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Sökning: WFRF:(Rizzuto Debora)

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1.
  • Akugizibwe, Roselyne, et al. (författare)
  • Multimorbidity Patterns and Unplanned Hospitalisation in a Cohort of Older Adults
  • 2020
  • Ingår i: Journal of Clinical Medicine. - : MDPI AG. - 2077-0383. ; 9:12
  • Tidskriftsartikel (refereegranskat)abstract
    • The presence of multiple chronic conditions (i.e., multimorbidity) increases the risk of hospitalisation in older adults. We aimed to examine the association between different multimorbidity patterns and unplanned hospitalisations over 5 years. To that end, 2,250 community-dwelling individuals aged 60 years and older from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K) were studied. Participants were grouped into six multimorbidity patterns using a fuzzy c-means cluster analysis. The associations between patterns and outcomes were tested using Cox models and negative binomial models. After 5 years, 937 (41.6%) participants experienced at least one unplanned hospitalisation. Compared to participants in the unspecific multimorbidity pattern, those in the cardiovascular diseases, anaemia and dementia pattern, the psychiatric disorders pattern and the metabolic and sleep disorders pattern presented with a higher hazard of first unplanned hospitalisation (hazard ratio range: 1.49-2.05; p < 0.05 for all), number of unplanned hospitalisations (incidence rate ratio (IRR) range: 1.89-2.44; p < 0.05 for all), in-hospital days (IRR range: 1.91-3.61; p < 0.05 for all), and 30-day unplanned readmissions (IRR range: 2.94-3.65; p < 0.05 for all). Different multimorbidity patterns displayed a differential association with unplanned hospital care utilisation. These findings call for a careful primary care follow-up of older adults with complex multimorbidity patterns.
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2.
  • Arthur Hvidtfeldt, Ulla, et al. (författare)
  • Long-term exposure to fine particle elemental components and lung cancer incidence in the ELAPSE pooled cohort
  • 2021
  • Ingår i: Environmental Research. - : Elsevier BV. - 0013-9351 .- 1096-0953. ; 193
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: An association between long-term exposure to fine particulate matter (PM2.5) and lung cancer has been established in previous studies. PM2.5 is a complex mixture of chemical components from various sources and little is known about whether certain components contribute specifically to the associated lung cancer risk. The present study builds on recent findings from the Effects of Low-level Air Pollution: A Study in Europe (ELAPSE) collaboration and addresses the potential association between specific elemental components of PM2.5 and lung cancer incidence.Methods: We pooled seven cohorts from across Europe and assigned exposure estimates for eight components of PM2.5 representing non-tail pipe emissions (copper (Cu), iron (Fe), and zinc (Zn)), long-range transport (sulfur (S)), oil burning/industry emissions (nickel (Ni), vanadium (V)), crustal material (silicon (Si)), and biomass burning (potassium (K)) to cohort participants' baseline residential address based on 100 m by 100 m grids from newly developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status).Results: The pooled study population comprised 306,550 individuals with 3916 incident lung cancer events during 5,541,672 person-years of follow-up. We observed a positive association between exposure to all eight components and lung cancer incidence, with adjusted HRs of 1.10 (95% CI 1.05, 1.16) per 50 ng/m(3) PM2.5 K, 1.09 (95% CI 1.02, 1.15) per 1 ng/m3 PM2.5 Ni, 1.22 (95% CI 1.11, 1.35) per 200 ng/m(3) PM2.5 S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m(3) PM2.5 V. Effect estimates were largely unaffected by adjustment for nitrogen dioxide (NO2). After adjustment for PM2.5 mass, effect estimates of K, Ni, S, and V were slightly attenuated, whereas effect estimates of Cu, Si, Fe, and Zn became null or negative.Conclusions: Our results point towards an increased risk of lung cancer in connection with sources of combustion particles from oil and biomass burning and secondary inorganic aerosols rather than non-exhaust traffic emissions. Specific limit values or guidelines targeting these specific PM2.5 components may prove helpful in future lung cancer prevention strategies.
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3.
