RESUMO
In this study, we evaluated the effect of low and high molecular weight polycyclic aromatic hydrocarbons (PAHs),
Assuntos
Aspergillus/crescimento & desenvolvimento , Benzo(a)pireno/farmacologia , Micélio/efeitos dos fármacos , Fenantrenos/farmacologia , Hidrocarbonetos Policíclicos Aromáticos/farmacologia , Pirenos/farmacologia , Esporos Fúngicos/efeitos dos fármacos , Trichoderma/crescimento & desenvolvimento , Aspergillus/efeitos dos fármacos , Aspergillus/metabolismo , Biodegradação Ambiental , Hidrocarbonetos Policíclicos Aromáticos/metabolismo , Microbiologia do Solo , Poluentes do Solo , Trichoderma/efeitos dos fármacos , Trichoderma/metabolismoRESUMO
Epidemiologic studies have suggested the association between environmental exposure to volatile organic compounds (VOCs) and polycyclic aromatic hydrocarbons (PAHs) and the increased risk of incurring asthma. Yet there is little data regarding the relationship between personal exposure to air pollution and the incidence of asthma in children. This study was designed to evaluate the effect of exposure to air pollution on children with asthma by using exposure biomarkers. We assessed the exposure level to VOCs by measuring urinary concentrations of hippuric acid and muconic acid, and PAHs by 1-OH pyrene and 2-naphthol in 30 children with asthma and 30 children without asthma (control). The mean level of hippuric acid was 0.158+/-0.169micromol/mol creatinine in the asthma group and 0.148+/-0.249micromol/mol creatinine in the control group, with no statistical significance noted (p=0.30). The mean concentration of muconic acid was higher in the asthma group than in the control group (7.630+/-8.915micromol/mol creatinine vs. 3.390+/-4.526micromol/mol creatinine p=0.01). The mean level of urinary 1-OHP was higher in the asthma group (0.430+/-0.343micromol/mol creatinine) than the control group (0.239+/-0.175micromol/mol creatinine), which was statistically significant (p=0.03). There was no difference in the mean concentration of 2-NAP between the two groups (9.864+/-10.037micromol/mol in the asthma group vs. 9.157+/-9.640micromol/mol in the control group, p=0.96). In conclusion, this study suggests that VOCs and PAHs have some role in asthma.
Assuntos
Pré-Escolar , Feminino , Humanos , Masculino , Poluentes Atmosféricos/farmacologia , Asma/fisiopatologia , Estudos de Casos e Controles , Creatinina/urina , Hipuratos/urina , Naftóis/urina , Compostos Orgânicos/química , Hidrocarbonetos Policíclicos Aromáticos/farmacologia , Pirenos/metabolismo , Ácido Sórbico/análogos & derivados , VolatilizaçãoRESUMO
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous in the environment and originate from incomplete combustion process of organic materials. These compounds are bioactivated to reactive metabolites which bind covalently to DNA and subsequently initiate carcinogenesis. PAHs have been well established as an enzyme inducer of cytochrome P450 (CYP) such as CYP1A1 and CYP1A2. Caffeine is primarily metabolized by CYP1A2 to paraxanthine, so it has been used as a specific probe for assessing CYP1A2 activity. The purpose of this study was to compare CYP1A2 activity in female subjects that were automobile exhaust exposed and non-automobile exhaust exposed using serum paraxanthine/caffeine ratio as an index. Each subject took a 180 mg single oral dose of caffeine solution. Blood samples were collected before and 5 hours after caffeine intake. Serum samples were separated by centrifugation and stored at -20 degrees C until analysis by high performance liquid chromatography (HPLC). Carbon monoxide (CO) level in blood was also detected using spectrophotometer. The results showed that serum paraxanthine/caffeine ratio in exposed subjects was significantly higher than non-exposed subjects (mean +/- SE of 0.45 +/- 0.05 and 0.33 +/- 0.03, respectively; p < 0.05). CO level in exposed subjects was also significantly higher than non-exposed subjects (mean +/- SE of 4.03 +/- 0.21 and 3.01 +/- 0.18, respectively; p < 0.05). Conclusion: Paraxanthine/caffeine ratio, as an index for CYP1A2 activity, can be used to determine PAHs exposure. Automobile exhaust exposed subjects demonstrated significantly higher CYP1A2 activity than that of the non-exposed subjects. Exposed subjects have a possibly higher risk of chemical carcinogenesis.