The neighbourhood social environment and alcohol use among urban and rural Scottish adolescents.
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ABSTRACT: Objectives
This research examined the relationship between neighbourhood social environmental characteristics and drinking outcomes among a sample of urban and rural adolescents.Methods
From a sample of 1558 Scottish secondary schoolchildren, surveyed as part of the 2010 Health Behaviour in School-aged Children study, we modelled three drinking outcomes on a variety of neighbourhood conditions, including social cohesion, disorder, alcohol outlet density, deprivation, and urban/rurality. Nested and cross-classified multilevel logistic regressions were specified.Results
An urban-to-rural gradient was found with non-urban adolescents exhibiting higher odds of having ever drank. Neighbourhood social cohesion related to having ever drank. Among drinkers, those living in accessible small towns had higher odds of weekly drinking and drunkenness compared to urban areas. Higher odds of drunkenness were also found in remote rural areas. Those residing in the least deprived areas had lower odds of weekly drinking.Conclusions
In Scotland, inequalities exist in adolescent alcohol use by urban/rurality and neighbourhood social conditions. Findings support regional targeting of public health efforts to address inequalities. Future work is needed to develop and evaluate intervention and prevention approaches for neighbourhoods at risk.
SUBMITTER: Martin G
PROVIDER: S-EPMC6353998 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Atmospheric particulate matter (PM) is a recognized risk factor for the global burden of disease in human populations. We are presenting here the application of toxicogenomics in the evaluation of the toxic effects of organic content of atmospheric particle matter (PM), from urban and rural environments (city of Barcelona and village of La Pobla, NE Spain), using the developing zebrafish embryo. The main goal is to identify the metabolic pathways involved in the adverse effects observed in zebrafish embryos exposed to PM organic content from urban and rural environments, also allowing the selection of genes of interest that are differentially expressed. The relevance of particle size to the PM toxicity is also addressed. Indeed, the zebrafish embryos were exposed to PM of aerodynamic diameter larger than 7.2 μm and smaller than 0.5 μm (PM10 and PM0.5, respectively). PM0.5 concentrated biological and toxic activities linked to organic substances. Transcriptomic analyses showed strong induction of the AhR signalling pathway (a.k.a. dioxin-like activity) for embryos exposed to both rural and urban extracts, correlating with the concentrations of PAHs. Urban extracts, with strong contribution of traffic emissions, specifically de-regulated oxidative stress-related genes, as well as pancreatic and eye-lens specific genes, two organs known to be affected by air pollution in humans. Exposure to rural extracts, with high contribution of wood burning emissions, affected genes implicated in basic cellular functions, in agreement with their strong embryotoxicity. Extracts from rural and urban samples elicited both common and specific transcriptome responses, suggesting different potentially adverse outcomes depending on PM source and composition. The authors thank the financial support of the Spanish Ministry (project TEA-PARTICLE, grant number CGL2011-29621) and the Portuguese Foundation for Science and Technology for the doctoral grant of Sofia R. Mesquita (SFRH/BD/80710/2011) funded by the Program POPH-QREN through the Portuguese Ministry of Education and Science and the European Social Fund, and support through project PEst-C/MAR/LA0015/2013.
2015-10-26 | GSE53522 | GEO
Project description:BACKGROUND:For people living with HIV (PLWH), alcohol use is harmful and may be influenced by unique challenges faced by PLWH living in rural areas. We describe patterns of alcohol use across rurality among PLWH. METHODS:Veterans Aging Cohort Study electronic health record data were used to identify patients with HIV (ICD-9 codes for HIV or AIDS) who completed AUDIT-C alcohol screening between February 1, 2008, and September 30, 2014. Regression models estimated and compared 4 alcohol use outcomes (any use [AUDIT-C > 0] and alcohol use disorder [AUD; ICD-9 codes for abuse or dependence] diagnoses among all PLWH, and AUDIT-C risk categories: lower- [1-3 men/1-2 women], moderate- [4-5 men/3-5 women], higher- 6-7]), and severe-risk [8-12], and heavy episodic drinking (HED; ?1 past-year occasion) among PLWH reporting use) across rurality (urban, large rural, small rural) and census-defined region. FINDINGS:Among 32,699 PLWH (29,540 urban, 1,301 large rural, and 1,828 small rural), both any alcohol use and AUD were highest in urban areas, although this varied across region. Predicted prevalence of any alcohol use was 54.1% (53.5%-54.7%) in urban, 49.6% (46.9%-52.3%) in large rural, and 50.6% (48.3%-52.9%) in small rural areas (P < .01). Predicted prevalence of AUD was 14.4% (14.0%-14.8%) in urban, 11.8% (10.0%-13.5%) in large rural, and 12.3% (10.8%-13.8%) in small rural areas (P < .01). Approximately 12% and 25% had higher- or severe-risk drinking and HED, respectively, but neither differed across rurality. CONCLUSION:Though some variation across rurality and region was observed, alcohol-related interventions are needed for PLWH across all geographic locations.
