Review Highlights Air Pollution’s Role in Atherosclerosis
Published in the journal Atherosclerosis
Overview
A recent review article published in Atherosclerosis highlights how air pollution, especially fine particulate matter (PM2.5), contributes to the development and progression of atherosclerosis. This chronic condition underlies many cardiovascular diseases (CVDs), which cause over 20 million deaths annually worldwide. The article calls for urgent global action to mitigate air pollution and its cardiovascular consequences.
Background
Atherosclerosis involves the buildup of lipids and inflammatory cells in artery walls, leading to plaques that can rupture and cause strokes or heart attacks. While lifestyle factors are well-known risks, environmental pollutants are increasingly recognized as major contributors.
Air pollution consists of harmful gases (NO2, SO2, CO, O3) and particles (PM10, PM2.5, ultrafine particles). These pollutants are linked to oxidative stress, inflammation, and vascular damage. PM2.5 is particularly dangerous due to its small size and chemical composition.
Link to Atherosclerosis
Numerous studies connect long-term PM2.5 exposure to early markers of atherosclerosis, including increased carotid intima-media thickness (CIMT), coronary artery calcification (CAC), and arterial stiffness. Some evidence also suggests early-life exposure can cause vascular changes in children.
Despite some inconsistencies and data gaps—especially for gases and in low-income regions—the overall literature strongly supports the role of air pollution in both developing and worsening atherosclerosis.
Biological Mechanisms
Lipid Alteration: PM2.5 raises LDL (“bad”) cholesterol and impairs HDL (“good”) cholesterol.
Oxidative Stress: Pollutants generate reactive oxygen species that damage cells and modify lipids.
Systemic Inflammation: Airborne particles trigger immune responses that promote plaque growth.
Endothelial Dysfunction: Pollutants damage blood vessel linings, increasing permeability and white blood cell adhesion.
Plaque Destabilization: PM exposure activates enzymes that weaken plaques and increase clotting risks.
Future Directions
Researchers urge more long-term studies, especially in underrepresented regions, using advanced imaging and personal air monitors. Investigations should explore emerging pollutants (e.g., microplastics, tire wear particles), the role of climate change, and interactions with factors like diet, noise, and heat.
Evaluating personal and policy-level interventions—such as air purifiers or low-emission zones—is also critical to reducing cardiovascular risks linked to air pollution.
