stationary-site monitors is consistent with a similar study showing significant effects for exposure to EC with exhaled nitric oxide in children with asthma: Delfino et al. (2006) also found significant associations with same- day and 2-day moving average concentrations of personal EC, but only with 1-day lag and 2-day moving average concentrations for cen- tral-site EC measurements. Although previous studies have investi- gated effects on PEF because of its ease in collection and its correlation with FEV1, our study had the advantage of investigating both of these lung function metrics directly meas- ured simultaneously. Our results support those of other studies finding associations of lung function change with exposure to PM pollution: both PM2.5 mass (Delfino et al. 2004, 2008; Suglia et al. 2008) and the EC fraction (McCreanor et al. 2007; Suglia et al. 2008). Reductions in lung function found in this work may underestimate the full effects because during the times children experienced the most severe symptoms, they were unable to blow into the spirometer. For instance, on five afternoon occasions, lung function mea- surements were missing when the same child recorded substantial symptoms. Furthermore, we did not obtain sufficient data on rescue medication, which may also have masked lung function effects. Increased frequency of as-needed medication use has itself been asso- ciated with exposure to air pollution (Gent et al. 2003; Rabinovitch et al. 2006; Thurston et al. 1997; Trasande and Thurston 2005; Von Klot et al. 2002). Cough Traffic air pollution and asthma We also investigated the effects of copol- lutants. We found a significant association of increased risk of wheeze with O3 concentra- tion at 1-day lag, even when the highest O3 concentrations were excluded. Risks of other symptoms were also elevated, but were not statistically significant. Associations of both same-day and lag effects of O3 concentrations with adverse respiratory health are widely doc- umented in the literature (Thurston and Bates 2003; U.S. EPA 2008). SO2 gas, a marker of fresh diesel exhaust in the South Bronx (sam- pling took place in warm, nonheating seasons and before regulations mandating low-sul- fur diesel), was also significantly associated with increased risk of symptoms. Although the associations we found with O3 and SO2 may have their own implications for respira- tory health, they did not confound the sig- nificant symptom associations found with EC in copollutant models. In addition, there is recent evidence of a biological interaction of exposure to DEP and O3 in the lung (Bosson et al. 2008). Furthermore, the association we found with SO2 is consistent with a role for diesel in our findings with EC, because the copresence of diesel SO2 with DEP may potentiate the respiratory effects of the diesel aerosols. Study limitations. A significant limitation of this study is the relatively small number of subjects studied because feasibility issues allowed us to enroll only 40 study partici- pants. Future studies enrolling more subjects may help narrow the uncertainty around the effect estimates we found in the present study, Wheeze of the integrated time periods (Figure 2), and school-hour weekday sulfur concentrations were not associated with either of the after- noon lung function metrics. Thus, school-site sulfur concentrations were not confounders of the EC–asthma symptom associations. Discussion The present analyses indicate that personal exposure to the EC portion of PM2.5, which in our exposure assessment analysis was strongly affected by diesel exhaust emissions in this locale (Spira-Cohen et al. 2010), is most associated with several adverse respiratory outcomes in a group of inner-city elementary school children with asthma. Symptom sever- ity was the most complete health record and yielded the most consistent results, showing a significant increase in risk with increasing exposure to EC concentrations. Associations between adverse symptoms and PM2.5 mass, measured both via the personal backpacks and at the school site, were, in general, in the same direction as for EC but had larger p-values. Measures of BC soot have previously been linked specifically with decreased lung func- tion (Suglia et al. 2008) and with markers of lung inflammation, such as exhaled nitric oxide (Delfino et al. 2006; Kulkarni et al. 2006). Among healthy children, reduced lung function has been associated with car- bon content in the lungs (Kulkarni et al. 2006), and EC concentrations with deficits in lung growth in children 10–18 years of age (Gauderman et al. 2004). A study of very young children in NYC found associations of cough during the cold/flu season with central- site EC concentrations, but not with PM2.5 (Patel et al. 2009). Short-term exposures to DEP also led to the enhancement of aller- gic inflammation (Diaz-Sanchez et al. 1997; Pourazar et al. 2005). The findings of the present study provide further evidence to sup- port the hypothesis that previous associations of asthma exacerbations with traffic are due to exposure to the DEP fraction of PM. EC is also associated with very small PM (< 1 µm) with larger surface area (U.S. EPA 2004). The strongest and most consistent asso- ciations we found were for personal EC expo- sures with increased risk of asthma-related symptoms, which were statistically signifi- cantly associated with increased same-day per- sonal EC concentrations. We found not only strong associations with same-day concentra- tions, but also a significant increase in risk of cough with a 1-day lag and the largest relative risks for wheeze and cough with a 2-day aver- age EC concentration. These associations sug- gest a possible delay in the onset of symptoms and/or possible cumulative effects because triggers for asthma reactions can contribute to both immediate and late-phase responses. Our finding of significant lag effects with Figure 2. Relative risks (RR) (with 95% CIs) of cough (A), wheeze (B), shortness of breath (C), and total symptom (D) severity scores associated with the school-site integrated measurements of sulfur, EC, and PM2.5. Measurements were taken from 0700 hr to 1400 hr (start hour = 7) and from 1400 hours to 0700 hours (start hour = 2). Sulfur and PM2.5: n = 615 for 0700 hours to 1400 hours; n = 605 for 1400 hours to 0700 hours. EC: n = 635 for 0700 hours to 1400 hours; n = 625 for 1400 hours to 0700 hours. RR of total symptoms for 0700 hours to 1400 hours sulfur = 1.0 (95% CI, 0.99–1.00). Environmental Health Perspectives • volume 119 | number 4 | April 2011 563 1.8 1.6 1.4 RR1.2 1.0 0.8 1.8 1.6 1.4 1.0 0.8 RR1.2 Start hour: 7 2 Sulfur 7 2 EC Shortness of breath Start hour: 7 2 Sulfur 7 2 EC Exposure 7 2 PM2.5 7 2 PM2.5 1.8 1.6 1.4 1.0 0.8 RR1.2 1.8 1.6 1.4 1.0 0.8 RR1.2 Start hour: 7 2 Sulfur 7 2 EC 7 2 PM2.5 Total symptoms Start hour: 7 2 Sulfur 7 2 EC Exposure 7 2 PM2.5