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Extreme heat and ozone are co-occurring exposures that independently and synergistically increase the risk of respiratory disease. To our knowledge, no joint warning systems consider both risks; understanding their interactive effect can warrant use of comprehensive warning systems to reduce their burden. We examined heterogeneity in joint effects (on the additive scale) between heat and ozone at small geographical scales. A within-community matched design with a Bayesian hierarchical model was applied to study this association at the zip code level. Spatially varying relative risks due to interaction (RERI) were quantified to consider joint effects. Determinants of the spatial variability of effects were assessed using a random effects metaregression to consider the role of demographic/neighborhood characteristics that are known effect modifiers. A total of 817,354 unscheduled respiratory hospitalizations occurred in California from 2004 to 2013 in the May to September period. RERIs revealed no additive interaction when considering overall joint effects. However, when considering the zip code level, certain areas observed strong joint effects. A lower median income, higher percentage of unemployed residents, and exposure to other air pollutants within a zip code drove stronger joint effects; a higher percentage of commuters who walk/bicycle, a marker for neighborhood wealth, showed decreased effects. Results indicate the importance of going beyond average measures to consider spatial variation in the health burden of these exposures and predictors of joint effects. This information can be used to inform early warning systems that consider both heat and ozone to protect populations from these deleterious effects in identified areas.
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Contaminantes Atmosféricos/toxicidad , Calor Extremo , Hospitalización/estadística & datos numéricos , Ozono/toxicidad , Sistema Respiratorio/fisiopatología , Contaminantes Atmosféricos/análisis , Teorema de Bayes , California , Humanos , Ozono/análisis , RiesgoRESUMEN
BACKGROUND: This study capitalized on coal and oil facility retirements to quantify their potential effects on fine particulate matter (PM2.5) concentrations and cardiorespiratory hospitalizations in affected areas using a generalized synthetic control method. METHODS: We identified 11 coal and oil facilities in California that retired between 2006 and 2013. We classified zip code tabulation areas (ZCTA) as exposed or unexposed to a facility retirement using emissions information, distance, and a dispersion model. We calculated weekly ZCTA-specific PM2.5 concentrations based on previously estimated daily time-series PM2.5 concentrations from an ensemble model, and weekly cardiorespiratory hospitalization rates based on hospitalization data collected by the California Department of Health Care Access and Information. We estimated the average differences in weekly average PM2.5 concentrations and cardiorespiratory hospitalization rates in four weeks after each facility retirement between the exposed ZCTAs and the synthetic control using all unexposed ZCTAs (i.e., the average treatment effect among the treated [ATT]) and pooled ATTs using meta-analysis. We conducted sensitivity analyses to consider different classification schemes to distinguish exposed from unexposed ZCTAs, including aggregating outcomes with different time intervals and including a subset of facilities with reported retirement date confirmed via emission record. RESULTS: The pooled ATTs were 0.02 µg/m3 (95% confidence interval (CI): -0.25 to 0.29 µg/m3) and 0.34 per 10,000 person-weeks (95%CI: -0.08 to 0.75 per 10,000 person-weeks) following the facility closure for weekly PM2.5 and cardiorespiratory hospitalization rates, respectively. Our inferences remained the same after conducting sensitivity analyses. CONCLUSIONS: We demonstrated a novel approach to study the potential benefits associated with industrial facility retirements. The declining contribution of industrial emissions to ambient air pollution in California may explain our null findings. We encourage future research to replicate this work in regions with different industrial activities.
