with the wildfire duration defined as 2 weeks or 1 week of peak intensity instead of 3 weeks to assess sensitivity to the duration of the wildfire event, but main effects were not substantively altered (data not shown). Among births in census tracts proximal to monitors with higher average PM10 during the wildfire event, the estimated decrement in birth weight associated with pregnancy (any trimester) during the event was 6.6 g (95% CI: –11.0, –2.2). In tracts more proximal to mon- itors with average PM10 levels < 40 µg/m3, the estimated decrement in birth weight asso- ciated with pregnancy during the event was 5.9 g (95% CI: –9.2, –2.6). These estimates were not discernibly different from each other [see Supplemental Material, Table S3 (http:// dx.doi.org/10.1289/ehp.1104515)]. Seasonality and trend. Over the entire period, 2001–2005, we found a secular decline in mean birth weight of 6.9 g/year (95% CI: –7.6, –6.2) [see Supplemental Material, Table S1 (http://dx.doi.org/10.1289/ehp.1104515)]. Those conceived in Q3 (July–September) had the highest estimated mean weight at birth, 11.9 g (95% CI: 9.0, 14.7) more than infants conceived in Q1 (January–March), the referent time period. Infants conceived in Q1 weighed the least. When we conducted a sensitivity analysis, using an alternate model with seasonal effects parameterized as a cosinor, the magnitude of the seasonal effect was comparable (11.6 g; 95% CI: 7.7, 15.5), as was the relative timing (i.e., phase) of highest birth weight, with the maximum occurring on 4 August (95% CI: 29 July, 7 August) [see Supplemental Material, Table S2 (http://dx.doi.org/10.1289/ ehp.1104515)]. Goodness-of-fit and residuals. The adjusted R2 for the full model was 0.109. We plotted residuals versus fitted values and constructed a quantile probability plot to verify that the residual distribution was normal. We did not observe any heteroskedasticity of the residuals (data not shown). Discussion We observed a slight reduction in estimated mean birth weight among term infants exposed in utero to the 2003 California wildfires. The strongest estimated effect was observed for second-trimester exposure, fol- lowed by third-trimester exposure. Climate change scientists predict that wildfires will increase in frequency and magni- tude as global temperatures increase and rain- fall patterns change (Westerling and Bryant 2008; Westerling et al. 2006). These increases in wildfire events are projected to add to atmospheric pollution in the western United States under various climate change scenarios (Spracklen et al. 2009). In California, smoke impacts are already a required consideration Environmental Health Perspectives • volume 120 | number 9 | September 2012 in the planning and execution of preventive wildfire management activities, such as pre- scribed burns. For example, forest manage- ment professionals are required to assess the likely direction of smoke plumes and gauge their potential for impact on smoke sensitive areas (State of California 2001). Kochi et al. (2010) make the case that optimal wildfire management policy should explicitly include estimates of health-related and economic costs of wildfire smoke exposure. Potential etiologic pathways. At least two categories of etiologic pathways plausibly link maternal wildfire exposure with lower birth weight: biological (exposure to air pollution from the fires) and psychosocial (stress caused by direct or indirect consequences of wild- fires). A combination of the two is also plausi- ble. We cannot differentiate the contributions of these two pathways here, because we were not able to quantify daily air pollution expo- sures for each birth, or individual or ecologi- cal indicators of maternal stress. Nevertheless, our results may reflect the potential conjoint effect of these two pathways. Among the biological mechanisms hypothe- sized as having a possible effect on intrauterine growth rate are hypoxia and/or oxidative stress resulting from exposure to woodsmoke con- stituents, including carbon monoxide and PM (Siddiqui et al. 2008), alteration of maternal– placental exchanges, endocrine disruption, and oxidative stress pathways leading to alteration of maternal host–defense mechanisms and sub- sequently higher risk of infections (Slama et al. 2008). Reviews on the topic have found lim- ited applicable research from animal and toxi- cological studies to distinguish these possible mechanisms (Ritz and Wilhelm 2008; Slama et al. 2008; Woodruff et al. 2009). Human studies of the acute effects of wildfire smoke exposure on firefighters have demonstrated inflammatory responses and pulmonary func- tion test declines (e.g., Swiston et al. 2008). Human experiments in which healthy non- smokers were exposed to woodsmoke under controlled conditions, with concentrations of PM2.5 > 240 µg/m3 for up to 4 hr, resulted in elevated levels of blood and urine biomark- ers indicating oxidative stress and pulmonary inflammation in the lower airways (Barregard et al. 2006, 2008; Sällsten et al. 2006). More recent experiments confirmed biomarkers of systemic and pulmonary inflammation in Reduced birth weight following wildfire blood and lavage, but found no effect on pul- monary function or self-reported symptoms, and minimal effects on indices of heart rate variability (Ghio et al. 2012). Psychosocial aspects of wildfire exposure may also contribute to adverse health out- comes, although this is an understudied topic (Kumagai et al. 2004). Several studies have observed signs of fetal stress and adverse birth outcomes in the aftermath of disasters such as earthquakes (Weissman et al. 1989), ship- wrecks (Catalano and Hartig 2001), and ter- rorist attacks (Catalano et al. 2005). Plausible causes of stress in the wake of wildfires include loss of property, shelter, money, and other basic individual resources; physical incapacita- tion or injury; and disruption of sharing and support networks (Fowler 2003). Further analyses with methods that bet- ter characterize individual-level pollution exposures and psychosocial stress would be required to distinguish the relative contribu- tion of the two pathways. Exposure misclassification. Our study cap- tured temporal variation in wildfire exposure, but was limited in its ability to account for spatial variation. The SoCAB includes areas that were likely not directly exposed to heavy smoke plumes or to significant concentra- tions of diffused smoke. Because we relied on administrative vital statistics records, we were not able to assess whether mothers resided within the air basin throughout their preg- nancies, or determine how much time they spent at their primary residence. Meteorology, time–activity patterns, and variations in the built environment likely all contributed to variations in individual exposures, and there- fore to exposure misclassification. Because our study did not capture variations in exposure among the exposed, we could not evaluate dose–response relationships. A relatively small number of highly exposed mothers in this region may have been affected to a greater degree than our estimates would predict. When we conducted a sensitivity analysis that distinguished between births located in higher versus lower PM10 tracts during the wildfire event, we observed that the decrease in birth weight associated with gestational wildfire exposure was similar between these two populations. This result may be attribut- able to the fact that monitoring results could not adequately capture differences in ambient Table 2. Estimated effect of wildfire event during gestation on birth weight (g), by trimester. Unadjusted model Adjusted model Trimester of exposure Third (≥ 29 weeks) Second (17–28 weeks) First (1–16 weeks) Any trimester Effect (g) –7.9 –17.1 –3.9 –8.8 95% CI (–12.8, –3.1) (–21.9, –12.3) (–7.8, 0.0) (–11.5, –6.1) Effect (g) –7.0 –9.7 –3.3 –6.1 Adjusted model includes terms for fetal sex, gestational age, parity, maternal age, maternal education, maternal race/ ethnicity, secular trend, and season. 95% CI (–11.8, –2.2) (–14.5, –4.8) (–7.2, 0.6) (–8.7, –3.5) 1343