{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T11:26:57Z","timestamp":1790508417837,"version":"4.1.0"},"reference-count":52,"publisher":"American Chemical Society (ACS)","issue":"4","license":[{"start":{"date-parts":[[2017,12,29]],"date-time":"2017-12-29T00:00:00Z","timestamp":1514505600000},"content-version":"vor","delay-in-days":3627,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2008,4,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Blood pressure (BP) may be implicated in associations observed between ambient particulate matter and cardiovascular morbidity and mortality. This study examined cross-sectional associations between short-term ambient fine particles (particulate matter \u2264 2.5 \u03bcm in aerodynamic diameter; PM2.5) and BP: systolic (SBP), diastolic (DBP), mean arterial (MAP), and pulse pressure (PP).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>The study sample included 5,112 persons 45\u201384 years of age, free of cardiovascular disease at the Multi-Ethnic Study of Atherosclerosis baseline examination (2000\u20132002). Data from U.S. Environmental Protection Agency monitors were used to estimate ambient PM2.5 exposures for the preceding 1, 2, 7, 30, and 60 days. Roadway data were used to estimate local exposures to traffic-related particles.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Results from linear regression found PP and SBP positively associated with PM2.5. For example, a 10-\u03bcg\/m3 increase in PM2.5 30-day mean was associated with 1.12 mmHg higher pulse pressure [95% confidence interval (CI), 0.28\u20131.97] and 0.99 mmHg higher systolic BP (95% CI, \u20130.15 to 2.13), adjusted for age, sex, race\/ethnicity, income, education, body mass index, diabetes, cigarette smoking and environmental tobacco smoke, alcohol use, physical activity, medications, atmospheric pressure, and temperature. Results were much weaker and not statistically significant for MAP and DBP. Although traffic-related variables were not themselves associated with BP, the association between PM2.5 and BP was stronger in the presence of higher traffic exposure.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Higher SBP and PP were associated with ambient levels of PM2.5 and the association was stronger in the presence of roadway traffic, suggesting that impairment of blood pressure regulation may play a role in response to air pollution.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1289\/ehp.10899","type":"journal-article","created":{"date-parts":[[2008,1,22]],"date-time":"2008-01-22T16:10:36Z","timestamp":1201018236000},"page":"486-491","source":"Crossref","is-referenced-by-count":230,"title":["Associations between Recent Exposure to Ambient Fine Particulate Matter and Blood Pressure in the Multi-Ethnic Study of Atherosclerosis (MESA)"],"prefix":"10.1021","volume":"116","author":[{"given":"Amy H.","family":"Auchincloss","sequence":"first","affiliation":[{"name":"Department of Epidemiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ana V.","family":"Diez Roux","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. Timothy","family":"Dvonch","sequence":"additional","affiliation":[{"name":"Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick L.","family":"Brown","sequence":"additional","affiliation":[{"name":"Department of Atmospheric Sciences, School of Engineering, University of Michigan, Ann Arbor, Michigan, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. Graham","family":"Barr","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Epidemiology, Columbia University Medical Center, New York, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martha L.","family":"Daviglus","sequence":"additional","affiliation":[{"name":"Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr.","given":"David C.","family":"Goff","sequence":"additional","affiliation":[{"name":"Department of Public Health Sciences, School of Medicine, Wake Forest University, Winston-Salem, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joel D.","family":"Kaufman","sequence":"additional","affiliation":[{"name":"Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, Washington, 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