  • Calderón-Larrañaga, Amaia, et al. (författare)
  • Assessing and Measuring Chronic Multimorbidity in the Older Population : A Proposal for Its Operationalization
  • 2017
  • Ingår i: The journals of gerontology. Series A, Biological sciences and medical sciences. - : Oxford University Press (OUP). - 1079-5006 .- 1758-535X. ; 72:10, s. 1417-1423
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundAlthough the definition of multimorbidity as the simultaneous presence of two or more chronic diseases is well established, its operationalization is not yet agreed. This study aims to provide a clinically driven comprehensive list of chronic conditions to be included when measuring multimorbidity. MethodsBased on a consensus definition of chronic disease, all four-digit level codes from the International Classification of Diseases, 10th revision (ICD-10) were classified as chronic or not by an international and multidisciplinary team. Chronic ICD-10 codes were subsequently grouped into broader categories according to clinical criteria. Last, we showed proof of concept by applying the classification to older adults from the Swedish National study of Aging and Care in Kungsholmen (SNAC-K) using also inpatient data from the Swedish National Patient Register.ResultsA disease or condition was considered to be chronic if it had a prolonged duration and either (a) left residual disability or worsening quality of life or (b) required a long period of care, treatment, or rehabilitation. After applying this definition in relation to populations of older adults, 918 chronic ICD-10 codes were identified and grouped into 60 chronic disease categories. In SNAC-K, 88.6% had >= 2 of these 60 disease categories, 73.2% had >= 3, and 55.8% had >= 4.ConclusionsThis operational measure of multimorbidity, which can be implemented using either or both clinical and administrative data, may facilitate its monitoring and international comparison. Once validated, it may enable the advancement and evolution of conceptual and theoretical aspects of multimorbidity that will eventually lead to better care.
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4.
  • Calderón-Larrañaga, Amaia, et al. (författare)
  • Rapidly developing multimorbidity and disability in older adults : does social background matter?
  • 2018
  • Ingår i: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 283:5, s. 489-499
  • Tidskriftsartikel (refereegranskat)abstract
    • Background. Multimorbidity is among the most disabling geriatric conditions. In this study, we explored whether a rapid development of multi morbidity potentiates its impact on the functional independence of older adults, and whether different sociodemographic factors play a role beyond the rate of chronic disease accumulation. Methods. A random sample of persons aged >= 60 years (n = 2387) from the Swedish National study on Aging and Care in Kungsholmen (SNAC-K) was followed over 6 years. The speed of multimorbidity development was estimated as the rate of chronic disease accumulation (linear mixed models) and further dichotomized into the upper versus the three lower rate quartiles. Binomial negative mixed models were used to analyse the association between speed of multimorbidity development and disability (impaired basic and instrumental activities of daily living), expressed as the incidence rate ratio (IRR). The effect of sociodemographic factors, including sex, education, occupation and social network, was investigated. Results. The risk of new activity impairment was higher among participants who developed multi morbidity faster (IRR 2.4, 95% Cl 1.9-3.1) compared with those who accumulated diseases more slowly overtime, even after considering the baseline number of chronic conditions. Only female sex (IRR for women vs. men 1.6, 95% Cl 1.2-2.0) and social network (IRR for poor vs. rich social network 1.7, 95% Cl 1.3-2.2) showed an effect on disability beyond the rate of chronic disease accumulation. Conclusions. Rapidly developing multimorbidity is a negative prognostic factor for disability. However, sociodemographic factors such as sex and social network may determine older adults' reserves of functional ability, helping them to live independently despite the rapid accumulation of chronic conditions.
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5.
  • Chen, Jie, et al. (författare)
  • Long-term exposure to ambient air pollution and bladder cancer incidence in a pooled European cohort : the ELAPSE project
  • 2022
  • Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 126:10, s. 1499-1507
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The evidence linking ambient air pollution to bladder cancer is limited and mixed.Methods: We assessed the associations of bladder cancer incidence with residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight PM2.5 elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in a pooled cohort (N = 302,493). Exposures were primarily assessed based on 2010 measurements and back-extrapolated to the baseline years. We applied Cox proportional hazard models adjusting for individual- and area-level potential confounders.Results: During an average of 18.2 years follow-up, 967 bladder cancer cases occurred. We observed a positive though statistically non-significant association between PM2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93–1.27) per 5 µg/m3 for 2010 exposure and 1.06 (95% CI: 0.99–1.14) for baseline exposure. Effect estimates for NO2, BC and O3 were close to unity. A positive association was observed with PM2.5 zinc (HR 1.08; 95% CI: 1.00–1.16 per 10 ng/m3).Conclusions: We found suggestive evidence of an association between long-term PM2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM2.5 suggests the importance of industrial emissions.
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6.
