Associations between 25 Lung Cancer Risk–Related SNPs and Polycyclic Aromatic Hydrocarbon–Induced Genetic Damage in Coke Oven Workers

Dai, Xiayun; Deng, Siyun; Wang, Tian; Qiu, Gaokun; Li, Jun; Yang, Binyao; Feng, Wei; He, Xiaosheng; Deng, Qifei; Ye, Jian; Zhang, Wangzhen; He, Meian; Zhang, Xiaomin; Guo, Huan; Wu, Tangchun

doi:10.1158/1055-9965.epi-13-1251

Cited by 19 publications

(9 citation statements)

References 45 publications

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“…We did not find any significant differences in levels of plasma BPDE‐Alb adducts and lymphocytic MN frequencies between smokers and non‐smokers in this occupational cohort. A possible reason was that when comparing with cigarette smoking, coke oven emissions contain much higher concentrations of PAHs, which may cover the role of smoking in generating BPDE‐Alb; moreover, the genetic damage of coke oven workers in the current study might be determined by high‐occupational exposure to PAHs rather than tobacco smoke, which was also consistent with results of our recent studies .…”

Section: Discussionsupporting

confidence: 90%

The interaction of APEX1 variant with polycyclic aromatic hydrocarbons on increasing chromosome damage and lung cancer risk among male Chinese

Wei

et al. 2014

Molecular Carcinogenesis

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Polycyclic aromatic hydrocarbons (PAHs) are the most significant contributors to tobacco-induced lung carcinogenesis. Apurinic/apyrimidinic endonuclease 1 (APE1) is a central enzyme in the removal of apurinic/apyrimidinic sites caused by DNA damaging agents. This study aimed to investigate the potential interaction of APEX1 polymorphisms and PAHs on genetic damage and lung cancer risk among male Chinese. We recruited an occupational cohort of 922 male coke oven workers and determined their DNA damage levels by calculating the lymphocytic micronucleus (MN) frequencies. Two well-studied APEX1 polymorphisms (-307A > C and Asp148Glu) and their associations with MN frequencies were examined. The impact of MN-related single nucleotide polymorphism (SNP) on lung cancer risk was further investigated in two case-control studies including 1634 male lung cancer patients and 1678 controls. It was shown that, the APEX1 148Glu allele was associated with significantly higher MN frequencies than 148Asp allele, with strongest associations among the highest PAH-exposure workers (P = 0.008). The APEX1 148Glu allele was also associated with increased lung cancer risk among male smokers, especially among heavy smokers in both case-control studies (odd ratio: 4.40, 95%CI: 3.29-5.72). In addition, APEX1 148Glu variant interacts with smoking in increasing male lung cancer risk, as measured by the attributable proportion due to interaction, which was 0.23 (95%CI: 0.06-0.39). This study showed evidence on interaction between APEX1 148Glu variant and cigarette smoking in increasing lung cancer susceptibility among male Chinese, which may be due to the synergistic effects of APEX1 148Glu and PAHs in increasing chromosome damage levels. The results provide a new insight into gene-interactions in lung carcinogenesis.

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Section: Discussionsupporting

confidence: 90%

The interaction of APEX1 variant with polycyclic aromatic hydrocarbons on increasing chromosome damage and lung cancer risk among male Chinese

Wei

et al. 2014

Molecular Carcinogenesis

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“…In a study from China [34], coke oven workers were found to have 25 lung cancer risk related SNPs which correlated with polycyclic hydrocarbon induced genetic damage. In a study of variants of the nicotinic receptor genes and the association with both smoking dependence and adenocarcinoma of the lung, two CHRNA3 SNPs were most associated with nicotine dependence and adenocarcinoma of the lung [35].…”

Section: Methodsmentioning

confidence: 99%

Germline mutations predisposing to non-small cell lung cancer

et al. 2015

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Lung cancer in multiple first degree relatives had previously been attributed to smoking and to inherited enzymes associated with increased activation of carcinogens in smoke. There was not clear agreement on the significance of the testing methods for lung cancer susceptibility. More recent studies have identified germline mutations associated with lung cancer even in the absence of smoking and other mutations with plausible explanations for their association with lung cancer caused by smoking. At this time, the clinical significance of the various germline mutations for screening and the implications for therapy are not certain. This review summarizes the currently identified germline mutations associated with lung cancer, but this growing area of research will very likely identify further significant mutations as well.

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“…Genome-wide association studies (GWAS) have identified multiple single-nucleotide polymorphisms (SNPs) associated with lung cancer. Lung cancer risk-associated SNPs and their correlations with PAH exposure were associated with 8-OHdG levels and Micronuclei (MN) frequency [38]. PAHs are established lung carcinogens and may cause mitochondrial toxicity.…”

Section: Biomarkers and Coke Oven Workersmentioning

confidence: 99%

“…These researchers established associations between SNPs and genetic damage caused by polycyclic aromatic hydrocarbons (PAHs). Lung cancer risk-associated SNPs and their correlations with PAH exposure were associated with urinary 8-hydroxydeoxyguanosine (8-OHdG) levels and micronucleus (MN) frequency [38].…”

Section: Relationship Between Different Biomarkers and Vital Statusmentioning

confidence: 99%

Environmental Monitoring of PAHs Exposure, Biomarkers and Vital Status in Coke Oven Workers

Vimercati

Bisceglia

Cavone

et al. 2020

IJERPH

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A follow-up study of a cohort of workers from a coke plant compared with a control group from the same industrial area was conducted in 2019. The recruitment and environmental and biomarker measurements were performed during 1993/1994. The environmental concentrations of polycyclic aromatic hydrocarbons (PAH), B(a)P, pyrene and nitro-PAH were measured. Personal data were collected via an individual semi-structured questionnaire by a trained physician. All biomarkers were measured after a specific blood drawing for every test. Significant risks (ORs) were observed for nitro-PAH (≥0.12 µg/m3) [OR = 7.96 (1.01–62.82)], urinary 1-hydroxypyrene (1-OHpy) (≥0.99 µmoles/moles of creatinine) [OR = 11.71 (1.47–92.90)], PAH DNA adducts (P32) (≥2.69 adducts/108 nucleotides) [OR = 5.46 (1.17–25.58)], total nitro-PAH hemoglobin adducts (≥161.68 fg/µg of Hb) [OR = 5.92 (1.26–27.86)], sister chromatid exchange (SCE) with TCR (≥377.84 SCE/cell chromosomes) [OR = 13.06 (3.95–93.10)], sister chromatid exchange with T (≥394.72 total SCE) [OR = 13.06 (3.95–93.10)], and sister chromatid exchange with X (≥8.19 mean SCE) [OR = 13.06 (3.95–93.10)]. Significant risk of death for all causes and chromosomal aberrations (48 h) (OR = 7.19 [1.19–43.44]) or micronuclei in culture at 48 h (OR = 3.86 [1.04–14.38]) were also found.

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Associations between 25 Lung Cancer Risk–Related SNPs and Polycyclic Aromatic Hydrocarbon–Induced Genetic Damage in Coke Oven Workers

Cited by 19 publications

References 45 publications

The interaction of APEX1 variant with polycyclic aromatic hydrocarbons on increasing chromosome damage and lung cancer risk among male Chinese

The interaction of APEX1 variant with polycyclic aromatic hydrocarbons on increasing chromosome damage and lung cancer risk among male Chinese

Germline mutations predisposing to non-small cell lung cancer

Environmental Monitoring of PAHs Exposure, Biomarkers and Vital Status in Coke Oven Workers

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