BACKGROUND OF THE STUDY
Earlier studies have generally relied on simple measures of traffic proximity and density to estimate exposure and have not found an association between air pollution and asthma incidence (Ciccone et al. 1998; English et al. 1999; Wjst et al. 1993). More recent studies have used modeling approaches that provide high -resolution estimates of neighborhood-scale variations in air pollution. Several studies using this approach have observed increases in asthma incidence or asthma symptoms for children exposed to higher levels of traffic-related air pollution (Brauer etal. 2002, 2007; Gauderman et al. 2005; McConnell et al. 2006; Morgenstern et al. 2008; Zmirou et al. 2004). However, not all such studies of this type have reported consistent associations (Gehring et al. 2002; Zmirou et al. 2004).
Pre- and postbirth exposures to environmental tobacco smoke (ETS) are inde-pendently associated with increased asthma incidence (Haberg et al. 2007). Although air pollution exposures before 2–3 years of age appear to be most important for asthma devel-opment (McConnell et al. 2006; Zmirou et al. 2004), the effect of prebirth (or in utero) expo-sure has not to our knowledge been examined. One exception is a study of polyclyclic aro-matic hydrocarbon exposure, which has been examined in conjunction with ETS (Miller et al. 2004).
In the first population-based birth cohort study to explore the relationship between ambient air pollution exposure and the risk of asthma incidence, we examined the effect of in utero and first-year exposures to ambi-ent air pollutants, estimated at the individual level, on the risk of asthma diagnosis in chil-dren up to 3 and 4 years of age. Pollutant exposures investigated were carbon monoxide (CO), nitrogen oxides [nitric oxide (NO) and nitrogen dioxide (NO2 )], particulate matter [≤ 10 µm and ≤ 2.5 µm in aerodynamic diam-eter (PM10 and PM 2.5)], ozone (O3), sulfur dioxide (SO2), black carbon, woodsmoke, and proximity to roads and point sources.
1.2 STATEMENT OF THE PROBLEM
Asthma is the most common chronic disease in childhood [World Health Organization (WHO) 2006]. Its prevalence is high and has generally increased worldwide over the latter part of the 20th century (Asher et al. 2006; WHO 2006). Although explanations for relatively rapid changes in prevalence are unknown, environmental factors, independently and jointly with genetic factors, are thought to be responsible. Although air pollution has been consistently shown to exacerbate existing asthma (English et al. 1999; Lipsett et al. 1997; McConnell et al. 1999, 2006; Nicolai et al. 2003; Norris et al. 1999), there are few investigations of asthma onset and air pollution despite the hypothesized link with exposure to outdoor air pollution (Institute of Medicine 2000; von Mutius 2000).
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