TY - JOUR
T1 - Short-term exposure to ambient air pollution and circulating biomarkers of endothelial cell activation
T2 - The Framingham Heart Study
AU - Li, Wenyuan
AU - Dorans, Kirsten S.
AU - Wilker, Elissa H.
AU - Rice, Mary B.
AU - Ljungman, Petter L.
AU - Schwartz, Joel D.
AU - Coull, Brent A.
AU - Koutrakis, Petros
AU - Gold, Diane R.
AU - Keaney, John F.
AU - Vasan, Ramachandran S.
AU - Benjamin, Emelia J.
AU - Mittleman, Murray A.
N1 - Funding Information:
This publication was made possible by U.S. Environmental Protection Agency (USEPA) Grant ( RD‐835872‐01 ) through the Harvard University USEPA sponsored Air, Climate & Environment (ACE) Centre. The contents of the study are solely the responsibility of the grantee and do not necessarily represent the official views of the USEPA. Further, USEPA does not endorse the purchase of any commercial products or services mentioned in the publication. Funding of the inflammation markers was through 1R01 HL64753 , R01 HL076784 , 1R01 AG028321 , 1R01 HL128914 , 2R01 HL092577 , and 1P50 HL120163. Funding of the Framingham Heart Study was via HHSN268201500001I and N01-HC-25195 . This work was also supported by the National Institute of Environmental Health Sciences ( NIEHS ) Grants P01 ES09825 and P30 ES000002 , and the National Institute of General Medical Sciences Grant 1P20GM109036-01A1 .
Publisher Copyright:
© 2018 Elsevier Inc.
PY - 2019/4
Y1 - 2019/4
N2 - Background: 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. Methods: 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 (PM2.5), black carbon (BC), sulfate (SO42-), nitrogen oxides (NOx), 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. Results: We found negative associations of PM2.5 and BC with P-selectin, of ozone with MCP-1, and of SO42- and NOx with osteoprotegerin. At the 5-day moving average, a 5 µg/m3 higher PM2.5 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 NOx was associated with 2.0% (95% CI: − 3.6, − 0.4) lower levels of osteoprotegerin. Conclusions: 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.
AB - Background: 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. Methods: 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 (PM2.5), black carbon (BC), sulfate (SO42-), nitrogen oxides (NOx), 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. Results: We found negative associations of PM2.5 and BC with P-selectin, of ozone with MCP-1, and of SO42- and NOx with osteoprotegerin. At the 5-day moving average, a 5 µg/m3 higher PM2.5 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 NOx was associated with 2.0% (95% CI: − 3.6, − 0.4) lower levels of osteoprotegerin. Conclusions: 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.
KW - Air pollution
KW - Biomarker
KW - Endothelial dysfunction
KW - Environment
KW - Epidemiology
KW - Inflammation
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U2 - 10.1016/j.envres.2018.10.027
DO - 10.1016/j.envres.2018.10.027
M3 - Article
C2 - 30654247
AN - SCOPUS:85059864547
VL - 171
SP - 36
EP - 43
JO - Environmental Research
JF - Environmental Research
SN - 0013-9351
ER -