scholarly journals Exposure to medium and high ambient levels of ozone causes adverse systemic inflammatory and cardiac autonomic effects

2015 ◽  
Vol 308 (12) ◽  
pp. H1499-H1509 ◽  
Author(s):  
Mehrdad Arjomandi ◽  
Hofer Wong ◽  
Aneesh Donde ◽  
Jessica Frelinger ◽  
Sarah Dalton ◽  
...  

Epidemiological evidence suggests that exposure to ozone increases cardiovascular morbidity. However, the specific biological mechanisms mediating ozone-associated cardiovascular effects are unknown. To determine whether short-term exposure to ambient levels of ozone causes changes in biomarkers of cardiovascular disease including heart rate variability (HRV), systemic inflammation, and coagulability, 26 subjects were exposed to 0, 100, and 200 ppb ozone in random order for 4 h with intermittent exercise. HRV was measured and blood samples were obtained immediately before (0 h), immediately after (4 h), and 20 h after (24 h) each exposure. Bronchoscopy with bronchoalveolar lavage (BAL) was performed 20 h after exposure. Regression modeling was used to examine dose-response trends between the endpoints and ozone exposure. Inhalation of ozone induced dose-dependent adverse changes in the frequency domains of HRV across exposures consistent with increased sympathetic tone [increase of (parameter estimate ± SE) 0.4 ± 0.2 and 0.3 ± 0.1 in low- to high-frequency domain HRV ratio per 100 ppb increase in ozone at 4 h and 24 h, respectively ( P = 0.02 and P = 0.01)] and a dose-dependent increase in serum C-reactive protein (CRP) across exposures at 24 h [increase of 0.61 ± 0.24 mg/l in CRP per 100 ppb increase in ozone ( P = 0.01)]. Changes in HRV and CRP did not correlate with ozone-induced local lung inflammatory responses (BAL granulocytes, IL-6, or IL-8), but changes in HRV and CRP were associated with each other after adjustment for age and ozone level. Inhalation of ozone causes adverse systemic inflammatory and cardiac autonomic effects that may contribute to the cardiovascular mortality associated with short-term exposure.

Author(s):  
Sona Margaryan ◽  
Armenuhi Hyusyan ◽  
Anush Martirosyan ◽  
Shushan Sargsian ◽  
Gayane Manukyan

AbstractBackgroundAlthough it is widely accepted that catecholamines and estrogens influence immunity and have consequences for health, their effect on innate immunity (e.g. monocytes and neutrophils) is still not fully investigated.Materials and methodsOur study aimed to analyze the production of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, monocyte chemoattractant protein (MCP)-1 and IL-8 by whole blood cells following short-term exposure to epinephrine (Epi) and 17β-estradiol (E2) in the presence or absence of lipopolysaccharide (LPS). We also evaluated the in vitro effect of these hormones on expression of β2 integrin (CD11b/CD18) and L-selectin (CD62L) by circulating neutrophils and monocytes in the blood of healthy subjects.ResultsEpi has shown a potential to modulate the production of pro-inflammatory mediators. Its exposure resulted in significantly increased production of IL-8 in a dose-dependent manner. On the contrary, a dose-dependent suppression of LPS-induced production of IL-1β, IL-8, and MCP-1 by Epi was observed. In neutrophils, a modest rise in CD11b expression was observed after Epi exposure. Simultaneously, Epi suppressed LPS-induced expression of CD11b and CD18. In monocytes, Epi suppressed LPS-induced expression of C11b. E2 inhibited LPS-induced TNF-α production and caused a significant decrease in CD62L expression in both cell populations. No significant changes were observed after double exposure of cells with Epi and E2.ConclusionsThus, our results show that Epi and E2 differentially modulate the innate immune response and have a dual effect on cytokine modulation. The findings suggest that the observed immunoregulatory role of Epi and E2 may influence the outcome in endotoxin responses and can be critical in the regulation of inflammatory responses.


Author(s):  
Mehrdad Arjomandi ◽  
Hofer Wong ◽  
Aneesh Donde ◽  
Karron Power ◽  
Nina Holland ◽  
...  

