Effect of inhaled sulphur dioxide and carbon particles on heart rate variability and markers of inflammation and coagulation in human subjects

H. C. Routledge, S. Manney, R. M. Harrison, Jonathan Geoffrey Ayres, J. Townend

    Research output: Contribution to journalArticle

    76 Citations (Scopus)

    Abstract

    Objective: To measure the inflammatory and autonomic responses of healthy humans and patients with coronary artery disease to controlled concentrations of two specific components of vehicle derived air pollution, carbon particles and sulphur dioxide (SO2).

    Methods: Placebo controlled, double blind, random order human challenge study examining the effects of carbon particles (50 mu g/m(3)) and SO2 (200 parts per billion (ppb)) on heart rate variability (HRV) and circulating markers of inflammation and coagulation in healthy volunteers and patients with stable angina.

    Results: In healthy volunteers, markers of cardiac vagal control did not fall in response to particle exposure but, compared with the response to air, increased transiently immediately after exposure ( root mean square of successive RR interval differences (RMSSD) 15 ( 5) ms with carbon particles and 4 ( 3) ms) with air, p< 0.05). SO2 exposure resulted in no immediate change but a significant reduction in HRV markers of cardiac vagal control at four hours ( RMSSD 22 (3.6) ms with air, 27 (2.7) ms with SO2, p< 0.05). No such changes were seen in patients with stable angina. Neither pollutant caused any change in markers of inflammation or coagulation at zero, four, or 24 hours.

    Conclusion: In healthy volunteers, short term exposure to pure carbon particles does not cause adverse effects on HRV or a systemic inflammatory response. The adverse effects of vehicle derived particulates are likely to be caused by more reactive species found on the particle surface. SO2 exposure does, however, reduce cardiac vagal control, a response that would be expected to increase susceptibility to ventricular arrhythmia.

    Original languageEnglish
    Pages (from-to)220-227
    Number of pages7
    JournalHeart
    Volume92
    DOIs
    Publication statusPublished - Feb 2006

    Keywords

    • PARTICULATE AIR-POLLUTION
    • HEALTHY-HUMAN VOLUNTEERS
    • MYOCARDIAL-INFARCTION
    • MORTALITY
    • EXPOSURE
    • ASSOCIATION
    • BLOOD
    • INTERVENTION
    • INCREASES
    • RESPONSES

    Cite this

    Effect of inhaled sulphur dioxide and carbon particles on heart rate variability and markers of inflammation and coagulation in human subjects. / Routledge, H. C.; Manney, S.; Harrison, R. M.; Ayres, Jonathan Geoffrey; Townend, J.

    In: Heart, Vol. 92, 02.2006, p. 220-227.

    Research output: Contribution to journalArticle

    Routledge, H. C. ; Manney, S. ; Harrison, R. M. ; Ayres, Jonathan Geoffrey ; Townend, J. / Effect of inhaled sulphur dioxide and carbon particles on heart rate variability and markers of inflammation and coagulation in human subjects. In: Heart. 2006 ; Vol. 92. pp. 220-227.
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    abstract = "Objective: To measure the inflammatory and autonomic responses of healthy humans and patients with coronary artery disease to controlled concentrations of two specific components of vehicle derived air pollution, carbon particles and sulphur dioxide (SO2).Methods: Placebo controlled, double blind, random order human challenge study examining the effects of carbon particles (50 mu g/m(3)) and SO2 (200 parts per billion (ppb)) on heart rate variability (HRV) and circulating markers of inflammation and coagulation in healthy volunteers and patients with stable angina.Results: In healthy volunteers, markers of cardiac vagal control did not fall in response to particle exposure but, compared with the response to air, increased transiently immediately after exposure ( root mean square of successive RR interval differences (RMSSD) 15 ( 5) ms with carbon particles and 4 ( 3) ms) with air, p< 0.05). SO2 exposure resulted in no immediate change but a significant reduction in HRV markers of cardiac vagal control at four hours ( RMSSD 22 (3.6) ms with air, 27 (2.7) ms with SO2, p< 0.05). No such changes were seen in patients with stable angina. Neither pollutant caused any change in markers of inflammation or coagulation at zero, four, or 24 hours.Conclusion: In healthy volunteers, short term exposure to pure carbon particles does not cause adverse effects on HRV or a systemic inflammatory response. The adverse effects of vehicle derived particulates are likely to be caused by more reactive species found on the particle surface. SO2 exposure does, however, reduce cardiac vagal control, a response that would be expected to increase susceptibility to ventricular arrhythmia.",
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    author = "Routledge, {H. C.} and S. Manney and Harrison, {R. M.} and Ayres, {Jonathan Geoffrey} and J. Townend",
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    T1 - Effect of inhaled sulphur dioxide and carbon particles on heart rate variability and markers of inflammation and coagulation in human subjects

    AU - Routledge, H. C.

