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Background: Chronic exposure to air pollutants is associated with increased risk of cardiovascular disease (CVD) among adults. However, little is known about how air pollution may affect the development of subclinical atherosclerosis in younger populations. Carotid artery intima-media thickness (CIMT) is a measure of subclinical atherosclerosis that provides insight into early CVD pathogenesis., Methods: In a pilot study of 70 participants from the Southern California Children's Health Study, we investigated CIMT progression from childhood to adulthood. Using carotid artery ultrasound images obtained at age 10 and follow-up images at age 21-22, we examined associations between childhood ambient and traffic-related air pollutants with changes in CIMT over time and attained adult CIMT using linear mixed-effects models adjusted for potential confounders. Average residential childhood exposures (i.e., birth to time of measurement at 10-11 years) were assigned for regional, ambient pollutants (ozone, nitrogen dioxide, particulate matter, interpolated from regulatory air monitoring data) and traffic-related nitrogen oxides (NO x ) by road class (modeled using the CALINE4 line source dispersion model). Traffic density was calculated within a 300-m residential buffer., Results: For each 1 standard deviation (SD) increase in childhood traffic-related total NO x exposure, we observed greater yearly rate of change in CIMT from childhood to adulthood (β: 2.17 μm/yr, 95% CI: 0.78-3.56). Increases in annual rate of CIMT change from childhood to adulthood also were observed with freeway NO x exposure (β: 2.24 μm/yr, 95% CI: 0.84-3.63) and traffic density (β: 2.11 μm/yr, 95% CI: 0.79-3.43). Traffic exposures were also related to increases in attained CIMT in early adulthood. No associations of CIMT change or attained level were observed with ambient pollutants., Conclusions: Overall, we observed adverse changes in CIMT over time in relation to childhood traffic-related NO x exposure and traffic density in our study population. While these results must be cautiously interpreted given the limited sample size, the observed associations of traffic measures with CIMT suggest a need for future studies to more fully explore this relationship.

Background: Air pollution exposure has been shown to increase the risk of obesity and metabolic dysfunction in animal models and human studies. However, the metabolic pathways altered by air pollution exposure are unclear, especially in adolescents and young adults who are at a critical period in the development of cardio-metabolic diseases., Objectives: The aim of this study was to examine the associations between air pollution exposure and indices of fatty acid and amino acid metabolism., Methods: A total of 173 young adults (18-23 years) from eight Children's Health Study (CHS) Southern California communities were examined from 2014 to 2018. Near-roadway air pollution (NRAP) exposure (freeway and non-freeway) and regional air pollution exposure (nitrogen dioxide, ozone and particulate matter) during one year before the study visit were estimated based on participants' residential addresses. Serum concentrations of 64 targeted metabolites including amino acids, acylcarnitines, non-esterified fatty acid (NEFA) and glycerol were measured in fasting serum samples. Principal component analysis of metabolites was performed to identify metabolite clusters that represent key metabolic pathways. Mixed effects models were used to analyze the associations of air pollution exposure with metabolomic principal component (PC) scores and individual metabolite concentrations adjusting for potential confounders., Results: Higher lagged one-year averaged non-freeway NRAP exposure was associated with higher concentrations of NEFA oxidation byproducts and higher NEFA-related PC score (all p's ≤ 0.038). The effect sizes were larger among obese individuals (interaction p = 0.047). Among females, higher freeway NRAP exposure was also associated with a higher NEFA-related PC score (p = 0.042). Among all participants, higher freeway NRAP exposure was associated with a lower PC score for lower concentrations of short- and median-chain acylcarnitines (p = 0.044)., Conclusions: Results of this study indicate that NRAP exposure is associated with altered fatty acid metabolism, which could contribute to the metabolic perturbation in obese youth., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Evidence suggests that childhood near-roadway air pollution (NRAP) exposures contribute to increased body mass index (BMI); however, effects of NRAP exposure during the vulnerable periods including in utero and first year of life have yet to be established. In this study, we examined whether exposure to elevated concentrations of NRAP during in utero and/or first year of life increase childhood BMI growth., Methods: Participants in the Children's Health Study enrolled from 2002 to 2003 with annual visits over a four-year period and who changed residences before study entry were included (n = 2318). Annual height and weight were measured and lifetime residential NRAP exposures including in utero and first year of life periods were estimated by nitrogen oxides (NO x ) using the California line-source dispersion model. Linear mixed effects models assessed in utero or first year near-road freeway and non-freeway NO x exposures and BMI growth after adjusting for age, sex, race/ethnicity, parental education, Spanish questionnaire, and later childhood near-road NO x exposure., Results: A two-standard deviation difference in first year of life near-road freeway NO x exposure was associated with a 0.1 kg/m 2 (95% confidence interval (CI): 0.03, 0.2) faster increase in BMI growth per year and a 0.5 kg/m 2 (95% CI: 0.02, 0.9) higher attained BMI at age 10 years., Conclusions: Higher exposure to early life NRAP increased the rate of change of childhood BMI and resulted in a higher attained BMI at age 10 years that were independent of later childhood exposures. These findings suggest that elevated early life NRAP exposures contribute to increased obesity risk in children.