  • Chen, Jie, et al. (författare)
  • Long-Term Exposure to Source-Specific Fine Particles and Mortality-A Pooled Analysis of 14 European Cohorts within the ELAPSE Project
  • 2022
  • Ingår i: Environmental Science and Technology. - : American Chemical Society (ACS). - 0013-936X .- 1520-5851. ; 56:13, s. 9277-9290
  • Tidskriftsartikel (refereegranskat)abstract
    • We assessed mortality risks associated with sourcespecific fine particles (PM2.5) in a pooled European cohort of 323,782 participants. Cox proportional hazard models were applied to estimate mortality hazard ratios (HRs) for source-specific PM2.5 identified through a source apportionment analysis. Exposure to 2010 annual average concentrations of source-specific PM2.5 components was assessed at baseline residential addresses. The source apportionment resulted in the identification of five sources: traffic, residual oil combustion, soil, biomass and agriculture, and industry. In single-source analysis, all identified sources were significantly positively associated with increased natural mortality risks. In multisource analysis, associations with all sources attenuated but remained statistically significant with traffic, oil, and biomass and agriculture. The highest association per interquartile increase was observed for the traffic component (HR: 1.06; 95% CI: 1.04 and 1.08 per 2.86 mu g/m(3) increase) across five identified sources. On a 1 mu g/m(3) basis, the residual oil-related PM2.5 had the strongest association (HR: 1.13; 95% CI: 1.05 and 1.22), which was substantially higher than that for generic PM2.5 mass, suggesting that past estimates using the generic PM2.5 exposure response function have underestimated the potential clean air health benefits of reducing fossil-fuel combustion. Source-specific associations with cause-specific mortality were in general consistent with findings of natural mortality.
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7.
  • Cole-Hunter, Thomas, et al. (författare)
  • Long-term air pollution exposure and Parkinson's disease mortality in a large pooled European cohort : An ELAPSE study
  • 2023
  • Ingår i: Environment International. - : Elsevier BV. - 0160-4120 .- 1873-6750. ; 171
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The link between exposure to ambient air pollution and mortality from cardiorespiratory diseases is well established, while evidence on neurodegenerative disorders including Parkinson’s Disease (PD) remains limited.Objective: We examined the association between long-term exposure to ambient air pollution and PD mortality in seven European cohorts.Methods: Within the project ‘Effects of Low-Level Air Pollution: A Study in Europe’ (ELAPSE), we pooled data from seven cohorts among six European countries. Annual mean residential concentrations of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), and ozone (O3), as well as 8 PM2.5 components (copper, iron, potassium, nickel, sulphur, silicon, vanadium, zinc), for 2010 were estimated using Europe-wide hybrid land use regression models. PD mortality was defined as underlying cause of death being either PD, secondary Parkinsonism, or dementia in PD. We applied Cox proportional hazard models to investigate the associations between air pollution and PD mortality, adjusting for potential confounders.Results: Of 271,720 cohort participants, 381 died from PD during 19.7 years of follow-up. In single-pollutant analyses, we observed positive associations between PD mortality and PM2.5 (hazard ratio per 5 µg/m3: 1.25; 95% confidence interval: 1.01–1.55), NO2 (1.13; 0.95–1.34 per 10 µg/m3), and BC (1.12; 0.94–1.34 per 0.5 × 10-5m-1), and a negative association with O3 (0.74; 0.58–0.94 per 10 µg/m3). Associations of PM2.5, NO2, and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM2.5 remained robust when adjusted for NO2 (1.24; 0.95–1.62) or BC (1.28; 0.96–1.71), whereas associations with NO2 or BC attenuated to null. O3 associations remained negative, but no longer statistically significant in models with PM2.5. We detected suggestive positive associations with the potassium component of PM2.5.Conclusion: Long-term exposure to PM2.5, at levels well below current EU air pollution limit values, may contribute to PD mortality.
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8.
