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Association between satellite-based estimates of long-term PM2.5 exposure and coronary artery disease.

ABSTRACT: BACKGROUND:Epidemiological studies have identified associations between long-term PM2.5 exposure and cardiovascular events, though most have relied on concentrations from central-site air quality monitors. METHODS:We utilized a cohort of 5679 patients who had undergone cardiac catheterization at Duke University between 2002-2009 and resided in North Carolina. We used estimates of daily PM2.5 concentrations for North Carolina during the study period based on satellite derived Aerosol Optical Depth (AOD) measurements and PM2.5 concentrations from ground monitors, which were spatially resolved with a 10×10km resolution, matched to each patient's residential address and averaged for the year prior to catheterization. The Coronary Artery Disease (CAD) index was used to measure severity of CAD; scores >23 represent a hemodynamically significant coronary artery lesion in at least one major coronary vessel. Logistic regression modeled odds of having CAD or an MI with each 1?g/m(3) increase in annual average PM2.5, adjusting for sex, race, smoking status and socioeconomic status. RESULTS:In adjusted models, a 1?g/m(3) increase in annual average PM2.5 was associated with an 11.1% relative increase in the odds of significant CAD (95% CI: 4.0-18.6%) and a 14.2% increase in the odds of having a myocardial infarction (MI) within a year prior (95% CI: 3.7-25.8%). CONCLUSIONS:Satellite-based estimates of long-term PM2.5 exposure were associated with both coronary artery disease (CAD) and incidence of myocardial infarction (MI) in a cohort of cardiac catheterization patients.

SUBMITTER: McGuinn LA

PROVIDER: S-EPMC4706491 | biostudies-literature | 2016 Feb

REPOSITORIES: biostudies-literature

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Association between satellite-based estimates of long-term PM2.5 exposure and coronary artery disease.

McGuinn Laura A LA Ward-Caviness Cavin K CK Neas Lucas M LM Schneider Alexandra A Diaz-Sanchez David D Cascio Wayne E WE Kraus William E WE Hauser Elizabeth E Dowdy Elaine E Haynes Carol C Chudnovsky Alexandra A Koutrakis Petros P Devlin Robert B RB

Environmental research 20151121

<h4>Background</h4>Epidemiological studies have identified associations between long-term PM2.5 exposure and cardiovascular events, though most have relied on concentrations from central-site air quality monitors.<h4>Methods</h4>We utilized a cohort of 5679 patients who had undergone cardiac catheterization at Duke University between 2002-2009 and resided in North Carolina. We used estimates of daily PM2.5 concentrations for North Carolina during the study period based on satellite derived Aeros ...[more]

PMID: 26613345

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Project description:BackgroundExposure measurement error is a central concern in air pollution epidemiology. Given that studies have been using ambient air pollution predictions as proxy exposure measures, the potential impact of exposure error on health effect estimates needs to be comprehensively assessed.ObjectivesWe aimed to generate wide-ranging scenarios to assess direction and magnitude of bias caused by exposure errors under plausible concentration-response relationships between annual exposure to fine particulate matter [PM ≤2.5μm in aerodynamic diameter (PM2.5)] and all-cause mortality.MethodsIn this simulation study, we use daily PM2.5 predictions at 1-km2 spatial resolution to estimate annual PM2.5 exposures and their uncertainties for ZIP Codes of residence across the contiguous United States between 2000 and 2016. We consider scenarios in which we vary the error type (classical or Berkson) and the true concentration-response relationship between PM2.5 exposure and mortality (linear, quadratic, or soft-threshold-i.e., a smooth approximation to the hard-threshold model). In each scenario, we generate numbers of deaths using error-free exposures and confounders of concurrent air pollutants and neighborhood-level covariates and perform epidemiological analyses using error-prone exposures under correct specification or misspecification of the concentration-response relationship between PM2.5 exposure and mortality, adjusting for the confounders.ResultsWe simulate 1,000 replicates of each of 162 scenarios investigated. In general, both classical and Berkson errors can bias the concentration-response curve toward the null. The biases remain small even when using three times the predicted uncertainty to generate errors and are relatively larger at higher exposure levels.DiscussionOur findings suggest that the causal determination for long-term PM2.5 exposure and mortality is unlikely to be undermined when using high-resolution ambient predictions given that the estimated effect is generally smaller than the truth. The small magnitude of bias suggests that epidemiological findings are relatively robust against the exposure error. In practice, the use of ambient predictions with a finer spatial resolution will result in smaller bias. https://doi.org/10.1289/EHP10389.

