A comparison of the mainstream smoke chemistry and mutagenicity of a representative sample of the US cigarette market with two Kentucky reference cigarettes (K1R4F and K1R5F)

Chepiga, T.A; Morton, Michael J.; Murphy, Patricia A.; Avalos, Jerry; Bombick, Betsy; Doolittle, David J.; Borgerding, Michael F.; Swauger, James E.

doi:10.1016/s0278-6915(00)00086-7

Cited by 127 publications

(80 citation statements)

References 14 publications

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“…Fischer et al showed that there was no correlation between levels of NNK in mainstream smoke and tar yield of German cigarettes, using the FTC method, although Chepiga et al did observe a correlation in U.S. cigarettes (5,24). Fischer et al proposed that the total volume drawn through a cigarette was the main factor influencing NNK delivery (25).…”

Section: Discussionmentioning

confidence: 99%

“…Cigarettes are currently classified into three categories based on tar measurements using the FTC method. Cigarettes with tar levels of >14.5 mg are called ''regular,'' those with >6.5 to 14.5 mg tar are termed ''light,'' and those with V6.5 mg tar are called ''ultralight'' (5). Inherent in this terminology is the implied message that light and ultralight cigarettes are less harmful.…”

Section: Introductionmentioning

confidence: 99%

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Similar Uptake of Lung Carcinogens by Smokers of Regular, Light, and Ultralight Cigarettes

Hecht

Murphy

Carmella

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

119

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Cigarette design has changed markedly over the past 60 years and sales-weighed levels of tar and nicotine have decreased. Currently, cigarettes are classified as regular (>14.5 mg tar), light (>6.5-14.5 mg tar), and ultralight (V V 6.5 mg tar), based on a Federal Trade Commission -specified machine-smoking protocol. Epidemiologic studies suggest that there is no difference in lung cancer risk among people who smoke light or ultralight cigarettes compared with regular cigarettes, but the uptake of lung carcinogens in smokers of these types of cigarettes has never been reported. We recruited 175 smokers, who filled out a tobacco use questionnaire in which their current brand was identified as regular, light, or ultralight. Urine samples were collected and analyzed for 1-hydroxypyrene (1-HOP), total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL plus its glucuronides) and total cotinine (cotinine plus its glucuronides). 1-HOP and total NNAL are biomarkers of uptake of polycyclic aromatic hydrocarbons and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, lung carcinogens in cigarette smoke. Total cotinine is a biomarker of nicotine uptake. There were no statistically significant differences in urinary levels of 1-HOP, total NNAL, and total cotinine in smokers of regular, light, and ultralight cigarettes, whether the results were expressed per mg urinary creatinine, per mL of urine, or per mg creatinine divided by cigarettes per day. Levels of machine measured tar were available for the cigarettes smoked by 149 of the subjects. There was no correlation between levels of tar and any of the biomarkers. These results indicate that lung carcinogen and nicotine uptake, as measured by urinary 1-HOP, total NNAL, and total cotinine is the same in smokers of regular, light, and ultralight cigarettes. The results are consistent with epidemiologic studies that show no difference in lung cancer risk in smokers of these cigarettes.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Similar Uptake of Lung Carcinogens by Smokers of Regular, Light, and Ultralight Cigarettes

Hecht

Murphy

Carmella

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

119

View full text Add to dashboard Cite

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“…Its sales-weighted concentration in current 'full-flavored' cigarettes is about 9 ng per cigarette (Chepiga et al, 2000). The abundant literature on BaP tends to diminish attention to other PAH such as dibenz [a,h]anthracene, 5-methylchrysene, and dibenzo[a,i]pyrene which are substantially stronger lung tumorigens than BaP in mice or hamsters, but occur in lower concentrations in cigarette smoke than does BaP (Nesnow et al, 1995;Sellakumar and Shubik, 1974).…”

Section: Tobacco Smoke Carcinogens and Cancermentioning

confidence: 99%

“…NNK is the most abundant systemic lung carcinogen in cigarette smoke. Multiple international studies definitively document the presence of NNK in cigarette smoke; its sales-weighted concentration in current 'full-flavored cigarettes' is 131 ng/ cigarette (Chepiga et al, 2000;Spiegelhalder and Bartsch, 1996;Hecht and Hoffmann, 1988).…”

Section: Tobacco Smoke Carcinogens and Cancermentioning

confidence: 99%

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Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers

et al. 2002

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It is estimated that cigarette smoking kills over 1 000 000 people each year by causing lung cancer as well as many other neoplasmas. p53 mutations are frequent in tobaccorelated cancers and the mutation load is often higher in cancers from smokers than from nonsmokers. In lung cancers, the p53 mutational patterns are different between smokers and nonsmokers with an excess of G to T transversions in smoking-associated cancers. The prevalence of G to T transversions is 30% in smokers' lung cancer but only 12% in lung cancers of nonsmokers. A similar trend exists, albeit less marked, in laryngeal cancers and in head and neck cancers. This type of mutation is infrequent in most other tumors aside from hepatocellular carcinoma. At several p53 mutational hotspots common to all cancers, such as codons 248 and 273, a large fraction of the mutations are G to T events in lung cancers but are almost exclusively G to A transitions in non-tobacco-related cancers. Two important classes of tobacco smoke carcinogens are the polycyclic aromatic hydrocarbons (PAH) and the nicotine-derived nitrosamines. Recent studies have indicated that there is a strong coincidence of G to T transversion hotspots in lung cancers and sites of preferential formation of PAH adducts along the p53 gene. Endogenously methylated CpG dinucleotides are the preferred sites for G to T transversions, accounting for more than 50% of such mutations in lung tumors. The same dinucleotide, when present within CpGmethylated mutational reporter genes, is the target of G to T transversion hotspots in cells exposed to the model PAH compound benzo[a]pyrene-7,8-diol-9,10-epoxide. As summarized here, a number of other tobacco smoke carcinogens also can cause G to T transversion mutations. The available data suggest that p53 mutations in lung cancers can be attributed to direct DNA damage from cigarette smoke carcinogens rather than to selection of pre-existing endogenous mutations.

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Cyanide

Pulster¹,

Hillman²

2015

Hamilton &Amp; Hardy's Industrial Toxicology

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A comparison of the mainstream smoke chemistry and mutagenicity of a representative sample of the US cigarette market with two Kentucky reference cigarettes (K1R4F and K1R5F)

Cited by 127 publications

References 14 publications

Similar Uptake of Lung Carcinogens by Smokers of Regular, Light, and Ultralight Cigarettes

Similar Uptake of Lung Carcinogens by Smokers of Regular, Light, and Ultralight Cigarettes

Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers

Cyanide

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