Cardiovascular Effects of Short Term Exposure to Fields of Electricity Power Transmission

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.

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Retinal Microvascular Response to Short-Term Exposure to Particulate Matters As an Indicator of Cardiovascular Effects in Work Environments

Journal of Environmental Health and Sustainable Development ◽

10.18502/jehsd.v6i1.5763 ◽

2021 ◽

Author(s):

Fatemeh Aminaei ◽

Mohammad Javad Zare Sakhvidi ◽

Hamideh Mihanpour ◽

Mojtaba Moghaddasi ◽

Mahdiyeh Shafieizadeh Bafghi

Keyword(s):

Large Scale ◽

Cardiovascular Effects ◽

Particulate Matters ◽

Short Term ◽

Cardiovascular Parameters ◽

Short Term Exposure ◽

Significant Difference ◽

Inhalable Dust ◽

Kolmogorov Smirnov ◽

Retinal Artery

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00849.2014 ◽

2015 ◽

Vol 308 (12) ◽

pp. H1499-H1509 ◽

Cited By ~ 38

Author(s):

Mehrdad Arjomandi ◽

Hofer Wong ◽

Aneesh Donde ◽

Jessica Frelinger ◽

Sarah Dalton ◽

...

Keyword(s):

Inflammatory Responses ◽

Intermittent Exercise ◽

Cardiovascular Effects ◽

Random Order ◽

Ozone Exposure ◽

Short Term ◽

Ozone Level ◽

Short Term Exposure ◽

Dose Dependent ◽

Ambient Levels

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.

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The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648027 ◽

1976 ◽

Vol 36 (01) ◽

pp. 221-229 ◽

Cited By ~ 16

Author(s):

Charles A. Schiffer ◽

Caroline L. Whitaker ◽

Morton Schmukler ◽

Joseph Aisner ◽

Steven L. Hilbert

Keyword(s):

Platelet Count ◽

Platelet Aggregation ◽

Dimethyl Sulfoxide ◽

Platelet Function ◽

Platelet Volume ◽

Short Term ◽

Platelet Factor ◽

Short Term Exposure ◽

Structural Abnormalities

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

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