ORIGINAL ARTICLES

Hourly variation in fine particle exposure is associated with transiently increased risk of ST segment depression

T Lanki^1,2, G Hoek³, K L Timonen⁴, A Peters², P Tiittanen¹, E Vanninen⁴, J Pekkanen^1,5

¹ Environmental Epidemiology Unit, National Public Health Institute (KTL), Kuopio, Finland
² Institute of Epidemiology, Helmholtz Zentrum München, Munich, Germany
³ Institute for Risk Assessment Sciences (IRAS), Utrecht University, Utrecht, the Netherlands
⁴ Department of Clinical Physiology and Nuclear Medicine, Kuopio University and Kuopio University Hospital, Kuopio, Finland
⁵ School of Public Health and Clinical Nutrition, University of Kuopio, Kuopio, Finland

Timo Lanki, National Public Health Institute (KTL), Environmental Epidemiology Unit, PO Box 95, FI-70701 Kuopio, Finland; timo.lanki{at}ktl.fi

Objectives: To evaluate whether hourly changes in fine particle (PM_2.5, 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 PM_2.5 exposure and outdoor levels of PM_2.5 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 PM_2.5 concentrations, but not outdoor ultrafine particle counts, were associated with ST segment depressions. The odds ratio (per 10 µg/m³) for personal PM_2.5 concentration during the hour preceding a clinic visit was 3.26 (95% CI 1.07 to 9.99) and for 4 h average outdoor PM_2.5 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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