Is Long-term Exposure to Air Pollution Associated with Episodic Memory? A Longitudinal Study from Northern Sweden.
Ontology highlight
ABSTRACT:
SUBMITTER: Oudin A
PROVIDER: S-EPMC5630578 | biostudies-literature | 2017 Oct
REPOSITORIES: biostudies-literature
Publications
Is Long-term Exposure to Air Pollution Associated with Episodic Memory? A Longitudinal Study from Northern Sweden.
Oudin Anna A Forsberg Bertil B Lind Nina N Nordin Steven S Oudin Åström Daniel D Sundström Anna A Nordin Maria M
Scientific reports 20171006 1
Associations between long-term exposure to ambient air pollution and cognitive function have been observed in a few longitudinal studies. Our aim was to investigate the association between long-term exposure to air pollution and episodic memory, a marker of early cognitive decline. We used data from the Betula study in Northern Sweden, and included participants 60 to 85 of age at inclusion, 1,469 persons in total. The participants were followed for up to 22 years, five years apart between 1988 a ...[more]
Similar Datasets
Project description:BackgroundFew studies have explored the role of air pollution in neurodegenerative processes, especially various types of dementia. Our aim was to evaluate the association between long-term exposure to air pollution and first hospitalization for dementia subtypes in a large administrative cohort.MethodsWe selected 350,844 subjects (free of dementia) aged 65-100 years at inclusion (21/10/2001) and followed them until 31/12/2013. We selected all subjects hospitalized for the first time with primary or secondary diagnoses of various forms of dementia. We estimated the exposure at residence using land use regression models for nitrogen oxides (NOx, NO2) and particulate matter (PM) and a chemical transport model for ozone (O3). We used Cox models to estimate the association between exposure and first hospitalization for dementia and its subtypes: vascular dementia (Vd), Alzheimer's disease (Ad) and senile dementia (Sd).ResultsWe selected 21,548 first hospitalizations for dementia (7497 for Vd, 7669 for Ad and 7833 for Sd). Overall, we observed a negative association between exposure to NO2 (10 μg/m3) and dementia hospitalizations (HR = 0.97; 95% CI: 0.96-0.99) and a positive association between exposure to O3, NOx and dementia hospitalizations, (O3: HR = 1.06; 95% CI: 1.04-1.09 per 10 μg/m3; NOx: HR = 1.01; 95% CI: 1.00-1.02 per 20 μg/m3).H. Exposure to NOx, NO2, PM2.5, and PM10 was positively associated with Vd and negatively associated with Ad. Hospitalization for Sd was positively associated with exposure to O3 (HR = 1.20; 95% CI: 1.15-1.24 per 10 μg/m3).ConclusionsOur results showed a positive association between exposure to NOx and O3 and hospitalization for dementia and a negative association between NO2 exposure and hospitalization for dementia. In the analysis by subtype, exposure to each pollutants (except O3) demonstrated a positive association with vascular dementia, while O3 exposure was associated with senile dementia. The results regarding vascular dementia are a clear indication that the brain effects of air pollution are linked with vascular damage.
| S-EPMC6689157 | biostudies-literature
Project description:BackgroundEpisodic memory decline varies by age and underlying neuropathology. Whether ambient air pollution contributes to the heterogeneity of episodic memory decline in older populations remains unclear.ObjectivesWe estimated associations between air pollution exposures and episodic memory decline according to pollutant, exposure time window, age, and latent class subgroups defined by episodic memory trajectories.MethodsParticipants were from the Women's Health Initiative Memory Study-Epidemiology of Cognitive Health Outcomes. Older women (n=2,056; 74-92 years of age) completed annual (2008-2018) episodic memory assessments using the telephone-based California Verbal Learning Test (CVLT). We estimated 3-y average fine particulate matter [PM with an aerodynamic diameter of ≤2.5μm (PM2.5)] and nitrogen dioxide (NO2) exposures at baseline and 10 y earlier (recent and remote exposures, respectively), using regionalized national universal kriging. Separate latent class mixed models were used to estimate associations between interquartile range increases in exposures and CVLT trajectories in women ≤80 and >80 years of age, adjusting for covariates.ResultsTwo latent classes were identified for women ≤80 years of age (n=828), "slow-decliners" {slope=-0.12/y [95% confidence interval (CI): -0.23, -0.01] and "fast-decliners" [slope=-1.79/y (95% CI: -2.08, -1.50)]}. In the slow-decliner class, but not the fast-decliner class, PM2.5 exposures were associated with a greater decline in CVLT scores over time, with a stronger association for recent vs. remote exposures [-0.16/y (95% CI: -2.08, -0.03) per 2.88 μg/m3 and -0.11/y (95% CI: -0.22, 0.01) per 3.27 μg/m3, respectively]. Among women ≥80 years of age (n=1,128), the largest latent class comprised "steady-decliners" [slope=-1.35/y (95% CI: -1.53, -1.17)], whereas the second class, "cognitively resilient", had no decline in CVLT on average. PM2.5 was not associated with episodic memory decline in either class. A 6.25-ppb increase in recent NO2 was associated with nonsignificant acceleration of episodic memory decline in the ≤80-y-old fast-decliner class [-0.21/y (95% CI: -0.45, 0.04)], and in the >80-y-old cognitively resilient class [-0.10/y (95% CI: -0.24, 0.03)] and steady-decliner class [-0.11/y (95% CI: -0.27, 0.05)]. Associations with recent NO2 exposure in women >80 years of age were stronger and statistically significant when 267 women with incident probable dementia were excluded [e.g., -0.12/y (95% CI: -0.22, -0.02) for the cognitively resilient class]. In contrast with changes in CVLT over time, there were no associations between exposures and CVLT scores during follow-up in any subgroup.DiscussionIn a community-dwelling U.S. population of older women, associations between late-life exposure to ambient air pollution and episodic memory decline varied by age-related cognitive trajectories, exposure time windows, and pollutants. https://doi.org/10.1289/EHP7668.
| S-EPMC8437247 | biostudies-literature
Project description:Background and purposeLong-term exposure to ambient air pollution is associated with higher risk of cardiovascular disease and stroke. We hypothesized that long-term exposure to air pollution would be associated with magnetic resonance imaging markers of subclinical cerebrovascular disease.MethodsParticipants were 1075 stroke-free individuals aged ≥50 years drawn from the magnetic resonance imaging subcohort of the Northern Manhattan Study who had lived at the same residence for at least 2 years before magnetic resonance imaging. Cross-sectional associations between ambient air pollution and subclinical cerebrovascular disease were analyzed.ResultsWe found an association between distance to roadway, a proxy for residential exposure to traffic pollution, and white matter hyperintensity volume; however, after adjusting for risk factors, this relationship was no longer present. All other associations between pollutant measures and white matter hyperintensity volume were null. There was no clear association between exposure to air pollutants and subclinical brain infarcts or total cerebral brain volume.ConclusionsWe found no evidence that long-term exposure to ambient air pollution is independently associated with subclinical cerebrovascular disease in an urban population-based cohort.
| S-EPMC5487287 | biostudies-literature
Project description:IntroductionLong-term air pollution exposure contributes to mortality but there are few studies examining effects of very long-term (>25 years) exposures.MethodsThis study investigated modelled air pollution concentrations at residence for 1971, 1981, 1991 (black smoke (BS) and SO2) and 2001 (PM10) in relation to mortality up to 2009 in 367,658 members of the longitudinal survey, a 1% sample of the English Census. Outcomes were all-cause (excluding accidents), cardiovascular (CV) and respiratory mortality.ResultsBS and SO2 exposures remained associated with mortality decades after exposure-BS exposure in 1971 was significantly associated with all-cause (OR 1.02 (95% CI 1.01 to 1.04)) and respiratory (OR 1.05 (95% CI 1.01 to 1.09)) mortality in 2002-2009 (ORs expressed per 10 μg/m(3)). Largest effect sizes were seen for more recent exposures and for respiratory disease. PM10 exposure in 2001 was associated with all outcomes in 2002-2009 with stronger associations for respiratory (OR 1.22 (95% CI 1.04 to 1.44)) than CV mortality (OR 1.12 (95% CI 1.01 to 1.25)). Adjusting PM10 for past BS and SO2 exposures in 1971, 1981 and 1991 reduced the all-cause OR to 1.16 (95% CI 1.07 to 1.26) while CV and respiratory associations lost significance, suggesting confounding by past air pollution exposure, but there was no evidence for effect modification. Limitations include limited information on confounding by smoking and exposure misclassification of historic exposures.ConclusionsThis large national study suggests that air pollution exposure has long-term effects on mortality that persist decades after exposure, and that historic air pollution exposures influence current estimates of associations between air pollution and mortality.
| S-EPMC4819629 | biostudies-literature
Project description:Long-term exposure to air pollution is associated with age-related diseases. We explored the association between accelerated biological aging and air pollution, a potential mechanism linking air pollution and health. We estimated long-term exposure to PM10, PM2.5, PM2.5 absorbance/black carbon (BC), and NOx via land-use regression models in individuals from the KORA F4 cohort. Accelerated biological aging was assessed using telomere length (TeloAA) and three epigenetic measures: DNA methylation age acceleration (DNAmAA), extrinsic epigenetic age acceleration (correlated with immune cell counts, EEAA), and intrinsic epigenetic age acceleration (independent of immune cell counts, IEAA). We also investigated sex-specific associations between air pollution and biological aging, given the published association between sex and aging measures. In KORA an interquartile range (0.97 µg/m3) increase in PM2.5 was associated with a 0.33 y increase in EEAA (CI = 0.01, 0.64; P = 0.04). BC and NOx (indicators or traffic exposure) were associated with DNAmAA and IEAA in women, while TeloAA was inversely associated with BC in men. We replicated this inverse BC-TeloAA association in the Normative Aging Study, a male cohort based in the USA. A multiple phenotype analysis in KORA F4 combining all aging measures showed that BC and PM10 were broadly associated with biological aging in men. Thus, we conclude that long-term exposure to air pollution is associated with biological aging measures, potentially in a sex-specific manner. However, many of the associations were relatively weak and further replication of overall and sex-specific associations is warranted.
| S-EPMC5342683 | biostudies-literature
Project description:Background and Purpose- China bears a heavy burden of stroke because of its large population of elderly people and the propensity for stroke. Previous studies have examined the association between air pollution and stroke mortality or hospital admission. However, the global evidence for adverse effects of air pollution on survival after stroke is scarce. Methods- We used the first national hospital-based prospective registry cohort of stroke in China, which included 12 291 ischemic stroke patients who visited hospitals during 2007 to 2008. All patients were followed for 1-year poststroke. Deaths during the follow-up period were recorded. Participants' 3-year prestroke exposures to ambient PM1, PM2.5, PM10 (particulate matter with aerodynamic diameters ≤1, ≤2.5, and ≤10 μm, respectively) and NO2 (nitrogen dioxide) were estimated by machine learning algorithms with satellite remote sensing, land use information, and meteorological data. Cox proportional hazards models were used to examine the association between air pollution and survival after ischemic stroke. Results- In total, 1649 deaths were identified during the 1-year follow-up period. After controlling for potential confounders, significant associations were observed between exposure to PM1 and PM2.5 and incident fatal ischemic stroke. The corresponding hazard ratios and 95% CIs associated with 10 µg/m3 increase in PM1 and PM2.5 were 1.05 (1.02-1.09) and 1.03 (1.00-1.06), respectively. No significant association was observed for PM10 or NO2 (hazard ratios and 95% CIs, 1.01 [1.00-1.03] and 1.03 [0.99-1.06], respectively). Higher hazard ratios (and 95% CIs) were observed for male, elderly and obese individuals. Conclusions- Prestroke exposure to PM1 and PM2.5 was associated with increased incident fatal ischemic stroke in the year following an ischemic stroke in China. Improved air quality may be beneficial for people to recover from stroke.
| S-EPMC6389419 | biostudies-literature
Project description:BackgroundSeveral studies have shown the health effects of air pollutants, especially in China, North American and Western European countries. But longitudinal cohort studies focused on health effects of long-term air pollution exposure are still limited in Southeast Asian countries where sources of air pollution, weather conditions, and demographic characteristics are different. The present study examined the association between long-term exposure to air pollution and self-reported morbidities in participants of the Thai cohort study (TCS) in Bangkok metropolitan region (BMR), Thailand.MethodsThis longitudinal cohort study was conducted for 9 years from 2005 to 2013. Self-reported morbidities in this study included high blood pressure, high blood cholesterol, and diabetes. Air pollution data were obtained from the Thai government Pollution Control Department (PCD). Particles with diameters ≤10 μm (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), ozone (O3), and carbon monoxide (CO) exposures were estimated with ordinary kriging method using 22 background and 7 traffic monitoring stations in BMR during 2005-2013. Long-term exposure periods to air pollution for each subject was averaged as the same period of person-time. Cox proportional hazards models were used to examine the association between long-term air pollution exposure with self-reported high blood pressure, high blood cholesterol, diabetes. Results of self-reported morbidity were presented as hazard ratios (HRs) per interquartile range (IQR) increase in PM10, O3, NO2, SO2, and CO.ResultsAfter controlling for potential confounders, we found that an IQR increase in PM10 was significantly associated with self-reported high blood pressure (HR = 1.13, 95% CI: 1.04, 1.23) and high blood cholesterol (HR = 1.07, 95%CI: 1.02, 1.12), but not with diabetes (HR = 1.05, 95%CI: 0.91, 1.21). SO2 was also positively associated with self-reported high blood pressure (HR = 1.22, 95%CI: 1.08, 1.38), high blood cholesterol (HR = 1.20, 95%CI: 1.11, 1.30), and diabetes (HR = 1.21, 95%CI: 0.92, 1.60). Moreover, we observed a positive association between CO and self-reported high blood pressure (HR = 1.07, 95%CI: 1.00, 1.15), but not for other diseases. However, self-reported morbidities were not associated with O3 and NO2.ConclusionsLong-term exposure to air pollution, especially for PM10 and SO2 was associated with self-reported high blood pressure, high blood cholesterol, and diabetes in subjects of TCS. Our study supports that exposure to air pollution increases cardiovascular disease risk factors for younger population.
| S-EPMC7768181 | biostudies-literature
Project description:BackgroundLong-term exposures to air pollution has been reported to be associated with inflammation and oxidative stress. However, the underlying metabolic mechanisms remain poorly understood.ObjectivesWe aimed to determine the changes in the blood metabolome and thus the metabolic pathways associated with long-term exposure to outdoor air pollution and ambient temperature.MethodsWe quantified metabolites using mass-spectrometry based global untargeted metabolomic profiling of plasma samples among men from the Normative Aging Study (NAS). We estimated the association between long-term exposure to PM2.5, NO2, O3, and temperature (annual average of central site monitors) with metabolites and their associated metabolic pathways. We used multivariable linear mixed-effect regression models (LMEM) while simultaneously adjusting for the four exposures and potential confounding and correcting for multiple testing. As a reduction method for the intercorrelated metabolites (outcome), we further used an independent component analysis (ICA) and conducted LMEM with the same exposures.ResultsMen (N?=?456) provided 648 blood samples between 2000 and 2016 in which 1158 metabolites were quantified. On average, men were 75.0?years and had an average body mass index of 27.7?kg/m2. Almost all men (97%) were not current smokers. The adjusted analysis showed statistically significant associations with several metabolites (58 metabolites with PM2.5, 15 metabolites with NO2, and 6 metabolites with temperature) while no metabolites were associated with O3. One out of five ICA factors (factor 2) was significantly associated with PM2.5. We identified eight perturbed metabolic pathways with long-term exposure to PM2.5 and temperature: glycerophospholipid, sphingolipid, glutathione, beta-alanine, propanoate, and purine metabolism, biosynthesis of unsaturated fatty acids, and taurine and hypotaurine metabolism. These pathways are related to inflammation, oxidative stress, immunity, and nucleic acid damage and repair.ConclusionsUsing a global untargeted metabolomic approach, we identified several significant metabolites and metabolic pathways associated with long-term exposure to PM2.5, NO2 and temperature. This study is the largest metabolomics study of long-term air pollution, to date, the first study to report a metabolomic signature of long-term temperature exposure, and the first to use ICA in the analysis of both.
| S-EPMC7788989 | biostudies-literature
Project description:BackgroundExposure to air pollution has been consistently associated with cardiovascular morbidity and mortality, but mechanisms remain uncertain. Associations with blood pressure (BP) may help to explain the cardiovascular effects of air pollution.ObjectiveWe examined the cross-sectional relationship between long-term (annual average) residential air pollution exposure and BP in the National Institute of Environmental Health Sciences' Sister Study, a large U.S. cohort study investigating risk factors for breast cancer and other outcomes.MethodsThis analysis included 43,629 women 35-76 years of age, enrolled 2003-2009, who had a sister with breast cancer. Geographic information systems contributed to satellite-based nitrogen dioxide (NO2) and fine particulate matter (? 2.5 ?m; PM2.5) predictions at participant residences at study entry. Generalized additive models were used to examine the relationship between pollutants and measured BP at study entry, adjusting for cardiovascular disease risk factors and including thin plate splines for potential spatial confounding.ResultsA 10-?g/m(3) increase in PM2.5 was associated with 1.4-mmHg higher systolic BP (95% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no significant association with diastolic BP. A 10-ppb increase in NO2 was associated with a 0.4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure.ConclusionsLong-term PM2.5 and NO2 exposures were associated with higher blood pressure. On a population scale, such air pollution-related increases in blood pressure could, in part, account for the increases in cardiovascular disease morbidity and mortality seen in prior studies.
| S-EPMC4590742 | biostudies-literature
Project description:Air pollutants (AP) play a role in subclinical inflammation, and are associated with cardiovascular morbidity and mortality. Metabolic syndrome (MetS) is inflammatory and precedes cardiovascular morbidity and type 2 diabetes. Thus, a positive association between AP and MetS may be hypothesized. We explored this association, (taking into account, pathway-specific MetS definitions), and its potential modifiers in Swiss adults. We studied 3769 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults, reporting at least four-hour fasting time before venepuncture. AP exposures were 10-year mean residential PM10 (particulate matter <10μm in diameter) and NO2 (nitrogen dioxide). Outcomes included MetS defined by World Health Organization (MetS-W), International Diabetes Federation (MetS-I) and Adult Treatment Panel-III (MetS-A) using four- and eight-hour fasting time limits. We also explored associations with individual components of MetS. We applied mixed logistic regression models to explore these associations. The prevalence of MetS-W, MetS-I and MetS-A were 10%, 22% and 18% respectively. Odds of MetS-W, MetS-I and MetS-A increased by 72% (51-102%), 31% (11-54%) and 18% (4-34%) per 10μg/m3 increase in 10-year mean PM10. We observed weaker associations with NO2. Associations were stronger among physically-active, ever-smokers and non-diabetic participants especially with PM10 (p<0.05). Associations remained robust across various sensitivity analyses including ten imputations of missing observations and exclusion of diabetes cases. The observed associations between AP exposure and MetS were sensitive to MetS definitions. Regarding the MetS components, we observed strongest associations with impaired fasting glycemia, and positive but weaker associations with hypertension and waist-circumference-based obesity. Cardio-metabolic effects of AP may be majorly driven by impairment of glucose homeostasis, and to a less-strong extent, visceral adiposity. Well-designed prospective studies are needed to confirm these findings.
| S-EPMC4478007 | biostudies-literature