Article Text
Abstract
Objectives Elevated ozone levels have been associated with cardiovascular morbidity and mortality. We investigated the effects of ozone on heart rate (HR) and repolarisation parameters in potentially susceptible populations.
Methods Between March 2007 and December 2008, 363 ECG recordings including >2000 1 h intervals were measured in 64 individuals with type 2 diabetes or impaired glucose tolerance and in 46 healthy individuals with a potential genetic predisposition on the detoxification pathways from Augsburg, Germany. Associations between 1 h averages of ozone and HR, Bazett-corrected QT-interval (QTc), T-wave amplitude and T-wave complexity were analysed using additive mixed models. A variable indicating season and participants' location during the 1 h ECG recordings (summer and outdoors vs winter or indoors) was used as a potential ozone effect modifier.
Results We observed concurrent and 1–4 h lagged increases in HR of 0.5–0.7% for each 20 μg/m3 increase in ozone. These effects were stronger (1.0–1.2%) when participants were outdoors during the summer. We detected in all participants a concurrent (−1.31%; 95% CI −2.19% to −0.42%) and 1 h lagged (−1.32%; −2.19% to −0.45%) T-wave flattening. Elevated ozone levels were associated with 1 h (2.12%; 0.81 to 3.52) and 2 h lagged (1.89%; 0.55% to 3.26%) increases in T-wave complexity. However, no effects were seen for QTc. Ozone effects were generally more pronounced in individuals with metabolic disorders than a potential genetic predisposition.
Conclusions Changes in repolarisation might contribute to underlying pathophysiological changes associated with the link between elevated ozone levels and reported adverse cardiovascular outcomes.
- Ozone
- repolarisation
- panel study
- cardiovascular
- statistics
- epidemiology
- meta-analysis
- longitudinal studies
- time series study
- climate
- bayesian statistics
- volatile organic compounds (VOCs)
- polyaromatic hydrocarbons (PAHs)
- PM10-PM2.5-ultrafine
- environment
- air pollution
- respiratory
- noise
- public health
- risk assessment
- mortality studies
- mathematical models
- exposure monitoring
- pollution
- particulates
- diesel fumes
- aerosols
- diabetes mellitus
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- Ozone
- repolarisation
- panel study
- cardiovascular
- statistics
- epidemiology
- meta-analysis
- longitudinal studies
- time series study
- climate
- bayesian statistics
- volatile organic compounds (VOCs)
- polyaromatic hydrocarbons (PAHs)
- PM10-PM2.5-ultrafine
- environment
- air pollution
- respiratory
- noise
- public health
- risk assessment
- mortality studies
- mathematical models
- exposure monitoring
- pollution
- particulates
- diesel fumes
- aerosols
- diabetes mellitus
Footnotes
Funding This research has been funded wholly or in part by the United States Environmental Protection Agency through STAR (‘Science to Achieve Results’) grant RD 832415 to the University of Rochester. It has not been subjected to the Agency's required peer and policy review and therefore does not necessarily reflect the views of the Agency and no official endorsement should be inferred. This study was also supported in part by a grant from the German Federal Ministry of Education and Research (BMBF) to the German Center for Diabetes Research (DZD e.V.). The KORA research platform (KORA, Cooperative Health Research in the Region of Augsburg) and the MONICA Augsburg studies were initiated and financed by the Helmholtz Zentrum München, German Research Center for Environmental Health (formerly GSF, National Research Center for Environment and Health), which is funded by the German Federal Ministry of Education and Research and by the State of Bavaria.
Competing interests None.
Ethics approval This study was conducted with the approval of Ethics Commission of the Bavarian Chamber of Physicians (‘Bayerische Landesaerztekammer’).
Provenance and peer review Not commissioned; externally peer reviewed.
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