Slim cigarette smoking in Urban China: Who are the early adopters and why?
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ABSTRACT:
SUBMITTER: Wang J
PROVIDER: S-EPMC8277019 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:OBJECTIVES: Millions of children and adolescents in rural China are left behind as their parents move away for work. Little is known about the impact of parental migration on their smoking and self-efficacy. This study explores the associations among parental migration, self-efficacy and smoking. METHODS: A cross-sectional study was conducted among middle school students in Liangying Township, Guangdong, China. Socio-demographic and parental migration characteristics, as well as adolescent past 30-day smoking and self-efficacy level were collected using a self-administered questionnaire. Univariate and multivariate analyses were performed to estimate the risk of parental migration features for smoking and self-efficacy. Hierarchical regression was fitted to examine the relationship among parental migration, self-efficacy and smoking. RESULTS: 2609 students (93.4%) participated into the study, 44% of who were with parents who had ever been or were currently migrating. Smoking prevalence was 9.7% in boys and 0.9% in girls. Paternal migration was protective for adolescent smoking, whilst maternal migration increased the risk. Both paternal and maternal migration had adverse effects on self-efficacy, a strong influencing factor for smoking. No significant relationship was found between other migration features and smoking and self-efficacy. The smoking risk of maternal migration was partly mediated by self-efficacy. There were no differences between boys and girls. CONCLUSIONS: Our findings suggest that adolescents whose mothers migrate from home to work elsewhere are at elevated risk for smoking. Improving self-efficacy may be an effective means to keep adolescents away from smoking, especially for those with maternal migration.
| S-EPMC3592888 | biostudies-other
Project description:Rural areas of the United States have a higher smoking prevalence than urban areas. However, no recent studies have rigorously examined potential changes in this disparity over time or whether the disparity can be explained by demographic or psychosocial characteristics associated with smoking. The present study used yearly cross sectional data from the National Survey on Drug Use and Health from 2007 through 2014 to examine cigarette smoking trends in rural versus urban areas of the United States. The analytic sample included 303,311 respondents. Two regression models were built to examine (a) unadjusted rural and urban trends in prevalence of current smoking and (b) whether differences remained after adjusting for demographic and psychosocial characteristics. Results of the unadjusted model showed disparate and diverging cigarette use trends during the 8-year time period. The adjusted model also showed diverging trends, initially with no or small differences that became more pronounced across the 8-year period. We conclude that differences reported in earlier studies may be explained by differences in rural versus urban demographic and psychosocial risk factors, while more recent and growing disparities appear to be related to other factors. These emergent differences may be attributable to policy-level tobacco control and regulatory factors that disproportionately benefit urban areas such as enforcement of regulations around the sale and marketing of tobacco products and treatment availability. Strong federal policies and targeted or tailored interventions may be important to expanding tobacco control and regulatory benefits to vulnerable populations including rural Americans.
| S-EPMC5600673 | biostudies-literature
Project description:BackgroundWhile the heritability of cigarette smoking and nicotine dependence (ND) is well-documented, the contribution of specific genetic variants to specific phenotypes has not been closely examined. The objectives of this study were to test the associations between 321 tagging single-nucleotide polymorphisms (SNPs) that capture common genetic variation in 24 genes, and early smoking and ND phenotypes in novice adolescent smokers, and to assess if genetic predictors differ across these phenotypes.MethodsIn a prospective study of 1294 adolescents aged 12-13 years recruited from ten Montreal-area secondary schools, 544 participants who had smoked at least once during the 7-8 year follow-up provided DNA. 321 single-nucleotide polymorphisms (SNPs) in 24 candidate genes were tested for an association with number of cigarettes smoked in the past 3 months, and with five ND phenotypes (a modified version of the Fagerstrom Tolerance Questionnaire, the ICD-10 and three clusters of ND symptoms representing withdrawal symptoms, use of nicotine for self-medication, and a general ND/craving symptom indicator).ResultsThe pattern of SNP-gene associations differed across phenotypes. Sixteen SNPs in seven genes (ANKK1, CHRNA7, DDC, DRD2, COMT, OPRM1, SLC6A3 (also known as DAT1)) were associated with at least one phenotype with a p-value <0.01 using linear mixed models. After permutation and FDR adjustment, none of the associations remained statistically significant, although the p-values for the association between rs557748 in OPRM1 and the ND/craving and self-medication phenotypes were both 0.076.ConclusionsBecause the genetic predictors differ, specific cigarette smoking and ND phenotypes should be distinguished in genetic studies in adolescents. Fifteen of the 16 top-ranked SNPs identified in this study were from loci involved in dopaminergic pathways (ANKK1/DRD2, DDC, COMT, OPRM1, and SLC6A3).ImpactDopaminergic pathways may be salient during early smoking and the development of ND.
