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Hourly variation in fine particle exposure is associated with transiently increased risk of ST segment depression
  1. T Lanki1,2,
  2. G Hoek3,
  3. K L Timonen4,
  4. A Peters2,
  5. P Tiittanen1,
  6. E Vanninen4,
  7. J Pekkanen1,5
  1. 1
    Environmental Epidemiology Unit, National Public Health Institute (KTL), Kuopio, Finland
  2. 2
    Institute of Epidemiology, Helmholtz Zentrum München, Munich, Germany
  3. 3
    Institute for Risk Assessment Sciences (IRAS), Utrecht University, Utrecht, the Netherlands
  4. 4
    Department of Clinical Physiology and Nuclear Medicine, Kuopio University and Kuopio University Hospital, Kuopio, Finland
  5. 5
    School of Public Health and Clinical Nutrition, University of Kuopio, Kuopio, Finland
  1. Timo Lanki, National Public Health Institute (KTL), Environmental Epidemiology Unit, PO Box 95, FI-70701 Kuopio, Finland; timo.lanki{at}ktl.fi

Abstract

Objectives: To evaluate whether hourly changes in fine particle (PM2.5, diameter<2.5 µm) exposure or outdoor particle concentrations are associated with rapid ischaemic responses.

Methods: 41 non-smoking elderly people with coronary heart disease were followed up with biweekly clinic visits in Helsinki, Finland. The occurrence of ST segment depressions >0.1 mV was recorded during submaximal exercise tests. Hourly variations in personal PM2.5 exposure and outdoor levels of PM2.5 and ultrafine particles (<0.1 µm) were recorded for 24 h before a clinic visit. Associations between particulate air pollution and ST segment depressions were evaluated using logistic regression.

Results: Both personal and outdoor PM2.5 concentrations, but not outdoor ultrafine particle counts, were associated with ST segment depressions. The odds ratio (per 10 µg/m3) for personal PM2.5 concentration during the hour preceding a clinic visit was 3.26 (95% CI 1.07 to 9.99) and for 4 h average outdoor PM2.5 it was 2.47 (95% CI 1.05 to 5.85).

Conclusions: Even very short-term elevations in fine particle exposure might increase the risk of myocardial ischaemia. The precise mechanism is still unknown but could involve changes in autonomic nervous control of the heart.

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Footnotes

  • Competing interests: None.

  • Funding: The main funding sources of the study were the European Union (ENV4-CT97-0568), the Academy of Finland (53307) and the National Technology Fund (40715/01). In addition, the corresponding author received personal grants from the Helsingin Sanomat Foundation and the Finnish Cultural Foundation.

  • Ethics approval: The study protocol was approved by the ethics committee of the National Public Health Institute.

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