Abstract
This study was carried out to examine the association between exposure to polycyclic aromatic hydrocarbon with traffic exhaust and biomarkers of lipid peroxidation and antioxidant levels among highway toll station workers. We conducted a cross-sectional study of 47 female highway toll station workers exposed to traffic exhausts and 27 female classroom trainees as a reference group. Exposure assessment was based on a biomarker of polycyclic aromatic hydrocarbon exposure, urinary 1-hydroxypyrene-glucuronide (1-OHPG). Urinary isoprostane was assayed as a biomarker of lipid peroxidation, and plasma antioxidative capacity of lipid-soluble substances (ACL) and water-soluble substances (ACW) was measured. The median concentration of urinary isoprostane was higher among the exposed non-smokers (4.63 ng/mL) compared with the reference non-smokers (3.52 ng/mL, difference: 0.91, 95% CI –0.15 to 1.98) (Wilcoxon rank-sum test: p = 0.04). The median concentration of ACW among non-smoking exposed subjects (37.9 μg/mL Trolox equivalent) was lower than that of the reference non-smokers (86.3 μg/mL). Adjusting for confounding effects by linear regression, a change in log(isoprostane) concentration was significantly related to a unit change in log(1-OHPG) (regression coefficient [ß], β = 0.14, 95% CI 0.07 to 0.21). Exposure to polycyclic aromatic hydrocarbon is associated with increased lipid peroxidation and reduced antioxidative capacity in toll station workers.
Highlights
A large body of epidemiologic research provides evidence that short-term exposure to air pollution is associated with increased cardiovascular mortality and morbidity (Donaldson et al 2001; Dockery, 2001; Dominici et al, 2006)
We recently studied toll workers exposed to high levels of PM2.5 from traffic exhausts and found elevated levels of urinary 8-hydroxydeoxyguanosine (8-OHdG), a biomarker of oxidative DNA damage, and plasma nitric oxide polycyclic aromatic hydrocarbons (PAHs) (NO) compared with unexposed subjects (Lai et al, 2005)
The results of the present study indicate an increased amount of lipid peroxidation, measured as urinary isoprostane, in subjects working under conditions of potential oxidative stress due to exposure to polycyclic aromatic hydrocarbons related to traffic exhausts compared with a reference group of women without occupational exposure
Summary
A large body of epidemiologic research provides evidence that short-term exposure to air pollution is associated with increased cardiovascular mortality and morbidity (Donaldson et al 2001; Dockery, 2001; Dominici et al, 2006). Raupach and colleagues (2006) proposed a model linking second-hand smoke to acute coronary syndromes This model may have some relevance to traffic-related air pollution, which contains some of the same gaseous and particulate combustion products. According to this model, oxidants in tobacco smoke and traffic exhausts, as well as free radicals released endogenously from activated neutrophils, play a central role in the causal pathway leading first to vascular inflammation and to platelet. Squadrito and colleagues (2007) suggested that semiquinone radicals, present in fine particles (PM2.5), undergo redox cycling, thereby reducing oxygen and generating reactive oxygen species (ROS) These ROS cause oxidative stress at the site of deposition and produce deleterious effects in the lung
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