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1.
Environ Health Perspect ; 129(10): 107002, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34605674

RESUMO

BACKGROUND: Transportation noise is increasingly acknowledged as a cardiovascular risk factor, but the evidence base for an association with stroke is sparse. OBJECTIVE: We aimed to investigate the association between transportation noise and stroke incidence in a large Scandinavian population. METHODS: We harmonized and pooled data from nine Scandinavian cohorts (seven Swedish, two Danish), totaling 135,951 participants. We identified residential address history and estimated road, railway, and aircraft noise for all addresses. Information on stroke incidence was acquired through linkage to national patient and mortality registries. We analyzed data using Cox proportional hazards models, including socioeconomic and lifestyle confounders, and air pollution. RESULTS: During follow-up (median=19.5y), 11,056 stroke cases were identified. Road traffic noise (Lden) was associated with risk of stroke, with a hazard ratio (HR) of 1.06 [95% confidence interval (CI): 1.03, 1.08] per 10-dB higher 5-y mean time-weighted exposure in analyses adjusted for individual- and area-level socioeconomic covariates. The association was approximately linear and persisted after adjustment for air pollution [particulate matter (PM) with an aerodynamic diameter of ≤2.5µm (PM2.5) and NO2]. Stroke was associated with moderate levels of 5-y aircraft noise exposure (40-50 vs. ≤40 dB) (HR=1.12; 95% CI: 0.99, 1.27), but not with higher exposure (≥50 dB, HR=0.94; 95% CI: 0.79, 1.11). Railway noise was not associated with stroke. DISCUSSION: In this pooled study, road traffic noise was associated with a higher risk of stroke. This finding supports road traffic noise as an important cardiovascular risk factor that should be included when estimating the burden of disease due to traffic noise. https://doi.org/10.1289/EHP8949.

2.
BMJ ; 374: n1904, 2021 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-34470785

RESUMO

OBJECTIVE: To investigate the associations between air pollution and mortality, focusing on associations below current European Union, United States, and World Health Organization standards and guidelines. DESIGN: Pooled analysis of eight cohorts. SETTING: Multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE) in six European countries. PARTICIPANTS: 325 367 adults from the general population recruited mostly in the 1990s or 2000s with detailed lifestyle data. Stratified Cox proportional hazard models were used to analyse the associations between air pollution and mortality. Western Europe-wide land use regression models were used to characterise residential air pollution concentrations of ambient fine particulate matter (PM2.5), nitrogen dioxide, ozone, and black carbon. MAIN OUTCOME MEASURES: Deaths due to natural causes and cause specific mortality. RESULTS: Of 325 367 adults followed-up for an average of 19.5 years, 47 131 deaths were observed. Higher exposure to PM2.5, nitrogen dioxide, and black carbon was associated with significantly increased risk of almost all outcomes. An increase of 5 µg/m3 in PM2.5 was associated with 13% (95% confidence interval 10.6% to 15.5%) increase in natural deaths; the corresponding figure for a 10 µg/m3 increase in nitrogen dioxide was 8.6% (7% to 10.2%). Associations with PM2.5, nitrogen dioxide, and black carbon remained significant at low concentrations. For participants with exposures below the US standard of 12 µg/m3 an increase of 5 µg/m3 in PM2.5 was associated with 29.6% (14% to 47.4%) increase in natural deaths. CONCLUSIONS: Our study contributes to the evidence that outdoor air pollution is associated with mortality even at low pollution levels below the current European and North American standards and WHO guideline values. These findings are therefore an important contribution to the debate about revision of air quality limits, guidelines, and standards, and future assessments by the Global Burden of Disease.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Poluição do Ar/efeitos adversos , Doenças Cardiovasculares/mortalidade , Exposição Ambiental/efeitos adversos , Doenças não Transmissíveis/mortalidade , Europa (Continente) , Humanos
3.
BMJ Open ; 11(9): e046040, 2021 09 08.
Artigo em Inglês | MEDLINE | ID: mdl-34497075

