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Hourly variation in fine particle exposure is associated with transiently increased risk of ST segment depression
  1. Timo Lanki (timo.lanki{at}
  1. National Public Health Institute (KTL), Finland
    1. Gerard Hoek (g.hoek{at}
    1. Institute for Risk Assessment Sciences (IRAS), Utrecht University, Netherlands
      1. Kirsi L Timonen (kirsi.timonen{at}
      1. Kuopio University Hospital; Kuopio University, Finland
        1. Annette Peters (peters{at}
        1. Helmholtz Zentrum München, Germany
          1. Pekka Tiittanen (pekka.tiittanen{at}
          1. National Public Health Institute (KTL), Finland
            1. Esko Vanninen (esko.vanninen{at}
            1. Kuopio University Hospital; Kuopio University, Finland
              1. Juha Pekkanen (juha.pekkanen{at}
              1. National Public Health Institute (KTL); Kuopio University, Finland


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

                Methods Forty-one non-smoking elderly persons with coronary heart disease were followed up with biweekly clinic visits and air pollution measurements in Helsinki, Finland. The occurrence of ST segment depressions >0.1 mV was recorded during submaximal exercise test. Hourly variations in personal PM2.5 exposure and outdoor levels of PM2.5 and ultrafine particles (<0.1 µm) were recorded during 24-hrs before the 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. Odds ratio [per 10 µg/m3] for personal PM2.5 concentration during the hour preceding clinic visit was 3.26, 95% CI: 1.07-9.99, and for 4-h average outdoor PM2.5 2.47, 95% CI 1.05-5.85.

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

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