Associations between outdoor temperature and markers of inflammation: a cohort study.
Associations between outdoor temperature and markers of inflammation: a cohort study.
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DOI：
10.1186/1476-069x-9-42
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发表时间：
2010-07-23
期刊：
影响因子：
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通讯作者：
Schwartz J
中科院分区：
文献类型：
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作者：
Halonen JI;Zanobetti A;Sparrow D;Vokonas PS;Schwartz J
环境温度与心血管疾病死亡率之间的关系已得到充分证实。这项研究调查了炎症是否可能是导致与温度相关的心血管死亡的机制的一部分。研究人群包括673名男性，平均年龄74.6岁，居住在大波士顿地区。他们大约每4年进行一次检查，并在2000-2008年（共1254次就诊）抽取血液样本进行炎症标志物分析。我们使用混合效应模型来估计环境温度与多种炎症标志物（c反应蛋白、白细胞计数、可溶性血管细胞粘附分子-1、可溶性细胞间粘附分子-1、肿瘤坏死因子α和白细胞介素-1β、-6和-8）之间的关系。模型中使用了每个受试者的随机截点和几个可能的混杂因素，包括与燃烧有关的空气污染和臭氧。我们发现c反应蛋白与温度相关，有0到1天的滞后和长达4周的累积反应。我们观察到，在四周的移动平均温度中，每降低5°C， C反应蛋白增加24.9%[95%置信区间（CI）： 7.36, 45.2]。我们还观察到温度与可溶性细胞间粘附分子-1 （4.52%,95% CI: 1.05, 8.10，超过4周的移动平均值）以及温度与可溶性血管细胞粘附分子-1 （6.60%,95% CI: 1.31, 12.2，超过4周的移动平均值）之间存在类似的关联。惩罚样条模型没有偏离线性。温度和其他炎症指标之间没有关联。在老年男性中，长期暴露在低温环境中与炎症标志物水平升高有关。这表明炎症标志物是中间过程的一部分，这可能导致与冷有关的心血管死亡，而不是与热有关的心血管死亡。
Associations between ambient temperature and cardiovascular mortality are well established. This study investigated whether inflammation could be part of the mechanism leading to temperature-related cardiovascular deaths. The study population consisted of a cohort of 673 men with mean age of 74.6 years, living in the greater Boston area. They were seen for examination roughly every 4 years, and blood samples for inflammation marker analyses were drawn in 2000-2008 (total of 1254 visits). We used a mixed effects model to estimate the associations between ambient temperature and a variety of inflammation markers (C-reactive protein, white blood cell count, soluble Vascular Cell Adhesion Molecule-1, soluble Intercellular Adhesion Molecule-1, tumor necrosis factor alpha, and interleukins -1β, -6 and -8). Random intercept for each subject and several possible confounders, including combustion-related air pollution and ozone, were used in the models. We found a 0 to 1 day lagged and up to 4 weeks cumulative responses in C-reactive protein in association with temperature. We observed a 24.9% increase [95% Confidence interval (CI): 7.36, 45.2] in C-reactive protein for a 5°C decrease in the 4 weeks' moving average of temperature. We observed similar associations also between temperature and soluble Intercellular Adhesion Molecule-1 (4.52%, 95% CI: 1.05, 8.10, over 4 weeks' moving average), and between temperature and soluble Vascular Cell Adhesion Molecule-1 (6.60%, 95% CI: 1.31, 12.2 over 4 weeks' moving average). Penalized spline models showed no deviation from linearity. There were no associations between temperature and other inflammation markers. Cumulative exposure to decreased temperature is associated with an increase in inflammation marker levels among elderly men. This suggests that inflammation markers are part of intermediate processes, which may lead to cold-, but not heat-, related cardiovascular deaths.