| S-EPMC4278712 | biostudies-literature
Project description:BackgroundSystematic data regarding adolescent smoking are needed at the national level to support evidence-based tobacco control in China. The goal of this study was to estimate smoking prevalence among Chinese adolescents using published data.MethodsPublished studies were located electronically from the commonly used databases in Chinese and English, complemented by manual searching. Forty-five studies were selected of the 9771 retrieved from the databases. These studies targeted adolescents aged 12-17 or middle/high school students, were conducted during the 1981-2010, and had adequate data for meta-analysis. The 45 selected studies covered 52 sites in different parts of China. Smoking rates were estimated using the sample-weighted and random effect method.ResultsThe estimated prevalence rate of lifetime smoking (ever smoked) varied within a narrow range (39.04%-46.03%) for males and progressively increased from 2.47% in 1981-1985 to 19.72% in 2001-2005 for females. The prevalence rate of current (30-day) smoking for males declined from 26.62% in 1981-1985 to 10.86% in 1996-2000 before increasing again. The prevalence of current smoking for females increased from 0.29% in 1981-1985 to 3.26% in 2006-2010.ConclusionsThe high levels of male smoking and the rapid increase in female smoking indicate growing burdens from tobacco-related diseases, underscoring the urgent need to strengthen adolescent tobacco control in China.
| S-EPMC4454929 | biostudies-literature
Project description:Atmospheric fine particulate matter (PM2.5) causes severe haze in China and is regarded as a threat to human health. The health effects of PM2.5 vary location by location due to the variation in size distribution, chemical com position, and sources. In this study, the cytotoxicity effect, oxidative stress, and gene expression regulation of PM2.5 in Chengdu and Chongqing, two typical urban areas in southern China, were evaluated. Urban PM2.5 in summer and winter significantly inhibited cell viability and increased reactive oxygen species (ROS) levels in A549 cells. Notably, PM2.5 in winter exhibited higher cytotoxicity and ROS level than summer. Moreover, in this study, PM2.5 commonly induced cancer-related gene expression such as cell adhesion molecule 1(PECAM1), interleukin 24 (IL24), and cytochrome P450 (CYP1A1); meanwhile, PM2.5 commonly acted on cancer-related biological functions such as cell-substrate junction, cell-cell junction, and focal adhesion. In partic ular, PM2.5 in Chengdu in summer had the highest carcinogenic potential among PM2.5 at the two sites in summer and winter. Importantly, cancer-related genes were uniquely targeted by PM2.5, such as epithelial splicing regu latory protein 1 (ESRP1) and membrane-associated ring-CH-type finger 1 (1-Mar) by Chengdu summer PM2.5; collagen type IX alpha 3 chain (COL9A3) by Chengdu winter PM2.5; SH2 domain-containing 1B (SH2D1B) by Chongqing summer PM2.5; and interleukin 1 receptor-like 1 (IL1RL1) and zinc finger protein 42 (ZNF423) by Chongqing winter PM2.5. Meanwhile, important cancer-related biological functions were specially induced by PM2.5, such as cell cycle checkpoint by Chengdu summer PM2.5; macromolecule methylation by Chengdu win ter PM2.5; endoplasmic reticulum-Golgi intermediate compartment membrane by Chongqing summer PM2.5;and cellular lipid catabolic process by Chongqing winter PM2.5. Conclusively, in the typical urban areas of southern China, both summer and winter PM2.5 illustrated significant gene regulation effects. This study contrib utes to evaluating the adverse health effects of PM2.5 in southern China and providing public health suggestions for policymakers.
