Contribution of tailpipe and non-tailpipe traffic sources to quasi-ultrafine, fine and coarse particulate matter in southern California.

Exposure to traffic-related air pollution (TRAP) in the near-roadway environment is associated with multiple adverse health effects. To characterize the relative contribution of tailpipe and non-tailpipe TRAP sources to particulate matter (PM) in the quasi-ultrafine (PM0.2), fine (PM2.5) and coarse (PM2.5-10) size fractions and identify their spatial determinants in southern California (CA). Month-long integrated PM0.2, PM2.5 and PM2.5-10 samples (n = 461, 265 and 298, respectively) were collected across cool and warm seasons in 8 southern CA communities (2008-9). Concentrations of PM mass, elements, carbons and major ions were obtained. Enrichment ratios (ER) in PM0.2 and PM10 relative to PM2.5 were calculated for each element. The Positive Matrix Factorization model was used to resolve and estimate the relative contribution of TRAP sources to PM in three size fractions. Generalized additive models (GAMs) with bivariate loess smooths were used to understand the geographic variation of TRAP sources and identify their spatial determinants. EC, OC, and B had the highest median ER in PM0.2 relative to PM2.5. Six, seven and five sources (with characteristic species) were resolved in PM0.2, PM2.5 and PM2.5-10, respectively. Combined tailpipe and non-tailpipe traffic sources contributed 66%, 32% and 18% of PM0.2, PM2.5 and PM2.5-10 mass, respectively. Tailpipe traffic emissions (EC, OC, B) were the largest contributor to PM0.2 mass (58%). Distinct gasoline and diesel tailpipe traffic sources were resolved in PM2.5. Others included fuel oil, biomass burning, secondary inorganic aerosol, sea salt, and crustal/soil. CALINE4 dispersion model nitrogen oxides, trucks and intersections were most correlated with TRAP sources. The influence of smaller roadways and intersections became more apparent once Long Beach was excluded. Non-tailpipe emissions constituted ~8%, 11% and 18% of PM0.2, PM2.5 and PM2.5-10, respectively, with important exposure and health implications. Future efforts should consider non-linear relationships amongst predictors when modeling exposures. Implications: Vehicle emissions result in a complex mix of air pollutants with both tailpipe and non-tailpipe components. As mobile source regulations lead to decreased tailpipe emissions, the relative contribution of non-tailpipe traffic emissions to near-roadway exposures is increasing. This study documents the presence of non-tailpipe abrasive vehicular emissions (AVE) from brake and tire wear, catalyst degradation and resuspended road dust in the quasi-ultrafine (PM0.2), fine and coarse particulate matter size fractions, with contributions reaching up to 30% in PM0.2 in some southern California communities. These findings have important exposure and policy implications given the high metal content of AVE and the efficiency of PM0.2 at reaching the alveolar region of the lungs and other organ systems once inhaled. This work also highlights important considerations for building models that can accurately predict tailpipe and non-tailpipe exposures for population health studies.

Estimating ambient-origin PM2.5 exposure for epidemiology: observations, prediction, and validation using personal sampling in the Multi-Ethnic Study of Atherosclerosis.

OBJECTIVES: We aim to characterize the qualities of estimation approaches for individual exposure to ambient-origin fine particulate matter (PM2.5), for use in epidemiological studies. METHODS: The analysis incorporates personal, home indoor, and home outdoor air monitoring data and spatio-temporal model predictions for 60 participants from the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air). We compared measurement-based personal PM2.5 exposure with several measured or predicted estimates of outdoor, indoor, and personal exposures. RESULTS: The mean personal 2-week exposure was 7.6 (standard deviation 3.7) µg/m3. Outdoor model predictions performed far better than outdoor concentrations estimated using a nearest-monitor approach (R = 0.63 versus R = 0.43). Incorporating infiltration indoors of ambient-derived PM2.5 provided better estimates of the measurement-based personal exposures than outdoor concentration predictions (R = 0.81 versus R = 0.63) and better scaling of estimated exposure (mean difference 0.4 versus 5.4 µg/m3 higher than measurements), suggesting there is value to collecting data regarding home infiltration. Incorporating individual-level time-location information into exposure predictions did not increase correlations with measurement-based personal exposures (R = 0.80) in our sample consisting primarily of retired persons. CONCLUSIONS: This analysis demonstrates the importance of incorporating infiltration when estimating individual exposure to ambient air pollution. Spatio-temporal models provide substantial improvement in exposure estimation over a nearest monitor approach.