Background: Traffic-related air pollution (TRAP) exposure has been linked to type 2 diabetes and metabolic dysfunction in humans. Animal studies suggest that air pollutants may alter the composition of the gut microbiota, which may negatively impact metabolic health through changes in the composition and/or function of the gut microbiome., Objectives: The primary aim of this study was to determine whether elevated TRAP exposure was correlated with gut bacterial taxa in overweight and obese adolescents from the Meta-AIR (Metabolic and Asthma Incidence Research) study. The secondary aim was to examine whether gut microbial taxa correlated with TRAP were also correlated with risk factors for type 2 diabetes (e.g., fasting glucose levels). We additionally explored whether correlations between TRAP and these metabolic risk factors could be explained by the relative abundance of these taxa., Methods: Participants (17-19 years; n=43) were enrolled between 2014 and 2016 from Southern California. The CALINE4 line dispersion model was used to model prior year residential concentrations of nitrogen oxides (NOx) as a marker of traffic emissions. The relative abundance of fecal microbiota was characterized by 16S rRNA sequencing and spearman partial correlations were examined after adjusting for body fat percent., Results: Freeway TRAP was correlated with decreased Bacteroidaceae (r=-0.48; p=0.001) and increased Coriobacteriaceae (r=0.48; p<0.001). These same taxa were correlated with fasting glucose levels, including Bacteroidaceae (r=-0.34; p=0.04) and Coriobacteriaceae (r=0.41; p<0.01). Further, freeway TRAP was positively correlated fasting glucose (r=0.45; p=0.004) and Bacteroidaceae and Coriobacteriaceae explained 24% and 29% of the correlation between TRAP and fasting glucose levels., Conclusions: Increased TRAP exposure was correlated with gut microbial taxa and fasting glucose levels. Gut microbial taxa that were correlated with TRAP partially explained the correlation between TRAP and fasting glucose levels. These results suggest that exposure to air pollutants may negatively impact metabolic health via alterations in the gut microbiota., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Background: Emerging evidence indicates that the near-roadway air pollution (NRAP) mixture contributes to CHD, yet few studies have evaluated the associated costs., Objective: We integrated an assessment of NRAP-attributable CHD in Southern California with new methods to value the associated mortality and hospitalizations., Methods: Based on population-weighted residential exposure to NRAP (traffic density, proximity to a major roadway and elemental carbon), we estimated the inflation-adjusted value of NRAP-attributable mortality and costs of hospitalizations that occurred in 2008. We also estimated anticipated costs in 2035 based on projected changes in population and in NRAP exposure associated with California's plans to reduce greenhouse gas emissions. For comparison, we estimated the value of CHD mortality attributable to PM less than 2.5μm in diameter (PM 2.5 ) in both 2008 and 2035., Results: The value of CHD mortality attributable to NRAP in 2008 was between $3.8 and $11.5 billion, 23% (major roadway proximity) to 68% (traffic density) of the $16.8 billion attributable to regulated regional PM 2.5 . NRAP-attributable costs were projected to increase to $10.6 to $22 billion in 2035, depending on the NRAP metric. Cost of NRAP-attributable hospitalizations for CHD in 2008 was $48.6 million and was projected to increase to $51.4 million in 2035., Conclusions: We developed an economic framework that can be used to estimate the benefits of regulations to improve air quality. CHD attributable to NRAP has a large economic impact that is expected to increase by 2035, largely due to an aging population. PM 2.5 -attributable costs may underestimate total value of air pollution-attributable CHD., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Background: Several studies have estimated the burden of coronary heart disease (CHD) mortality from ambient regional particulate matter ≤ 2.5 μm (PM2.5). The burden of near-roadway air pollution (NRAP) generally has not been examined, despite evidence of a causal link with CHD., Objective: We investigated the CHD burden from NRAP and compared it with the PM2.5 burden in the California South Coast Air Basin for 2008 and under a compact urban growth greenhouse gas reduction scenario for 2035., Methods: We estimated the population attributable fraction and number of CHD events attributable to residential traffic density, proximity to a major road, elemental carbon (EC), and PM2.5 compared with the expected disease burden if the population were exposed to background levels of air pollution., Results: In 2008, an estimated 1,300 CHD deaths (6.8% of the total) were attributable to traffic density, 430 deaths (2.4%) to residential proximity to a major road, and 690 (3.7%) to EC. There were 1,900 deaths (10.4%) attributable to PM2.5. Although reduced exposures in 2035 should result in smaller fractions of CHD attributable to traffic density, EC, and PM2.5, the numbers of estimated deaths attributable to each of these exposures are anticipated to increase to 2,500, 900, and 2,900, respectively, due to population aging. A similar pattern of increasing NRAP-attributable CHD hospitalizations was estimated to occur between 2008 and 2035., Conclusion: These results suggest that a large burden of preventable CHD mortality is attributable to NRAP and is likely to increase even with decreasing exposure by 2035 due to vulnerability of an aging population. Greenhouse gas reduction strategies developed to mitigate climate change offer unexploited opportunities for air pollution health co-benefits.