| S-EPMC6502702 | biostudies-literature
Project description:Atmospheric particulate matter (PM) is a recognized risk factor for the global burden of disease in human populations. We are presenting here the application of toxicogenomics in the evaluation of the toxic effects of organic content of atmospheric particle matter (PM), from urban and rural environments (city of Barcelona and village of La Pobla, NE Spain), using the developing zebrafish embryo. The main goal is to identify the metabolic pathways involved in the adverse effects observed in zebrafish embryos exposed to PM organic content from urban and rural environments, also allowing the selection of genes of interest that are differentially expressed. The relevance of particle size to the PM toxicity is also addressed. Indeed, the zebrafish embryos were exposed to PM of aerodynamic diameter larger than 7.2 μm and smaller than 0.5 μm (PM10 and PM0.5, respectively). PM0.5 concentrated biological and toxic activities linked to organic substances. Transcriptomic analyses showed strong induction of the AhR signalling pathway (a.k.a. dioxin-like activity) for embryos exposed to both rural and urban extracts, correlating with the concentrations of PAHs. Urban extracts, with strong contribution of traffic emissions, specifically de-regulated oxidative stress-related genes, as well as pancreatic and eye-lens specific genes, two organs known to be affected by air pollution in humans. Exposure to rural extracts, with high contribution of wood burning emissions, affected genes implicated in basic cellular functions, in agreement with their strong embryotoxicity. Extracts from rural and urban samples elicited both common and specific transcriptome responses, suggesting different potentially adverse outcomes depending on PM source and composition. The authors thank the financial support of the Spanish Ministry (project TEA-PARTICLE, grant number CGL2011-29621) and the Portuguese Foundation for Science and Technology for the doctoral grant of Sofia R. Mesquita (SFRH/BD/80710/2011) funded by the Program POPH-QREN through the Portuguese Ministry of Education and Science and the European Social Fund, and support through project PEst-C/MAR/LA0015/2013. The PM filter samples used in the present study were PM10 and PM0.5 from the urban site - total of 4 samples from 2 sampling months; and PM0.5 from the rural site - total of 2 samples from 2 sampling months (PM10 samples from the rural site were not tested due to their very low concentration in organic compounds, and insignificant biological activity, previously measured). Sampling occurred during the cold periods of the year 2012/2013. The organic fraction of PM samples was extracted by sonication using a mixture of dichloromethane:methanol. Then, the extracts were filtered, evaporated and re-dissolved in Dimethyl sulfoxide (DMSO). Zebrafish fertilized eggs were exposed to PM organic extracts (0.2% DMSO) from the urban and rural sites from 24 to 120h post-fertilization. Total RNA was isolated from whole embryos (pools of 20 individuals), using Trizol reagent protocol (Invitrogen Life Technologies, Carlsberg, CA). The microarray study was performed using the Agilent Two-colour D. rerio Oligo Microarray v3 platform, following the Agilent Microarray â?? Based Gene Expression Analysis protocol. Three biological replicates were performed for each PM sample and controls. Biological replicates, a technical replicate and a self-to-self, were simultaneously amplified and labelled using Cyanine 3 (Cy3) and Cyanine 5 (Cy5) dye. After cRNA purification (RNeasy Kit, Quiagen GmbH, Hilden, Germany), the cRNA concentration and labelling were quantified in the NanoDrop spectrophotometer, obtaining incorporation rates in the range of 15-20pmol of cyanide dye/µl cRNA and yield values > 0.825ug, as recommended. cRNA was fragmented and hybridized in 4x44K arrays, for 17h at 65oC. After the hybridization the array slides were washed, and immediately scanned using Microarray Scanner Agilent G2505C system. Data was extracted using Agilent Feature Extraction Software v10.5.1.1, and the quality of microarray data was evaluated using the Quality Control report provided by Agilent Software. Based on the microarray data analysis, 22 primers were selected and designed using Primer Express 2.0 software (Applied Biosystems, Foster City, CA). Genes were quantified by real-time PCR to validate the microarray data, and a subset of 13 genes were further selected by their robust behaviour in the validation assays, allowing to differentiate the toxic potential of PM from urban and rural sources.
