Cardiovascularand Inflammatory Consequences of Short-term Exposure to Air Pollution

  • Getahun Bero Bedada

    Student thesis: Phd

    Abstract

    Much previous work on air pollution epidemiology has studied end-stage outcomessuch as mortality or severe ill health warranting emergency admission, often based onclinical criteria prone to misclassification, and usually without accompanying study ofthe mediating mechanisms. Therefore this work has three specific objectives: firstly, toassess the effects of short-term exposure to particles and gases on acute coronarysyndrome (ACS), by measuring the levels of cardiac troponin T (cTnT), a highlysensitive and specific marker of myocardial damage in patients admitted to hospital forchest pain of myocardial origin; secondly, to investigate the effects of short-termchanges 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 arange of mediators or markers in a putative susceptible population.Two case-crossover studies were conducted to study the association between short-termchanges in air pollutants and ischaemic cardiac events and TIA. Hospital data onadmissions were analysed for actual or suspected ischaemic events and the associatedcTnT levels were obtained. For the TIA project, data on 709 subjects were obtainedfrom five TIA centres clustered around Manchester and Liverpool. In the third project apanel of 35 type 2 diabetes mellitus patients were prospectively followed fortnightly fora total of four visits. At each visit blood was collected to measure markers ofinflammation, coagulation and endothelial function. In all three projects ambient airpollution data were obtained from background monitoring networks and in the thirdproject 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 greater than or equal to 1 ng/ml). Bothparticulate and gaseous pollutants were associated with admission for ACS. The twolargest 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). Associationsbetween pollution and ACS admissions were the strongest for women, those above theage of 65 years and in the cooler season.Project 2: In the Manchester dataset, exposure to nitric oxide (NO) was associated withoccurrence of TIA, while no effect was observed for Liverpool data. Subgroup analysisreveals that CO, NO and NO2 were more strongly related to the occurrence of TIA inparticipants above the age of 65 years and male patients.Project 3: No consistent association was observed between measured biomarkers and airpollutants using exposure data from ambient monitoring stations. In contrast, significantassociation between personal PM2.5 and interleukin-6 (IL-6) was observed. Similarly,personal PM2.5 had large but non-significant positive associations with high sensitivityC-reactive protein and fibrinogen.The results of this study reveal that short-term changes in particulate and gaseouspollution are related to the risk of admission for ACS as demonstrated by a specificmarker hitherto not used for this purpose. It provides limited evidence for an associationbetween changes in ambient NO concentration (which may have been a surrogate foranother pollutant), and the occurrence of TIA, which had not previously been studied asan air pollution outcome, and increase in IL-6, a major pro-inflammatory marker. TheIL-6 response to personal PM2.5 provides evidence in support of the link betweenambient levels of particles/gases and cardiopulmonary morbidity and mortality.
    Date of Award31 Dec 2010
    Original languageEnglish
    Awarding Institution
    • The University of Manchester
    SupervisorRaymond Agius (Supervisor) & Adrian Hirst (Supervisor)

    Keywords

    • Air pollution, acute coronary syndrome, stroke, transient ischaemic attack, inflammatory markers, personal exposure

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