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社区老年人群个体、室内及室外PM2.5暴露特征及与健康风险评估关联性

Indoor, outdoor, and personal exposure to PM2.5 and associated health risk in community-dwelling elderly residents in Fuzhou city, 2021: a cross-sectional study

  • 摘要:
    目的 分析福州市某社区老年人群细颗粒物PM2.5个体、室内、室外的暴露特征及与健康风险评估的关联。
    方法 以福州市某社区为现场,在夏冬季分别对140名和107名老年人进行连续3日的个体、室内和室外PM2.5暴露测量,同时开展环境因素及健康状况问卷调查。采用美国环保局推荐的健康风险评估模型评估健康风险。
    结果 福州市社区老年人群个体、室内和室外PM2.5日均暴露浓度分别为61.83、41.37、32.00 µg/m3,呈现个体 > 室内 > 室外浓度。个体PM2.5浓度夏季高于冬季(71.78 µg/m3 vs. 50.72 µg/m3),室内外PM2.5浓度夏季低于冬季(室内:38.43 µg/m3 vs. 49.76 µg/m3,室外:32.00 µg/m3 vs. 34.53 µg/m3)。室内外PM2.5浓度较低时(室内:< 57.95 µg/m3,室外:< 49.38 µg/m3),个体浓度明显高于室内外浓度;室内外PM2.5浓度较高时,个体浓度近似于室内外浓度。多环芳烃(PAHs)和金属组分的暴露健康风险呈现个体高于室内外、冬季高于夏季。PAHs对个体具有潜在致癌风险(冬季:12.74 × 10 – 6,夏季1.673 × 10 – 6);金属元素Mn,As和Cd具有非致癌风险(均HQ > 1);As,Ni,Cd和Pb对个体具有潜在致癌风险,其中As具有致癌风险(夏季:128.272 × 10 – 6,冬季:226.214 × 10 – 6)。
    结论 室内外PM2.5浓度较低时,采用室内外浓度代替个体浓度会低估个体真实的暴露水平;室内外PM2.5浓度较高时,采用室内外浓度可近似于个体暴露水平。基于精准个体PM2.5及其组分暴露水平进行健康风险评估,可减少因暴露评估不准确而导致的人群健康效应偏差。

     

    Abstract:
    Objective To investigate personal total, indoor, outdoor exposure to particulate matter less than 2.5 μm in aerodynamic diameter (PM2.5) and health risks associated with the exposure among community-dwelling elderly in Fuzhou city.
    Methods A total of 247 residents (≥ 60 years of age, living at the current residence for at least 3 years, without serious respiratory/circulatory disease and without disability) were recruited from a community in Fuzhou city, Fujian province, using random sampling stratified by residential floor. Three-day continuous sampling of PM2.5 was performed by using a personal particulate sampler, a constant-temperature, constant-flow particulate sampler in the living room, and an automatic outdoor particulate sampler within 2 km of the participants' homes during the winter season for 140 participants and during the summer season for 107 participants in 2021. All participants were interviewed with a questionnaire on demographics, living conditions, health status, lifestyle behaviors, and activities during the PM2.5 sampling period. PM2.5 concentration was measured with the weighing method; polycyclic aromatic hydrocarbons (PAHs) and metal elemental components in collected PM2.5 were determined by ultra-high performance liquid chromatography and inductively coupled plasma mass spectrometry. The health risk associated with PAHs and metals in PM2.5 was assessed by using the health risk assessment model recommended by the United States Environmental Protection Agency.
    Results The mean daily exposure concentrations of PM2.5 for the participants were 61.83 µg/m3 for personal exposure, 41.37 µg/m3 for indoor exposure, and 32.00 µg/m3 for outdoor exposure, with descending order of personal, indoor, and outdoor exposure concentrations. The total personal PM2.5 exposure concentration was higher in summer than in winter (71.78 µg/m3 vs. 50.72 µg/m3), while the personal indoor and outdoor PM2.5 exposure concentrations were lower in summer than in winter (indoor: 38.43 µg/m3 vs. 49.76 µg/m3, outdoor: 32.00 µg/m3 vs. 34.53 µg/m3). When personal indoor and outdoor PM2.5 concentrations were low (indoor < 57.95 µg/m3, outdoor < 49.38 µg/m3), the total personal exposure concentrations were significantly higher than the personal indoor and outdoor exposure concentrations; when personal indoor and outdoor PM2.5 concentrations were high, the total personal exposure concentration was close to the personal indoor and outdoor exposure concentrations. The health risks of exposure to PAHs and metal constituents in PM2.5 were higher for total personal exposure than for personal indoor and outdoor exposure, and higher in winter than in summer. Exposure to PAHs in PM2.5 posed a potential carcinogenic risk to the participants, with excess lifetime cancer risks (ELCRs) of 12.74 × 10 – 6 and 1.673 × 10 – 6 for winter and summer exposure, respectively. Exposure to manganese, arsenic, and cadmium in PM2.5 posed non-carcinogenic risks to the participants, all with health quotients greater than 1. Exposure to arsenic, nickel, cadmium, and lead in PM2.5 posed potential carcinogenic risks to the participants, with ELCRs of 128.272 × 10 – 6 and 226.214 × 10 – 6 for summer and winter arsenic exposure, respectively.
    Conclusions When indoor and outdoor PM2.5 concentrations are low, taking indoor and outdoor concentrations as a surrogate for total personal exposure concentrations will underestimate actual personal exposure; when indoor and outdoor PM2.5 concentrations are high, using indoor and outdoor concentrations may approximate total personal exposure. Health risk assessment based on accurate personal exposure to PM2.5 and its constituents can reduce the bias in population health effects caused by inaccurate exposure assessment.

     

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