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Purpose: 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. Methods: 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. Results: 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). Conclusions: Our findings quantitatively demonstrate that workers exposed to coke oven fumes and smoking will cause more serious DNA oxidative damage. [ABSTRACT FROM AUTHOR]

Purpose: To assess changes in oxidative DNA damage and lung function amongst a group of foundry workers resulting from an engineering intervention to reduce air respirable dust in their working environment. Methods: We studied all 22 workers recruited from a typical small Taiwanese iron foundry plant before and 3 months after improvements to air exhaust control. The effectiveness of the air exhaust intervention in reducing respirable dust and SiO was determined by personal breathing-zone air sampling. Initial baseline biomarker measurements were taken of lung function and urinary 8-hydroxy-deoxyguanosine (8-OHdG) in all of the workers, with follow-up measurements taken 3 months after the engineering control was put in place. Generalized estimating equations were used to assess the effect of the intervention on lung function and oxidative DNA damage. Results: Following the intervention, respirable dust density decreased from 2.87 ± 1.38 mg/m to 1.60 ± 0.70 mg/m ( p = 0.07), and SiO concentration decreased from 0.43 ± 0.25 mg/m to 0.18 ± 0.11 mg/m ( p < 0.05). Compared to initial baseline, significant improvements were found in lung function (FVC, FEV1, FVC%pred and FEV1%pred) amongst the workers after the engineering intervention. A significant increase in concentration of urinary 8-OHdG was observed after the engineering intervention in smokers, but not in non-smokers. Conclusions: These findings indicate that reductions in workplace respirable dust and SiO concentration can result in improved lung function amongst foundry workers. [ABSTRACT FROM AUTHOR]

In order to investigate a role of paraoxonase 1 ( PON1) polymorphism in organophosphorus (OP)-induced 8-hydroxydeoxyguanosine (8-OHdG) levels, urinary metabolites of OP, PON1 genotypes, and 8-OHdG levels in leukocyte and urine were measured in OP indoor insecticide sprayers and controls in summer and winter. The study population contained 18 male sprayers and age-matched 18 male controls. Sprayers were primarily exposed to OP insecticides (mainly fenitrothion, dichlorvos, chlorpyrifos, and diazinon), and partially to pyrethroids (mainly permethrin) and carbamates (mainly propoxur). Urinary metabolites of OP were measured by gas chromatography-mass spectrometry. 8-OHdG levels in leukocyte and urine were measured by ELISA kit. PON1 genotype was identified using allele-specific fluorogenic TaqMan probes. The mean concentrations of urinary dimethyl phosphate (DMP) and total dialkyl phosphates (DAP) in summer and those of 8-OHdG in summer and winter were significantly higher in OP sprayers than controls. This resulted in a significant positive correlation between 8-OHdG levels and urinary DMP or DAP, suggesting a correlation between OP metabolites and production of oxidative stress. Of PON1 genotypes, incidences of Q/Q, Q/R, and R/R types were 17, 39, and 44% in OP sprayers and controls, respectively. Although PON1 polymorphism did not contribute to the leukocyte and urinary 8-OHdG levels, the urinary OP metabolite concentrations in summer showed a significant decrease as the number Q allele decreased. These results indicate that an increase in OP metabolites is associated with a high level of oxidative stress in OP sprayers, although the contribution of the PON1 polymorphism to the metabolism of OP is still unclear. [ABSTRACT FROM AUTHOR]

Oxidative DNA damage is considered to play an important role in pathophysiological processes, ageing and cancer. So far major interest has been on measuring 8-hydroxy-2′-deoxyguanosine (8-OHdG), the preferred methods relying on HPLC or GC-mass spectrometry. The high biological relevance of 8-OHdG is due to its ability to induce G→T transversions, which are among the most frequent somatic mutations found in human cancers. Effects of workplace exposures on the level of white blood cell 8-OHdG or urinary 8-OHdG have been reported with controversial results. Exposures examined include asbestos, azo-dyes, benzene, fine particulate matter (PM2.5), glassworks, polycyclic aromatic hydrocarbons (PAHs), rubber manufacturing, silica, metals, styrene, toluene and xylenes. The available data indicate that there is still a lack of well established dose-response relations between occupational or environmental exposures and the induction of 8-OHdG. Smoking has been most consistently identified as a confounder for 8-OHdG, but various occupational studies did not reveal higher levels of 8-OHdG in smokers. Despite the conflicting results, the reported studies show promise for 8-OHdG as a biomarker of oxidative stress associated with chemical exposure. However, there are critical aspects related to the analytical challenge, artifactual production of 8-OHdG, inter- and intra-individual variation, confounding factors and inter-laboratory differences, implying that further work is needed to reach a consensus on the background level of 8-OHdG. [ABSTRACT FROM AUTHOR]

Objectives: To investigate the effect of dioxin on the formation of oxidative DNA damage and urinary mutagenicity, we measured the concentrations of serum dioxins and lymphocytic 8-hydroxydeoxyguanosine (8-OH-dG) in 57 male waste incinerator workers, urinary 8-OH-dG and urinary mutagenicity in 29 male waste incinerator workers. Methods: Information about the subjects was obtained from a questionnaire. Concentrations of polychlorinated dibenzo- p-dioxin (PCDD), polychlorinated dibenzofuran (PCDF), and coplanar-polychlorinated-biphenyl (Co-PCB) in serum samples from the workers were measured with a high-resolution gas chromatograph /high-resolution mass spectrometer. Lymphocytic and urinary 8-OH-dG levels were measured with a high-performance liquid chromatography-electrochemical detector system. The urinary mutagenicity was measured with umu assay. Results: The lymphocytic 8-OH-dG level showed a negative association with the serum dioxin level (total value of TEQ-PCDD, PCDF, and Co-PCB). Urinary 8-OH-dG did not show correlation with serum dioxin level, but showed positive correlation with the smoking index. Conclusions: With respect to the subjects‘ serum dioxin level, dioxin did not increase the urinary 8-OH-dG level by oxidative DNA damage, but upregulation of the primary defenses with oxidative damage and/or DNA repair system activity might have occurred. [ABSTRACT FROM AUTHOR]

Objective. To investigate the potential for exposure to polycyclic aromatic hydrocarbons (PAHs) to induce oxidative DNA damage, we conducted a cross-sectional study in coke-oven workers employed at an iron–steel factory. Methods. The study population contained 119 coke-oven workers from different work areas of the oven and 38 controls. Personal information on age, employment duration, smoking habit and alcohol consumption was obtained at an interview. Leukocyte 8-hydroxydeoxyguanosine (8-OHdG) was measured by high performance liquid chromatography with electrochemical detection. Leukocyte aromatic DNA adducts as effective dose, and urinary 1-hydroxypyren as internal dose, were also measured, and used to analyze the relationship of 8-OHdG with other biomarkers for PAH exposure, tobacco smoke and alcohol consumption. Results. The leukocyte 8-OHdG revealed a wide inter-individual variation. The highest 8-OHdG level was detected in bottom-workers of the coke-oven. There were significant differences among the four different work areas (P=0.02). We could not find significant correlation between 8-OHdG levels and urinary 1-hydroxypyrene, but a weakly positive correlation was found between 8-OHdG and leukocyte aromatic DNA adducts among all subjects (r=0.19 P=0.03). We could not observe any effect of smoking and alcohol drinking on 8-OHdG production. Conclusion. We could not find clear evidence that PAH exposure induces oxidative DNA damage. [ABSTRACT FROM AUTHOR]

Objective: To determine the potential for asphalt fume exposure to increase DNA damage, we conducted a cross-sectional study of roofers involved in the application of roofing asphalt. Methods: DNA strand breaks and the ratio of 8-hydroxydeoxyguanosine (8-OHdG) to 2-deoxyguanosine (dG) were measured in peripheral blood leukocytes of roofers. In addition, urinary excretion of 8-OHdG and 8-epi-prostaglandin F2α (8-epi-PGF) was also measured. The study population consisted of 26 roofers exposed to roofing asphalt and 15 construction workers not exposed to asphalt during the past 5 years. A subset of asphalt roofers (n=19) was exposed to coal-tar pitch dust (coal tar) during removal of existing roofs prior to applying hot asphalt. Personal air monitoring was performed for one work-week to measure exposure to total particulates, benzene-soluble fraction of total particulates, and polycyclic aromatic compounds (PACs). Urinary 1-OH-pyrene levels were measured as an internal biomarker of PAC exposure. Results: Full-shift breathing zone measurements for total particulates, benzene-solubles and PACs were significantly higher for coal-tar exposed workers than for roofers not exposed to coal tar. Similarly, urinary 1-OH-pyrene levels were higher in coal-tar exposed roofers than roofers not exposed to coal tar. Total particulates or benzene-soluble fractions were not associated with urinary 1-OH-pyrene, but PAC exposure was highly correlated with urinary 1-OH-pyrene. When stratified by 1-OH-pyrene excretion, DNA strand breaks increased in a dose-dependent manner, and leukocyte 8-OHdG/dG decreased in a dose-dependent manner. Significant changes in DNA damage appeared to be linked to PACs from coal-tar exposure, although asphalt fume alone was associated with a small but significant increase in urinary 1-OH-pyrene and DNA strand breaks. Conclusions: Results are consistent with previous reports that asphalt or coal-tar exposure can cause DNA damage. Urinary 8-epi-PGF remained relatively constant during the week for virtually all subjects, regardless of exposure indicating that neither asphalt nor coal-tar exposure induces an overt oxidative stress. A small, but statistically significant increase in 8OHdG was evident in end-of-week urine samples compared with start-of-week urine samples in roofers exposed to coal-tar. The increase in urinary 8OHdG coupled with the decrease in leukocyte 8-OHdG/dG, suggests that coal-tar exposure induces protective or repair mechanisms that result in reduced levels of steady-state oxidative-DNA damage. [ABSTRACT FROM AUTHOR]