RISK EFFECTS OF NEAR-ROADWAY POLLUTANTS AND ASTHMA STATUS ON BRONCHITIC SYMPTOMS IN CHILDREN.

BACKGROUND: Bronchitic symptoms in children pose a significant clinical and public health burden. Exposures to criteria air pollutants affect bronchitic symptoms, especially in children with asthma. Less is known about near-roadway exposures. METHODS: Bronchitic symptoms (bronchitis, chronic cough, or phlegm) in the past 12 months were assessed annually with 8 to 9 years of follow-up on 6757 children from the southern California Children's Health Study. Residential exposure to freeway and non-freeway near-roadway air pollution was estimated using a line-source dispersion model. Mixed-effects logistic regression models were used to relate near-roadway air pollutant exposures to bronchitic symptoms among children with and without asthma. RESULTS: Among children with asthma, a two standard deviation increase in non-freeway exposures (odds ratio [OR]: 1.44; 95% confidence interval [CI]: 1.17-1.78) and freeway exposures (OR: 1.31; 95% CI: 1.06-1.60) were significantly associated with increased risk of bronchitic symptoms. Among children without asthma, only non-freeway exposures had a significant association (OR: 1.14; 95% CI: 1.00-1.29). Associations were strongest among children living in communities with lower regional particulate matter. CONCLUSIONS: Near-roadway air pollution was associated with bronchitic symptoms, especially among children with asthma and those living in communities with lower regional particulate matter. Better characterization of traffic pollutants from non-freeway roads is needed since many children live in close proximity to this source.

Prenatal Air Pollution Exposures, DNA Methyl Transferase Genotypes, and Associations with Newborn LINE1 and Alu Methylation and Childhood Blood Pressure and Carotid Intima-Media Thickness in the Children's Health Study.

BACKGROUND: Although exposure to ambient air pollutants increases cardiovascular disease risk in adults little is known about the effects of prenatal exposure. Genetic variation and epigenetic alterations are two mechanisms that may influence the effects of early-life exposures on cardiovascular phenotypes. OBJECTIVES: We investigated whether genetic and epigenetic variation modify associations between prenatal air pollution on markers of cardiovascular risk in childhood. METHODS: We used linear regression analysis to investigate the associations between prenatal pollutants (PM2.5, PM10, NO2, O3), long interspersed nuclear elements (LINE1) and AluYb8 DNA methylation levels measured in newborn blood spot tests, and carotid intima-media thickness (CIMT) and blood pressure (BP) in 459 participants as part of the Children's Health Study. Interaction terms were also included to test for effect modification of these associations by genetic variation in methylation reprogramming genes. RESULTS: Prenatal exposure to NO2 in the third trimester of pregnancy was associated with higher systolic BP in 11-year-old children. Prenatal exposure to multiple air pollutants in the first trimester was associated with lower DNA methylation in LINE1, whereas later exposure to O3 was associated with higher LINE1 methylation levels in newborn blood spots. The magnitude of associations with prenatal air pollution varied according to genotype for 11 SNPs within DNA methyltransferase 1 (DNMT1), DNA methyltransferase 3 Beta (DNMT3B), Tet methylcytosine dioxygenase 2 (TET2), and Thymine DNA glycosylase (TDG) genes. Although first-trimester O3 exposure was not associated with CIMT and systolic BP overall, associations within strata of DNMT1 or DNMT3B were observed, and the magnitude and the direction of these associations depended on DNMT1 genotypes. CONCLUSIONS: Genetic and epigenetic variation in DNA methylation reprogramming genes and in LINE1 retrotransposons may play important roles in downstream cardiovascular consequences of prenatal air pollution exposure. Citation: Breton CV, Yao J, Millstein J, Gao L, Siegmund KD, Mack W, Whitfield-Maxwell L, Lurmann F, Hodis H, Avol E, Gilliland FD. 2016. Prenatal air pollution exposures, DNA methyl transferase genotypes, and associations with newborn LINE1 and Alu methylation and childhood blood pressure and carotid intima-media thickness in the Children's Health Study. Environ Health Perspect 124:1905-1912; http://dx.doi.org/10.1289/EHP181.

