E-cigarette and hookah adoption patterns: Is the harm reduction theory just so much smoke?
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ABSTRACT:
SUBMITTER: Ford EW
PROVIDER: S-EPMC7244911 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Alteration of innate immune cells in the lungs can promote loss of peripheral tolerance that leads to autoimmune responses in cigarette smokers. Development of autoimmunity in smokers with emphysema is also strongly linked to the expansion of autoreactive T helper (Th) cells expressing interferon gamma (Th1), and interleukin 17A (Th17). However, the mechanisms responsible for enhanced self-recognition and reduced immune tolerance in smoker with emphysema remain less clear. Here we show that C1q, a component of the complement protein 1 complex (C1), is downregulated in lung CD1a+ antigen presenting cells (APCs) isolated from emphysematous human, and mouse lung APCs after chronic cigarette smoke exposure. C1q potentiated the function of APCs to differentiate CD4+ T cells to Tregs, while it inhibited Th17 cell development and proliferation. Mice deficient in C1q that were exposed to chronic smoke exhibited exaggerated lung inflammation marked by increased Th17 cells, while reconstitution of C1q in the lungs enhanced Tregs abundance, dampened smoke-induced lung inflammation, and reversed established emphysema. Our findings demonstrate that cigarette smoke-mediated loss of C1q could play a key role in reduced peripheral tolerance, which could be explored to treat emphysema.
| S-EPMC6629245 | biostudies-other
Project description:Rationale: The effects of hookah smoke on respiratory epithelia have not been well characterized. Objectives: To characterize and compare the effects of hookah tobacco smoke and conventional cigarette smoke on the epigenome and transcriptome of human respiratory epithelia. Methods: Normal human small airway epithelial cells and cyclin-dependent kinase 4/human telomerase reverse transcriptase–immortalized human bronchial epithelial cells were cultured for 5 days in normal media in the presence or absence of water pipe condensates or cigarette smoke condensates under relevant exposure conditions. CyQUANT assay (Thermo Fisher Scientific), RNA sequencing, quantitative reverse transcriptase–polymerase chain reaction, and Western blotting techniques were used to examine/compare the effects of hookah and cigarette smoke on cell proliferation, messenger RNA/microRNA expression, and global histone marks. Results: Water pipe condensates– and cigarette smoke condensates–mediated, dose-dependent growth-inhibitory effects in cultured respiratory epithelial cells were measured. Under conditions mediating equipotent mild to moderate growth-inhibitory effects, water pipe condensates as well as cigarette smoke condensates decreased histone H4 lysine 15 acetylation (H4K16ac) and histone H4 lysine 20 trimethylation (H4K20me3) levels in small airway epithelial cells and human bronchial epithelial cells; these histone alterations are putative “hallmarks of cancer.” RNA sequencing analysis demonstrated that cigarette smoke condensates and water pipe condensates mediated dose-dependent alterations in gene expression in small airway epithelial cells and human bronchial epithelial cells. A total of 873 genes were commonly regulated (fold change >2) by water pipe condensates (1.0 mg/ml) and cigarette smoke condensates (0.05 mg/ml) in small airway epithelial cells, whereas a total of 1,577 genes were commonly regulated by water pipe condensates (1.0 mg/ml) and cigarette smoke condensates (0.05 mg/ml) in human bronchial epithelial cells. Ingenuity Pathway Analysis (QIAGEN Bioinformatics) of the 100 genes commonly regulated by water pipe condensates and cigarette smoke condensates in small airway epithelial cells and human bronchial epithelial cells demonstrated that the top three activated upstream regulators are cigarette smoke (z-score?=?2.577), benzo[a]pyrene (z-score?=?2.905), and nuclear factor (erythroid-derived 2)-like 2 (NFE2L2, Nrf2) (z-score?=?2.531). Analysis of downstream effects indicated that growth of epithelial tissue was predicted to be increased (z-score?=?2.813; P?<?0.001). The top three canonical pathways included xenobiotic metabolism signaling, aryl hydrocarbon receptor signaling, and nicotine degradation III. Conclusions: These preliminary findings strongly suggest that hookah tobacco is not a safe alternative to cigarettes, and warrant further evaluation of the epigenomic effects of hookah smoke in human respiratory epithelia using our established laboratory models and correlative analyses in hookah smokers.