RESUMO

OBJECTIVES: To estimate concentration-response relationships for particulate matter (PM) and black carbon (BC) in relation to mortality in cohorts from three Swedish cities with comparatively low pollutant levels. SETTING: Cohorts from Gothenburg, Stockholm and Umeå, Sweden. DESIGN: High-resolution dispersion models were used to estimate annual mean concentrations of PM with aerodynamic diameter ≤10 µm (PM10) and ≤2.5 µm (PM2.5), and BC, at individual addresses during each year of follow-up, 1990-2011. Moving averages were calculated for the time windows 1-5 years (lag1-5) and 6-10 years (lag6-10) preceding the outcome. Cause-specific mortality data were obtained from the national cause of death registry. Cohort-specific HRs were estimated using Cox regression models and then meta-analysed including a random effect of cohort. PARTICIPANTS: During the study period, 7 340 cases of natural mortality, 2 755 cases of cardiovascular disease (CVD) mortality and 817 cases of respiratory and lung cancer mortality were observed among in total 68 679 individuals and 689 813 person-years of follow-up. RESULTS: Both PM10 (range: 6.3-41.9 µg/m3) and BC (range: 0.2-6.8 µg/m3) were associated with natural mortality showing 17% (95% CI 6% to 31%) and 9% (95% CI 0% to 18%) increased risks per 10 µg/m3 and 1 µg/m3 of lag1-5 exposure, respectively. For PM2.5 (range: 4.0-22.4 µg/m3), the estimated increase was 13% per 5 µg/m3, but less precise (95% CI -9% to 40%). Estimates for CVD mortality appeared higher for both PM10 and PM2.5. No association was observed with respiratory mortality. CONCLUSION: The results support an effect of long-term air pollution on natural mortality and mortality in CVD with high relative risks also at low exposure levels. These findings are relevant for future decisions concerning air quality policies.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Carbono , Causas de Morte , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Humanos , Material Particulado/efeitos adversos , Material Particulado/análise , Suécia/epidemiologia
4.
Lancet Planet Health ; 5(9): e620-e632, 2021 09.
Artigo em Inglês | MEDLINE | ID: mdl-34508683

RESUMO

BACKGROUND: Long-term exposure to outdoor air pollution increases the risk of cardiovascular disease, but evidence is unclear on the health effects of exposure to pollutant concentrations lower than current EU and US standards and WHO guideline limits. Within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we investigated the associations of long-term exposures to fine particulate matter (PM2·5), nitrogen dioxide (NO2), black carbon, and warm-season ozone (O3) with the incidence of stroke and acute coronary heart disease. METHODS: We did a pooled analysis of individual data from six population-based cohort studies within ELAPSE, from Sweden, Denmark, the Netherlands, and Germany (recruited 1992-2004), and harmonised individual and area-level variables between cohorts. Participants (all adults) were followed up until migration from the study area, death, or incident stroke or coronary heart disease, or end of follow-up (2011-15). Mean 2010 air pollution concentrations from centrally developed European-wide land use regression models were assigned to participants' baseline residential addresses. We used Cox proportional hazards models with increasing levels of covariate adjustment to investigate the association of air pollution exposure with incidence of stroke and coronary heart disease. We assessed the shape of the concentration-response function and did subset analyses of participants living at pollutant concentrations lower than predefined values. FINDINGS: From the pooled ELAPSE cohorts, data on 137 148 participants were analysed in our fully adjusted model. During a median follow-up of 17·2 years (IQR 13·8-19·5), we observed 6950 incident events of stroke and 10 071 incident events of coronary heart disease. Incidence of stroke was associated with PM2·5 (hazard ratio 1·10 [95% CI 1·01-1·21] per 5 µg/m3 increase), NO2 (1·08 [1·04-1·12] per 10 µg/m3 increase), and black carbon (1·06 [1·02-1·10] per 0·5 10-5/m increase), whereas coronary heart disease incidence was only associated with NO2 (1·04 [1·01-1·07]). Warm-season O3 was not associated with an increase in either outcome. Concentration-response curves indicated no evidence of a threshold below which air pollutant concentrations are not harmful for cardiovascular health. Effect estimates for PM2·5 and NO2 remained elevated even when restricting analyses to participants exposed to pollutant concentrations lower than the EU limit values of 25 µg/m3 for PM2·5 and 40 µg/m3 for NO2. INTERPRETATION: Long-term air pollution exposure was associated with incidence of stroke and coronary heart disease, even at pollutant concentrations lower than current limit values. FUNDING: Health Effects Institute.

