Multi-alkylated Polynuclear Aromatic Hydrocarbons of Tobacco Smoke: Separation and Identification

Snook, M. E.; Severson, Ray F.; Arrendale, Richard F.; Higman, Howard C.; Chortyk, O. T.

doi:10.2478/cttr-2013-0452

Cited by 16 publications

(20 citation statements)

References 8 publications

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“…For cyclopenta[ c,d ]pyrene and dibenzo[ a,l ]pyrene, there are very limited or no data on their quantities in cigarette smoke, and fairly limited data have been presented for dibenz[ a,h ]anthracene 6. There are multiple PAH in cigarette smoke possibly including unidentified carcinogens 46–48…”

Section: Lung Carcinogens In Cigarette Smokementioning

confidence: 99%

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Lung carcinogenesis by tobacco smoke

Hecht

2012

Intl Journal of Cancer

392

299

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Cigarette smoke is a complex mixture of chemicals including multiple genotoxic lung carcinogens. The classic mechanisms of carcinogen metabolic activation to DNA adducts, leading to miscoding and mutations in critical growth control genes, applies to this mixture but some aspects are difficult to establish because of the complexity of the exposure. This paper discusses certain features of this mechanism including the role of nicotine and its receptors; lung carcinogens, co-carcinogens and related substances in cigarette smoke; structurally characterized DNA adducts in the lungs of smokers; the mutational consequences of DNA adduct formation in smokers’ lungs; and biomarkers of nicotine and carcinogen uptake as related to lung cancer. While there are still uncertainties which may never be fully resolved, the general mechanisms by which cigarette smoking causes lung cancer are well understood and provide insights relevant to prevention of lung cancer, the number one cancer killer in the world, causing 1.37 million deaths per year.

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Section: Lung Carcinogens In Cigarette Smokementioning

confidence: 99%

“…6 There are multiple PAH in cigarette smoke possibly including unidentified carcinogens. [46][47][48]…”

Section: Variants In Nicotinic Acetylcholine Receptor Subunit Genes Cmentioning

confidence: 99%

Lung carcinogenesis by tobacco smoke

Hecht

2012

Intl Journal of Cancer

392

299

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“…Other carcinogens not evaluated by IARC are also likely to be present. For example, among the PAH, multiple alkylated and high molecular-weight compounds have been detected, but are incompletely characterized with respect to their carcinogenicity (Snook et al, 1978). Eighteen Nnitrosamines are present in cigarette smoke (Hoffmann et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

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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“…1 Consequently, the 16 priority PAHs or their subsets in ETS were investigated concerning their levels, compositions, 1,6,9 and toxicity, 5 as well as the influence of smoking conditions and cigarette design on the chemical delivery. 7,10,11 However, as cigarette smoke is a complex mixture with multiple classes of chemical compounds, more PAHs, such as alkylated and sulfur/oxygen (S/O) PAHs, also exist in cigarette smoke, 12,13 either being possible human carcinogens or promoters for the carcinogenicity of other PAHs. 6 Previous studies have evidenced that some alkylated and S/O PAHs were more toxic than their parent ones.…”

Section: ■ Introductionmentioning

confidence: 99%

Parent, Alkylated, and Sulfur/Oxygen-Containing Polycyclic Aromatic Hydrocarbons in Mainstream Smoke from 13 Brands of Chinese Cigarettes

Gao

Wang

et al. 2015

Environ. Sci. Technol.

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China has the world's largest population of smokers with serious health consequences, yet we know a very limited spectrum of hazardous chemicals in cigarette smoke even for carcinogenic polycyclic aromatic hydrocarbons (PAHs). Here, we chose 13 popular cigarette brands sold in China markets, collected particulate matters in mainstream smoke using filter pads and an automatic smoking machine, and analyzed 56 PAHs, including 31 parent, 18 alkylated, and 7 sulfur/oxygen-containing PAHs (S/O PAHs). The 56 PAHs in mainstream smoke totaled from 244.2 ± 28.5 to 10254.8 ± 481.5 ng cig −1 ; parent, alkylated, and S/O PAHs shared 16−23%, 64−74%, and 6−18%, respectively. Benzo[a]pyrene (BaP) ranged 1.1−41.6 ng cig −1 , while BaP equivalent concentrations (BaP eq ) ranged 3.6− 120.2 ng cig −1 , but contributions to BaP eq by individual carcinogenic PAH species varied with cigarette brands. When these cigarette smoke source profiles were pooled together with those of other combustion ones available in the literature, we found that widely used diagnostic ratios of parent PAHs failed to distinguish cigarette smoke from other combustion sources, except that the ratio indeno [1,2,3-cd]pyrene/(indeno[1,2,3-cd]pyrene + benzo[g,h,i]perylene) can largely separate cigarette smoke from vehicular emissions and that the ratio of Retene/(Retene + chrysene) can further discriminate cigarette smoke from coal combustion when alkylated PAHs are involved.

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Multi-alkylated Polynuclear Aromatic Hydrocarbons of Tobacco Smoke: Separation and Identification

Cited by 16 publications

References 8 publications

Lung carcinogenesis by tobacco smoke

Lung carcinogenesis by tobacco smoke

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

Parent, Alkylated, and Sulfur/Oxygen-Containing Polycyclic Aromatic Hydrocarbons in Mainstream Smoke from 13 Brands of Chinese Cigarettes

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