Urinary 1-hydroxypyrene and smoking are determinants of LINE-1 and AhRR promoter methylation in coke oven workers

Yang, Jin; Li, Yanli; Zhang, Huitao; Zhang, Hongjie; Wang, Wubin; Fan, Yanfeng

doi:10.1016/j.mrgentox.2018.01.001

Cited by 14 publications

(8 citation statements)

References 37 publications

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“…Tekpli [18] reported smoking was associated with CYP1A1 methylation. Other studies suggested PAH exposure was related to DNA methylation [33–35]. In our study, we observed smoking and 1-OHP co-exposure was associated with CYP1A1 hypomethylation, further proved that smokers exposed to PAH were more likely to lower CYP1A1 methylation levels, which were consisted with other studies.…”

Section: Discussionsupporting

confidence: 89%

CYP1A1 methylation mediates the effect of smoking and occupational polycyclic aromatic hydrocarbons co-exposure on oxidative DNA damage among Chinese coke-oven workers

Li¹,

Li²,

Zhang³

et al. 2019

Environ Health

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Background Multiple factors, including co-exposure between lifestyle and environmental risks, are important in susceptibility to oxidative DNA damage. However, the underlying mechanism is not fully understood. This study was undertaken to evaluate whether Cytochrome P4501A1 ( CYP1A1 ) methylation can mediate the co-exposure effect between smoking and occupational polycyclic aromatic hydrocarbons (PAH) in development of oxidative DNA damage. Methods We explored the associations between smoking and occupational PAH co-exposure effect, CYP1A1 methylation and oxidative DNA damage among 500 workers from a coke-oven plant in China. Urine biomarkers of PAH exposure (1-hydroxypyrene, 1-OHP; 2-hydroxynaphthalene, 2-NAP; 2-hydroxyfluorene, 2-FLU; and 9-hydroxyphenanthren, 9-PHE) and a marker of oxidative DNA damage (8-hydroxy- 2′- deoxyguanosine, 8-OHdG) were measured by high performance liquid chromatography. CYP1A1 methylation was measured by pyrosequencing. Finally, mediation analysis was performed to investigate whether CYP1A1 methylation mediated smoking and occupational PAH co-exposure effect on oxidative DNA damage. Results We observed significant associations of smoking and 1-OHP co-exposure with CYP1A1 hypomethylation (OR: 1.87, 95% CI: 1.01–3.47) and high 8-OHdG (OR: 2.13, 95% CI: 1.14–3.97). There was a significant relationship between CYP1A1 hypomethylation and high 8-OHdG (1st vs. 3rd tertile = 1.58, 95% CI: 1.01–2.47, P for trend = 0.046). In addition, mediation analysis suggested CYP1A1 hypomethylation could explain 13.6% of effect of high 8-OHdG related to smoking and 1-OHP co-exposure. Conclusions Our findings suggested that the co-exposure effect of smoking and occupational PAH could increase the risk of oxidative DNA damage by a mechanism partly involving CYP1A1 hypomethylation. Electronic supplementary material The online version of this article (10.1186/s12940-019-0508-0) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 89%

CYP1A1 methylation mediates the effect of smoking and occupational polycyclic aromatic hydrocarbons co-exposure on oxidative DNA damage among Chinese coke-oven workers

Li¹,

Li²,

Zhang³

et al. 2019

Environ Health

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“…Finally, DNA methylation may be one of the potential mechanisms involved in naphthalene-induced adverse effects on birth outcomes. Several studies have demonstrated that exposure to PAHs can change the methylation of specific genes and global genomic DNA methylation [44–46]. Previous studies have also revealed that the presence of maternal 2-OH NAP is associated with lower methylation levels within the Alu and LINE-1 [47].…”