Unlabelled: We hypothesized that chronic exposures to traffic combustion products may lower bone mineral density (BMD). We found that proximity to freeways was associated with reduced BMD. Our findings suggest that traffic-related pollution may contribute to the occurrence of osteopenia and osteoporosis., Introduction: Adults residing in rural areas have been linked with higher BMD. We aimed to determine if this difference is due in part to air pollution by examining the relationships between traffic metrics and ambient air pollution with total body and pelvic BMD., Methods: Mexican American adults (n = 1,175; mean 34 years; 72 % female) who had participated in the BetaGene study of air pollution, obesity, and insulin resistance were included in this analysis. Total body and pelvic BMD were estimated using dual-energy X-ray absorptiometry. Traffic and ambient air pollutant exposures were estimated at residences using location and ambient monitoring data. Variance component models were used to analyze the associations between residential distance to the nearest freeway and ambient air pollutants with BMD., Results: Residential proximity to a freeway was associated with lower total body BMD (p-trend = 0.01) and pelvic BMD (p-trend = 0.03) after adjustment for age, sex, weight, and height. The adjusted mean total body and pelvic BMD in participants living within 500 m of a freeway were 0.02 and 0.03 g/cm(2) lower than participants living greater than 1,500 m from a freeway. These associations did not differ significantly by age, sex, or obesity status. Results were similar after further adjustment for body fat and weekly physical activity minutes. Ambient air pollutants (NO2, O3, and PM2.5) were not significantly associated with BMD., Conclusions: Traffic-related exposures in overweight and obese Mexican Americans may adversely affect BMD. Our findings indicate that long-term exposures to traffic may contribute to the occurrence of osteoporosis and its consequences.

Unlabelled: To assess accountability and effectiveness of air regulatory policies, we reviewed more than 20 years of monitoring data, emissions estimates, and regulatory policies across several southern California communities participating in a long-term study of children's health. Between 1994 and 2011, air quality improved for NO2 and PM2.5 in virtually all the monitored communities. Average NO2 declined 28% to 53%, and PM2.5 decreased 13% to 54%. Year-to-year PM2.5 variability at lower pollution sites was large compared to changes in long-term trends. PM10 and O3 decreases were largest in communities that were initially among the most polluted. Trends in annual average NO2, PM2.5, and PM10 concentrations in higher pollution communities were generally consistent with NOx, ROG, SOx, PM2.5, and PM10 emissions decreases. Reductions observed at one of the higher PM2.5 sites, Mira Loma, were generally within the range expected from reductions observed in ROG, NOx, SOx, and PM2.5 emissions. Despite a 38% increase in regional motor vehicle activity, vigorous economic growth, and a 30% population increase, total estimated emissions of NOx, ROG, SOx, PM2.5, and PM10 decreased by 54%, 65%, 40%, 21%, and 15%, respectively, during the 20-year time period. Emission control strategies in California have achieved dramatic reductions in ambient NO2, O3, PM2.5, and PM10. However, additional reductions will still be needed to achieve current health-based clean air standards., Implications: For many cities facing the challenge of reducing air pollution to meet health-based standards, the emission control policies and pollution reduction programs adopted in southern California should serve as an example of the potential success of aggressive, comprehensive, and integrated approaches. Policies targeting on-road mobile emissions were the single most important element for observed improvements in the Los Angeles region. However, overall program success was the result of a much broader approach designed to achieve emission reductions across all major pollutants and emissions categories.

