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机场相关超细颗粒物暴露对哮喘成人肺功能和炎症的短期影响。

Short-term effects of airport-associated ultrafine particle exposure on lung function and inflammation in adults with asthma.

机构信息

Division of Environmental Health, Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Division of Environmental Health, Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

出版信息

Environ Int. 2018 Sep;118:48-59. doi: 10.1016/j.envint.2018.05.031. Epub 2018 May 26.

DOI:10.1016/j.envint.2018.05.031
PMID:29800768
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6368339/
Abstract

BACKGROUND

Exposure to ultrafine particles (UFP, particles with aerodynamic diameter < 100 nm) is associated with reduced lung function and airway inflammation in individuals with asthma. Recently, elevated UFP number concentrations (PN) from aircraft landing and takeoff activity were identified downwind of the Los Angeles International Airport (LAX) but little is known about the health impacts of airport-related UFP exposure.

METHODS

We conducted a randomized crossover study of 22 non-smoking adults with mild to moderate asthma in Nov-Dec 2014 and May-Jul 2015 to investigate short-term effects of exposure to LAX airport-related UFPs. Participants conducted scripted, mild walking activity on two occasions in public parks inside (exposure) and outside (control) of the high UFP zone. Spirometry, multiple flow exhaled nitric oxide, and circulating inflammatory cytokines were measured before and after exposure. Personal UFP PN and lung deposited surface area (LDSA) and stationary UFP PN, black carbon (BC), particle-bound PAHs (PB-PAH), ozone (O), carbon dioxide (CO) and particulate matter (PM) mass were measured. Source apportionment analysis was conducted to distinguish aircraft from roadway traffic related UFP sources. Health models investigated within-subject changes in outcomes as a function of pollutants and source factors.

RESULTS

A high two-hour walking period average contrast of ~34,000 particles·cm was achieved with mean (std) PN concentrations of 53,342 (25,529) and 19,557 (11,131) particles·cm and mean (std) particle size of 28.7 (9.5) and 33.2 (11.5) at the exposure and control site, respectively. Principal components analysis differentiated airport UFPs (PN), roadway traffic (BC, PB-PAH), PM mass (PM, PM), and secondary photochemistry (O) sources. A standard deviation increase in the 'Airport UFPs' factor was significantly associated with IL-6, a circulating marker of inflammation (single-pollutant model: 0.21, 95% CI = 0.08-0.34; multi-pollutant model: 0.18, 0.04-0.32). The 'Traffic' factor was significantly associated with lower Forced Expiratory Volume in 1 s (FEV) (single-pollutant model: -1.52, -2.28 to -0.77) and elevated sTNFrII (single-pollutant model: 36.47; 6.03-66.91; multi-pollutant model: 64.38; 6.30-122.46). No consistent associations were observed with exhaled nitric oxide.

CONCLUSIONS

To our knowledge, our study is the first to demonstrate increased acute systemic inflammation following exposure to airport-related UFPs. Health effects associated with roadway traffic exposure were distinct. This study emphasizes the importance of multi-pollutant measurements and modeling techniques to disentangle sources of UFPs contributing to the complex urban air pollution mixture and to evaluate population health risks.

摘要

背景

暴露于超细颗粒(UFP,空气动力学直径 < 100nm 的颗粒)与哮喘患者的肺功能降低和气道炎症有关。最近,在洛杉矶国际机场(LAX)下风处发现飞机起降活动产生的 UFP 数量浓度(PN)升高,但人们对机场相关 UFP 暴露的健康影响知之甚少。

方法

我们于 2014 年 11 月至 12 月和 2015 年 5 月至 7 月期间对 22 名非吸烟、患有轻度至中度哮喘的成年人进行了一项随机交叉研究,以研究暴露于 LAX 机场相关 UFP 的短期影响。参与者在公园内(暴露组)和公园外(对照组)进行了两次脚本化的、轻度的步行活动。在暴露前后测量肺活量、多次呼出的一氧化氮、循环炎症细胞因子。测量个人 UFP PN 和肺沉积表面积(LDSA)以及固定 UFP PN、黑碳(BC)、颗粒结合多环芳烃(PB-PAH)、臭氧(O)、二氧化碳(CO)和颗粒物(PM)质量。进行源分配分析以区分飞机和道路交通相关 UFP 源。健康模型研究了污染物和源因素对结果的影响。

结果

通过高两小时步行期平均对比约 34000 个粒子·cm 实现了约 34000 个粒子·cm 的高浓度,暴露和对照点的 PN 浓度分别为 53342(25529)和 19557(11131)个粒子·cm,平均(标准偏差)粒径分别为 28.7(9.5)和 33.2(11.5)。主成分分析区分了机场 UFPs(PN)、道路交通(BC、PB-PAH)、PM 质量(PM、PM)和二次光化学反应(O)源。“机场 UFPs”因子的标准偏差增加与炎症的循环标志物 IL-6 显著相关(单污染物模型:0.21,95%CI=0.08-0.34;多污染物模型:0.18,0.04-0.32)。“交通”因子与用力呼气量第一秒(FEV)降低呈显著相关(单污染物模型:-1.52,-2.28 至-0.77)和 sTNFrII 升高(单污染物模型:36.47;6.03-66.91;多污染物模型:64.38;6.30-122.46)。未观察到与呼出的一氧化氮有一致的关联。

结论

据我们所知,我们的研究首次证明了暴露于机场相关 UFP 后急性全身炎症增加。与道路交通暴露相关的健康影响是不同的。本研究强调了多污染物测量和建模技术的重要性,以便于分解导致复杂城市空气污染混合物的 UFP 源,并评估人群健康风险。

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