Barclay J L, Miller B G, Dick S, Dennekamp M, Ford I, Hillis G S, Ayres J G, Seaton A
Department of Cardiology, Aberdeen Royal Infirmary, UK.
Occup Environ Med. 2009 May;66(5):325-34. doi: 10.1136/oem.2008.039032. Epub 2008 Nov 18.
To investigate preclinical adverse effects of ambient particulate air pollution and nitrogen oxides in patients with heart failure.
A cohort of 132 non-smoking patients living in Aberdeen, Scotland, with stable chronic heart failure were enrolled in a repeated-measures panel study. Patients with atrial fibrillation or pacemakers were excluded. Participants were studied for 3 days every 2 months for up to 1 year with monitoring of pollutant exposure and concurrent measurements of pathophysiological responses. Measurements included daily area concentration of particulate matter with a median aerodynamic diameter of <10 micrometres (PM(10)), particle number concentration (PNC) and nitrogen oxides; daily estimated personal concentration of particulate matter with a median aerodynamic diameter of <2.5 micrometres (PM(2.5)) and PNC exposures; and 3-day cumulative personal nitrogen dioxide (NO(2)). Concurrent meteorological data were recorded. Blood was taken at the end of each 3-day block for assays of markers of endothelial activation, inflammation and coagulation. Cardiac rhythm was monitored by ambulatory Holter monitor during the final 24 h of each block.
The average 24 h background ambient PM(10) ranged from 7.4 to 68 microg.m(-3) and PNC from 454 to 11 283 particles.cm(-3). No associations were demonstrated between the incidence of arrhythmias, heart rate variability or haematological/biochemical measures and any variations in pollutant exposures at any lags.
Assuming that low-level pollution affects the parameters measured, these findings may suggest a beneficial effect of modern cardioprotective therapy, which may modify responses to external risk factors. Widespread use of such drugs in susceptible populations may in future reduce the adverse effects of air pollution on the heart.
研究环境细颗粒物空气污染和氮氧化物对心力衰竭患者的临床前不良影响。
一项重复测量的群组研究纳入了132名居住在苏格兰阿伯丁、患有稳定慢性心力衰竭的非吸烟患者。排除患有心房颤动或使用起搏器的患者。参与者每2个月接受3天的研究，为期1年，监测污染物暴露情况，并同时测量病理生理反应。测量内容包括空气动力学直径中位数<10微米的颗粒物（PM10）的每日区域浓度、颗粒数浓度（PNC）和氮氧化物；空气动力学直径中位数<2.5微米的颗粒物（PM2.5）的每日估计个人浓度和PNC暴露量；以及3天累积个人二氧化氮（NO2）。记录同期气象数据。在每个3天时间段结束时采集血液，用于检测内皮激活、炎症和凝血标志物。在每个时间段的最后24小时，通过动态心电图监测仪监测心律。
24小时背景环境PM10的平均浓度范围为7.4至68微克·立方米(-3)，PNC范围为454至11283颗粒·立方厘米(-3)。在任何滞后时间，心律失常发生率、心率变异性或血液学/生物化学指标与污染物暴露的任何变化之间均未显示出相关性。
假设低水平污染会影响所测量的参数，这些发现可能表明现代心脏保护疗法具有有益作用，可能会改变对外部危险因素的反应。这类药物在易感人群中的广泛使用未来可能会减少空气污染对心脏的不良影响。
