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Spatiotemporally‐Resolved Air Exchange Rate as a Modifier of Acute Air Pollution‐Related Morbidity in AtlantaMorbidity in Atlanta
Citation:
Sarnat, J., S. Sarnat, W. Flanders, H. Chang, J. Mulholland, L. Baxter, V. Isakov, AND H. Ozkaynak. Spatiotemporally‐Resolved Air Exchange Rate as a Modifier of Acute Air Pollution‐Related Morbidity in AtlantaMorbidity in Atlanta. Journal of Exposure Science and Environmental Epidemiology . Nature Publishing Group, London, Uk, 23(6):606-615, (2013).
Impact/Purpose:
The National Exposure Research Laboratory′s (NERL′s) Human Exposure and Atmospheric Sciences Division (HEASD) conducts research in support of EPA′s mission to protect human health and the environment. HEASD′s research program supports Goal 1 (Clean Air) and Goal 4 (Healthy People) of EPA′s strategic plan. More specifically, our division conducts research to characterize the movement of pollutants from the source to contact with humans. Our multidisciplinary research program produces Methods, Measurements, and Models to identify relationships between and characterize processes that link source emissions, environmental concentrations, human exposures, and target-tissue dose. The impact of these tools is improved regulatory programs and policies for EPA.
Description:
Epidemiological studies frequently use central site concentrations as surrogates of exposure to air pollutants. Variability in air pollutant infiltration due to differential air exchange rates (AERs) is potentially a major factor affecting the relationship between central site concentrations and actual exposure, and may thus influence observed health risk estimates. In this analysis, we examined AER as an effect modifier of associations between several urban air pollutants and corresponding emergency department (ED) visits for asthma and wheeze during a four-year study period (January 1999- December 2002) for a 186 ZIP code area in metro Atlanta. We found positive associations for the interaction between AER and pollution on asthma ED visits for both CO and NOx indicating significant or near-significant effect modification by AER on the pollutant risk ratio estimates. In contrast, the interaction term between PM2.5 and AER on asthma ED visits was negative and significant. However, alternative distributional tertile analyses showed PM2.5 and AER epidemiological model results to be similar to those found for NOx and CO (namely, increasing RRs with increasing AERs when ambient PM2.5 concentrations were below the highest tertile of their distribution). Despite the fact that O3 was a strong independent predictor of asthma ED visits in our main analysis, we found no O3 - AER effect modification. To our knowledge, our findings for CO, NOx, and PM2.5, are the first to provide an indication of short-term (i.e., daily) effect modification of multiple air pollution-related risk associations with daily changes in AER. While limited to one outcome category in a single large urban locale, the findings suggest that the use of relatively simple and easy-to-derive AER surrogates may reflect intraurban differences in short-term exposures to pollutants of ambient origin.
URLs/Downloads:
AER EPI FINAL FINAL JESEE MAIN TEXT_SUBMITTED_SECOND.REV1_CLEAN.PDF (PDF, NA pp, 892.626 KB, about PDF)Journal of Exposure Science & Environmental Epidemiology
