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Cyanoethyl mercapturic acid (CEMA) is a urinary metabolite of acrylonitrile, a toxicant found in substantial quantities in cigarette smoke, but not in non-combusted products such as e-cigarettes or smokeless tobacco and rarely in the diet or in the general human environment. Thus, we hypothesized that CEMA is an excellent biomarker of combusted tobacco product use. We tested this hypothesis by analyzing CEMA in the urine of 1259 cigarette smokers (urinary cotinine ≥25 ng/mL) and 1191 nonsmokers. The analyses of CEMA and cotinine were performed by validated liquid chromatography-tandem mass spectrometry methods. Logistic regression was fit for log-transformed CEMA to construct the receiver operating characteristic curve. We found that a CEMA cutpoint of 27 pmol/mL urine differentiated cigarette smokers from nonsmokers with sensitivity and specificity greater than 99%. The use of different cotinine cutpoints to define smokers (10-30 ng/mL) had little effect on the results. CEMA is a highly reliable urinary biomarker to identify users of combusted tobacco products such as cigarettes as opposed to users of non-combusted products, medicinal nicotine, or nonusers of tobacco products. CEMA can be used to distinguish users of combusted tobacco products from non-combusted products such as e-cigarettes, smokeless tobacco, and medicinal nicotine. Levels of CEMA in the urine of people who use these non-combusted products are extremely low, in contrast to cotinine.

Background Article 20 of the EU Tobacco Products Directive [TPD] stipulates that e-cigarette packets and refill products must carry a nicotine addiction health warning. Although previous studies conducted in North America have found that perceived harm, addictiveness and intention to use declined following exposure to e-cigarette health warnings, possible effects of the TPD health warnings on smokers and non-smokers has not been studied. This study will investigate the effects of the EU TPD e-cigarette health warnings and a comparative harm message (COMP; developed specifically for this study) on smokers’ and non-smokers’ perceptions of harm, addictiveness and social acceptability of e-cigarettes. Additionally, the potential effects of the TPD warnings and the COMP on smokers’ intentions to purchase and use e-cigarettes will be explored. Methods/design A sample of 2400 UK residents will be recruited in this experimental, randomised design, with Smoking status (Smoker vs. Non-smoker), TPD presence (TPD1 vs. TPD2 vs. No-TPD) and COMP presence (Presence vs. Absence) as between subjects independent variables, and Time (pre-post exposure of images) as a within subjects factor. Dependent variables comprise self-reported perceived harm, addictiveness, social acceptability, e-cigarettes’ effectiveness, intentions to purchase and use e-cigarettes. Cigarette dependence, previous e-cigarette exposure, and baseline intentions to quit will be measured as covariates. Discussion Health warnings, such as those implemented by the TPD, may help to prevent non-smokers from e-cigarettes use, but it is possible that they may inadvertently deter smokers from initiating use and substituting their tobacco smoking for e-cigarettes use if their content is deemed too negative. It is hoped that this study will help identify the most effective message or combination of messages that encourage use among smokers without promoting use among non-smokers. Trial registration ISRCTN registry ISRCTN76967031 ; date of registration: 23/10/18.

This study assessed how electronic cigarette (ECIG) characteristics amenable to regulation—namely nicotine content, flavor, and modified risk messages—impact ECIG use susceptibility, harm/addiction perceptions, and abuse liability indices among combustible tobacco cigarette (CTC) smokers and non-smokers. CTC smokers and non-smokers varying in ECIG use recruited via Amazon Mechanical Turk (MTurk) completed an online survey in 2016 (analytic n = 706). Participants were randomly assigned to one of eight conditions differing in ECIG characteristics: nicotine content (no, low, high), flavor (menthol, tobacco, fruit), or modified risk message (reduced harm, reduced carcinogen exposure). Regressions assessed ECIG susceptibility, harm/addiction perceptions, and abuse liability indices (purchase task measures of breakpoint/intensity) within each regulatory domain (nicotine content, flavor, message) and their interactions with CTC/ECIG status. Differential effects on ECIG susceptibility, harm/addiction perceptions, and abuse liability indices were observed by regulatory domain with many effects moderated by CTC/ECIG status. ECIG nicotine content and flavor conditions were the most influential across outcomes. Greater nicotine content, tobacco-flavored and reduced carcinogen exposure ECIGs were more highly preferred by CTC smokers with some differing preferences for non-users. Findings reinforce consideration of discrete ECIG preferences across tobacco use status to improve regulatory efficacy.

