Effects of ambient air pollution on symptoms of asthma in Seattle-area children enrolled in the CAMP study.
Effects of ambient air pollution on symptoms of asthma in Seattle-area children enrolled in the CAMP study.
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DOI：
10.1289/ehp.001081209
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发表时间：
2000-12
影响因子：
10.4
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中科院分区：
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我们对居住在大西雅图、华盛顿地区的133名哮喘儿童（5-13岁）进行了平均58天（范围28-112天）的观察，以筛选入组儿童哮喘管理项目（CAMP）研究。从研究日记中获得每日哮喘症状的自我报告，并在边缘重复测量logistic回归模型中与环境空气污染水平进行比较。我们将哮喘症状日定义为儿童报告至少一次轻度哮喘发作的任何一天。所有分析均控制了受试者特异性变量[年龄、种族、性别、基线身高和FEV（1）PC（20）浓度（1秒内用力呼气量减少20%所需的乙酰甲胆碱激发浓度）]和潜在的时间依赖性混杂因素（星期几、季节和温度）。由于参与者的观察期不同，我们估计了受试者之间和受试者内部的空气污染物影响。我们主要关注的是受试者内效应：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几率的影响。在单一污染物模型中，群体平均估计值表明，一氧化碳每增加1 ppm，滞后1天，增加30% [95%置信区间（CI），11-52%]，滞后1天，增加18%[95%置信区间（CI），11-52%]。（95% CI，5-33%）增加10微克/立方米（3）的同一天颗粒物< 1.0微米（PM（1.0）），而< 10 microm的颗粒物（PM（10））每增加10微克/立方米（μ g/m3），则增加11%（95%CI，3-20%），滞后1天。以前一天的哮喘症状为条件，我们估计与CO、PM（1.0）和PM（10）增加相关的哮喘症状几率分别增加25%（95% CI，10-42%）、14%（95% CI，4-26%）和10%（95% CI，3-16%）。我们没有发现二氧化硫（SO（2））和哮喘症状的几率之间有任何联系。在多污染物模型中，单独的污染物的影响较小。CO和PM增加的总体影响（1。0)哮喘症状的几率增加31%（95% CI，11-55%）。我们的结论是，有一个在短期的空气污染水平的变化之间的关联，作为指数的PM和CO，并在西雅图儿童哮喘症状的发生。虽然PM对哮喘的影响已经在其他研究中发现，但CO可能是加重哮喘的车辆废气和其他燃烧副产物的标志物。
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.