2015-10-26 | E-GEOD-53522 | biostudies-arrayexpress
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Project description:Adolescents who are particularly sensitive to social stress may be vulnerable to earlier alcohol consumption and related problems. Although a small literature supports this contention, previous studies mostly relied on retrospective self-report. The current study used discrete-time survival analysis (DTSA) to test whether real-time social stress responding (via laboratory induction) and social anxiety symptoms predicted 12-month alcohol onset in an alcohol-naïve sample of young female adolescents. Anxiety elicited by the task was expected to predict greater and earlier rates of alcohol incidence, particularly among girls with higher levels of self-reported social anxiety symptoms. Participants were 104 community-recruited girls (ages 12-15 years) who completed a modified Trier Social Stress Test and questionnaires; follow-up calls were conducted at 3, 6, 9, and 12 months after the laboratory visit. Self-reported anxiety was assessed in response to the stressor following acclimation (baseline), instruction (anticipation), and speech (posttask). By 12 months, 30.8% of the sample had consumed a full alcoholic beverage. The DTSA revealed that girls with higher levels of social anxiety and greater elevations in anticipatory (but not posttask) anxiety compared to baseline had earlier alcohol initiation. This is the first study to examine the role of both laboratory-induced anxious responding and retrospective reports of social anxiety as prospective predictors of alcohol incidence. These preliminary findings suggest that adolescent girls who are more sensitive to social stress may be at risk for experimenting with alcohol earlier than their peers. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
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Project description:The molecular basis of evolutionary change is assumed to be genetic variation. However, growing evidence suggests that epigenetic mechanisms, such as DNA methylation, may also be involved in evolutionary change. An important first step in evaluating this hypothesis is to test for the presence of epigenetic variation between natural populations living under different environmental conditions. In the current study we explored variation between populations of Darwin’s finches living in adjacent “urban” and “rural” environments on Santa Cruz Island in the Galápagos. We tested for morphological, genetic, and epigenetic differences between the urban and rural populations of each of two species of ground finches, Geospiza fortis and G. fuliginosa. Using data collected from more than 1000 birds, we found significant morphological differences between populations of G. fortis, but not G. fuliginosa. We did not find genetic differences between populations of either species, based on comparisons of copy number variation (CNV). In contrast, we did find epigenetic differences between the urban and rural populations of both species, based on DNA methylation analysis. We explored genomic features and gene associations of the differentially methylated regions (DMR), as well as their possible functional significance. In summary, our study documents local population epigenetic variation within species of Darwin’s finches.
2017-01-07 | GSE87825 | GEO
Project description:Investigations of social-genetic effects, whereby a social partner's genotype affects another's outcomes, can be confounded by the influence of the social partner's rearing environment. We used marital information on more than 300,000 couples from Swedish national data to disentangle social-genetic from rearing-environment effects for alcohol use disorder (AUD). Using observational and extended-family designs, we found that (a) marriage to a spouse with a predisposition toward AUD (as indexed by a parental history of AUD) increased risk for developing AUD; (b) this increased risk was not explained by socioeconomic status, the spouse's AUD status, or contact with the spouse's parents; and (c) this increased risk reflected the psychological consequences of the spouse having grown up with an AUD-affected parent (i.e., a rearing-environment effect) rather than a social-genetic effect. Findings illustrate that a spouse's rearing-environment exposures may confer risk for AUD.
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