2006 ◽  
Vol 38 (3) ◽  
pp. 267-275 ◽  
Author(s):  
Barbara PAWLIK-SKOWROŃSKA ◽  
O. William PURVIS ◽  
Jacek PIRSZEL ◽  
Tadeusz SKOWROŃSKI

Cellular responses to copper stress were investigated for the first time in a saxicolous lichen species, Lecanora polytropa (Hoffm.) Rabenh. Bright blue-green apothecia accumulated up to 1·3% Cu on a dry weight basis (205 μ mol Cu g−1), c. 50% in an exchangeable form. A bright turquoise-blue layer extended beneath the hymenium into the medulla, above and between a dentate photobiont layer. Oxalic (1·88 μ mol g−1), citric (0·83 μ mol g−1) and lower concentrations of malic (0·45 μ mol g−1) acids were determined by GC/MS analysis. Short-term exposure to high Cu2+ concentrations (40 and 400 μ mol g−1) under non-complexing conditions caused a dose-dependent decrease in chlorophyll a content; chlorophyll b and total carotenoid contents remained constant. The phaeophytinization quotient remained unchanged during Cu2+ exposure. Analysis of thiol peptides confirmed glutathione was reduced (GSH) in native L. polytropa (0·538 μ mol g−1), and phytochelatins (PC2 and PC3) oxidised. Short-term exposure to 40 μ mol g−1 Cu2+ oxidised c. 28% of the glutathione pool; oxidised phytochelatin concentrations remained unchanged. This is the first report of phytochelatin production and thiol peptide status in a crustose lichen. These represent two possible detoxification mechanisms in this Cu-tolerant species. Copper complexation by low molecular mass organic acids and non-protein thiols do not entirely account for its tolerance.


1990 ◽  
Vol 69 (1) ◽  
pp. 245-250 ◽  
Author(s):  
J. M. Fouke ◽  
R. A. DeLemos ◽  
M. J. Dunn ◽  
E. R. McFadden

Short-term exposure to 0.5 parts per million (ppm) ozone has been shown to cause an increase in respiratory resistance in primates that can be diminished by 50% with pretreatment with cromolyn sodium. Because of the known membrane-stabilizing effects of cromolyn and the resultant inhibition of mediator production, we hypothesized a role for the products of arachidonic acid (AA) metabolism in these events. We exposed five adult male baboons to 0.5 ppm ozone on two occasions, once with cromolyn pretreatment and once without. Pulmonary resistance (RL) was monitored and bronchoalveolar lavage (BAL) was performed before and after each exposure. The BAL was analyzed for a stable hydrolysis product of prostacyclin, 6-keto-prostaglandin (PG) F1 alpha, PGE2, a stable hydrolysis product of thromboxane (Tx) A2, TxB2, and PGF2 alpha. RL increased after ozone exposure (1.62 +/- 0.23 to 3.77 +/- 0.51 cmH2O.l-1.s, difference 2.15; P less than 0.02), and this effect was partially blocked by cromolyn (1.93 +/- 0.09 to 3.18 +/- 0.40 cmH2O.l-1.s, difference 1.25; P less than 0.02). The base-line levels of the metabolites of AA in the BAL were as follows (in pg/ml): 6-keto-PGF1 alpha 72.78 +/- 12.6, PGE2 145.92 +/- 30.52, TxB2 52.52 +/- 9.56, and PGF2 alpha 22.28 +/- 5.42. Ozone exposure had no effect on the level of any of these prostanoids (P = NS). These studies quantify the magnitude of cyclooxygenase products of AA metabolism in BAL from baboon lungs and demonstrate that changes in the levels of these mediators in BAL are not prerequisites for ozone-induced increases in respiratory resistance.(ABSTRACT TRUNCATED AT 250 WORDS)


1979 ◽  
Vol 184 (2) ◽  
pp. 203-214 ◽  
Author(s):  
Harald L. Guenther ◽  
Hannelore E. Guenther ◽  
Herbert Fleisch

