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PM2.5 来源解析的氧化剂生成能力。

Oxidant generation capacity of source-apportioned PM2.5.

机构信息

Eckerd College, St Petersburg, Florida, USA.

出版信息

Inhal Toxicol. 2010 Dec;22 Suppl 2(0 2):29-36. doi: 10.3109/08958378.2010.509368. Epub 2010 Sep 16.

Abstract

While many studies found associations between ambient particulate matter (PM) and morbidity or mortality outcomes, it is unclear whether these associations were dependent on the composition of PM, which varies with the source of that PM. We address this knowledge gap by conducting a time-series PM-health effects assessment that specifically investigates the role of source-apportioned fine PM (PM2.5) on the oxidant generation capacity that might be responsible for respiratory and cardiovascular health outcomes. Daily PM2.5 composition speciation and black carbon (BC) measurements, conducted in rural New York for 303 days between March 2003 and January 2005, were analyzed using factor analysis source-apportionment model, and five source categories (transported aerosol/secondary sulfate, resuspended soil, metals, residual oil combustion, and industrial/incineration) were identified. After the exposure of human epithelial cells (BEAS-2B) to these PM2.5 samples, cellular nuclear factor-κB (NF-κB) activation showed a relatively significant association Ni (concentration averaging 38 ng/m(3)), and weaker but still significant correlations with Ba (13 ng/m(3)), Mn (9 ng/m(3)), and Fe (500 ng/m(3)). The single-source regression analysis of NF-κB signal showed significant association with metal source only. Our results showed that metals in PM2.5 were the important source for cellular oxidant generation and may be responsible for subsequent health effects associate with particle air pollution.

摘要

虽然许多研究发现环境颗粒物(PM)与发病率或死亡率之间存在关联,但目前尚不清楚这些关联是否取决于 PM 的组成,而 PM 的组成因 PM 的来源而异。我们通过进行时间序列 PM-健康效应评估来解决这一知识空白,该评估专门研究了源分配细颗粒物(PM2.5)对氧化剂生成能力的作用,而氧化剂生成能力可能是导致呼吸和心血管健康结果的原因。在 2003 年 3 月至 2005 年 1 月的 303 天内,在纽约农村进行了每日 PM2.5 成分谱和黑碳(BC)测量,并使用因子分析源分配模型对其进行了分析,确定了五个来源类别(传输气溶胶/二次硫酸盐、再悬浮土壤、金属、残余油燃烧和工业/焚烧)。将这些 PM2.5 样本暴露于人体上皮细胞(BEAS-2B)后,细胞核因子-κB(NF-κB)的激活显示出与 Ni(平均浓度为 38ng/m3)相对显著的关联,与 Ba(13ng/m3)、Mn(9ng/m3)和 Fe(500ng/m3)也存在较弱但仍显著的相关性。NF-κB 信号的单源回归分析显示与金属源存在显著关联。我们的结果表明,PM2.5 中的金属是细胞氧化剂生成的重要来源,可能是导致随后与颗粒空气污染相关的健康影响的原因。

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