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Refined ambient PM2.5 exposure surrogates and the risk of myocardial infarction

Journal of Exposure Science & Environmental Epidemiology volume 23, pages 573–580 (2013)Cite this article

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Abstract

Using a case-crossover study design and conditional logistic regression, we compared the relative odds of transmural (full-wall) myocardial infarction (MI) calculated using exposure surrogates that account for human activity patterns and the indoor transport of ambient PM2.5 with those calculated using central-site PM2.5 concentrations to estimate exposure to PM2.5 of outdoor origin (exposure to ambient PM2.5). Because variability in human activity and indoor PM2.5 transport contributes exposure error in epidemiologic analyses when central-site concentrations are used as exposure surrogates, we refer to surrogates that account for this variability as “refined” surrogates. As an alternative analysis, we evaluated whether the relative odds of transmural MI associated with increases in ambient PM2.5 is modified by residential air exchange rate (AER), a variable that influences the fraction of ambient PM2.5 that penetrates and persists indoors. Use of refined exposure surrogates did not result in larger health effect estimates (ORs=1.10–1.11 with each interquartile range (IQR) increase), narrower confidence intervals, or better model fits compared with the analysis that used central-site PM2.5. We did observe evidence for heterogeneity in the relative odds of transmural MI with residential AER (effect-modification), with residents of homes with higher AERs having larger ORs than homes in lower AER tertiles. For the level of exposure-estimate refinement considered here, our findings add support to the use of central-site PM2.5 concentrations for epidemiological studies that use similar case-crossover study designs. In such designs, each subject serves as his or her own matched control. Thus, exposure error related to factors that vary spatially or across subjects should only minimally impact effect estimates. These findings also illustrate that variability in factors that influence the fraction of ambient PM2.5 in indoor air (e.g., AER) could possibly bias health effect estimates in study designs for which a spatiotemporal comparison of exposure effects across subjects is conducted.

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Acknowledgements

This research was funded, in part, by the US Environmental Protection Agency (Cooperative Agreement CR-83407201-0), NIEHS-sponsored UMDNJ Center for Environmental Exposures and Disease (NIEHS P30ES005022), and the New Jersey Agricultural Experiment Station. Natasha Hodas was supported by a Graduate Assistance in Areas of National Need Fellowship and an EPA STAR Fellowship. Although this work was reviewed by EPA and approved for publication, it may not necessarily reflect official agency policy.

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Authors and Affiliations

  1. Department of Environmental Sciences, Rutgers University, New Brunswick, New Jersey, USA

    Natasha Hodas & Barbara J Turpin

  2. Environmental Technologies Division, Lawrence Berkeley National Laboratory, Berkeley, California, USA

    Melissa M Lunden

  3. National Exposure Research Laboratory, United States Environmental Protection Agency, Research Triangle Park, North Carolina, USA

    Lisa K Baxter, Halûk Özkaynak & Janet Burke

  4. Department of Biostatistics, University of Medicine and Dentistry of New Jersey, School of Public Health, Piscataway, New Jersey, USA

    Pamela Ohman-Strickland

  5. Department of Public Health Sciences, University of Rochester, School of Medicine and Dentistry, Rochester, New York, USA

    Kelly Thevenet-Morrison & David Q Rich

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Hodas, N., Turpin, B., Lunden, M. et al. Refined ambient PM2.5 exposure surrogates and the risk of myocardial infarction. J Expo Sci Environ Epidemiol 23, 573–580 (2013). https://doi.org/10.1038/jes.2013.24

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