Effects of a Nicotine Fact Sheet on Perceived Risk of Nicotine and E-Cigarettes and Intentions to Seek Information About and Use E-Cigarettes
Name:
ijerph-17-00131-v2.pdf
Size:
306.8Kb
Format:
PDF
Description:
Final Published Version
Publisher
MDPICitation
Yang, B.; Owusu, D.; Popova, L. Effects of a Nicotine Fact Sheet on Perceived Risk of Nicotine and E-Cigarettes and Intentions to Seek Information About and Use E-Cigarettes. Int. J. Environ. Res. Public Health 2020, 17, 131.Rights
Copyright © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
We examined how a nicotine fact sheet influenced smokers' beliefs about nicotine and electronic cigarettes (e-cigarettes), a potentially less harmful alternative to conventional cigarettes. In an exploratory online experiment, 756 US adult current and recent former smokers (quit in the past 2 years) were randomized to view a nicotine fact sheet or control messages (bottled water ads). Effects of the nicotine fact sheet on perceived nicotine addictiveness, nicotine risk, comparative risk of e-cigarettes, and dual use intentions were analyzed using log-Poisson regression with robust error. Linear regression analyzed effects on perceived absolute risk and switching and information seeking intentions about e-cigarettes. Compared to control, the nicotine fact sheet doubled the probability of disagreeing that nicotine is the main cause of smoking-related disease (26.2% vs. 12.7%, RR = 2.06, 95% CI = 1.51, 2.82, p < 0.001). However, nearly three quarters of participants viewing the nicotine fact sheet still thought that nicotine is the main cause of smoking-related disease. The nicotine fact sheet increased smokers' intentions to seek information about e-cigarettes (b = 0.45, 95% CI = 0.15, 0.74, p = 0.003). We did not find evidence suggesting unintended consequences of the nicotine fact sheet on smokers' e-cigarettes risk perceptions or use intentions (e.g., increased dual use intentions or reduced absolute e-cigarette risk perception).Note
Open access journalISSN
1661-7827PubMed ID
31878111Version
Final published versionScopus Count
Collections
Except where otherwise noted, this item's license is described as Copyright © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
Related items
Showing items related by title, author, creator and subject.
-
Genotoxicity Study on Nicotine and Nicotine-Derived Nitrosamine by Accelerator Mass SpectrometryWe have studied DNA adduction with 14C-labe1ed nicotine and nicotine-derived nitrosamine, 4-(methylnitrosamino)1-(3-pyridyl)-1-butanone (NNK), by accelerator mass spectrometry (AMS) in mouse liver at doses equivalent to lowlevel exposure of humans. The dose ranges of nicotine and NNK administered were from 0.4g to 4.0x 10^2 micrograms kg b.w.-1, and from 0.1 micrograms to 2.0x10^4 micrograms kg b.w.-1, respectively. In the exposure of mice to either nicotine or NNK, the number of DNA adducts increased linearly with increasing dose. The detection limit of DNA adducts was 1 adduct per 1011 nucleotide molecules. This limit is 1-4 orders of magnitude lower than that of other techniques used for quantification of DNA adducts. The results of our animal experiments enabled us to speculate that nicotine is a potential carcinogen. According to the procedure for 14C-labeled-NNK synthesis, we discuss the ultimate chemical speciation of NNK bound to DNA. From the animal tests we derived a directly perceivable relation between tobacco consumption and DNA adduction as the carcinogenic risk assessment.
