Urban-rural and socioeconomic status: Impact on multimorbidity prevalence in hospitalized patients.
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ABSTRACT: Objective
The aim of this study was to describe multimorbidity prevalence in hospitalized adults, by urban-rural area of residence and socioeconomic status (SES).Methods
Linked hospital episode data were used. Adults (≥18 years) admitted to hospital as an inpatient during 2014 in Grampian, Scotland, were included. Conditions were identified from admissions during the 5 years prior to the first admission in 2014. Multimorbidity was defined as ≥2 conditions and measured using Tonelli et al. based on International Classification of Diseases-10 coding (preselected list of 30 conditions). We used proportions and 95% confidence intervals (CIs) to summarize the prevalence of multimorbidity by age group, sex, urban-rural category and deprivation. The association between multimorbidity and patient characteristics was assessed using the χ 2 test.Results
Forty one thousand five hundred and forty-five patients were included (median age 62, 52.6% female). Overall, 27.4% (95% CI 27.0, 27.8) of patients were multimorbid. Multimorbidity prevalence was 28.8% (95% CI 28.1, 29.5) in large urban versus 22.0% (95% CI 20.9, 23.3) in remote rural areas and 28.7% (95% CI 27.2, 30.3) in the most deprived versus 26.0% (95% CI 25.2, 26.9) in the least deprived areas. This effect was consistent in all age groups, but not statistically significant in the age group 18-29 years. Multimorbidity increased with age but was similar for males and females.Conclusion
Given the scarcity of research into the effect of urban-rural area and SES on multimorbidity prevalence among hospitalized patients, these findings should inform future research into new models of care, including the consideration of urban-rural area and SES.
SUBMITTER: Robertson L
PROVIDER: S-EPMC7171988 | 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:BackgroundUrbanization is often cited as a main cause of increasing BMIs in low- and middle-income countries (LMICs), and urban residents in LMICs tend to have higher BMIs than do rural residents. However, urban-rural differences may be driven by differences in socioeconomic status (SES).ObjectiveUsing nationally representative data collected at 2 time points in 38 LMICs, we assessed the association between urban residence and BMI before and after adjustment for measures of individual- and household-level SES.DesignWe conducted a cross-sectional analysis of nationally representative samples of 678,471 nonpregnant women aged 15-49 y, with 225,312 women in the earlier round of surveys conducted between 1991 and 2004 and 453,159 women in the later round conducted between 1998 and 2010. We used linear and ordered multinomial analysis with a country fixed effect to obtain a pooled estimate and a country-stratified analysis.ResultsWe found that mean BMI (kg/m²) in less-developed countries was generally higher within urban areas (excess BMI associated with urban residence before wealth index adjustment: 1.55; 95% CI: 1.52, 1.57). However, the urban association was attenuated after SES was accounted for (association after adjustment: 0.44; 95% CI: 0.41, 0.47). Individual- and household-level SES measures were independently and positively associated with BMI.ConclusionThe association between urban residence and obesity in LMICs is driven largely by higher individual- and community-level SES in urban areas, which suggests that urban residence alone may not cause increased body weight in developing countries.
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| S-EPMC4060853 | biostudies-other
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
Project description:ObjectiveTo investigate the relationship between socioeconomic factors and bronchiolitis severity among hospitalized infants.MethodsWe performed a 17-center, prospective cohort study from 2011 to 2014. Children <1 year old hospitalized with bronchiolitis were enrolled. Socioeconomic factors included estimated median household income (MHI) per home ZIP code, parent-reported household income, number of adults and children in household, and insurance type. We defined higher bronchiolitis severity as receipt of intensive care treatment. Multivariable logistic regression was used to analyze the association between socioeconomic factors and bronchiolitis severity, with the final model adjusted for potential clustering by site.ResultsIn multivariable models adjusted for demographic and clinical characteristics, estimated MHI was the socioeconomic factor most strongly associated with severity. Compared to infants with an intermediate MHI ($40,000-$79,999), odds of receiving intensive care treatment were significantly higher for those with MHI of ≥$80,000 (aOR 2.05, 95% CI 1.19-3.53). No significant associations were found for the other socioeconomic factors (all P > .30). While there were no significant differences in clinical presentation between income groups (all P > .25) or in receipt of mechanical ventilation alone (P = .98), infants with estimated MHI ≥$80,000 were significantly more likely to specifically have been admitted to the intensive care unit (P = .01).ConclusionsIn this multicenter study of infants hospitalized with bronchiolitis, we identified higher median household income as a risk factor for intensive care treatment. This work may yield important biological or nonbiological insights for the future management of infants with bronchiolitis.
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