Lung cancer in never smokers (LCINS) is a common cause of cancer mortality but its genomic landscape is poorly characterized. Here high-coverage whole-genome sequencing of 232 LCINS showed 3 subtypes defined by copy number aberrations. The dominant subtype (piano), which is rare in lung cancer in smokers, features somatic UBA1 mutations, germline AR variants and stem cell-like properties, including low mutational burden, high intratumor heterogeneity, long telomeres, frequent KRAS mutations and slow growth, as suggested by the occurrence of cancer drivers’ progenitor cells many years before tumor diagnosis. The other subtypes are characterized by specific amplifications and EGFR mutations (mezzo-forte) and whole-genome doubling (forte). No strong tobacco smoking signatures were detected, even in cases with exposure to secondhand tobacco smoke. Genes within the receptor tyrosine kinase–Ras pathway had distinct impacts on survival; five genomic alterations independently doubled mortality. These findings create avenues for personalized treatment in LCINS. Whole-genome sequencing of lung cancer in never smokers identifies different copy number subtypes and shows a lack of tobacco smoking signatures, even in cases exposed to secondhand smoke.

Cigarette smoke first interacts with the lung through the cellularly diverse airway epithelium and goes on to drive development of most chronic lung diseases. Here, through single cell RNA-sequencing analysis of the tracheal epithelium from smokers and non-smokers, we generate a comprehensive atlas of epithelial cell types and states, connect these into lineages, and define cell-specific responses to smoking. Our analysis infers multi-state lineages that develop into surface mucus secretory and ciliated cells and then contrasts these to the unique specification of submucosal gland (SMG) cells. Accompanying knockout studies reveal that tuft-like cells are the likely progenitor of both pulmonary neuroendocrine cells and CFTR-rich ionocytes. Our smoking analysis finds that all cell types, including protected stem and SMG populations, are affected by smoking through both pan-epithelial smoking response networks and hundreds of cell-specific response genes, redefining the penetrance and cellular specificity of smoking effects on the human airway epithelium. Chronic lung diseases are characterized by molecular and cellular composition changes. Here the authors use single-cell RNA sequencing to map cell type-specific changes in human tracheal epithelium related to smoking, and to provide evidence for a tuft-like progenitor for pulmonary neuroendocrine cells and ionocytes.

Through the use of an innovative method to identify original publications, we conducted a meta-analysis of all epidemiological studies evaluating the association between second-hand smoke (SHS) exposure and breast cancer risk among female non-smokers published in English up to October 2022. Pooled relative risks (RR) were obtained through the use of random-effects models. Dose–response relationships were derived using log-linear functions. Out of 73 identified eligible studies, 63 original articles were included in the meta-analysis. The pooled RR for breast cancer for overall exposure to SHS was 1.24 (95% confidence interval, CI, 1.15–1.34, number of articles, n  = 52). Regarding the setting of exposure, RRs were 1.17 (95% CI 1.08–1.27, n  = 37) for SHS exposure at home, 1.03 (95% CI 0.98–1.08, n  = 15) at the workplace, 1.24 (95% CI 1.11–1.37, n  = 16) at home or workplace, and 1.45 (95% CI 1.16–1.80, n  = 13) for non-specified settings. The risk of breast cancer increased linearly with higher duration (RR 1.29; 95% CI 1.04–1.59 for 40 years of SHS exposure, n  = 12), intensity (RR 1.38; 95% CI 1.14–1.67 for 20 cigarettes of SHS exposure per day, n  = 6), and pack-years (RR 1.50; 95% CI 0.92–2.45 for 40 SHS pack-years, n  = 6) of SHS exposure. This meta-analysis shows a statistically significant excess risk of breast cancer in women exposed to SHS.

Background Chronic obstructive pulmonary disease (COPD) is a prevalent chronic disorder in China, impacting a significant proportion of individuals aged > 40 years. In China, the prevalence of and risk factors for COPD among non-smokers remain largely unexplored. In this study, we aimed to determine the prevalence of COPD in non-smokers within the Chinese population and identify potential risk factors associated with COPD in non-smokers. Methods Web of Science, PubMed, Embase, Chinese WanFang, Chinese China National Knowledge Infrastructure, and Weipu databases from inception to August 5, 2024, were searched. Studies reporting the percentage of never-smokers among those diagnosed with COPD and investigations exploring the risk factors associated with COPD in never-smokers in China were examined. Summary proportions and odds ratios (OR), along with their corresponding 95% confidence intervals (95% CI), were measured. Results In total, 112 investigations with 491,812 participants were included. The percentage of never-smokers in people with COPD was 41.1% (95% CI: 37.5–44.6%). The prevalence of never-smokers among males diagnosed with COPD was 22.3% (95% CI: 18.8–25.7%), which differed from that among women (81.3%, 95% CI: 75.3–87.2%). The results showed an association between the utilization of biomass fuel and the occurrence of COPD in never-smokers (OR: 1.25, 95% CI: 1.06–1.44). Among never-smokers, the data showed a close association between being underweight (OR: 1.89, 95% CI: 1.78–2.00), tuberculosis history (OR: 1.71, 95% CI: 1.53–1.88) and COPD. Never-smokers living in rural areas or those with low educational status were more susceptible to COPD. Conclusion This review confirmed the highly different proportions of never-smokers among male and female patients with COPD. Trial registration PROSPERO: CRD42023420786.

