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Background. The Thai government has been developing its Eastern Economic Corridor (EEC), which spans three provinces, with the aim of improving connections with other Asian nations. Since this strategic development, the number of trucks, private car, and passenger car registrations have continued to grow, with a corresponding increase in related to benzene, toluene, ethylbenzene, and xylene (BTEX). Objectives. This study aims to compare the levels of trans, trans-muconic acid (t, t MA); toluene (TU); mandelic acid (MA); and methyl hippuric acid (MHA) in the urine of gas station employees, considering demographic and occupational factors. Material and methods. These employees worked either near or away from the fuel dispenser, and there 100 people in each group. Data were collected using interviews and testing environmental air and urine samples for benzene, toluene, ethyl benzene, and xylene (BTEX). Results. The results showed that BTEX concentrations were just detectable in all 200 cases (100%). The mean (±SD) urine level of t, t MA was 449.28 (±213.32) μg/g creatinine, while the median (min-max) was 428.23 (95.58-1202.56) μg/g creatinine. The mean TU was 0.011 (0.001) mg/L, while the median (min-max) was 0.011 (0.010-0.013) mg/L. MA levels were higher inside the pollution control zone than they were outside the zone (p=.009). Employees who practiced poor personal hygiene had relatively high urinary toluene and MHA levels (p=.009) and those who did not wear personal protective equipment (PPE) had relatively high MA levels (p=.040). Conclusion. The results of this study revealed statistically significant biomarkers influencing the levels of t, t MA; TU; MA; and MHA in urine. The recommendations of this study are that employers should provide their employees with suitable PPE, check regularly to ensure that it is worn, and strongly encourage employees to take care of their sanitation. Employees should take appropriate breaks and days off to minimize their exposure to BTEX.
DNA is constantly damaged and repaired in living cells. The repair products of the oxidative DNA lesions, i.e. oxidised nucleosides and bases, are poor substrates for the enzymes involved in nucleotide synthesis, are fairly water soluble, and generally excreted into the urine without further metabolism. Among the possible products, 8-oxo-2'-deoxyguanosine, 8-oxoguanine, thymine glycol, thymidine glycol and, 5-hydroxymethyluracil have so far been identified in urine. It should be emphasised that the excretion of the repair products in urine represents the average rate of damage in the total body whereas the level of oxidised bases in nuclear DNA is a concentration measurement in that specific tissuećells in the moment of sampling. The rate of oxidative DNA modifications has been studied in humans by means of the repair products as urinary biomarkers, particularly with respect to 8-oxo-2'-deoxyguanosine. The data obtained so far indicate that the important determinants of the oxidative damage rate include tobacco smoking, oxygen consumption and some inflammatory diseases whereas diet composition, energy restriction and antioxidant supplements have but a minimal influence, possibly with the exception of yet unidentified phytochemicals, e.g. from cruciferous vegetables. The data are consistent with the experimentally based notion that oxidative DNA damage is an important mutagenic and apparently carcinogenic factor. However, the proof of a causal relationship in humans is still warranted. In the future the use of biomarkers may provide this evidence and allow further investigations on the qualitative and quantitative importance of oxidative DNA modification and carcinogenesis in man, as well as elucidate possible preventive measures.
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