宁波市某城区大气PM2.5中PAHs源解析及健康风险评估
Source apportionment and health risk assessment of polycyclic aromatic hydrocarbons in PM2.5 in an urban area of Ningbo
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摘要:
目的 调查宁波市某城区大气PM2.5中多环芳烃（PAHs）污染水平，判断其来源，评估其对人群的潜在健康风险。
方法 于2016年每月10—17日（9月采样时间为8—15日），在宁波市江北区儿童医院4层楼顶平台采集颗粒物样本，采用高效液相色谱法测定不同季节大气PM2.5中16种PAHs水平。采用特定PAHs比值来判断PM2.5中PAHs来源。采用美国环境保护署超级基金风险评估指南推荐的吸入模型对PAHs进行人群健康风险评估。
结果 PM2.5年均质量浓度为54 μg/m3，超过标准限值（35 μg/m3）。PM2.5中16种PAHs每日总质量浓度介于1.60~31.26ng/m3，平均6.11ng/m3。PM2.5中BaP年均质量浓度为0.50ng/m3，未超过我国环境空气质量标准（1 ng/m3），但其日均质量浓度超标率为2.1%。16种PAHs总质量浓度季节分布呈冬季高、夏季低。从特定比值判断，该采样点大气PM2.5中PAHs主要来源于汽油燃烧。人群吸入PM2.5中PAHs无致癌风险（Risk=0.54×10-6），而有非致癌风险（HQ=1.06）。
结论 该采样点存在大气PM2.5污染，人群通过吸入途径暴露于PM2.5中PAHs无致癌风险，但有非致癌风险。
Abstract:Objective To investigate the pollution levels of polycyclic aromatic hydrocarbons (PAHs) in PM2.5 in an urban area of Ningbo, identify their sources, and evaluate their potential health risks.
Methods Particulate matter samples were collected from the four-storey roof platform of Ningbo Jiangbei Children's Hospital from 10th to 17th of every month except September (from 8th to 15th) in 2016. High performance liquid chromatography was used to determine the levels of 16 polycyclic aromatic hydrocarbons (PAHs) in collected atmospheric PM2.5 samples. PAHs ratios were used to identify sources of PAHs. The inhalation model recommended by Risk Assessment Guideline for Superfund of the US Environmental Protection Agency was used to assess the health risks of PAHs.
Results The average annual concentration of PM2.5 was 54 μg/m3, exceeding the national limit (35 μg/m3). The total concentrations of 16 PAHs in PM2.5 were between 1.60 and 31.26 ng/m3, and the average value was 6.11 ng/m3. The average annual concentration of BaP in PM2.5 was 0.50 ng/m3, which did not exceed the ambient air quality standard of China (1 ng/m3), but the unqualified rate of daily average concentration was 2.1%. The total concentrations of 16 PAHs were high in winter and low in summer. According to the predetermined diagnostic ratios, the PAHs in PM2.5 at the selected sampling site were mainly derived from gasoline combustion. There was no carcinogenic risk (Risk=0.54×10-6) but was non-carcinogenic risk (HQ=1.06) if populations were exposed to the sampled PAHs in PM2.5.
Conclusion PM2.5 pollution is identified at the sampling site. Exposure to PAHs in PM2.5 by inhaling in the selected area poses no human carcinogenic risk but has human non-carcinogenic risk.
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