| S-EPMC5946508 | biostudies-literature
Project description:Nicotine, an addictive drug, is present in all forms of tobacco products, including hookah tobacco, which is not yet regulated in the United States. This study aimed to investigate the uptake of nicotine in hookah smokers and non-smokers exposed to secondhand smoke (SHS) at indoor hookah social events in natural settings where hookah tobacco was smoked exclusively. We quantified cotinine, a metabolite of nicotine, in the urine of 105 hookah smokers and 103 non-smokers. Participants provided spot urine samples the morning of and the morning after attending an indoor hookah-only smoking social event at a hookah lounge or in a private home. Following a social event where exclusively hookah tobacco was smoked, urinary cotinine levels increased significantly 8.5 times (geometric mean (GM): 16.0 ng/mg to 136.1 ng/mg) among hookah smokers, and 2.5 times (GM: 0.4 ng/mg to 1.0 ng/mg) among non-smokers exposed exclusively to hookah tobacco SHS. Among hookah smokers, the highest increase in urinary cotinine levels post a hookah event was found in occasional hookah smokers in which GM levels increased significantly 31.2 times post smoking (from 2.0 ng/mg to 62.3 ng/mg). Reported reasons for preference to smoke hookah at home by hookah smokers who attended a hookah social event in a private home included recreational purposes, socializing with friends and family, 'Me' time and relaxing at home, more comfortable to smoke hookah at home, owning a hookah and hookah tobacco, eating and drinking while smoking hookah, and saving money by smoking at home and not going to hookah lounges. Hookah tobacco smoke is a source of substantial nicotine exposure. Our results call for protecting hookah smokers' and non-smokers' health by requiring accurate hookah tobacco labels, raising taxes on hookah tobacco, reducing the spread of hookah lounges, and encouraging voluntary bans on smoking hookah tobacco in private homes.
| S-EPMC5967845 | biostudies-literature
Project description:OBJECTIVE:Susceptibility to cigarette smoking has been used since the mid-1990s as a measure to identify youth at risk of cigarette initiation. However, it is unclear how well this measure predicts future smoking among electronic (e-)cigarette or hookah users, or among those in tobacco-friendly social environments. METHODS:We used prospective data from the Southern California Children's Health Study to evaluate the performance (sensitivity, specificity, predictive value) of a composite index assessing susceptibility to smoking, and to evaluate whether performance of the measure differed by use of e-cigarettes or hookah, or immersion in a tobacco-friendly social environment. Susceptibility to cigarette smoking was measured in 11th/12th grade (2014) among never cigarette-smokers (N=1266); follow-up data on smoking initiation were obtained approximately 16 months later. RESULTS:Overall, 16.4% of youth initiated smoking between baseline and follow-up. The sensitivity of the susceptibility to smoking index was low (46.4%), and specificity was high (79.0%). No difference in sensitivity was observed by baseline e-cigarette use; specificity was higher among never e- cigarette users. Differences in negative predictive value (NPV) and positive predictive value (PPV) were also observed by baseline e-cigarette and hookah use. Specificity was generally lower, and sensitivity was generally higher for those in tobacco-friendly social environments. CONCLUSIONS:Our findings suggest that use of the susceptibility to smoking index in cross-sectional studies of older adolescents to identify those likely to begin smoking may be inappropriate for those using alternative tobacco products (e.g., e-cigarettes or hookah).
