Long-term low-level air pollution is associated with subclinical endothelial dysfunction, the initial and critical step leading to adverse cardiovascular outcomes, even at exposure levels below current regulatory targets.
Key Findings
Results
Air pollutant concentrations in the study region decreased significantly from 2010 to 2015, with 6-year levels averaging below current regulatory thresholds.
PM10, PM2.5, NO2, and BC all decreased over the study period (p < 0.0001).
Six-year average levels were: PM10 = 15.9 µg/m³, PM2.5 = 12.8 µg/m³, NO2 = 14.3 µg/m³, and BC = 1.04 µg/m³.
By 2015, concentrations had declined further to PM10 = 14.6 µg/m³, PM2.5 = 11.5 µg/m³, NO2 = 12.0 µg/m³, and BC = 0.85 µg/m³.
The study population consisted of 453 Flemish participants (47.7% women; mean age 52.8 years).
Results
Dmax (maximal difference in pulse amplitude between test and control fingers) was inversely correlated with PM2.5 regardless of adjustment for cardiovascular risk factors.
The association between Dmax and PM2.5 was statistically significant irrespective of risk factor adjustment.
Associations of Rmax with PM2.5 and associations of both Dmax and Rmax with other pollutants (PM10, NO2, BC) were weaker but consistently inverse (p values < 0.10).
Endothelial function was assessed by finger photoplethysmography after 5 minutes of ischaemia.
Mixed models accounting for co-residence were used to relate air pollutants to the endothelial function outcomes.
Results
The association between endothelial dysfunction and PM10 and PM2.5 weakened over the 6-year study period, paralleling the declining pollutant concentrations.
Association sizes of both Rmax and Dmax with PM10 and PM2.5 weakened over 6 years (p ≤ 0.044).
This temporal weakening of associations paralleled the decreasing air pollutant levels observed from 2010 to 2015.
The pattern suggests that improvements in air quality corresponded with attenuated endothelial dysfunction associations.
Results
Higher Rmax and Dmax (better endothelial function) were associated with a significantly reduced risk of a composite cardiovascular endpoint over up to 10 years of follow-up.
The risk of a composite cardiovascular endpoint decreased with higher Rmax and Dmax (p ≤ 0.043).
Hazard ratios for the composite cardiovascular endpoint ranged from 0.31 to 0.49 for higher endothelial function measures.
Proportional hazards regression was used to relate cardiovascular endpoints to endothelial function measures.
Follow-up extended up to 10 years, during which endothelial dysfunction predicted cardiovascular disease.
Results
Geographical analysis revealed that spatial patterns of endothelial dysfunction followed the spatial gradients in PM2.5 across residential addresses.
Residential air pollution was estimated using high-resolution spatiotemporal interpolation linked to participants' residential addresses.
Endothelial dysfunction mapped onto PM2.5 spatial gradients in the geographic analysis.
This spatial correlation supports a causal relationship between residential PM2.5 exposure and endothelial dysfunction.
Conclusions
Even at low exposure levels below WHO and EU clean-air targets, air pollution remained associated with subclinical endothelial dysfunction.
The study was conducted in the context of recently updated WHO and EU clean-air targets.
Average PM2.5 exposure (12.8 µg/m³ over 6 years) was at or below current EU limit values.
The authors characterize endothelial dysfunction as 'the initial and critical step leading to adverse cardiovascular outcomes.'
The findings indicate residual cardiovascular risk from air pollution even at relatively low contemporary exposure levels.
What This Means
This research suggests that even at relatively low levels of air pollution — below or near current regulatory limits in Europe — long-term residential exposure is linked to subtle damage to the inner lining of blood vessels, known as endothelial dysfunction. The study followed 453 adults in Flanders, Belgium, from 2010 to 2015, measuring their exposure to common air pollutants (fine particles, nitrogen dioxide, and black carbon) and assessing blood vessel health using a non-invasive finger test that measures how blood flow recovers after brief restriction. The researchers found that people exposed to higher levels of fine particulate matter (PM2.5) consistently showed worse blood vessel function, and this pattern held up even after accounting for other cardiovascular risk factors like age, smoking, and blood pressure.
Importantly, the study also found that as air quality improved over the 6-year period — with pollutant levels declining measurably — the strength of the association between pollution and blood vessel damage also weakened. This suggests that reducing air pollution may lead to improvements in vascular health at the population level. Furthermore, the degree of blood vessel dysfunction measured at baseline predicted who went on to develop cardiovascular disease over up to 10 years of follow-up, with people who had better vascular function having roughly half to one-third the cardiovascular risk of those with poorer function.
This research matters because it provides evidence that air pollution harms cardiovascular health even at exposure levels that are considered relatively 'clean' by current standards, and that endothelial dysfunction — an early, detectable sign of vascular damage — serves as a meaningful link between pollution exposure and eventual heart disease. The findings support ongoing efforts by the WHO and European Union to tighten clean-air standards, suggesting that further reductions in air pollution could meaningfully reduce population-level cardiovascular risk.
Yang Z, Martens D, An D, Shi H, Wang Y, Yu Y, et al.. (2026). Endothelial function in relation to low-level chronic residential air pollution in a general population: a cohort study.. Blood pressure. https://doi.org/10.1080/08037051.2026.2724736