Fine particulate matter and intima media thickness: Role of endothelial function biomarkers

Ambient fine particulate matter (PM_2.5) is a risk factor for atherosclerosis disease. We aimed to assess whether nitric oxide stable metabolites (NOx) and l-arginine mediate the association between PM_2.5 and carotid intima media thickness (cIMT) increase.

We selected 251 participants from the control group of GEA (Genetics of Atheroslerosis Disease Mexican) study (2008-2013) in Mexico City. Mediation models were carried out using pathway analyses, a special case of structural equation models.

The median concentration of PM_2.5 area under the curve (auc) was 25.2 µg/m³ (interquartile range: 24.2-26.4 µg/m³). Employing participants with observed values for both biomarkers (n = 117), the total effect of PM_2.5auc on mean cIMT at bilateral, right, and left was 19.27 µm (95% confidence interval [CI]: 5.77, 32.78; P value = 0.005), 12.69 µm (95% CI: 0.67, 24.71; P value = 0.039), and 25.86 µm (95% CI: 3.18, 48.53; P value = 0.025) per each 1 µg/m³ increase of PM_2.5auc. The direct effect of PM_2.5auc (per 1 µg/m³ increase) was 18.89 µm (95% CI: 5.37, 32.41; P value = 0.006) for bilateral, 13.65 µm (95% CI: 0.76, 26.55; P value = 0.038) for right, and 24.13 µm (95% CI: 3.22, 45.03; P value = 0.024) for left. The indirect effects of NOx and l-arginine were not statistically significant showing that endothelial function biomarkers did not mediate PM_2.5 and cIMT associations. Although l-arginine was not a mediator in the PM_2.5 and cIMT pathway, a decrease in l-arginine was significantly associated with PM_2.5auc.

In this study of adults from Mexico City, we found that PM_2.5 was associated with an increase in cIMT at bilateral, left, and right, and these associations were not mediated by endothelial function biomarkers (l-arginine and NOx).