<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li W</submitter><funding>U.S. Environmental Protection Agency</funding><funding>NIA NIH HHS</funding><funding>NIEHS NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>NIEHS</funding><funding>Framingham Heart Study</funding><funding>National Institute of General Medical Sciences</funding><funding>NIGMS NIH HHS</funding><pagination>36-43</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6478022</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>171</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Short-term exposure to air pollution has been associated with cardiovascular events, potentially by promoting endothelial cell activation and inflammation. A few large-scale studies have examined the associations and have had mixed results.&lt;h4>Methods&lt;/h4>We included 3820 non-current smoking participants (mean age 56 years, 54% women) from the Framingham Offspring cohort examinations 7 (1998-2001) and 8 (2005-2008), and Third Generation cohort examination 1 (2002-2005), who lived within 50 km of a central monitoring station. We calculated the 1- to 7-day moving averages of fine particulate matter (PM&lt;sub>2.5&lt;/sub>), black carbon (BC), sulfate (SO&lt;sub>4&lt;/sub>&lt;sup>2-&lt;/sup>), nitrogen oxides (NO&lt;sub>x&lt;/sub>), and ozone before examination visits. We used linear mixed effect models for P-selectin, monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule 1, lipoprotein-associated phospholipase A2 activity and mass, and osteoprotegerin that were measured up to twice, and linear regression models for CD40 ligand and interleukin-18 that were measured once, adjusting for demographics, life style and clinical factors, socioeconomic position, time, and meteorology.&lt;h4>Results&lt;/h4>We found negative associations of PM&lt;sub>2.5&lt;/sub> and BC with P-selectin, of ozone with MCP-1, and of SO&lt;sub>4&lt;/sub>&lt;sup>2-&lt;/sup> and NO&lt;sub>x&lt;/sub> with osteoprotegerin. At the 5-day moving average, a 5 µg/m&lt;sup>3&lt;/sup> higher PM&lt;sub>2.5&lt;/sub> was associated with 1.6% (95% CI: - 2.8, - 0.3) lower levels of P-selectin; a 10 ppb higher ozone was associated with 1.7% (95% CI: - 3.2, - 0.1) lower levels of MCP-1; and a 20 ppb higher NO&lt;sub>x&lt;/sub> was associated with 2.0% (95% CI: - 3.6, - 0.4) lower levels of osteoprotegerin.&lt;h4>Conclusions&lt;/h4>We did not find evidence of positive associations between short-term air pollution exposure and endothelial cell activation. On the contrary, short-term exposure to higher levels of ambient pollutants were associated with lower levels of P-selectin, MCP-1, and osteoprotegerin in the Framingham Heart Study.</pubmed_abstract><journal>Environmental research</journal><pubmed_title>Short-term exposure to ambient air pollution and circulating biomarkers of endothelial cell activation: The Framingham Heart Study.</pubmed_title><pmcid>PMC6478022</pmcid><funding_grant_id>R01 AG028321</funding_grant_id><funding_grant_id>P01 ES009825</funding_grant_id><funding_grant_id>P20 GM109036</funding_grant_id><funding_grant_id>1P20GM109036-01A1</funding_grant_id><funding_grant_id>R01 ES029846</funding_grant_id><funding_grant_id>2R01 HL092577</funding_grant_id><funding_grant_id>HHSN268201500001C</funding_grant_id><funding_grant_id>P30 ES000002</funding_grant_id><funding_grant_id>1R01 AG028321</funding_grant_id><funding_grant_id>N01-HC-25195</funding_grant_id><funding_grant_id>R01 HL076784</funding_grant_id><funding_grant_id>P50 HL120163</funding_grant_id><funding_grant_id>R01 HL092577</funding_grant_id><funding_grant_id>1R01 