5.
Aging (Albany NY) ; 13(15): 19186-19206, 2021 08 12.
Artigo em Inglês | MEDLINE | ID: mdl-34383709

RESUMO

BACKGROUND: This study aimed to detect health trajectories after age 60, and to explore to what extent individual and social factors may contribute to healthier aging. METHODS: Twelve-year health trajectories were identified in subjects from the Swedish National Study on Aging and Care in Kungsholmen (N=3108), integrating five indicators of disease, physical and cognitive function, and disability through nominal response models. Growth mixture models were applied to explore health trajectories in terms of rate and pattern of change. Baseline information about health-related behaviors and the social context was collected through standardized questionnaires. The strength of the associations was estimated using logistic regression, and their impact through population attributable fractions (PAF). RESULTS: Three trajectories were identified grouping 78%, 18%, and 4% of people with respectively increasing rates of health decline. Compared to the best trajectory, subjects in the middle and worst trajectories became functionally dependent 12.0 (95% CI: 11.4-12.6) and 12.1 (95% CI: 11.5-12.7) years earlier, respectively. Insufficient physical activity (OR: 3.38, 95% CI: 2.58-4.42), financial strain (OR: 2.76, 95% CI: 1.77-4.30), <12 years education (OR: 1.53, 95% CI: 1.14-2.04), low social connections (OR: 1.45, 95% CI: 1.09-1.94), low social participation (OR: 1.39, 95% CI: 1.06-1.83) and a body mass index ≥25 (OR: 1.34, 95% CI: 1.03-1.75) were associated with belonging to the middle/worst trajectories. The highest PAFs were observed for insufficient physical activity (27.1%), low education (19.3%) and low social participation (15.9%); a total PAF of 66.1% was obtained. CONCLUSIONS: Addressing the social determinants of health in its broadest sense, complementarily considering life-long factors belonging to the socioeconomic, psychosocial, and behavioral dimensions, should be central to any strategy aimed at fostering health in older age.

6.
Clin Nutr ; 40(8): 4838-4844, 2021 08.
Artigo em Inglês | MEDLINE | ID: mdl-34358824

RESUMO

BACKGROUND & AIMS: Healthy diet has been associated with decreased mortality, but its impact on survival without disability is less clear. We aimed to investigate the association between the Nordic Prudent Diet Pattern (NPDP) and dementia- and disability-free survival, and to assess its interaction with other healthy lifestyle behaviors. METHODS: Within the Swedish National Study on Aging and Care-Kungsholmen, 2290 dementia- and disability-free adults aged ≥60 were followed up to 12 years to detect survival free from dementia (standard criteria) and disability (Katz's Activities of Daily Living). NPDP index was assessed at baseline with a 98-item food frequency questionnaire (characterized mainly by more frequent intakes of vegetable, fruit, cooking, cereals, whole grains, fish, and water) and was further categorized into tertiles (low, moderate, or high). Information on lifestyle factors was collected via baseline questionnaire. A favorable (vs unfavorable) lifestyle profile was determined based on smoking status, social network and physical activity. Data were analyzed using Cox proportional hazard regression models and Laplace regression. RESULTS: During the follow-up, 1074 participants survived without dementia and disability (614 died, 518 became disabled, and 84 developed dementia). Compared to low NPDP adherence, the hazard ratio (HR) of high NPDP adherence was 1.19 (95% CI 1.04-1.34) for dementia- and disability-free survival. High NPDP adherence prolonged lifespan without mental and physical disability by an average of 1.24 years (95% CI 0.11-2.37). Further, among participants with high NPDP adherence, a favorable lifestyle profile was associated with an even higher HR (1.96, 95% CI 1.52-2.42) of dementia- and disability-free survival, corresponding to an average of 3.80 (95% CI 2.25-5.35) years longer life compared to those with low NPDP adherence and an unfavorable lifestyle profile. CONCLUSION: High adherence to NPDP prolongs survival with good mental and physical function for more than one year, and this could increase to almost four years with a favorable lifestyle.

