Fine particulate air pollution and the progression of carotid intima-medial thickness: a prospective cohort study from the multi-ethnic study of atherosclerosis and air pollution

• Published in: PLoS medicine 2013-04, Vol.10 (4), p.e1001430
• Main Authors: Adar, Sara D, Sheppard, Lianne, Vedal, Sverre, Polak, Joseph F, Sampson, Paul D, Diez Roux, Ana V, Budoff, Matthew, Jacobs, Jr, David R, Barr, R Graham, Watson, Karol, Kaufman, Joel D
• Format: Article
• Language: English
• Subjects: Aged; Air pollution; Air Pollution - adverse effects; Air Pollution - analysis; Atherosclerosis; Atherosclerosis - etiology; Atherosclerosis - pathology; Blood pressure; Cardiovascular disease; Carotid artery; Carotid Intima-Media Thickness; Cohort Studies; Cross-Sectional Studies; Development and progression; Disease Progression; Earth Sciences; Economic indicators; Environmental Exposure - adverse effects; Environmental Exposure - analysis; Female; Health aspects; Heart; Human beings; Humans; Hypotheses; Influence on nature; Male; Medicine; Metropolitan areas; Middle Aged; Outdoor air quality; Particles; Particulate Matter - adverse effects; Particulate Matter - analysis; Physiological aspects; Studies; Time Factors; Ultrasonic imaging
• ISSN: 1549-1676; 1549-1277; 1549-1676
• DOI: 10.1371/journal.pmed.1001430

Fine particulate matter (PM2.5) has been linked to cardiovascular disease, possibly via accelerated atherosclerosis. We examined associations between the progression of the intima-medial thickness (IMT) of the common carotid artery, as an indicator of atherosclerosis, and long-term PM2.5 concentrations in participants from the Multi-Ethnic Study of Atherosclerosis (MESA). MESA, a prospective cohort study, enrolled 6,814 participants at the baseline exam (2000-2002), with 5,660 (83%) of those participants completing two ultrasound examinations between 2000 and 2005 (mean follow-up: 2.5 years). PM2.5 was estimated over the year preceding baseline and between ultrasounds using a spatio-temporal model. Cross-sectional and longitudinal associations were examined using mixed models adjusted for confounders including age, sex, race/ethnicity, smoking, and socio-economic indicators. Among 5,362 participants (5% of participants had missing data) with a mean annual progression of 14 µm/y, 2.5 µg/m(3) higher levels of residential PM2.5 during the follow-up period were associated with 5.0 µm/y (95% CI 2.6 to 7.4 µm/y) greater IMT progressions among persons in the same metropolitan area. Although significant associations were not found with IMT progression without adjustment for metropolitan area (0.4 µm/y [95% CI -0.4 to 1.2 µm/y] per 2.5 µg/m(3)), all of the six areas showed positive associations. Greater reductions in PM2.5 over follow-up for a fixed baseline PM2.5 were also associated with slowed IMT progression (-2.8 µm/y [95% CI -1.6 to -3.9 µm/y] per 1 µg/m(3) reduction). Study limitations include the use of a surrogate measure of atherosclerosis, some loss to follow-up, and the lack of estimates for air pollution concentrations prior to 1999. This early analysis from MESA suggests that higher long-term PM2.5 concentrations are associated with increased IMT progression and that greater reductions in PM2.5 are related to slower IMT progression. These findings, even over a relatively short follow-up period, add to the limited literature on air pollution and the progression of atherosclerotic processes in humans. If confirmed by future analyses of the full 10 years of follow-up in this cohort, these findings will help to explain associations between long-term PM2.5 concentrations and clinical cardiovascular events.