The purpose of the study was to assess tobacco smoking habits among nursing students and how these are influenced by family members and cohabitants.

Some studies show that truck drivers use tobacco and other stimulants to stay awake as they drive. Despite their increased risks for many of tobacco-related health disparities, there is limited engagement of truck drivers in smoking cessation programs. The objective of this study was to describe smoking characteristics and identify their preferred smoking cessation methods among truck drivers.

No abstract available

In jails and prisons worldwide, older adults are among the fastest growing demographic groups. Criminal justice-involved populations smoke tobacco at high rates. Older adults are also disproportionate smokers and have more difficulty quitting smoking than other age groups. Yet, little is known about tobacco use or knowledge and attitudes toward smoking cessation among the growing population of incarcerated older adults.

Heated tobacco products (HTPs) are designed to heat tobacco to a high enough temperature to release aerosol, without burning it or producing smoke. They differ from e-cigarettes because they heat tobacco leaf/sheet rather than a liquid. Companies who make HTPs claim they produce fewer harmful chemicals than conventional cigarettes. Some people report stopping smoking cigarettes entirely by switching to using HTPs, so clinicians need to know whether they are effective for this purpose and relatively safe. Also, to regulate HTPs appropriately, policymakers should understand their impact on health and on cigarette smoking prevalence.

For the identification of genes associated with smoking initiation and current smoking, genome-wide association analyses were carried out in 3497 subjects. Significant genes that replicated in three independent samples (n = 405, 5810, and 1648) were visualized into a biologically meaningful network showing cellular location and direct interaction of their proteins. Several interesting groups of proteins stood out, including glutamate receptors (e.g., GRIN2B, GRIN2A, GRIK2, GRM8), proteins involved in tyrosine kinase receptor signaling (e.g., NTRK2, GRB14), transporters (e.g., SLC1A2, SLC9A9) and cell-adhesion molecules (e.g., CDH23). We conclude that a network-based genome-wide association approach can identify genes influencing smoking behavior.

We evaluated associations of smoking heaviness markers and the effects of smoking cessation on the intestinal microbiota and cardiovascular disease risk factors in current smokers undertaking a quit attempt. Participants were current smokers enrolled in a prospective randomized clinical trial of smoking cessation therapies with visits at baseline, 2, and 12 weeks. Genomic DNA was extracted from fecal samples followed by 16S rRNA gene sequencing and analysis using the QIIME2 software workflow. Relative abundances of bacterial taxa and alpha- and beta-diversity measures were used for comparisons. The 36 smokers were (mean (standard deviation)) 51.5 (11.1) years old (42% male) and smoked 15.1 (6.4) cigarettes per day for 22.7 (11.9) pack-years. Relative abundances of the phylum Actinobacteria correlated with pack-years (rho = -0.44, p = 0.008) and Cyanobacteria correlated with CO levels (rho = 0.39, p = 0.021). After 12 weeks, relative abundances of the phylum Bacteroidetes increased (pANCOVA = 0.048) and Firmicutes decreased (pANCOVA = 0.036) among abstainers compared to continuing smokers. Increases in alpha-diversity were associated with heart rates (rho = -0.59, p = 0.037), systolic blood pressures (rho = -0.58, p = 0.043), and C-reactive protein (rho = -0.60, p = 0.034). Smoking cessation led to minor changes in the intestinal microbiota. It is unclear if the proven health benefits of smoking cessation lead to salutary changes in the intestinal microbiota.

The nicotine metabolite ratio (NMR) as measured by the ratio of 3'hydroxycotinine to cotinine has been examined in relation to tobacco use patterns including cigarettes per day and quit success to determine its role in nicotine dependence. We examined the NMR in relation to smoking topography and tested the hypothesis that normal metabolizers have a greater total daily puff volume than slow metabolizers.

Genes encoding the receptors involved in the dopaminergic and serotonergic pathways are potential candidates in the mechanisms of nicotine addiction.

No abstract available

Nicotine addiction is associated with dysregulated inhibitory control (IC), mediated by corticothalamic circuitry including the right inferior frontal gyrus (rIFG). Among sated smokers, worse IC task performance and greater IC-related rIFG activity have been shown to be associated with greater relapse vulnerability. The present study investigated the effects of smoking abstinence on associations between IC task performance, rIFG activation, and smoking behavior. Smokers (N = 26, 15 female) completed an IC task (Go/Go/No-go) during fMRI scanning followed by a laboratory-based smoking relapse analog task (SRT) on two visits: once when sated and once following 24 h of smoking abstinence. During the SRT, smokers were provided with monetary rewards for incrementally delaying smoking. A significant main effect of No-go accuracy on latency to smoke during the SRT was observed when collapsing across smoking states (abstinent vs. sated). Similarly, a significant main effect of IC-related activation in rIFG on SRT performance was observed across states. The main effect of state, however, was non-significant in both of these models. Furthermore, the interaction between smoking state and No-go accuracy on SRT performance was non-significant, indicating a similar relationship between IC and lapse vulnerability under both sated and abstinent conditions. The state X rIFG activation interaction on SRT performance was likewise non-significant. Post-hoc whole brain analyses indicated that abstinence resulted in greater IC-related activity in the right middle frontal gyrus (MFG) and insula. Activation during IC in these regions was significantly associated with decreased No-go accuracy. Moreover, greater abstinence induced activity in right MFG during IC was associated with smoking sooner on the SRT. These findings are bolstered by the extant literature on the effects of nicotine on executive function and also contribute novel insights on how individual differences in behavioral and neuroimaging measures of IC may influence relapse propensity independent of smoking state.

It is possible that some people who quit smoking experience improved mental health after cessation and therefore remain abstinent, whereas other people who quit may experience worse mental health after cessation and therefore be more likely to relapse to smoking. Thus, in this study we aimed to examine the association between an enduring change in mental health following the cessation period and future risk of relapse.

Currently, most college campuses across the U.S. in some way address on-campus cigarette smoking, mainly through policies that restrict smoking on campus premises. However, it is not well understood whether college-level anti-smoking policies help reduce cigarette smoking among students. In addition, little is known about policies that may have an impact on student smoking behavior. This study attempted to address these issues through a literature review.

Smoking is associated with negative health of skin and increased signs of facial ageing. We aimed to address two questions about smoking and appearance: (1) does facial appearance alone provide an indication of smoking status, and (2) how does smoking affect the attractiveness of faces? We used faces of identical twins discordant for smoking, and prototypes made by averaging the faces of the twins. In Task 1, we presented exemplar twin sets and same sex prototypes side-by-side and participants (n = 590) indicated which face was the smoker. Participants were blind to smoking status. In Task 2 a separate sample (n = 580) indicated which face was more attractive. For the exemplar twin sets, there was inconclusive evidence participants selected the smoking twin as the smoker more often, or selected the non-smoking twin as the more attractive more often. For the prototypes, however, participants clearly selected the smoking prototypes as the smoker more often, and the non-smoking prototypes as the more attractive. Prototypical faces of non-smokers are judged more attractive, and prototypical faces of smokers are correctly identified as smokers more often than prototypical faces of matched smokers/non-smokers [corrected]. We discuss the possible use of these findings in smoking behaviour change interventions.

In the last decade Poland has successfully carried out effective anti-tobacco campaigns and introduced tobacco control legislation. This comprehensive strategy has focused on the general population and has led to a considerable decrease in tobacco consumption. Prisoners constitute a relatively small part of the entire Polish population and smoking habits in this group have been given little attention. The aim of the study was to assess the prevalence of cigarette smoking in Polish male prisoners, factors determining smoking in this group, prisoners' attitudes towards smoking cessation, and to evaluate prisoners' perception of different anti-tobacco measures.

Tobacco smoking is the cause of many preventable diseases and premature deaths in the UK and around the world. It poses enormous health- and non-health-related costs to the affected individuals, employers, and the society at large. The World Health Organization (WHO) estimates that, globally, smoking causes over US$500 billion in economic damage each year.

Chronic cigarette smoking is associated with numerous abnormalities in brain neurobiology, but few studies specifically investigated the chronic effects of smoking (compared to the acute effects of smoking, nicotine administration, or nicotine withdrawal) on cerebral perfusion (i.e., blood flow). Predominately middle-aged male (47 ± 11 years of age) smokers (n = 34) and non-smokers (n = 27) were compared on regional cortical perfusion measured by continuous arterial spin labeling magnetic resonance studies at 4 Tesla. Smokers showed significantly lower perfusion than non-smokers in the bilateral medial and lateral orbitofrontal cortices, bilateral inferior parietal lobules, bilateral superior temporal gyri, left posterior cingulate, right isthmus of cingulate, and right supramarginal gyrus. Greater lifetime duration of smoking (adjusted for age) was related to lower perfusion in multiple brain regions. The results indicated smokers showed significant perfusion deficits in anterior cortical regions implicated in the development, progression, and maintenance of all addictive disorders. Smokers concurrently demonstrated reduced blood flow in posterior brain regions that show morphological and metabolic aberrations as well as elevated beta amyloid deposition demonstrated by those with early stage Alzheimer disease. The findings provide additional novel evidence of the adverse effects of cigarette smoking on the human brain.

No abstract available

This investigation offers insights into system-wide pathological processes induced in response to cigarette smoke exposure by determining its influences at the gene expression level.

Recent studies have identified biomarkers of chronological age based on DNA methylation levels. Since active smoking contributes to a wide spectrum of aging-related diseases in adults, this study intended to examine whether active smoking exposure could accelerate the DNA methylation age in forms of age acceleration (AA, residuals of the DNA methylation age estimate regressed on chronological age). We obtained the DNA methylation profiles in whole blood samples by Illumina Infinium Human Methylation450 Beadchip array in two independent subsamples of the ESTHER study and calculated their DNA methylation ages by two recently proposed algorithms. None of the self-reported smoking indicators (smoking status, cumulative exposure and smoking cessation time) or serum cotinine levels was significantly associated with AA. On the contrary, we successfully confirmed that 66 out of 150 smoking-related CpG sites were associated with AA, even after correction for multiple testing (FDR <0.05). We further built a smoking index (SI) based on these loci and demonstrated a monotonic dose-response relationship of this index with AA. In conclusion, DNA methylation-based biological indicators for current and past smoking exposure, but not self-reported smoking information or serum cotinine levels, were found to be related to DNA methylation defined AA. Further research should address potential mechanisms underlying the observed patterns, such as potential reflections of susceptibility to environmental hazards in both smoking related methylation changes and methylation defined AA.