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Contaminantes Atmosféricos , Contaminación del Aire , Humanos , Contaminantes Atmosféricos/análisis , Jubilación , Carbón Mineral , Contaminación del Aire/análisis , Material Particulado/análisis , California , Centrales EléctricasRESUMEN
BACKGROUND: Although slow gait speed is an established risk factor for falls, few studies have evaluated change in gait speed as a predictor of falls or considered variability in effects by cognitive status. Change in gait speed may be a more useful metric because of its potential to identify decline in function. In addition, older adults with mild cognitive impairment are at an elevated risk of falls. The purpose of this research was to quantify the association between 12-month change in gait speed and falls in the subsequent 6 months among older adults with and without mild cognitive impairment. METHODS: Falls were self-reported every six months, and gait speed was ascertained annually among 2,776 participants in the Ginkgo Evaluation of Memory Study (2000-2008). Adjusted Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI) for fall risk relative to a 12-month change in gait speed. RESULTS: Slowing gait speed over 12 months was associated with increased risk of one or more falls (HR:1.13; 95% CI: 1.02 to 1.25) and multiple falls (HR:1.44; 95% CI: 1.18 to 1.75). Quickening gait speed was not associated with risk of one or more falls (HR 0.97; 95% CI: 0.87 to 1.08) or multiple falls (HR 1.04; 95% CI: 0.84 to 1.28), relative to those with a less than 0.10 m/s change in gait speed. Associations did not vary by cognitive status (pinteraction = 0.95 all falls, 0.25 multiple falls). CONCLUSIONS: Decline in gait speed over 12 months is associated with an increased likelihood of falls among community-dwelling older adults, regardless of cognitive status. Routine checks of gait speed at outpatient visits may be warranted as a means to focus fall risk reduction efforts.
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Disfunción Cognitiva , Vida Independiente , Humanos , Anciano , Estudios Retrospectivos , Marcha , Estudios de Cohortes , Velocidad al Caminar , Disfunción Cognitiva/diagnóstico , Disfunción Cognitiva/epidemiologíaRESUMEN
INTRODUCTION: Growing evidence implicates air pollution as a risk factor for dementia, but prior work is limited by challenges in diagnostic accuracy and assessing exposures in the decades prior to disease development. We evaluated the impact of long-term fine particulate matter (PM2.5 ) exposures on incident dementia (all-cause, Alzheimer's disease [AD], and vascular dementia [VaD]) in older adults. METHODS: A panel of neurologists adjudicated dementia cases based on extensive neuropsychological testing and magnetic resonance imaging. We applied validated fine-scale air pollutant models to reconstructed residential histories to assess exposures. RESULTS: An interquartile range increase in 20-year PM2.5 was associated with a 20% higher risk of dementia (95% confidence interval [CI]: 5%, 37%) and an increased risk of mixed VaD/AD but not AD alone. DISCUSSION: Our findings suggest that air pollutant exposures over decades contribute to dementia and that effects of current exposures may be experienced years into the future.
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Contaminantes Atmosféricos , Contaminación del Aire , Enfermedad de Alzheimer , Demencia Vascular , Humanos , Anciano , Ginkgo biloba , Contaminación del Aire/efectos adversos , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Enfermedad de Alzheimer/epidemiología , Enfermedad de Alzheimer/inducido químicamente , Material Particulado/efectos adversos , Material Particulado/análisis , Demencia Vascular/epidemiologíaRESUMEN
INTRODUCTION: No evidence exists about the impact of air pollution reduction on incidence of dementia. The aim of this study was to quantify how air quality improvement leads to dementia-incidence benefits. METHODS: In the French Three-City cohort (12 years of follow-up), we used parametric g-computation to quantify the expected number of prevented dementia cases under different hypothetical interventions with particulate matter measuring <2.5 µm (PM2.5 ) reductions. RESULTS: Among 7051 participants, 789 participants developed dementia. The median PM2.5 reduction between 1990 and 2000 was 12.2 (µg/m3 ). Such a reduction reduced the risk of all-cause dementia (hazard ratio [HR], 0.85; 95% confidence interval [CI], 0.76 to 0.95). If all study participants were enjoying a hypothetical reduction of more than 13.10 µg/m3 (median reduction observed in the city of Montpellier), the rate difference was -0.37 (95% CI, -0.57 to -0.17) and the rate ratio was 0.67 (95% CI, 0.50 to 0.84). DISCUSSION: These findings highlight the possible substantial benefits of reducing air pollution in the prevention of dementia.
