Early pulmonary response is critical for extra-pulmonary carbon nanoparticle mediated effects: comparison of inhalation versus intra-arterial infusion exposures in mice View Full Text


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Article Info

DATE

2017-06-20

AUTHORS

Koustav Ganguly, Dariusch Ettehadieh, Swapna Upadhyay, Shinji Takenaka, Thure Adler, Erwin Karg, Fritz Krombach, Wolfgang G. Kreyling, Holger Schulz, Otmar Schmid, Tobias Stoeger

ABSTRACT

BackgroundThe death toll associated with inhaled ambient particulate matter (PM) is attributed mainly to cardio-vascular rather than pulmonary effects. However, it is unclear whether the key event for cardiovascular impairment is particle translocation from lung to circulation (direct effect) or indirect effects due to pulmonary particle-cell interactions. In this work, we addressed this issue by exposing healthy mice via inhalation and intra-arterial infusion (IAI) to carbon nanoparticles (CNP) as surrogate for soot, a major constituent of (ultrafine) urban PM.MethodsEquivalent surface area CNP doses in the blood (30mm2 per animal) were applied by IAI or inhalation (lung-deposited dose 10,000mm2; accounting for 0.3% of lung-to-blood CNP translocation). Mice were analyzed for changes in hematology and molecular markers of endothelial/epithelial dysfunction, pro-inflammatory reactions, oxidative stress, and coagulation in lungs and extra-pulmonary organs after CNP inhalation (4 h and 24 h) and CNP infusion (4 h). For methodological reasons, we used two different CNP types (spark-discharge and Printex90), with very similar physicochemical properties [≥98 and ≥95% elemental carbon; 10 and 14 nm primary particle diameter; and 800 and 300 m2/g specific surface area] for inhalation and IAI respectively.ResultsMild pulmonary inflammatory responses and significant systemic effects were observed following 4 h and 24 h CNP inhalation. Increased retention of activated leukocytes, secondary thrombocytosis, and pro-inflammatory responses in secondary organs were detected following 4 h and 24 h of CNP inhalation only. Interestingly, among the investigated extra-pulmonary tissues (i.e. aorta, heart, and liver); aorta revealed as the most susceptible extra-pulmonary target following inhalation exposure. Bypassing the lungs by IAI however did not induce any extra-pulmonary effects at 4 h as compared to inhalation.ConclusionsOur findings indicate that extra-pulmonary effects due to CNP inhalation are dominated by indirect effects (particle-cell interactions in the lung) rather than direct effects (translocated CNPs) within the first hours after exposure. Hence, CNP translocation may not be the key event inducing early cardiovascular impairment following air pollution episodes. The considerable response detected in the aorta after CNP inhalation warrants more emphasis on this tissue in future studies. More... »

PAGES

19

References to SciGraph publications

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  • Journal

    TITLE

    Particle and Fibre Toxicology

    ISSUE

    1

    VOLUME

    14

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1186/s12989-017-0200-x

    DOI

    http://dx.doi.org/10.1186/s12989-017-0200-x

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1086114248

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28637465


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    345 Institute of Lung Biology and Disease, Comprehensive Pneumology Center, Helmholtz Zentrum München, German Research Center for Environmental Health, D85764, Neuherberg, Germany
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    347 grid-institutes:grid.4714.6 schema:alternateName Unit of Lung and Airway Research, Institute of Environmental Medicine (IMM), Karolinska Institutet, SE-171 77, Stockholm, Sweden
    348 Unit of Work Environment Toxicology, Institute of Environmental Medicine (IMM), Karolinska Institutet, SE-171 77, Stockholm, Sweden
    349 schema:name Unit of Lung and Airway Research, Institute of Environmental Medicine (IMM), Karolinska Institutet, SE-171 77, Stockholm, Sweden
    350 Unit of Work Environment Toxicology, Institute of Environmental Medicine (IMM), Karolinska Institutet, SE-171 77, Stockholm, Sweden
    351 rdf:type schema:Organization
    352 grid-institutes:grid.5252.0 schema:alternateName Walter Brendel Centre of Experimental Medicine, Ludwig-Maximilians-Universität, D81377, Munich, Germany
    353 schema:name Walter Brendel Centre of Experimental Medicine, Ludwig-Maximilians-Universität, D81377, Munich, Germany
    354 rdf:type schema:Organization
     




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