評估郵差個人暴露於交通空氣污染物質對心血管功能的影響

Abstract

許多毒理學與流行病學的研究已經指出交通相關的污染物質會增加心血管的致死率的風險以及影響心血管的功能，特別是一些易感受族群者，像是老年人或已患有心血管疾病的病人。然而之前的研究往往採用固定點，例如一般測站的採樣結果作為個人暴露，這樣會造成暴露評估上的誤差。因此，此研究一共從新莊郵局徵選了18位健康的郵務人員；這群受測者在外出送信的過程中會配戴個人五階微粒採樣器以及直讀式臭氧儀。健康方面採用外出回來時的心跳變異性的五種指標（HRV）以及血管彈性的指標（CAVI）。每位受測者當他們騎車送信時自星期一到星期五進行連續五天的採樣。我們採用混合式受體模式(linear mixed-effect models)進行暴露與健康評估。監測站的採樣與個人暴露結果有差異，測站會低估個人的微粒暴露特別是小的微粒（直徑小於0.25μm），但會高估個人的臭氧暴露。大微粒的個人暴露預測只跟固定測站的數據以及溫度或濕度有關。針對小微粒的個人暴露預測，選取固定測站小微粒的濃度以及個人和主要道路間的距離、風速和溫度可以提高預測能力，縱相關係數（longitudinal correlation）可自0.61提升到0.85。至於個人即時性臭氧的暴露預測則可藉由固定側站的臭氧及一氧化碳濃度，人到測站的距離或車速作為變相，縱相關係數可自0.41提升到0.51。個人小微粒的暴露會造成心跳變異速率(HRV)相關指標的下降，但個人臭氧的暴露只會造成SDNN此單一指標的上升；又以小微粒對心跳變異速率的影響較為重要。每升高17.46μg/m3會造成14.50%的SDNN下降。至於血管彈性指標則與個人臭氧和大微粒有相關性。每上升20ppb的臭氧會造成5.31%血管彈性指標上升。因此交通污染物質確實對人體的心血管功能造成傷害，且不同的物質像大微粒，小微粒或臭氧對人體造成危害的途徑是不相同的。採用個人採樣器有助於此個人暴露與健康上的研究。

Although traffic-related pollutants have been associated with increased cardiovascular mortality and affected the cardiovascular functions, most studies used the central site monitoring data as surrogates for personal exposure. To examine the associations between traffic-related air pollution and cardiovascular functions, we used the personal five-sized-fraction particular matter sampler (PCIS; cut point: 2.5, 1.0, 0.5 and 0.25 μm) and personal real-time ozone monitor to assess personal exposure. We recruited 18 healthy adults from the Sinjhuang Post Office in Taipei County, Taiwan. We sampled PM and ozone when they worked outside by motorcycles. In this exploratory study, the health endpoints of those subjects were postsample HRV indices and Cardiao-ankle vascular index (CAVI) as an arterial stiffness index. We used mixed-effect models to estimate the personal exposure from fixed-site data and also to estimate the health effects from personal particles and ozone exposure. The fixed site monitoring data underestimated personal PM exposure, especially for the small particles with diameter < 0.25μm (different ratio = 1.72). However, fixed site data overestimated personal ozone exposure (different ratio = -0.23). The models including fixed-site PM data, distance to the major road, wind speed, temperature were increased the correlation from 0.61 to 0.85 for small particles with aerodynamic diameter less than 0.25μm. Large particle only was associated significantly (p value <0.05) with temperature and relative humidity in the fixed-effect models after adjusting fixed-site PM data. The fixed site O3, CO, distance from fixed-site station or speed were chosen as the variables for estimate the real-time personal ozone exposure (r = 0.50). We also found that increased exposure to small particles (<0.25μm) was associated with decreased HRV indices but increased ozone exposure significantly was associated with increased SDNN. For a 17.46μg/m3 increase in PM <0.25&micro;m, SDNN decreased 14.50%. However, ozone and PM between 1.0 to2.5μm were associated with increased Cardio-ankle vascular index (CAVI). An interquartile increase of 20ppb in the average ozone exposure was associated with 5.31% increase in CAVI. Different size-fraction PM and ozone exposure were associated with cardiovascular effects. Large PM, small PM and ozone have different pathway to affect the health response. The use of personal exposure improved the association between health outcomes and exposure and decrease the misclassification.