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Contaminantes Atmosféricos , Contaminación del Aire , Demencia , Humanos , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Mejoramiento de la Calidad , Exposición a Riesgos Ambientales , Contaminación del Aire/efectos adversos , Material Particulado/análisis , Demencia/epidemiología , Demencia/prevención & controlRESUMEN
This study aimed to investigate the role of cardiovascular health (CVH) and vascular events as potential contributors to socioeconomic inequalities in dementia using causal mediation analyses. We used data from the Three-City Cohort, a French population-based study with 12 years of follow-up, with active search of dementia cases and validated diagnosis. Individual socioeconomic status was assessed using education, occupation and income. A CVH score as defined by the American Heart Association and incident vascular events were considered separately as mediators. We performed multi-level Cox proportional and Aalen additive hazard regression models to estimate the total effects of socioeconomic status on dementia risk. To estimate natural direct and indirect effects through CVH and vascular events, we applied two distinct weighting methods to quantify the role of CVH and vascular events: Inverse Odds Ratio Weighting (IORW) and Marginal Structural Models (MSM) respectively. Among 5581 participants, the risk of dementia was higher among participants with primary education (HR 1.60, 95%CI 1.44-1.78), blue-collar workers (HR 1.62, 95%CI 1.43-1.84) and with lower income (HR 1.23, 95%CI 1.09-1.29). Using additive models, 571 (95% CI 288-782) and 634 (95% CI 246-1020) additional cases of dementia per 100 000 person and year were estimated for primary education and blue-collar occupation, respectively. Using IORW, the CVH score mediate the relationship between education or income, and dementia (proportion mediated 17% and 26%, respectively). Yet, considering vascular events as mediator, MSM generated indirect effects that were smaller and more imprecise. Socioeconomic inequalities in dementia risk were observed but marginally explained by CVH or vascular events mediators.
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Enfermedades Cardiovasculares/complicaciones , Demencia/diagnóstico , Conductas Relacionadas con la Salud , Clase Social , Determinantes Sociales de la Salud , Anciano , Enfermedades Cardiovasculares/epidemiología , Demencia/epidemiología , Demencia/etiología , Femenino , Disparidades en el Estado de Salud , Indicadores de Salud , Humanos , Masculino , Análisis de Mediación , Características de la Residencia/estadística & datos numéricosRESUMEN
Exposure to ambient fine particulate matter (particulate matter ≤2.5 µm in aerodynamic diameter (PM2.5)) during pregnancy is associated with preterm birth (PTB), a leading cause of infant morbidity and mortality. Results from studies attempting to identify etiologically relevant exposure periods of vulnerability have been inconsistent, possibly because of failure to consider the time-to-event nature of the outcome and lagged exposure effects of PM2.5. In this study, we aimed to identify critical exposure windows for weekly PM2.5 exposure and PTB in California using California birth cohort data from 2005-2010. Associations were assessed using distributed-lag Cox proportional hazards models. We assessed effect-measure modification by race/ethnicity by calculating the weekly relative excess risk due to interaction. For a 10-µg/m3 increase in PM2.5 exposure over the entire period of gestation, PTB risk increased by 11% (hazard ratio = 1.11, 95% confidence interval: 1.09, 1.14). Gestational weeks 17-24 and 36 were associated with increased vulnerability to PM2.5 exposure. We find that non-Hispanic black mothers may be more susceptible to effects of PM2.5 exposure than non-Hispanic white mothers, particularly at the end of pregnancy. These findings extend our knowledge about the existence of specific exposure periods during pregnancy that have the greatest impact on preterm birth.
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Contaminantes Atmosféricos/efectos adversos , Exposición Materna/efectos adversos , Material Particulado/efectos adversos , Nacimiento Prematuro/etiología , Adolescente , Adulto , Negro o Afroamericano , California , Estudios de Cohortes , Femenino , Humanos , Modelos Teóricos , Embarazo , Resultado del Embarazo , Trimestres del Embarazo , Nacimiento Prematuro/etnología , Modelos de Riesgos Proporcionales , Adulto JovenRESUMEN
BACKGROUND: Low exposure to ultraviolet radiation (UVR) from sunlight may be a risk factor for developing multiple sclerosis (MS). Possible pathways may be related to effects on immune system function or vitamin D insufficiency, as UVR plays a role in the production of the active form of vitamin D in the body. OBJECTIVE: This study examined whether lower levels of residential UVR exposure from sunlight were associated with increased MS risk in a cohort of radiologic technologists. METHODS: Participants in the third and fourth surveys of the US Radiologic Technologists (USRT) Cohort Study eligible (N = 39,801) for analysis provided complete residential histories and reported MS diagnoses. MS-specialized neurologists conducted medical record reviews and confirmed 148 cases. Residential locations throughout life were matched to satellite data from NASA's Total Ozone Mapping Spectrometer (TOMS) project to estimate UVR dose. RESULTS: Findings indicate that MS risk increased as average lifetime levels of UVR exposures in winter decreased. The effects were consistent across age groups <40 years. There was little indication that low exposures during summer or at older ages were related to MS risk. CONCLUSION: Our findings are consistent with the hypothesis that UVR exposure reduces MS risk and may ultimately suggest prevention strategies.