Prenatal Air Pollution Exposure and Early Cardiovascular Phenotypes in Young Adults.

Exposure to ambient air pollutants increases risk for adverse cardiovascular health outcomes in adults. We aimed to evaluate the contribution of prenatal air pollutant exposure to cardiovascular health, which has not been thoroughly evaluated. The Testing Responses on Youth (TROY) study consists of 768 college students recruited from the University of Southern California in 2007-2009. Participants attended one study visit during which blood pressure, heart rate and carotid artery arterial stiffness (CAS) and carotid artery intima-media thickness (CIMT) were assessed. Prenatal residential addresses were geocoded and used to assign prenatal and postnatal air pollutant exposure estimates using the U.S. Environmental Protection Agency's Air Quality System (AQS) database. The associations between CAS, CIMT and air pollutants were assessed using linear regression analysis. Prenatal PM10 and PM2.5 exposures were associated with increased CAS. For example, a 2 SD increase in prenatal PM2.5 was associated with CAS indices, including a 5% increase (ß = 1.05, 95% CI 1.00-1.10) in carotid stiffness index beta, a 5% increase (ß = 1.05, 95% CI 1.01-1.10) in Young's elastic modulus and a 5% decrease (ß = 0.95, 95% CI 0.91-0.99) in distensibility. Mutually adjusted models of pre- and postnatal PM2.5 further suggested the prenatal exposure was most relevant exposure period for CAS. No associations were observed for CIMT. In conclusion, prenatal exposure to elevated air pollutants may increase carotid arterial stiffness in a young adult population of college students. Efforts aimed at limiting prenatal exposures are important public health goals.

Time-location patterns of a diverse population of older adults: the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air).

The primary aim of this analysis was to present and describe questionnaire data characterizing time-location patterns of an older, multiethnic population from six American cities. We evaluated the consistency of results from repeated administration of this questionnaire and between this questionnaire and other questionnaires collected from participants of the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air). Participants reported spending most of their time inside their homes (average: 121 h/week or 72%). More than 50% of the participants reported spending no time in several of the location options, including at home outdoors, at work/volunteer/school locations indoors or outdoors, or in "other" locations outdoors. We observed consistency between self-reported time-location patterns from repeated administration of the time-location questionnaire and compared with other survey instruments. Comparisons with national cohorts demonstrated the differences in time-location patterns in the MESA Air cohort due to differences in demographics, but the data showed similar trends in patterns by age, gender, season, and employment status. This study was the first to explicitly examine the time-location patterns in an older, multiethnic population and the first to add data on Chinese participants. These data can be used to inform future epidemiological research of MESA Air and other studies that include diverse populations.

Emissions reduction policies and recent trends in Southern California's ambient air quality.

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.

NOS1 methylation and carotid artery intima-media thickness in children.

