Air pollution and blood markers of cardiovascular risk.
Air pollution and blood markers of cardiovascular risk.
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DOI：
10.1289/ehp.01109s3405
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发表时间：
2001-06
影响因子：
10.4
通讯作者：
中科院分区：
文献类型：
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最近的研究表明，空气污染与每年成千上万的心血管过早死亡有关。这些协会的机制仍不清楚。在这项研究中，我们研究了美国全国人口样本中心血管风险血液标志物与空气污染之间的关系。在美国第三次全国健康和营养检查调查（NHANES III）中，将空气污染浓度合并到受试者中，并检查了与纤维蛋白原水平和血小板和白色血细胞计数的关联。NHANES III中的受试者是美国人口的代表性样本。回归控制年龄，种族，性别，体重指数，目前吸烟，每天吸烟数量。复杂的调查设计处理使用混合模型与随机抽样现场效果。在单一污染物模型中，PM（10）（空气动力学质量中值直径小于10微米的颗粒物）与所有三种结果相关（p< 0.05）：二氧化硫（SO（2））仅与白色细胞计数显著相关，二氧化氮（NO（2））与血小板计数和纤维蛋白原显著相关，臭氧与任何结果均无关。在双污染物模型中，PM（10）仍然是控制SO（2）的白色细胞计数的重要预测因子，但反之亦然。PM（10）在含NO（2）的血小板计数模型中具有边缘显著性，并且NO（2）系数的符号反转。这些结果在控制室内暴露（木柴炉、环境烟草烟雾、煤气炉、壁炉）、饮食风险因素（饱和脂肪、酒精、咖啡因摄入量、n-3脂肪酸）和血清胆固醇的情况下是稳定的。影响的程度是适度的[例如，13 μ g/dL的纤维蛋白原，PM（下标）10（/下标）的四分位数范围（IQR）变化，95%置信区间（CI）4.6-22.1 mg/dL]。然而，对于相同的IQR变化，纤维蛋白原处于前10%的比值比为1.77（95%CI 1.26-2.49）。这些效应为死亡率研究提供了相当大的生物相容性。PM（10），而不是气态空气污染物，与心血管风险的血液标志物相关，这可能解释与早期死亡的流行病学联系。
Recent studies have linked air pollution to tens of thousands of premature cardiovascular deaths per year. The mechanisms of such associations remain unclear. In this study we examine the association between blood markers of cardiovascular risk and air pollution in a national sample of the U.S. population. Air pollution concentrations were merged to subjects in the Third National Health and Nutrition Examination Survey (NHANES III) in the United States, and the association with fibrinogen levels and counts of platelets and white blood cells were examined. The subjects in NHANES III are a representative sample of the U.S. population. Regressions controlled for age, race, sex, body mass index, current smoking, and number of cigarettes per day. The complex survey design was dealt with using mixed models with a random sampling site effect. In single-pollutant models, PM(10) (particulate matter with a mass median aerodynamic diameter less than 10 microm) was associated with all three outcomes (p< 0.05): Sulfur dioxide (SO(2)) was significantly associated only with white cell counts, nitrogen dioxide (NO(2)) with platelet counts and fibrinogen, and ozone with none of the outcomes. In two-pollutant models, PM(10) remained a significant predictor of white cell counts controlling for SO(2) but not vice versa. PM(10) was marginally significant in a model for platelet counts with NO(2), and the sign of the NO(2) coefficient was reversed. These results were stable with control for indoor exposures (wood stoves, environmental tobacco smoke, gas stoves, fireplaces), dietary risk factors (saturated fat, alcohol, caffeine intake, n-3 fatty acids), and serum cholesterol. The magnitude of the effects are modest [e.g., 13 microg/dL fibrinogen for an interquartile range (IQR) change in PM(subscript)10(/subscript), 95% confidence interval (CI) 4.6-22.1 mg/dL]. However, the odds ratio of being in the top 10% of fibrinogen for the same IQR change was 1.77 (95% CI 1.26-2.49). These effects provide considerable biologic plausibility to the mortality studies. PM(10), but not gaseous air pollutants, is associated with blood markers of cardiovascular risk, and this may explain epidemiologic associations with early deaths.