Background: Emerging evidence suggests that near-roadway air pollution (NRP) exposure causes childhood asthma. The associated costs are not well documented., Objective: We estimated the cost of childhood asthma attributable to residential NRP exposure and regional ozone (O3) and nitrogen dioxide (NO2) levels in Los Angeles County. We developed a novel approach to apportion the costs between these exposures under different pollution scenarios., Methods: We integrated results from a study of willingness to pay to reduce the burden of asthma with results from studies of health care use and charges to estimate the costs of an asthma case and exacerbation. We applied those costs to the number of asthma cases and exacerbations caused by regional pollution in 2007 and to hypothetical scenarios of a 20% reduction in regional pollution in combination with a 20% reduction or increase in the proportion of the total population living within 75 m of a major roadway., Results: Cost of air pollution-related asthma in Los Angeles County in 2007 was $441 million for O3 and $202 million for NO2 in 2010 dollars. Cost of routine care (care in absence of exacerbation) accounted for 18% of the combined NRP and O3 cost and 39% of the combined NRP and NO2 cost; these costs were not recognized in previous analyses. NRP-attributable asthma accounted for 43% (O3) to 51% (NO2) of the total annual cost of exacerbations and routine care associated with pollution. Hypothetical scenarios showed that costs from increased NRP exposure might offset savings from reduced regional pollution., Conclusions: Our model disaggregates the costs of regional pollution and NRP exposure and illustrates how they might vary under alternative exposure scenarios. The cost of air pollution is a substantial burden on families and an economic loss for society., (Copyright © 2014 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Background: Biologically plausible mechanisms link traffic-related air pollution to metabolic disorders and potentially to obesity. Here we sought to determine whether traffic density and traffic-related air pollution were positively associated with growth in body mass index (BMI = kg/m2) in children aged 5-11 years., Methods: Participants were drawn from a prospective cohort of children who lived in 13 communities across Southern California (N = 4550). Children were enrolled while attending kindergarten and first grade and followed for 4 years, with height and weight measured annually. Dispersion models were used to estimate exposure to traffic-related air pollution. Multilevel models were used to estimate and test traffic density and traffic pollution related to BMI growth. Data were collected between 2002-2010 and analyzed in 2011-12., Results: Traffic pollution was positively associated with growth in BMI and was robust to adjustment for many confounders. The effect size in the adjusted model indicated about a 13.6% increase in annual BMI growth when comparing the lowest to the highest tenth percentile of air pollution exposure, which resulted in an increase of nearly 0.4 BMI units on attained BMI at age 10. Traffic density also had a positive association with BMI growth, but this effect was less robust in multivariate models., Conclusions: Traffic pollution was positively associated with growth in BMI in children aged 5-11 years. Traffic pollution may be controlled via emission restrictions; changes in land use that promote jobs-housing balance and use of public transit and hence reduce vehicle miles traveled; promotion of zero emissions vehicles; transit and car-sharing programs; or by limiting high pollution traffic, such as diesel trucks, from residential areas or places where children play outdoors, such as schools and parks. These measures may have beneficial effects in terms of reduced obesity formation in children.

Background: Few previous studies examined the impact of prenatal air pollution exposures on fetal development based on ultrasound measures during pregnancy., Methods: In a prospective birth cohort of more than 500 women followed during 1993-1996 in Los Angeles, California, we examined how air pollution impacts fetal growth during pregnancy. Exposure to traffic related air pollution was estimated using CALINE4 air dispersion modeling for nitrogen oxides (NOx) and a land use regression (LUR) model for nitrogen monoxide (NO), nitrogen dioxide (NO2) and NOx. Exposures to carbon monoxide (CO), NO2, ozone (O3) and particles <10μm in aerodynamic diameter (PM10) were estimated using government monitoring data. We employed a linear mixed effects model to estimate changes in fetal size at approximately 19, 29 and 37 weeks gestation based on ultrasound., Results: Exposure to traffic-derived air pollution during 29 to 37 weeks was negatively associated with biparietal diameter at 37 weeks gestation. For each interquartile range (IQR) increase in LUR-based estimates of NO, NO2 and NOx, or freeway CALINE4 NOx we estimated a reduction in biparietal diameter of 0.2-0.3mm. For women residing within 5km of a monitoring station, we estimated biparietal diameter reductions of 0.9-1.0mm per IQR increase in CO and NO2. Effect estimates were robust to adjustment for a number of potential confounders. We did not observe consistent patterns for other growth endpoints we examined., Conclusions: Prenatal exposure to traffic-derived pollution was negatively associated with fetal head size measured as biparietal diameter in late pregnancy., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Congenital anomalies are a leading cause of infant mortality and are important contributors to subsequent morbidity. Studies suggest associations between environmental contaminants and some anomalies, although evidence is limited. We aimed to investigate whether ambient air pollutant and traffic exposures in early gestation contribute to the risk of selected congenital anomalies in the San Joaquin Valley of California, 1997-2006. Seven exposures and 5 outcomes were included for a total of 35 investigated associations. We observed increased odds of neural tube defects when comparing the highest with the lowest quartile of exposure for several pollutants after adjusting for maternal race/ethnicity, education, and multivitamin use. The adjusted odds ratio for neural tube defects among those with the highest carbon monoxide exposure was 1.9 (95% confidence interval: 1.1, 3.2) compared with those with the lowest exposure, and there was a monotonic exposure-response across quartiles. The highest quartile of nitrogen oxide exposure was associated with neural tube defects (adjusted odds ratio = 1.8, 95% confidence interval: 1.1, 2.8). The adjusted odds ratio for the highest quartile of nitrogen dioxide exposure was 1.7 (95% confidence interval: 1.1, 2.7). Ozone was associated with decreased odds of neural tube defects. Our results extend the limited body of evidence regarding air pollution exposure and adverse birth outcomes.

