A national cohort study (2000-2018) of long-term air pollution exposure and incident dementia in older adults in the United States.
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ABSTRACT:
SUBMITTER: Shi L
PROVIDER: S-EPMC8604909 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Growing evidence suggests that fine particulate matter (PM2.5) likely increases the risks of dementia, yet little is known about the relative contributions of different constituents. Here, we conducted a nationwide population-based cohort study (2000 to 2017) by integrating the Medicare Chronic Conditions Warehouse database and two independently sourced datasets of high-resolution PM2.5 major chemical composition, including black carbon (BC), organic matter (OM), nitrate (NO3-), sulfate (SO42-), ammonium (NH4+), and soil dust (DUST). To investigate the impact of long-term exposure to PM2.5 constituents on incident all-cause dementia and Alzheimer's disease (AD), hazard ratios for dementia and AD were estimated using Cox proportional hazards models, and penalized splines were used to evaluate potential nonlinear concentration-response (C-R) relationships. Results using two exposure datasets consistently indicated higher rates of incident dementia and AD for an increased exposure to PM2.5 and its major constituents. An interquartile range increase in PM2.5 mass was associated with a 6 to 7% increase in dementia incidence and a 9% increase in AD incidence. For different PM2.5 constituents, associations remained significant for BC, OM, SO42-, and NH4+ for both end points (even after adjustments of other constituents), among which BC and SO42- showed the strongest associations. All constituents had largely linear C-R relationships in the low exposure range, but most tailed off at higher exposure concentrations. Our findings suggest that long-term exposure to PM2.5 is significantly associated with higher rates of incident dementia and AD and that SO42-, BC, and OM related to traffic and fossil fuel combustion might drive the observed associations.
| S-EPMC9910468 | biostudies-literature
Project description:We describe spatial patterns in environmental injustice and inequality for residential outdoor nitrogen dioxide (NO2) concentrations in the contiguous United States. Our approach employs Census demographic data and a recently published high-resolution dataset of outdoor NO2 concentrations. Nationally, population-weighted mean NO2 concentrations are 4.6 ppb (38%, p<0.01) higher for nonwhites than for whites. The environmental health implications of that concentration disparity are compelling. For example, we estimate that reducing nonwhites' NO2 concentrations to levels experienced by whites would reduce Ischemic Heart Disease (IHD) mortality by ∼7,000 deaths per year, which is equivalent to 16 million people increasing their physical activity level from inactive (0 hours/week of physical activity) to sufficiently active (>2.5 hours/week of physical activity). Inequality for NO2 concentration is greater than inequality for income (Atkinson Index: 0.11 versus 0.08). Low-income nonwhite young children and elderly people are disproportionately exposed to residential outdoor NO2. Our findings establish a national context for previous work that has documented air pollution environmental injustice and inequality within individual US metropolitan areas and regions. Results given here can aid policy-makers in identifying locations with high environmental injustice and inequality. For example, states with both high injustice and high inequality (top quintile) for outdoor residential NO2 include New York, Michigan, and Wisconsin.
| S-EPMC3988057 | biostudies-literature
Project description:China is the world's largest emitter of anthropogenic air pollutants, and measurable amounts of Chinese pollution are transported via the atmosphere to other countries, including the United States. However, a large fraction of Chinese emissions is due to manufacture of goods for foreign consumption. Here, we analyze the impacts of trade-related Chinese air pollutant emissions on the global atmospheric environment, linking an economic-emission analysis and atmospheric chemical transport modeling. We find that in 2006, 36% of anthropogenic sulfur dioxide, 27% of nitrogen oxides, 22% of carbon monoxide, and 17% of black carbon emitted in China were associated with production of goods for export. For each of these pollutants, about 21% of export-related Chinese emissions were attributed to China-to-US export. Atmospheric modeling shows that transport of the export-related Chinese pollution contributed 3-10% of annual mean surface sulfate concentrations and 0.5-1.5% of ozone over the western United States in 2006. This Chinese pollution also resulted in one extra day or more of noncompliance with the US ozone standard in 2006 over the Los Angeles area and many regions in the eastern United States. On a daily basis, the export-related Chinese pollution contributed, at a maximum, 12-24% of sulfate concentrations over the western United States. As the United States outsourced manufacturing to China, sulfate pollution in 2006 increased in the western United States but decreased in the eastern United States, reflecting the competing effect between enhanced transport of Chinese pollution and reduced US emissions. Our findings are relevant to international efforts to reduce transboundary air pollution.
