Sack Coralynn, Wang Meng, Knutson Victoria, Gassett Amanda, Hoffman Eric A, Sheppard Lianne, Barr R Graham, Kaufman Joel D, Smith Benjamin
Department of Medicine.
Department of Environmental and Occupational Health Sciences, and.
Am J Respir Crit Care Med. 2024 Jun 1;209(11):1351-1359. doi: 10.1164/rccm.202307-1248OC.
Airway tree morphology varies in the general population and may modify the distribution and uptake of inhaled pollutants. We hypothesized that smaller airway caliber would be associated with emphysema progression and would increase susceptibility to air pollutant-associated emphysema progression. MESA (Multi-Ethnic Study of Atherosclerosis) is a general population cohort of adults 45-84 years old from six U.S. communities. Airway tree caliber was quantified as the mean of airway lumen diameters measured from baseline cardiac computed tomography (CT) (2000-2002). Percentage emphysema, defined as percentage of lung pixels below -950 Hounsfield units, was assessed up to five times per participant via cardiac CT scan (2000-2007) and equivalent regions on lung CT scan (2010-2018). Long-term outdoor air pollutant concentrations (particulate matter with an aerodynamic diameter ⩽2.5 μm, oxides of nitrogen, and ozone) were estimated at the residential address with validated spatiotemporal models. Linear mixed models estimated the association between airway tree caliber and emphysema progression; modification of pollutant-associated emphysema progression was assessed using multiplicative interaction terms. Among 6,793 participants (mean ± SD age, 62 ± 10 yr), baseline airway tree caliber was 3.95 ± 1.1 mm and median (interquartile range) of percentage emphysema was 2.88 (1.21-5.68). In adjusted analyses, 10-year emphysema progression rate was 0.75 percentage points (95% confidence interval, 0.54-0.96%) higher in the smallest compared with largest airway tree caliber quartile. Airway tree caliber also modified air pollutant-associated emphysema progression. Smaller airway tree caliber was associated with accelerated emphysema progression and modified air pollutant-associated emphysema progression. A better understanding of the mechanisms of airway-alveolar homeostasis and air pollutant deposition is needed.
气道树形态在普通人群中存在差异,可能会改变吸入污染物的分布和摄取。我们假设较小的气道管径与肺气肿进展相关,并会增加对空气污染物相关的肺气肿进展的易感性。动脉粥样硬化多民族研究(MESA)是一项来自美国六个社区的45 - 84岁成年人的普通人群队列研究。气道树管径通过从基线心脏计算机断层扫描(CT)(2000 - 2002年)测量的气道腔直径的平均值进行量化。肺气肿百分比定义为低于-950亨氏单位的肺像素百分比,每位参与者通过心脏CT扫描(2000 - 2007年)和肺部CT扫描(2010 - 2018年)的等效区域评估多达五次。使用经过验证的时空模型估计居住地址的长期室外空气污染物浓度(空气动力学直径≤2.5μm的颗粒物、氮氧化物和臭氧)。线性混合模型估计气道树管径与肺气肿进展之间的关联;使用乘法交互项评估污染物相关的肺气肿进展的改变。在6793名参与者(平均±标准差年龄,62±10岁)中,基线气道树管径为3.95±1.1mm,肺气肿百分比的中位数(四分位间距)为2.88(1.21 - 5.68)。在调整分析中,与最大气道树管径四分位数相比,最小四分位数的10年肺气肿进展率高0.75个百分点(95%置信区间,0.54 - 0.96%)。气道树管径也改变了空气污染物相关的肺气肿进展。较小的气道树管径与加速的肺气肿进展以及改变的空气污染物相关的肺气肿进展相关。需要更好地了解气道 - 肺泡稳态和空气污染物沉积的机制。