Southwest Center for Occupational and Environmental Health, 1200 Herman Pressler Dr., Houston, TX 77030, USA; Division of Epidemiology, Human Genetics and Environmental Sciences, University of Texas School of Public Health, 1200 Herman Pressler Dr., Houston, TX 77030, USA.
Southwest Center for Occupational and Environmental Health, 1200 Herman Pressler Dr., Houston, TX 77030, USA; Division of Epidemiology, Human Genetics and Environmental Sciences, University of Texas School of Public Health, 1200 Herman Pressler Dr., Houston, TX 77030, USA.
Environ Res. 2014 May;131:50-8. doi: 10.1016/j.envres.2014.02.013. Epub 2014 Mar 20.
We investigated associations of short-term changes in ambient ozone (O3), fine particulate matter (PM2.5) and nitrogen dioxide (NO2) concentrations and the timing of new-onset asthma, using a large, high-risk population in an area with historically high ozone levels.
The study population included 18,289 incident asthma cases identified among Medicaid-enrolled children in Harris County Texas between 2005-2007, using Medicaid Analytic Extract enrollment and claims files. We used a time-stratified case-crossover design and conditional logistic regression to assess the effect of increased short-term pollutant concentrations on the timing of asthma onset.
Each 10 ppb increase in ozone was significantly associated with new-onset asthma during the warm season (May-October), with the strongest association seen when a 6-day cumulative average period was used as the exposure metric (odds ratio [OR]=1.05, 95% confidence interval [CI], 1.02-1.08). Similar results were seen for NO2 and PM2.5 (OR=1.07, 95% CI, 1.03-1.11 and OR=1.12, 95% CI, 1.03-1.22, respectively), and PM2.5 also had significant effects in the cold season (November-April), 5-day cumulative lag (OR=1.11. 95% CI, 1.00-1.22). Significantly increased ORs for O3 and NO2 during the warm season persisted in co-pollutant models including PM2.5. Race and age at diagnosis modified associations between ozone and onset of asthma.
Our results indicate that among children in this low-income urban population who developed asthma, their initial date of diagnosis was more likely to occur following periods of higher short-term ambient pollutant levels.
我们研究了短期环境臭氧(O3)、细颗粒物(PM2.5)和二氧化氮(NO2)浓度变化与新发病例哮喘发作时间之间的关系,该研究在一个历史上臭氧水平较高的地区使用了一个大型高危人群。
本研究人群包括 2005-2007 年在德克萨斯州哈里斯县参加医疗补助计划的儿童中确定的 18289 例新发病例哮喘,使用医疗补助分析提取登记和索赔文件。我们使用时间分层病例交叉设计和条件逻辑回归来评估短期污染物浓度增加对哮喘发作时间的影响。
臭氧每增加 10ppb 与暖季(5 月至 10 月)新发病例哮喘显著相关,当使用 6 天累积平均期作为暴露指标时,关联最强(比值比 [OR]=1.05,95%置信区间 [CI],1.02-1.08)。NO2 和 PM2.5 也有类似的结果(OR=1.07,95%CI,1.03-1.11 和 OR=1.12,95%CI,1.03-1.22),PM2.5 在冷季(11 月至 4 月)也有显著影响,5 天累积滞后(OR=1.11,95%CI,1.00-1.22)。在包括 PM2.5 在内的共污染物模型中,暖季臭氧和 NO2 的 OR 显著增加。臭氧与哮喘发病之间的关联在种族和诊断时年龄上有所不同。
我们的研究结果表明,在该低收入城市人群中患有哮喘的儿童中,他们的初始诊断日期更有可能出现在短期环境污染物水平较高的时期之后。