| S-EPMC3918792 | biostudies-literature
Project description:BackgroundAir pollution may cause inflammatory and oxidative stress damage to the brain, leading to neurodegenerative disease. The association between air pollution and dementia, and modification by apolipoprotein E genotype 4 (APOE-ε4) has yet to be fully investigated.ObjectivesTo examine associations of air pollution with three types of incident dementias (Alzheimer's disease (AD), frontotemporal dementia (FTD), and vascular dementia (VAD)), and their potential modification by APOE-ε4 genotype.MethodsThe UK Biobank enrolled >500,000 participants (2006-2010) with ongoing follow-up. We used annual averages of air pollution (PM2.5, PM10, PM2.5-10, PM2.5absorbance, NO2, NOX) for 2010 scaled to interquartile ranges (IQR). We included individuals aged ≥60 years, with no dementia diagnosis prior to January 1, 2010. Time to incident dementia and follow-up time were reported from baseline (January 01, 2010) to last censor event (death, last hospitalization, or loss to follow-up). Cox proportional hazard ratios (HR) and 95% confidence intervals (95% CI) were calculated to estimate the association of air pollutants and incident dementia, and modification of these associations by APOE-ε4.ResultsOur sample included 187,194 individuals (including N = 680 AD, N = 377 VAD, N = 63 FTD) with a mean follow-up of 7.04 years. We observed consistent associations of PM2.5 with greater risk of all-cause dementia (HR = 1.17, 95% CI: 1.10, 1.24) and AD (HR = 1.17, 95% CI: 1.06, 1.29). NO2 was also associated with greater risk of any incident dementia (HR = 1.18, 95% CI: 1.10, 1.25), AD (HR = 1.15, 95% CI: 1.04, 1.28) and VAD (HR = 1.18, 95% CI: 1.03, 1.35). APOE-ε4 did not modify the association between any air pollutants and dementia.DiscussionPM2.5 and NO2 levels were associated with several types of dementia, and these associations were not modified by APOE-ε4. Findings from the UK Biobank support and extend to other epidemiological evidence for the potential association of air pollutants with detrimental brain health during aging.
| S-EPMC8976829 | biostudies-literature
Project description:BackgroundAmbient air pollution exposure has been associated with dementia. Additionally, epidemiologic evidence supports associations between air pollution and diabetes as well as diabetes and dementia. Thus, an indirect pathway between air pollution and dementia may exist through metabolic dysfunction.ObjectiveTo investigate whether local traffic-related air pollution (TRAP) influences incident dementia and cognitive impairment, non-dementia (CIND) in a cohort of older Mexican Americans. We also assess how much of this estimated effect might be mediated through type 2 diabetes (T2DM).MethodsIn a 10-year, prospective study of Latinos (n = 1,564), we generated TRAP-NOx as a surrogate for pollution from local traffic sources at participants' residences during the year prior to enrollment. We used Cox proportional hazards modeling and mediation analysis to estimate the effects of TRAP-NOx on dementia and/or CIND and indirect pathways operating through T2DM.ResultsHigher TRAP-NOx was associated with incident dementia (HR = 1.55 for the highest versus lower tertiles, 95% CI = 1.04, 2.55). Higher TRAP-NOx was also associated with T2DM (OR = 1.62, 95% CI = 1.27, 2.05); furthermore, T2DM was associated with dementia (HR = 1.94, 95% CI = 1.42, 2.66). Mediation analysis indicated that 20% of the estimated effect of TRAP-NOx on dementia/CIND was mediated through T2DM.ConclusionOur results suggest that exposure to local traffic-related air pollution is associated with incident dementia. We also estimated that 20% of this effect is mediated through T2DM. Thus, ambient air pollution might affect brain health via direct damage as well as through indirect pathways related to diabetes and metabolic dysfunction.
