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Title: Cardiovascular & inflammatory consequences of short-term exposure to air pollution
Author: Bero Bedada, Getahun
ISNI:       0000 0004 2691 3588
Awarding Body: University of Manchester
Current Institution: University of Manchester
Date of Award: 2010
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Much previous work on air pollution epidemiology has studied end-stage outcomes such as mortality or severe ill health warranting emergency admission, often based on clinical criteria prone to misclassification, and usually without accompanying study of the mediating mechanisms. Therefore this work has three specific objectives: firstly, to assess the effects of short-term exposure to particles and gases on acute coronary syndrome (ACS), by measuring the levels of cardiac troponin T (cTnT), a highly sensitive and specific marker of myocardial damage in patients admitted to hospital for chest pain of myocardial origin; secondly, to investigate the effects of short-term changes in ambient air pollution on the occurrence of transient ischaemic attacks (TIA); finally, to investigate the effects of ambient and personal exposure to air pollutants on a range of mediators or markers in a putative susceptible population. Two case-crossover studies were conducted to study the association between short-term changes in air pollutants and ischaemic cardiac events and TIA. Hospital data on admissions were analysed for actual or suspected ischaemic events and the associated cTnT levels were obtained. For the TIA project, data on 709 subjects were obtained from five TIA centres clustered around Manchester and Liverpool. In the third project a panel of 35 type 2 diabetes mellitus patients were prospectively followed fortnightly for a total of four visits. At each visit blood was collected to measure markers of inflammation, coagulation and endothelial function. In all three projects ambient air pollution data were obtained from background monitoring networks and in the third project personal exposure to PM2.5 was measured. Project 1: Of 28,622 admissions, 17.5% were ACS with myocyte necrosis (cTnT 0.03-1ng/ml) and 1004 (3.5%) were cases of myocardial infarction (cTnT ≥ 1 ng/ml). Both particulate and gaseous pollutants were associated with admission for ACS. The two largest effects per interquartile increase of exposure were observed with PM10 with ORof 1.14 (95% CI: 1.05-1.24) and with SO2, OR 1.11 (95% CI: 1.00-1.23). Associations between pollution and ACS admissions were the strongest for women, those above the age of 65 years and in the cooler season. Project 2: In the Manchester dataset, exposure to nitric oxide (NO) was associated with occurrence of TIA, while no effect was observed for Liverpool data. Subgroup analysis reveals that CO, NO and NO2 were more strongly related to the occurrence of TIA in participants above the age of 65 years and male patients. Project 3: No consistent association was observed between measured biomarkers and air pollutants using exposure data from ambient monitoring stations. In contrast, significant association between personal PM2.5 and interleukin-6 (IL-6) was observed. Similarly, personal PM2.5 had large but non-significant positive associations with high sensitivity C-reactive protein and fibrinogen. The results of this study reveal that short-term changes in particulate and gaseous pollution are related to the risk of admission for ACS as demonstrated by a specific marker hitherto not used for this purpose. It provides limited evidence for an association between changes in ambient NO concentration (which may have been a surrogate for another pollutant), and the occurrence of TIA, which had not previously been studied as an air pollution outcome, and increase in IL-6, a major pro-inflammatory marker. The IL-6 response to personal PM2.5 provides evidence in support of the link between ambient levels of particles/gases and cardiopulmonary morbidity and mortality.
Supervisor: Agius, Raymond ; Hirst, Adrian Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available
Keywords: Air pollution ; acute coronary syndrome ; stroke ; transient ischaemic attack ; inflammatory markers ; personal exposure