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Title: Airborne particulate matter exposure and urinary albumin excretion: The Multi-Ethnic Study of Atherosclerosis
Authors: O'Neill, MS
Diez Roux, AV
Auchincloss, AH
Green Franklin, TL
Jacobs Jr., DR
Astor, BC
Dvonch, JT
Kaufman, JD
Issue Date: 2007
Publisher: Occupational and Environmental Medicine
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 (g/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 g/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 g/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.
Appears in Collections:Environmental Health Sciences, Department of (SPH)
Epidemiology, Department of (SPH)

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