    AU - Manney, S.

    AU - Harrison, R. M.

    AU - Ayres, Jonathan Geoffrey

    AU - Townend, J.

    PY - 2006/2

    Y1 - 2006/2

    N2 - Objective: To measure the inflammatory and autonomic responses of healthy humans and patients with coronary artery disease to controlled concentrations of two specific components of vehicle derived air pollution, carbon particles and sulphur dioxide (SO2).Methods: Placebo controlled, double blind, random order human challenge study examining the effects of carbon particles (50 mu g/m(3)) and SO2 (200 parts per billion (ppb)) on heart rate variability (HRV) and circulating markers of inflammation and coagulation in healthy volunteers and patients with stable angina.Results: In healthy volunteers, markers of cardiac vagal control did not fall in response to particle exposure but, compared with the response to air, increased transiently immediately after exposure ( root mean square of successive RR interval differences (RMSSD) 15 ( 5) ms with carbon particles and 4 ( 3) ms) with air, p< 0.05). SO2 exposure resulted in no immediate change but a significant reduction in HRV markers of cardiac vagal control at four hours ( RMSSD 22 (3.6) ms with air, 27 (2.7) ms with SO2, p< 0.05). No such changes were seen in patients with stable angina. Neither pollutant caused any change in markers of inflammation or coagulation at zero, four, or 24 hours.Conclusion: In healthy volunteers, short term exposure to pure carbon particles does not cause adverse effects on HRV or a systemic inflammatory response. The adverse effects of vehicle derived particulates are likely to be caused by more reactive species found on the particle surface. SO2 exposure does, however, reduce cardiac vagal control, a response that would be expected to increase susceptibility to ventricular arrhythmia.

    AB - Objective: To measure the inflammatory and autonomic responses of healthy humans and patients with coronary artery disease to controlled concentrations of two specific components of vehicle derived air pollution, carbon particles and sulphur dioxide (SO2).Methods: Placebo controlled, double blind, random order human challenge study examining the effects of carbon particles (50 mu g/m(3)) and SO2 (200 parts per billion (ppb)) on heart rate variability (HRV) and circulating markers of inflammation and coagulation in healthy volunteers and patients with stable angina.Results: In healthy volunteers, markers of cardiac vagal control did not fall in response to particle exposure but, compared with the response to air, increased transiently immediately after exposure ( root mean square of successive RR interval differences (RMSSD) 15 ( 5) ms with carbon particles and 4 ( 3) ms) with air, p< 0.05). SO2 exposure resulted in no immediate change but a significant reduction in HRV markers of cardiac vagal control at four hours ( RMSSD 22 (3.6) ms with air, 27 (2.7) ms with SO2, p< 0.05). No such changes were seen in patients with stable angina. Neither pollutant caused any change in markers of inflammation or coagulation at zero, four, or 24 hours.Conclusion: In healthy volunteers, short term exposure to pure carbon particles does not cause adverse effects on HRV or a systemic inflammatory response. The adverse effects of vehicle derived particulates are likely to be caused by more reactive species found on the particle surface. SO2 exposure does, however, reduce cardiac vagal control, a response that would be expected to increase susceptibility to ventricular arrhythmia.

    KW - PARTICULATE AIR-POLLUTION

    KW - HEALTHY-HUMAN VOLUNTEERS

    KW - MYOCARDIAL-INFARCTION

    KW - MORTALITY

    KW - EXPOSURE

    KW - ASSOCIATION

    KW - BLOOD

    KW - INTERVENTION

    KW - INCREASES

    KW - RESPONSES

    U2 - 10.1136/HRT.2004.051672

    DO - 10.1136/HRT.2004.051672

    M3 - Article

    VL - 92

    SP - 220

    EP - 227

    JO - Heart

    JF - Heart

    SN - 1355-6037

    ER -