The impact of smoking in Crohn's disease: no smoke without fire.
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ABSTRACT:
SUBMITTER: Aldhous MC
PROVIDER: S-EPMC5517176 | biostudies-other | 2010 Oct
REPOSITORIES: biostudies-other
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Project description:Background People who smoke with serious mental illness carry disproportionate costs from smoking, including poor health and premature death from tobacco-related illnesses. Hospitals in New Zealand are ostensibly smoke-free; however, some mental health wards have resisted implementing this policy. Aim This study explored smoking in acute metal health wards using data emerging from a large sociological study on modern acute psychiatric units. Methods Eighty-five in-depth, semi-structured interviews were conducted with staff and service users from four units. Data were analysed using a social constructionist problem representation approach. Results Although high-level smoke-free policies were mandatory, most participants disregarded these policies and smoking occurred in internal courtyards. Staff reasoned that acute admissions were not the time to quit smoking, citing the sceptres of distress and possibly violence; further, they found smoking challenging to combat. Inconsistent enforcement of smoke-free policies was common and problematic. Many service users also rejected smoke-free policies; they considered smoking facilitated social connections, alleviated boredom, and helped them feel calm in a distressing environment – some started or increased smoking following admission. A minority viewed smoking as a problem; a fire hazard, or pollutant. No one mentioned its health risks. Conclusion Psychiatric wards remain overlooked corners where hospital smoke-free policies are inconsistently applied or ignored. Well-meaning staff hold strong but anachronistic views about smoking. To neglect smoking cessation support for people with serious mental illness is discriminatory and perpetuates health and socioeconomic inequities. However, blanket applications of generic policy are unlikely to succeed. Solutions may include myth-busting education for service users and staff, local champions, and strong managerial support and leadership, with additional resourcing during transition phases. Smoke-free policies need consistent application with non-judgemental NRT and, potentially, other treatments. Smoking cessation would be supported by better designed facilities with more options for alleviating boredom, expressing autonomy, facilitating social connections, and reducing distress.
| S-EPMC8592473 | biostudies-literature
Project description:Background/aimsCurrent models of Crohn's disease (CD) describe an inappropriate immune response to gut microbiota in genetically susceptible individuals. NOD2 variants are strongly associated with development of CD, and NOD2 is part of the innate immune response to bacteria. This study aimed to identify differences in fecal microbiota in CD patients and non-IBD controls stratified by NOD2 genotype.MethodsPatients with CD and non-IBD controls of known NOD2 genotype were identified from patients in previous UK IBD genetics studies and the Cambridge bioresource (genotyped/phenotyped volunteers). Individuals with known CD-associated NOD2 mutations were matched to those with wild-type genotype. We obtained fecal samples from patients in clinical remission with low fecal calprotectin (<250 µg/g) and controls without gastrointestinal disease. After extracting DNA, the V1-2 region of 16S rRNA genes were polymerase chain reaction (PCR)-amplified and sequenced. Analysis was undertaken using the mothur package. Volatile organic compounds (VOC) were also measured.ResultsNinety-one individuals were in the primary analysis (37 CD, 30 bioresource controls, and 24 household controls). Comparing CD with nonIBD controls, there were reductions in bacterial diversity, Ruminococcaceae, Rikenellaceae, and Christensenellaceae and an increase in Enterobacteriaceae. No significant differences could be identified in microbiota by NOD2 genotype, but fecal butanoic acid was higher in Crohn's patients carrying NOD2 mutations.ConclusionsIn this well-controlled study of NOD2 genotype and fecal microbiota, we identified no significant genotype-microbiota associations. This suggests that the changes associated with NOD2 genotype might only be seen at the mucosal level, or that environmental factors and prior inflammation are the predominant determinant of the observed dysbiosis in gut microbiota.
| S-EPMC6176884 | biostudies-literature
Project description:: Our objective is to assess the effect of genetic and environmental factors on Crohn's disease location.: We identified 628 patients with Crohn's disease within the Washington University database (April 2005 through February 2010) that had complete information on 31 Crohn's disease-associated genotypes and clinical information on disease location (L1 to L4), smoking, sex, race, and age at diagnosis. For statistical reasons, the 3 major NOD2 alleles (rs2066844, rs2066845, and rs2066847) were grouped together. Logistic regression incorporating all of the genotypes and clinical covariates, including smoking, was performed with stepwise variable selection and by best subset selection.: Stepwise variable selection selected 3 major covariates, composite NOD2 genotype, smoking, and TNFSF15 genotype, which are also the 3 covariates selected by the best subset method. Whereas the NOD2 genotype and smoking are positively associated with ileal (L1 + L3) disease, the TNFSF15 genotype is positively associated with isolated colonic (L2) disease.: The ability to detect disease site associations in this single-center study may be limited by the population size, low allelic frequency, and/or low odds ratio of certain Crohn's disease risk alleles.: These results indicate that NOD2 genotype, smoking status, and TNFSF15 genotype should be included as covariates in assessing the effect of genetic and environmental factors on Crohn's disease site location.
