Environmental tobacco smoke exposure and ischaemic heart disease: an evaluation of the evidence

Environmental tobacco smoke exposure and ischaemic heart disease: an evaluation of the evidence
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DOI:
10.1136/bmj.315.7114.973
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发表时间:
1997-10-18
影响因子:
105.7
通讯作者:
Wald, NJ
Wald, NJ
中科院分区:
医学1区
文献类型:
--
作者:
Law, MR;Morris, JK;Wald, NJ

文献摘要

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目的:估计暴露于环境烟草烟雾引起的缺血性心脏病的风险,并解释为什么相关的过量风险几乎是每天吸烟20支的一半,而暴露于环境烟草烟雾的风险仅为吸烟的1%左右。设计:荟萃分析所有已发表的19项可接受的缺血性心脏病风险研究,包括与吸烟者一起生活的终身不吸烟者和与非吸烟者一起生活的人的缺血性心脏病风险研究,5项吸烟和缺血性心脏病的大型前瞻性研究,以及血小板聚集研究和烟草烟雾暴露饮食研究。结果:在65岁时,与暴露于环境烟草烟雾相关的缺血性心脏病的相对风险为1.30(95%可信区间为1.22至1.38)。在同一年龄,每天吸一根烟的估计相对风险相似(1.39(1.18至1.64)),而每天吸20根烟的估计相对风险为1.78(1.31至2.44)。两项独立的分析表明,与吸烟者生活在一起的非吸烟者的饮食使他们患缺血性心脏病的风险高出6%,因此环境中吸烟的直接影响是使风险增加23%(14%至33%),因为1.30/1.06 = 1.23。血小板聚集为低剂量效应提供了一种合理且定量一致的机制。在实验中,暴露于环境中的烟草烟雾导致血小板聚集增加,预计会产生急性效应,使缺血性心脏病的风险增加34%。结论:吸入他人的烟雾是导致缺血性心脏病的重要且可避免的原因,它会使一个人患缺血性心脏病的风险增加四分之一。
Objectives: To estimate the risk of ischaemic heart disease caused by exposure to environmental tobacco smoke and to explain why the associated excess risk is almost half that of smoking 20 cigarettes per day when the exposure is only about 1% that of smoking.Design: Meta-analysis of all 19 acceptable published studies of risk of ischaemic heart disease in lifelong non-smokers who live with a smoker and in those who live with a non-smoker, five large prospective studies of smoking and ischaemic heart disease, and studies of platelet aggregation and studies of diet according to exposure to tobacco smoke.Results: The relative risk of ischaemic heart disease associated with exposure to environmental tobacco smoke was 1.30 (95% confidence interval 1.22 to 1.38) at age 65. At the same age the estimated relative risk associated with smoking one cigarette per day was similar (1.39 (1.18 to 1.64)), while for 20 per day it was 1.78 (1.31 to 2.44). Two separate analyses indicated that non-smokers who live with smokers eat a diet that places them at a 6% higher risk of ischaemic heart disease, so the direct effect of environmental tobacco smoke is to increase risk by 23% (14% to 33%), since 1.30/1.06 = 1.23. Platelet aggregation provides a plausible and quantitatively consistent mechanism for the low dose effect. The increase in platelet aggregation produced experimentally by exposure to environmental tobacco smoke would be expected to have acute effects increasing the risk of ischaemic heart disease by 34%.Conclusion: Breathing other people's smoke is an important and avoidable cause of ischaemic heart disease, increasing a person's risk by a quarter.