7.
Age Ageing ; 2021 Jul 03.
Artigo em Inglês | MEDLINE | ID: mdl-34228784

RESUMO

BACKGROUND: the aim of this study was to examine the cross-sectional and longitudinal associations of different multimorbidity patterns with physical frailty in older adults. METHODS: we used data from the Swedish National study on Aging and Care in Kungsholmen to generate a physical frailty measure, and clusters of participants with similar multimorbidity patterns were identified through fuzzy c-means cluster analyses. The cross-sectional association (n = 2,534) between multimorbidity clusters and physical frailty was measured through logistic regression analyses. Six- (n = 2,122) and 12-year (n = 2,140) longitudinal associations were determined through multinomial logistic regression analyses. RESULTS: six multimorbidity patterns were identified at baseline: psychiatric diseases; cardiovascular diseases, anaemia and dementia; sensory impairments and cancer; metabolic and sleep disorders; musculoskeletal, respiratory and gastrointestinal diseases; and an unspecific pattern lacking any overrepresented diseases. Cross-sectionally, each pattern was associated with physical frailty compared with the unspecific pattern. Over 6 years, the psychiatric diseases (relative risk ratio [RRR]: 3.04; 95% confidence intervals [CI]: 1.59-5.79); cardiovascular diseases, anaemia and dementia (RRR 2.25; 95% CI: 1.13-4.49) and metabolic and sleep disorders (RRR 1.99; 95% CI: 1.25-3.16) patterns were associated with incident physical frailty. The cardiovascular diseases, anaemia and dementia (RRR: 4.81; 95% CI: 1.59-14.60); psychiatric diseases (RRR 2.62; 95% CI: 1.45-4.72) and sensory impairments and cancer (RRR 1.87; 95% CI: 1.05-3.35) patterns were more associated with physical frailty, compared with the unspecific pattern, over 12 years. CONCLUSIONS: we found that older adults with multimorbidity characterised by cardiovascular and neuropsychiatric disease patterns are most susceptible to developing physical frailty.

8.
Int J Cancer ; 149(11): 1887-1897, 2021 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-34278567

RESUMO

Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the "Effects of low-level air pollution: A study in Europe" (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO2 ), particulate matter with diameter <2.5 µm (PM2.5 ), black carbon (BC), warm-season ozone (O3 ), and eight elemental components of PM2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European-wide hybrid land-use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer-free adults at baseline, 512 developed liver cancer during a mean follow-up of 18.1 years. We observed positive linear associations between NO2 (hazard ratio, 95% confidence interval: 1.17, 1.02-1.35 per 10 µg/m3 ), PM2.5 (1.12, 0.92-1.36 per 5 µg/m3 ), and BC (1.15, 1.00-1.33 per 0.5 10-5 /m) and liver cancer incidence. Associations with NO2 and BC persisted in two-pollutant models with PM2.5 . Most components of PM2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM2.5 or NO2 . Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards.

9.
Eur Respir J ; 57(6)2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-34088754

RESUMO

BACKGROUND: Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter <2.5 µm (PM2.5), nitrogen dioxide (NO2) and black carbon (BC) with asthma incidence in adults. METHODS: We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders. RESULTS: Of 98 326 participants, 1965 developed asthma during a mean follow-up of 16.6 years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04-1.43) per 5 µg·m-3 for PM2.5, 1.17 (95% CI 1.10-1.25) per 10 µg·m-3 for NO2 and 1.15 (95% CI 1.08-1.23) per 0.5×10-5 m-1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM2.5 and NO2. NO2 and BC estimates remained unchanged in two-pollutant models with PM2.5, whereas PM2.5 estimates were attenuated to unity. The concentration-response curves showed no evidence of a threshold. CONCLUSIONS: Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Asma , Adulto , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Criança , Exposição Ambiental/análise , Europa (Continente) , Humanos , Incidência , Material Particulado/análise , Suécia
10.
Age Ageing ; 50(5): 1657-1665, 2021 09 11.
Artigo em Inglês | MEDLINE | ID: mdl-34120170

RESUMO

BACKGROUND: this article investigates the association between life satisfaction and disability-free survival, and explores the roles of chronic diseases and healthy lifestyle in this association. METHOD: a cohort of 2,116 functionally independent adults aged ≥60 was followed up to 12 years. At baseline, life satisfaction was assessed with the Life Satisfaction Index A (LSI-A). Disability-free survival was defined as the survival till the first occurrence of either death, dementia or physical disability. Information on lifestyle factors was collected via questionnaire. Chronic diseases were ascertained through clinical examinations at baseline and each follow-up. Data were analysed using Cox proportional hazard regression models and Laplace regression. RESULTS: over follow-up, 1,121 participants died, developed dementia, or became disabled. High LSI-A versus Low LSI-A had a lower risk of death, dementia and physical disability (hazard ratio [HR] 0.79, 95% confidence intervals [CI] 0.67-0.94), and had a longer disability-free period by 1.73 (95% CI 0.18-3.32) years. In mediation analysis, accumulation of chronic diseases mediated 17.8% of the association between LSI-A and disability-free survival. In joint effect analysis, participants with high LSI-A and a favourable lifestyle profile had a HR of 0.53 (95% CI 0.41-0.69) for the composite endpoint, and lived 3.2 (95% CI 1.35-5.11) disability-free years longer than those with low life satisfaction and an unfavourable lifestyle profile. DISCUSSION: high life satisfaction is independently associated with longer disability-free survival. This association is partially mediated by a lower burden of chronic diseases and is reinforced by healthy lifestyle.