Traffic-related air pollution is recognized as an important contributor to health problems. Epidemiologic analyses suggest that prenatal exposure to traffic-related air pollutants may be associated with adverse birth outcomes; however, there is insufficient evidence to conclude that the relation is causal. The Study of Air Pollution, Genetics and Early Life Events comprises all births to women living in 4 counties in California's San Joaquin Valley during the years 2000-2006. The probability of low birth weight among full-term infants in the population was estimated using machine learning and targeted maximum likelihood estimation for each quartile of traffic exposure during pregnancy. If everyone lived near high-volume freeways (approximated as the fourth quartile of traffic density), the estimated probability of term low birth weight would be 2.27% (95% confidence interval: 2.16, 2.38) as compared with 2.02% (95% confidence interval: 1.90, 2.12) if everyone lived near smaller local roads (first quartile of traffic density). Assessment of potentially causal associations, in the absence of arbitrary model assumptions applied to the data, should result in relatively unbiased estimates. The current results support findings from previous studies that prenatal exposure to traffic-related air pollution may adversely affect birth weight among full-term infants.

Background: The emerging consensus that exposure to near-roadway traffic-related pollution causes asthma has implications for compact urban development policies designed to reduce driving and greenhouse gases., Objectives: We estimated the current burden of childhood asthma-related disease attributable to near-roadway and regional air pollution in Los Angeles County (LAC) and the potential health impact of regional pollution reduction associated with changes in population along major traffic corridors., Methods: The burden of asthma attributable to the dual effects of near-roadway and regional air pollution was estimated, using nitrogen dioxide and ozone as markers of urban combustion-related and secondary oxidant pollution, respectively. We also estimated the impact of alternative scenarios that assumed a 20% reduction in regional pollution in combination with a 3.6% reduction or 3.6% increase in the proportion of the total population living near major roads, a proxy for near-roadway exposure., Results: We estimated that 27,100 cases of childhood asthma (8% of total) in LAC were at least partly attributable to pollution associated with residential location within 75 m of a major road. As a result, a substantial proportion of asthma-related morbidity is a consequence of near-roadway pollution, even if symptoms are triggered by other factors. Benefits resulting from a 20% regional pollution reduction varied markedly depending on the associated change in near-roadway proximity., Conclusions: Our findings suggest that there are large and previously unappreciated public health consequences of air pollution in LAC and probably in other metropolitan areas with dense traffic corridors. To maximize health benefits, compact urban development strategies should be coupled with policies to reduce near-roadway pollution exposure.

Air quality has emerged as a key determinant of important health outcomes in children and adults. This study aims to identify factors that influence local, within-community air quality, and to build a model for traffic-related air pollution (TRP).We utilized concentrations of NO(2), NO, and total oxides of nitrogen (NO(x)), which were measured at 942 locations in 12 southern California communities. For each location, population density, elevation, land-use, and several indicators of traffic were calculated. A spatial random effects model was used to study the relationship of these predictors to each TRP.Variation in TRP was strongly correlated with traffic on nearby freeways and other major roads, and also with population density and elevation. After accounting for traffic, categories of land-use were not associated with the pollutants. Traffic had a larger relative impact in small urban (low regional pollution) communities than in large urban (high regional pollution) communities. For example, our best fitting model explained 70% of the variation in NO(x) in large urban areas and 76% in small urban areas. Compared with living at least 1,500 m from a freeway, living within 250 m of a freeway was associated with up to a 41% increase in TRP in a large urban area, and up to a 75% increase in small urban areas.Thus, traffic strongly affects local air quality in large and small urban areas, which has implications for exposure assessment and estimation of health risks.

Rationale: Emerging evidence indicates that psychosocial stress enhances the effect of traffic exposure on the development of asthma., Objectives: We hypothesized that psychosocial stress would also modify the effect of traffic exposure on lung function deficits., Methods: We studied 1,399 participants in the Southern California Children's Health Study undergoing lung function testing (mean age, 11.2 yr). We used hierarchical mixed models to assess the joint effect of traffic-related air pollution and stress on lung function., Measurements and Main Results: Psychosocial stress in each child's household was assessed based on parental response to the perceived stress scale (range, 0-16) at study entry. Exposures to nitric oxide, nitrogen dioxide, and total oxides of nitrogen (NOx), surrogates of the traffic-related pollution mixture, were estimated at schools and residences based on a land-use regression model. Among children from high-stress households (parental perceived stress scale > 4) deficits in FEV1 of 4.5 (95% confidence interval, -6.5 to -2.4) and of 2.8% (-5.7 to 0.3) were associated with each 21.8 ppb increase in NOx at homes and schools, respectively. These pollutant effects were significantly larger in the high-stress compared with lower-stress households (interaction P value 0.007 and 0.05 for residential and school NOx, respectively). No significant NOx effects were observed in children from low-stress households. A similar pattern of association was observed for FVC. The observed associations for FEV1 and FVC remained after adjusting for sociodemographic factors and after restricting the analysis to children who do not have asthma., Conclusions: A high-stress home environment is associated with increased susceptibility to lung function effects of air pollution both at home and at school.