Objectives: The present study was performed to investigate the relationship between work-related factors, including psychological stress, and the formation of a type of oxidative DNA damage, 8-hydroxydeoxyguanosine (8-OH-dG), in order to examine their possible risk factor for occupational carcinogenesis. Methods: A total of 54 healthy workers (27 male and 27 female, aged 41.2 ± 12.5 years) in a company were investigated for 8-OH-dG levels in the peripheral blood leukocytes at the time of a questionnaire survey regarding several factors, such as working hours, workload, fatigue, sleep, psychological stress and the prospect of alleviating it. Subjects were limited to non-smoking and non-drinking workers to exclude the influence of cigarette smoking and alcohol drinking, which have been reported to have associations with the formation of 8-OH-dG. Results: The levels of 8-OH-dG in female subjects were significantly related to the perceived workload (F=5.56, P=0.010), the perceived psychological stress (F=6.15, P=0.007), and the impossibility of alleviating stress (F=3.82, P=0.048). No associations were observed in male subjects. Conclusions: Psychological stress and perceived overwork appear to be related to the pathogenesis of cancer via the formation of 8-OH-dG, particularly in female workers. [ABSTRACT FROM AUTHOR]

Objective: To examine radical-induced DNA damage and its elimination in workers exposed to quartz and in patients with silicosis, and to assess the relationship of these effects to lung function. Methods: Blood and spontaneous urine samples were obtained from active, quartz-exposed workers without silicosis (n=63), and from retired workers with silicosis (n=42). Levels of 8-hydroxydeoxyguanosine (8-OHdG) were determined in peripheral blood leukocyte DNA and urine, by the use of high-performance liquid chromatography coupled with ultra violet- (UV) and electrochemical detection. Results: No significant differences in the mean levels of 8-OHdG in leukocyte DNA and of urinary excretion of 8-OHdG were found between silicosis patients and quartz-exposed healthy workers. However, in the group of silicosis patients with increased oxidative DNA damage the urinary excretion of 8-OHdG was lower than in the corresponding group of active workers without silicosis. In the case of silicosis, urinary 8-OHdG correlated positively, and 8-OHdG in DNA correlated negatively, with forced expiratory volume in one second (FEV1) and forced vital capacity (FVC). Healthy workers with a personally estimated high dust exposure in the workplace showed higher levels of 8-OHdG in DNA than did workers with moderate dust exposure. No association of 8-OHdG formation and/or elimination with duration of employment, field of activity, smoking or age was found. Conclusion: Our findings suggest that a less effective repair of 8-OHdG is associated with a higher degree of pulmonary airway obstruction in patients with silicosis. [ABSTRACT FROM AUTHOR]

Previous epidemiological studies have indicated that industrial art glass workers have increased mortality risks for certain types of cancer and for cardio-and cerebrovascular disease. To test the hypothesis that increased oxidative stress might contribute to these increased mortality risks, the urinary levels of the lipid peroxidation product, malondialdehyde (MDA), and the oxidative DNA adduct, 8-hydroxydeoxyguanosine (8OHdG) were determined in 343 workers (230 men and 113 women) from the art glass industry in the southeast of Sweden. Of the study subjects, 199 (181 men and 18 women) were engaged in the process of glass production and were regarded as exposed, whereas the remainders performed clerical, warehouse and other service work and were regarded as unexposed. One hundred and sixteen were smokers (75 men and 41 women) and 215 were non-smokers (142 men and 73 women). The findings indicate that (a) exposure to industrial art glass work per se does not cause any major oxidative stress as measured by urinary levels of MDA and 8OHdG, (b) the effects from smoking per se are limited to increased lipid peroxidation among men, and (c) joint exposure to industrial art glass work and smoking may cause increased lipid peroxidation among men and increased DNA hydroxylation among both men and women. While these findings provide no evidence for increased oxidative stress due to industrial art glass work per se, the increased 8OHdG excretion in workers who smoke may be associated with a higher risk of developing free radical-dependent degenerative disease including cancer [ABSTRACT FROM AUTHOR]