Dataset Information

The impacts of including information about the number of carcinogens in smoke on standardized cigarette packs in the UK.

ABSTRACT:

Background

Since May 2017, standardized packaging has been mandatory in the UK, with packs required to display an 'information message' explaining that there are more than 70 carcinogens in tobacco smoke.

Methods

Three waves of a longitudinal online survey in the UK with smokers pre-standardized packaging (Wave 1: April-May 2016) and followed up post-standardized packaging (Wave 2: September-November 2017, Wave 3: May-July 2019). Of the 6233 smokers at Wave 1, 4293 responded at Wave 2 and 3175 at Wave 3. We explored knowledge of the number of carcinogens in smoke, and whether knowing that smoke contains more than 70 carcinogens mediated change in the belief that the dangers of smoking are exaggerated (risk perception), stubbing out cigarettes, quit intentions and quitting. As the information message is larger on roll-your-own packs than on cigarette packs, as the packs are larger, we also explored whether there was any difference in knowing that smoke contains more than 70 carcinogens between exclusive cigarette smokers and exclusive roll-your-own smokers.

Results

Knowledge that there are over 70 carcinogens in smoke increased among smokers across waves, with the increase from Waves 1 to 3 greater for exclusive roll-your-own smokers than exclusive cigarette smokers (adjusted odds ratio=1.44; 95% CI 1.03-2.03). Knowledge that there are over 70 carcinogens in smoke mediated higher risk perception but not stubbing cigarettes out, quit intentions or quitting.

Conclusions

The information message improved knowledge of how many carcinogens are in smoke, particularly among exclusive roll-your-own smokers, and this was linked to higher risk perception.

SUBMITTER: Moodie C

PROVIDER: S-EPMC8546877 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature

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Publications

The impacts of including information about the number of carcinogens in smoke on standardized cigarette packs in the UK.

Moodie Crawford C Best Catherine C Critchlow Nathan N Hitchman Sara S Stead Martine M McNeill Ann A

European journal of public health 20211001 5

<h4>Background</h4>Since May 2017, standardized packaging has been mandatory in the UK, with packs required to display an 'information message' explaining that there are more than 70 carcinogens in tobacco smoke.<h4>Methods</h4>Three waves of a longitudinal online survey in the UK with smokers pre-standardized packaging (Wave 1: April-May 2016) and followed up post-standardized packaging (Wave 2: September-November 2017, Wave 3: May-July 2019). Of the 6233 smokers at Wave 1, 4293 responded at Wa ...[more]

PMID: 34519345

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Project description:Background:Mitochondrial dysfunction is an important component of the aging process and has been implicated in the development of many human diseases. Mitochondrial DNA copy number (mtDNAcn), an indirect biomarker of mitochondrial function, is sensitive to oxidative damage. Few population-based studies have investigated the impact of fruit and vegetable consumption and cigarette smoke (2 major sources of exogenous antioxidants and oxidants) on leukocyte mtDNAcn. Objectives:We investigated the association between fruit and vegetable consumption, cigarette smoke, and leukocyte mtDNAcn based on data from the Nurses' Health Study (NHS). Methods:Data from 2769 disease-free women in the NHS were used to examine the cross-sectional associations between dietary sources of antioxidants, cigarette smoke, and leukocyte mtDNAcn. In vitro cell-based experiments were conducted to support the findings from the population-based study. Results:In the multivariable-adjusted model, both whole-fruit consumption and intake of flavanones (a group of antioxidants abundant in fruit) were positively associated with leukocyte mtDNAcn (P-trend = 0.005 and 0.02, respectively), whereas pack-years of smoking and smoking duration were inversely associated with leukocyte mtDNAcn (P-trend = 0.01 and 0.007, respectively). These findings are supported by in vitro cell-based experiments showing that the administration of naringin, a major flavanone in fruit, led to a substantial increase in mtDNAcn in human leukocytes, whereas exposure to nicotine-derived nitrosamine ketone, a key carcinogenic ingredient of cigarette smoke, resulted in a significant decrease in mtDNAcn of cells (all P < 0.05). Further in vitro studies showed that alterations in leukocyte mtDNAcn were functionally linked to the modulation of mitochondrial biogenesis and function. Conclusions:Fruit consumption and intake of dietary flavanones were associated with increased leukocyte mtDNAcn, whereas cigarette smoking was associated with decreased leukocyte mtDNAcn, which is a promising biomarker for oxidative stress-related health outcomes.

Project description:Mutations in somatic cells are inflicted by both extrinsic and intrinsic sources and contribute over time to cancer. Tobacco smoke contains chemical carcinogens that have been causatively implicated with cancers of the lung and head & neck1,2. APOBEC family DNA cytosine deaminases have emerged as endogenous sources of mutation in cancer, with hallmark mutational signatures (SBS2/SBS13) that often co-occur in tumors of tobacco smokers with an equally diagnostic mutational signature (SBS4)3,4. Here we challenge the dogma that mutational processes are thought to occur independently and with additive impact by showing that 4-nitroquinoline 1-oxide (NQO), a model carcinogen for tobacco exposure, sensitizes cells to APOBEC3B (A3B) mutagenesis and leads to synergistic increases in both SBS2 mutation loads and oral carcinomas in vivo. NQO-exposed/A3B-expressing animals exhibit twice as many head & neck lesions as carcinogen-exposed wildtype animals. This increase in carcinogenesis is accompanied by a synergistic increase in mutations from APOBEC signature SBS2, but not from NQO signature SBS4. Interestingly, a large proportion of A3B-catalyzed SBS2 mutations occurs as strand-coordinated pairs within 32 nucleotides of each other in transcribed regions, suggesting a mechanism in which removal of NQO-DNA adducts by nucleotide excision repair exposes short single-stranded DNA tracts to enzymatic deamination. These highly enriched pairs of APOBEC signature mutations are termed didyma (Greek for twins) and are mechanistically distinct from other types of clustered mutation (omikli and kataegis). Computational analyses of lung and head & neck tumor genomes show that both APOBEC mutagenesis and didyma are elevated in cancers from smokers compared to non-smokers. APOBEC signature mutations and didyma are also elevated in normal lung tissues in smokers prior to cancer initiation. Collectively, these results indicate that DNA adducting mutagens in tobacco smoke can amplify DNA damage and mutagenesis by endogenous APOBEC enzymes and, more broadly, suggest that mutational mechanisms can interact synergistically in both cancer initiation and promotion.

Dataset Information

The impacts of including information about the number of carcinogens in smoke on standardized cigarette packs in the UK.

Background

Methods

Results

Conclusions

Publications

The impacts of including information about the number of carcinogens in smoke on standardized cigarette packs in the UK.

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