Synergistic Increase of Oxidative Stress and Tumor Markers in PAH-Exposed Workers

Gao, Meili; Chen, Lei; Li, Yongfei; Xue, Xiaochang; Chen, Lan; Wang, Lina; Shah, Walayat; Kong, Yu

doi:10.7314/apjcp.2014.15.17.7105

Cited by 13 publications

(10 citation statements)

References 55 publications

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“…One probable explanation of this finding is that cigarette smoke contains about 50 potent carcinogens, including PAHs, nicotine, and other organic chemicals (Pryor, 1997) that are capable of increasing oxygen free-radical production and lipid peroxidation. Gao et al (2014) also noticed that smoking led to higher MDA concentrations in : correlation coefficient, model; 8-OHdG: 8-oxo-2 0 -deoxyguanosine; MDA: malondialdehyde. a Model using stepwise method and an adjusting tail moment, 8-oxodG, and MDA content (excluding control individuals).…”

Section: Discussionmentioning

confidence: 86%

“…One probable explanation of this finding is that cigarette smoke contains about 50 potent carcinogens, including PAHs, nicotine, and other organic chemicals (Pryor, 1997) that are capable of increasing oxygen free-radical production and lipid peroxidation. Gao et al (2014) also noticed that smoking led to higher MDA concentrations in PAH-exposed workers. Alcohol also enhances the production of ROS and causes lipid peroxidation, either directly or by exhausting antioxidative defense substances, which can induce oxidative DNA damage in humans (Guo and Ren, 2010).…”

Section: Discussionmentioning

confidence: 89%

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A multibiomarker approach to evaluate the effect of polyaromatic hydrocarbon exposure on oxidative and genotoxic damage in tandoor workers

et al. 2019

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We conducted a cohort study of tandoor workers to evaluate the relationship between the biomarkers of oxidative and genotoxic damage and exposure to polyaromatic hydrocarbons. A series of oxidative and genotoxic damage biomarkers, including urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG), malondialdehyde (MDA) content, and tail moment (TM) by comet assay, was studied. A total of 76 tandoor workers and 79 demographically matched healthy individuals as controls were included. Our results showed that the tandoor workers had significantly higher urinary levels of 1-hydroxypyrene, urinary 8-OHdG, MDA content, and TM compared with the control population. The concentration of all these biomarkers increased with age in the control population as well as tandoor workers. In tandoor workers, significant variation in MDA, 8-oxodG (8-oxo-2′-deoxyguanosine) and TM concentration was detected between smokers (5.08 ± 1.72 nmol/mL, 16.01 ± 4.94 ng/mg creatinine, and 5.87 ± 0.98 µm, respectively) and nonsmokers (3.84 ± 0.98 nmol/mL, 13.74 ± 3.60 ng/mg creatinine, and 5.32 ± 0.69 µm, respectively). A similar pattern was obtained for the control population. We did not obtain significant variations for alcoholics and tobacco chewers. A significant increase in all these three biomarkers was observed with the increase in the period of work exposure in tandoor workers. Multivariate regression analysis also revealed that urinary 8-oxodG, MDA, and TM were statistically significantly related to age and period of work exposure. Overall, the present study showed that the exposure to wood smoke in tandoor workers under occupational conditions led to increased DNA damage because of oxidative stress and genotoxicity. These biomarkers, therefore, are good indices to assess oxidative DNA damage in these workers exposed to occupational genotoxicants. It is also necessary to make preventive changes in work conditions and lifestyle, which will help these occupational workers to lead a healthy life.

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Section: Discussionmentioning

confidence: 86%

“…One probable explanation of this finding is that cigarette smoke contains about 50 potent carcinogens, including PAHs, nicotine, and other organic chemicals (Pryor, 1997) that are capable of increasing oxygen free-radical production and lipid peroxidation. Gao et al (2014) also noticed that smoking led to higher MDA concentrations in PAH-exposed workers. Alcohol also enhances the production of ROS and causes lipid peroxidation, either directly or by exhausting antioxidative defense substances, which can induce oxidative DNA damage in humans (Guo and Ren, 2010).…”

Section: Discussionmentioning

confidence: 89%

A multibiomarker approach to evaluate the effect of polyaromatic hydrocarbon exposure on oxidative and genotoxic damage in tandoor workers

et al. 2019

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“…We do not deny the possibility of deficiency of vitamin C implicated to the rising level of oxidative DNA damage in people who eat grilled food (Figure 1). Moreover, the genetic profile of biotransformation carcinogens from grilled meat may play a role in activation and produce free electrons and elevated 8-OHdG [20,35,36]. Thus, reactive free electrons deplete vitamin C.…”

Section: Discussionmentioning

confidence: 99%

Diet contains carcinogens and deficiency of vitamin C determines the level of oxidative DNA damage among Jakarta toll collectors

Laelasari

Kusnoputranto²,

Budiawan

et al. 2018

biomedicalresearch

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Consuming meat food products that undergo high-temperature combustion is able to provide opportunities exposed to carcinogenic substances and leads to oxidative stress. Oxidative stress is also a precondition for the occurrence of DNA damage and cancer can be detected by the presence of 8hydroxy-'2-deoxyguanosine (8OHdG). The study aimed to investigate whether the high prevalence of oxidative stress in Jakarta highway toll collector is independently or causally implicated in deficiency of vitamin C and the grilled food as the third factor modified the association. A cross-sectional study and urinary 8-OHdG was detected using the Enzyme-Link Immunosorbent Assay (ELISA) method on 161 toll gate collectors. The study found a strong relationship between grilled food and 8-OHdG (p-value 0.037); prevalence risk ratio (PRR) 2.01 (95% CI 1.044-3.890). However, relationship between variable vitamin C and the 8-OHdG stratified by grilled food founded inverse negatively, it was due to the high frequency of subjects 8-OHdG presented significantly with the deficiency of vitamin C. There was not enough intake of vitamin C among people who ate grilled food. Mantel-Haenzel formula was calculated and the estimation found the condition of independence from the test were X 2 MH =0.843 among the group who consumed the grilled food. The association between intake of grilled food and oxidative stress is the mere result of the effect of deficiency of vitamin C. Special attention should be given to minimize diet containing various carcinogens like the meat grilling process with a high temperature to decrease degenerative diseases and cancer risk in sub-population with high expose to air pollution.

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“…Smoking can significantly modify the effects of urinary 1-hydroxypyrene on high concentrations of urinary 8-OHdG during coexposure to both light or heavy smoking and high 1-hydroxypyrene levels [32]. Urinary 1-hydroxypyrene is a useful biomarker for evaluating total PAH exposure, and coke oven workers with heavy smoking showed more serious DNA oxidative damage than nonsmokers [33][34][35]. Measurement of BPDE-I-DNA adduct levels in coke plant workers is essential in determining cancer risk due to high exposure to PAHs, particularly B[a]P [29].…”

Section: Biomarkers and Coke Oven Workersmentioning

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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Synergistic Increase of Oxidative Stress and Tumor Markers in PAH-Exposed Workers

Cited by 13 publications

References 55 publications

A multibiomarker approach to evaluate the effect of polyaromatic hydrocarbon exposure on oxidative and genotoxic damage in tandoor workers

A multibiomarker approach to evaluate the effect of polyaromatic hydrocarbon exposure on oxidative and genotoxic damage in tandoor workers

Diet contains carcinogens and deficiency of vitamin C determines the level of oxidative DNA damage among Jakarta toll collectors

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

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