The authors conducted a case-control survey nested within a birth cohort and collected detailed risk factor information to assess the extent to which residual confounding and exposure misclassification may impact air pollution effect estimates. Using a survey of 2,543 of 6,374 women sampled from a cohort of 58,316 eligible births in 2003 in Los Angeles County, California, the authors estimated with logistic regression and two-phase models the effects of pregnancy period-specific air pollution exposure on the odds of preterm birth. For the first trimester, the odds of preterm birth consistently increased with increasing carbon monoxide exposures and also at high levels of exposure to particulate matter less than or equal to 2.5 microm in diameter (>21.4 microg/m(3)), regardless of type of data (cohort/sample) or covariate adjustment (carbon monoxide exposures of >1.25 ppm increased the odds by 21-25%). Women exposed to carbon monoxide above 0.91 ppm during the last 6 weeks of pregnancy experienced increased odds of preterm birth. Crude and birth certificate covariate-adjusted results for carbon monoxide differed from each other. However, further adjustment for risk factors assessed in the survey did not change effect estimates for short-term pollutant averages appreciably, except for time-activity patterns, which strengthened the observed associations. These results confirm the importance of reducing exposure misclassification when evaluating the effect of traffic-related pollutants that vary spatially.

Epidemiologic studies addressing the relationship between ambient air pollution and fetal development are accumulating worldwide. Studies conducted in China (Wang et al. 1997;Xu et al. 1995), Brazil (Pereira et al. 1998), the Czech Republic (Bobak and Leon 1999;Dejmek et al. 1999;Perera et al. 1999), Mexico (Loomis et al. 1999), Korea (Ha et al. 2001), and the United States (Woodruff et al. 1997) linked ambient air pollution exposure during pregnancy with term low birth weight (LBW), intrauterine growth retardation (IUGR), preterm birth, and perinatal mortality. We recently reported that increases in carbon monoxide, particulate matter < 10 µm in aerodynamic diameter (PM 10 ), and ozone concentrations during vulnerable pregnancy periods increased the risk of term LBW (Ritz and Yu 1999), preterm delivery (Ritz et al. 2000), and certain cardiac malformations, such as ventricular septal defects (Ritz et al. 2002). CO is released directly in motor vehicle exhaust and does not react readily in the atmosphere to form other compounds. Fine (< 2.5 µm) and ultrafine (< 0.1 µm) particles are also released directly in vehicle exhaust but undergo physical and chemical transformations in the atmosphere as they disperse from the roadway (Zhu et al. 2002). The consistently observed associations between ambient CO concentrations and adverse birth outcomes in our previous studies suggest that compounds in motor vehicle exhaust (either CO or associated compounds such as fine and ultrafine particles) may affect fetal development.In our previous studies (Ritz and Yu 1999;Ritz et al. 2000Ritz et al. , 2002, air pollution exposure assessment was based on measurements taken at ambient monitoring stations during specific pregnancy periods. Although such measures may adequately reflect average exposure of pregnant women to background air pollution concentrations in their neighborhood, they may not take into account differential exposure within neighborhoods due to proximity to heavy-traffic roadways and freeways. Women residing closer to these sources may experience greater exposure to potentially toxic compounds released directly in vehicle exhaust or formed in the atmosphere adjacent to roadways. Therefore, we examined whether residential proximity to heavy-traffic roadways, such as freeways and major arterials, during pregnancy was associated with the risk of term LBW and preterm birth in infants born to women living in Los Angeles County, California, between 1994-1996 using a case-control study design. MethodsSubjects. We used birth certificates, provided by the California Department of Health Services (Sacramento, CA), to identify study subjects and to determine their gestational age, birth weight, and values for covariates included in our analyses. We included infants born to women living in the 28 Los Angeles County zip codes evaluated in earlier work (Ritz and Yu 1999;Ritz et al. 2000) and 84 additional zip codes selected to capture areas intersected by freeways and major arterials and collectors (Figure 1). Overall we included...