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Esclerosis Múltiple/epidemiología , Luz Solar , Rayos Ultravioleta , Adulto , Estudios de Cohortes , Femenino , Mapeo Geográfico , Humanos , Masculino , Personal de Laboratorio Clínico , Persona de Mediana Edad , Esclerosis Múltiple/prevención & control , Riesgo , Tecnología RadiológicaRESUMEN
BACKGROUND: Studies suggesting a protective effect of estrogen in neurodegenerative diseases prompted us to investigate this relationship in progressive supranuclear palsy (PSP). METHODS: This case-control study evaluated the self-reported reproductive characteristics and estrogen of 150 women with PSP and 150 age-matched female controls who participated in the Environmental Genetic-PSP study. Conditional logistic regression models were generated to examine associations of PSP with estrogen. RESULTS: There was no association between years of estrogen exposure duration and PSP. There was a suggestion of an inverse association between composite estrogen score and PSP that did not reach statistical significance (P = .06). Any exposure to estrogen replacement therapy halved the risk of PSP (odds ratio = 0.52; 95% confidence interval = 0.30-0.92; P = .03). Among PSP cases, earlier age at menarche was associated with better performance on Hoehn and Yahr stage (ß = -0.60; SE = 0.26; P = .02) and Unified Parkinson's Disease Rating Scale II score (ß = -5.19; SE = 2.48; P = .04) at clinical examination. CONCLUSIONS: This case-control study suggests a protective role of lifetime estrogen exposure in PSP. Future studies will be needed to confirm this association. © 2018 International Parkinson and Movement Disorder Society.
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Estrógenos/efectos adversos , Interacción Gen-Ambiente , Parálisis Supranuclear Progresiva/inducido químicamente , Parálisis Supranuclear Progresiva/genética , Anciano , Estudios de Casos y Controles , Femenino , Humanos , Modelos Logísticos , Persona de Mediana Edad , América del Norte , Autoinforme , Parálisis Supranuclear Progresiva/epidemiología , Encuestas y CuestionariosRESUMEN
BACKGROUND: Endotoxin, a contaminant of cotton dust, is an experimental model for parkinsonism (PS). METHODS: We investigated associations between exposures to endotoxin, solvents, magnetic fields, and night shift work, and neurologist-determined PS among Shanghai women textile workers, including 537 retired cotton factory workers ages ≥50 years and an age-matched reference group of 286 retired textile workers not exposed to cotton dust. Repeat exams were conducted 2.5 years after enrollment among 467 cotton workers and 229 reference workers. RESULTS: We identified 39 prevalent PS cases and 784 non-cases. No consistent or statistically significant associations were observed for endotoxin, solvents, magnetic fields, or shift work with PS risk, severity, or progression. CONCLUSIONS: Despite the null findings, additional studies of endotoxin exposure and risk of PS in other well-characterized occupational cohorts are warranted in view of toxicological evidence that endotoxin is a pathogenic agent and its widespread occurrence in multiple industries worldwide.
