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Airborne particulate matter exposure and urinary albumin excretion: the Multi-Ethnic Study of Atherosclerosis
  1. M S O’Neill1,2,
  2. A V Diez-Roux1,
  3. A H Auchincloss1,
  4. T G Franklin1,
  5. D R Jacobs, Jr3,4,
  6. B C Astor5,
  7. J T Dvonch2,
  8. J Kaufman6
  1. 1
    Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI, USA
  2. 2
    Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, MI, USA
  3. 3
    Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis, MN, USA
  4. 4
    Department of Nutrition, University of Oslo, Oslo, Norway
  5. 5
    Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA
  6. 6
    Department of Environmental and Occupational Health Sciences, University of Washington School of Public Health, Seattle, WA, USA
  1. Dr Marie S O’Neill, University of Michigan School of Public Health, 6631 SPH Tower, 109 South Observatory, Ann Arbor, MI 48109-2029, USA; marieo{at}umich.edu

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 (μg/m3) was estimated from ambient monitors for 1 month, 2 months and two decades before visit one. We regressed recent and chronic (20 year) particulate matter (PM) exposure on urinary albumin/creatinine ratio (UACR, mg/g) and microalbuminuria at first examination, controlling for age, race/ethnicity, sex, smoking, second-hand smoke exposure, body mass index and dietary protein (n = 3901). 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 or microalbuminuria (per 10 μg/m3 increment of chronic PM10 exposure, mean difference in log UACR = −0.02 (95% CI −0.07 to 0.03) and relative probability of having microalbuminuria = 0.92 (95% CI 0.77 to 1.08)) We found only weak evidence that albuminuria was accelerated among those chronically exposed to particles: each 10 μg/m3 increment in chronic PM10 exposure was associated with a 1.14 relative probability of developing microalbuminuria over 3–4 years, although 95% confidence intervals included the null (95% CI 0.96 to 1.36).

Conclusions: UACR is not a strong mechanistic marker for the possible influence of air pollution on cardiovascular health in this sample.

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Footnotes

  • Competing interests: None.

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