Barcelona Institute for Global Health (ISGlobal-CREAL), Barcelona, Spain; Center for Energy Development and Health, Colorado State University, CO, USA; Department of Environmental and Radiological Health Sciences, Colorado State University, CO, USA.
Centre for Environmental Policy, Imperial College London, London, UK.
Environ Int. 2018 Feb;111:247-259. doi: 10.1016/j.envint.2017.11.024. Epub 2017 Dec 30.
Exposure to air pollution is known to affect both short and long-term outcomes of the cardiopulmonary system; however, findings on short-term outcomes have been inconsistent and often from isolated and long-term rather than coexisting and short-term exposures, and among susceptible/unhealthy rather than healthy populations.
We aimed to investigate separately the annual, daily and daily space-time-activity-weighted effect of ambient air pollution, as well as confounding or modification by other environmental (including noise) or space-time-activity (including total daily physical activity) exposures, on cardiopulmonary outcomes in healthy adults.
Participants (N=57: 54% female) had indicators of cardiopulmonary outcomes [blood pressure (BP), pulse (HR) and heart rate variability (HRV {SDNN}), and lung function (spirometry {FEV, FVC, SUM})] measured on four different mornings (at least five days apart) in a clinical setting between 2011 and 2014. Spatiotemporal ESCAPE-LUR models were used to estimate daily and annual air pollution exposures (including PM, PM, but not Ozone {derived from closest station}) at participant residential and occupational addresses. Participants' time-activity diaries indicated time spent at either address to allow daily space-time-activity-weighted estimates, and capture total daily physical activity (total-PA {as metabolic-equivalents-of-task, METs}), in the three days preceding health measurements. Multivariate-adjusted linear mixed-effects models (using either annual or daily estimates) were adjusted for possible environmental confounders or mediators including levels of ambient noise and greenness. Causal mediation analysis was also performed separately considering these factors as well as total-PA. All presented models are controlled by age, height, sex and season.
An increase in 5μg/m of daily space-time-activity-weighted PM exposure was statistically significantly associated with a 4.1% reduction in total heart rate variability (SDNN; p=0.01), and remained robust after adjusting for suspected confounders [except for occupational-address noise (β=-2.7, p=0.20)]. An increase in 10ppb of annual mean Ozone concentration at the residential address was statistically significantly associated with an increase in diastolic BP of 6.4mmHg (p<0.01), which lost statistical significance when substituted with daily space-time-activity-weighted estimates. As for pulmonary function, an increase in 10μg/m of annual mean PM concentration at the residential address was significantly associated with a 0.3% reduction in FVC (p<0.01) and a 0.5% reduction in SUM (p<0.04), for which again significance was lost when substituted for daily space-time-activity-weighted estimates These associations with pulmonary function remained robust after adjusting for suspected confounders, including annual Ozone, as well as total-PA and bioaerosol (pollen and fungal spore) levels (but not residential-neighborhood greenness {β=-0.22, p=0.09; β=-0.34, p=0.15, respectively}). Multilevel mediation analysis indicated that the proportion mediated as a direct effect on cardiopulmonary outcomes by suspected confounders (including total-PA, residential-neighborhood greenness, and occupational-address noise level) from primary exposures (including PM, PM, and O) was not statistically significant.
Our findings suggest that increased daily space-time-activity-weighted PM exposure levels significantly adversely affect cardiac autonomic modulation (as reduced total HRV) among healthy adults. Additionally, increased annual levels at the residential address of Ozone and PM significantly increase diastolic blood pressure and reduce lung function, respectively, among healthy adults. These associations typically remained robust when adjusting for suspected confounders. Occupational-address noise and residential-neighborhood greenness levels, however, were seen as mediators of cardiovascular and pulmonary outcomes, respectively. Total daily physical activity was not seen as a mediator of any of the studied outcomes, which supports the promotion of active mobility within cities.
众所周知,空气污染暴露会影响心肺系统的短期和长期结果;然而,关于短期结果的发现一直不一致,而且往往来自孤立的、长期的而不是共存的、短期的暴露,以及易感/不健康的人群而不是健康的人群。
我们旨在分别研究环境污染物(包括噪声)或时空活动(包括总日常体力活动)暴露对健康成年人心肺结果的短期、每日和每日时空活动加权效应,以及其他环境污染物(包括噪声)或时空活动(包括总日常体力活动)暴露的混杂或修饰作用。
参与者(N=57:54%为女性)在 2011 年至 2014 年期间在临床环境中进行了四次不同的早晨(至少相隔五天)的心肺结果[血压(BP)、脉搏(HR)和心率变异性(HRV{SDNN})]测量。使用时空 ESCAPE-LUR 模型来估计参与者居住和工作地址的每日和年度空气污染暴露(包括 PM2.5、PM10,但不包括衍生自最近的监测站的臭氧)。参与者的时间活动日记表明他们在这两个地址的时间分配,以允许进行每日时空活动加权估计,并在健康测量前三天内捕捉总日常体力活动(总-PA{作为代谢等效任务,METs})。多变量调整的线性混合效应模型(使用年度或每日估计值)调整了可能的环境混杂因素或中介因素,包括环境噪声和绿化水平。因果中介分析也分别考虑了这些因素以及总-PA。所有呈现的模型均由年龄、身高、性别和季节控制。
每日时空活动加权 PM 暴露增加 5μg/m 与总心率变异性(SDNN)降低 4.1%呈统计学显著相关(p=0.01),并且在调整疑似混杂因素后仍然稳健[除了工作地址噪声(β=-2.7,p=0.20)]。居住地址的年平均臭氧浓度增加 10ppb 与舒张压升高 6.4mmHg 呈统计学显著相关(p<0.01),当用每日时空活动加权估计值替代时,这种关联失去了统计学意义。至于肺功能,居住地址的年平均 PM10 浓度增加 10μg/m 与 FVC 降低 0.3%(p<0.01)和 SUM 降低 0.5%(p<0.04)显著相关,当用每日时空活动加权估计值替代时,这种关联仍然稳健。这些与肺功能的关联在调整疑似混杂因素后仍然稳健,包括年平均臭氧、总-PA 和生物气溶胶(花粉和真菌孢子)水平(但不包括居住区域绿化水平{β=-0.22,p=0.09;β=-0.34,p=0.15})。多层次中介分析表明,疑似混杂因素(包括总-PA、居住区域绿化水平和工作地址噪声水平)对初级暴露(包括 PM2.5、PM10 和 O)的直接影响在心肺结果中所占的比例没有统计学意义。
我们的研究结果表明,每日时空活动加权 PM 暴露水平的增加显著影响健康成年人的心脏自主调节(表现为总 HRV 降低)。此外,居住地址的年平均臭氧和 PM10 水平的增加分别显著增加舒张压和降低肺功能,分别在健康成年人中。当调整疑似混杂因素时,这些关联通常仍然稳健。然而,工作地址噪声和居住区域绿化水平分别被视为心血管和肺部结果的中介。总日常体力活动未被视为任何研究结果的中介,这支持在城市中促进积极的流动性。