Toxicological analysis of low-nicotine and nicotine-free cigarettes

Chen, Jinguo; Higby, Richard; Tian, Defa; D, Tan; Johnson, Michael D.; Xiao, Yingxian; Kellar, Kenneth J.; Feng, Shibao; Shields, Peter G.

doi:10.1016/j.tox.2008.05.009

Cited by 36 publications

(38 citation statements)

References 45 publications

(55 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nitrosamines and polycyclic aromatic amines are considered important chemical agents able to promote genetic insult as far as carcinogenesis [15]. In this regard, it has been postulated that nicotine attenuates the acute toxic effects of tobacco condensate in cultured human epithelial cells [29]. …”

Section: Discussionmentioning

confidence: 99%

Cytogenetic Biomonitoring in Buccal Mucosa Cells from Young Smokers

et al. 2015

View full text Add to dashboard Cite

Objective: Nowadays, much attention has been focused on the search for new non-invasive methodologies able to predict malignant transformation of oral mucosa cells. The aim of the present study was to comparatively evaluate DNA damage (micronucleus) and cellular death (pyknosis, karyolysis and karyorrhexis) in exfoliated oral mucosa cells from smokers and non-smokers in buccal mucosa cells. Study Design: A total of 24 young, healthy smokers and 14 non-smokers were included in this setting. Individuals had epithelial cells from the cheek mechanically exfoliated, placed in fixative and dropped in clean slides which were checked for the above nuclear phenotypes. Results: Smokers presented more (p < 0.05) micronucleated oral mucosa cells than non-smokers. Tobacco smoke was not able to increase other nuclear alterations closely related to cytotoxicity such as karyorrhexis, pyknosis and karyolysis. Conclusion: In summary, these data indicate that the cigarette is able to induce micronuclei in oral mucosa cells, so the micronucleus test is a suitable method for predicting oral cancer risk.

show abstract

Section: Discussionmentioning

confidence: 99%

Cytogenetic Biomonitoring in Buccal Mucosa Cells from Young Smokers

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Such products are assumed to be able to control/reduce or even eliminate nicotine delivery, and reduce toxicity or mutagenicity of cigarette smoke. However, some studies have found that the new cigarettes may be actually more harmful than the conventional ones due to compensatory smoking patterns and/or specific device designs of some PREPs (Brooks et al, 2005;Laugesen & Fowles, 2006;Chen et al, 2008;Lin et al, 2009Lin et al, , 2010among others). In fact, PREPs with tobacco reconstitution and new device designs may also alter a smoker's puffing and post-puffing behavior, smoke particle characteristics (e.g., size distribution, hygroscopity), and exposure conditions (i.e., temperature, humidity, and number concentrations).…”

Section: Introductionmentioning

confidence: 99%

Size-change and deposition of conventional and composite cigarette smoke particles during inhalation in a subject-specific airway model

Zhang

Kleinstreuer

Hyun

2012

Journal of Aerosol Science

View full text Add to dashboard Cite

“…Smoking harms nearly every organ in the body, causing many diseases and reducing the health of smokers in general (Das, 2003; Department of Health and Human Services [U.S.], 2004). Cigarette smoke contains more than 4000 chemicals, including more than 60 carcinogens (Chen et al, 2008). Comparisons of different cigarette types have clearly demonstrated differences in the chemical composition of the smoke as a function of additives (Baker et al, 2004a), paper type (Baker et al, 2004b), tobacco processing (Martin et al, 2003), and other manufacturer-specific features (Harris, 2001).…”

mentioning

confidence: 99%

“…However, there is also evidence for compensatory behavioral changes (increased puff volume and frequency and increased numbers of cigarettes smoked) (Djordjevic et al, 2000;Kabat, 2003) that result in altered smoke composition (Counts et al, 2005) and increased exposure to harmful components of cigarette smoke. Of potentially greater concern is evidence that cigarette smoke condensates (CSC) from low-nicotine cigarettes are more toxic to normal human bronchial epithelial (NHBE) cells than CSC from high-nicotine cigarettes, possibly due to nicotine-mediated suppression of apoptotic pathways (Chen et al, 2008). Therefore, understanding the consequences of differences in smoke composition as a function of cigarette design and smoking behavior is important in reducing the health burden of cigarette smoking.…”

mentioning

confidence: 99%

Effects Of 10 Cigarette Smoke Condensates On Primary Human Airway Epithelial Cells By Comparative Gene And Cytokine Expression Studies

Pickett¹,

Seagrave²,

Boggs³

et al. 2010

D23. Recent Advances on Smoking Health Effects

View full text Add to dashboard Cite

Cigarettes vary in tobacco blend, filter ventilation, additives, and other physical and chemical properties, but little is known regarding potential differences in toxicity to a smoker's airway epithelia. We compared changes in gene expression and cytokine production in primary normal human bronchial epithelial cells following treatment for 18 h with cigarette smoke condensates (CSCs) prepared from five commercial and four research cigarettes, at doses of~4 mg/ml nicotine. Nine of the CSCs were produced under a standard International Organization for Standardization smoking machine regimen and one was produced by a more intense smoking machine regimen. Isolated messenger RNA (mRNA) was analyzed by microarray hybridization, and media was analyzed for secreted cytokines and chemokines. Twenty-one genes were differentially expressed by at least 9 of the 10 CSCs by more than twofold, including genes encoding detoxifying and antioxidant proteins. Cytochrome P450, family 1, subfamily A, polypeptide 1 (CYP1A1) and NAD(P)H dehydrogenase, quinone 1 (NQO-1) were selected for validation with quantitative real-time PCR (qRT-PCR) and Western blot analyses. NQO-1 expression determined with microarrays, qRT-PCR, and Western blotting differed among the CSC types, with good correlation among the different assays. CYP1A1 mRNA levels varied substantially, but there was little correlation with the protein levels. For each CSC, the three most induced and three most repressed genes were identified. These genes may be useful as markers of exposure to that particular cigarette type. Furthermore, differences in interleukin-8 secretion were observed. These studies lay the foundation for future investigations to analyze differences in the responses of in vivo systems to tobacco products marketed with claims of reduced exposure or reduced harm.

show abstract

Toxicological analysis of low-nicotine and nicotine-free cigarettes

Abstract: Low-nicotine and nicotine-free cigarettes are commercially available under the brand-name Quest®.

Cited by 36 publications

References 45 publications

Cytogenetic Biomonitoring in Buccal Mucosa Cells from Young Smokers

Cytogenetic Biomonitoring in Buccal Mucosa Cells from Young Smokers

Size-change and deposition of conventional and composite cigarette smoke particles during inhalation in a subject-specific airway model

Effects Of 10 Cigarette Smoke Condensates On Primary Human Airway Epithelial Cells By Comparative Gene And Cytokine Expression Studies

Contact Info

Product

Resources

About