| S-EPMC7591265 | biostudies-literature
Project description:Foodborne outbreaks reported to national surveillance systems represent a subset of all outbreaks in the United States; not all outbreaks are detected, investigated, and reported. We described the structural factors and outbreak characteristics of outbreaks reported during 2009-2018. We categorized states (plus DC) as high (highest quintile), middle (middle 3 quintiles), or low (lowest quintile) reporters on the basis of the number of reported outbreaks per 10 million population. Analysis revealed considerable variation across states in the number and types of foodborne outbreaks reported. High-reporting states reported 4 times more outbreaks than low reporters. Low reporters were more likely than high reporters to report larger outbreaks and less likely to implicate a setting or food vehicle; however, we did not observe a significant difference in the types of food vehicles identified. Per capita funding was strongly associated with increased reporting. Investments in public health programming have a measurable effect on outbreak reporting.
| S-EPMC9155876 | biostudies-literature
Project description:BackgroundDisparities in exposure to air pollution by race-ethnicity and by socioeconomic status have been documented in the United States, but the impacts of declining transportation-related air pollutant emissions on disparities in exposure have not been studied in detail.ObjectiveThis study was designed to estimate changes over time (2000 to 2010) in disparities in exposure to outdoor concentrations of a transportation-related air pollutant, nitrogen dioxide (NO2), in the United States.MethodsWe combined annual average NO2 concentration estimates from a temporal land use regression model with Census demographic data to estimate outdoor exposures by race-ethnicity, socioeconomic characteristics (income, age, education), and by location (region, state, county, urban area) for the contiguous United States in 2000 and 2010.ResultsEstimated annual average NO2 concentrations decreased from 2000 to 2010 for all of the race-ethnicity and socioeconomic status groups, including a decrease from 17.6 ppb to 10.7 ppb (-6.9 ppb) in nonwhite [non-(white alone, non-Hispanic)] populations, and 12.6 ppb to 7.8 ppb (-4.7 ppb) in white (white alone, non-Hispanic) populations. In 2000 and 2010, disparities in NO2 concentrations were larger by race-ethnicity than by income. Although the national nonwhite-white mean NO2 concentration disparity decreased from a difference of 5.0 ppb in 2000 to 2.9 ppb in 2010, estimated mean NO2 concentrations remained 37% higher for nonwhites than whites in 2010 (40% higher in 2000), and nonwhites were 2.5 times more likely than whites to live in a block group with an average NO2 concentration above the WHO annual guideline in 2010 (3.0 times more likely in 2000).ConclusionsFindings suggest that absolute NO2 exposure disparities by race-ethnicity decreased from 2000 to 2010, but relative NO2 exposure disparities persisted, with higher NO2 concentrations for nonwhites than whites in 2010. https://doi.org/10.1289/EHP959.
| S-EPMC5915204 | biostudies-literature
Project description:PURPOSE:To conduct the first epidemiologic study prospectively examining the association between particulate matter air pollution?<?2.5 µm in diameter (PM2.5) exposure and hepatocellular carcinoma (HCC) risk in the U.S. METHODS:Surveillance, Epidemiology, and End Results (SEER) provided information on HCC cases diagnosed between 2000 and 2014 from 16 population-based cancer registries across the U.S. Ambient PM2.5 exposure was estimated by linking the SEER county with a spatial PM2.5 model using a geographic information system. Poisson regression with robust variance estimation was used to calculate incidence rate ratios and 95% confidence intervals (CIs) for the association between ambient PM2.5 exposure per 10 µg/m3 increase and HCC risk adjusting for individual-level age at diagnosis, sex, race, year of diagnosis, SEER registry, and county-level information on health conditions, lifestyle, demographic, socioeconomic, and environmental factors. RESULTS:Higher levels of ambient PM2.5 exposure were associated with a statistically significant increased risk for HCC (n?=?56,245 cases; adjusted IRR per 10 µg/m3 increase?=?1.26, 95% CI 1.08, 1.47; p?<?0.01). CONCLUSIONS:If confirmed in studies with individual-level PM2.5 exposure and risk factor information, these results suggest that ambient PM2.5 exposure may be a risk factor for HCC in the U.S.
