Eicosapentaenoic acid appears to counteract harmful CV effects from air pollution
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Key takeaways:
- Eicosapentaenoic acid (EPA) restored function in endothelial cells exposed to urban or fine air pollution particle matters.
- Agents containing EPA may be able to be used to combat CV effects of air pollution.
Eicosapentaenoic acid, the active ingredient in certain omega-3 fatty acids, promoted anti-inflammatory, cytoprotective and lipid changes in endothelial cells exposed to air pollution, researchers reported.
In a study funded in part by Amarin, which makes icosapent ethyl (Vascepa), a pharmaceutical-grade omega-3 fatty acid containing eicosapentaenoic acid (EPA), the researchers investigated whether EPA restores function in endothelial cells exposed to urban or fine air pollution particles of matter.
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The CV hazards of air pollution
“Air pollution has been identified by the most recent Global Burden of Disease Study as the fourth leading contributor to global mortality. Cardiovascular disease, especially atherothrombotic events, accounts for the majority of these deaths,” R. Preston Mason, PhD, MBA, a member of the cardiovascular division at Brigham and Women’s Hospital and president and founder of Elucida Research, and Samuel C.R. Sherratt, PhD, senior research scientist at Elucida Research, told Healio. “Exposure to fine particulate matter (PM) air pollution ( 2.5 µm in mean diameter) causes both acute and chronic tissue injury as a result of their efficient penetration and toxic chemical constituents, including inorganic transition metals, elemental and organic carbons, and biological residuals such as endotoxin. Transitional metals and polycyclic aromatic hydrocarbons in PMs produce a surge in reactive oxygen species that lead to inflammation and systemic tissue damage. Fine PMs are able to penetrate into the bloodstream where they contribute to atherosclerotic changes and increased risk for myocardial infarction and stroke. For more than a decade, our laboratory has been investigating the biological effects of omega-3 fatty acids, especially EPA, in models of CV disease. Among our published findings is the observation that EPA and its bioactive metabolites reverse vascular endothelial cell dysfunction through multiple mechanisms, including reductions in reactive oxygen species, preserved membrane stability, increased nitric oxide bioavailability and broad anti-inflammatory actions.
“As air pollution PMs damage pulmonary and vascular endothelial cells through oxidative stress and inflammatory processes, we were interested in testing EPA in human tissue following exposure to such PMs. We were also inspired by investigations conducted by the Environmental Protection Agency showing that omega-3 fatty acid supplementation can reverse dyslipidemia and abnormalities in cardiac function among test subjects systematically exposed to air pollution PMs,” they told Healio.
Urban PMs modified nine of 12 proteins and fine PMs modified 13 of 36 proteins linked to platelet and neutrophil degranulation pathways, and caused a decrease of more than 50% in the stimulated release ratio of nitric oxide to peroxynitrite (P < .001), the researchers found.
However, treatment of endothelial cells exposed to those PMs with EPA altered expressions of proteins found in inflammatory pathways and increased the expression of heme oxygenase-1, a cytoprotective protein, by 2.1-fold (P = .024), according to the researchers.
In addition, EPA reduced elevations in soluble intercellular adhesion molecule-1 levels by 22% (P < .01) and improved the release ratio of nitric oxide to peroxynitrite by more than 35% (P < .05), they found.
‘Mechanistic insights’
“These findings provide mechanistic insights for cardiologists into the role of air pollution PMs in atherothrombotic disease, especially the role of endothelial dysfunction, oxidative stress and inflammation,” Mason and Sherratt told Healio. “This research also supports a potential role for EPA in reducing or even reversing such effects due to its broad biological actions and metabolic products that improve endothelial cell function. These findings may also contribute to our understanding of EPA as administered in a highly purified ethyl ester (icosapent ethyl) in reducing clinical events in outcome trials. The benefits of EPA may be due to improved endothelial function, reduced oxidative stress and anti-inflammatory actions.”
References:
- Abohashem S, et al. Eur Heart J. 2021;doi:10.1093/eurheartj/ehaa982.
- Bhatt DL, et al. N Engl J Med. 2019;doi:10.1056/NEJMoa1812792.
- Ferecatu I, et al. Part Fibre Toxicol. 2010;doi:10.1186/1743-8977-7-18.
- Franklin BA, et al. Curr Probl Cardiol. 2015;doi:10.1016/j.cpcardiol.2015.01.003.
- Lodovici M, et al. J Toxicol. 2011;doi:10.1155/2011/487074.
- Newman JD, et al. J Am Coll Cardiol. 2020;doi:10.1016.j.jacc.2020.10.020.
- Rajagopalan S, et al. Circulation. 2020;doi:10.1161/CIR.0000000000000931.
- Sherratt SCR, et al. Curr Athero Rep. 2023;doi:10.1007/s11883-022-01075-x.
- Tong H, et al. Environ Health Perspect. 2012;doi:10.1289/ehp.1104472.
- Yokoyama M, et al. Lancet. 2007;doi:10.1016/S1040-6736(07)60527-3.
For more information:
R. Preston Mason, PhD, MBA, can be reached at rpmason@elucidaresearch.com.
Samuel C.R. Sherratt, PhD, can be reached at ssherratt@elucidaresearch.com.
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