Karr Catherine, Lumley Thomas, Shepherd Kristen, Davis Robert, Larson Timothy, Ritz Beate, Kaufman Joel
Department of Pediatrics, University of Washington, Seattle, Washington 98104, USA.
Environ Health Perspect. 2006 Feb;114(2):277-81. doi: 10.1289/ehp.8313.
We examined the association of infant bronchiolitis with acute exposure to ambient air pollutants.
We employed a time-stratified case-crossover method and based the exposure windows on a priori, biologically based hypotheses.
We evaluated effects in 19,901 infants in the South Coast Air Basin of California in 1995-2000 with a hospital discharge record for bronchiolitis in the first year of life (International Classification of Diseases, 9th Revision, CM466.1).
EVALUATIONS/MEASUREMENTS: Study subjects' ZIP code was linked to ambient air pollution monitors to derive exposures. We estimated the risk of bronchiolitis hospitalization associated with increases in wintertime ambient air pollutants using conditional logistic regression.
We observed no increased risk after acute exposure to particulate matter < or = 2.5 microm in aerodynamic diameter (PM2.5), carbon monoxide, or nitrogen dioxide. PM2.5 exposure models suggested a 26-41% increased risk in the most premature infants born at gestational ages between 25 and 29 weeks; however, these findings were based on very small numbers.
We found little support for a link between acute increases in ambient air pollution and infant bronchiolitis except modestly increased risk for PM2.5 exposure among infants born very prematurely. In these infants, the periods of viral acquisition and incubation concurred with the time of increased risk. RELEVANCE TO PROFESSIONAL PRACTICE: We present novel data for the infant period and the key respiratory disease of infancy, bronchiolitis. Incompletely explained trends in rising bronchiolitis hospitalization rates and increasing number of infants born prematurely underscore the importance of evaluating the impact of ambient air pollution in this age group in other populations and studies.
我们研究了婴儿细支气管炎与急性暴露于环境空气污染物之间的关联。
我们采用了时间分层病例交叉法,并根据先验的生物学假设确定暴露窗口。
我们评估了1995年至2000年加利福尼亚州南海岸空气盆地19901名婴儿的情况,这些婴儿在出生第一年有细支气管炎的医院出院记录(国际疾病分类,第9版,CM466.1)。
评估/测量:研究对象的邮政编码与环境空气污染监测器相关联以得出暴露情况。我们使用条件逻辑回归估计了与冬季环境空气污染物增加相关的细支气管炎住院风险。
在急性暴露于空气动力学直径小于或等于2.5微米的颗粒物(PM2.5)、一氧化碳或二氧化氮后,我们未观察到风险增加。PM2.5暴露模型表明,孕周在25至29周之间出生的最早产婴儿风险增加26%至41%;然而,这些发现基于非常少的病例数。
我们发现环境空气污染急性增加与婴儿细支气管炎之间的联系几乎没有依据,除了极早产婴儿中PM2.5暴露风险略有增加。在这些婴儿中,病毒感染和潜伏期与风险增加的时间一致。与专业实践的相关性:我们提供了婴儿期和婴儿期关键呼吸道疾病细支气管炎的新数据。细支气管炎住院率上升和早产婴儿数量增加的趋势未得到充分解释,这凸显了在其他人群和研究中评估环境空气污染对该年龄组影响的重要性。