Dataset Information

Association between African Dust Transport and Acute Exacerbations of COPD in Miami.

ABSTRACT: BACKGROUND:Air pollution is increasingly recognized as a risk factor for acute exacerbation of chronic obstructive pulmonary disease (COPD). Changing climate and weather patterns can modify the levels and types of air pollutants. For example, dust outbreaks increase particulate air pollution. OBJECTIVE:This paper examines the effect of Saharan dust storms on the concentration of coarse particulate matter in Miami, and its association with the risk of acute exacerbation of COPD (AECOPD). METHODS:In this prospective cohort study, 296 COPD patients (with 313 events) were followed between 2013 and 2016. We used Light Detection and Ranging (LIDAR) and satellite-based Aerosol Optical Depth (AOD) to identify dust events and quantify particulate matter (PM) exposure, respectively. Exacerbation events were modeled with respect to location- and time-lagged dust and PM exposures, using multivariate logistic regressions. MEASUREMENTS AND MAIN RESULTS:Dust duration and intensity increased yearly during the study period. During dust events, AOD increased by 51% and particulate matter ?2.5 µm in aerodynamic diameter (PM2.5) increased by 25%. Adjusting for confounders, ambient temperature and local PM2.5 exposure, one-day lagged dust exposure was associated with 4.9 times higher odds of two or more (2+ hereto after) AECOPD events (odds ratio = 4.9; 95% CI = 1.8-13.4; p < 0.001). Ambient temperature exposure also showed a significant association with 2+ and 3+ AECOPD events. The risk of AECOPD lasted up to 15 days after dust exposure, declining from 10× higher on day 0 to 20% higher on day 15. CONCLUSIONS:Saharan dust outbreaks observed in Miami elevate the concentration of PM and increase the risk of AECOPD in COPD patients with recurring exacerbations.

SUBMITTER: Gutierrez MP

PROVIDER: S-EPMC7464868 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Association between African Dust Transport and Acute Exacerbations of COPD in Miami.

Gutierrez Miguel Pardinas MP Zuidema Paquita P Mirsaeidi Mehdi M Campos Michael M Kumar Naresh N

Journal of clinical medicine 20200803 8

<h4>Background</h4>Air pollution is increasingly recognized as a risk factor for acute exacerbation of chronic obstructive pulmonary disease (COPD). Changing climate and weather patterns can modify the levels and types of air pollutants. For example, dust outbreaks increase particulate air pollution.<h4>Objective</h4>This paper examines the effect of Saharan dust storms on the concentration of coarse particulate matter in Miami, and its association with the risk of acute exacerbation of COPD (AE ...[more]

PMID: 32756441

Similar Datasets

Project description:BackgroundThe majority of patients with chronic obstructive pulmonary disease (COPD) suffer from comorbid cardiovascular (CV) disease. Accumulating evidence suggests a temporal association between COPD exacerbations and acute CV events, possibly due to lung hyperinflation, increased hypoxemia and systemic inflammation. The aims of the study were to estimate the risk of (1) acute CV events [acute myocardial infarction (AMI), CV-related death] or stroke in the months following a COPD exacerbation and (2) COPD exacerbation in the months following an acute CV event.MethodsA systematic literature review of observational studies published since 2000 was conducted by searching literature databases (Medline and Embase). Studies were eligible if conducted in adults with COPD, exposed to either COPD exacerbation or acute CV events, with outcomes of acute CV events or COPD exacerbation reported. Studies were appraised for relevance, bias and quality. Meta-analyses, using random-effect models, were performed for each outcome of interest, thus providing a pooled relative risk (RR) and its 95% confidence interval.ResultsEight studies were identified, of which seven were used for the meta-analyses examining the risk of CV events 1-3 months after an exacerbation compared with none. For stroke (six studies), RR was 1.68 (95% CI = 1.19-2.38). For AMI (six studies), RR was 2.43 (95% CI = 1.40-4.20). No studies exploring risk of exacerbation following an acute CV event were identified.ConclusionThis meta-analysis identified a markedly increased risk of stroke or AMI within a relatively short period of time following a COPD exacerbation. Although the underlying mechanisms are not fully elucidated, patients with COPD should be monitored for risk of CV outcomes after exacerbations. In addition, preventing exacerbations may decrease the risk of subsequent acute CV events.RegistrationThe study protocol was published via PROSPERO: International Prospective Register of Systematic Reviews (#CRD42020211055).

Project description:BackgroundExacerbations of chronic obstructive pulmonary disease (COPD) are associated with accelerated loss of lung function and death. Identification of patients at risk for these events, particularly those requiring hospitalization, is of major importance. Severe pulmonary hypertension is an important complication of advanced COPD and predicts acute exacerbations, though pulmonary vascular abnormalities also occur early in the course of the disease. We hypothesized that a computed tomographic (CT) metric of pulmonary vascular disease (pulmonary artery enlargement, as determined by a ratio of the diameter of the pulmonary artery to the diameter of the aorta [PA:A ratio] of >1) would be associated with severe COPD exacerbations.MethodsWe conducted a multicenter, observational trial that enrolled current and former smokers with COPD. We determined the association between a PA:A ratio of more than 1 and a history at enrollment of severe exacerbations requiring hospitalization and then examined the usefulness of the ratio as a predictor of these events in a longitudinal follow-up of this cohort, as well as in an external validation cohort. We used logistic-regression and zero-inflated negative binomial regression analyses and adjusted for known risk factors for exacerbation.ResultsMultivariate logistic-regression analysis showed a significant association between a PA:A ratio of more than 1 and a history of severe exacerbations at the time of enrollment in the trial (odds ratio, 4.78; 95% confidence interval [CI], 3.43 to 6.65; P<0.001). A PA:A ratio of more than 1 was also independently associated with an increased risk of future severe exacerbations in both the trial cohort (odds ratio, 3.44; 95% CI, 2.78 to 4.25; P<0.001) and the external validation cohort (odds ratio, 2.80; 95% CI, 2.11 to 3.71; P<0.001). In both cohorts, among all the variables analyzed, a PA:A ratio of more than 1 had the strongest association with severe exacerbations.ConclusionsPulmonary artery enlargement (a PA:A ratio of >1), as detected by CT, was associated with severe exacerbations of COPD. (Funded by the National Heart, Lung, and Blood Institute; ClinicalTrials.gov numbers, NCT00608764 and NCT00292552.).