| S-EPMC5940508 | biostudies-literature
Project description:ImportancePrior studies on the association between fine particulate matter with diameters 2.5 μm or smaller (PM2.5) and probability of death have not applied multilevel analysis disaggregating data for US census tract, states, and counties, nor tested its interaction by socioeconomic status (SES). Such an approach could provide a more refined identification and targeting of populations exposed to increased risk from PM2.5.ObjectiveTo assess the association between PM2.5 and age-specific mortality risk (ASMR) using disaggregated data at the census tract level and evaluate such association according to census tract SES.Design, setting, and participantsThis nationwide cross-sectional study used a linkage of 3 different data sets. ASMR for the period of 2010 to 2015 was obtained from the National Center for Health Statistic, SES data covering a period from 2006 to 2016 came from the American Community Survey, and mean PM2.5 exposure levels from 2010 to 2015 were derived from well-validated atmospheric chemistry and machine learning models. Data were analyzed in April 2021.ExposuresThe main exploratory variable was mean census tract-level long-term exposure to PM2.5 from 2010 to 2015.Main outcomes and measuresThe primary outcome was census tract-level ASMR. Multilevel models were used to quantify the geographic variation in ASMR at levels of census tract, county, and state. Additional analysis explored the interaction of SES in the association of ASMR with PM2.5 exposure.ResultsData from 67 148 census tracts nested in 3087 counties and 50 states were analyzed. The association between exposure to PM2.5 and ASMR varied substantially across census tracts. The magnitude of such association also varied across age groups, being higher among adults and older adults. Census tracts accounted for most of the total geographic variation in mortality risk (range, 77.0%-94.2%). ASMR was higher in deciles with greater PM2.5 concentration. For example, ASMR for age 75 to 84 years was 54.6 per 1000 population higher in the decile with the second-highest PM2.5 concentration than in the decile with the lowest PM2.5 concentration. The ASMR, PM2.5 concentrations, and magnitude of the association between both were higher in the census tracts with the lowest SES.Conclusions and relevanceThis cross-sectional study found that census tracts with lower SES presented higher PM2.5 concentrations. ASMR and air pollution varied substantially across census tracts. There was an association between air pollution and ASMR across all age groups in the United States. These findings suggest that equitable public policies aimed at improving air quality are needed and important to increase life expectancy.
| S-EPMC9131742 | biostudies-literature
Project description:BACKGROUND:In recent years (2000-2007), ambient levels of fine particulate matter (PM2.5) have continued to decline as a result of interventions, but the decline has been at a slower rate than previous years (1980-2000). Whether these more recent and slower declines of PM2.5 levels continue to improve life expectancy and whether they benefit all populations equally is unknown. METHODS:We assembled a data set for 545 U.S. counties consisting of yearly county-specific average PM2.5, yearly county-specific life expectancy, and several potentially confounding variables measuring socioeconomic status, smoking prevalence, and demographic characteristics for the years 2000 and 2007. We used regression models to estimate the association between reductions in PM2.5 and changes in life expectancy for the period from 2000 to 2007. RESULTS:A decrease of 10 ?g/m in the concentration of PM2.5 was associated with an increase in mean life expectancy of 0.35 years (SD = 0.16 years, P = 0.033). This association was stronger in more urban and densely populated counties. CONCLUSIONS:Reductions in PM2.5 were associated with improvements in life expectancy for the period from 2000 to 2007. Air pollution control in the last decade has continued to have a positive impact on public health.
| S-EPMC3521092 | biostudies-literature