Effects of exposure to polycyclic aromatic hydrocarbons and heavy metals on the oxidative stress, inflammation and DNA methylation among traffic conductors

Abstract

Background: Exposure to traffic-related air pollutants, including polycyclic aromatic hydrocarbons (PAHs) and heavy metals, has been associated with the etiology and prognosis of many diseases including cardiovascular events. However, the specific causal agents and underlying mechanisms for different adverse health effects remain unclear. Objectives: The aims of this study were to examine the relations of exposure to PAHs (1-hydroxypyrene-glucuronide, 1-OHPG) and metals (cadmium, Cd; nickel, Ni; lead, Pb; and copper, Cu) with lipid peroxidation (4-hydroxynonenal, 4-HNE), inflammation (high-sensitive C-creative protein, hs-CRP), endothelial function (vascular cell adhesion molecule-1,VCAM-1; intercellular adhesion molecule-1, ICAM-1), DNA damage (8-hydroxydeoxyguanosine, 8-OHdG) and DNA methylation (long interspersed nuclear element-1, LINE-1). Methods: we recruited 91 traffic conductors and 53 indoor official workers between May 2009 and June 2011 in Taipei, Taiwan. Post-shift blood and urine samples from 2 consecutive days were collected. The urine samples were analyzed for 1-OHPG, Cd, Ni, As, Pb, Cu, and 8-OHdG. The blood samples were measured for HNE, hs-CRP, VCAM-1, ICAM-1, and LINE-1. We constructed a linear mixed model to assess these associations adjusted for covariates. Results: We found that urinary 1-OHPG levels were positively associated with urinary 8-OHdG levels (β=0.09, p=0.026), and urinary 8-OHdG levels were negatively associated with LINE-1 methylation levels (β= -0.85, p=0.021) among traffic conductors. Significant positive relations between urinary As and Pb levels and HNE levels, and between all urinary metals levels and ICAM-1 levels, and between urinary Pb levels and VCAM-1 levels, as well as between urinary Ni levels and hs-CRP levels were observed in traffic conductors. Conclusions: Exposure to PAHs and metals could increase the burden of oxidative stress and inflammation, and oxidative stress could result in global DNA hypomethylation.