Dataset Information

Neighborhood sociodemographic effects on the associations between long-term PM2.5 exposure and cardiovascular outcomes and diabetes.

ABSTRACT: Introduction:Exposure to PM2.5 air pollution and neighborhood-level sociodemographic characteristics are associated with cardiovascular disease and possibly diabetes. However, the joint effect of sociodemographics and PM2.5 on these outcomes is uncertain. Methods:We examined whether clusters of sociodemographic characteristics modified effects of long-term PM2.5 exposure on coronary artery disease (CAD), myocardial infarction (MI), hypertension, and diabetes. We used medical records data from 2192 cardiac catheterization patients residing in North Carolina and assigned to one of six previously-determined clusters. For each participant, we estimated annual PM2.5 exposure at their primary residence using a hybrid model with a 1 km2 resolution. We used logistic regression models adjusted for age, sex, body mass index, and smoking status, to assess cluster-specific associations with PM2.5 and to determine if there were interactions between cluster and PM2.5 on outcomes. Results:Compared to cluster 3 (OR 0.93, 95% CI 0.82-1.07; urban, low proportion of black individuals and high socioeconomic status), we observed greater associations between PM2.5 and hypertension in clusters 1 (OR 1.22, 95% CI 0.99-1.50, pint 0.03) and 2 (OR 1.64, 95% CI 1.16-2.32, pint 0.003), which were urban, high proportion of black individuals, and low socioeconomic status. PM2.5 was associated with MI (OR 1.29, 95% CI 1.16-1.42) but not diabetes, regardless of cluster and was associated with CAD in cluster 3 (OR 1.15, 95% CI 1.00, 1.31) and overall (OR 1.07, 95% CI 0.98, 1.17). Discussion:Areas of relative disadvantage have a stronger association between PM2.5 and hypertension compared to areas of relative advantage.

SUBMITTER: Weaver AM

PROVIDER: S-EPMC6415293 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Neighborhood sociodemographic effects on the associations between long-term PM<sub>2.5</sub> exposure and cardiovascular outcomes and diabetes.

Weaver Anne M AM McGuinn Laura L Neas Lucas L Mirowsky Jaime J Devlin Robert B RB Dhingra Radhika R Ward-Caviness Cavin C Cascio Wayne E WE Kraus William E WE Hauser Elizabeth R ER Di Qian Q Schwartz Joel J Diaz-Sanchez David D

Environmental epidemiology (Philadelphia, Pa.) 20190201 1

<h4>Introduction</h4>Exposure to PM<sub>2.5</sub> air pollution and neighborhood-level sociodemographic characteristics are associated with cardiovascular disease and possibly diabetes. However, the joint effect of sociodemographics and PM<sub>2.5</sub> on these outcomes is uncertain.<h4>Methods</h4>We examined whether clusters of sociodemographic characteristics modified effects of long-term PM<sub>2.5</sub> exposure on coronary artery disease (CAD), myocardial infarction (MI), hypertension, an ...[more]