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Endotoxinas/análisis , Enfermedades Profesionales/epidemiología , Exposición Profesional/análisis , Trastornos Parkinsonianos/epidemiología , Industria Textil , Adulto , China/epidemiología , Polvo/análisis , Endotoxinas/toxicidad , Femenino , Gossypium , Humanos , Persona de Mediana Edad , Enfermedades Profesionales/etiología , Exposición Profesional/efectos adversos , Trastornos Parkinsonianos/etiologíaRESUMEN
Background: Growing evidence links air pollution exposure to the risk of dementia. We hypothesized that hypertension may partially mediate this effect. Methods: We previously documented an association between air pollution and dementia in the Ginkgo Evaluation of Memory Study, a randomized, placebo-controlled trial of 3069 adults ≥75 years across four US sites who were evaluated for dementia every 6 months from 2000-2008. We utilized a two-stage regression approach for causal mediation analysis to decompose the total effect of air pollution on dementia into its natural direct and indirect effect through prevalent hypertension. Exposure to air pollution in the 10 or 20 years before enrollment was assigned using estimates from fine-scale spatial-temporal models for PM2.5, PM10, and NO2. We used Poisson regression models for hypertension and Cox proportional hazard models for time-to-incident all-cause dementia, adjusting for a priori confounders. Results: Participants were free of mild cognitive impairment at baseline (n = 2564 included in analyses); 69% had prevalent hypertension at baseline. During follow-up, 12% developed all-cause dementia (Alzheimer's disease [AD] = 212; vascular dementia with or without AD [VaD/AD mixed] = 97). We did not find an adverse effect of any air pollutant on hypertension. Hypertension was associated with VaD/AD mixed (HR, 1.92 [95% CI = 1.14, 3.24]) but not AD. We did not observe mediation through hypertension for the effect of any pollutant on dementia outcomes. Conclusions: The lack of mediated effect may be due to other mechanistic pathways and the minimal effect of air pollution on hypertension in this cohort of older adults.
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BACKGROUND: Falls contribute to impairments in activities of daily living (ADLs), resulting in significant declines in the quality of life, safety, and functioning of older adults. Understanding the magnitude and duration of the effect of falls on ADLs, as well as identifying the characteristics of older adults more likely to have post-fall ADL impairment is critical to inform fall prevention and post-fall intervention. The purpose of this study is to 1) Quantify the association between falls and post-fall ADL impairment and 2) Model trajectories of ADL impairment pre- and post-fall to estimate the long-term impact of falls and identify characteristics of older adults most likely to have impairment. METHOD: Study participants were from the Ginkgo Evaluation of Memory Study, a randomized controlled trial in older adults (age 75+) in the United States. Self-reported incident falls and ADL scores were ascertained every 6 months over a 7-year study period. We used Cox proportional hazards analyses (n = 2091) to quantify the association between falls and ADL impairment and latent class trajectory modeling (n = 748) to visualize trajectories of ADL impairment pre-and post-fall. RESULTS: Falls reported in the previous 6 months were associated with impairment in ADLs (HR: 1.42; 95% CI 1.32, 1.52) in fully adjusted models. Based on trajectory modeling (n = 748), 19% (n = 139) of participants had increased, persistent ADL impairment after falling. Participants who were female, lived in a neighborhood with higher deprivation, or experienced polypharmacy were more likely to have ADL impairment post-fall. CONCLUSIONS: Falls are associated with increased ADL impairment, and this impairment can persist over time. It is crucial that all older adults, and particularly those at higher risk of post-fall ADL impairment have access to comprehensive fall risk assessment and evidence-based fall prevention interventions, to help mitigate the negative impacts on ADL function.
