Smoking modify the effects of polycyclic aromatic hydrocarbons exposure on oxidative damage to DNA in coke oven workers

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

doi:10.1007/s00420-017-1206-2

Cited by 26 publications

(12 citation statements)

References 45 publications

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“…Our study revealed smoking and 1-OHP co-exposure was positively related to high 8-OHdG levels, indicating smokers, which are occupational exposed to PAH in the long term, may have more serious oxidative damage to DNA. These results were consistent with the previously reported findings [15].…”

Section: Discussionsupporting

confidence: 94%

“…Smoking has a strong effect on oxidative DNA damage, and PAH exposure is also related to oxidative DNA damage among occupational workers and general population [11–14]. There is a dose-dependent relationship of smoking and PAH metabolites in the risk of oxidative damage to DNA [15]. However, a challenge remains to fully understand the molecular mechanism of lifestyle - environmental factors between smoking and occupational PAH co-exposure effect on oxidative DNA damage.…”

Section: Introductionmentioning

confidence: 99%

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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: 94%

Section: Introductionmentioning

confidence: 99%

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

Self Cite

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“…Thus, multiple urine sample measurements should be used in future studies to evaluate the individual long-term exposure to environmental PAH. Accumulative epidemiologic studies also use single-point urinary PAH metabolites as internal exposure biomarkers, and random single-point PAH metabolites can be used to evaluate PAH exposure levels [47, 50]. Third, none of the birth outcomes considered the population standard for expected growth, which was mainly because the features of recruited subjects were not suitable for considering the clinical relevance in our study.…”

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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“…This is also the case of the fisherman of the second observation who was a smoker and exposed to diesel exhaust; a case study on lung cancer among Swedish dockworkers exposed to diesel exhaust and smoking confirmed a strong interaction between these two factors [16]. Similarly, it is well established that in workers exposed to polycyclic aromatic hydrocarbons, smoking causes more serious DNA oxidative damage than in non-exposed individuals, which may play the pivotal role in the carcinogenic mechanism of lung cancer [17].…”

Section: Discussionmentioning

confidence: 99%

Occupational lung cancer among fisherman: a triple case report

Ghailan

Ftouh

2018

International Maritime Health

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Smoking modify the effects of polycyclic aromatic hydrocarbons exposure on oxidative damage to DNA in coke oven workers

Abstract: Our findings quantitatively demonstrate that workers exposed to coke oven fumes and smoking will cause more serious DNA oxidative damage.

Cited by 26 publications

References 45 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

Occupational lung cancer among fisherman: a triple case report

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