Exposure to ultrafine carbon particles at levels below detectable pulmonary inflammation affects cardiovascular performance in spontaneously hypertensive rats

Upadhyay, Swapna; Stoeger, Tobias; Harder, Volkar; Thomas, Ronald F.; Schladweiler, Mette C.; Semmler‐Behnke, Manuela; Takenaka, Shinji; Karg, Erwin; Reitmeir, Peter; Bäder, Michael; Stampfl, Andreas; Kodavanti, Urmila P.; Schulz, Holger

doi:10.1186/1743-8977-5-19

Cited by 43 publications

(62 citation statements)

References 57 publications

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“…In spontaneously hypertensive rats exposed to similar ultrafine carbon particles (172 µg/m 3 for 24 hours), blood pressure and heart rate increased with a lag of 1-3 days. Inflammatory markers in lavage fluid, lung tissue, and blood were unaffected, but mRNA expression of hemeoxygenase-1, endothelin-1, endothelin receptors, tissue factor, and plasminogen activator inhibitor in the lung showed a significant induction (Upadhyay et al, 2008), which is an indication of a cardiovascular (or even systemic) effect without adverse effects at the port of entry -that is, the lung. Given differences in the deposited dose in the respiratory systems of rats and human beings, the concentration used in this study is high, but not unrealistic when extrapolated to human exposures.…”

Section: Toxicological Studiesmentioning

confidence: 95%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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This document presents answers to 24 questions relevant to reviewing European policies on air pollution and to addressing health aspects of these policies. The answers were developed by a large group of scientists engaged in the WHO project "Review of evidence on health aspects of air pollution -REVIHAAP". The experts reviewed and discussed the newly accumulated scientific evidence on the adverse effects on health of air pollution, formulating science-based answers to the 24 questions. Extensive rationales for the answers, including the list of key references, are provided. The review concludes that a considerable amount of new scientific information on the adverse effects on health of particulate matter, ozone and nitrogen dioxide, observed at levels commonly present in Europe, has been published in recent years. This new evidence supports the scientific conclusions of the WHO air quality guidelines, last updated in 2005, and indicates that the effects in some cases occur at air pollution concentrations lower than those serving to establish these guidelines. It also provides scientific arguments for taking decisive actions to improve air quality and reduce the burden of disease associated with air pollution in Europe.This publication arises from the project REVIHAAP and has been co-funded by the European Union. Keywords AIR POLLUTANTS AIR POLLUTION -ADVERSE EFFECTS ENVIRONMENT AND PUBLIC HEALTH EVIDENCE BASED PRACTICE GUIDELINES HEALTH POLICYAddress requests about publications of the WHO Regional Office for Europe to: Publications WHO Regional Office for Europe Scherfigsvej 8 DK-2100 Copenhagen Ø, Denmark Alternatively, complete an online request form for documentation, health information, or for permission to quote or translate, on the Regional Office web site (http://www.euro.who.int/pubrequest). © World Health Organization 2013All rights reserved. The Regional Office for Europe of the World Health Organization welcomes requests for permission to reproduce or translate its publications, in part or in full.The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate borderlines for which there may not yet be full agreement.The mention of specific companies or of certain manufacturers products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters.All reasonable precautions have been taken by the World Health Organization to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either express or implied. ...

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Section: Toxicological Studiesmentioning

confidence: 95%

A rapid assessment of the impact of hazard reduction burning around Sydney, May 2016

Broome¹,

Johnston

Horsley

et al. 2016

Medical Journal of Australia

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“…353 Recently, ultrafine carbon particles were shown to increase BP in spontaneously hypertensive rats 1 to 3 days after a 24-hour exposure. 354 This response occurred concomitant with increased ET-1 messenger ribonucleic acid levels in lung tissue and small elevations in plasma renin concentration and angiotensin I and II in the systemic circulation. These findings further support the idea that ET may play a role in cardiovascular responses to PM exposure and suggest that activation of the renin-angiotensin system may also be involved.…”

Section: Systemic and Pulmonary Hypertensionmentioning

confidence: 99%

“…416 These include the relevance of the dosages delivered to cardiovascular organs, the consequences of particle constituent modifications after interactions with lung tissue/fluids and plasma components, the means of transport within the circulation (eg, protein bound or within cells), 417 and the time course and ultimate sites of PM sequestration. It is also possible that increases in some vasoactive mediators or molecules with adverse effects on cardiovascular tissue, such as ET-1, [351][352][353][354] may occur in the lung and systemic circulation without the need for antecedent lung inflammation. Moreover, the 3 general pathways represent a simplification of complicated biological processes.…”

mentioning

confidence: 99%

Particulate Matter Air Pollution and Cardiovascular Disease

Brook¹,

Rajagopalan²,

Pope³

et al. 2010

Circulation

5,194

3,225

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Abstract-In 2004, the first American Heart Association scientific statement on "Air Pollution and Cardiovascular Disease" concluded that exposure to particulate matter (PM) air pollution contributes to cardiovascular morbidity and mortality. In the interim, numerous studies have expanded our understanding of this association and further elucidated the physiological and molecular mechanisms involved. The main objective of this updated American Heart Association scientific statement is to provide a comprehensive review of the new evidence linking PM exposure with cardiovascular disease, with a specific focus on highlighting the clinical implications for researchers and healthcare providers. The writing group also sought to provide expert consensus opinions on many aspects of the current state of science and updated suggestions for areas of future research. On the basis of the findings of this review, several new conclusions were reached, including the following: Exposure to PM Ͻ2.5 m in diameter (PM 2.5 ) over a few hours to weeks can trigger cardiovascular disease-related mortality and nonfatal events; longer-term exposure (eg, a few years) increases the risk for cardiovascular mortality to an even greater extent than exposures over a few days and reduces life expectancy within more highly exposed segments of the population by several months to a few years; reductions in PM levels are associated with decreases in cardiovascular mortality within a time frame as short as a few years; and many credible pathological mechanisms have been elucidated that lend biological plausibility to these findings. It is the opinion of the writing group that the overall evidence is consistent with a causal relationship between PM 2.5 exposure and cardiovascular morbidity and mortality. This body of evidence has grown and been strengthened substantially since the first American Heart Association scientific statement was published. Finally, PM 2.5 exposure is deemed a modifiable factor that contributes to cardiovascular morbidity and mortality. (Circulation. 2010;121:2331-2378.)

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“…In other studies, increases in heart rate have been noted after a lag of 2 or 3 days following ultrafi ne carbon PM exposure in hypertensive rats; however, the test material used in this study was distinct from that of studies discussed above (Upadhyay et al, 2008 ). Cardiac arrhythmias are related to heart rate changes, and, therefore, recently experimental studies have focused on heart dysrhythm.…”

mentioning

confidence: 70%

“…There remains signifi cant discordance in the data obtained among different studies because of varied physicochemistry and concentrations of the test materials used, different methods and durations of exposures, and the animal models selected as the objects of study for health effects. The majority of studies have evaluated circulating biomarkers; electrocardiographic changes; aortic plaque formation; and, occasionally, a spectrum of markers of oxidative stress or vascular thrombosis (Chuang et al, 2007 ;Liu et al, 2007 ;Yue et al, 2007 ;Araujo et al, 2008 ;Upadhyay et al, 2008 ). Most of the studies that have shown changes in biomarkers as a result of PM exposure have not involved dose -related exposure levels.…”

Section: Experimental Evidencementioning

confidence: 99%