Delfino, RJ; Gillen, DL; Staimer, N; Arhami, M; Polidori, A; Sioutas, C; Longhurst, J
Rationale: Associations between ST-segment depression and ambient air pollution have been reported primarily in studies using in-clinic ECGs. Few studies use ambulatory ECG monitoring, which allows an assessment of hourly exposure-response relations. Furthermore, little is known about differences in ECG changes in relation to two predominant organic fractions of particulate matter <2.5 μm (PM2.5): primary organic aerosols (POA) emitted directly from combustion sources and secondary consisting partly of photochemical reactions products involving reactive anthropogenic and biogenic volatile organic compounds. We here report on a panel cohort of 38 elderly with coronary artery disease living in four retirement communities in the Los Angeles air basin, where vehicular traffic is the predominant source of POA.
Methods: Ambulatory ECG data were not used the remainder (26 of 64 of subjects) on digoxin, or with conduction abnormalities precluding interpretation of ST changes. Subjects were followed for up to 10 days with 24-hour ambulatory ECG. Eighteen of 38 subjects developed ischemic, defined as planar or down-sloping shift of ≥1.0 mm lasting >60 seconds. We measured hourly air pollutant exposures in the outdoor environment of each retirement community, including criteria pollutant gases, particle number (PN), PM2.5 mass, PM2.5 elemental and organic carbon (EC, OC), and black carbon (BC). Primary and secondary OC (OCpri, SOC) were estimated from total OC representing POA and SOA, respectively. The odds of an ischemic ST-segment event were analyzed with generalized estimating equation models controlling for temperature. Exposures were mean centered by community and seasonal phase of study.
Results: ST depression was positively associated with exposure to PM2.5, BC, EC, OCpri, CO, and NOx, but not SOC, total OC, PN or O3. Associations were found for exposure averages in the last 24 hours through at least 3-day average exposures. ST depression also was associated significantly with the last 4-hr and 8-hr average BC and NOx-NO2. For example, per interquartile increase of 1.02 μg/m^3 BC, the OR for ST depression was 3.26 (95% CI: 1.32, 8.10) for 3-d average BC, and 1.37 (95% CI: 1.01, 1.86) for 8-hr average BC.
Conclusions: Traffic-related air pollution appears to be related to cardiac ischemia as evidenced by ST-segment depression in ambulatory ECG data among a susceptible population. We found no evidence that photochemically-related aerosols or gases as indicated by SOC or ozone, respectively, were associated with ST-segment depression. These findings are coherent with similar findings in this panel for circulating biomarkers of inflammation.