BACKGROUND: Nitric oxide (NO) plays an important role in cardiovascular health by maintaining and regulating vascular tone and blood flow. Epigenetic regulation of NO synthase (NOS), the genes responsible for NO production, may affect cardiovascular disease, including the development of atherosclerosis in children. METHODS AND RESULTS: We measured percentage DNA methylation using bisulfite conversion and pyrosequencing assays on DNA from buccal cells provided by 377 participants of the Children's Health Study on whom carotid artery intima-media thickness (CIMT) measurements were also collected. We examined a total of 16 CpG loci located within NOS1, NOS2A, NOS3, ARG1, and ARG2 genes responsible for NO production. CIMT was measured using high-resolution B-mode carotid ultrasound. The association between percentage DNA methylation in ARG and NOS genes with CIMT was evaluated using linear regression adjusted for sex, ethnicity, body mass index, age at CIMT, town of residence, and experimental plate for pyrosequencing reactions. Differences in the association by ethnicity and ancestral group were also evaluated. For a 1% increase in average DNA methylation of NOS1, CIMT increased by 1.2 µm (P=0.02). This association was greater in Hispanic children of Native American descent (ß=2.3; P=0.004) than in non-Hispanic whites (ß=0.3; P=0.71) or Hispanic whites (ß=1.0; P=0.35). CONCLUSIONS: DNA methylation of NOS1 has a plausible role in atherogenesis through regulation of NO production, although ancestry may alter the magnitude of this association.

Spatial Variation in Particulate Matter Components over a Large Urban Area.

To characterize exposures to particulate matter (PM) and its components, we performed a large sampling study of small-scale spatial variation in size-resolved particle mass and composition. PM was collected in size ranges of < 0.2, 0.2-to-2.5, and 2.5-to-10 µm on a scale of 100s to 1000s of meters to capture local sources. Within each of eight Southern California communities, up to 29 locations were sampled for rotating, month-long integrated periods at two different times of the year, six months apart, from Nov 2008 through Dec 2009. Additional sampling was conducted at each community's regional monitoring station to provide temporal coverage over the sampling campaign duration. Residential sampling locations were selected based on a novel design stratified by high- and low-predicted traffic emissions and locations over- and under-predicted from previous dispersion model and sampling comparisons. Primary vehicle emissions constituents, such as elemental carbon (EC), showed much stronger patterns of association with traffic than pollutants with significant secondary formation, such as PM2.5 or water soluble organic carbon. Associations were also stronger during cooler times of the year (Oct through Mar). Primary pollutants also showed greater within-community spatial variation compared to pollutants with secondary formation contributions. For example, the average cool-season community mean and standard deviation (SD) for EC were 1.1 and 0.17 µg/m3, respectively, giving a coefficient of variation (CV) of 18%. For PM2.5, average mean and SD were 14 and 1.3 µg/m3, respectively, with a CV of 9%. We conclude that within-community spatial differences are important for accurate exposure assessment of traffic-related pollutants.

HDL anti-oxidant function associates with LDL level in young adults.

OBJECTIVES: The primary objective was to evaluate predictors of HDL anti-oxidant function in young adults. BACKGROUND: High-density lipoprotein (HDL) cholesterol is considered a protective factor for cardiovascular disease (CVD). However, increased levels are not always associated with decreased cardiovascular risk. A better understanding of the importance of HDL functionality and how it affects CVD risk is needed. METHODS: Fifty non-Hispanic white subjects from the Testing Responses on Youth (TROY) study were randomly selected to investigate whether differences in HDL anti-oxidant function are associated with traditional cardiovascular risk factors, including carotid intima media thickness (CIMT), arterial stiffness and other inflammatory/metabolic parameters. HDL anti-oxidant capacity was evaluated by assessing its ability to inhibit low-density lipoprotein (LDL) cholesterol oxidation by air using a DCF-based fluorescent assay and expressed as a HDL oxidant index (HOI). The associations between HOI and other variables were assessed using both linear and logistic regression. RESULTS: Eleven subjects (25%) had an HOI ≥ 1, indicating a pro-oxidant HDL. Age, LDL, high sensitivity C-reactive protein (hsCRP), and paraoxonase activity (PON1), but not HDL, were all associated with HOI level in univariate linear regression models. In multivariate models that mutually adjusted for these variables, LDL remained the strongest predictor of HOI (0.13 increase in HOI per 1 SD increase in LDL, 95% CI 0.04, 0.22). Atherogenic index of plasma, pulse pressure, homocysteine, glucose, insulin, CIMT and measurements of arterial stiffness were not associated with HOI in this population. CONCLUSIONS: These results suggest LDL, hsCRP and DBP might predict HDL anti-oxidant function at an early age.