Assuntos
Pessoas com Deficiência , Satisfação Pessoal , Doença Crônica , Estudos de Coortes , Estilo de Vida Saudável , Humanos
11.
Environ Health Perspect ; 129(4): 47009, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33844598

RESUMO

BACKGROUND: Inconsistent associations between long-term exposure to particles with an aerodynamic diameter ≤2.5 µm [fine particulate matter (PM2.5)] components and mortality have been reported, partly related to challenges in exposure assessment. OBJECTIVES: We investigated the associations between long-term exposure to PM2.5 elemental components and mortality in a large pooled European cohort; to compare health effects of PM2.5 components estimated with two exposure modeling approaches, namely, supervised linear regression (SLR) and random forest (RF) algorithms. METHODS: We pooled data from eight European cohorts with 323,782 participants, average age 49 y at baseline (1985-2005). Residential exposure to 2010 annual average concentration of eight PM2.5 components [copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V), and zinc (Zn)] was estimated with Europe-wide SLR and RF models at a 100×100 m scale. We applied Cox proportional hazards models to investigate the associations between components and natural and cause-specific mortality. In addition, two-pollutant analyses were conducted by adjusting each component for PM2.5 mass and nitrogen dioxide (NO2) separately. RESULTS: We observed 46,640 natural-cause deaths with 6,317,235 person-years and an average follow-up of 19.5 y. All SLR-modeled components were statistically significantly associated with natural-cause mortality in single-pollutant models with hazard ratios (HRs) from 1.05 to 1.27. Similar HRs were observed for RF-modeled Cu, Fe, K, S, V, and Zn with wider confidence intervals (CIs). HRs for SLR-modeled Ni, S, Si, V, and Zn remained above unity and (almost) significant after adjustment for both PM2.5 and NO2. HRs only remained (almost) significant for RF-modeled K and V in two-pollutant models. The HRs for V were 1.03 (95% CI: 1.02, 1.05) and 1.06 (95% CI: 1.02, 1.10) for SLR- and RF-modeled exposures, respectively, per 2 ng/m3, adjusting for PM2.5 mass. Associations with cause-specific mortality were less consistent in two-pollutant models. CONCLUSION: Long-term exposure to V in PM2.5 was most consistently associated with increased mortality. Associations for the other components were weaker for exposure modeled with RF than SLR in two-pollutant models. https://doi.org/10.1289/EHP8368.

12.
J Alzheimers Dis ; 80(2): 591-599, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33579834

RESUMO

BACKGROUND: A growing but contrasting evidence relates air pollution to cognitive decline. The role of cerebrovascular diseases in amplifying this risk is unclear. OBJECTIVES: 1) Investigate the association between long-term exposure to air pollution and cognitive decline; 2) Test whether cerebrovascular diseases amplify this association. METHODS: We examined 2,253 participants of the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). One major air pollutant (particulate matter ≤2.5µm, PM2.5) was assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. The speed of cognitive decline (Mini-Mental State Examination, MMSE) was estimated as the rate of MMSE decline (linear mixed models) and further dichotomized into the upper (25%fastest cognitive decline), versus the three lower quartiles. The cognitive scores were used to calculate the odds of fast cognitive decline per levels of PM2.5 using regression models and considering linear and restricted cubic splines of 10 years exposure before the baseline. The potential modifier effect of cerebrovascular diseases was tested by adding an interaction term in the model. RESULTS: We observed an inverted U-shape relationship between PM2.5 and cognitive decline. The multi-adjusted piecewise regression model showed an increased OR of fast cognitive decline of 81%(95%CI = 1.2-3.2) per interquartile range difference up to mean PM2.5 level (8.6µg/m3) for individuals older than 80. Above such level we observed no further risk increase (OR = 0.89;95%CI = 0.74-1.06). The presence of cerebrovascular diseases further increased such risk by 6%. CONCLUSION: Low to mean PM2.5 levels were associated with higher risk of accelerated cognitive decline. Cerebrovascular diseases further amplified such risk.