| S-EPMC5803381 | biostudies-literature
Project description:INTRODUCTION:Use of tobacco products among adolescents is a major global public health concern. Given the changing landscape of tobacco product use and the lack of epidemiologic data to inform tobacco prevention and control strategies in Kuwait, this study sought to estimate the prevalence and patterns of electronic cigarette (e-cigarette), conventional cigarette, and hookah use among adolescents in Kuwait. Moreover, exposure to secondhand smoke (SHS) and secondhand aerosol (SHA) from e-cigarettes was assessed. METHODS:This cross-sectional study enrolled high school students (n=1565; 16-19 years) across Kuwait. Current (past 30-day) use of e-cigarettes, conventional cigarettes, and hookah were assessed through self-reported data. Additionally, current (past 7-day) exposure to SHS and SHA in households and public places were ascertained. Associations were evaluated using Poisson regression, and adjusted prevalence ratios (APRs) and 95% confidence intervals (CIs) were estimated. RESULTS:Overall, 26.4% (402/1525), 25.1% (383/1525), and 20.9% (318/1525) of the study participants were current e-cigarette users, conventional cigarette smokers, and hookah smokers, respectively. Current use of any tobacco product was reported by 35.1% (535/1525) of the total study participants. The prevalence of concurrent triple use of 'e-cigarettes, conventional cigarettes, and hookah' was estimated to be 12.8% (195/1525). Also, among the study participants, 41.9% (619/1479) were exposed to household SHS, 32.0% (469/1465) were exposed to household SHA, and 62.2% (916/1472) were exposed to SHS and/or SHA in public places. Male adolescents were more likely than females to be current e-cigarette users (APR=5.19; 95% CI: 4.09-6.57), conventional cigarette smokers (APR=5.42; 95% CI: 4.26-6.90), and hookah smokers (APR=3.43; 95% CI: 2.72- 4.32). CONCLUSIONS:A substantial proportion of adolescents in Kuwait are currently using tobacco products and being exposed to SHS/SHA. The findings emphasize the need to continue monitoring all forms of tobacco product use among adolescents and to strengthen tobacco prevention and control programs.
| S-EPMC7398596 | biostudies-literature
Project description:IntroductionAcrolein is a highly ciliatoxic agent, a toxic respiratory irritant, a cardiotoxicant, and a possible carcinogen present in tobacco smoke including hookah tobacco.Methods105 hookah smokers and 103 non-smokers attended exclusively hookah smoking social events at either a hookah lounge or private home, and provided urine samples the morning of and the morning after the event. Samples were analyzed for 3-hydroxypropylmercapturic acid (3-HPMA), a metabolite of acrolein.ResultsGeometric mean (GM) urinary 3-HPMA levels in hookah smokers and non-smokers exposed to secondhand smoke (SHS) increased significantly, 1.41 times, 95% CI = 1.15 to 1.74 and 1.39 times, 95% CI = 1.16 to 1.67, respectively, following a hookah social event. The highest increase (1.68 times, 95% CI = 1.15 to 2.45; p = 0.007) in 3-HPMA post a hookah social event was among daily hookah smokers (GM, from 1991 pmol/mg to 3348 pmol/mg). Pre-to-post event change in urinary 3-HPMA was significantly positively correlated with pre-to-post event change in urinary cotinine among hookah smokers at either location of hookah event, (ρ = 0.359, p = 0.001), and among non-smokers in hookah lounges (ρ = 0.369, p = 0.012).ConclusionsHookah tobacco smoke is a source of acrolein exposure. Findings support regulating hookah tobacco products including reducing humectants and sugar additives, which are precursors of acrolein under certain pyrolysis conditions. We suggest posting health warning signs for indoor smoking in hookah lounges, and encouraging voluntary bans of smoking hookah tobacco in private homes.ImplicationsOur study is the first to quantify the increase in acrolein exposure in hookah smokers and non-smokers exposed to exclusively hookah tobacco SHS at hookah social events in homes or hookah lounges. Our findings provide additional support for regulating hookah tobacco product content, protecting non-smokers' health by posting health warning signs for indoor smoking in hookah lounges, and encouraging home bans on hookah tobacco smoking to safeguard vulnerable residents.
| S-EPMC5896480 | biostudies-literature
Project description:Carbonyls are harmful and potentially harmful constituents (HPHCs) in mainstream cigarette smoke (MSS). Carbonyls, including formaldehyde and acrolein, are carcinogenic or mutagenic in a dose-dependent manner. Past studies demonstrate significant reduction of HPHCs by charcoal filtration. However, limits of charcoal filtration and cigarette design have not yet been investigated in a systematic manner. Objective data is needed concerning the feasibility of HPHC reduction in combustible filtered cigarettes. This systematic study evaluates the effect of charcoal filtration on carbonyl reduction in MSS. We modified filters of ten popular cigarette products with predetermined quantities (100-400 mg) of charcoal in a plug-space-plug configuration. MSS carbonyls, as well as total particulate matter, tar, nicotine, carbon monoxide (TNCO), and draw resistance were quantified. Significant carbonyl reductions were observed across all cigarette products as charcoal loading increased. At the highest charcoal loadings, carbonyls were reduced by nearly 99%. Tar and nicotine decreased modestly (<20%) compared to reductions in carbonyls. Increased draw resistance was significant at only the highest charcoal loadings. This work addresses information gaps in the science base that can inform the evaluation of charcoal filtration as an available technological adaptation to cigarette design which reduces levels of carbonyls in MSS.
