Dataset Information

Association of long-term air pollution with ventricular conduction and repolarization abnormalities.

ABSTRACT: BACKGROUND:Short-term exposure to air pollution may affect ventricular repolarization, but there is limited information on how long-term exposures might affect the surface ventricular electrocardiographic (ECG) abnormalities associated with cardiovascular events. We carried out a study to determine whether long-term air pollution exposure is associated with abnormalities of ventricular repolarization and conduction in adults without known cardiovascular disease. METHODS:A total of 4783 participants free of clinical cardiovascular disease in the Multi-Ethnic Study of Atherosclerosis underwent 12-lead ECG examinations, cardiac-computed tomography, and calcium scoring, as well as estimation of air pollution exposure using a finely resolved spatiotemporal model to determine long-term average individual exposure to fine particulate matter (PM(2.5)) and proximity to major roadways. We assessed ventricular electrical abnormalities including presence of QT prolongation (Rautaharju QTrr criteria) and intraventricular conduction delay (QRS duration >120 milliseconds). We used logistic regression to determine the adjusted relationship between air pollution exposures and ECG abnormalities. RESULTS:A 10-?g/m³ increase in estimated residential PM(2.5) was associated with an increased odds of prevalent QT prolongation (adjusted odds ratio [OR] = 1.6 [95% confidence interval (CI) = 1.2-2.2]) and intraventricular conduction delay (1.7 [1.0-2.6]), independent of coronary-artery calcium score. Living near major roadways was not associated with ventricular electrical abnormalities. No evidence of effect modification by traditional risk factors or study site was observed. CONCLUSIONS:This study demonstrates an association between long-term exposure to air pollution and ventricular repolarization and conduction abnormalities in adults without clinical cardiovascular disease, independent of subclinical coronary arterial calcification.

SUBMITTER: Van Hee VC

PROVIDER: S-EPMC3197855 | biostudies-literature | 2011 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Association of long-term air pollution with ventricular conduction and repolarization abnormalities.

Van Hee Victor C VC Szpiro Adam A AA Prineas Ronald R Neyer Jonathan J Watson Karol K Siscovick David D Kyun Park Sung S Kaufman Joel D JD

Epidemiology (Cambridge, Mass.) 20111101 6

<h4>Background</h4>Short-term exposure to air pollution may affect ventricular repolarization, but there is limited information on how long-term exposures might affect the surface ventricular electrocardiographic (ECG) abnormalities associated with cardiovascular events. We carried out a study to determine whether long-term air pollution exposure is associated with abnormalities of ventricular repolarization and conduction in adults without known cardiovascular disease.<h4>Methods</h4>A total of ...[more]

PMID: 21918454

Similar Datasets

Project description:Importance:Emerging yet contrasting evidence associates air pollution with incident dementia, and the potential role of cardiovascular disease (CVD) in this association is unclear. Objective:To investigate the association between long-term exposure to air pollution and dementia and to assess the role of CVD in that association. Design, Setting, and Participants:Data for this cohort study were extracted from the ongoing Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), a longitudinal population-based study with baseline assessments from March 21, 2001, through August 30, 2004. Of the 5111 randomly selected residents in the Kungsholmen district of Stockholm 60 years or older and living at home or in institutions, 521 were not eligible (eg, due to death before the start of the study or no contact information). Among the remaining 4590 individuals, 3363 (73.3%) were assessed. For the current analysis, 2927 participants who did not have dementia at baseline were examined, with follow-up to 2013 (mean [SD] follow-up time, 6.01?[2.56] years). Follow-up was completed February 18, 2013, and data were analyzed from June 26, 2018, through June 20, 2019. Exposures:Two major air pollutants (particulate matter ?2.5 ?m [PM2.5] and nitrogen oxide [NOx]) were assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. Main Outcomes and Measures:The hazard of dementia was estimated using Cox proportional hazards regression models. The potential of CVD (ie, atrial fibrillation, ischemic heart disease, heart failure, and stroke) to modify and mediate the association between long-term exposure to air pollution and dementia was tested using stratified analyses and generalized structural equation modeling. Results:At baseline, the mean (SD) age of the 2927 participants was 74.1 (10.7) years, and 1845 (63.0%) were female. Three hundred sixty-four participants with incident dementia were identified. The hazard of dementia increased by as much as 50% per interquartile range difference in mean pollutant levels during the previous 5 years at the residential address (hazard ratio [HR] for difference of 0.88 ?g/m3 PM2.5, 1.54 [95% CI, 1.33-1.78]; HR for difference of 8.35 ?g/m3 NOx, 1.14 [95% CI, 1.01-1.29]). Heart failure (HR for PM2.5, 1.93 [95% CI, 1.54-2.43]; HR for NOx, 1.43 [95% CI, 1.17-1.75]) and ischemic heart disease (HR for PM2.5, 1.67 [95% CI, 1.32-2.12]; HR for NOx, 1.36 [95% CI, 1.07-1.71]) enhanced the dementia risk, whereas stroke appeared to be the most important intermediate condition, explaining 49.4% of air pollution-related dementia cases. Conclusions and Relevance:This study found that long-term exposure to air pollution was associated with a higher risk of dementia. Heart failure and ischemic heart disease appeared to enhance the association between air pollution and dementia, whereas stroke seemed to be an important intermediate condition between the association of air pollution exposure with dementia.