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Actividades Cotidianas , Calidad de Vida , Anciano , Femenino , Humanos , Masculino , Estudios de Cohortes , Estudios Retrospectivos , Ensayos Clínicos Controlados Aleatorios como AsuntoRESUMEN
Air pollution has been linked to Alzheimer's disease and related dementias (ADRD), but the mechanisms connecting air pollution to ADRD have not been firmly established. Air pollution may cause oxidative stress and neuroinflammation and contribute to the deposition of amyloid beta (Aß) in the brain. We examined the association between fine particulate matter<2.5 µm in diameter (PM2.5), particulate matter<10 µm in diameter (PM10), nitrogen dioxide (NO2), and plasma based measures of Aß1-40, Aß1-42 and Aß1-42/Aß1-40 using data from 3044 dementia-free participants of the Ginkgo Evaluation of Memory Study (GEMS). Air pollution exposures were estimated at residential addresses that incorporated address histories dating back to 1980, resulting in one-, five-, 10- and 20- year exposure averages. Aß was measured at baseline (2000-2002) and then again at the end of the study (2007-2008) allowing for linear regression models to assess cross-sectional associations and linear random effects models to evaluate repeated measures. After adjustment for socio-demographic and behavioral covariates, we found small positive associations between each air pollutant and Aß1-40 but no association with Aß1-42 or the ratio measures in cross sectional analysis. In repeat measures analysis, we found larger positive associations between each air pollutant and all three outcomes. We observed a 4.43% (95% CI 3.26%, 5.60%) higher Aß1-40 level, 9.73% (6.20%, 13.38%) higher Aß1-42 and 1.57% (95% CI: 0.94%, 2.20%) higher Aß1-42/Aß1-40 ratio associated with a 2 µg/m3 higher 20-year average PM2.5. Associations with other air pollutants were similar. Our study contributes to the broader evidence base on air pollution and ADRD biomarkers by evaluating longer air pollution exposure averaging periods to better mimic disease progression and provides a modifiable target for ADRD prevention.
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Contaminantes Atmosféricos , Contaminación del Aire , Humanos , Anciano , Péptidos beta-Amiloides/análisis , Estudios Transversales , Ginkgo biloba , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Material Particulado/efectos adversos , Material Particulado/análisis , Dióxido de Nitrógeno/efectos adversos , Dióxido de Nitrógeno/análisis , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisisRESUMEN
Evidence suggests exposure to air pollution increases the risk of dementia. Cognitively stimulating activities and social interactions, made available through the social environment, may slow cognitive decline. We examined whether the social environment buffers the adverse effect of air pollution on dementia in a cohort of older adults. Methods: This study draws from the Ginkgo Evaluation of Memory Study. Participants aged 75 years and older were enrolled between 2000 and 2002 and evaluated for dementia semi-annually through 2008. Long-term exposure to particulate matter and nitrogen dioxide was assigned from spatial and spatiotemporal models. Census tract-level measures of the social environment and individual measures of social activity were used as measures of the social environment. We generated Cox proportional hazard models with census tract as a random effect and adjusted for demographic and study visit characteristics. Relative excess risk due to interaction was estimated as a qualitative measure of additive interaction. Results: This study included 2,564 individuals. We observed associations between increased risk of dementia and fine particulate matter (µg/m3), coarse particulate matter (µg/m3), and nitrogen dioxide (ppb); HRs per 5 unit increase were 1.55 (1.01, 2.18), 1.31 (1.07, 1.60), and 1.18 (1.02, 1.37), respectively. We found no evidence of additive interaction between air pollution and the neighborhood social environment. Conclusions: We found no consistent evidence to suggest a synergistic effect between exposure to air pollution and measures of the social environment. Given the many qualities of the social environment that may reduce dementia pathology, further examination is encouraged.
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Introduction: Research focusing on cognitive aging and dementia is a global endeavor. However, cross-national differences in cognition are embedded in other sociocultural differences, precluding direct comparisons of test scores. Such comparisons can be facilitated by co-calibration using item response theory (IRT). The goal of this study was to explore, using simulation, the necessary conditions for accurate harmonization of cognitive data. Method: Neuropsychological test scores from the US Health and Retirement Study (HRS) and the Mexican Health and Aging Study (MHAS) were subjected to IRT analysis to estimate item parameters and sample means and standard deviations. These estimates were used to generate simulated item response patterns under 10 scenarios that adjusted the quality and quantity of linking items used in harmonization. IRT-derived factor scores were compared to the known population values to assess bias, efficiency, accuracy, and reliability of the harmonized data. Results: The current configuration of HRS and MHAS data was not suitable for harmonization, as poor linking item quality led to large bias in both cohorts. Scenarios with more numerous and higher quality linking items led to less biased and more accurate harmonization. Discussion: Linking items must possess low measurement error across the range of latent ability for co-calibration to be successful. HIGHLIGHTS: We developed a statistical simulation platform to evaluate the degree to which cross-sample harmonization accuracy varies as a function of the quality and quantity of linking items.Two large studies of aging-one in Mexico and one in the United States-use three common items to measure cognition.These three common items have weak correspondence with the ability being measured and are all low in difficulty.Harmonized scores derived from the three common linking items will provide biased and inaccurate estimates of cognitive ability.Harmonization accuracy is greatest when linking items vary in difficulty and are strongly related to the ability being measured.
