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Airborne particulate matter exposure and urinary albumin excretion: The Multi-Ethnic Study of Atherosclerosis
  1. Marie S. O'Neill (marieo{at}umich.edu)
  1. University of Michigan, United States
    1. Ana V Diez-Roux (adiezrou{at}umich.edu)
    1. University of Michigan, United States
      1. Amy H. Auchincloss (aauchinc{at}umich.edu)
      1. University of Michigan, United States
        1. Tracy G. Franklin (greentl{at}umich.edu)
        1. University of Michigan, United States
          1. David R. Jacobs Jnr (jacobs{at}epi.umn.edu)
          1. University of Minnesota, United States
            1. Brad C Astor (bastor{at}jhsph.edu)
            1. Johns Hopkins University, United States
              1. J. Timothy Dvonch (dvonch{at}umich.edu)
              1. University of Michigan, United States
                1. Joel Kaufman (joelk{at}u.washington.edu)
                1. University of Washington, United States

                  Abstract

                  Objectives: Understanding mechanistic pathways linking airborne particle exposure to cardiovascular health is important for causal inference and setting environmental standards. We evaluated whether urinary albumin excretion, a subclinical marker of microvascular function which predicts cardiovascular events, was associated with ambient particle exposure. Methods: Urinary albumin and creatinine were measured among members of the Multi-Ethnic Study of Atherosclerosis at three visits during 2000-2004. Exposure to PM2.5 and PM10 (ƒÝg/m3) was estimated from ambient monitors for one month, two months and two decades before visit one. We regressed recent and chronic (20 year) PM exposure on urinary albumin/creatinine ratio (UACR) (mg/g) and microalbuminuria at first exam, controlling for age; race/ethnicity; sex; smoking; secondhand smoke exposure; body mass index; and dietary protein (n=3,901). We also evaluated UACR changes and development of microalbuminuria between the first, and second and third visits which took place at 1.5 to 2 year intervals in relation to chronic PM exposure prior to baseline using mixed models. Results: Chronic and recent particle exposures were not associated with current UACR nor microalbuminuria {per 10 ƒÝg/m3 increment of chronic PM10 exposure, mean difference in log UACR = -0.02 (CI: -0.07, 0.03) and relative probability of having microalbuminuria = 0.92 (CI: 0.77, 1.08)} We found only weak evidence that albuminuria was accelerated among those chronically exposed to particles: each 10 ƒÝg/m3 increment in chronic PM10 exposure was associated with a 1.14 relative probability of developing microalbuminuria over 3-4 years, though 95% confidence intervals (CI) included the null (0.96, 1.36). Conclusions: UACR is not a strong mechanistic marker for air pollution¡¦s possible influence on cardiovascular health in this sample.

                  • cardiovascular disease
                  • environmental air pollutants
                  • epidemiology

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