  • Ding, Mozhu, et al. (författare)
  • Tracing temporal trends in dementia incidence over 25 years in central Stockholm, Sweden
  • 2020
  • Ingår i: Alzheimer's & Dementia. - : Wiley. - 1552-5260 .- 1552-5279. ; 16:5, s. 770-778
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Recent reports from high-income countries have suggested a declining incidence of dementia.Methods: Trends in dementia incidence over 25 years among people >= 75 years of age were examined using two population-based cohort studies: the Kungsholmen Project (KP, n = 1473, 1987-1998) and the Swedish National study on Aging and Care in Kungsholmen (SNAC-K, n = 1746, 2001-2013).Results: We identified 440 (29.9%) and 388 (22.2%) incident dementia cases in the KP and SNAC-K cohorts, respectively. The incidence of dementia declined by 30% (hazard ratio [HR] = 0.70; 95% confidence interval [CI] 0.61-0.80) during the second decade. Adjustment of education, psychosocial working conditions, lifestyle, and vascular diseases did not substantially change the results (HR = 0.77, 95% CI 0.65-0.90). This decline was observed particularly in women and people with elementary education.Discussion: Our study provides direct evidence of a declining trend in dementia incidence. Improved cognitive reserve and cardiovascular health could partially explain the decline.
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9.
  • Dintica, Christina S., et al. (författare)
  • Impaired olfaction is associated with cognitive decline and neurodegeneration in the brain
  • 2019
  • Ingår i: Neurology. - 0028-3878 .- 1526-632X. ; 92:7, s. e700-e709
  • Tidskriftsartikel (refereegranskat)abstract
    • ObjectiveWe aimed to examine whether impaired olfaction is associated with cognitive decline and indicators of neurodegeneration in the brain of dementia-free older adults.MethodsWithin the Rush Memory and Aging Project, 380 dementia-free participants (mean age = 78 years) were followed for up to 15 years, and underwent MRI scans. Olfactory function was assessed using the Brief Smell Identification Test (B-SIT) at baseline, and categorized as anosmia (B-SIT <6), hyposmia (B-SIT 6-10 in men and 6-10.25 in women), and normal (B-SIT 10.25-12 in men and 10.5-12 in women). Cognitive function was annually assessed with a battery of 21 tests, from which composite scores were derived. Structural total and regional brain volumes were estimated. Data were analyzed using linear regression and mixed-effects models.ResultsAt study entry, 138 (36.3%) had normal olfactory function, 213 (56.1%) had hyposmia, and 29 (7.6%) had anosmia. In multiadjusted mixed-effects models, hyposmia (beta = -0.03, 95% confidence interval [CI] -0.05 to -0.02) and anosmia (beta = -0.13, 95% CI -0.16 to -0.09) were associated with faster rate of cognitive decline compared to normal olfaction. On MRI, impaired olfaction (hyposmia or anosmia) was related to smaller volumes of the hippocampus (beta = -0.19, 95% CI -0.33 to -0.05), and in the entorhinal (beta = -0.16, 95% CI -0.24 to -0.08), fusiform (beta = -0.45, 95% CI -0.78 to -0.14), and middle temporal (beta = -0.38, 95% CI -0.72 to -0.01) cortices.ConclusionImpaired olfaction predicts faster cognitive decline and might indicate neurodegeneration in the brain among dementia-free older adults.
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10.
  • Dintica, Christina S., et al. (författare)
  • The relation of poor mastication with cognition and dementia risk : a population-based longitudinal study
  • 2020
  • Ingår i: Aging. - : Impact Journals LLC. - 1945-4589 .- 1945-4589. ; 12:9, s. 8536-8548
  • Tidskriftsartikel (refereegranskat)abstract
    • We investigated the effect of poor masticatory ability on cognitive trajectories and dementia risk in older adults. 544 cognitively intact adults aged =50 were followed for up to 22 years. Cognitive domains (verbal, spatial/fluid, memory, and perceptual speed) were assessed at baseline and follow-ups. Dementia was ascertained according to standard criteria. Masticatory ability was assessed using the Eichner Index and categorized according to the number of posterior occlusal zones: A (all four), B (3-1), and C (none).At baseline, 147 (27.0%) participants were in Eichner category A, 169 (31.1%) in B and 228 (41.9%) in C. After the age of 65, participants in Eichner category B and C showed an accelerated decline in spatial/fluid abilities (beta: -0.16, 95% CI: -0.30 to -0.03) and (beta: -0.15, 95% CI: -0.28 to -0.02), respectively. Over the follow-up, 52 incident dementia cases were identified. Eichner categories B or C were not associated with an increased risk of dementia, compared to category A (Hazard Ratio [HR]: 0.83, 95% CI: 0.39 to 1.76 and HR: 0.63, 95% CI: 0.30 to 1.29, respectively).Poor masticatory ability is associated with an accelerated cognitive decline in fluid/spatial abilities, however it was not related to a higher risk of dementia.
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