Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA.
Environ Health. 2010 Jul 23;9:42. doi: 10.1186/1476-069X-9-42.
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 -1beta, -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 degrees 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.
环境温度与心血管死亡率之间的关联已得到充分证实。本研究旨在探讨炎症是否可能是导致与温度相关的心血管死亡的机制之一。
研究人群由 673 名年龄在 74.6 岁左右的男性组成,居住在大波士顿地区。他们每 4 年接受一次检查,并在 2000-2008 年期间采集了 1254 次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各种炎症标志物(C 反应蛋白、白细胞计数、可溶性血管细胞黏附分子-1、可溶性细胞间黏附分子-1、肿瘤坏死因子-α以及白细胞介素-1β、-6 和 -8)之间的关联。模型中使用了每个受试者的随机截距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 反应蛋白与温度之间存在 0 至 1 天的滞后和长达 4 周的累积反应。我们发现,在 4 周的移动平均温度中,温度每下降 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黏附分子-1(4.52%,95%CI:1.05,8.10,4 周移动平均)之间以及温度与可溶性血管细胞黏附分子-1(6.60%,95%CI:1.31,12.2,4 周移动平均)之间也存在类似的关联。惩罚样条模型显示没有偏离线性。温度与其他炎症标志物之间没有关联。
累积暴露于低温与老年男性炎症标志物水平的升高有关。这表明炎症标志物是中间过程的一部分,可能导致与冷有关的心血管死亡,但与热无关。