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环境木烟及其他颗粒物污染物与心脏病患者全身炎症、凝血和血栓形成生物标志物之间的关联。

Associations between ambient wood smoke and other particulate pollutants and biomarkers of systemic inflammation, coagulation and thrombosis in cardiac patients.

作者信息

Croft Daniel P, Cameron Scott J, Morrell Craig N, Lowenstein Charles J, Ling Frederick, Zareba Wojciech, Hopke Philip K, Utell Mark J, Thurston Sally W, Thevenet-Morrison Kelly, Evans Kristin A, Chalupa David, Rich David Q

机构信息

Division of Pulmonary and Critical Care, Department of Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY, USA.

Division of Cardiology, Department of Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY, USA.

出版信息

Environ Res. 2017 Apr;154:352-361. doi: 10.1016/j.envres.2017.01.027. Epub 2017 Feb 4.

DOI:10.1016/j.envres.2017.01.027
PMID:28167447
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5375102/
Abstract

BACKGROUND

Increased particulate air pollution has been associated with both an increased risk of myocardial infarction (MI) and adverse changes in cardiac biomarkers. Up to 30% of ambient wintertime fine particles (PM) in Rochester, NY are from wood burning. Our study examined associations between ambient levels of a marker of wood smoke (Delta-C) and other particulate air pollutants and biomarkers of inflammation, coagulation and thrombosis.

METHODS

We measured blood concentrations of C-reactive protein (CRP), D-dimer, fibrinogen, P-selectin, platelet factor 4 (PF-4), von Willebrand factor (vWF), and myeloperoxidase (MPO) of 135 patients undergoing cardiac catheterization during the winters of 2011-2013. We coupled these data with hourly ambient concentrations of Delta-C, black carbon (BC; marker of traffic pollution), and ultrafine (10-100nm; UFP), accumulation mode (100-500nm; AMP), and fine particles (<2.5µm; PM). Using linear regression models, we estimated the change in each biomarker associated with increased pollutant concentrations at intervals between 1 and 96h preceding blood collection.

RESULTS

Each 0.13µg/m increase in Delta-C concentration in the prior 12h was associated with a 0.91% increase in fibrinogen levels (95% CI=0.23%, 1.59%), but unexpectedly in the prior 48h, each 0.17µg/m increase in Delta-C concentration was associated with a 2.75% decrease in MPO levels (95% CI=-5.13%,-0.37%). We did not see associations between Delta-C concentrations and any other biomarkers. Interquartile range (IQR) increases in PM BC, UFP, and AMP concentrations were generally associated with increased CRP and fibrinogen, but not PF4, D-dimer, vWF, or P-selectin.

CONCLUSIONS

In a population of cardiac patients, we noted adverse changes in fibrinogen associated with increased concentrations of a marker of wood smoke. Increases in PM, BC, AMP, and UFP concentrations in the previous 96h were also associated with adverse changes in markers of systemic inflammation and coagulation, but not with markers of endothelial cell dysfunction or platelet activation.

摘要

背景

空气中颗粒物污染增加与心肌梗死(MI)风险升高及心脏生物标志物的不良变化均相关。在纽约州罗切斯特市,冬季环境中高达30%的细颗粒物(PM)来自木材燃烧。我们的研究检测了木烟标志物(Delta-C)的环境水平与其他颗粒物空气污染物以及炎症、凝血和血栓形成生物标志物之间的关联。

方法

我们测量了2011 - 2013年冬季接受心脏导管插入术的135例患者血液中C反应蛋白(CRP)、D-二聚体、纤维蛋白原、P-选择素、血小板因子4(PF-4)、血管性血友病因子(vWF)和髓过氧化物酶(MPO)的浓度。我们将这些数据与Delta-C、黑碳(BC;交通污染标志物)以及超细颗粒物(10 - 100nm;UFP)、积聚模态颗粒物(100 - 500nm;AMP)和细颗粒物(<2.5µm;PM)的每小时环境浓度相结合。使用线性回归模型,我们估计了在采血前1至96小时的时间间隔内,每种生物标志物随污染物浓度升高的变化情况。

结果

在之前12小时内,Delta-C浓度每增加0.13µg/m³与纤维蛋白原水平升高0.91%相关(95%置信区间=0.23%,1.59%),但出乎意料的是,在之前48小时内,Delta-C浓度每增加0.17µg/m³与MPO水平降低2.75%相关(95%置信区间=-5.13%,-0.37%)。我们未发现Delta-C浓度与任何其他生物标志物之间存在关联。PM、BC、UFP和AMP浓度的四分位数间距(IQR)增加通常与CRP和纤维蛋白原升高相关,但与PF4、D-二聚体、vWF或P-选择素无关。

结论

在心脏病患者群体中,我们注意到纤维蛋白原的不良变化与木烟标志物浓度升高有关。在之前96小时内,PM、BC、AMP和UFP浓度升高也与全身炎症和凝血标志物的不良变化相关,但与内皮细胞功能障碍或血小板活化标志物无关。

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