Association of Exposure to Particular Matter and Carotid Intima-Media Thickness: A Systematic Review and Meta-Analysis

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Background: Long time exposure to particular matter has been linked to myocardial infarction, stroke and blood pressure, but its association with atherosclerosis is not clear. This meta-analysis was aimed at assessing whether PM _2.5 and PM ₁₀ have an effect on subclinical atherosclerosis measured by carotid intima-media thickness (CIMT). Methods: Pubmed, Ovid Medline, Embase and NICK between 1948 and 31 March 2015 were searched by combining the keywords about exposure to the outcome related words. The random-effects model was applied in computing the change of CIMT and their corresponding 95% confidence interval (95% CI). The effect of potential confounding factors was assessed by stratified analysis and the impact of traffic proximity was also estimated. Results: Among 56 identified studies, 11 articles satisfied the inclusion criteria. In overall analysis increments of 10 μg/m ³ in PM _2.5 and PM ₁₀ were associated with an increase of CIMT (16.79 μm; 95% CI, 4.95–28.63 μm and 4.13 μm; 95% CI, −5.79–14.04 μm, respectively). Results shown in subgroup analysis had reference value for comparing with those of the overall analysis. The impact of traffic proximity on CIMT was uncertain. Conclusions: Exposure to PM _2.5 had a significant association with CIMT and for women the effect may be more obvious.

Related collections

Most cited references 51

Record: found
Abstract: found
Article: not found

Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

C. Pope, Richard Burnett, George Thurston … (2004)

Epidemiologic studies have linked long-term exposure to fine particulate matter air pollution (PM) to broad cause-of-death mortality. Associations with specific cardiopulmonary diseases might be useful in exploring potential mechanistic pathways linking exposure and mortality. General pathophysiological pathways linking long-term PM exposure with mortality and expected patterns of PM mortality with specific causes of death were proposed a priori. Vital status, risk factor, and cause-of-death data, collected by the American Cancer Society as part of the Cancer Prevention II study, were linked with air pollution data from United States metropolitan areas. Cox Proportional Hazard regression models were used to estimate PM-mortality associations with specific causes of death. Long-term PM exposures were most strongly associated with mortality attributable to ischemic heart disease, dysrhythmias, heart failure, and cardiac arrest. For these cardiovascular causes of death, a 10-microg/m3 elevation in fine PM was associated with 8% to 18% increases in mortality risk, with comparable or larger risks being observed for smokers relative to nonsmokers. Mortality attributable to respiratory disease had relatively weak associations. Fine particulate air pollution is a risk factor for cause-specific cardiovascular disease mortality via mechanisms that likely include pulmonary and systemic inflammation, accelerated atherosclerosis, and altered cardiac autonomic function. Although smoking is a much larger risk factor for cardiovascular disease mortality, exposure to fine PM imposes additional effects that seem to be at least additive to if not synergistic with smoking.

0 comments Cited 584 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Pathophysiology of coronary artery disease.

Peter Libby, Pierre Théroux (2005)

During the past decade, our understanding of the pathophysiology of coronary artery disease (CAD) has undergone a remarkable evolution. We review here how these advances have altered our concepts of and clinical approaches to both the chronic and acute phases of CAD. Previously considered a cholesterol storage disease, we currently view atherosclerosis as an inflammatory disorder. The appreciation of arterial remodeling (compensatory enlargement) has expanded attention beyond stenoses evident by angiography to encompass the biology of nonstenotic plaques. Revascularization effectively relieves ischemia, but we now recognize the need to attend to nonobstructive lesions as well. Aggressive management of modifiable risk factors reduces cardiovascular events and should accompany appropriate revascularization. We now recognize that disruption of plaques that may not produce critical stenoses causes many acute coronary syndromes (ACS). The disrupted plaque represents a "solid-state" stimulus to thrombosis. Alterations in circulating prothrombotic or antifibrinolytic mediators in the "fluid phase" of the blood can also predispose toward ACS. Recent results have established the multiplicity of "high-risk" plaques and the widespread nature of inflammation in patients prone to develop ACS. These findings challenge our traditional view of coronary atherosclerosis as a segmental or localized disease. Thus, treatment of ACS should involve 2 overlapping phases: first, addressing the culprit lesion, and second, aiming at rapid "stabilization" of other plaques that may produce recurrent events. The concept of "interventional cardiology" must expand beyond mechanical revascularization to embrace preventive interventions that forestall future events.