| S-EPMC3403696 | biostudies-literature
Project description:There is considerable evidence that inhaled toxicants such as cigarette smoke can cause both irreversible changes to the genetic material (DNA mutations) and putatively reversible changes to the epigenetic landscape (changes in the DNA methylation and chromatin modification state). The diseases that are believed to involve genetic and epigenetic perturbations include lung cancer, chronic obstructive pulmonary disease (COPD), and cardiovascular disease (CVD), all of which are strongly linked epidemiologically to cigarette smoking. In this review, we highlight the significance of genomics and epigenomics in these major smoking-related diseases. We also summarize the in vitro and in vivo findings on the specific perturbations that smoke and its constituent compounds can inflict upon the genome, particularly on the pulmonary system. Finally, we review state-of-the-art genomics and new techniques such as high-throughput sequencing and genome-wide chromatin assays, rapidly evolving techniques which have allowed epigenetic changes to be characterized at the genome level. These techniques have the potential to significantly improve our understanding of the specific mechanisms by which exposure to environmental chemicals causes disease. Such mechanistic knowledge provides a variety of opportunities for enhanced product safety assessment and the discovery of novel therapeutic interventions.
| S-EPMC3491444 | biostudies-literature
Project description:BackgroundThe development and course of Crohn's disease (CD) is related to both genetic and environmental factors. Smoking has been found to exacerbate the course of CD by increasing the risk of developing fistulas and strictures as well as the need for surgery, possibly because of an interaction between smoking or nicotine on macrophage function and the intestinal microvasculature. Several genes are involved in the pathogenesis of CD, and in this study the gene expression differences of the descending colonic mucosa were investigated in CD (smokers or never smokers) and controls (smokers or never smokers).AimTo identify any difference in gene expression of the descending colonic mucosa between smoking and never-smoking CD patients (and controls) by determining genetic expression profiles from microarray analysis.MethodsFifty-seven specimens were obtained by routine colonoscopy from the included material: CD smokers (n = 28) or never-smokers (n = 14) as compared to fifteen healthy controls (8 smokers and 7 never-smokers). RNA was isolated and gene expression assessed with Affymetrix GeneChip Human Genome U133 Plus 2.0. Data were analyzed by principal component analysis (PCA), Wilcoxon rank sum test and multiple linear regressions. Real-time (RT) PCR was subsequently applied to verify microarray results.ResultsThe PCA analysis showed no intrinsic clustering of smokers versus never-smokers. However, when Wilcoxon rank sum test corrected with Q values were performed, six known genes were significantly expressed differently in the inflamed CD smokers as compared to the inflamed CD never-smokers: ring finger protein 138 (RNF138), metalothionein 2A (MT2A) and six transmembrane epithelial antigen of the prostate 3 (STEAP3), SA hypertension-associated homolog, PGM2L1 and KCNJ2. The subsequent RT-PCR-analyses verified, however, that only RNF138, MT2A and STEAP3 were significantly up-regulated in CD smokers in specimens with inflammatory activity of the descending colon.ConclusionsThe present study demonstrates that the genes, RNF138, MT2A, and STEAP3 are differently expressed in the inflamed descending colon of smoking versus never-smoking CD patients, which might be of relevance for the poorer clinical course among CD smokers. Many gastroenterologists are still not totally aware of the benefits of smoking cessation in relation to CD, and do not put much effort into getting the patients to quit, therefore more information on the negative effects of smoking, seems warranted.
| S-EPMC2708910 | biostudies-literature
Project description:BackgroundSmoke-free ordinances (SFO) have been shown to be effective public health interventions, but there is limited data on the impact SFO on lung cancer outcomes. We explored the effect of county-level SFO strength with smoking prevalence and lung cancer incidence in Indiana.MethodsWe obtained county-level lung cancer incidence from the Indiana State Cancer Registry and county-level characteristics from the Indiana Tobacco Prevention and Cessation Commission's policy database between 1995 and 2016. Using generalized estimating equations, we performed multivariable analyses of smoking prevalence and age-adjusted lung cancer rates with respect to the strength of smoke-free ordinances at the county level over time.ResultsOf Indiana's 92 counties, 24 had a SFO by 2011. In 2012, Indiana enacted a state-wide SFO enforcing at least moderate level SFO protection. Mean age-adjusted lung cancer incidence per year was 76.8 per 100,000 population and mean smoking prevalence per year was 25% during the study period. Counties with comprehensive or moderate SFO had a smoking prevalence 1.2% (95% CI [-1.88, -0.52]) lower compared with counties with weak or no SFO. Counties that had comprehensive or moderate SFO also had an 8.4 (95% CI [-11.5, -5.3]) decrease in new lung cancer diagnosis per 100,000 population per year compared with counties that had weak or no SFO.ConclusionCounties with stronger smoke-free air ordinances were associated with decreased smoking prevalence and fewer new lung cancer cases per year. Strengthening SFO is paramount to decreasing lung cancer incidence.
| S-EPMC8051804 | biostudies-literature
Project description:BackgroundImplementation of smoke free policies has potentially substantial effects on health by reducing secondhand smoke exposure. However little is known about whether the introduction of anti-smoking legislation translates into decreased secondhand smoke exposure. We examined whether smoking bans impact rates of secondhand smoke exposure in public places and rates of complete workplace smoking restriction.MethodsCanadian Community Health Survey was used to obtain secondhand smoking exposure rates in 15 Ontario municipalities. Data analysis included descriptive summaries and 95% confidence intervals were calculated and compared across groupsResultsAcross all studied municipalities, secondhand smoke exposure in public places decreased by 4.7% and workplace exposure decreased by 2.3% between the 2003 and 2005 survey years. The only jurisdiction to implement a full ban from no previous ban was also the only setting that experienced significant decreases in both individual exposure to secondhand smoke in a public place (-17.3%, 95% CI -22.8, -11.8) and workplace exposure (-18.1%, 95% CI -24.9, -11.3). Exposures in vehicles and homes declined in almost all settings over time.ConclusionsImplementation of a full smoking ban was associated with the largest decreases in secondhand smoke exposure while partial bans and changes in existing bans had inconsistent effects. In addition to decreasing exposure in public places as would be expected from legislation, bans may have additional benefits by decreasing rates of current smokers and decreasing exposures to secondhand smoke in private settings.
| S-EPMC3064640 | biostudies-literature
Project description:Little research has examined the effects of high concentration, medium-duration smoke exposure on cardiovascular health. We investigated whether six weeks of exposure to smoke from the 2014 Hazelwood coal mine fire in Victoria (Australia), was associated with long-term clinical or subclinical cardiovascular disease approximately four years later, in adult residents of the towns of Morwell (exposed, n = 336) and Sale (unexposed, n = 162). The primary outcome was serum high sensitivity (hs) C-reactive protein (CRP). Blood pressure, electrocardiogram, flow mediated dilatation and serum levels of hs-troponin, N-terminal pro B-type natriuretic peptide and lipids were secondary outcomes. There was no significant difference in weighted median hsCRP levels between exposed and unexposed participants (1.9 mg/L vs. 1.6 mg/L, p = 0.273). Other outcomes were comparable between the groups. hsCRP was associated in a predictable manner with current smoking, obesity and use of lipid-lowering therapy. Four years after a 6-week coal mine fire, this study found no association between smoke exposure and markers of clinical or subclinical cardiovascular disease in exposed adults.
| S-EPMC7914645 | biostudies-literature
Project description:It is suggested that subtyping of complex inflammatory diseases can be based on genetic susceptibility and relevant environmental exposure (G+E). We propose that using matched cellular phenotypes in human subjects and corresponding preclinical models with the same G+E combinations is useful to this end. As an example, defective Paneth cells can subtype Crohn's disease (CD) subjects; Paneth cell defects have been linked to multiple CD susceptibility genes and are associated with poor outcome. We hypothesized that CD susceptibility genes interact with cigarette smoking, a major CD environmental risk factor, to trigger Paneth cell defects. We found that both CD subjects and mice with ATG16L1T300A (T300A; a prevalent CD susceptibility allele) developed Paneth cell defects triggered by tobacco smoke. Transcriptional analysis of full-thickness ileum and Paneth cell-enriched crypt base cells showed the T300A-smoking combination altered distinct pathways, including proapoptosis, metabolic dysregulation, and selective downregulation of the PPAR? pathway. Pharmacologic intervention by either apoptosis inhibitor or PPAR? agonist rosiglitazone prevented smoking-induced crypt apoptosis and Paneth cell defects in T300A mice and mice with conditional Paneth cell-specific knockout of Atg16l1. This study demonstrates how explicit G+E can drive disease-relevant phenotype and provides rational strategies for identifying actionable targets.
| S-EPMC6205411 | biostudies-literature
Project description:Thirdhand smoke (THS) residue results from secondhand smoke, and is emerging as a distinct public health hazard, particularly for medically fragile pediatric patients living with smokers. THS is difficult to remove and readily reacts with other pollutants to form carcinogens and ultrafine particles. This study investigated THS found in homes of high-risk infants admitted to a neonatal intensive care unit and their association with characteristics (eg, number of household smokers) hypothesized to influence THS.Baseline data from 141 hospitalized infants' homes were analyzed, along with follow-up data (n = 22) to explore household smoking characteristics and THS changes in response to indoor smoking ban policies.Households with an indoor ban, in which not more than 10 cigarettes/d were smoked, had the lowest levels of THS contamination compared to homes with no ban (P < .001) and compared to homes with an indoor ban in which greater numbers of cigarettes were smoked (P < .001). Importantly, homes with an indoor ban in which at least 11 cigarettes/d were smoked were not different from homes without a ban. The follow-up sample of 22 homes provided initial evidence indicating that, unless a ban was implemented, THS levels in homes continued to increase over time.Preliminary longitudinal data suggest that THS may continue to accumulate in homes over time and household smoking bans may be protective. However, for homes with high occupant smoking levels, banning indoor smoking may not be fully adequate to protect children from THS. Unless smoking is reduced and bans are implemented, medically fragile children will be exposed to the dangers of THS.
| S-EPMC5896819 | biostudies-literature