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

BACKGROUND: 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. METHODS: 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. RESULTS: The median concentration of PM(2.5) area under the curve (auc) was 25.2 µg/m(3) (interquartile range: 24.2-26.4 µg/m(3)). 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/m(3) increase of PM(2.5auc). The direct effect of PM(2.5auc) (per 1 µg/m(3) 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). CONCLUSIONS: 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).