Electric Power Research Institute, Palo Alto, California, USA.
Environ Health Perspect. 2011 Apr;119(4):474-80. doi: 10.1289/ehp.1002831. Epub 2010 Dec 15.
Exposure to fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] is linked to adverse cardiopulmonary health effects; however, the responsible constituents are not well defined.
We used a rat model to investigate linkages between cardiac effects of concentrated ambient particle (CAP) constituents and source factors using a unique, highly time-resolved data set.
Spontaneously hypertensive rats inhaled Detroit Michigan, CAPs during summer or winter (2005-2006) for 13 consecutive days. Electrocardiogram data were recorded continuously, and heart rate (HR) and heart rate variability (HRV) metrics were derived. Extensive CAP characterization, including use of a Semicontinuous Elements in Aerosol Sampler (SEAS), was performed, and positive matrix factorization was applied to investigate source factors.
Mean CAP exposure concentrations were 518 μg/m(3) and 357 μg/m(3) in the summer and winter, respectively. Significant reductions in the standard deviation of the normal-to-normal intervals (SDNN) in the summer were strongly associated with cement/lime, iron/steel, and gasoline/diesel factors, whereas associations with the sludge factor and components were less consistent. In winter, increases in HR were associated with a refinery factor and its components. CAP-associated HR decreases in winter were linked to sludge incineration, cement/lime, and coal/secondary sulfate factors and most of their associated components. Specific relationships for increased root mean square of the standard deviation of successive normal-to-normal intervals (RMSSD) in winter were difficult to determine because of lack of consistency between factors and associated constituents.
Our results indicate that specific modulation of cardiac function in Detroit was most strongly linked to local industrial sources. Findings also highlight the need to consider both factor analytical results and component-specific results when interpreting findings.
暴露于细颗粒物[空气动力学直径≤2.5μm（PM2.5）]与不良心肺健康影响有关，但负责的成分尚未明确定义。
我们使用大鼠模型，使用独特的、高度时间分辨数据集，研究浓缩环境颗粒（CAP）成分的心脏效应与来源因素之间的联系。
自发性高血压大鼠在夏季或冬季（2005-2006 年）连续 13 天吸入底特律密歇根州的 CAP。连续记录心电图数据，并得出心率（HR）和心率变异性（HRV）指标。进行了广泛的 CAP 特性描述，包括使用半连续元素气溶胶采样器（SEAS），并应用正矩阵因子分析来研究来源因素。
夏季和冬季的平均 CAP 暴露浓度分别为 518μg/m(3)和 357μg/m(3)。夏季正常到正常间隔标准差（SDNN）的显著降低与水泥/石灰、铁/钢和汽油/柴油因素密切相关，而与污泥因素及其成分的相关性不太一致。冬季 HR 的增加与炼油厂因素及其成分有关。冬季 CAP 相关的 HR 降低与污泥焚烧、水泥/石灰和煤/二次硫酸盐因素及其大多数相关成分有关。由于缺乏因素和相关成分之间的一致性，冬季 RMSSD 的均方根标准差的增加的特定关系很难确定。
我们的结果表明，底特律特定的心脏功能调节与当地工业来源最为密切相关。研究结果还强调，在解释研究结果时，需要同时考虑因子分析结果和成分特异性结果。
