Department of Environmental and Occupational Health, University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania, USA.
Department of Environmental and Occupational Health, Drexel University Dornsife School of Public Health, Philadelphia, Pennsylvania, USA.
Environ Health Perspect. 2021 May;129(5):57007. doi: 10.1289/EHP7089. Epub 2021 May 17.
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.
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.
Circulating interleukin (IL)-6, C-reactive protein (CRP) (), and lipopolysaccharide stimulated production of , IL-6, and tumor necrosis factor () 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 ()] 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.
There were no significant correlations between circulating and stimulated measures of inflammation. Significant positive associations were found between exposure to and BC with stimulated production of IL-6, , and . Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of and . No pollutants were associated with circulating IL-6 or CRP levels.
Exposure to , 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.
慢性暴露于空气污染可能使免疫系统变得活跃,增加对免疫刺激的炎症反应,并为炎症性疾病(包括哮喘和心血管疾病)的风险增加提供途径。尽管长期暴露于环境空气污染与循环炎症标志物的增加有关,但尚不清楚它是否与炎症反应的程度有关。
本研究旨在检查慢性环境污染物暴露与健康成年人队列中循环和刺激炎症介质水平之间的关系。
在成人健康与行为 II 队列中测量了循环白细胞介素(IL)-6、C 反应蛋白(CRP)()和脂多糖刺激产生的、IL-6 和肿瘤坏死因子()。使用混合分散土地利用回归模型,为每个居住地址估算细颗粒物(空气动力学直径小于或等于 2.5μm 的颗粒物())和成分(黑碳(BC)和铅(Pb)、锰(Mn)、锌(Zn)和铁(Fe))。使用线性回归检查污染物暴露与炎症指标之间的关系;模型调整了年龄、性别、种族、教育、吸烟、体重指数和采血月份。
循环和刺激炎症指标之间没有显著相关性。暴露于和 BC 与刺激产生的 IL-6、和呈显著正相关。Pb、Mn、Fe 和 Zn 暴露与刺激产生的和呈正相关。没有污染物与循环 IL-6 或 CRP 水平相关。
暴露于、BC、Pb、Mn、Fe 和 Zn 与刺激免疫细胞产生的炎症介质增加有关。相比之下,污染物暴露与循环炎症标志物无关。这些结果表明,慢性暴露于某些污染物可能使免疫细胞产生更大的炎症反应,可能导致炎症性疾病的风险增加。https://doi.org/10.1289/EHP7089。