SAIMSARA Journal

Machine-Readable Science • ISSN 3054-3991

Air Pollution and Atherosclerosis from PM2.5 to Traffic Pollution: Scoping Review with ☸️SAIMSARA.

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Cardiac & Vascular Health

Issue 1, Volume 1, 2026

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DOI: 10.62487/saimsaracf5686c9

Editorial note
• Last update: 2026-05-18 16:19:23
What is this paper about
Air pollution is not just background exposure — this evidence map shows how PM2.5 and traffic-related pollution repeatedly align with CIMT progression, coronary calcium, plaque phenotype, cardiovascular events, and mechanistic vascular injury. Built from 96 references and 186 original studies, the full map gives a practical view of which vascular endpoints are most consistently affected, which populations appear vulnerable, and where prevention or exposure-reduction research should move next.
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Abstract: To map and synthesize original research on the relationship between air pollution exposure and atherosclerosis, emphasizing vascular imaging outcomes, clinical atherosclerotic disease, susceptible populations, and mechanistic pathways supported by human, animal, and laboratory evidence. The review uses 96 references and builds its evidence map from 186 original studies with 1807331 total participants/sample observations (topic-deduplicated ΣN). This scoping review indicates that long-term exposure to air pollution, particularly PM2.5 and traffic-related mixtures, is consistently associated with subclinical and clinical atherosclerosis across imaging, biomarker, and outcome studies. The most recurrent signal links higher PM2.5 with accelerated vascular injury, exemplified by 5.0 µm/year greater carotid intima-media thickness progression per 2.5 µg/m³ PM2.5 and a hazard ratio of 1.77 for incident atherosclerosis under long-term multi-pollutant exposure. Converging mechanistic evidence supports a role for oxidative stress, systemic inflammation, and endothelial dysfunction as plausible biological intermediaries, while susceptibility appears heightened in children, menopausal women, and patients with established coronary disease. Although some lower-exposure cohorts reported null associations, the overall pattern supports integrating exposure history into cardiovascular prevention. Future work should prioritize harmonized longitudinal imaging studies and intervention trials testing whether exposure reduction meaningfully slows atherosclerotic progression.

Keywords: Air pollution; Atherosclerosis; Particulate matter; PM2.5; Nitrogen dioxide; Carotid intima-media thickness; Coronary plaque; Traffic-related pollution; Cardiovascular disease; Oxidative stress

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