Abstract

Background:

Chronic exposure to air pollution may prime the immune system to be reactive, increasing inflammatory responses to immune stimulation and providing a pathway to increased risk for inflammatory diseases, including asthma and cardiovascular disease. Although long-term exposure to ambient air pollution has been associated with increased circulating markers of inflammation, it is unknown whether it also relates to the magnitude of inflammatory response.

Objectives:

The aim of this study was to examine associations between chronic ambient pollution exposures and circulating and stimulated levels of inflammatory mediators in a cohort of healthy adults.

Methods:

Circulating interleukin (IL)-6, C-reactive protein (CRP) ($n=392$), and lipopolysaccharide stimulated production of $\text{IL-}1\mathrm{\beta }$, IL-6, and tumor necrosis factor $\left(\text{TNF}\right)\text{-}\mathrm{\alpha }$ ($n=379$) were measured in the Adult Health and Behavior II cohort. Fine particulate matter [particulate matter with aerodynamic diameter less than or equal to 2.5 μm (${\mathrm{PM}}_{2.5}$)] and constituents [black carbon (BC), and lead (Pb), manganese (Mn), zinc (Zn), and iron (Fe)] were estimated for each residential address using hybrid dispersion land use regression models. Associations between pollutant exposures and inflammatory measures were examined using linear regression; models were adjusted for age, sex, race, education, smoking, body mass index, and month of blood draw.

Results:

There were no significant correlations between circulating and stimulated measures of inflammation. Significant positive associations were found between exposure to ${\mathrm{PM}}_{2.5}$ and BC with stimulated production of IL-6, $\text{IL-}1\mathrm{\beta }$, and $\text{TNF-}\mathrm{\alpha }$. Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of $\text{IL-}1\mathrm{\beta }$ and $\text{TNF-}\mathrm{\alpha }$. No pollutants were associated with circulating IL-6 or CRP levels.

Discussion:

Exposure to ${\mathrm{PM}}_{2.5}$, BC, Pb, Mn, Fe, and Zn was associated with increased production of inflammatory mediators by stimulated immune cells. In contrast, pollutant exposure was not related to circulating markers of inflammation. These results suggest that chronic exposure to some pollutants may prime immune cells to mount larger inflammatory responses, possibly contributing to increased risk for inflammatory disease. https://doi.org/10.1289/EHP7089

中文翻译：

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一群中年成年人的长期环境空气污染暴露以及循环和刺激的炎症介质

摘要

背景：

长期暴露于空气污染可能会使免疫系统产生反应，增加对免疫刺激的炎症反应，并为增加炎症性疾病（包括哮喘和心血管疾病）的风险提供途径。尽管长期暴露于环境空气污染与炎症循环标志物增加有关，但尚不清楚它是否也与炎症反应的程度有关。

目标：

本研究的目的是检查健康成人队列中慢性环境污染暴露与炎症介质的循环和刺激水平之间的关联。

方法：

循环白细胞介素 (IL)-6、C 反应蛋白 (CRP) ($n=392$) 和脂多糖刺激产生 $\text{IL-}1\mathrm{\beta }$, IL-6, 和肿瘤坏死因子 $\left(\text{肿瘤坏死因子}\right)\text{——}\mathrm{\alpha }$ ($n=379$) 是在成人健康和行为 II 队列中测量的。细颗粒物[空气动力学直径小于或等于2.5μm（${\mathrm{下午}}_{2.5}$)] 和成分 [黑碳 (BC) 和铅 (Pb)、锰 (Mn)、锌 (Zn) 和铁 (Fe)] 使用混合分散土地利用回归模型估算每个住宅地址。使用线性回归检查污染物暴露与炎症测量之间的关联；模型根据年龄、性别、种族、教育、吸烟、体重指数和抽血月份进行了调整。

结果：

循环和刺激的炎症指标之间没有显着相关性。发现暴露之间存在显着的正相关${\mathrm{下午}}_{2.5}$ 和 BC 刺激产生 IL-6， $\text{IL-}1\mathrm{\beta }$， 和 $\text{肿瘤坏死因子-}\mathrm{\alpha }$. Pb、Mn、Fe 和 Zn 暴露与刺激产生$\text{IL-}1\mathrm{\beta }$ 和 $\text{肿瘤坏死因子-}\mathrm{\alpha }$. 没有污染物与循环 IL-6 或 CRP 水平相关。

讨论：

接触 ${\mathrm{下午}}_{2.5}$、BC、Pb、Mn、Fe 和 Zn 与受刺激的免疫细胞产生的炎症介质增加有关。相比之下，污染物暴露与炎症的循环标志物无关。这些结果表明，长期接触某些污染物可能会促使免疫细胞产生更大的炎症反应，这可能会增加患炎症性疾病的风险。https://doi.org/10.1289/EHP7089