- Original article
2007: MD, MI & MN in U.S. & Norway: Scientific Paper: Airborne particulate matter exposure and urinary albumin excretion: the Multi-Ethnic Study of Atherosclerosis
- M S O’Neill1,2,
- A V Diez-Roux1,
- A H Auchincloss1,
- T G Franklin1,
- D R Jacobs, Jr3,4,
- B C Astor5,
- J T Dvonch2,
- J Kaufman6
+ Author Affiliations
1 Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI, USA
2 Department of Environmental Health Sciences, University of Michigan School of Public Health, Ann Arbor, MI, USA
3 Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis, MN, USA
4 Department of Nutrition, University of Oslo, Oslo, Norway
5 Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA
6 Department of Environmental and Occupational Health Sciences, University of Washington School of Public Health, Seattle, WA, USA
- Dr Marie S O’Neill, University of Michigan School of Public Health, 6631 SPH Tower, 109 South Observatory, Ann Arbor, MI 48109-2029, USA; email@example.com
- Accepted 9 November 2007
- Published Online First 21 November 2007
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.