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Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress.

ABSTRACT: Air pollution is associated with significant adverse health effects, including increased cardiovascular morbidity and mortality. Exposure to particulate matter with an aerodynamic diameter of <2.5 microm (PM(2.5)) increases ischemic cardiovascular events and promotes atherosclerosis. Moreover, there is increasing evidence that the smallest pollutant particles pose the greatest danger because of their high content of organic chemicals and prooxidative potential. To test this hypothesis, we compared the proatherogenic effects of ambient particles of <0.18 microm (ultrafine particles) with particles of <2.5 microm in genetically susceptible (apolipoprotein E-deficient) mice. These animals were exposed to concentrated ultrafine particles, concentrated particles of <2.5 microm, or filtered air in a mobile animal facility close to a Los Angeles freeway. Ultrafine particle-exposed mice exhibited significantly larger early atherosclerotic lesions than mice exposed to PM(2.5) or filtered air. Exposure to ultrafine particles also resulted in an inhibition of the antiinflammatory capacity of plasma high-density lipoprotein and greater systemic oxidative stress as evidenced by a significant increase in hepatic malondialdehyde levels and upregulation of Nrf2-regulated antioxidant genes. We conclude that ultrafine particles concentrate the proatherogenic effects of ambient PM and may constitute a significant cardiovascular risk factor.

SUBMITTER: Araujo JA

PROVIDER: S-EPMC3014059 | biostudies-literature | 2008 Mar

REPOSITORIES: biostudies-literature

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Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress.

Araujo Jesus A JA Barajas Berenice B Kleinman Michael M Wang Xuping X Bennett Brian J BJ Gong Ke Wei KW Navab Mohamad M Harkema Jack J Sioutas Constantinos C Lusis Aldons J AJ Nel Andre E AE

Circulation research 20080117 5

Air pollution is associated with significant adverse health effects, including increased cardiovascular morbidity and mortality. Exposure to particulate matter with an aerodynamic diameter of <2.5 microm (PM(2.5)) increases ischemic cardiovascular events and promotes atherosclerosis. Moreover, there is increasing evidence that the smallest pollutant particles pose the greatest danger because of their high content of organic chemicals and prooxidative potential. To test this hypothesis, we compar ...[more]

PMID: 18202315

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Project description:BackgroundIncreased particulate air pollution has been associated with both an increased risk of myocardial infarction (MI) and adverse changes in cardiac biomarkers. Up to 30% of ambient wintertime fine particles (PM2.5) in Rochester, NY are from wood burning. Our study examined associations between ambient levels of a marker of wood smoke (Delta-C) and other particulate air pollutants and biomarkers of inflammation, coagulation and thrombosis.MethodsWe measured blood concentrations of C-reactive protein (CRP), D-dimer, fibrinogen, P-selectin, platelet factor 4 (PF-4), von Willebrand factor (vWF), and myeloperoxidase (MPO) of 135 patients undergoing cardiac catheterization during the winters of 2011-2013. We coupled these data with hourly ambient concentrations of Delta-C, black carbon (BC; marker of traffic pollution), and ultrafine (10-100nm; UFP), accumulation mode (100-500nm; AMP), and fine particles (<2.5µm; PM2.5). Using linear regression models, we estimated the change in each biomarker associated with increased pollutant concentrations at intervals between 1 and 96h preceding blood collection.ResultsEach 0.13µg/m3 increase in Delta-C concentration in the prior 12h was associated with a 0.91% increase in fibrinogen levels (95% CI=0.23%, 1.59%), but unexpectedly in the prior 48h, each 0.17µg/m3 increase in Delta-C concentration was associated with a 2.75% decrease in MPO levels (95% CI=-5.13%,-0.37%). We did not see associations between Delta-C concentrations and any other biomarkers. Interquartile range (IQR) increases in PM2.5, BC, UFP, and AMP concentrations were generally associated with increased CRP and fibrinogen, but not PF4, D-dimer, vWF, or P-selectin.ConclusionsIn a population of cardiac patients, we noted adverse changes in fibrinogen associated with increased concentrations of a marker of wood smoke. Increases in PM2.5, BC, AMP, and UFP concentrations in the previous 96h were also associated with adverse changes in markers of systemic inflammation and coagulation, but not with markers of endothelial cell dysfunction or platelet activation.