Background: Little is known about environmental causes and contributing factors for autism. Basic science and epidemiologic research suggest that oxidative stress and inflammation may play a role in disease development. Traffic-related air pollution, a common exposure with established effects on these pathways, contains substances found to have adverse prenatal effects., Objectives: We examined the association between autism and proximity of residence to freeways and major roadways during pregnancy and near the time of delivery, as a surrogate for air pollution exposure., Methods: Data were from 304 autism cases and 259 typically developing controls enrolled in the Childhood Autism Risks from Genetics and the Environment (CHARGE) study. The mother's address recorded on the birth certificate and trimester-specific addresses derived from a residential history obtained by questionnaire were geocoded, and measures of distance to freeways and major roads were calculated using ArcGIS software. Logistic regression models compared residential proximity to freeways and major roads for autism cases and typically developing controls., Results: Adjusting for sociodemographic factors and maternal smoking, maternal residence at the time of delivery was more likely be near a freeway (≤ 309 m) for cases than for controls [odds ratio (OR)=1.86; 95% confidence interval (CI), 1.04-3.45]. Autism was also associated with residential proximity to a freeway during the third trimester (OR=2.22; CI, 1.16-4.42). After adjustment for socioeconomic and sociodemographic characteristics, these associations were unchanged. Living near other major roads at birth was not associated with autism., Conclusions: Living near a freeway was associated with autism. Examination of associations with measured air pollutants is needed.

Background: Two recent case-control studies in Italy reported that long-term exposure to particulate air pollution or living near major traffic roads was associated with an increased risk of deep vein thrombosis (DVT). No prospective evidence exists on the possible association between long-term traffic-related air pollution and incident venous thromboembolism (VTE)., Objectives: To examine the association between long-term traffic exposure and incident VTE in a population-based prospective cohort study., Methods: We studied 13,143 middle-aged men and women in the Atherosclerosis Risk in Communities Study without a history of DVT or pulmonary embolism at baseline examination (1987-1989). The Geographical Information System-mapped traffic density and distance to major roads in the four study communities served as measures of traffic exposure. We examined the association between traffic exposure and incident VTE with proportional hazards regression models., Results: A total of 405 subjects developed VTE in 2005. Traffic density was not significantly associated with VTE. Relative to those in the lowest quartile of traffic density, the adjusted hazard ratios across increasing quartiles were 1.18 (95% confidence interval [CI] 0.88-1.57), 0.99 (95% CI 0.74-1.34) and 1.14 (95% CI 0.86-1.51) (P-value for trend across quartiles = 0.64). For residents living within 150 m of major roads, as compared with subjects living further away, the adjusted hazard ratio was 1.16 (95% CI 0.95-1.42, P = 0.14)., Conclusions: This first prospective study in the general population does not support an association between air pollution exposure or traffic proximity and risk of DVT. More data may be needed to clarify whether traffic or air pollution influences the risk of VTE., (© 2011 International Society on Thrombosis and Haemostasis.)

Background: Traffic-related air pollution has been associated with adverse cardiorespiratory effects, including increased asthma prevalence. However, there has been little study of effects of traffic exposure at school on new-onset asthma., Objectives: We evaluated the relationship of new-onset asthma with traffic-related pollution near homes and schools., Methods: Parent-reported physician diagnosis of new-onset asthma (n = 120) was identified during 3 years of follow-up of a cohort of 2,497 kindergarten and first-grade children who were asthma- and wheezing-free at study entry into the Southern California Children's Health Study. We assessed traffic-related pollution exposure based on a line source dispersion model of traffic volume, distance from home and school, and local meteorology. Regional ambient ozone, nitrogen dioxide (NO(2)), and particulate matter were measured continuously at one central site monitor in each of 13 study communities. Hazard ratios (HRs) for new-onset asthma were scaled to the range of ambient central site pollutants and to the residential interquartile range for each traffic exposure metric., Results: Asthma risk increased with modeled traffic-related pollution exposure from roadways near homes [HR 1.51; 95% confidence interval (CI), 1.25-1.82] and near schools (HR 1.45; 95% CI, 1.06-1.98). Ambient NO(2) measured at a central site in each community was also associated with increased risk (HR 2.18; 95% CI, 1.18-4.01). In models with both NO(2) and modeled traffic exposures, there were independent associations of asthma with traffic-related pollution at school and home, whereas the estimate for NO(2) was attenuated (HR 1.37; 95% CI, 0.69-2.71)., Conclusions: Traffic-related pollution exposure at school and homes may both contribute to the development of asthma.

Objectives: As part of a community-based participatory research effort, we estimated the preventable burden of childhood asthma associated with air pollution in the southern California communities of Long Beach and Riverside., Methods: We calculated attributable fractions for 2 air pollution reduction scenarios to include assessment of the newly recognized health effects associated with residential proximity to major roads and impact from ship emissions., Results: Approximately 1600 (9%) of all childhood asthma cases in Long Beach and 690 (6%) in Riverside were attributed to traffic proximity. Ship emissions accounted for 1400 (21%) bronchitis episodes and, in more modest proportions, health care visits for asthma. Considerably greater reductions in asthma morbidity could be obtained by reducing nitrogen dioxide and ozone concentrations to levels found in clean coastal communities., Conclusions: Both Long Beach and Riverside have heavy automobile traffic corridors as well as truck traffic and regional pollution originating in the Los Angeles-Long Beach port complex, the largest in the United States. Community-based quantitative risk analyses can improve our understanding of health problems and help promote public health in transportation planning.