2022-10-30 | GSE216512 | GEO
Project description:PurposeThe practice of "genomic" (or "personalized") medicine requires the availability of appropriate diagnostic testing. Our study objective was to identify the reasons for health systems to bring next-generation sequencing into their clinical laboratories and to understand the process by which such decisions were made. Such information may be of value to other health systems seeking to provide next-generation sequencing testing to their patient populations.MethodsA standardized open-ended interview was conducted with the laboratory medical directors and/or department of pathology chairs of 13 different academic institutions in 10 different states.ResultsGenomic testing for cancer dominated the institutional decision making, with three primary reasons: more effective delivery of cancer care, the perceived need for institutional leadership in the field of genomics, and the premise that genomics will eventually be cost-effective. Barriers to implementation included implementation cost; the time and effort needed to maintain this newer testing; challenges in interpreting genetic variants; establishing the bioinformatics infrastructure; and curating data from medical, ethical, and legal standpoints. Ultimate success depended on alignment with institutional strengths and priorities and working closely with institutional clinical programs.ConclusionThese early adopters uniformly viewed genomic analysis as an imperative for developing their expertise in the implementation and practice of genomic medicine.
| S-EPMC4262758 | biostudies-literature
Project description:COVID-19 vaccine hesitancy is currently-one of the main obstacles to worldwide herd immunity and socioeconomic recovery. Because vaccine coverage can vary between and within countries, it is important to identify sources of variation so that policies can be tailored to different population groups. In this paper, we analyze the results from a survey designed and implemented in order to identify early adopters and laggers in six big cities located in Argentina, Colombia, Chile, Ecuador, Peru, and Dominican Republic. We find that trust in government and science, accurate knowledge about the value of vaccination and vaccine effects, and perceived risk of getting sick is associated with a higher probability to get vaccinated. We also identify potential laggers such as women and populations with high education but low knowledge about vaccines. We discuss specific strategies to promote vaccination among these populations groups as well as more general strategies designed to gain trust. These findings are specific to the context of Latin America insofar as the underlying factors associated with the choice to be vaccinated vary significantly by location and in relation to individual-level factors.
| S-EPMC9584855 | biostudies-literature
Project description:Introduction:This study examines the associations between early onset of e-cigarette use and cigarette smoking and other substance use behaviors among US adolescents. Methods:Data were collected via self-administered questionnaires from a nationally representative sample of 2299 US high school seniors attending public and private high schools during the spring of their senior year in 2015 as part of the Monitoring the Future study. Results:A higher percentage of adolescents who began using e-cigarettes in ninth grade or earlier (early onset) were found to report current and lifetime cigarette smoking and other substance use relative to those individuals who never used e-cigarettes or those who began using e-cigarettes later in the 12th grade. Multivariate logistic regression analyses indicated that the adjusted odds of alcohol use, cigarette smoking, marijuana use, nonmedical prescription drug use, and other illicit drug use among early onset e-cigarette users were significantly greater than those for individuals never having used e-cigarettes (adjusted odds ratios [AORs] ranged 9.5-70.6, p < .001). While these associations were significant for both experimental and frequent e-cigarette users, the effects of early onset were stronger among frequent e-cigarette users. Similarly, the odds of these substance use behaviors (except alcohol) among early onset e-cigarette users were also significantly greater than the odds for later onset e-cigarette users (AORs ranged 2.8-4.1, p < .05). Conclusions:Early onset of e-cigarette use was significantly associated with increased odds of cigarette smoking and other substance use behaviors. E-cigarette use is often preceded by alcohol use, cigarette smoking, and marijuana use, suggesting that more long-term prospective studies are warranted. Implications:To date, no studies have examined the probability of cigarette smoking and other substance use behaviors as a function of age at onset of e-cigarette use. In the present study, early onset of e-cigarette use was significantly associated with increased odds of cigarette smoking and other substance use behaviors. The findings reinforce the importance of addressing a wide range of substances including alcohol, traditional cigarettes, and marijuana when developing early primary prevention efforts to reduce e-cigarette use among youth.
