 to 18 months of continued NRT use for relapse prevention (5), and other studies also indicate that this use is cost effective (6). An important question of considerable interest that remains today, however, is whether NRT can be recommended for long-term use, even years, to continue to promote smoking abstinence. The answer to this question requires both an efficacy and safety assessment. In this context, NRT conceptually has substantial benefits compared with long-term smoking but also, as explained later and addressed in this issue of the journal, laboratory studies suggest a potential for nicotine to foster the development of cancer.The premise of long-term NRT use is that it would prevent smoking relapse, and the risks would be limited to maintaining nicotine addiction, but without the adverse consequences of continued smoking, such as increased lung cancer risk. Like the consideration of other long-term medications, on face value it is a simple risk-benefits equation. In actuality, however, this question is not simple to answer because the risk can be considered in 3 different contexts and comparator groups namely: (i) what is the risk o...

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“…Low-nitrogen tobacco blends have been reported to result in the reduction of some biologically active aromatic nitrogen compounds in tobacco smoke (Hoffmann et al, 1980;Schmeltz and Hoffmann, 1977;Benner et al, 1968) and low-nitrogen tobacco blends have exhibited reduced mutagenicity in bacteria compared to higher nitrogen tobacco blends (Munoz et al, 1968;Mizusaki et al, 1977). The low-nitrogen tobacco blend used in this study reduced mutagenic potential in the Salmonella strain TA98 compared to the experimental cigarette in the study containing a standard commercial tobacco blend.…”

Section: Discussionmentioning

confidence: 81%

Evaluation of the Genotoxic and Cytotoxic Potential of Mainstream Whole Smoke and Smoke Condensate from a Cigarette Containing a Novel Carbon Filter

Bombick

Ayres

et al. 1997

Toxicol Sci

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A novel carbon filter has been developed which primarily reduces the amount of certain vapor phase constituents of tobacco smoke with greater efficiency than the charcoal filters of cigarettes currently in the market In vitro indicators of genotoxic and cytotoxic potential were used to compare the cigarette smoke condensate (particulate phase) or whole cigarette smoke (vapor phase and particulate phase) from cigarettes containing the novel carbon filter with smoke condensate or whole smoke from commercial or prototype cigarettes not containing the novel carbon filter. Ames bacterial mutagenicity, sister chromatid exchange (SCE) in Chinese hamster ovary (CHO) cells, and neutral red cytotoxicity assays in CHO cells were utilized to assess the genotoxic and cytotoxic potential of the cigarette smoke condensates. SCE and neutral red cytotoxicity assays were utilized to assess the genotoxic and cytotoxic potential of the whole smoke. As expected, the novel carbon filter did not significantly affect the genotoxic or cytotoxic activity of the smoke condensate, although we did observe that the use of low-nitrogen tobacco reduced the mutagenicity of the condensate in Salmonella typhimurium strain TA98. However, the whole smoke from cigarettes containing the novel carbon filter demonstrated significant reductions in genotoxic and cytotoxic potential compared to cigarettes without the novel carbon filter. The toxicity of the smoke was correlated (r = 0.7662 for cytotoxicity and r -0.7562 for SCE induction) to the aggregate mass of several vapor phase components (acetone, acetaldehyde, acrolein, acrylonitrile, 1, ammonia, NO,, HCN, benzene, isoprene, and formaldehyde) in the smoke of the cigarettes utilized in this study. In conclusion, this novel carbon filter, which significantly reduced the amount of carbonyls and other volatiles in mainstream cigarette smoke, resulted in significant reductions in the genotoxic and cytotoxic activity of the smoke as measured by these assays.S 1997 Society of Toxicology.

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Relation between chemical constituents of tobacco and mutagenic activity of cigarette smoke condensate

Cited by 83 publications

References 7 publications

Toxicological analysis of low-nicotine and nicotine-free cigarettes

Toxicological analysis of low-nicotine and nicotine-free cigarettes

Long-term Nicotine Replacement Therapy: Cancer Risk in Context

Evaluation of the Genotoxic and Cytotoxic Potential of Mainstream Whole Smoke and Smoke Condensate from a Cigarette Containing a Novel Carbon Filter

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