Assuntos
Poluentes Atmosféricos/efeitos adversos , Disfunção Cognitiva/etiologia , Material Particulado/efeitos adversos , Idoso , Poluição do Ar , Transtornos Cerebrovasculares/epidemiologia , Disfunção Cognitiva/epidemiologia , Exposição Ambiental , Feminino , Humanos , Estudos Longitudinais , Masculino , Testes de Estado Mental e Demência , Pessoa de Meia-Idade , Tamanho da Partícula , Fatores Socioeconômicos , Suécia/epidemiologia
13.
J Am Med Dir Assoc ; 22(10): 2184-2189.e1, 2021 10.
Artigo em Inglês | MEDLINE | ID: mdl-33556330

RESUMO

OBJECTIVES: The aim was to evaluate patterns of multimorbidity that increase the risk of institutionalization in older persons, also exploring the potential buffering effect of formal and informal care. DESIGN: Prospective cohort study. SETTING AND PARTICIPANTS: The population-based Swedish National study on Aging and Care in Kungsholmen, Stockholm, Sweden. MEASURES: In total, 2571 community-dwelling older adults were grouped at baseline according to their underlying multimorbidity patterns, using a fuzzy c-means cluster algorithm, and followed up for 6 years to test the association between multimorbidity patterns and institutionalization. RESULTS: Six patterns of multimorbidity were identified: psychiatric diseases; cardiovascular diseases, anemia, and dementia; metabolic and sleep disorders; sensory impairments and cancer; musculoskeletal, respiratory, and gastrointestinal diseases; and an unspecific pattern including diseases of which none were overrepresented. In total, 110 (4.3%) participants were institutionalized during the follow-up, ranging from 1.7% in the metabolic and sleep disorders pattern to 8.4% in the cardiovascular diseases, anemia, and dementia pattern. Compared with the unspecific pattern, only the cardiovascular diseases, anemia, dementia pattern was significantly associated with institutionalization [relative risk ratio (RRR) = 2.23; 95% confidence interval (CI) 1.07‒4.65)], after adjusting for demographic characteristics and disability status at baseline. In stratified analyses, those not receiving formal care in the psychiatric diseases pattern (RRR 3.34; 95% CI 1.20‒9.32) and those not receiving formal or informal care in the 'cardiovascular diseases, anemia, dementia' pattern (RRR 2.99; 95% CI 1.20‒7.46; RRR 2.79; 95% CI 1.16‒6.71, respectively) had increased risks of institutionalization. CONCLUSIONS AND IMPLICATIONS: Older persons suffering from specific multimorbidity patterns have a higher risk of institutionalization, especially if they lack formal or informal care. Interventions aimed at preventing the clustering of diseases could reduce the associated burden on residential long-term care. Formal and informal care provision may be effective strategies in reducing the risk of institutionalization.

14.
Alzheimers Dement ; 17(5): 768-776, 2021 05.
Artigo em Inglês | MEDLINE | ID: mdl-33403740

RESUMO

INTRODUCTION: We investigate dementia risk in older adults with different disease patterns and explore the role of inflammation and apolipoprotein E (APOE) genotype. METHODS: A total of 2,478 dementia-free participants with two or more chronic diseases (ie, multimorbidity) part of the Swedish National study on Aging and Care in Kungsholmen (SNAC-K) were grouped according to their multimorbidity patterns and followed to detect clinical dementia. The potential modifier effect of C-reactive protein (CRP) and apolipoprotein E (APOE) genotype was tested through stratified analyses. RESULTS: People with neuropsychiatric, cardiovascular, and sensory impairment/cancer multimorbidity had increased hazards for dementia compared to the unspecific (Hazard ration (HR) 1.66, 95% confidence interval [CI] 1.13-2.42; 1.61, 95% CI 1.17-2.29; 1.32, 95% CI 1.10-1.71, respectively). Despite the lack of statistically significant interaction, high CRP increased dementia risk within these patterns, and being APOE ε4 carriers heightened dementia risk for neuropsychiatric and cardiovascular multimorbidity. DISCUSSION: Individuals with neuropsychiatric, cardiovascular, and sensory impairment/cancer patterns are at increased risk for dementia and APOE ε4, and inflammation may further increase the risk. Identifying such high-risk groups might allow tailored interventions for dementia prevention.

