Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • The urinary levels of OHP among the exposed workers were

    2021-10-16

    The urinary levels of 1-OHP among the exposed workers were higher than those reported for a Brazilian group of charcoal workers (0.07 μmol mol creatinine) exposed to wood smoke (Kato et al., 2004), and for nonsmoking bus drivers (0.19 μmol mol creatinine) and nonsmoking mail carriers (0.11 μmol mol creatinine) in a Danish population (Hansen et al., 2004). Nevertheless, these levels were lower than those reported for nonsmoking Italian coke-oven workers (0.94 μmol mol creatinine), who were engaged in various tasks (Clonfero et al., 1995), and for nonsmoking Korean coke-oven workers (2.81 μmol mol creatinine) (Nan et al., 2001). The observed levels of 1-OHP in the sample of exposed workers were also lower than those of nonsmoking individuals exposed to diesel exhaust, including workers of the diesel plants (2.18 μmol mol creatinine) and street vendors (2.18 μmol mol creatinine) in the urban area of Santiago, Chile (Adonis et al., 2003). Our results showed that the Carmofur of 1-OHP was significantly lower in the older individuals of the non-exposed group. Breathing behavior could be responsible for this effect (Jacob and Seidel, 2002). However, no such effect was observed in the exposed sugarcane workers; hence, this decrease may be an artifact. The levels of 1-OHP were higher in the exposed workers carrying the CYP1A1⁎2A, ⁎2B, ⁎4 and GSTP1 polymorphisms, but the difference was not significant. Our results are in agreement with Pan et al. (1998), who found no influence of the GSTM1 or CYP1A1 (Ile/Val) polymorphisms on 1-OHP excretion in a group of 99 Chinese coke-oven workers. Likewise, no influence of the CYP1A1⁎2A and ⁎2B and GSTM1 genetic polymorphisms on the urinary levels of 1-OHP was detected in workers of two electric steel plants and an iron foundry that were exposed to high levels of PAHs (Apostoli et al., 2003). Hemminki et al. (1997) also found no influence of genotypes GSTM1 or CYP1A1 on urinary 1-pyreno levels in foundry workers. In contrast, gene–environment interactions with the excretion of 1-OHP were confirmed by Alexandrie et al. (2000) in aluminum smelter workers, where the CYP1A1⁎2B and GSTM1 polymorphisms were found to have a significant influence on 1-OHP excretion. These authors also showed that total particulate-associated PAH exposure, use of respiratory protection devices and metabolizing genotype for the CYP1A1 and GSTM1 genes significantly determined urinary excretion of 1-OHP. Our study showed no significant differences in the urinary levels of 1-OHP in individuals with a null GSTM1 genotype. This finding is in agreement with Merlo et al. (1998). Actually, GSTM1 activity is not directly linked to the metabolism of 1-OHP, which is, in fact, mainly excreted as a glucuronide conjugate. Nevertheless, Alexandrie et al. (2000), Adonis et al. (2003), and Apostoli et al. (2003), who demonstrated an effect of polymorphism on urinary 1-OHP levels, explained the positive correlation observed between the null genotype and 1-OHP excretion by suggesting that a deficiency in GSTM1 activity may increase the glucuronidation pathway, as a result of accumulation of PAH derivatives that are not conjugated with glutathione and which may cause the induction of CYP1A1 and increase 1-OHP. Considering that the main routes of occupational exposure to PAHs are inhalation and cutaneous absorption (Alexandrie et al., 2000), and that extra-hepatic CYP1A1 is primarily expressed in the lung, it can be suggested that people working in polluted places, such as sugarcane fields that were burnt, are exposed to high levels of inhalable particle matter and PAHs, and might therefore be at high risk to develop long-term effects such as lung cancer. This effect might be regulated by individual differences in the efficiency to metabolize PAHs such as BaP or pyrene (Adonis et al., 2003). The urinary excretion of 1-OHP in workers has shown a high degree of interindividual variation (Alexandrie et al., 2000, Einistö et al., 1990) that may be explained by genetic, environmental and/or lifestyle factors. Metabolic activation and detoxification processes have been shown to be crucial for individual susceptibility to the exposure to genotoxic carcinogens and to influence the excretion of mutagens in urine. For example, glutathione S-transferases (GSTs) are important for detoxifying a number of mutagenic compounds, including metabolites of PAHs.