Project description:Chronic obstructive pulmonary disease (COPD) is the third-leading cause of death worldwide. Identifying COPD-associated DNA methylation marks in African-Americans may contribute to our understanding of racial disparities in COPD susceptibility. We determined differentially methylated genes and co-methylation network modules associated with COPD in African-Americans recruited during exacerbations of COPD and smoking controls from the Pennsylvania Study of Chronic Obstructive Pulmonary Exacerbations (PA-SCOPE) cohort.We assessed DNA methylation from whole blood samples in 362 African-American smokers in the PA-SCOPE cohort using the Illumina Infinium HumanMethylation27 BeadChip Array. Final analysis included 19302 CpG probes annotated to the nearest gene transcript after quality control. We tested methylation associations with COPD case-control status using mixed linear models. Weighted gene comethylation networks were constructed using weighted gene coexpression network analysis (WGCNA) and network modules were analyzed for association with COPD.There were five differentially methylated CpG probes significantly associated with COPD among African-Americans at an FDR less than 5 %, and seven additional probes that approached significance at an FDR less than 10 %. The top ranked gene association was MAML1, which has been shown to affect NOTCH-dependent angiogenesis in murine lung. Network modeling yielded the "yellow" and "blue" comethylation modules which were significantly associated with COPD (p-value 4?×?10-10 and 4?×?10-9, respectively). The yellow module was enriched for gene sets related to inflammatory pathways known to be relevant to COPD. The blue module contained the top ranked genes in the concurrent differential methylation analysis (FXYD1/LGI4, gene significance p-value 1.2?×?10-26; MAML1, p-value 2.0?×?10-26; CD72, p-value 2.1?×?10-25; and LPO, p-value 7.2?×?10-25), and was significantly associated with lung development processes in Gene Ontology gene-set enrichment analysis.We identified 12 differentially methylated CpG sites associated with COPD that mapped to biologically plausible genes. Network module comethylation patterns have identified candidate genes that may be contributing to racial differences in COPD susceptibility and severity. COPD-associated comethylation modules contained genes previously associated with lung disease and inflammation and recapitulated known COPD-associated genes. The genes implicated by differential methylation and WGCNA analysis may provide mechanistic targets contributing to COPD susceptibility, exacerbations, and outcomes among African-Americans.Trial Registration: NCT00774176 , Registry: ClinicalTrials.gov, URL: www.clinicaltrials.gov , Date of Enrollment of First Participant: June 2004, Date Registered: 04 January 2008 (retrospectively registered).

Project description:BackgroundObservational studies suggest that beta-blockers may reduce the risk of exacerbations and death in patients with moderate or severe chronic obstructive pulmonary disease (COPD), but these findings have not been confirmed in randomized trials.MethodsIn this prospective, randomized trial, we assigned patients between the ages of 40 and 85 years who had COPD to receive either a beta-blocker (extended-release metoprolol) or placebo. All the patients had a clinical history of COPD, along with moderate airflow limitation and an increased risk of exacerbations, as evidenced by a history of exacerbations during the previous year or the prescribed use of supplemental oxygen. We excluded patients who were already taking a beta-blocker or who had an established indication for the use of such drugs. The primary end point was the time until the first exacerbation of COPD during the treatment period, which ranged from 336 to 350 days, depending on the adjusted dose of metoprolol.ResultsA total of 532 patients underwent randomization. The mean (±SD) age of the patients was 65.0±7.8 years; the mean forced expiratory volume in 1 second (FEV1) was 41.1±16.3% of the predicted value. The trial was stopped early because of futility with respect to the primary end point and safety concerns. There was no significant between-group difference in the median time until the first exacerbation, which was 202 days in the metoprolol group and 222 days in the placebo group (hazard ratio for metoprolol vs. placebo, 1.05; 95% confidence interval [CI], 0.84 to 1.32; P = 0.66). Metoprolol was associated with a higher risk of exacerbation leading to hospitalization (hazard ratio, 1.91; 95% CI, 1.29 to 2.83). The frequency of side effects that were possibly related to metoprolol was similar in the two groups, as was the overall rate of nonrespiratory serious adverse events. During the treatment period, there were 11 deaths in the metoprolol group and 5 in the placebo group.ConclusionsAmong patients with moderate or severe COPD who did not have an established indication for beta-blocker use, the time until the first COPD exacerbation was similar in the metoprolol group and the placebo group. Hospitalization for exacerbation was more common among the patients treated with metoprolol. (Funded by the Department of Defense; BLOCK COPD ClinicalTrials.gov number, NCT02587351.).

Dataset Information

Association between African Dust Transport and Acute Exacerbations of COPD in Miami.

Publications

Association between African Dust Transport and Acute Exacerbations of COPD in Miami.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets