Studies have found associations between PM2.5 and cardiovascular events. The role of different components of PM2.5 is not well understood. We used linear mixed-effects models with the adaptive LASSO penalty to select PM2.5 species and source(s), separately, that may be associated with markers of inflammation and endothelial dysfunction, with adjustment for age, obesity, smoking, statin use, diabetes mellitus, temperature, and season as fixed effects in a large longitudinal cohort of elderly men. We also analyzed these associations with source apportionment models and examined genetic pathway–air pollution interactions within three relevant pathways (oxidative stress, metal processing, and endothelial function). We found that independent of PM2.5 mass vanadium (V) was associated with intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). An IQR increase (3.2 ng/m3) in 2-day moving average V was associated with a 2.5% (95% CI: 1.2–3.8%) change in ICAM-1 and a 3.9% (95% CI: 2.2–5.7%) change in VCAM-1, respectively. In addition, an oil combustion source rich in V was linked to these adhesion molecules. People with higher allelic risk profiles related to oxidative stress may have greater associations (P-value of interaction=0.11). Our findings suggest that particles derived from oil combustion may be associated with inflammation and endothelial dysfunction, and it is likely that oxidative stress plays a role in the associations.
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This study was supported by the National Institute of Environmental Health Sciences Grants ES00002 and ES015172-01, and the US Environmental Protection Agency Grant RD-834798-01. Its contents are solely the responsibility of the grantee and do not necessarily represent the official views of the funders. Furthermore, the funders do not endorse the purchase of any commercial products or services mentioned in the publication. Dr. David Sparrow was supported by a VA Research Career Scientist award. The VA Normative Aging Study is supported by the Cooperative Studies Program/Epidemiology Research and Information Centers of the US Department of Veterans Affairs and is a component of the Massachusetts Veterans Epidemiology Research and Information Center, Boston, Massachusetts.
The authors declare no conflict of interest.
Supplementary Information accompanies the paper on the Journal of Exposure Science and Environmental Epidemiology website
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Dai, L., Bind, MA., Koutrakis, P. et al. Fine particles, genetic pathways, and markers of inflammation and endothelial dysfunction: Analysis on particulate species and sources. J Expo Sci Environ Epidemiol 26, 415–421 (2016). https://doi.org/10.1038/jes.2015.83
- endothelial dysfunction
- fine particulate matter
- genetic pathway
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