Shmool Jessie Loving Carr, Kinnee Ellen, Sheffield Perry Elizabeth, Clougherty Jane Ellen
University of Pittsburgh Graduate School of Public Health, Department of Environmental and Occupational Health, 100 Technology Drive, Ste. 350, Pittsburgh, PA 15219, USA.
Icahn School of Medicine at Mount Sinai, DPM, 1 Gustave L. Levy Pl., Box 1057, New York, NY 10029, USA.
Environ Res. 2016 May;147:108-14. doi: 10.1016/j.envres.2016.01.020. Epub 2016 Feb 6.
Childhood asthma morbidity has been associated with short-term air pollution exposure. To date, most investigations have used time-series models, and it is not well understood how exposure misclassification arising from unmeasured spatial variation may impact epidemiological effect estimates. Here, we develop case-crossover models integrating temporal and spatial individual-level exposure information, toward reducing exposure misclassification in estimating associations between air pollution and child asthma exacerbations in New York City (NYC).
Air pollution data included: (a) highly spatially-resolved intra-urban concentration surfaces for ozone and co-pollutants (nitrogen dioxide and fine particulate matter) from the New York City Community Air Survey (NYCCAS), and (b) daily regulatory monitoring data. Case data included citywide hospital records for years 2005-2011 warm-season (June-August) asthma hospitalizations (n=2353) and Emergency Department (ED) visits (n=11,719) among children aged 5-17 years. Case residential locations were geocoded using a multi-step process to maximize positional accuracy and precision in near-residence exposure estimates. We used conditional logistic regression to model associations between ozone and child asthma exacerbations for lag days 0-6, adjusting for co-pollutant and temperature exposures. To evaluate the effect of increased exposure specificity through spatial air pollution information, we sequentially incorporated spatial variation into daily exposure estimates for ozone, temperature, and co-pollutants.
Percent excess risk per 10ppb ozone exposure in spatio-temporal models were significant on lag days 1 through 5, ranging from 6.5 (95% CI: 0.2-13.1) to 13.0 (6.0-20.6) for inpatient hospitalizations, and from 2.9 (95% CI: 0.1-5.7) to 9.4 (6.3-12.7) for ED visits, with strongest associations consistently observed on lag day 2. Spatio-temporal excess risk estimates were consistently but not statistically significantly higher than temporal-only estimates on lag days 0-3.
Incorporating case-level spatial exposure variation produced small, non-significant increases in excess risk estimates. Our modeling approach enables a refined understanding of potential measurement error in temporal-only versus spatio-temporal air pollution exposure assessments. As ozone generally varies over much larger spatial scales than that observed within NYC, further work is necessary to evaluate potential reductions in exposure misclassification for populations spanning wider geographic areas, and for other pollutants.
儿童哮喘发病率与短期空气污染暴露有关。迄今为止,大多数调查都使用时间序列模型,而对于因未测量的空间变异导致的暴露错误分类如何影响流行病学效应估计,人们还了解甚少。在此,我们开发了整合时间和空间个体水平暴露信息的病例交叉模型,以减少在估计纽约市(NYC)空气污染与儿童哮喘急性发作之间的关联时的暴露错误分类。
空气污染数据包括:(a)来自纽约市社区空气调查(NYCCAS)的臭氧和共污染物(二氧化氮和细颗粒物)的高空间分辨率城市内部浓度表面,以及(b)每日监管监测数据。病例数据包括2005 - 2011年暖季(6月至8月)5至17岁儿童全市范围的医院记录,其中哮喘住院病例(n = 2353)和急诊科(ED)就诊病例(n = 11719)。使用多步骤过程对病例居住地点进行地理编码,以在近居住暴露估计中最大化位置准确性和精度。我们使用条件逻辑回归对滞后0至6天的臭氧与儿童哮喘急性发作之间的关联进行建模,并对共污染物和温度暴露进行调整。为了评估通过空间空气污染信息提高暴露特异性的效果,我们将空间变异依次纳入臭氧、温度和共污染物的每日暴露估计中。
时空模型中每10 ppb臭氧暴露的超额风险百分比在滞后1至5天具有统计学意义,住院病例的超额风险百分比范围为6.5(95% CI:0.2 - 13.1)至13.0(6.0 - 20.6),急诊科就诊病例的超额风险百分比范围为2.9(95% CI:0.1 - 5.7)至9.4(6.3 - 12.7),在滞后第2天始终观察到最强的关联。在滞后0至3天,时空超额风险估计始终但无统计学显著高于仅时间模型的估计。
纳入病例水平的空间暴露变异使超额风险估计有小幅、不显著的增加。我们的建模方法有助于更精确地理解仅时间与时空空气污染暴露评估中潜在的测量误差。由于臭氧通常在比纽约市内观察到的更大空间尺度上变化,因此有必要进一步开展工作,以评估跨更广泛地理区域的人群以及其他污染物在暴露错误分类方面的潜在减少情况。