Association between polycyclic aromatic hydrocarbon exposure and blood lipid levels: the indirect effects of inflammation and oxidative stress

Abstract

Although previous studies have indicated polycyclic aromatic hydrocarbons (PAHs) as cardiovascular health risk factors, evidence linking exposure to PAHs and blood lipids is still lacking, and the mechanism remains largely unknown. In this study, we evaluated the association between human internal exposure to PAHs and blood lipid levels in adults, as well as the indirect effects of inflammation and oxidative stress. The internal exposure of PAHs was assessed by determining serum PAHs and their hydroxylated metabolites (OH-PAHs) in the paired urine samples. Multivariable linear regression results demonstrated significant positive associations of individual PAHs and OH-PAHs with blood lipid biomarkers. The Bayesian kernel machine regression model revealed positive joint effects of PAH internal exposure on the fasting blood glucose, low-density lipoprotein cholesterol, total cholesterol, and total triglyceride, as well as an increased ratio of apolipoprotein B to apolipoprotein A1. In evaluating individual effects, serum phenanthrene played the most significant role in the association of increased PAH exposure with elevated fasting blood glucose. Quantile g-computation demonstrated the significant change in the levels of apolipoprotein B, ratio of apolipoprotein B to apolipoprotein A1, low-density lipoprotein cholesterol, and total cholesterol per quartile increase in PAH internal exposure. The restricted cubic spline analysis demonstrated the non-linear relationship between individual PAHs and OH-PAHs on blood lipid biomarkers. The mediation analysis indicated that PAH exposure may affect blood lipids not directly, but rather indirectly through intermediate inflammation and oxidative stress. The results demonstrated a significant association between increased PAH exposure levels and elevated blood lipids, highlighting the indirect effects of inflammation and oxidative stress.

Keywords: Blood lipids; Inflammation; Mediation analysis; Oxidative stress; Polycyclic aromatic hydrocarbons.