Huan Guo

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Organization: Huazhong University of Science and Technology
Department: Department of Occupational and Environmental Health
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Co-reporter:Yansen Bai, Wei Feng, Suhan Wang, Xiao Zhang, Wangzhen Zhang, Meian He, Xiaomin Zhang, Tangchun Wu, and Huan Guo
Environmental Science & Technology 2016 Volume 50(Issue 2) pp:951-960
Publication Date(Web):December 24, 2015
DOI:10.1021/acs.est.5b03945
Essential metals play important roles in maintaining cellular homeostasis, but the effects of their interaction with the environmental pollutants are still not very well-known in human subjects. The aim of this study was to evaluate the roles of essential metals and their interactions with polycyclic aromatic hydrocarbons (PAHs) on chromosome damage, an early carcinogenic event. A total of 1245 male workers were included in this study and the levels of 11 urinary essential metals, 12 urinary PAH metabolites, plasma concentrations of benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts, and lymphocyte micronucleus (MN) frequencies were monitored. We found that zinc (Zn), selenium (Se), and strontium (Sr) have significant inverse dose–response relationships with MN frequencies (all P < 0.05). Furthermore, the protective roles of Zn, Se, and Sr were mainly shown among subjects with high levels of BPDE-Alb adducts. Significant effect modification of BPDE-Alb adducts on the associations of Zn, Se, and Sr with MN frequencies was observed (all Pinteraction < 0.05). Our study showed evidence that Zn, Se, and Sr play protective roles in reducing chromosome damage, and these effects can be modified by PAH exposure levels. These findings add potential evidence for the preventive effects of Zn, Se, and Sr against carcinogenesis in human subjects.
Co-reporter:Dan Kuang, Wangzhen Zhang, Qifei Deng, Xiao Zhang, Kun Huang, Lei Guan, Die Hu, Tangchun Wu, and Huan Guo
Environmental Science & Technology 2013 Volume 47(Issue 13) pp:7446
Publication Date(Web):June 7, 2013
DOI:10.1021/es401639x
Polycyclic aromatic hydrocarbons (PAHs) are known to induce reactive oxygen species and oxidative stress, but the dose–response relationships between exposure to PAHs and oxidative stress levels have not been established. In this study, we recruited 1333 male coke oven workers, monitored the levels of environmental PAHs, and measured internal PAH exposure biomarkers including 12 urinary PAH metabolites and plasma benzo[a]pyrene-r-7,t-8,t-9,c-10-tetrahydotetrol-albumin (BPDE-Alb) adducts, as well as the two oxidative biomarkers urinary 8-hydroxydeoxyguanosine (8-OHdG) and 8-iso-prostaglandin-F2α (8-iso-PGF2α). We found that the total concentration of urinary PAH metabolites and plasma BPDE-Alb adducts were both significantly associated with increased 8-OHdG and 8-iso-PGF2α in both smokers and nonsmokers (all p < 0.05). This exposure-response effect was also observed for most PAH metabolites (all ptrend < 0.01), except for 4-hydroxyphenanthrene and 8-OHdG (ptrend = 0.108). Furthermore, it was shown that only urinary 1-hydroxypyrene has a significant positive association with both 8-OHdG and 8-iso-PGF2α after a Bonferroni correction (p < 0.005). Our results indicated that urinary ΣOH-PAHs and plasma BPDE-Alb adducts can result in significant dose-related increases in oxidative damage to DNA and lipids. Furthermore, when a multianalyte method is unavailable, our findings demonstrate that urinary 1-hydroxypyrene is a useful biomarker for evaluating total PAHs exposure and assessing oxidative damage in coke oven workers.
Benzo[10,11]chryseno[3,4-b]oxirene-7,8-diol,7,8,8a,9a-tetrahydro-, (7R,8S,8aS,9aR)-rel-
Prosta-5,13-dien-1-oicacid, 9,11,15-trihydroxy-, (5Z,8b,9a,11a,13E,15S)-
Guanosine,2'-deoxy-7,8-dihydro-8-oxo-
Benzo[pqr]tetraphen-3-ol
4-HYDROXY-PHENANTHRENE
9H-Fluoren-2-ol
1-Phenanthrenol
Phenanthren-3-ol
Phenanthren-2-ol
Phenanthren-9-ol