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家庭空气污染与炎症血液标志物:一项横断面分析。

Household air pollution and blood markers of inflammation: A cross-sectional analysis.

机构信息

Department of Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.

Center for Global Non-Communicable Disease Research and Training, Johns Hopkins University, Baltimore, MD, USA.

出版信息

Indoor Air. 2021 Sep;31(5):1509-1521. doi: 10.1111/ina.12814. Epub 2021 Mar 22.

DOI:10.1111/ina.12814
PMID:33749948
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8380676/
Abstract

Household air pollution (HAP) from biomass stoves is a leading risk factor for cardiopulmonary outcomes; however, its toxicity pathways and relationship with inflammation markers are poorly understood. Among 180 adult women in rural Peru, we examined the cross-sectional exposure-response relationship between biomass HAP and markers of inflammation in blood using baseline measurements from a randomized trial. We measured markers of inflammation (CRP, IL-6, IL-10, IL-1β, and TNF-α) with dried blood spots, 48-h kitchen area concentrations and personal exposures to fine particulate matter (PM ), black carbon (BC), and carbon monoxide (CO), and 48-h kitchen concentrations of nitrogen dioxide (NO ) in a subset of 97 participants. We conducted an exposure-response analysis between quintiles of HAP levels and markers of inflammation. Markers of inflammation were more strongly associated with kitchen area concentrations of BC than PM . As expected, kitchen area BC concentrations were positively associated with TNF-α (pro-inflammatory) concentrations and negatively associated with IL-10, an anti-inflammatory marker, controlling for confounders in single- and multi-pollutant models. However, contrary to expectations, kitchen area BC and NO concentrations were negatively associated with IL-1β, a pro-inflammatory marker. No associations were identified for IL-6 or CRP, or for any marker in relation to personal exposures.

摘要

家庭燃烧生物质产生的空气污染(HAP)是心肺疾病的主要风险因素;然而,其毒性途径及其与炎症标志物的关系尚不清楚。在秘鲁农村的 180 名成年女性中,我们使用一项随机试验的基线测量结果,检验了生物质 HAP 与血液中炎症标志物之间的横断面暴露反应关系。我们通过干血斑测量了炎症标志物(CRP、IL-6、IL-10、IL-1β 和 TNF-α),并在 97 名参与者的亚组中测量了 48 小时厨房区域浓度和个人暴露于细颗粒物(PM )、黑碳(BC)和一氧化碳(CO)以及 48 小时厨房浓度的二氧化氮(NO )。我们在 HAP 水平五分位数和炎症标志物之间进行了暴露反应分析。炎症标志物与厨房区域 BC 浓度的相关性强于 PM 。如预期的那样,厨房区域 BC 浓度与促炎标志物 TNF-α浓度呈正相关,与抗炎标志物 IL-10 浓度呈负相关,在单污染物和多污染物模型中控制了混杂因素。然而,与预期相反,厨房区域 BC 和 NO 浓度与促炎标志物 IL-1β 呈负相关。在个人暴露与任何标志物之间都没有发现 IL-6 或 CRP 或任何标志物的关联。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e77d/8380676/000e162a91de/nihms-1699903-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e77d/8380676/000e162a91de/nihms-1699903-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e77d/8380676/000e162a91de/nihms-1699903-f0001.jpg

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