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颗粒物空气污染与血管反应性:公交站研究

Particulate air pollution and vascular reactivity: the bus stop study.

作者信息

Dales Robert, Liu Ling, Szyszkowicz Mietek, Dalipaj Mary, Willey Jeff, Kulka Ryan, Ruddy Terrence D

机构信息

Health Canada, A.L. 4602C, 400 Cooper Street, Room 2045, Ottawa, ON, Canada K1A 0K9.

出版信息

Int Arch Occup Environ Health. 2007 Nov;81(2):159-64. doi: 10.1007/s00420-007-0199-7. Epub 2007 May 11.

Abstract

OBJECTIVE

Particulate air pollution is associated with cardiovascular morbidity but mechanisms are not well understood. We tested the effects on vascular reactivity of exposure to fine particulates matter mass (PM(2.5)), number of particles <or=1 microm/m(3) (PM(1.0)) and nitrogen dioxide concentration (NO(2)).

METHOD

About 39 healthy volunteers sat outside for 2 h at two different Ottawa bus stops. Flow-mediated vasodilation (FMD) of the brachial artery was then measured by ultrasound and expressed as: (maximum artery diameter after release of a blood pressure cuff inflated above systolic pressure-baseline resting diameter)/baseline resting diameter.

RESULTS

A 30 microg/m(3) increase in PM(2.5) exposure corresponded to a 0.48% reduction in FMD, P=0.05 representing a 5% relative change in the maximum ability to dilate. Results were consistent between the two bus stops and not sensitive to type of analysis. No significant association was found between FMD and NO(2), PM(1.0) or traffic density.

CONCLUSION

PM(2.5) may reduce the capacity to vasodilate, a potential explanation for the documented association with cardiovascular morbidity.

摘要

目的

空气污染颗粒物与心血管疾病发病率相关,但其机制尚未完全明确。我们测试了暴露于细颗粒物质量(PM(2.5))、直径小于或等于1微米/立方米的颗粒物数量(PM(1.0))以及二氧化氮浓度(NO(2))对血管反应性的影响。

方法

约39名健康志愿者在渥太华两个不同的公交站点户外坐2小时。然后通过超声测量肱动脉的血流介导的血管舒张(FMD),并表示为:(收缩压以上充气的血压袖带松开后动脉最大直径 - 基线静息直径)/基线静息直径。

结果

PM(2.5)暴露量每增加30微克/立方米,FMD降低0.48%,P = 0.05,代表最大舒张能力相对变化5%。两个公交站点的结果一致,且对分析类型不敏感。未发现FMD与NO(2)、PM(1.0)或交通密度之间存在显著关联。

结论

PM(2.5)可能会降低血管舒张能力,这可能是其与心血管疾病发病率相关的一个潜在解释。

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