PMID: 30882060

Similar Datasets

Project description:BackgroundAir pollution exposures have been shown to adversely impact health through a number of biological pathways associated with glucose metabolism. However, few studies have evaluated the associations between air pollution and glycosylated hemoglobin (HbA1c) levels. Further, no studies have evaluated these associations in US populations or investigated whether associations differ in diabetic as compared to non-diabetic populations. To address this knowledge gap, we investigated the associations between airborne fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and HbA1c levels in both diabetic and non-diabetic older Americans. We also examined the impact of PM2.5 and NO2 on prevalent diabetes mellitus (DM) in this cohort.MethodsWe used multilevel logistic and linear regression models to evaluate the association between long-term average air pollutant levels and prevalence of DM and HbA1c levels, respectively, among 4121 older (57+ years) Americans enrolled in the National Social Life, Health, and Aging Project between 2005 and 2011. All models adjusted for age, sex, body mass index, smoking status, race, household income, education level, neighborhood socioeconomic status, geographic region, urbanicity and diabetic medication use. We estimated participant-specific exposures to PM2.5 on a six-kilometer grid covering the conterminous U.S. using spatio-temporal models, and to NO2 using nearest measurements from the Environmental Protection Agency's Air Quality System. HbA1c levels were measured for participants in each of two data collection waves from dried blood spots and log-transformed prior to analysis. Participants were considered diabetic if they had HbA1c values≥6.5% or reported taking diabetic medication.ResultsThe prevalence of diabetes at study entry was 22.2% (n=916) and the mean HbA1c was 6.0±1.1%. Mean one-year moving average PM2.5 and NO2 exposures were 10.4±3.0μg/m3 and 13.1±7.0 ppb, respectively. An inter-quartile range (IQR, 3.9μg/m3) increase in one-year moving average PM2.5 was positively associated with increased diabetes prevalence (prevalence odds ratio, POR 1.35, 95% CI: 1.19, 1.53). Similarly, an IQR (8.6 ppb) increase in NO2 was also significantly associated with diabetes prevalence (POR 1.27, 95% CI: 1.10, 1.48). PM2.5 (1.8%±0.6%, p<0.01) and NO2 (2.0%±0.7%, p<0.01) exposures were associated with higher HbA1c levels in diabetic participants, while only NO2 was significantly associated with HbA1c in non-diabetic participants (0.8%±0.2%, p<0.01). Significant dose response relationships were identified for both pollutants in diabetic participants and for NO2 in non-diabetic participants.Conclusions/interpretationsIn a cohort of older men and women in the United States, PM2.5 and NO2 exposures were significantly associated with prevalence of DM and increased HbA1c levels among both non-diabetic and diabetic participants. These associations suggest that air pollution could be a key risk factor for abnormal glucose metabolism and diabetes in the elderly.

Project description:Background & aimsExisting evidence suggests that long-term exposure to ambient fine particulate pollution (PM2.5) may increase metabolic dysfunction-associated fatty liver disease (MAFLD) risk. However, there is still limited evidence on the association of PM2.5 constituents with MAFLD. Therefore, this study explores the associations between the five main chemical constituents of PM2.5 and MAFLD to provide more explicit information on the liver exposome.MethodsA total of 76,727 participants derived from the China Multi-Ethnic Cohort, a large-scale epidemic survey in southwest China, were included in this study. Multiple linear regression models were used to estimate the pollutant-specific association with MAFLD. Weighted quantile sum regression was used to evaluate the joint effect of the pollutant-mixture on MAFLD and identify which constituents contribute most to it.ResultsThree-year exposure to PM2.5 constituents was associated with a higher MAFLD risk and more severe liver fibrosis. Odds ratios for MAFLD were 1.480, 1.426, 1.294, 1.561, 1.618, and 1.368 per standard deviation increase in PM2.5, black carbon, organic matter, ammonium, sulfate, and nitrate, respectively. Joint exposure to the five major chemical constituents was also positively associated with MAFLD (odds ratio 1.490, 95% CI 1.360-1.632). Nitrate contributed most to the joint effect of the pollutant-mixture. Further stratified analyses indicate that males, current smokers, and individuals with a high-fat diet might be more susceptible to ambient PM2.5 exposure than others.ConclusionsLong-term exposure to PM2.5 and its five major chemical constituents may increase the risk of MAFLD. Nitrate might contribute most to MAFLD, which may provide new clues for liver health. Males, current smokers, and participants with high-fat diets were more susceptible to these associations.Impact and implicationsThis large-scale epidemiologic study explored the associations between constituents of fine particulate pollution (PM2.5) and metabolic dysfunction-associated fatty liver disease (MAFLD), and further revealed which constituents play a more important role in increasing the risk of MAFLD. In contrast to previous studies that examined the effects of PM2.5 as a whole substance, this study carefully explored the health effects of the individual constituents of PM2.5. These findings could (1) help researchers to identify the specific particles responsible for hepatotoxicity, and (2) indicate possible directions for policymakers to efficiently control ambient air pollution, such as targeting the sources of nitrate pollution.

