■大多数现有研究仅调查了建筑环境对呼吸系统疾病的直接影响。然而,越来越多的证据表明,城市的建筑环境通过影响空气污染对公众健康有间接影响。探索"城市建成环境-空气污染-呼吸系统疾病"的级联机制,对于营造健康的呼吸环境具有重要意义,这就是本研究的目的。
■本研究收集了2015-2017年武汉市同济医院呼吸系统疾病患者的临床资料。此外,每日空气污染水平(二氧化硫(SO2),二氧化氮(NO2),颗粒物(PM2.5,PM10),和臭氧(O3),气象数据(平均温度和相对湿度),收集了城市建筑环境的数据。我们使用Spearman相关性来研究空气污染与气象变量之间的关系;使用分布滞后非线性模型(DLNM)来研究呼吸系统疾病之间的短期关系。空气污染物,和气象因素;使用多尺度地理加权回归模型(MGWR)研究了建筑环境中空间异质性对空气污染的影响。
■在研究期间,呼吸系统疾病的平均水平(平均年龄54岁)为每天15.97人,其中男性(平均年龄57岁)为9.519,女性(平均年龄48岁)为6.451;PM10,PM2.5,NO2,SO2和O3的24小时平均水平分别为78.056μg/m3,71.962μg/m3,54.468μg/m3,12.898μg/m3和46.904μg/m3;在PM10和SO2之间的相关性最高(r=0.762,p=0.01其次是NO2和PM2.5(r=0.73,p<0.01),PM10和PM2.5(r=0.704,p<0.01)。我们观察到NO2对呼吸系统疾病的显著滞后效应,对于滞后0天和滞后1天,NO2浓度增加10μg/m3相当于呼吸系统疾病增加1.009%(95%CI:1.001,1.017%)和1.005%(95%CI:1.001,1.011%)。NO2的空间分布受高密度城市发展(人口密度,建筑密度,购物服务设施数量,建设用地,这四个因素的带宽为43),而绿地和公园可以有效减少空气污染(R2=0.649)。
■以前的研究集中在空气污染对呼吸系统疾病的影响以及建筑环境对空气污染的影响,本研究将这三个方面结合起来,探讨它们之间的关系。此外,对“建筑环境-空气污染-呼吸系统疾病”级联机制的理论进行了实际研究,并分解为具体的实验步骤,这在以前的研究中没有发现。此外,我们观察到NO2对呼吸系统疾病的滞后效应和NO2分布中建筑环境的空间异质性。
Most existing studies have only investigated the direct effects of the built environment on respiratory diseases. However, there is mounting evidence that the built environment of cities has an indirect influence on public health via influencing air pollution. Exploring the \"urban built environment-air pollution-respiratory diseases\" cascade mechanism is important for creating a healthy respiratory environment, which is the aim of this study.
The study gathered clinical data from 2015 to 2017 on patients with respiratory diseases from Tongji Hospital in Wuhan. Additionally, daily air pollution levels (sulfur dioxide (SO2), nitrogen dioxide (NO2), particulate matter (PM2.5, PM10), and ozone (O3)), meteorological data (average temperature and relative humidity), and data on urban built environment were gathered. We used Spearman correlation to investigate the connection between air pollution and meteorological variables; distributed lag non-linear model (DLNM) was used to investigate the short-term relationships between respiratory diseases, air pollutants, and meteorological factors; the impacts of spatial heterogeneity in the built environment on air pollution were examined using the multiscale geographically weighted regression model (MGWR).
During the study period, the mean level of respiratory diseases (average age 54) was 15.97 persons per day, of which 9.519 for males (average age 57) and 6.451 for females (average age 48); the 24 h mean levels of PM10, PM2.5, NO2, SO2 and O3 were 78.056 μg/m3, 71.962 μg/m3, 54.468 μg/m3, 12.898 μg/m3, and 46.904 μg/m3, respectively; highest association was investigated between PM10 and SO2 (r = 0.762, p < 0.01), followed by NO2 and PM2.5 (r = 0.73, p < 0.01), and PM10 and PM2.5 (r = 0.704, p < 0.01). We observed a significant lag effect of NO2 on respiratory diseases, for lag 0 day and lag 1 day, a 10 μg/m3 increase in NO2 concentration corresponded to 1.009% (95% CI: 1.001, 1.017%) and 1.005% (95% CI: 1.001, 1.011%) increase of respiratory diseases. The spatial distribution of NO2 was significantly influenced by high-density urban development (population density, building density, number of shopping service facilities, and construction land, the bandwidth of these four factors are 43), while green space and parks can effectively reduce air pollution (R2 = 0.649).
Previous studies have focused on the effects of air pollution on respiratory diseases and the effects of built environment on air pollution, while this study combines these three aspects and explores the relationship between them. Furthermore, the theory of the \"built environment-air pollution-respiratory diseases\" cascading mechanism is practically investigated and broken down into specific experimental steps, which has not been found in previous studies. Additionally, we observed a lag effect of NO2 on respiratory diseases and spatial heterogeneity of built environment in the distribution of NO2.