0 comments Cited 365 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Association of coronary heart disease incidence with carotid arterial wall thickness and major risk factors: the Atherosclerosis Risk in Communities (ARIC) Study, 1987-1993.

L E Chambless, G Heiss, A Folsom … (1997)

Few studies have determined whether greater carotid artery intima-media thickness (IMT) in asymptomatic individuals is associated prospectively with increased risk of coronary heart disease (CHD). In the Atherosclerosis Risk in Communities Study, carotid IMT, an index of generalized atherosclerosis, was defined as the mean of IMT measurements at six sites of the carotid arteries using B-mode ultrasound. The authors assessed its relation to CHD incidence over 4-7 years of follow-up (1987-1993) in four US communities (Forsyth County, North Carolina; Jackson, Mississippi; Minneapolis, Minnesota; and Washington County, Maryland) from samples of 7,289 women and 5,552 men aged 45-64 years who were free of clinical CHD at baseline. There were 96 incident events for women and 194 for men. In sex-specific Cox proportional hazards models adjusted only for age, race, and center, the hazard rate ratio comparing extreme mean IMT (> or = 1 mm) to not extreme (< 1 mm) was 5.07 for women (95% confidence interval 3.08-8.36) and 1.85 for men (95% confidence interval 1.28-2.69). The relation was graded (monotonic), and models with cubic splines indicated significant nonlinearity. The strength of the association was reduced by including major CHD risk factors, but remained elevated at higher IMT. Up to 1 mm mean IMT, women had lower adjusted annual event rates than did men, but above 1 mm their event rate was closer to that of men. Thus, mean carotid IMT is a noninvasive predictor of future CHD incidence.

0 comments Cited 328 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Paul B. Tchounwou: Role: Academic Editor

Journal

Journal ID (nlm-ta): Int J Environ Res Public Health

Journal ID (iso-abbrev): Int J Environ Res Public Health

Journal ID (publisher-id): ijerph

Title: International Journal of Environmental Research and Public Health

Publisher: MDPI

ISSN (Print): 1661-7827

ISSN (Electronic): 1660-4601

Publication date (Electronic): 15 October 2015

Publication date (Print): October 2015

Volume: 12

Issue: 10

Pages: 12924-12940

Affiliations

[1 ]Department of Cardiology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100730, China; E-Mails: lxlryyc@ 123456sina.com (X.L.); lianhui1988@ 123456163.com (H.L.); yanping.ruan@ 123456163.com (Y.R.); 18911122174@ 123456163.com (R.L.); zhaoxy0909@ 123456sina.com (X.Z.)

[2 ]Leeds Institute of Cardiovascular & Metabolic Medicine, University of Leeds, Leeds LS2 9JT, UK; E-Mail: medmnr@ 123456leeds.ac.uk

Author notes

[* ]Author to whom correspondence should be addressed; E-Mail: Fan@ 123456pumch.cn ; Tel.: +86-10-6915-5066; Fax: +86-10-6915-5068.

Article

Publisher ID: ijerph-12-12924

DOI: 10.3390/ijerph121012924

PMC ID: 4627008

PubMed ID: 26501300

SO-VID: a7290a47-682d-4e56-a490-0a8d75d64198

License:

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

Association of Exposure to Particular Matter and Carotid Intima-Media Thickness: A Systematic Review and Meta-Analysis

Read this article at

Abstract

Related collections

Global Health Next Generation Network

Most cited references 51

Cardiovascular mortality and long-term exposure to particulate air pollution: epidemiological evidence of general pathophysiological pathways of disease.

Pathophysiology of coronary artery disease.

Association of coronary heart disease incidence with carotid arterial wall thickness and major risk factors: the Atherosclerosis Risk in Communities (ARIC) Study, 1987-1993.

Author and article information

Contributors

Journal

Affiliations

Author notes

Article

History

Categories

Comments

Comment on this article

Similar content 393

Cited by 10

Most referenced authors 1,750