意大利撒丁岛小学生低水平环境苯暴露和氧化 DNA 损伤的生物标志物。
Biomarkers of Low-Level Environmental Exposure to Benzene and Oxidative DNA Damage in Primary School Children in Sardinia, Italy.
机构信息
Department of Medical Sciences and Public Health, University of Cagliari, Monserrato, 092109 Cagliari, Italy.
Department of Biomedical and Dental Sciences and Morpho-Functional Imaging, University of Messina, 98122 Messina, Italy.
出版信息
Int J Environ Res Public Health. 2021 Apr 27;18(9):4644. doi: 10.3390/ijerph18094644.
BACKGROUND
The main anthropic sources of exposure to airborne benzene include vehicular traffic, cigarette smoke, and industrial emissions.
METHODS
To detect early genotoxic effects of environmental exposure to benzene, we monitored environmental, personal, and indoor airborne benzene in children living in an urban area and an area near a petrochemical plant. We also used urinary benzene and S-phenylmercapturic acid (S-PMA) as biomarkers of benzene exposure and urinary 8-hydroxydeoxyguanosine (8-OHdG) as a biomarker of early genotoxic effects.
RESULTS
Although always below the European Union limit of 5 μg/m, airborne benzene levels were more elevated in the indoor, outdoor, and personal samples from the industrial surroundings compared to the urban area ( = 0.026, = 0.005, and = 0.001, respectively). Children living in the surroundings of the petrochemical plant had urinary benzene values significantly higher than those from the urban area in both the morning and evening samples ( = 0.01 and = 0.02, respectively). Results of multiple regression modelling showed that age was a significant predictor of 8-OHdG excretion, independent of the sampling hour. Moreover, at the low exposure level experienced by the children participating in this study, neither personal or indoor airborne benzene level, nor personal monitoring data, affected 8-OHdG excretion.
CONCLUSIONS
Our results suggest the importance of biological monitoring of low-level environmental exposure and its relation to risk of genotoxic effects among children.
背景
空气中苯的主要人为暴露源包括机动车交通、香烟烟雾和工业排放。
方法
为了检测环境苯暴露的早期遗传毒性效应，我们监测了居住在城市地区和石化厂附近地区的儿童的环境、个人和室内空气苯。我们还将尿苯和 S-苯巯基尿酸（S-PMA）用作苯暴露的生物标志物，将尿 8-羟基脱氧鸟苷（8-OHdG）用作早期遗传毒性效应的生物标志物。
结果
尽管始终低于欧盟规定的 5μg/m，但与城市地区相比，石化厂周边地区的室内、室外和个人样本中的空气苯水平更高（=0.026、=0.005 和=0.001，分别）。石化厂周边地区的儿童在早晨和晚上的尿液苯值均明显高于城市地区（=0.01 和=0.02，分别）。多元回归模型结果显示，年龄是 8-OHdG 排泄的一个重要预测因子，独立于采样时间。此外，在参与本研究的儿童所经历的低暴露水平下，个人或室内空气苯水平或个人监测数据均未影响 8-OHdG 的排泄。
结论
我们的研究结果表明，生物监测低水平环境暴露及其与儿童遗传毒性效应风险的关系非常重要。
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