| S-EPMC5448414 | biostudies-literature
Project description:Hookah smoking is one of the major indoor sources of benzene, toluene, ethylbenzene, and xylenes (BTEX). This study aimed to investigate the potential exposure to BTEX among primary school children, particularly those exposed to hookah smoke. This cross-sectional study was conducted in Khesht, one of the southwestern cities in Iran, in mid-June 2020. Totally, 50 primary school children exposed to hookah smoke were chosen as the case group and 50 primary school children were selected as the control group. Urinary un-metabolized BTEX was measured by a headspace gas chromatography mass spectrometry (GC-MS). Additionally, a detailed questionnaire was used to gather data and information from the students' parents. The mean levels of urinary benzene, toluene, ethylbenzene, m,p-xylene, and o-xylene were 1.44, 5.87, 2.49, 6.93, and 7.17 μg/L, respectively in the exposed children. Urinary BTEX was 3.93-folds higher in the case group than in the controls (p<0.05). Household cleaning products, the floor on which the house was located, children's sleeping place, and playing outdoors were found to be important factors in predicting urinary BTEX levels. Overall, it was found necessary to avoid indoor smoking to prevent the emission of BTEX compounds via exhaled mainstream smoke and to protect vulnerable non-smokers, especially children, from exposure to second-hand and third-hand smoke.
| S-EPMC9100313 | biostudies-literature
Project description:Waterpipe smoking is becoming more popular worldwide and there is a pressing need to better characterize the exposure of smokers to chemical compounds present in the mainstream smoke. We report real-time measurements of mainstream smoke for carbon monoxide, volatile organic compounds and nanoparticle size distribution and chemical composition using a custom dilution flow tube. A conventional tobacco mixture, a dark leaf unwashed tobacco and a nicotine-free herbal tobacco were studied. Results show that carbon monoxide is present in the mainstream smoke and originates primarily from the charcoal used to heat the tobacco. Online measurements of volatile organic compounds in mainstream smoke showed an overwhelming contribution from glycerol. Gas phase analysis also showed that very little filtration of the gas phase products is provided by the percolation of mainstream smoke through water. Waterpipe smoking generated high concentrations of 4-100 nm nanoparticles, which were mainly composed of sugar derivatives and especially abundant in the first 10 min of the smoking session. These measured emissions of volatiles and particles are compared with those from a reference cigarette (3R4F) and represent the equivalent of the emission of one or more entire cigarettes for a single puff of hookah smoke. Considerations related to the health impacts of waterpipe smoking are discussed.
| S-EPMC7546025 | biostudies-literature
Project description:This study evaluated the hypothesis that smoke from harm reduction cigarettes impedes attachment and proliferation of H9 human embryonic stem cells (hESCs). Smoke from three harm reduction brands was compared with smoke from a conventional brand. Doses of smoke were measured in puff equivalents (PE) (1 PE = the amount of smoke in one puff that dissolves in 1 ml of medium). Cytotoxic doses were determined using morphological criteria and trypan blue staining, and apoptosis was confirmed using Magic Red staining. Attachment and proliferation of hESC were followed at a noncytotoxic dose in time-lapse videos collected using BioStation technology. Data were mined from videos either manually or using video bioinformatics subroutines developed with CL-Quant software. Mainstream (MS) and sidestream (SS) smoke from conventional and harm reduction cigarettes induced apoptosis in hESC colonies at 1 PE. At 0.1 PE (noncytotoxic), SS smoke from all brands inhibited attachment of hESC colonies to Matrigel with the strongest inhibition occurring in harm reduction brands. At 0.1 PE, SS smoke, but not MS smoke, from all brands inhibited hESC growth, and two harm reduction brands were more potent than the conventional brand. In general, hESC appeared more sensitive to smoke than their mouse ESC counterparts. Although harm reduction cigarettes are often marketed as safer than conventional brands, our assays show that SS smoke from harm reduction cigarettes was at least as potent or in some cases more potent than smoke from a conventional brand and that SS smoke was more inhibitory than MS smoke in all assays.
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