15.
Environ Res ; 193: 110568, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33278469

RESUMO

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/m3 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/m3 PM2.5 S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m3 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.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Pulmonares , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Ambiental/análise , Europa (Continente)/epidemiologia , Humanos , Incidência , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/epidemiologia , Material Particulado/análise
16.
J Gerontol A Biol Sci Med Sci ; 76(1): 157-163, 2021 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-32569349

RESUMO

BACKGROUND: Longitudinal studies describing centenarians' health trajectories are currently lacking. We compared health trajectories of older adults becoming centenarians and their shorter-living counterparts in terms of chronic diseases, disability, and cognitive decline. METHODS: We identified 3,573 individuals participating in the Kungsholmen Project and the Swedish National Study on Aging and Care in Kungsholmen who lived <100 years and 222 who survived to their 100th birthday. Trajectories of chronic diseases, disability (impaired activities of daily living), and cognitive status were obtained via linear mixed models over 13 years. RESULTS: Centenarians had fewer chronic diseases than noncentenarians. Before age 85, centenarians showed slower health changes. In centenarians, multimorbidity, disability, and cognitive impairment occurred 4 to 9 years later than in noncentenarians. After age 85, the speed of accumulation of chronic diseases, disabilities, and cognitive decline accelerated in centenarians. At age 100, 39% of the centenarians were cognitively intact and 55% had escaped disability. Only 5% were free of multimorbidity at age 100. When compared with their shorter lived counterparts, in terms of years spent in poor health, centenarians experienced more years with multimorbidity (9.4 vs 6.8 years; p < .001), disability (4.3 vs 3.1 years; p = .005), and cognitive impairment (6.3 vs 4.3 years; p < .001). CONCLUSIONS: Older people who become centenarians present a delay in the onset of morbidity, but spend more years in this condition compared to their shorter lived peers. The observation of older adults' health trajectories might help to forecast healthier aging, and plan future medical and social care delivery.

17.
Age Ageing ; 50(2): 480-487, 2021 02 26.
Artigo em Inglês | MEDLINE | ID: mdl-32706849

RESUMO

BACKGROUND: It remains unclear whether and to what extent health behaviours may prolong survival and compress the period of survival with disability. OBJECTIVE: To identify modifiable health behaviours that are associated with later disability onset and longer disability-free survival. DESIGN: This population-based cohort study used data from the Swedish National Study on Ageing and Care in Kungsholmen (SNAC-K) ranging between 2001 and 2016. SETTING AND SUBJECTS: A total of 3,041 disability-free adults aged ≥60 years were followed up to 15 years. METHODS: Data on health behaviours were collected at baseline. Information on limitations in activities of daily living was obtained at baseline and during the follow-up. Laplace regression was used to model the median age at death and disability occurrence as a function of health behaviours. RESULTS: Never smoking, moderate alcohol drinking, rich social network and high leisure activity were individually related to longer survival by 1-3 years. Participants with high leisure activity lived 1.6 years (95% CI: 0.9-2.3) more without a disability. After combining lifestyle factors, social network, and leisure activities into a 4-level 'health behaviour profile', people with the healthiest behaviour profile lived 2.8 years (95% CI: 1.3-4.2) longer, had disability 3.5 years (95% CI: 1.7-5.3) later and lived 0.7 years (95% CI, 0.4-1.1) more without a disability compared to those with the least healthy behaviours profile. CONCLUSIONS: These findings suggest that health behaviours could prolong the lifespan, and leisure activities may further compress years lived with disability among older adults.