To quantify the relation between smoking cessation after a first cardiovascular (CV) event and risk of recurrent CV events and mortality. Data were available from 4,673 patients aged 61 ± 8.7 years, with a recent (≤1 year) first manifestation of arterial disease participating in the SMART-cohort. Cox models were used to quantify the relation between smoking status and risk of recurrent major atherosclerotic cardiovascular events (MACE including stroke, MI and vascular mortality) and mortality. In addition, survival according to smoking status was plotted, taking competing risk of non-vascular mortality into account. A third of the smokers stopped after their first CV event. During a median of 7.4 (3.7–10.8) years of follow-up, 794 patients died and 692 MACE occurred. Compared to patients who continued to smoke, patients who quit had a lower risk of recurrent MACE (adjusted HR 0.66, 95% CI 0.49–0.88) and all-cause mortality (adjusted HR 0.63, 95% CI 0.48–0.82). Patients who reported smoking cessation on average lived 5 life years longer and recurrent MACE occurred 10 years later. In patients with a first CV event >70 years, cessation of smoking had improved survival which on average was comparable to former or never smokers. Irrespective of age at first CV event, cessation of smoking after a first CV event is related to a substantial lower risk of recurrent vascular events and all-cause mortality. Since smoking cessation is more effective in reducing CV risk than any pharmaceutical treatment of major risk factors, it should be a key objective for patients with vascular disease.

Background We examined the association between active and passive smoking and lung cancer risk and the population attributable fraction (PAF) of lung cancer due to active smoking, in the Norwegian Women and Cancer Study, a nationally representative prospective cohort study. Methods We followed 142,508 women, aged 31–70 years, who completed a baseline questionnaire between 1991 and 2007, through linkages to national registries through December 2015. We used Cox proportional hazards models, to estimate hazard ratios (HRs) with 95% confidence intervals (CIs). We calculated PAF to indicate what proportion of lung cancer cases could have been prevented in the absence of smoking. Results During the more than 2.3 million person-years of observation, we ascertained 1507 lung cancer cases. Compared with never smokers, current (HR 13.88, 95% CI 10.18–18.91) smokers had significantly increased risk of lung cancer. Female never smokers exposed to passive smoking had a 1.3-fold (HR 1.34, 95% CI 0.89–2.01) non- significantly increased risk of lung cancer, compared with never smokers. The PAF of lung cancer was 85.3% (95% CI 80.0–89.2). Conclusion More than 8 in 10 lung cancer cases could have been avoided in Norway, if the women did not smoke.

Background E-cigarette use prevalence has grown rapidly in the US. Despite the popularity of these products, few acute exposure toxicity studies exist, and studies on long-term pulmonary health effects are limited. E-cigarette users who are never combustible cigarette smokers (sole users) constitute a unique group of young adults that may be at increased risk of bronchial hyperreactivity and development of asthma. Given the public health concern about the potential pulmonary health effects of sole e-cigarette use, we aimed to examine the association between e-cigarette use and asthma among never combustible cigarette smokers. Methods We pooled 2016 and 2017 data of the Behavioral Risk Factor Surveillance System (BRFSS), a large, cross-sectional telephone survey of adults aged 18 years and older in the U.S. We included 402,822 participants without any history of combustible cigarette smoking (defined as lifetime smoking < 100 cigarettes) and with complete self-reported information on key variables. Current e-cigarette use, further classified as daily or occasional use, was the primary exposure. The main outcome, asthma, was defined as self-reported history of asthma. We assess the relationship of sole e-cigarette use with asthma using multivariable logistic regression adjusting for age, sex, race, income, level of education and body mass index. Results Of 402,822 never combustible cigarette smokers, there were 3103 (0.8%) current e-cigarette users and 34,074 (8.5%) with asthma. The median age group of current e-cigarette users was 18–24 years. Current e-cigarette use was associated with 39% higher odds of self-reported asthma compared to never e-cigarette users (Odds Ratio [OR], 1.39; 95% confidence interval: 1.15, 1.68). There was a graded increased odds of having asthma with increase of e-cigarette use intensity. The odds ratio of self-reported asthma increased from 1.31 (95% confidence interval: 1.05, 1.62) in occasional users to 1.73 (95% confidence interval: 1.21, 2.48) in daily e-cigarette users, compared to never e-cigarette users. Conclusion Our findings from a large, nationally representative survey suggest increased odds of asthma among never combustible smoking e-cigarette users. This may have potential public health implications, providing a strong rationale to support future longitudinal studies of pulmonary health in young e-cigarette-using adults.