Section: Discussionmentioning

confidence: 99%

Maternal urinary 2-hydroxynaphthalene and birth outcomes in Taiyuan, China

Nie

Cheng

et al. 2018

Environ Health

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BackgroundNaphthalene is the simplest polycyclic aromatic hydrocarbon (PAH). It is easily emitted into the atmosphere, posing a significant risk to human health. However, limited studies have described the impact of naphthalene exposure on birth outcomes. In this study, we investigated the association between the maternal urinary metabolites of naphthalene, 2-hydroxynaphthalene (2-OH NAP), and birth outcomes.MethodIn the present study, four urinary PAH metabolites were measured in 263 pregnant women during late pregnancy. Multiple linear regression analysis was used to analyze the relationship between the concentrations of 2-OH NAP and birth outcomes, and restricted cubic spline models were further used to examine the shapes of the dose-response association.ResultGeneral linear models showed that prenatal urinary 2-OH NAP was associated with lower birth weight (BW) (− 4.38% for the high vs. low exposure group of 2-OH NAP; p for trend = 0.049) and higher cephalization index (CI) (4.30% for the high vs. low exposure group of 2-OH NAP; p for trend = 0.038). These associations were linear and significant when 2-OH NAP was modeled as a continuous variable in restricted cubic spline models (P linear = 0.0293 for 2-OH NAP and BW; P linear = 0.0326 for 2-OH NAP and CI). Multiple linear regression data indicated that each 1 ln-unit increase in 2-OH NAP was significantly associated with a 2.09 g/cm increase in the CI. The associations among 2-OH NAP, BW, and CI were also observed in a subset of participants residing close to arterial traffic.ConclusionOur data indicated that prenatal exposure to naphthalene had an adverse effect on fetal birth outcomes, especially the brain development index. Reduced exposure to naphthalene may improve newborn health outcomes. In Taiyuan, naphthalene may result from traffic pollution.Electronic supplementary materialThe online version of this article (10.1186/s12940-018-0436-4) contains supplementary material, which is available to authorized users.

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“…Epigenetic changes include DNA methylation, non-coding RNAs (such as microRNAs), chromatin remodeling, and histone modifications (Tammen et al, 2013). In this regard, several studies have established an association between epigenetic modifications and exposure to PAHs (Alegría-Torres et al, 2013;Zhang et al, 2016;Li et al, 2018;Yang et al, 2018). Alegría-Torres et al (2013) found a negative association between DNA methylation of the interleukin 12 and p53 gene promoters and urinary 1-OHP (using a PAHs exposure biomarker) levels in Mexican male brick manufacturers.…”

Section: Introductionmentioning

confidence: 99%

Expression levels of circulating microRNAs‐126, ‐155, and ‐145 in Mexican women exposed to polycyclic aromatic hydrocarbons through biomass fuel use

Ruíz-Vera

Ochoa-Martínez

Pruneda-Álvarez

et al. 2019

Environ and Mol Mutagen

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Human exposure to polycyclic aromatic hydrocarbons (PAHs) has been considered a risk determinant for the development of cardiovascular diseases (CVD). Therefore, the aim of this study was to assess expression levels of vascular‐related miRNAs, miR‐126, miR‐155, and miR‐145, in plasma from women (aged 19–81 years) exposed (n = 100) and non‐exposed (n = 20) to PAHs via biomass combustion smoke.1‐hydroxypyrene (1‐OHP) was determined in urine as a biomarker of exposure to PAHs using high‐resolution liquid chromatography. Plasma expression levels of proposed miRNAs were determined by quantitative real‐time PCR. Additionally, traditional risk factors (age, blood pressure, serum lipid profile, blood glucose, and among others) associated with CVD were evaluated. Urinary 1‐OHP concentrations and plasma expression levels of miR‐126 and miR‐155 were significantly higher (P < 0.05) in women using wood as a fuel source in their homes (indoor) compared to women from the reference group (non‐exposed to biomass smoke). Besides, multivariate linear regression analyses revealed that miR‐126[β = 0.61; 95% confidence interval (0.32–0.90)] and miR‐155 [β = 0.45; 95% confidence interval (0.13–0.84)] expression levels were significantly associated with urinary 1‐OHP concentrations after being adjusted by traditional risk factors (P < 0.05). In contrast, no significant relationship was found between miR‐145 and urinary 1‐OHP levels. Furthermore, miRNAs assessed in this investigation are associated with CVD events. Consequently, actions to reduce exposure to PAHs in the evaluated population are warranted. Environ. Mol. Mutagen. 60:546–558, 2019. © 2019 Wiley Periodicals, Inc.

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Urinary 1-hydroxypyrene and smoking are determinants of LINE-1 and AhRR promoter methylation in coke oven workers

Cited by 14 publications

References 37 publications

CYP1A1 methylation mediates the effect of smoking and occupational polycyclic aromatic hydrocarbons co-exposure on oxidative DNA damage among Chinese coke-oven workers

CYP1A1 methylation mediates the effect of smoking and occupational polycyclic aromatic hydrocarbons co-exposure on oxidative DNA damage among Chinese coke-oven workers

Maternal urinary 2-hydroxynaphthalene and birth outcomes in Taiyuan, China

Expression levels of circulating microRNAs‐126, ‐155, and ‐145 in Mexican women exposed to polycyclic aromatic hydrocarbons through biomass fuel use

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