TY - JOUR
T1 - Long-term exposure to airborne particles and arterial stiffness
T2 - The multi-ethnic study of atherosclerosis (MESA)
AU - O'Neill, Marie S.
AU - Diez-Roux, Ana V.
AU - Auchincloss, Amy H.
AU - Shen, Mingwu
AU - Lima, João A.
AU - Polak, Joseph F.
AU - Graham Barr, R.
AU - Kaufman, Joel
AU - Jacobs, David R.
PY - 2011/6
Y1 - 2011/6
N2 - Background: Increased arterial stiffness could represent an intermediate subclinical outcome in the mechanistic pathway underlying associations between average long-term pollution exposure and cardiovascular events. Objective: We hypothesized that 20 years of exposure to particulate matter (PM) ≤ 2.5 and 10 μm in aerodynamic diameter (PM2.5 and PM10, respectively) would be positively associated with arterial stiffness in 3,996 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) who were seen at six U.S. study sites. Methods: We assigned pollution exposure during two decades preceding a clinical exam (2000-2002) using observed PM10 from monitors nearest participants' residences and PM10 and PM2.5 imputed from a space-time model. We examined three log-transformed arterial stiffness outcome measures: Young's modulus (YM) from carotid artery ultrasound and large (C1) and small (C2) artery vessel compliance from the radial artery pulse wave. All associations are expressed per 10 μg/m3 increment in PM and were adjusted for weather, age, sex, race, glucose, triglycerides, diabetes, waist:hip ratio, seated mean arterial pressure, smoking status, pack-years, cigarettes per day, environmental tobacco smoke, and physical activity. C1 and C2 models were further adjusted for heart rate, weight, and height. Results: Long-term average particle exposure was not associated with greater arterial stiffness measured by YM, C1, or C2, and the few associations observed were not robust across metrics and adjustment schemes. Conclusions: Long-term particle mass exposure did not appear to be associated with greater arterial stiffness in this study sample.
AB - Background: Increased arterial stiffness could represent an intermediate subclinical outcome in the mechanistic pathway underlying associations between average long-term pollution exposure and cardiovascular events. Objective: We hypothesized that 20 years of exposure to particulate matter (PM) ≤ 2.5 and 10 μm in aerodynamic diameter (PM2.5 and PM10, respectively) would be positively associated with arterial stiffness in 3,996 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) who were seen at six U.S. study sites. Methods: We assigned pollution exposure during two decades preceding a clinical exam (2000-2002) using observed PM10 from monitors nearest participants' residences and PM10 and PM2.5 imputed from a space-time model. We examined three log-transformed arterial stiffness outcome measures: Young's modulus (YM) from carotid artery ultrasound and large (C1) and small (C2) artery vessel compliance from the radial artery pulse wave. All associations are expressed per 10 μg/m3 increment in PM and were adjusted for weather, age, sex, race, glucose, triglycerides, diabetes, waist:hip ratio, seated mean arterial pressure, smoking status, pack-years, cigarettes per day, environmental tobacco smoke, and physical activity. C1 and C2 models were further adjusted for heart rate, weight, and height. Results: Long-term average particle exposure was not associated with greater arterial stiffness measured by YM, C1, or C2, and the few associations observed were not robust across metrics and adjustment schemes. Conclusions: Long-term particle mass exposure did not appear to be associated with greater arterial stiffness in this study sample.
KW - Air pollution
KW - Arterial stiffness
KW - Environmental air pollutants
KW - Epidemiology
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U2 - 10.1289/ehp.0901524
DO - 10.1289/ehp.0901524
M3 - Article
C2 - 21245016
AN - SCOPUS:79958794008
SN - 0091-6765
VL - 119
SP - 844
EP - 851
JO - Environmental Health Perspectives
JF - Environmental Health Perspectives
IS - 6
ER -