Literature DB >> 20407379

Long-term exposure to air pollution and vascular damage in young adults.

Virissa Lenters1, Cuno S Uiterwaal, Rob Beelen, Michiel L Bots, Paul Fischer, Bert Brunekreef, Gerard Hoek.   

Abstract

BACKGROUND: Long-term exposure to ambient air pollution has recently been linked to atherosclerosis and cardiovascular events. There are, however, very limited data in healthy young people. We examined the association between air pollutants and indicators of vascular damage in a cohort of young adults.
METHODS: We used data from the Atherosclerosis Risk in Young Adults study. We estimated exposure to nitrogen dioxide (NO2), particulate matter less than 2.5 microm in aerodynamic diameter (PM2.5), black smoke, sulfur dioxide (SO2), and various traffic indicators for participants' 2000 home addresses. Exposure for the year 2000 was estimated by land-use regression models incorporating regional background annual air pollution levels, land-use variables, population densities, and traffic intensities on nearby roads. Outcomes were common carotid artery intima-media thickness (n = 745), aortic pulse wave velocity (n = 524), and augmentation index (n = 729).
RESULTS: Exposure contrasts were substantial for NO2, SO2, and black smoke (5th-95th percentiles = 19.7 to 44.9, 2.5 to 5.2, and 8.6 to 19.4 microg/m3, respectively) and smaller for PM2.5 (16.5 to 19.9 microg/m3). The variability of carotid artery intima-media thickness was less than for pulse wave velocity and especially augmentation index (5-95th percentiles = 0.42 to 0.58 mm, 4.9 to 7.4 m/s and -12.3% to 27.3%, respectively). No associations were found between any of the pollutants or traffic indicators and carotid artery intima-media thickness, although PM2.5 effect estimates were in line with previous studies. We observed a 4.1% (95% confidence interval = 0.1% to 8.0%) increase in pulse wave velocity and a 37.6% (2.2% to 72.9%) increase in augmentation index associated with a 25 microg/m3 increase in NO2, and a 5.3% (0.1% to 10.4%) increase in pulse wave velocity with a 5 microg/m3 increase in SO2. PM2.5 and black smoke were not associated with either of these 2 outcomes.
CONCLUSIONS: Air pollution may accelerate arterial-wall stiffening in young adults. Small outcome variability and lack of residential mobility data may have limited the power to detect an effect on intima-media thickness.

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Year:  2010        PMID: 20407379     DOI: 10.1097/EDE.0b013e3181dec3a7

Source DB:  PubMed          Journal:  Epidemiology        ISSN: 1044-3983            Impact factor:   4.822


  43 in total

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2.  Development of outcome-based, multipollutant mobile source indicators.

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4.  Comparison of ultrasound-measured properties of the common carotid artery to tobacco smoke exposure in a cohort of Indonesian patients.

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Journal:  World J Emerg Med       Date:  2017

5.  Differential effects of inhalation exposure to PM2.5 on hypothalamic monoamines and corticotrophin releasing hormone in lean and obese rats.

Authors:  Priya Balasubramanian; Madhu P Sirivelu; Kathryn A Weiss; James G Wagner; Jack R Harkema; Masako Morishita; P S Mohankumar; Sheba M J Mohankumar
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6.  Five-year exposure to PM2.5 and ozone and subclinical atherosclerosis in late midlife women: The Study of Women's Health Across the Nation.

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7.  Residential Exposure to PM2.5 and Ozone and Progression of Subclinical Atherosclerosis Among Women Transitioning Through Menopause: The Study of Women's Health Across the Nation.

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8.  The value of using seasonality and meteorological variables to model intra-urban PM2.5 variation.

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9.  Prospective study of particulate air pollution exposures, subclinical atherosclerosis, and clinical cardiovascular disease: The Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air).

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10.  Changes in traffic exposure and the risk of incident myocardial infarction and all-cause mortality.

Authors:  Jaime E Hart; Eric B Rimm; Kathryn M Rexrode; Francine Laden
Journal:  Epidemiology       Date:  2013-09       Impact factor: 4.822

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