| S-EPMC6037083 | biostudies-other
Project description:Longitudinal analyses investigated (a) the co-occurrence of marijuana use and conventional cigarette smoking within time and (b) bidirectional associations between marijuana and conventional cigarette use in three developmental periods: adolescence, young adulthood, and adulthood. A cross-lag model was used to examine the bidirectional model of marijuana and conventional cigarette smoking frequency from ages 13 to 33 years. The bidirectional model accounted for gender, school-age economic disadvantage, childhood attention problems, and race. Marijuana use and conventional cigarette smoking were associated within time in decreasing magnitude and increased cigarette smoking predicted increased marijuana use during adolescence. A reciprocal relationship was found in the transition from young adulthood to adulthood, such that increased conventional cigarette smoking at age 24 years uniquely predicted increased marijuana use at age 27 years, and increased marijuana use at age 24 years uniquely predicted more frequent conventional cigarette smoking at age 27 years, even after accounting for other factors. The association between marijuana and cigarette smoking was found to developmentally vary in the current study. Results suggest that conventional cigarette smoking prevention efforts in adolescence and young adulthood could potentially lower the public health impact of both conventional cigarette smoking and marijuana use. Findings point to the importance of universal conventional cigarette smoking prevention efforts among adolescents as a way to decrease later marijuana use and suggest that a prevention effort focused on young adults as they transition to adulthood would lower the use of both cigarette and marijuana use.
| S-EPMC5505066 | biostudies-literature
Project description:BACKGROUND:DNA methylation leaves a long-term signature of smoking exposure and is one potential mechanism by which tobacco exposure predisposes to adverse health outcomes, such as cancers, osteoporosis, lung, and cardiovascular disorders. METHODS AND RESULTS:To comprehensively determine the association between cigarette smoking and DNA methylation, we conducted a meta-analysis of genome-wide DNA methylation assessed using the Illumina BeadChip 450K array on 15?907 blood-derived DNA samples from participants in 16 cohorts (including 2433 current, 6518 former, and 6956 never smokers). Comparing current versus never smokers, 2623 cytosine-phosphate-guanine sites (CpGs), annotated to 1405 genes, were statistically significantly differentially methylated at Bonferroni threshold of P<1×10-7 (18?760 CpGs at false discovery rate <0.05). Genes annotated to these CpGs were enriched for associations with several smoking-related traits in genome-wide studies including pulmonary function, cancers, inflammatory diseases, and heart disease. Comparing former versus never smokers, 185 of the CpGs that differed between current and never smokers were significant P<1×10-7 (2623 CpGs at false discovery rate <0.05), indicating a pattern of persistent altered methylation, with attenuation, after smoking cessation. Transcriptomic integration identified effects on gene expression at many differentially methylated CpGs. CONCLUSIONS:Cigarette smoking has a broad impact on genome-wide methylation that, at many loci, persists many years after smoking cessation. Many of the differentially methylated genes were novel genes with respect to biological effects of smoking and might represent therapeutic targets for prevention or treatment of tobacco-related diseases. Methylation at these sites could also serve as sensitive and stable biomarkers of lifetime exposure to tobacco smoke.
| S-EPMC5267325 | biostudies-literature