Yu O, Sheppard L, Lumley T, Koenig J Q, Shapiro G G
Department of Biostatistics, University of Washington, Seattle, Washington 98195-7232, USA.
Environ Health Perspect. 2000 Dec;108(12):1209-14. doi: 10.1289/ehp.001081209.
We observed a panel of 133 children (5-13 years of age) with asthma residing in the greater Seattle, Washington, area for an average of 58 days (range 28-112 days) during screening for enrollment in the Childhood Asthma Management Program (CAMP) study. Daily self-reports of asthma symptoms were obtained from study diaries and compared with ambient air pollution levels in marginal repeated measures logistic regression models. We defined days with asthma symptoms as any day a child reported at least one mild asthma episode. All analyses were controlled for subject-specific variables [age, race, sex, baseline height, and FEV(1) PC(20) concentration (methacholine provocative concentration required to produce a 20% decrease in forced expiratory volume in 1 sec)] and potential time-dependent confounders (day of week, season, and temperature). Because of variable observation periods for participants, we estimated both between- and within-subject air pollutant effects. Our primary interest was in the within-subject effects: the effect of air pollutant excursions from typical levels in each child's observation period on the odds of asthma symptoms. In single-pollutant models, the population average estimates indicated a 30% [95% confidence interval (CI), 11-52%] increase for a 1-ppm increment in carbon monoxide lagged 1 day, an 18% (95% CI, 5-33%) increase for a 10-microg/m(3) increment in same-day particulate matter < 1.0 microm (PM(1.0)), and an 11% (95% CI, 3-20%) increase for a 10-microg/m(3) increment in particulate matter < 10 microm (PM(10)) lagged 1 day. Conditional on the previous day's asthma symptoms, we estimated 25% (95% CI, 10-42%), 14% (95% CI, 4-26%), and 10% (95% CI, 3-16%) increases in the odds of asthma symptoms associated with increases in CO, PM(1.0), and PM(10), respectively. We did not find any association between sulfur dioxide (SO(2)) and the odds of asthma symptoms. In multipollutant models, the separate pollutant effects were smaller. The overall effect of an increase in both CO and PM(1. 0) was a 31% (95% CI, 11-55%) increase in the odds of symptoms of asthma. We conclude that there is an association between change in short-term air pollution levels, as indexed by PM and CO, and the occurrence of asthma symptoms among children in Seattle. Although PM effects on asthma have been found in other studies, it is likely that CO is a marker for vehicle exhaust and other combustion by-products that aggravate asthma.
我们观察了133名年龄在5至13岁之间的哮喘儿童，他们居住在华盛顿州大西雅图地区，在儿童哮喘管理项目（CAMP）研究的筛查阶段平均停留了58天（范围为28至112天）。通过研究日记获取哮喘症状的每日自我报告，并在边际重复测量逻辑回归模型中与环境空气污染水平进行比较。我们将有哮喘症状的日子定义为儿童报告至少一次轻度哮喘发作的任何一天。所有分析均针对个体特异性变量[年龄、种族、性别、基线身高和FEV(1) PC(20)浓度（使一秒用力呼气量降低20%所需的乙酰甲胆碱激发浓度）]以及潜在的时间依赖性混杂因素（星期几、季节和温度）进行了控制。由于参与者的观察期各不相同，我们估计了个体间和个体内的空气污染物影响。我们主要关注的是个体内影响：在每个儿童的观察期内，空气污染物偏离典型水平对哮喘症状发生几率的影响。在单污染物模型中，总体平均估计表明，一氧化碳滞后1天每增加1 ppm，增加30%[95%置信区间（CI），11 - 52%]；当日颗粒物<1.0微米（PM(1.0)）每增加10微克/立方米，增加18%（95% CI，5 - 33%）；颗粒物<10微米（PM(10)）滞后1天每增加10微克/立方米，增加11%（95% CI，3 - 20%）。以前一天的哮喘症状为条件，我们估计与一氧化碳、PM(1.0)和PM(10)增加相关的哮喘症状发生几率分别增加25%（95% CI，10 - 42%）、14%（95% CI，4 - 26%）和10%（95% CI，3 - 16%）。我们未发现二氧化硫（SO(2)）与哮喘症状发生几率之间存在任何关联。在多污染物模型中，各污染物的单独影响较小。一氧化碳和PM(1.0)同时增加的总体影响是哮喘症状发生几率增加31%（95% CI，11 - 55%）。我们得出结论，以PM和CO为指标的短期空气污染水平变化与西雅图儿童哮喘症状的发生之间存在关联。尽管在其他研究中已发现PM对哮喘有影响，但一氧化碳很可能是加重哮喘的车辆尾气和其他燃烧副产物的一个标志物。