18.
Environ Int ; 146: 106249, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33197787

RESUMO

BACKGROUND/AIM: Ambient air pollution has been associated with lung cancer, but the shape of the exposure-response function - especially at low exposure levels - is not well described. The aim of this study was to address the relationship between long-term low-level air pollution exposure and lung cancer incidence. METHODS: The "Effects of Low-level Air Pollution: a Study in Europe" (ELAPSE) collaboration pools seven cohorts from across Europe. We developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates for nitrogen dioxide (NO2), fine particulate matter (PM2.5), black carbon (BC), and ozone (O3) to assign exposure to cohort participants' residential addresses in 100 m by 100 m grids. 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). We fitted linear models, linear models in subsets, Shape-Constrained Health Impact Functions (SCHIF), and natural cubic spline models to assess the shape of the association between air pollution and lung cancer at concentrations below existing standards and guidelines. RESULTS: The analyses included 307,550 cohort participants. During a mean follow-up of 18.1 years, 3956 incident lung cancer cases occurred. Median (Q1, Q3) annual (2010) exposure levels of NO2, PM2.5, BC and O3 (warm season) were 24.2 µg/m3 (19.5, 29.7), 15.4 µg/m3 (12.8, 17.3), 1.6 10-5m-1 (1.3, 1.8), and 86.6 µg/m3 (78.5, 92.9), respectively. We observed a higher risk for lung cancer with higher exposure to PM2.5 (HR: 1.13, 95% CI: 1.05, 1.23 per 5 µg/m3). This association was robust to adjustment for other pollutants. The SCHIF, spline and subset analyses suggested a linear or supra-linear association with no evidence of a threshold. In subset analyses, risk estimates were clearly elevated for the subset of subjects with exposure below the EU limit value of 25 µg/m3. We did not observe associations between NO2, BC or O3 and lung cancer incidence. CONCLUSIONS: Long-term ambient PM2.5 exposure is associated with lung cancer incidence even at concentrations below current EU limit values and possibly WHO Air Quality Guidelines.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Pulmonares , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Exposição Ambiental/análise , Europa (Continente)/epidemiologia , Humanos , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/epidemiologia , Material Particulado/análise
19.
Environ Int ; 146: 106267, 2021 01.
Artigo em Inglês | MEDLINE | ID: mdl-33276316

RESUMO

BACKGROUND: Air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD), but evidence is sparse and inconsistent. OBJECTIVES: We examined the association between long-term exposure to low-level air pollution and COPD incidence. METHODS: Within the 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE) study, we pooled data from three cohorts, from Denmark and Sweden, with information on COPD hospital discharge diagnoses. Hybrid land use regression models were used to estimate annual mean concentrations of particulate matter with a diameter < 2.5 µm (PM2.5), nitrogen dioxide (NO2), and black carbon (BC) in 2010 at participants' baseline residential addresses, which were analysed in relation to COPD incidence using Cox proportional hazards models. RESULTS: Of 98,058 participants, 4,928 developed COPD during 16.6 years mean follow-up. The adjusted hazard ratios (HRs) and 95% confidence intervals for associations with COPD incidence were 1.17 (1.06, 1.29) per 5 µg/m3 for PM2.5, 1.11 (1.06, 1.16) per 10 µg/m3 for NO2, and 1.11 (1.06, 1.15) per 0.5 10-5m-1 for BC. Associations persisted in subset participants with PM2.5 or NO2 levels below current EU and US limit values and WHO guidelines, with no evidence for a threshold. HRs for NO2 and BC remained unchanged in two-pollutant models with PM2.5, whereas the HR for PM2.5 was attenuated to unity with NO2 or BC. CONCLUSIONS: Long-term exposure to low-level air pollution is associated with the development of COPD, even below current EU and US limit values and possibly WHO guidelines. Traffic-related pollutants NO2 and BC may be the most relevant.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Doença Pulmonar Obstrutiva Crônica , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Estudos de Coortes , Exposição Ambiental/análise , Europa (Continente)/epidemiologia , Humanos , Incidência , Material Particulado/análise , Material Particulado/toxicidade , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Doença Pulmonar Obstrutiva Crônica/etiologia , Suécia
20.
Eur Respir J ; 2020 Dec 10.
Artigo em Inglês | MEDLINE | ID: mdl-33303534

RESUMO

BACKGROUND: Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, while evidence is still insufficient. Within the multicentre project "Effects of Low-Level Air Pollution: A Study in Europe" (ELAPSE), we examined the associations of long-term exposures to particulate matter with diameter<2.5 µm (PM2.5), nitrogen dioxide (NO2), and black carbon (BC) with asthma incidence in adults. METHODS: We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders. RESULTS: Of 98 326 participants, 1965 developed asthma during a 16.6 years mean follow-up. We observed associations in fully adjusted models with hazard ratios and 95% confidence intervals of 1.22 (1.04-1.43) per 5 µg·m-3 for PM2.5, 1.17 (1.10-1.25) per 10 µg·m-3 for NO2, and 1.15 (1.08-1.23) per 0.5 10-5 m-1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the EU and US limit values and possibly WHO guidelines for PM2.5 and NO2. NO2 and BC estimates remained unchanged in two-pollutant models with PM2.5, whereas PM2.5 estimates were attenuated to unity. The concentration response curves showed no evidence of a threshold. CONCLUSIONS: Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.

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