HL128914</funding_grant_id><funding_grant_id>N01 HC025195</funding_grant_id><funding_grant_id>K23 ES026204</funding_grant_id><funding_grant_id>HHSN268201500001I</funding_grant_id><funding_grant_id>1R01 HL64753</funding_grant_id><funding_grant_id>N01HC25195</funding_grant_id><funding_grant_id>R01 HL128914</funding_grant_id><funding_grant_id>P01 ES09825</funding_grant_id><funding_grant_id>RD‐835872‐01</funding_grant_id><pubmed_authors>Schwartz JD</pubmed_authors><pubmed_authors>Vasan RS</pubmed_authors><pubmed_authors>Gold DR</pubmed_authors><pubmed_authors>Mittleman MA</pubmed_authors><pubmed_authors>Li W</pubmed_authors><pubmed_authors>Rice MB</pubmed_authors><pubmed_authors>Ljungman PL</pubmed_authors><pubmed_authors>Dorans KS</pubmed_authors><pubmed_authors>Coull BA</pubmed_authors><pubmed_authors>Koutrakis P</pubmed_authors><pubmed_authors>Keaney JF</pubmed_authors><pubmed_authors>Wilker EH</pubmed_authors><pubmed_authors>Benjamin EJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Short-term exposure to ambient air pollution and circulating biomarkers of endothelial cell activation: The Framingham Heart Study.</name><description>&lt;h4>Background&lt;/h4>Short-term exposure to air pollution has been associated with cardiovascular events, potentially by promoting endothelial cell activation and inflammation. A few large-scale studies have examined the associations and have had mixed results.&lt;h4>Methods&lt;/h4>We included 3820 non-current smoking participants (mean age 56 years, 54% women) from the Framingham Offspring cohort examinations 7 (1998-2001) and 8 (2005-2008), and Third Generation cohort examination 1 (2002-2005), who lived within 50 km of a central monitoring station. We calculated the 1- to 7-day moving averages of fine particulate matter (PM&lt;sub>2.5&lt;/sub>), black carbon (BC), sulfate (SO&lt;sub>4&lt;/sub>&lt;sup>2-&lt;/sup>), nitrogen oxides (NO&lt;sub>x&lt;/sub>), and ozone before examination visits. We used linear mixed effect models for P-selectin, monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule 1, lipoprotein-associated phospholipase A2 activity and mass, and osteoprotegerin that were measured up to twice, and linear regression models for CD40 ligand and interleukin-18 that were measured once, adjusting for demographics, life style and clinical factors, socioeconomic position, time, and meteorology.&lt;h4>Results&lt;/h4>We found negative associations of PM&lt;sub>2.5&lt;/sub> and BC with P-selectin, of ozone with MCP-1, and of SO&lt;sub>4&lt;/sub>&lt;sup>2-&lt;/sup> and NO&lt;sub>x&lt;/sub> with osteoprotegerin. At the 5-day moving average, a 5 µg/m&lt;sup>3&lt;/sup> higher PM&lt;sub>2.5&lt;/sub> was associated with 1.6% (95% CI: - 2.8, - 0.3) lower levels of P-selectin; a 10 ppb higher ozone was associated with 1.7% (95% CI: - 3.2, - 0.1) lower levels of MCP-1; and a 20 ppb higher NO&lt;sub>x&lt;/sub> was associated with 2.0% (95% CI: - 3.6, - 0.4) lower levels of osteoprotegerin.&lt;h4>Conclusions&lt;/h4>We did not find evidence of positive associations between short-term air pollution exposure and endothelial cell activation. On the contrary, short-term exposure to higher levels of ambient pollutants were associated with lower levels of P-selectin, MCP-1, and osteoprotegerin in the Framingham Heart Study.</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Apr</publication><modification>2024-02-14T19:51:02.274Z</modification><creation>2020-05-22T14:49:49Z</creation></dates><accession>S-EPMC6478022</accession><cross_references><pubmed>30654247</pubmed><doi>10.1016/j.envres.2018.10.027</doi></cross_references></HashMap>