Department of Environmental and Occupational Health, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, UPM Serdang 43400, Selangor, Malaysia.
Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, UPM Serdang 43400, Selangor, Malaysia.
Int J Environ Res Public Health. 2021 Mar 4;18(5):2575. doi: 10.3390/ijerph18052575.
This study aimed to assess the association of exposure to particle-bound (PM) polycyclic aromatic hydrocarbons (PAHs) with potential genotoxicity and cancer risk among children living near the petrochemical industry and comparative populations in Malaysia. PM samples were collected using a low-volume sampler for 24 h at three primary schools located within 5 km of the industrial area and three comparative schools more than 20 km away from any industrial activity. A gas chromatography-mass spectrometer was used to determine the analysis of 16 United States Environmental Protection Agency (USEPA) priority PAHs. A total of 205 children were randomly selected to assess the DNA damage in buccal cells, employing the comet assay. Total PAHs measured in exposed and comparative schools varied, respectively, from 61.60 to 64.64 ng m and from 5.93 to 35.06 ng m. The PAH emission in exposed schools was contributed mainly by traffic and industrial emissions, dependent on the source apportionment. The 95th percentiles of the incremental lifetime cancer risk estimated using Monte Carlo simulation revealed that the inhalation risk for the exposed children and comparative populations was 2.22 × 10 and 2.95 × 10, respectively. The degree of DNA injury was substantially more severe among the exposed children relative to the comparative community. This study reveals that higher exposure to PAHs increases the risk of genotoxic effects and cancer among children.
本研究旨在评估儿童在石化工业区附近及马来西亚其他地区的暴露于颗粒结合态（PM）多环芳烃（PAHs）与潜在遗传毒性和癌症风险之间的关联。在距离工业区 5 公里范围内的三所小学和距离任何工业活动 20 公里以上的三所比较学校，使用小体积采样器采集了 24 小时的 PM 样本。使用气相色谱-质谱联用仪对美国环保署（USEPA）优先 PAHs 的 16 种分析物进行了分析。共随机选择了 205 名儿童，采用彗星试验评估口腔细胞的 DNA 损伤情况。暴露组和对照组学校测量的总多环芳烃分别为 61.60 至 64.64ng/m 和 5.93 至 35.06ng/m。暴露组学校的 PAH 排放主要来自交通和工业排放，具体取决于源分配。使用蒙特卡罗模拟估计的增量终生癌症风险的第 95 百分位数表明，暴露儿童和对照组人群的吸入风险分别为 2.22×10 和 2.95×10。与对照组相比，暴露组儿童的 DNA 损伤程度更为严重。本研究表明，PAHs 暴露水平升高会增加儿童的遗传毒性效应和癌症风险。
