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俄亥俄州斯图本维尔的 PM2.5 对高血压大鼠心脏功能的影响取决于风向和特定来源。

PM2.5-induced changes in cardiac function of hypertensive rats depend on wind direction and specific sources in Steubenville, Ohio.

机构信息

University of Michigan, Ann Arbor, MI, USA.

出版信息

Inhal Toxicol. 2011 Jun;23(7):417-30. doi: 10.3109/08958378.2011.580387.

DOI:10.3109/08958378.2011.580387
PMID:21639710
Abstract

BACKGROUND

Increases in particulate matter less than 2.5 µm (PM(2.5)) in ambient air is linked to acute cardiovascular morbidity and mortality. Specific components and potential emission sources of PM(2.5) responsible for adverse health effects of cardiovascular function are unclear.

METHODS

Spontaneously hypertensive rats were implemented with radiotelemeters to record ECG responses during inhalation exposure to concentrated ambient particles (CAPs) for 13 consecutive days in Steubenville, OH. Changes in heart rate (HR) and its variability (HRV) were compared to PM(2.5) trace elements in 30-min time frames to capture acute physiological responses with real-time fluctuations in PM(2.5) composition. Using positive matrix factorization, six major source factors were identified: (i) coal/secondary, (ii) mobile sources, (iii) metal coating/processing, (iv) iron/steel manufacturing, (v) lead and (vi) incineration.

RESULTS

Exposure-related changes in HR and HRV were dependant on winds predominately from either the northeast (NE) or southwest (SW). During SW winds, the metal processing factor was associated with increased HR, whereas factors of incineration, lead and iron/steel with NE winds were associated with decreased HR. Decreased SDNN was dominated during NE winds by the incinerator factor, and with SW winds by the metal factor. Metals and mobile source factors also had minor impacts on decreased SDNN with NE winds. Individual elemental components loaded onto these factors generally showed significant associations, although there were some discrepancies.

CONCLUSIONS

Acute cardiovascular changes in response to ambient PM(2.5) exposure can be attributed to specific PM constituents and sources linked with incineration, metal processing, and iron/steel production.

摘要

背景

环境空气中小于 2.5 µm 的颗粒物(PM(2.5))的增加与急性心血管发病率和死亡率有关。导致心血管功能不良影响的 PM(2.5)的特定成分和潜在排放源尚不清楚。

方法

在俄亥俄州斯图本维尔,对自发性高血压大鼠实施无线电遥测,以在 13 天内连续记录吸入浓缩环境颗粒物(CAPs)时的心电图反应。将心率(HR)及其变异性(HRV)的变化与 PM(2.5)微量元素进行比较,以 30 分钟的时间框架捕捉 PM(2.5)成分实时波动的急性生理反应。使用正矩阵因子分解,确定了六个主要来源因素:(i)煤/二次,(ii)移动源,(iii)金属涂层/加工,(iv)钢铁制造,(v)铅和(vi)焚烧。

结果

与暴露相关的 HR 和 HRV 变化取决于主要来自东北(NE)或西南(SW)的风。在 SW 风期间,金属加工因子与 HR 增加有关,而在 NE 风期间,焚烧、铅和钢铁制造因子与 HR 降低有关。在 NE 风期间,SDNN 的降低主要由焚烧器因子主导,而在 SW 风期间则由金属因子主导。金属和移动源因子也对 NE 风下 SDNN 的降低有较小的影响。加载到这些因子上的个别元素成分通常显示出显著的关联,尽管存在一些差异。

结论

环境 PM(2.5)暴露引起的急性心血管变化可归因于与焚烧、金属加工和钢铁生产相关的特定 PM 成分和来源。

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