Project description:Background & aimNumerous studies have linked air pollution with cardiovascular diseases. Fewer studies examined the associations at low concentration levels or assessed potential modifiers. Some investigations only examined hospitalizations, which can miss incident cases. This study aims to address these gaps through a nationwide cohort study of Medicare enrollees.MethodsOur study cohort comprise all Medicare enrollees (≥65 years old) continuously enrolled in the fee-for-service program and both Medicare part A and B across the contiguous U.S. from 2000 to 2016. We examined the associations of population-weighted ZIP code-level annual average PM2.5, NO2, and warm-season O3 (May-October), with the first diagnoses of atrial fibrillation (AF), congestive heart failure (CHF), and stroke. We fit multi-pollutant Cox proportional hazards models adjusted for individual demographic characteristics and area-level covariates. We further examined these associations at low pollutant concentration levels and the potential effect modifications by race/ethnicity and comorbidities (diabetes, hypertension, hyperlipidemia).ResultsElevated PM2.5 and NO2 levels were associated with increased incidence of AF, CHF, and stroke. For each 1 μg/m3 increase in annual PM2.5, hazard ratios (HRs) were 1.0059 (95%CI: 1.0054-1.0064), 1.0260 (95%CI: 1.0256-1.0264), and 1.0279 (95%CI: 1.0274-1.0284), respectively. For each1 ppb increase in annual NO2, HRs are 1.0057 (95%CI: 1.0056-1.0059), 1.0112 (95%CI: 1.0110-1.0113), and 1.0095 (95%CI: 1.0093-1.0096), respectively. For warm-season O3, each 1 ppb increase was associated with increased incidence of CHF (HR=1.0035, 95%CI: 1.0033-1.0037) and stroke (HR=1.0026, 95%CI: 1.0023-1.0028). Larger magnitudes of HRs were observed when restricted to pollutants levels lower than NAAQS standards. Generally higher risks were observed for Black people and diabetics.ConclusionsLong-term exposure to PM2.5, NO2, and warm-season O3 were associated with increased incidence of cardiovascular diseases, even at low pollutant concentration levels. Black people and people with diabetes were found to be vulnerable populations.

Project description:BackgroundSeveral epidemiological studies have reported that long-term exposure to fine particulate matter (PM2.5) is associated with higher mortality. Evidence regarding contributions of PM2.5 constituents is inconclusive.ObjectivesWe assembled a data set of 12.5 million Medicare enrollees (≥ 65 years of age) to determine which PM2.5 constituents are a) associated with mortality controlling for previous-year PM2.5 total mass (main effect); and b) elevated in locations exhibiting stronger associations between previous-year PM2.5 and mortality (effect modification).MethodsFor 518 PM2.5 monitoring locations (eastern United States, 2000-2006), we calculated monthly mortality rates, monthly long-term (previous 1-year average) PM2.5, and 7-year averages (2000-2006) of major PM2.5 constituents [elemental carbon (EC), organic carbon matter (OCM), sulfate (SO42-), silicon (Si), nitrate (NO3-), and sodium (Na)] and community-level variables. We applied a Bayesian hierarchical model to estimate location-specific mortality rates associated with previous-year PM2.5 (model level 1) and identify constituents that contributed to the spatial variability of mortality, and constituents that modified associations between previous-year PM2.5 and mortality (model level 2), controlling for community-level confounders.ResultsOne-standard deviation (SD) increases in 7-year average EC, Si, and NO3- concentrations were associated with 1.3% [95% posterior interval (PI): 0.3, 2.2], 1.4% (95% PI: 0.6, 2.4), and 1.2% (95% PI: 0.4, 2.1) increases in monthly mortality, controlling for previous-year PM2.5. Associations between previous-year PM2.5 and mortality were stronger in combination with 1-SD increases in SO42- and Na.ConclusionsLong-term exposures to PM2.5 and several constituents were associated with mortality in the elderly population of the eastern United States. Moreover, some constituents increased the association between long-term exposure to PM2.5 and mortality. These results provide new evidence that chemical composition can partly explain the differential toxicity of PM2.5.

Dataset Information

Neighborhood sociodemographic effects on the associations between long-term PM2.5 exposure and cardiovascular outcomes and diabetes.

Publications

Neighborhood sociodemographic effects on the associations between long-term PM<sub>2.5</sub> exposure and cardiovascular outcomes and diabetes.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets