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Acute Exposure to Diesel Exhaust Increases Muscle Sympathetic Nerve Activity in Humans
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.ORCID-id: 0000-0002-8753-830X
Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Lungmedicin.
School of Medicine Western Sydney University Sydney NSW Australia.
Human Autonomic Neurophysiology Laboratory School of Medicine Baker Heart and Diabetes Institute Melbourne Vic. Australia; Department of Physiology School of Biomedical Sciences The University of Melbourne Melbourne Vic. Australia.
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2021 (Engelska)Ingår i: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, E-ISSN 2047-9980, Vol. 10, nr 10, artikel-id e018448Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Background: Diesel exhaust (DE) emissions are a major contributor to ambient air pollution and are strongly associated with cardiovascular morbidity and mortality. Exposure to traffic-related particulate matter is linked with acute adverse cardiovascular events; however, the mechanisms are not fully understood. We examined the role of the autonomic nervous system during exposure to DE that has previously only been indirectly investigated.

Methods and Results: Using microneurography, we measured muscle sympathetic nerve activity (MSNA) directly in the peroneal nerve of 16 healthy individuals. MSNA, heart rate, and respiration were recorded while subjects rested breathing filtered air, filtered air with an exposure mask, and standardized diluted DE (300 µg/m3) through the exposure mask. Heart rate variability was assessed from an ECG. DE inhalation rapidly causes an increase in number of MSNA bursts as well as the size of bursts within 10 minutes, peaking by 30 minutes (P<0.001), compared with baseline filtered air with an exposure mask. No significant changes occurred in heart rate variability indices during DE exposure; however, MSNA frequency correlated negatively with total power (r2=0.294, P=0.03) and low frequency (r2=0.258, P=0.045). Heart rate correlated positively with MSNA frequency (r2=0.268, P=0.04) and the change in percentage of larger bursts (burst amplitude, height >50% of the maximum burst) from filtered air with an exposure mask (r2=0.368, P=0.013).

Conclusions: Our study provides direct evidence for the rapid modulation of the autonomic nervous system after exposure to DE, with an increase in MSNA. The quick increase in sympathetic outflow may explain the strong epidemiological data associating traffic-related particulate matter to acute adverse cardiovascular events such as myocardial infarction.

Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02892279.

Ort, förlag, år, upplaga, sidor
Wiley-Blackwell Publishing Inc., 2021. Vol. 10, nr 10, artikel-id e018448
Nyckelord [en]
air pollution, autonomic nervous system, diesel, heart rate variability, muscle sympathetic nerve activity, sympatho‐excitation
Nationell ämneskategori
Kardiologi och kardiovaskulära sjukdomar
Identifikatorer
URN: urn:nbn:se:umu:diva-183918DOI: 10.1161/JAHA.120.018448ISI: 000651436300025PubMedID: 33942621Scopus ID: 2-s2.0-85106552074OAI: oai:DiVA.org:umu-183918DiVA, id: diva2:1560697
Forskningsfinansiär
Hjärt-LungfondenForte, Forskningsrådet för hälsa, arbetsliv och välfärdVästerbottens läns landstingTillgänglig från: 2021-06-04 Skapad: 2021-06-04 Senast uppdaterad: 2025-02-10Bibliografiskt granskad

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Rankin, Gregory D.Kabéle, MikaelSandström, ThomasBosson, Jenny A.

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Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Kardiologi och kardiovaskulära sjukdomar

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