Smoking modify the effects of polycyclic aromatic hydrocarbons exposure on oxidative damage to DNA in coke oven workers
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Coke oven emissions containing polycyclic aromatic hydrocarbons (PAHs) are predominant toxic constituents of particulate air pollution that have been linked to increased risk of lung cancer. Numerous epidemiological studies have suggested that oxidative DNA damage may play a pivotal role in the carcinogenic mechanism of lung cancer. Little is known about the effect of interaction between PAHs exposure and lifestyle on DNA oxidative damage.
The study population is composed by coke oven workers (365) and water treatment workers (144), and their urinary levels of four PAH metabolites and 8-hydroxydeoxyguanosine (8-OHdG) were determined. Airborne samples of exposed sites (4) and control sites (3) were collected, and eight carcinogenic PAHs were detected by high-performance liquid chromatography.
The median values of the sum of eight carcinogenic PAHs and BaP in exposed sites were significantly higher than control sites (P < 0.01). The study found that the urinary PAH metabolites were significantly elevated in coke oven workers (P < 0.01). Multivariate logistic regression analysis revealed that the risk of high levels of urinary 8-OHdG will increase with increasing age, cigarette consumption, and levels of urinary 1-hydroxypyrene, and P for trend were all <0.05. Smoking can significantly modify the effects of urinary 1-hydroxypyrene on high concentrations urinary 8-OHdG, during co-exposure to both light or heavy smoking and high 1-hydroxypyrene levels (OR 4.28, 95% CI 1.32–13.86 and OR 5.05, 95% CI 1.63–15.67, respectively).
Our findings quantitatively demonstrate that workers exposed to coke oven fumes and smoking will cause more serious DNA oxidative damage.
KeywordsPolycyclic aromatic hydrocarbons 1-Hydroxypyrene Smoking 8-Hydroxydeoxyguanosine
This work was supported by research funding from the National Nature Science Foundation of China (NSFC 81273041, 30901180). The authors declare that they have no conflict of interest.
- Besaratinia A, Van Schooten FJ, Schilderman PA, De Kok TM, Haenen GR, Van Herwijnen MH, Van Agen E, Pachen D, Kleinjans JC (2001) A multi-biomarker approach to study the effects of smoking on oxidative DNA damage and repair and antioxidative defense mechanisms. Carcinogenesis 22:395–401CrossRefGoogle Scholar
- Cadet J, Berger M, Douki T, Ravanat JL (1997) Oxidative damage to DNA: Formation, measurement, and biological significance. Rev Physiol Biochem Pharmacol 131:1–87Google Scholar
- Cao C, Lai T, Li M, Zhou H, Lv D, Deng Z, Ying S, Chen Z, Li W, Shen H (2016) Smoking-promoted oxidative DNA damage response is highly correlated to lung carcinogenesis. Oncotarget 7:18919–18926Google Scholar
- Crawford JO, Dixon K, Miller BG, Cherrie JW (2014) A review of the effectiveness of respirators in reducing exposure to polycyclic aromatic hydrocarbons for coke oven workers. Ann Occup Hyg 58:943–954Google Scholar
- Elovaara E, Vaananen V, Mikkola J (2003) Simultaneous analysis of naphthols, phenanthrols, and 1-hydroxypyrene in urine as biomarkers of polycyclic aromatic hydrocarbon exposure: Intraindividual variance in the urinary metabolite excretion profiles caused by intervention with beta-naphthoflavone induction in the rat. Arch Toxicol 77:183–193CrossRefGoogle Scholar
- Erhola M, Toyokuni S, Okada K, Tanaka T, Hiai H, Ochi H, Uchida K, Osawa T, Nieminen MM, Alho H, Kellokumpu-Lehtinen P (1997) Biomarker evidence of DNA oxidation in lung cancer patients: association of urinary 8-hydroxy-2′-deoxyguanosine excretion with radiotherapy, chemotherapy, and response to treatment. FEBS Lett 409:287–291CrossRefGoogle Scholar
- Gackowski D, Speina E, Zielinska M, Kowalewski J, Rozalski R, Siomek A, Paciorek T, Tudek B, Olinski R (2003) Products of oxidative DNA damage and repair as possible biomarkers of susceptibility to lung cancer. Cancer Res 63:4899–4902Google Scholar
- Haugen A, Becher G, Benestad C, Vahakangas K, Trivers GE, Newman MJ, Harris CC (1986) Determination of polycyclic aromatic hydrocarbons in the urine, benzo(a)pyrene diol epoxide-DNA adducts in lymphocyte DNA, and antibodies to the adducts in sera from coke oven workers exposed to measured amounts of polycyclic aromatic hydrocarbons in the work atmosphere. Cancer Res 46:4178–4183Google Scholar
- Moktar A, Singh R, Vadhanam MV, Ravoori S, Lillard JW, Gairola CG, Gupta RC (2011) Cigarette smoke condensate-induced oxidative DNA damage and its removal in human cervical cancer cells. Int J Oncol 39:941–947Google Scholar
- Palackal NT, Lee SH, Harvey RG, Blair IA, Penning TM (2002) Activation of polycyclic aromatic hydrocarbon trans-dihydrodiol proximate carcinogens by human aldo-keto reductase (akr1c) enzymes and their functional overexpression in human lung carcinoma (a549) cells. J Biol Chem 277:24799–24808CrossRefGoogle Scholar
- Rybka J, Kupczyk D, Kedziora-Kornatowska K, Pawluk H, Czuczejko J, Szewczyk-Golec K, Kozakiewicz M, Antonioli M, Carvalho LA, Kedziora J (2011) Age-related changes in an antioxidant defense system in elderly patients with essential hypertension compared with healthy controls. Redox Rep 16:71–77CrossRefGoogle Scholar
- Unwin J, Cocker J, Scobbie E, Chambers H (2006) An assessment of occupational exposure to polycyclic aromatic hydrocarbons in the uk. Ann Occup Hyg 50:395–403Google Scholar
- Yuan J, Chen L, Chen D, Guo H, Bi X, Ju Y, Jiang P, Shi J, Yu Z, Yang J, Li L, Jiang Q, Sheng G, Fu J, Wu T, Chen X (2008) Elevated serum polybrominated diphenyl ethers and thyroid-stimulating hormone associated with lymphocytic micronuclei in chinese workers from an e-waste dismantling site. Environ Sci Technol 42:2195–2200CrossRefGoogle Scholar