Project description:BACKGROUND:A growing body of epidemiological literature indicates that particulate matter (PM) air pollution exposure is associated with elevated Alzheimer's disease (AD) risk and may exacerbate AD-related cognitive decline. Of concern is exposure to the ultrafine PM (UFP) fraction (?100?nm), which deposits efficiently throughout the respiratory tract, has higher rates of translocation to secondary organs, like brain, and may induce inflammatory changes. We, therefore, hypothesize that exposure to UFPs will exacerbate cognitive deficits in a mouse model of AD. The present study assessed alterations in learning and memory behaviors in aged (12.5?months) male 3xTgAD and non-transgenic mice following a 2-week exposure (4-h/day, 4?days/week) to concentrated ambient UFPs using the Harvard ultrafine concentrated ambient particle system (HUCAPS) or filtered air. Beginning one month following exposure, locomotor activity, spatial learning and memory, short-term recognition memory, appetitive motivation, and olfactory discrimination were assessed. RESULTS:No effects on locomotor activity were found following HUCAPS exposure (number concentration, 1?×?104-4.7?×?105 particles/cm3; mass concentration, 29-132??g/m3). HUCAPS-exposed mice, independent of AD background, showed a significantly decreased spatial learning, mediated through reference memory deficits, as well as short-term memory deficits in novel object recognition testing. AD mice displayed diminished spatial working memory, potentially a result of olfactory deficits, and short-term memory. AD background modulated HUCAPS-induced changes on appetitive motivation and olfactory discrimination, specifically enhancing olfactory discrimination in NTg mice. Modeling variation in appetitive motivation as a covariate in spatial learning and memory, however, did not support the conclusion that differences in motivation significantly underlie changes in spatial learning and memory. CONCLUSIONS:A short-term inhalation exposure of aged mice to ambient UFPs at human-relevant concentrations resulted in protracted (testing spanning 1-6.5?months post-exposure) adverse effects on multiple memory domains (reference and short-term memory) independent of AD background. Impairments in learning and memory were present when accounting for potential covariates like motivational changes and locomotor activity. These results highlight the need for further research into the potential mechanisms underlying the cognitive effects of UFP exposure in adulthood.

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Project description:BACKGROUND: Studies have shown a relationship between air pollution and increased risk of cardiovascular morbidity and mortality. Due to the complexity of ambient air pollution composition, recent studies have examined the effects of co-exposure, particularly particulate matter (PM) and gas, to determine whether pollutant interactions alter (e.g. synergistically, antagonistically) the health response. This study examines the independent effects of fine (FCAPs) and ultrafine (UFCAPs) concentrated ambient particles on cardiac function, and determine the impact of ozone (O?) co-exposure on the response. We hypothesized that UFCAPs would cause greater decrement in mechanical function and electrical dysfunction than FCAPs, and that O? co-exposure would enhance the effects of both particle-types. METHODS: Conscious/unrestrained radiotelemetered mice were exposed once whole-body to either 190 ?g/m³ FCAPs or 140 ?g/m³ UFCAPs with/without 0.3 ppm O?; separate groups were exposed to either filtered air (FA) or O? alone. Heart rate (HR) and electrocardiogram (ECG) were recorded continuously before, during and after exposure, and cardiac mechanical function was assessed using a Langendorff perfusion preparation 24 hrs post-exposure. RESULTS: FCAPs alone caused a significant decrease in baseline left ventricular developed pressure (LVDP) and contractility, whereas UFCAPs did not; neither FCAPs nor UFCAPs alone caused any ECG changes. O? co-exposure with FCAPs caused a significant decrease in heart rate variability when compared to FA but also blocked the decrement in cardiac function. On the other hand, O? co-exposure with UFCAPs significantly increased QRS-interval, QTc and non-conducted P-wave arrhythmias, and decreased LVDP, rate of contractility and relaxation when compared to controls. CONCLUSIONS: These data suggest that particle size and gaseous interactions may play a role in cardiac function decrements one day after exposure. Although FCAPs?+?O? only altered autonomic balance, UFCAPs?+?O? appeared to be more serious by increasing cardiac arrhythmias and causing mechanical decrements. As such, O? appears to interact differently with FCAPs and UFCAPs, resulting in varied cardiac changes, which suggests that the cardiovascular effects of particle-gas co-exposures are not simply additive or even generalizable. Additionally, the mode of toxicity underlying this effect may be subtle given none of the exposures described here impaired post-ischemia recovery.

Project description:The main objective of this study was chemical characterization and source apportionment of the oxidative potential of ambient PM2.5 samples collected in an urban background area in Athens, Greece. Ambient PM2.5 samples were collected during the summer (June-September) of 2017 and winter (February-March) of 2018 at a residential, urban background site in the outlying neighborhood of the Demokritos National Laboratory in Athens, Greece. The collected PM samples were analyzed for their chemical constituents including metals and trace elements, water-soluble organic carbon (WSOC), elemental and organic carbon (EC/OC), and marker of biomass burning (i.e., levoglucosan). In addition, the DCFH in vitro assay was performed to determine the oxidative potential of the PM2.5 samples. We performed a series of statistical analyses, including Spearman rank-order correlation analysis, principal component analysis (PCA), and multi linear regression (MLR) to determine the most significant species (as source tracers) contributing to the oxidative potential of PM2.5. Our findings revealed that the intrinsic (per PM mass) and extrinsic (per m3 of air volume) oxidative potentials of the collected ambient PM2.5 samples were significantly higher than those measured in many urban areas around the world. The results of the MLR analyses indicated that the major pollution sources contributing to the oxidative potential of ambient PM2.5 were vehicular emissions (characterized by EC) (44%), followed by secondary organic aerosol (SOA) formation (characterized by WSOC) (16%), and biomass burning (characterized by levoglucosan) (9%). The oxidative potential of the collected ambient PM2.5 samples was also higher in summer compared to the winter, mainly due to higher concentrations of EC and WSOC during this season. Results from this study corroborate the impact of traffic and SOA on the oxidative potential of ambient PM2.5 in greater Athens area, and can be helpful in adopting appropriate public health policies regarding detrimental outcomes of exposure to PM2.5.

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Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress.

Publications

Ambient particulate pollutants in the ultrafine range promote early atherosclerosis and systemic oxidative stress.

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