Investigations were carried out to assess the effects of disodium 1-hydroxyethane-1,1-diphosphonate and disodium dichloromethanediphosphonate (compounds containing a P–C–P bond) on isolated rabbit articular chondrocytes in culture. Studies on growth behaviour showed that both diphosphonates displayed inhibitory actions, dichloromethanediphosphonate producing the larger effect. Both compounds inhibited the uptake of 2-deoxy-d-glucose, dichloromethanediphosphonate once more being the more potent of the two. The uptake of α-aminoisobutyrate was considerably increased by chondrocytes treated with dichloromethanediphosphonate, whereas 1-hydroxyethane-1,1-diphosphonate showed no effects. The biosynthesis of sulphated extracellular macromolecules secreted by the cells into the pericellular space as well as into the growth medium was greatly increased by dichloromethanediphosphonate but not by 1-hydroxyethane-1,1-diphosphonate. The stimulatory effect was dose-dependent. Short-term exposure of already confluent cells to dichloromethanediphosphonate as opposed to growing the cells to confluence in the presence of the diphosphonate revealed that the stimulatory effects were already evident after 24h, indicating that cell division is not necessarily required to produce the observed effects. The increment in proteoglycan synthesis was still evident with cells that were exposed continuously to the diphosphonate in primary as well as secondary culture. Pulse–chase experiments together with studies on the enzyme arylsulphatase revealed that the appearance of increased amounts of proteoglycans was the result of a stimulation in synthesis and not due to an inhibition in turnover.


2015 ◽  
Vol 35 (2) ◽  
pp. 829-840 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Priya Yuvaraju ◽  
Sumaya Beegam ◽  
Badreldin H Ali

Background/Aim: Water-pipe smoking (WPS) has acquired worldwide popularity, and is disseminating particularly rapidly in Europe and North America. However, little is known about the short-term cardiovascular effects of WPS. Methods: Presently, we assessed the short-term cardiovascular effects of nose-only exposure to mainstream WPS in BALB/c mice for 30 min/day for 5 consecutive days. Control mice were exposed to air. At the end of the exposure period, several cardiovascular endpoints were measured. Results: WPS did not affect the number of leukocytes and the plasma concentrations of C-reactive protein, tumor necrosis factor α (TNFα) and interleukin-6 (IL-6). Likewise, plasma levels of lipid peroxidation (LPO), reduced glutathione (GSH) and catalase were not affected by WPS. By contrast, WPS aggravated in vivo thrombosis by shortening the thrombotic occlusion time in pial arterioles and venules. The number of circulating platelets was reduced by WPS suggesting the occurrence of platelet aggregation in vivo. Elevated concentrations of fibrinogen and plasminogen activator inhibitor-1 were seen after the exposure to WPS. Blood samples taken from mice exposed to WPS and exposed to adenosine diphosphate showed more platelet aggregation. The heart concentrations of IL-6 and TNFα were augmented by WPS. Likewise, heart levels of LPO, reactive oxygen species and the antioxidants catalase and GSH were increased by WPS. However, the systolic blood pressure and heart rate were not affected by WPS. Conclusion: It can be concluded that short-term exposure to WPS exerts procoagulatory effects and induce cardiac inflammation and oxidative stress. At the time point investigated, there was no evidence for blood inflammation or oxidative stress.


Author(s):  
Fatemeh Aminaei ◽  
Mohammad Javad Zare Sakhvidi ◽  
Hamideh Mihanpour ◽  
Mojtaba Moghaddasi ◽  
Mahdiyeh Shafieizadeh Bafghi

Introduction: According to the literature, Central Retinal Arteriolar Equivalent (CRAE), Central Retinal Venular Equivalent (CRVE), and Artemio Venule Ratio (AVR) are three important markers in determining the changes of retinal artery. These markers are employed as an indicator of cardiovascular effects in workers. This study aimed to evaluate the changes in retinal micro vascular responses in workers exposed to short-term exposure to particulate matters caused by occupational processes using CRAE, CRVE, and AVR markers. Materials and Methods: In this study, 96 workers exposed to job-related pollution in a tile and ceramic company were investigated. Fundus photos of these people were analyzed via ARIA software using the related protocols. The data were investigated employing Kolmogorov–Smirnov and Mann-Whitney tests as well as the correlation and regression tests. Results: No significant difference was observed in the ocular parameters of smokers and non-smokers. Cardiovascular parameters had no significant correlation with CRAE and CRVE as well as breathable and inhalable dust; however, these parameters had a direct and significant correlation with AVR, PM10, and PM2.5 particles. Conclusion: The results did not show any changes in the retinal artery in workers who were exposed to job-related pollution. Moreover, no significant relationship was found between retinal artery changes and cardiovascular parameters. However, more large-scale studies are needed to clarify the relationship of particulate air pollutants with CRAE, CRVE, and AVR changes.


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