-
Nicotine and TNF alpha, modulators of T cell signaling-effects on T cell development in fetal thymus organ cultureT cell development is regulated by signals generated in the interactions between developing thymocytes and the thymic stroma. Using fetal thymus organ culture (FTOC) as a model of T cell development, we investigated the ability of two potent signal modulators to influence this process. These studies show that both nicotine and tumor necrosis factor-alpha have the ability to influence T cell receptor (TCR) signaling and the maturational capacity of treated cultures. FTOC treated with low concentrations of nicotine produced more immature T cells and fewer mature T cells. These expanded populations of cells also expressed CD69, CD95 (FAS) and elevated levels of recombinase activating genes (RAG). This phenotype reflects the fact that these cells have received a positive selection signal, are for apoptosis and are likely attempting secondary TCR rearrangements. Nicotine effects were partially blocked by the nicotinic antagonist, d-tubocurarine. Furthermore, d-tubocurarine alone blocked the development of T cells entirely, suggesting the presence of an endogenous ligand that may engage nicotinic acetylcholine receptors and regulate normal thymopoeisis. These observations underscore the linkage between the nervous and the immune systems, not only in terms of shared resources, but also in terms of direct interactions between these two systems. In another study we used FTOC and an associated in vitro Type 1 diabetes mellitus model to reconcile the role of TNF-alpha in thymopoiesis with its role in diabetes. Our data indicate that thymocytes from NOD FTOC express lower levels of TNF receptors and produce more TNF-alpha compared to non-diabetic C57BL/6 (B6) FTOC. Neutralization of endogenous TNF-alpha in NOD FTOC with a soluble TNF receptor (sTNF R1) rescued insulin production in our in vitro diabetes model. NOD FTOC treated with TNF-alpha produced greater numbers of mature T cells and a higher percentage of cells expressing CD95L (Fas ligand). Treatment with sTNF R1 had the opposite effect. TNF-alpha's known ability to attenuate TCR signaling coupled with these observations suggest that its overproduction in these animals may be driving T cells to maturity, altering the process of negative selection and ultimately enhancing the survival of potentially diabetogenic T cells resulting in disease susceptibility in these animals.
-
Heterologous Expression of Alpha 6*- Nicotinic Acetylcholine Receptors and the Natural Distribution of Alpha 6 SubunitsNicotinic acetylcholine receptors (nAChR) are neurotransmitter-gated ion channels that exist as a family of subtypes defined by unique subunit compositions. nAChR containing α6 subunits (α6*-nAChR) have attracted interest because α6 subunits are thought to be localized in brain regions implicated in reward, mood and drug dependence. To provide new information necessary toward a more complete understanding of roles of α6*-nAChR in neuropsychiatric health and disease, three lines of investigation were pursued. A set of stably transfected, human, immortalized cell lines were generated that heterologously express nAChR α6 subunits in combination with other nAChR subunits found in reward brain regions (nAChR subunit combinations α6β2, α6β4, α6β2β3, α6β4β3, α6β2β3α5, α6β4β3α5, α6α4β2β3 and α6α4β4β3). The α6α4β2β3 combination may have a functional response to epibatidine that differs from that of the α4β2 nAChR. A unique binding site was identified in cells transfected with the α6β4β3α5 nAChR subunit combination. Messenger RNA fluorescence in situ hybridization (mRNA FISH) studies established regional and celluar distribution of nAChR α6 subunit mRNA in the mouse brain. The third line of study extended this work to examine potential co-expression of nAChR α6 subunits and glutamic acid decarboxylase (GAD) or tyrosine hydroxylase (TH) as labels of GABAergic and dopaminergic/catecholaminergic neurons respectively, using tandem mRNA FISH and fluorescence immunohistochemistry. nAChR α6 subunit signal in the substantia nigra (SN) and ventral tegmental area (VTA) was congruent with previous studies. Message was also detected in the amydala, dentate gyrus, striatum, zona incerta, and cingulate, entorhinal, perirhinal, piriform, and prelimbic cortices. nAChR α6 mRNA was coexpressed with GAD in the amygdala, dentate gyrus, striatum, SN, VTA and cingulate, entorhinal, prelimbic and prelimbic cortices. TH was exclusively co-localized with nAChR α6 mRNA in the SN and VTA. Findings suggest extended roles for α6*-nAChR in the brain, particularly in the control of GABAergic neuronal activity and/or GABA release. These studies provide new insights into the composition of α6*-nAChR, the localization and cellular origins of nAChR α6 subunit expression. Data collected suggest roles for α6*-nAChR in many brain regions, including those involved in higher order processes involved in drug dependence and reward, and in modulation of inhibitory neurotransmission.
