4.7 Article

Short-term exposure to ambient air pollution and circulating biomarkers of endothelial cell activation: The Framingham Heart Study

Journal

ENVIRONMENTAL RESEARCH
Volume 171, Issue -, Pages 36-43

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.envres.2018.10.027

Keywords

Air pollution; Endothelial dysfunction; Inflammation; Biomarker; Environment; Epidemiology

Funding

  1. U.S. Environmental Protection Agency (USEPA) Grant through the Harvard University USEPA [RD-835872-01]
  2. National Institute of Environmental Health Sciences (NIEHS) [P01 ES09825, P30 ES000002]
  3. National Institute of General Medical Sciences [1P20GM109036-01A1]
  4. [1R01 HL64753]
  5. [R01 HL076784]
  6. [1R01 AG028321]
  7. [1R01 HL128914]
  8. [2R01 HL092577]
  9. [1P50 HL120163]
  10. [HHSN268201500001I]
  11. [N01-HC-25195]

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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 mu g/m(3) 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.

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