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Cognitive impacts of ambient air pollution in the National Social Health and Aging Project (NSHAP) cohort.

ABSTRACT: Pathways through which air pollution may impact cognitive function are poorly understood, particularly with regard to whether and how air pollution interacts with social and emotional factors to influence cognitive health.To examine the association between air pollutant exposures and cognitive outcomes among older adults participating in the National Social Life, Health, and Aging Project (NSHAP) cohort study.Measures of cognitive function, social connectedness, and physical and mental health were obtained for each NSHAP participant starting with Wave 1 of the study in 2005. Cognitive function was assessed using the Chicago Cognitive Function Measure (CCFM) for 3377 participants. Exposures to fine particles (PM2.5) were estimated for each participant using GIS-based spatio-temporal models, and exposures to nitrogen dioxide (NO2) were obtained from the nearest EPA monitors.In adjusted linear regression models, IQR increases in 1 to 7year PM2.5 exposures were associated with a 0.22 (95% CI: -0.44, -0.01) to a 0.25 (95% CI: -0.43, -0.06) point decrease in CCFM scores, equivalent to aging 1.6years, while exposures to NO2 were equivalent to aging 1.9years. The impacts of PM2.5 on cognition were modified by stroke, anxiety, and stress, and were mediated by depression. The impacts of NO2 were mediated by stress and effect modification by impaired activities of daily living for NO2 was found.Exposures to long-term PM2.5 and NO2 were associated with decreased cognitive function in our cohort of older Americans, and individuals who experienced a stroke or elevated anxiety were more susceptible to the effects of PM2.5 on cognition. Additionally, mediation results suggest that PM2.5 may impact cognition through pathways related to mood disorders.

SUBMITTER: Tallon LA

PROVIDER: S-EPMC6022397 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature

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Cognitive impacts of ambient air pollution in the National Social Health and Aging Project (NSHAP) cohort.

Tallon Lindsay A LA Manjourides Justin J Pun Vivian C VC Salhi Carmel C Suh Helen H

Environment international 20170406

<h4>Background</h4>Pathways through which air pollution may impact cognitive function are poorly understood, particularly with regard to whether and how air pollution interacts with social and emotional factors to influence cognitive health.<h4>Objective</h4>To examine the association between air pollutant exposures and cognitive outcomes among older adults participating in the National Social Life, Health, and Aging Project (NSHAP) cohort study.<h4>Methods</h4>Measures of cognitive function, so ...[more]

PMID: 28392067

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Project description:BackgroundAmbient fine particulate matter (PM2.5) is among the most prevalent sources of environmentally induced inflammation and oxidative stress, both of which are implicated in the pathogenesis of most mental disorders. Evidence, however, concerning the impact of PM2.5 on mental health is just emerging.ObjectiveWe examined the association between PM2.5 and current level of depressive and anxiety symptoms using a nationally representative probability sample (n = 4,008) of older, community-dwelling individuals living across the United States (the National Social Life, Health and Aging project).MethodsMental health was evaluated using validated, standardized questionnaires and clinically relevant cases were identified using well-established cutoffs; daily PM2.5 estimates were obtained using spatiotemporal models. We used generalized linear mixed models, adjusting for potential confounders, and explored effect modification.ResultsAn increase in PM2.5 was significantly associated with anxiety symptoms, with the largest increase for 180-days moving average (OR = 1.61; 95% CI: 1.35, 1.92) after adjusting for socioeconomic measures (SES); PM2.5 was positively associated with depressive symptoms, and significantly for 30-day moving average (OR = 1.16; 95% CI: 1.05, 1.29) upon SES adjustment. The observed associations were enhanced among individuals who had low SES and history of comorbidity. When considering mental health as chronic conditions, PM2.5 was significantly associated with incident depressive symptoms for all exposure windows examined, but with incident anxiety symptoms only for shorter exposure windows, which may be due to a drop in power resulting from the decreased between-subject variability in chronic PM2.5 exposure.ConclusionPM2.5 was associated with depressive and anxiety symptoms, with associations the strongest among individuals with lower SES or among those with certain health-related characteristics. Citation: Pun VC, Manjourides J, Suh H. 2017. Association of ambient air pollution with depressive and anxiety symptoms in older adults: results from the NSHAP study. Environ Health Perspect 125:342-348; http://dx.doi.org/10.1289/EHP494.

