TY - JOUR
T1 - Acute effects of fine particulate air pollution on ST segment height
T2 - A longitudinal study
AU - He, Fan
AU - Shaffer, Michele L.
AU - Rodriguez-Colon, Sol
AU - Bixler, Edward O.
AU - Vgontzas, Alexandros N.
AU - Williams, Ronald W.
AU - Wu, Rongling
AU - Cascio, Wayne E.
AU - Liao, Duanping
N1 - Funding Information:
This study is funded by NIEHS (1 R01 ES014010). The authors wish to thank Dr. David Mortara of Mortara Instrument, Inc. for providing the SuperECG software for the analysis of the electrocardiographic data. The research described in this article by the United States Environmental Protection Agency has not been subjected to Agency review and, therefore, does not necessarily reflect the review of the Agency and no official endorsement should be inferred.
PY - 2010
Y1 - 2010
N2 - Background. The mechanisms for the relationship between particulate air pollution and cardiac disease are not fully understood. Air pollution-induced myocardial ischemia is one of the potentially important mechanisms. Methods. We investigate the acute effects and the time course of fine particulate pollution (PM2.5) on myocardium ischemic injury as assessed by ST-segment height in a community-based sample of 106 healthy non-smokers. Twenty-four hour beat-to-beat electrocardiogram (ECG) data were obtained using a high resolution 12-lead Holter ECG system. After visually identifying and removing all the artifacts and arrhythmic beats, we calculated beat-to-beat ST-height from ten leads (inferior leads II, III, and aVF; anterior leads V3 and V4; septal leads V1 and V2; lateral leads I, V5, and V6,). Individual-level 24-hour real-time PM2.5concentration was obtained by a continuous personal PM 2.5monitor. We then calculated, on a 30-minute basis, the corresponding time-of-the-day specific average exposure to PM2.5for each participant. Distributed lag models under a linear mixed-effects models framework were used to assess the regression coefficients between 30-minute PM2.5and ST-height measures from each lead; i.e., one lag indicates a 30-minute separation between the exposure and outcome. Results. The mean (SD) age was 56 (7.6) years, with 41% male and 74% white. The mean (SD) PM 2.5exposure was 14 (22) g/m3. All inferior leads (II, III, and aVF) and two out of three lateral leads (I and V6), showed a significant association between higher PM2.5levels and higher ST-height. Most of the adverse effects occurred within two hours after PM2.5exposure. The multivariable adjusted regression coefficients (95% CI) of the cumulative effect due to a 10 g/m3 increase in Lag 0-4 PM2.5on ST-I, II, III, aVF and ST-V6 were 0.29 (0.01-0.56) V, 0.79 (0.20-1.39) V, 0.52 (0.01-1.05) V, 0.65 (0.11-1.19) V, and 0.58 (0.07-1.09) V, respectively, with all p < 0.05. Conclusions. Increased PM2.5concentration is associated with immediate increase in ST-segment height in inferior and lateral leads, generally within two hours. Such an acute effect of PM2.5may contribute to increased potential for regional myocardial ischemic injury among healthy individuals.
AB - Background. The mechanisms for the relationship between particulate air pollution and cardiac disease are not fully understood. Air pollution-induced myocardial ischemia is one of the potentially important mechanisms. Methods. We investigate the acute effects and the time course of fine particulate pollution (PM2.5) on myocardium ischemic injury as assessed by ST-segment height in a community-based sample of 106 healthy non-smokers. Twenty-four hour beat-to-beat electrocardiogram (ECG) data were obtained using a high resolution 12-lead Holter ECG system. After visually identifying and removing all the artifacts and arrhythmic beats, we calculated beat-to-beat ST-height from ten leads (inferior leads II, III, and aVF; anterior leads V3 and V4; septal leads V1 and V2; lateral leads I, V5, and V6,). Individual-level 24-hour real-time PM2.5concentration was obtained by a continuous personal PM 2.5monitor. We then calculated, on a 30-minute basis, the corresponding time-of-the-day specific average exposure to PM2.5for each participant. Distributed lag models under a linear mixed-effects models framework were used to assess the regression coefficients between 30-minute PM2.5and ST-height measures from each lead; i.e., one lag indicates a 30-minute separation between the exposure and outcome. Results. The mean (SD) age was 56 (7.6) years, with 41% male and 74% white. The mean (SD) PM 2.5exposure was 14 (22) g/m3. All inferior leads (II, III, and aVF) and two out of three lateral leads (I and V6), showed a significant association between higher PM2.5levels and higher ST-height. Most of the adverse effects occurred within two hours after PM2.5exposure. The multivariable adjusted regression coefficients (95% CI) of the cumulative effect due to a 10 g/m3 increase in Lag 0-4 PM2.5on ST-I, II, III, aVF and ST-V6 were 0.29 (0.01-0.56) V, 0.79 (0.20-1.39) V, 0.52 (0.01-1.05) V, 0.65 (0.11-1.19) V, and 0.58 (0.07-1.09) V, respectively, with all p < 0.05. Conclusions. Increased PM2.5concentration is associated with immediate increase in ST-segment height in inferior and lateral leads, generally within two hours. Such an acute effect of PM2.5may contribute to increased potential for regional myocardial ischemic injury among healthy individuals.
UR - https://www.scopus.com/pages/publications/78049474731
UR - https://www.scopus.com/inward/citedby.url?scp=78049474731&partnerID=8YFLogxK
U2 - 10.1186/1476-069X-9-68
DO - 10.1186/1476-069X-9-68
M3 - Article
C2 - 21059260
AN - SCOPUS:78049474731
SN - 1476-069X
VL - 9
JO - Environmental Health: A Global Access Science Source
JF - Environmental Health: A Global Access Science Source
IS - 1
M1 - 68
ER -