Effects of internal exposure to polycyclic aromatic hydrocarbons on lipids and mediation of oxidative stress pathways:a case-control study of ischemic stroke
Objective To understand the relationship between internal exposure to polycyclic aromatic hydrocarbons and blood lipids and the mediating role of oxidative stress pathways therein.Methods From November 2021 to June 2023,the patients with ischemic stroke and the control population were recruited at Xiqing Hospital and Yangliuqing Community Hospital in Tianjin,China,and 171 cases and 342 control population served as the study subjects.Urinary PAH metabolites,oxidative stress indicators 8-hydroxy-2'-deoxyguanosine(8-OHdG)and 3-nitrotyrosine(3-NT)were measured.Multiple linear regression was used to analyze the association between internal PAH exposure and blood lipids as well as oxidative stress indicators,and the mediating effect was used to analyze the mediating role of oxidative stress pathway in the alteration of blood lipids by internal PAH exposure.Results Total polycyclic aromatic hydrocarbon hydroxyl metabolites(ΣOH-PAHs)in the total study population was 187.02 μg/g Cr.ΣOH-PAHs levels were higher in the ischemic stroke group compared to the control group(P<0.001).ΣOH-Flu and ΣOH-PAHs were positively correlated with the ratio of low-density lipoproteins to high-density lipoproteins(LDL/HDL)(P<0.05).ΣOH-Flu was positively correlated with 8-OHdG.positive association(P<0.05),andΣOH-Nap,ΣOH-Flu,ΣOH-Phe,and ΣOH-PAHs were positively associated with 3-NT(P<0.05).8-OHdG mediated between the association of ΣOH-Flu and ΣOH-PAHs with LDL/HDL,with mediation ratios of 12.00%and 8.20%(P<0.05).3-NT was positively associated with the ratio of LDUHDL in the association of ΣOH-Flu and ΣOH-PAHs There was a mediating role between the association with LDUHDL with mediating proportions of 26.74%and 25.76%(P<0.05).Conclusion There is a significant correlation between internal PAH exposure and lipids,and the oxidative stress pathway may mediate the association between internal PAH exposure and lipids.