Harvard T.H. Chan School of Public Health, 677 Huntington Ave, Boston, MA 02115, United States; Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States.
Harvard T.H. Chan School of Public Health, 677 Huntington Ave, Boston, MA 02115, United States; Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States; Tulane School of Public Health and Tropical Medicine, New Orleans, LA, United States.
Environ Res. 2019 Apr;171:36-43. doi: 10.1016/j.envres.2018.10.027. Epub 2018 Oct 28.
Short-term exposure to air pollution has been associated with cardiovascular events, potentially by promoting endothelial cell activation and inflammation. A few large-scale studies have examined the associations and have had mixed results.
We included 3820 non-current smoking participants (mean age 56 years, 54% women) from the Framingham Offspring cohort examinations 7 (1998-2001) and 8 (2005-2008), and Third Generation cohort examination 1 (2002-2005), who lived within 50 km of a central monitoring station. We calculated the 1- to 7-day moving averages of fine particulate matter (PM), black carbon (BC), sulfate (SO), nitrogen oxides (NO), and ozone before examination visits. We used linear mixed effect models for P-selectin, monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule 1, lipoprotein-associated phospholipase A2 activity and mass, and osteoprotegerin that were measured up to twice, and linear regression models for CD40 ligand and interleukin-18 that were measured once, adjusting for demographics, life style and clinical factors, socioeconomic position, time, and meteorology.
We found negative associations of PM and BC with P-selectin, of ozone with MCP-1, and of SO and NO with osteoprotegerin. At the 5-day moving average, a 5 µg/m higher PM was associated with 1.6% (95% CI: - 2.8, - 0.3) lower levels of P-selectin; a 10 ppb higher ozone was associated with 1.7% (95% CI: - 3.2, - 0.1) lower levels of MCP-1; and a 20 ppb higher NO was associated with 2.0% (95% CI: - 3.6, - 0.4) lower levels of osteoprotegerin.
We did not find evidence of positive associations between short-term air pollution exposure and endothelial cell activation. On the contrary, short-term exposure to higher levels of ambient pollutants were associated with lower levels of P-selectin, MCP-1, and osteoprotegerin in the Framingham Heart Study.
短期暴露于空气污染与心血管事件有关,可能是通过促进内皮细胞激活和炎症。一些大规模研究已经检查了这些关联,结果喜忧参半。
我们纳入了弗雷明汉后代队列检查 7(1998-2001 年)和 8(2005-2008 年)以及第三代队列检查 1(2002-2005 年)中 3820 名非当前吸烟者(平均年龄 56 岁,54%为女性),这些人居住在距离中心监测站 50 公里以内。我们计算了检查前 1 至 7 天的细颗粒物(PM)、黑碳(BC)、硫酸盐(SO)、氮氧化物(NO)和臭氧的移动平均值。我们使用线性混合效应模型对 P-选择素、单核细胞趋化蛋白 1(MCP-1)、细胞间黏附分子 1、脂蛋白相关磷脂酶 A2 活性和质量以及骨保护素进行了测量,这些物质的测量次数最多为两次,而使用线性回归模型对 CD40 配体和白细胞介素-18 进行了一次测量,这些模型都经过了调整,以适应人口统计学、生活方式和临床因素、社会经济地位、时间和气象条件。
我们发现 PM 和 BC 与 P-选择素呈负相关,臭氧与 MCP-1 呈负相关,SO 和 NO 与骨保护素呈负相关。在 5 天移动平均值中,PM 每增加 5µg/m,P-选择素水平降低 1.6%(95%可信区间:-2.8,-0.3);臭氧每增加 10 ppb,MCP-1 水平降低 1.7%(95%可信区间:-3.2,-0.1);NO 每增加 20 ppb,骨保护素水平降低 2.0%(95%可信区间:-3.6,-0.4)。
我们没有发现短期空气污染暴露与内皮细胞激活之间存在正相关的证据。相反,在弗雷明汉心脏研究中,短期暴露于较高水平的环境污染物与 P-选择素、MCP-1 和骨保护素水平降低有关。