Project description:ImportanceThe level of coronary artery calcium (CAC) can effectively stratify cardiovascular risk in middle-aged and older adults, but its utility for young adults is unclear.ObjectivesTo determine the prevalence of CAC in adults aged 30 to 49 years and the subsequent association of CAC with coronary heart disease (CHD), cardiovascular disease (CVD), and all-cause mortality.Design, setting, and participantsA multicenter retrospective cohort study was conducted among 22 346 individuals from the CAC Consortium who underwent CAC testing (baseline examination, 1991-2010, with follow-up through June 30, 2014; CAC quantified using nonconrast, cardiac-gated computed tomography scans) for clinical indications and were followed up for cause-specific mortality. Participants were free of clinical CVD at baseline. Statistical analysis was performed from June 1, 2017, to May 31, 2018.Main outcomes and measuresThe prevalence of CAC and the subsequent rates of CHD, CVD, and all-cause mortality. Competing risks regression modeling was used to calculate multivariable-adjusted subdistribution hazard ratios for CHD and CVD mortality.ResultsThe sample of 22 346 participants (25.0% women and 75.0% men; mean [SD] age, 43.5 [4.5] years) had a high prevalence of hyperlipidemia (49.6%) and family history of CHD (49.3%) but a low prevalence of current smoking (11.0%) and diabetes (3.9%). The prevalence of any CAC was 34.4%, with 7.2% having a CAC score of more than 100. During follow-up (mean [SD], 12.7 [4.0] years), there were 40 deaths related to CHD, 84 deaths related to CVD, and 298 total deaths. A total of 27 deaths related to CHD (67.5%) occurred among individuals with CAC at baseline. The CHD mortality rate per 1000 person-years was 10-fold higher among those with a CAC score of more than 100 (0.69; 95% CI, 0.41-1.16) compared with those with a CAC score of 0 (0.07; 95% CI, 0.04-0.12). After multivariable adjustment, those with a CAC score of more than 100 had a significantly increased risk of CHD (subdistribution hazard ratio, 5.6; 95% CI, 2.5-12.7), CVD (subdistribution hazard ratio, 3.3; 95% CI, 1.8-6.2), and all-cause mortality (hazard ratio, 2.6; 95% CI, 1.9-3.6) compared with those with a CAC score of 0.Conclusions and relevanceIn a large sample of young adults undergoing CAC testing for clinical indications, 34.4% had CAC, and those with elevated CAC scores had significantly higher rates of CHD and CVD mortality. Coronary artery calcium may have potential utility for clinical decision-making among select young adults at elevated risk of cardiovascular disease.

Project description:Background Epidemiological studies demonstrating a relationship between gout and cardiovascular disease are older and predate modern cardiovascular preventive therapy. We assessed the contemporary association between gout and cardiovascular disease in patients with obstructive coronary artery disease. Methods and Results Data were from the Duke Databank for Cardiovascular Diseases, which followed up patients undergoing cardiac catheterization with obstructive coronary artery disease at Duke University Medical Center (1998-2013). We assessed the relationship between gout diagnosis at baseline or during follow-up and the primary composite outcome of cardiovascular death, myocardial infarction, or stroke, adjusting for differences in baseline clinical factors. Secondary end points included cardiovascular death and all-cause mortality. New, postbaseline, gout diagnosis was included as a time-dependent covariate. Among 17 201 patients, 1406 (8.2%) had baseline gout and a high burden of cardiovascular risk factors, but high rates of optimal medical therapy. Over a median follow-up of 6.4 years, gout diagnosis at time of catheterization was not associated with the primary outcome (hazard ratio [95% confidence interval], 1.05 [0.96-1.15]; P=0.31) or cardiovascular death (hazard ratio [95% confidence interval], 1.10 [0.99-1.22]; P=0.08), but was associated with increased all-cause mortality (hazard ratio [95% confidence interval], 1.13 [1.05-1.23]; P=0.002). After including new, postbaseline, gout diagnosis, the instantaneous risk of the primary outcome was significantly associated with prior gout diagnosis (hazard ratio [95% confidence interval], 1.15 [1.07-1.25]; P=0.0004). Conclusions A clinical history of gout is associated with worse outcomes in a contemporary population of patients with obstructive coronary artery disease. This increased risk exists despite high levels of optimal baseline cardiovascular disease medical therapy, suggesting that residual cardiovascular risk is not addressed by standard medical therapy.

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.

Dataset Information

Association between satellite-based estimates of long-term PM2.5 exposure and coronary artery disease.

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Association between satellite-based estimates of long-term PM2.5 exposure and coronary artery disease.

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