Project description:BackgroundBiventricular (BiV) pacing increases transmural repolarization heterogeneity due to epicardial to endocardial conduction from the left ventricular (LV) lead. However, limited evidence is available on concomitant changes in ventricular depolarization and repolarization and long-term outcomes of BiV pacing. Therefore, we investigated associations of BiV pacing-induced concomitant changes in ventricular depolarization and repolarization with mortality (i.e., LV assist device, heart transplantation, or all-cause mortality) and sustained ventricular arrhythmia endpoints.MethodsConsecutive BiV-defibrillator recipients with digital preimplantation and postimplantation electrocardiograms recorded between 2006 and 2015 at Duke University Medical Center were included. We calculated changes in QRS duration and corrected JT (JTc) interval and split them by median values. For simplicity, these variables were named QRSdecreased (≤ -12 ms), QRSincreased (> -12 ms), JTcdecreased (≤22 ms), and JTcincreased (> 22 ms) and subsequently used to construct four mutually exclusive groups.ResultsWe included 528 patients (median age, 68 years; male, 69%). No correlation between changes in QRS duration and JTc interval was observed (P = .295). Compared to QRSdecreased /JTcincreased , increased risk of the composite mortality endpoint was associated with QRSdecreased /JTcdecreased (hazard ratio [HR] = 1.62; 95% confidence interval [CI] = 1.09-2.43), QRSincreased /JTcdecreased (HR = 1.86; 95% CI = 1.27-2.71), and QRSincreased /JTcincreased (HR = 2.25; 95% CI = 1.52-3.35). No QRS/JTc group was associated with excess sustained ventricular arrhythmia risk (P = .400).ConclusionAmong BiV-defibrillator recipients, QRSdecreased /JTcincreased was associated with the most favorable long-term survival free of LV assist device, heart transplantation, and sustained ventricular arrhythmias. Our findings suggest that improved electrical resynchronization may be achieved by assessing concomitant changes in ventricular depolarization and repolarization.

Project description:BackgroundRecent studies suggest that household endotoxin and allergens can modify the impact of air pollutants on development of asthma; however, epidemiological evidence is limited and conflicting.ObjectivesTo investigate whether pet ownership modified the association between ambient air pollution and asthma in children.MethodsWe conducted a population-based cross-sectional study, the Seven Northeast Cities Study in China and recruited a total of 59,754 children from 94 schools during 2012-2013. Long-term air pollutant concentrations, including airborne particulate matter with a diameter of 1 μm or less (PM1 ), PM2.5 , PM10 , and nitrogen dioxide (NO2 ) from 2009 to 2012 were estimated using a random forest model. We collected information of respiratory health in children using the Epidemiologic Standardization Project Questionnaire of the American Thoracic Society (ATS-DLD-78-A). Regression models were used to evaluate associations between pet ownership and air pollution on asthma after adjusting for potential covariates.ResultsExposure to increasing levels of air pollutants was associated with higher prevalence of asthma, but associations were significantly attenuated in children who owned pets. For example, compared to children without pets, those who owned pets did not have an increased risk of symptoms of asthma (odds ratio, 1.01, 95% confidence interval: 0.78, 1.30), wheeze (0.96, 95% confidence interval [CI]: 0.76, 1.21), and cough (1.01, 95% CI: 0.87, 1.18) for each 10 µg/m3 increase in PM1 (P-int < 0.05). Similar trends were observed for other air pollutants. Dog and bird ownership decreased the associations of asthma and cough with air pollutant exposure. The main findings were consistent with a series of sensitivity analyses.ConclusionCurrent pet ownership may reduce the adverse impact of long-term air pollution on childhood asthma. Longitudinal studies are needed to confirm this finding which could have important implications for public health.