Project description:BackgroundExposure to air pollution was reported to affect glucose metabolism, increasing the risk of diabetes mellitus. We conducted an epidemiological study on glucose metabolism and air pollution by exploring the levels of fasting blood glucose (FBG) and hemoglobin A1c (HbA1c) with changes in ambient air quality, depending on the characteristics of the susceptible population.MethodsWe carried out a cross-sectional analysis of a nationally representative sample of 10,014 adults (4267 in male and 5747 in female) from the Korea National Health and Nutrition Examination Survey in 2012 and 2013 along with data from the Korean Air Quality Forecasting System. The analysis was performed using a generalized linear model stratified by sex, age, and presence of diabetes. We assessed the changes in FBG and HbA1c associated with exposures to particulate matter (PM10), fine particulate matter (PM2.5), and nitrogen dioxide (NO2) after controlling for confounders.ResultsThere were 1110 participants with diabetes (557 in male and 553 in female). Overall, the FBG level increased by 7.83?mg/dL (95% confidence interval [CI]: 2.80-12.87) per interquartile range (IQR) increment of NO2, 5.32?mg/dL (95% CI: 1.22-9.41) per IQR increment of PM10 at a moving average of 0-6?days, and 4.69?mg/dL (95% CI: 0.48-8.91) per IQR increment of PM2.5 at a moving average of 0-5?days. HbA1c increased by 0.57% (95% CI: 0.04-1.09) per IQR increment of PM10 at a moving average of 0-60?days and 0.34% (95% CI: 0.04-0.63) per IQR increment of PM2.5 at a moving average of 0-75?days. The change in FBG and HbA1c increased more in the diabetic group, especially in males aged 65?years or more. There was a strong association between elevation in diabetes-related parameters and exposure to air pollution.ConclusionsOur study provides scientific evidence supporting that short- and mid-term exposure to air pollution is associated with changes in biological markers related to diabetes. This finding suggests that the impact of air pollution should be reflected in chronic disease management when establishing local health care policies.

Project description:In utero air pollution exposure has been associated with adverse birth outcomes, yet effects of air pollutants on regulatory mechanisms in fetal growth and critical windows of vulnerability during pregnancy are not well understood. There is evidence that epigenetic alterations may contribute to these effects. DNA methylation (DNAm) based age estimators have been developed and studied extensively with health outcomes in recent years. Growing literature suggests environmental factors, such as air pollution and smoking, can influence epigenetic aging. However, little is known about the effect of prenatal air pollution exposure on epigenetic aging. In this study, we leveraged existing data on prenatal air pollution exposure and cord blood DNAm from 332 mother-child pairs in the Early Autism Risk Longitudinal Investigation (EARLI) and Markers of Autism Risk in Babies-Learning Early Signs (MARBLES), two pregnancy cohorts enrolling women who had a previous child diagnosed with autism spectrum disorder, to assess the relationship of prenatal exposure to air pollution and epigenetic aging at birth. DNAm age was computed using existing epigenetic clock algorithms for cord blood tissue-Knight and Bohlin. Epigenetic age acceleration was defined as the residual of regressing chronological gestational age on DNAm age, accounting for cell type proportions. Multivariable linear regression models and distributed lag models (DLMs), adjusting for child sex, maternal race/ethnicity, study sites, year of birth, maternal education, were completed. In the single-pollutant analysis, we observed exposure to PM2.5, PM10, and O3 during preconception period and pregnancy period were associated with decelerated epigenetic aging at birth. For example, pregnancy average PM10 exposure (per 10 unit increase) was associated with epigenetic age deceleration at birth (weeks) for both Knight and Bohlin clocks (β = -0.62, 95% CI: -1.17, -0.06; β = -0.32, 95% CI: -0.63, -0.01, respectively). Weekly DLMs revealed that increasing PM2.5 during the first trimester and second trimester were associated with decelerated epigenetic aging and that increasing PM10 during the preconception period was associated with decelerated epigenetic aging, using the Bohlin clock estimate. Prenatal ambient air pollution exposure, particularly in early and mid-pregnancy, was associated with decelerated epigenetic aging at birth.

Dataset Information

Cognitive impacts of ambient air pollution in the National Social Health and Aging Project (NSHAP) cohort.

Publications

Cognitive impacts of ambient air pollution in the National Social Health and Aging Project (NSHAP) cohort.

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