Effects of urban fine particulate matter and ozone on HDL functionality

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Abstract

Background

Exposures to ambient particulate matter (PM) are associated with increased morbidity and mortality. PM _2.5 (<2.5 μm) and ozone exposures have been shown to associate with carotid intima media thickness in humans. Animal studies support a causal relationship between air pollution and atherosclerosis and identified adverse PM effects on HDL functionality.

We aimed to determine whether brief exposures to PM _2.5 and/or ozone could induce effects on HDL anti-oxidant and anti-inflammatory capacity in humans.

Methods

Subjects were exposed to fine concentrated ambient fine particles (CAP) with PM _2.5 targeted at 150 μg/m ³, ozone targeted at 240 μg/m ³ (120 ppb), PM _2.5 plus ozone targeted at similar concentrations, and filtered air (FA) for 2 h, on 4 different occasions, at least two weeks apart, in a randomized, crossover study. Blood was obtained before exposures (baseline), 1 h after and 20 h after exposures. Plasma HDL anti-oxidant/anti-inflammatory capacity and paraoxonase activity were determined. HDL anti-oxidant/anti-inflammatory capacity was assessed by a cell-free fluorescent assay and expressed in units of a HDL oxidant index (HOI). Changes in HOI (ΔHOI) were calculated as the difference in HOI from baseline to 1 h after or 20 h after exposures.

Results

There was a trend towards bigger ΔHOI between PM _2.5 and FA 1 h after exposures ( p = 0.18) but not 20 h after. This trend became significant ( p <0.05) when baseline HOI was lower (<1.5 or <2.0), indicating decreased HDL anti-oxidant/anti-inflammatory capacity shortly after the exposures. There were no significant effects of ozone alone or in combination with PM _2.5 on the change in HOI at both time points. The change in HOI due to PM _2.5 showed a positive trend with particle mass concentration ( p = 0.078) and significantly associated with the slope of systolic blood pressure during exposures ( p = 0.005).

Conclusions

Brief exposures to concentrated PM _2.5 elicited swift effects on HDL anti-oxidant/anti-inflammatory functionality, which could indicate a potential mechanism for how particulate air pollution induces harmful cardiovascular effects.

Electronic supplementary material

The online version of this article (doi:10.1186/s12989-016-0139-3) contains supplementary material, which is available to authorized users.

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Most cited references 47

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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.

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Long-term air pollution exposure and acceleration of atherosclerosis and vascular inflammation in an animal model.

Qinghua Sun, Aixia Wang, Ximei Jin … (2005)

Recent studies have suggested a link between inhaled particulate matter exposure in urban areas and susceptibility to cardiovascular events; however, the precise mechanisms remain to be determined. To test the hypothesis that subchronic exposure to environmentally relevant particulate matter, even at low concentrations, potentiates atherosclerosis and alters vasomotor tone in a susceptible disease model. Between July 21, 2004, and January 12, 2005, 28 apolipoprotein E-/- (apoE-/-) mice were, based on randomized assignments, fed with normal chow or high-fat chow and exposed to concentrated ambient particles of less than 2.5 microm (PM2.5) or filtered air (FA) in Tuxedo, NY, for 6 hours per day, 5 days per week for a total of 6 months. Composite atherosclerotic plaque in the thoracic and abdominal aorta and vasomotor tone changes. In the high-fat chow group, the mean (SD) composite plaque area of PM2.5 vs FA was 41.5% (9.8%) vs 26.2% (8.6%), respectively (P<.001); and in the normal chow group, the composite plaque area was 19.2% (13.1%) vs 13.2% (8.1%), respectively (P = .15). Lipid content in the aortic arch measured by oil red-O staining revealed a 1.5-fold increase in mice fed the high-fat chow and exposed to PM2.5 vs FA (30.0 [8.2] vs 20.0 [7.0]; 95% confidence interval [CI], 1.21-1.83; P = .02). Vasoconstrictor responses to phenylephrine and serotonin challenge in the thoracic aorta of mice fed high-fat chow and exposed to PM2.5 were exaggerated compared with exposure to FA (mean [SE], 134.2% [5.2%] vs 100.9% [2.9%], for phenylephrine, and 156.0% [5.6%] vs 125.1% [7.5%], for serotonin; both P = .03); relaxation to the endothelium-dependent agonist acetylcholine was attenuated (mean [SE] of half-maximal dose for dilation, 8.9 [0.2] x 10(-8) vs 4.3 [0.1] x 10(-8), respectively; P = .04). Mice fed high-fat chow and exposed to PM2.5 demonstrated marked increases in macrophage infiltration, expression of the inducible isoform of nitric oxide synthase, increased generation of reactive oxygen species, and greater immunostaining for the protein nitration product 3-nitrotyrosine (all P<.001). In an apoE-/- mouse model, long-term exposure to low concentration of PM2.5 altered vasomotor tone, induced vascular inflammation, and potentiated atherosclerosis.

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Ambient Air Pollution and Atherosclerosis in Los Angeles

Nino Künzli, Michael Jerrett, Wendy J. Mack … (2004)

Associations have been found between long-term exposure to ambient air pollution and cardiovascular morbidity and mortality. The contribution of air pollution to atherosclerosis that underlies many cardiovascular diseases has not been investigated. Animal data suggest that ambient particulate matter (PM) may contribute to atherogenesis. We used data on 798 participants from two clinical trials to investigate the association between atherosclerosis and long-term exposure to ambient PM up to 2.5 μm in aerodynamic diameter (PM2.5). Baseline data included assessment of the carotid intima-media thickness (CIMT), a measure of subclinical atherosclerosis. We geocoded subjects’ residential areas to assign annual mean concentrations of ambient PM2.5. Exposure values were assigned from a PM2.5 surface derived from a geostatistical model. Individually assigned annual mean PM2.5 concentrations ranged from 5.2 to 26.9 μg/m3 (mean, 20.3). For a cross-sectional exposure contrast of 10 μg/m3 PM2.5, CIMT increased by 5.9% (95% confidence interval, 1–11%). Adjustment for age reduced the coefficients, but further adjustment for covariates indicated robust estimates in the range of 3.9–4.3% (p-values, 0.05–0.1). Among older subjects (≥60 years of age), women, never smokers, and those reporting lipid-lowering treatment at baseline, the associations of PM2.5 and CIMT were larger with the strongest associations in women ≥60 years of age (15.7%, 5.7–26.6%). These results represent the first epidemiologic evidence of an association between atherosclerosis and ambient air pollution. Given the leading role of cardiovascular disease as a cause of death and the large populations exposed to ambient PM2.5, these findings may be important and need further confirmation.

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Author and article information

Contributors

Jesus A. Araujo: (310) 825-3222 , (310) 206-9133 , JAraujo@mednet.ucla.edu

Journal

Journal ID (nlm-ta): Part Fibre Toxicol

Journal ID (iso-abbrev): Part Fibre Toxicol

Title: Particle and Fibre Toxicology

Publisher: BioMed Central (London )

ISSN (Electronic): 1743-8977

Publication date (Electronic): 24 May 2016

Publication date PMC-release: 24 May 2016

Publication date Collection: 2015

Volume: 13

Electronic Location Identifier: 26

Affiliations

[ ]Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, 10833 Le Conte Avenue, CHS 43-264, P.O. Box 951679, Los Angeles, CA 90095 USA

[ ]Department of Environmental Health Sciences, Fielding School of Public Health, University of California, Los Angeles, USA

[ ]Molecular Biology Institute, University of California, Los Angeles, CA USA

[ ]Environment Canada, Toronto, ON Canada

[ ]Southern Ontario Centre for Atmospheric Aerosol Research (SOCAAR), Toronto, ON Canada

[ ]Division of Occupational and Environmental Health, Dalla Lana School of Public Health, University of Toronto, Toronto, ON Canada

[ ]Department of Medicine, Faculty of Medicine, University of Toronto, Toronto, ON Canada

[ ]Li Ka Shing Knowledge Institute, St Michael’s Hospital, Toronto, ON Canada

[ ]Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, MI USA

Article

Publisher ID: 139

DOI: 10.1186/s12989-016-0139-3

PMC ID: 4879751

PubMed ID: 27221567

SO-VID: b7743aa6-3937-4abf-b013-b9311139d214

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 10 October 2015

Date accepted : 10 May 2016

Funding

Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;

Award ID: RO1ES016959

Award Recipient : Jesus A. Araujo

Funded by: FundRef http://dx.doi.org/http://dx.doi.org/10.13039/100000139, U.S. Environmental Protection Agency;

Award ID: CR830837

Funded by: FundRef http://dx.doi.org/http://dx.doi.org/10.13039/501100000023, Government of Canada;

Custom metadata

ScienceOpen disciplines: Toxicology

Keywords: high density lipoprotein (hdl),air pollution,hdl oxidant index (hoi),hdl function,fine particulate matter,cardiovascular,ozone

Data availability:

ScienceOpen disciplines: Toxicology

Keywords: high density lipoprotein (hdl), air pollution, hdl oxidant index (hoi), hdl function, fine particulate matter, cardiovascular, ozone

Effects of urban fine particulate matter and ozone on HDL functionality

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Abstract

Background

Methods

Results

Conclusions

Electronic supplementary material

Related collections

Pneumonia, sex, and the environment

Most cited references 47

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

Long-term air pollution exposure and acceleration of atherosclerosis and vascular inflammation in an animal model.

Ambient Air Pollution and Atherosclerosis in Los Angeles

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