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Stillbirths and complications from preterm birth are two of the leading causes of neonatal deaths across the globe. Lower- to middle-income countries (LMICs) are experiencing some of the highest rates of these adverse birth outcomes. Research has suggested that environmental determinants, such as extreme heat, can increase the risk of preterm birth and stillbirth. Under climate change, extreme heat events have become more severe and frequent and are occurring in differential seasonal patterns. Little is known about how extreme heat affects the risk of preterm birth and stillbirth in LMICs. Thus, it is imperative to examine how exposure to extreme heat affects adverse birth outcomes in regions with some of the highest rates of preterm and stillbirths. Most of the evidence linking extreme heat and adverse birth outcomes has been generated from high-income countries (HICs) notably because measuring temperature in LMICs has proven challenging due to the scarcity of ground monitors. The paucity of health data has been an additional obstacle to study this relationship in LMICs. In this study, globally gridded meteorological data was linked with spatially and temporally resolved Demographic and Health Surveys (DHS) data on adverse birth outcomes. A global analysis of 14 LMICs was conducted per a pooled time-stratified case-crossover design with distributed-lag nonlinear models to ascertain the relationship between acute exposure to extreme heat and PTB and stillbirths. We notably found that experiencing higher maximum temperatures and smaller diurnal temperature range during the last week before birth increased the risk of preterm birth and stillbirth. This study is the first global assessment of extreme heat events and adverse birth outcomes and builds the evidence base for LMICs.
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Calor Extremo , Nacimiento Prematuro , Países en Desarrollo , Calor Extremo/efectos adversos , Femenino , Humanos , Renta , Recién Nacido , Embarazo , Nacimiento Prematuro/epidemiología , Mortinato/epidemiologíaRESUMEN
Typically, progressive supranuclear palsy (PSP) is clinically characterized by slow vertical saccades or supranuclear gaze palsy, levodopa-resistant parkinsonism with predominant axial symptoms, and cognitive executive impairment. Over the past decades, various PSP phenotypes, including PSP with predominant parkinsonism, PSP with corticobasal syndrome, PSP with progressive gait freezing, and PSP with predominant frontal dysfunction, have been identified from pathologically confirmed cases. Expanding knowledge led to new diagnostic criteria for PSP that with increased disease awareness led to increased PSP prevalence estimates. The identification of environmental and modifiable risk factors creates an opportunity to intervene and delay the onset of PSP or slow disease progression. To date, despite the increasing number of publications assessing risk factors for PSP, few articles have focused on environmental and lifestyle risk factors for this disorder. In this article, we reviewed the literature investigating the relationship between PSP and several environmental and other modifiable lifestyle risk factors. In our review, we found that exposures to toxins related to diet, metals, well water, and hypertension were associated with increased PSP risk. In contrast, higher education and statins may be protective. Further case-control studies are encouraged to determine the exact role of these factors in the etiopathogenesis of PSP, which in turn would inform strategies to prevent and reduce the burden of PSP.
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BACKGROUND: Hispanics/Latinos in the United States are more likely to live in neighborhoods with greater exposure to air pollution and are projected to have the largest increase in dementia among race/ethnic minority groups. OBJECTIVE: We examined the associations of air pollution with performance on cognitive function tests in Hispanic/Latino adults. METHODS: We used data from the San Diego site of the Hispanic Community Health Study/Study of Latinos, an ongoing cohort of Hispanics/Latinos. This analysis focused on individuals ≥45 years of age who completed a neurocognitive battery examining overall mental status, verbal learning, memory, verbal fluency, and executive function (nâ=â2,089). Air pollution (PM2.5 and O3) before study baseline was assigned to participants' zip code. Logistic and linear regression were used to estimate the associations of air pollution on overall mental status and domain-specific standardized test scores. Models accounted for complex survey design, demographic, and socioeconomic characteristics. RESULTS: We found that for every 10µg/m3 increase in PM2.5, verbal fluency worsened (ß: -0.21 [95%CI: -0.68, 0.25]). For every 10 ppb increase in O3, verbal fluency and executive function worsened (ß: -0.19 [95%CI: -0.34, -0.03]; ß: -0.01 [95%CI: -0.01, 0.09], respectively). We did not identify any detrimental effect of pollutants on other domains. CONCLUSION: Although we found suggestions that air pollution may impact verbal fluency and executive function, we observed no consistent or precise evidence to suggest an adverse impact of air pollution on cognitive level among this cohort of Hispanic/Latino adults.
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Contaminación del Aire/efectos adversos , Cognición , Exposición a Riesgos Ambientales/efectos adversos , Adulto , Anciano , California , Estudios de Cohortes , Femenino , Hispánicos o Latinos , Humanos , Masculino , Persona de Mediana EdadRESUMEN
Air pollution may increase risk of Alzheimer's disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. Here, we constructed two national U.S. population-based cohorts of those aged ≥65 from the Medicare Chronic Conditions Warehouse (2000-2018), combined with high-resolution air pollution datasets, to investigate the association of long-term exposure to ambient fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) with dementia and AD incidence, respectively. We identified ~2.0 million incident dementia cases (N = 12,233,371; dementia cohort) and ~0.8 million incident AD cases (N = 12,456,447; AD cohort). Per interquartile range (IQR) increase in the 5-year average PM2.5 (3.2 µg/m3), NO2 (11.6 ppb), and warm-season O3 (5.3 ppb) over the past 5 years prior to diagnosis, the hazard ratios (HRs) were 1.060 (95% confidence interval [CI]: 1.054, 1.066), 1.019 (95% CI: 1.012, 1.026), and 0.990 (95% CI: 0.987, 0.993) for incident dementias, and 1.078 (95% CI: 1.070, 1.086), 1.031 (95% CI: 1.023, 1.039), and 0.982 (95%CI: 0.977, 0.986) for incident AD, respectively, for the three pollutants. For both outcomes, concentration-response relationships for PM2.5 and NO2 were approximately linear. Our study suggests that exposures to PM2.5 and NO2 are associated with incidence of dementia and AD.
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Contaminación del Aire/efectos adversos , Demencia/epidemiología , Exposición a Riesgos Ambientales/efectos adversos , Anciano , Anciano de 80 o más Años , Contaminantes Atmosféricos/efectos adversos , Contaminación del Aire/estadística & datos numéricos , Demencia/etiología , Exposición a Riesgos Ambientales/estadística & datos numéricos , Monitoreo del Ambiente/estadística & datos numéricos , Femenino , Estudios de Seguimiento , Humanos , Incidencia , Masculino , Material Particulado/efectos adversos , Factores de Riesgo , Estados Unidos/epidemiologíaRESUMEN
Wildfire smoke adversely impacts respiratory health as fine particles can penetrate deeply into the lungs. Epidemiological studies of differential impacts typically target population subgroups in terms of vulnerability to wildfire smoke. Such information is useful to customize smoke warnings and mitigation actions for specific groups of individuals. In addition to individual vulnerability, it is also important to assess spatial patterns of health impacts to identify vulnerable communities and tailor public health actions during wildfire smoke events. METHODS: We assess the spatiotemporal variation in respiratory hospitalizations in San Diego County during a set of major wildfires in 2007, which led to a substantial public health burden. We propose a spatial within-community matched design analysis, adapted to the study of wildfire impacts, coupled with a Bayesian Hierarchical Model, that explicitly considers the spatial variation of respiratory health associated with smoke exposure, compared to reference periods before and after wildfires. We estimate the signal-to-noise ratio to ultimately gauge the precision of the Bayesian model output. RESULTS: We find the highest excess hospitalizations in areas covered by smoke, mainly ZIP codes contained by and immediately downwind of wildfire perimeters, and that excess hospitalizations tend to follow the distribution of smoke plumes across space (ZIP codes) and time (days). CONCLUSIONS: Analyzing the spatiotemporal evolution of exposure to wildfire smoke is necessary due to variations in smoke plume extent, particularly in this region where the most damaging wildfires are associated with strong wind conditions.