Association between Residential Exposure to Air Pollution and Incident Coronary Heart Disease Is Not Mediated by Leukocyte Telomere Length: A UK Biobank Study.

Association between Residential Exposure to Air Pollution and Incident Coronary Heart Disease Is Not Mediated by Leukocyte Telomere Length: A UK Biobank Study.
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DOI:
10.3390/toxics11060489
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发表时间:
2023-05-28
期刊:
影响因子:
4.6
通讯作者:
Brugge D
Brugge D
中科院分区:
环境科学与生态学3区
文献类型:
--
作者:
Kuo CL;Liu R;Godoy LDC;Pilling LC;Fortinsky RH;Brugge D

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更高的空气污染暴露和更短的白细胞端粒长度(LTL)都与冠心病(CHD)风险增加有关,并共享合理的机制,包括炎症。LTL可作为空气污染暴露的生物标志物,并可进行干预以降低CHD的风险。据我们所知,我们是第一个测试的中介作用的LTL之间的关系,空气污染暴露和冠心病事件。使用英国生物银行(UKB)数据(n = 317,601),我们进行了一项前瞻性研究,将住宅空气污染暴露(PM2.5,PM10,NO2,NOx)和LTL与平均随访12.6年的冠心病事件联系起来。采用考克斯比例风险模型和惩罚样条函数的广义加性模型来模拟污染物浓度和LTL与冠心病事件的关系。我们发现空气污染暴露与LTL和CHD之间存在非线性关系。在较低范围内的污染物浓度与较长的LTL和降低冠心病的风险呈递减相关。然而,较低的污染物浓度与降低CHD风险之间的关联很少受到LTL(<3%)的介导。我们的研究结果表明,空气污染通过不涉及LTL的途径影响CHD。需要复制改进的空气污染测量,更准确地评估个人暴露。
Higher air pollution exposure and shorter leukocyte telomere length (LTL) are both associated with increased risk of coronary heart disease (CHD), and share plausible mechanisms, including inflammation. LTL may serve as a biomarker of air pollution exposure and may be intervened with to reduce the risk of CHD. To the best of our knowledge, we are the first to test the mediation effect of LTL in the relationship between air pollution exposure and incident CHD. Using the UK Biobank (UKB) data (n = 317,601), we conducted a prospective study linking residential air pollution exposure (PM2.5, PM10, NO2, NOx) and LTL to incident CHD during a mean follow-up of 12.6 years. Cox proportional hazards models and generalized additive models with penalized spline functions were used to model the associations of pollutant concentrations and LTL with incident CHD. We found non-linear associations of air pollution exposure with LTL and CHD. Pollutant concentrations in the lower range were decreasingly associated with longer LTL and reduced risk of CHD. The associations between lower pollutant concentrations and reduced risk of CHD, however, were minimally mediated by LTL (<3%). Our findings suggest that air pollution influences CHD through pathways that do not involve LTL. Replication is needed with improved measurements of air pollution that more accurately assesses personal exposure.
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DOI: 10.1126/science.aaz6876
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期刊: Science (New York, N.Y.)
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