Background: Exposure to traffic has been associated with asthma outcomes in children, but its effect on asthma in adults has not been well studied., Objective: To test the hypothesis that lung function and health status are associated with traffic exposures., Methods: We measured FEV(1) % predicted, general health status using the Physical Component Scale of the 12-item Short Form (SF-12 PCS), and quality of life (QoL) using the Marks Asthma Quality of Life questionnaire in a cohort of adults with asthma or rhinitis (n = 176; 145 with asthma). We assessed exposures to traffic by geocoding subjects' residential addresses and assigning distance to roadways. Associations between distance to nearest roadway and distance to nearest major roadway and FEV(1) % predicted or SF-12 PCS were studied by using linear regression., Results: FEV(1) % predicted was positively associated with distance from both nearest roadway (P = .01) and nearest major roadway (P = .02). SF-12 PCS and QoL were not significantly associated with either traffic variable. Adjustment for income, smoking, and obesity did not substantively change the associations of the traffic variables with FEV(1) % predicted (P = .04 for nearest roadway and P = .02 for nearest major roadway) and did not cause associations with either SF-12 PCS or QoL to become significant., Conclusions: Traffic exposure was associated with decreased lung function in adults with asthma.

Background: For people living close to busy roads, traffic is a major source of air pollution. Few prospective data have been published on the effects of long-term exposure to traffic on the incidence of coronary heart disease (CHD)., Objectives: In this article, we examined the association between long-term traffic exposure and incidence of fatal and nonfatal CHD in a population-based prospective cohort study., Methods: We studied 13,309 middle-age men and women in the Atherosclerosis Risk in Communities study, without previous CHD at enrollment, from 1987 to 1989 in four U.S. communities. Geographic information system-mapped traffic density and distance to major roads served as measures of traffic exposure. We examined the association between traffic exposure and incident CHD using proportional hazards regression models, with adjustment for background air pollution and a wide range of individual cardiovascular risk factors., Results: Over an average of 13 years of follow-up, 976 subjects developed CHD. Relative to those in the lowest quartile of traffic density, the adjusted hazard ratio (HR) in the highest quartile was 1.32 [95% confidence interval (CI), 1.06-1.65; p-value for trend across quartiles = 0.042]. When we treated traffic density as a continuous variable, the adjusted HR per one unit increase of log-transformed density was 1.03 (95% CI, 1.01-1.05; p = 0.006). For residents living within 300 m of major roads compared with those living farther away, the adjusted HR was 1.12 (95% CI, 0.95-1.32; p = 0.189). We found little evidence of effect modification for sex, smoking status, obesity, low-density lipoprotein cholesterol level, hypertension, age, or education., Conclusion: Higher long-term exposure to traffic is associated with incidence of CHD, independent of other risk factors. These prospective data support an effect of traffic-related air pollution on the development of CHD in middle-age persons.

Background: Traffic exposure is a major contributor to ambient air pollution for people living close to busy roads. The relationship between traffic exposure and lung function remains inconclusive in adults., Methods: A cross-sectional study was conducted to investigate the association between traffic exposure and lung function in the Atherosclerosis Risk in Communities (ARIC) study, a community based cohort of 15 792 middle aged men and women. Traffic density and distance to major roads were used as measures of traffic exposure., Results: After controlling for potential confounders including demographic factors, personal and neighbourhood level socioeconomic characteristics, cigarette smoking and background air pollution, higher traffic density was significantly associated with lower forced expiratory volume in 1 s (FEV1) and forced vital capacity (FVC) in women. Relative to the lowest quartile of traffic density, the adjusted differences across increasing quartiles were 5.1, -15.4 and -21.5 ml for FEV1 (p value of linear trend across the quartiles = 0.041) and 1.2, -23.4 and -34.8 ml for FVC (p trend = 0.010). Using distance from major roads as a simpler index of traffic related air pollution exposure, the FEV1 was -15.7 ml (95% CI -34.4 to 2.9) lower and the FVC was -24.2 ml (95% CI -46.2 to -2.3) lower for women living within 150 m compared with subjects living further away. There was no significant effect of traffic density or distance to major roads on lung function in men. The FEV1/FVC ratio was not significantly associated with traffic exposure in either men or women., Conclusions: This is the largest published study of traffic exposure and pulmonary function in adults to date. These results add to growing evidence that chronic exposure to traffic related air pollution may adversely affect respiratory health.