Project description:BACKGROUND:Malaysia has the highest rate of diabetes mellitus (DM) in the Southeast Asian region, and has ongoing air pollution and periodic haze exposure. METHODS:Diabetes data were derived from the Malaysian National Health and Morbidity Surveys conducted in 2006, 2011 and 2015. The air pollution data (NOx, NO2, SO2, O3 and PM10) were obtained from the Department of Environment Malaysia. Using multiple logistic and linear regression models, the association between long-term exposure to these pollutants and prevalence of diabetes among Malaysian adults was evaluated. RESULTS:The PM10 concentration decreased from 2006 to 2014, followed by an increase in 2015. Levels of NOx decreased while O3 increased annually. The air pollutant levels based on individual modelled air pollution exposure as measured by the nearest monitoring station were higher than the annual averages of the five pollutants present in the ambient air. The prevalence of overall diabetes increased from 11.4% in 2006 to 21.2% in 2015. The prevalence of known diabetes, underdiagnosed diabetes, overweight and obesity also increased over these years. There were significant positive effect estimates of known diabetes at 1.125 (95% CI, 1.042, 1.213) for PM10, 1.553 (95% CI, 1.328, 1.816) for O3, 1.271 (95% CI, 1.088, 1.486) for SO2, 1.124 (95% CI, 1.048, 1.207) for NO2, and 1.087 (95% CI, 1.024, 1.153) for NOx for NHMS 2006. The adjusted annual average levels of PM10 [1.187 (95% CI, 1.088, 1.294)], O3 [1.701 (95% CI, 1.387, 2.086)], NO2 [1.120 (95% CI, 1.026, 1.222)] and NOx [1.110 (95% CI, 1.028, 1.199)] increased significantly from NHMS 2006 to NHMS 2011 for overall diabetes. This was followed by a significant decreasing trend from NHMS 2011 to 2015 [0.911 for NO2, and 0.910 for NOx]. CONCLUSION:The findings of this study suggest that long-term exposure to O3 is an important associated factor of underdiagnosed DM risk in Malaysia. PM10, NO2 and NOx may have mixed effect estimates towards the risk of DM, and their roles should be further investigated with other interaction models. Policy and intervention measures should be taken to reduce air pollution in Malaysia.

Project description:Significant associations between air pollution (AP) and insulin resistance (IR) have been reported in limited populations or certain patient groups, but few studies have addressed this association in the general population, especially in Asians. Although abdominal fat is a major contributor to IR, previous studies have not fully controlled for its effect in the association between AP and IR. We investigated the association between exposure to AP and IR in Korean adults in the general population and whether this association is maintained even after controlling for the effects of abdominal fat, particularly visceral fat. This was a cross-sectional study. Data were obtained for Korean adults who participated in screening health checkups at Seoul National University Health Examination Center from 2006 to 2014. A total of 4251 men and women aged 22-84 years were included. IR was represented by the homeostasis model assessment of insulin resistance (HOMA-IR). Adiposity traits such as visceral adipose tissue (VAT) and subcutaneous adipose tissue areas were measured by computed tomography. We assessed the annual mean concentrations of air pollutants, including particulate matter with an aerodynamic diameter of 10 µm or less (PM10), nitrogen dioxide, sulfur dioxide, and carbon monoxide. HOMA-IR was significantly associated with increased annual mean exposure to PM10 in both men (β = 0.15; 95% CI 0.09, 0.22) and women (β = 0.16; 95% CI 0.09, 0.23), and these associations were maintained even after controlling for VAT area (both p < 0.05). The adjusted mean HOMA-IR increased gradually with the level of long-term PM10 exposure (low, intermediate, and high exposure) (all p for trend < 0.001) in the subgroup analysis. After adjusting for possible confounding factors, including VAT area, the annual mean exposure to PM10 was significantly associated with the presence of IR in both men (OR 1.18; 95% CI 1.03, 1.35) and women (OR 1.44; 95% CI 1.18, 1.76). Other air pollutants, such as NO2, SO2 and CO, did not show any significant associations with HOMA-IR or the presence of IR. Persistent exposure to PM10 is the main independent risk factor for IR and exhibits a dose-dependent association regardless of visceral fatness in both men and women.

Dataset Information

Association of long-term air pollution with ventricular conduction and repolarization abnormalities.

Publications

Association of long-term air pollution with ventricular conduction and repolarization abnormalities.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets