Longitudinal relationships of polycyclic aromatic hydrocarbons exposure and genetic susceptibility with blood lipid profiles

• Published in: Environment international Vol. 164; p. 107259
• Main Authors: Ma, Jixuan, Hao, Xingjie, Nie, Xiuquan, Yang, Shijie, Zhou, Min, Wang, Dongming, Wang, Bin, Cheng, Man, Ye, Zi, Xie, Yujia, Wang, Chaolong, Chen, Weihong
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Ltd 01.06.2022; Elsevier
• Subjects: Blood lipid; blood lipids; environment; genetic predisposition to disease; Genetic susceptibility; high density lipoprotein cholesterol; hyperlipidemia; low density lipoprotein cholesterol; metabolites; Polycyclic aromatic hydrocarbons; Polygenic risk scores; regression analysis; risk; Polygenic risk scores; Polycyclic aromatic hydrocarbons; Genetic susceptibility; Blood lipid
• ISSN: 0160-4120; 1873-6750; 1873-6750
• DOI: 10.1016/j.envint.2022.107259

[Display omitted] •Exposure to PAHs is associated with increased blood lipid profiles over 6 years.•Individual with higher lipid-PRS could be more susceptible to hyperlipidemias.•Higher lipid-PRS aggravate and modify blood lipid when exposure to PAHs. We aim to analyze the effects of polycyclic aromatic hydrocarbons (PAHs) exposure and genetic predisposition on blood lipid through a longitudinal epidemiological study. We enrolled 4,356 observations who participated at baseline (n = 2,435) and 6-year follow-up (n = 1,921) from Wuhan-Zhuhai cohort. Ten urinary PAHs metabolites and blood lipid (i.e., total cholesterol [TC], triglycerides [TG], low-density lipoprotein cholesterol [LDL-C], and high-density lipoprotein cholesterol [HDL-C]) were measured at both baseline and follow-up. The polygenic risk scores (PRS) of blood lipid were constructed by the corresponding genome-wide association studies. Linear mixed models were fit to identify associations between urinary PAHs metabolites, blood lipid, and lipid-PRSs in the repeated-measure analysis. Besides, longitudinal relationships of blood lipid with urinary PAHs metabolites and respective lipid-PRSs were examined by using linear regression models. Compared with subjects who had persistently low urinary total hydroxyphenanthrene (ΣOHPh), those with persistently high levels had an average increase of 0.137 mmol/l for TC and 0.129 mmol/l for LDL-C over 6 years. Each 1-unit increase of TC-, TG-, LDL-C-, and HDL-C-specific PRS were associated with an average increase of 0.438 mmol/l for TC, 0.264 mmol/l for TG, 0.198 mmol/l for LDL-C, and 0.043 mmol/l for HDL-C over 6 years, respectively. Compared with subjects who had low genetic risk and persistently low ΣOHPh, subjects with high LDL-specific PRS and persistently high ΣOHPh had an average increase of 0.652 mmol/l for LDL-C. Our results suggest that high-level ΣOHPh exposure is associated with an average increase of LDL-C over 6 years, and those relationships can be aggravated by a higher LDL-C-genetic risk. No significant relationships were observed between other PAHs metabolites (including hydroxynaphthalene, hydroxyfluorene, and hydroxypyrene) and blood lipid changes over 6 years. Our findings emphasize the importance of preventing PAHs exposure, particularly among those with a higher genetic predisposition of hyperlipidemia.