Background: The prevalence of autistic disorder (AD), a serious developmental condition, has risen dramatically over the past two decades, but high-quality population-based research addressing etiology is limited.Objectives: We studied the influence of exposures to traffic-related air pollution during pregnancy on the development of autism using data from air monitoring stations and a land use regression (LUR) model to estimate exposures.Methods: Children of mothers who gave birth in Los Angeles, California, who were diagnosed with a primary AD diagnosis at 3–5 years of age during 1998–2009 were identified through the California Department of Developmental Services and linked to 1995–2006 California birth certificates. For 7,603 children with autism and 10 controls per case matched by sex, birth year, and minimum gestational age, birth addresses were mapped and linked to the nearest air monitoring station and a LUR model. We used conditional logistic regression, adjusting for maternal and perinatal characteristics including indicators of SES.Results: Per interquartile range (IQR) increase, we estimated a 12–15% relative increase in odds of autism for ozone [odds ratio (OR) = 1.12, 95% CI: 1.06, 1.19; per 11.54-ppb increase] and particulate matter ≤ 2.5 µm (OR = 1.15; 95% CI: 1.06, 1.24; per 4.68-μg/m3 increase) when mutually adjusting for both pollutants. Furthermore, we estimated 3–9% relative increases in odds per IQR increase for LUR-based nitric oxide and nitrogen dioxide exposure estimates. LUR-based associations were strongest for children of mothers with less than a high school education.Conclusion: Measured and estimated exposures from ambient pollutant monitors and LUR model suggest associations between autism and prenatal air pollution exposure, mostly related to traffic sources.

BackgroundThere is a growing body of epidemiologic literature reporting associations between atmospheric pollutants and reproductive outcomes, particularly birth weight and gestational duration.ObjectivesThe objectives of our international workshop were to discuss the current evidence, to identify the strengths and weaknesses of published epidemiologic studies, and to suggest future directions for research.DiscussionParticipants identified promising exposure assessment tools, including exposure models with fine spatial and temporal resolution that take into account time–activity patterns. More knowledge on factors correlated with exposure to air pollution, such as other environmental pollutants with similar temporal variations, and assessment of nutritional factors possibly influencing birth outcomes would help evaluate importance of residual confounding. Participants proposed a list of points to report in future publications on this topic to facilitate research syntheses. Nested case–control studies analyzed using two-phase statistical techniques and development of cohorts with extensive information on pregnancy behaviors and biological samples are promising study designs. Issues related to the identification of critical exposure windows and potential biological mechanisms through which air pollutants may lead to intrauterine growth restriction and premature birth were reviewed.ConclusionsTo make progress, this research field needs input from toxicology, exposure assessment, and clinical research, especially to aid in the identification and exposure assessment of feto-toxic agents in ambient air, in the development of early markers of adverse reproductive outcomes, and of relevant biological pathways. In particular, additional research using animal models would help better delineate the biological mechanisms underpinning the associations reported in human studies.

BackgroundPreeclampsia is a major complication of pregnancy that can lead to substantial maternal and perinatal morbidity, mortality, and preterm birth. Increasing evidence suggests that air pollution adversely affects pregnancy outcomes. Yet few studies have examined how local traffic-generated emissions affect preeclampsia in addition to preterm birth.ObjectivesWe examined effects of residential exposure to local traffic-generated air pollution on preeclampsia and preterm delivery (PTD).MethodsWe identified 81,186 singleton birth records from four hospitals (1997–2006) in Los Angeles and Orange Counties, California (USA). We used a line-source dispersion model (CALINE4) to estimate individual exposure to local traffic-generated nitrogen oxides (NOx) and particulate matter < 2.5 μm in aerodynamic diameter (PM2.5) across the entire pregnancy. We used logistic regression to estimate effects of air pollution exposures on preeclampsia, PTD (gestational age < 37 weeks), moderate PTD (MPTD; gestational age < 35 weeks), and very PTD (VPTD; gestational age < 30 weeks).ResultsWe observed elevated risks for preeclampsia and preterm birth from maternal exposure to local traffic-generated NOx and PM2.5. The risk of preeclampsia increased 33% [odds ratio (OR) = 1.33; 95% confidence interval (CI), 1.18–1.49] and 42% (OR = 1.42; 95% CI, 1.26–1.59) for the highest NOx and PM2.5 exposure quartiles, respectively. The risk of VPTD increased 128% (OR = 2.28; 95% CI, 2.15–2.42) and 81% (OR = 1.81; 95% CI, 1.71–1.92) for women in the highest NOx and PM2.5 exposure quartiles, respectively.ConclusionExposure to local traffic-generated air pollution during pregnancy increases the risk of preeclampsia and preterm birth in Southern California women. These results provide further evidence that air pollution is associated with adverse reproductive outcomes.