Background: Whether local exposure to major roadways adversely affects lung-function growth during the period of rapid lung development that takes place between 10 and 18 years of age is unknown. This study investigated the association between residential exposure to traffic and 8-year lung-function growth., Methods: In this prospective study, 3677 children (mean age 10 years [SD 0.44]) participated from 12 southern California communities that represent a wide range in regional air quality. Children were followed up for 8 years, with yearly lung-function measurements recorded. For each child, we identified several indicators of residential exposure to traffic from large roads. Regression analysis was used to establish whether 8-year growth in lung function was associated with local traffic exposure, and whether local traffic effects were independent of regional air quality., Findings: Children who lived within 500 m of a freeway (motorway) had substantial deficits in 8-year growth of forced expiratory volume in 1 s (FEV(1), -81 mL, p=0.01 [95% CI -143 to -18]) and maximum midexpiratory flow rate (MMEF, -127 mL/s, p=0.03 [-243 to -11), compared with children who lived at least 1500 m from a freeway. Joint models showed that both local exposure to freeways and regional air pollution had detrimental, and independent, effects on lung-function growth. Pronounced deficits in attained lung function at age 18 years were recorded for those living within 500 m of a freeway, with mean percent-predicted 97.0% for FEV1 (p=0.013, relative to >1500 m [95% CI 94.6-99.4]) and 93.4% for MMEF (p=0.006 [95% CI 89.1-97.7])., Interpretation: Local exposure to traffic on a freeway has adverse effects on children's lung development, which are independent of regional air quality, and which could result in important deficits in attained lung function in later life.

Results from studies of traffic and childhood asthma have been inconsistent, but there has been little systematic evaluation of susceptible subgroups. In this study, we examined the relationship of local traffic-related exposure and asthma and wheeze in southern California school children (5-7 years of age). Lifetime history of doctor-diagnosed asthma and prevalent asthma and wheeze were evaluated by questionnaire. Parental history of asthma and child's history of allergic symptoms, sex, and early-life exposure (residence at the same home since 2 years of age) were examined as susceptibility factors. Residential exposure was assessed by proximity to a major road and by modeling exposure to local traffic-related pollutants. Residence within 75 m of a major road was associated with an increased risk of lifetime asthma [odds ratio (OR)=1.29; 95% confidence interval (CI), 1.01-1.86], prevalent asthma (OR=1.50; 95% CI, 1.16-1.95), and wheeze (OR=1.40; 95% CI, 1.09-1.78). Susceptibility increased in long-term residents with no parental history of asthma for lifetime asthma (OR=1.85; 95% CI, 1.11-3.09), prevalent asthma (OR=2.46; 95% CI, 0.48-4.09), and recent wheeze (OR=2.74; 95% CI, 1.71-4.39). The higher risk of asthma near a major road decreased to background rates at 150-200 m from the road. In children with a parental history of asthma and in children moving to the residence after 2 years of age, there was no increased risk associated with exposure. Effect of residential proximity to roadways was also larger in girls. A similar pattern of effects was observed with traffic-modeled exposure. These results indicate that residence near a major road is associated with asthma. The reason for larger effects in those with no parental history of asthma merits further investigation.

Background: Evidence for a causal relationship between traffic-related air pollution and asthma has not been consistent across studies, and comparisons among studies have been difficult because of the use of different indicators of exposure., Methods: We examined the association between traffic-related pollution and childhood asthma in 208 children from 10 southern California communities using multiple indicators of exposure. Study subjects were randomly selected from participants in the Children's Health Study. Outdoor nitrogen dioxide (NO2) was measured in summer and winter outside the home of each child. We also determined residential distance to the nearest freeway, traffic volumes on roadways within 150 meters, and model-based estimates of pollution from nearby roadways., Results: Lifetime history of doctor-diagnosed asthma was associated with outdoor NO2; the odds ratio (OR) was 1.83 (95% confidence interval=1.04-3.22) per increase of 1 interquartile range (IQR=5.7 ppb) in exposure. We also observed increased asthma associated with closer residential distance to a freeway (1.89 per IQR; 1.19-3.02) and with model-based estimates of outdoor pollution from a freeway (2.22 per IQR; 1.36-3.63). These 2 indicators of freeway exposure and measured NO2 concentrations were also associated with wheezing and use of asthma medication. Asthma was not associated with traffic volumes on roadways within 150 meters of homes or with model-based estimates of pollution from nonfreeway roads., Conclusions: These results indicate that respiratory health in children is adversely affected by local exposures to outdoor NO2 or other freeway-related pollutants.

Population growth and the proliferation of roadways in Southern California have facilitated a glut of mobile air pollution sources (cars and trucks), resulting in substantial atmospheric pollution. Despite successful efforts over the past 40 years to reduce pollution, an alarming set of health effects attributable to air pollution have been described in Southern California. The Children's Health Study indicates that reduced lung function growth, increased school absences, asthma exacerbation, and new-onset asthma are occurring at current levels of air pollution, with sizable economic consequences. We describe these findings and urge a more aggressive effort to reduce air pollution exposures to protect our children's health. Lessons from this "case study" have national implications.