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Acute effects of fine particulate air pollution on ST segment height: A longitudinal study

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...

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Detalles Bibliográficos
Autores principales: He, Fan, Shaffer, Michele L, Rodriguez-Colon, Sol, Bixler, Edward O, Vgontzas, Alexandros N, Williams, Ronald W, Wu, Rongling, Cascio, Wayne E, Liao, Duanping
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989950/
https://www.ncbi.nlm.nih.gov/pubmed/21059260
http://dx.doi.org/10.1186/1476-069X-9-68
Descripción
Sumario: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 (PM(2.5)) 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 PM(2.5 )concentration was obtained by a continuous personal PM(2.5 )monitor. We then calculated, on a 30-minute basis, the corresponding time-of-the-day specific average exposure to PM(2.5 )for each participant. Distributed lag models under a linear mixed-effects models framework were used to assess the regression coefficients between 30-minute PM(2.5 )and 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(2.5 )exposure was 14 (22) μg/m(3). All inferior leads (II, III, and aVF) and two out of three lateral leads (I and V6), showed a significant association between higher PM(2.5 )levels and higher ST-height. Most of the adverse effects occurred within two hours after PM(2.5 )exposure. The multivariable adjusted regression coefficients β (95% CI) of the cumulative effect due to a 10 μg/m(3 )increase in Lag 0-4 PM(2.5 )on ST-I, II, III, aVF and ST-V6 were 0.29 (0.01-0.56) μV, 0.79 (0.20-1.39) μV, 0.52 (0.01-1.05) μV, 0.65 (0.11-1.19) μV, and 0.58 (0.07-1.09) μV, respectively, with all p < 0.05. CONCLUSIONS: Increased PM(2.5 )concentration is associated with immediate increase in ST-segment height in inferior and lateral leads, generally within two hours. Such an acute effect of PM(2.5 )may contribute to increased potential for regional myocardial ischemic injury among healthy individuals.