Birth weight and carotid artery intima-media thickness.

OBJECTIVES: To determine the association between birth weight and carotid artery intima-media thickness (CIMT), a measure of atherogenesis, in a population of 11-year-old children. STUDY DESIGN: CIMT measured by high-resolution ultrasound, and birth registry data were available for 670 children of the Southern California Children's Health Study. Multivariate regression analyses were performed to investigate the association between birth weight and CIMT, with adjustment for child's health status and lifestyle, pregnancy information, and parental health. RESULTS: Mean CIMT was 0.57 mm (SD 0.04). We found a nonlinear association between birth weight and CIMT, with an increase in CIMT of 0.014 mm in the fifth (P value .01) compared with the third birth weight quintile. These associations were robust in subsample analyses in children considered normal-weight by gestational age or in term-born children. No significant association with CIMT was found for the lowest quintile. CONCLUSIONS: Greater birth weight was significantly associated with increased CIMT at age 11 years. No evidence for an impact of lower birth weight was found. The predictive value of childhood CIMT on future cardiovascular outcomes is largely unknown, but strong associations between childhood cardiovascular disease risk factors and adult vascular disease suggest that increased CIMT in childhood may be clinically important.

Childhood air pollutant exposure and carotid artery intima-media thickness in young adults.

BACKGROUND: Exposure to ambient air pollutants increases risk for cardiovascular health outcomes in adults. The contribution of childhood air pollutant exposure to cardiovascular health has not been thoroughly evaluated. METHODS AND RESULTS: The Testing Responses on Youth study consists of 861 college students recruited from the University of Southern California in 2007 to 2009. Participants attended 1 study visit during which blood pressure, heart rate, and carotid artery intima-media thickness (CIMT) were assessed. Self-administered questionnaires collected information about health and sociodemographic characteristics, and a 12-hour fasting blood sample was drawn for lipid and biomarker analyses. Residential addresses were geocoded and used to assign cumulative air pollutant exposure estimates based on data derived from the U.S. Environmental Protection Agency's Air Quality System database. The associations between CIMT and air pollutants were assessed using linear regression analysis. Mean CIMT was 603 µm (±54 SD). A 2 standard deviation (SD) increase in childhood (aged 0-5 years) or elementary school (aged 6-12 years) O(3) exposure was associated with a 7.8-µm (95% confidence interval, -0.3-15.9) or 10.1-µm (95% confidence interval, 1.8-18.5) higher CIMT, respectively. Lifetime exposure to O(3) showed similar but nonsignificant associations. No associations were observed for PM(2.5), PM(10), or NO(2), although adjustment for these pollutants strengthened the childhood O(3) associations. CONCLUSIONS: Childhood exposure to O(3) may be a novel risk factor for CIMT in a healthy population of college students. Regulation of air pollutants and efforts that focus on limiting childhood exposures continue to be important public health goals.

Modeling the residential infiltration of outdoor PM(2.5) in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air).

BACKGROUND: Epidemiologic studies of fine particulate matter [aerodynamic diameter ≤ 2.5 µm (PM(2.5))] typically use outdoor concentrations as exposure surrogates. Failure to account for variation in residential infiltration efficiencies (F(inf)) will affect epidemiologic study results. OBJECTIVE: We aimed to develop models to predict F(inf) for > 6,000 homes in the Multi-Ethnic Study of Atherosclerosis and Air Pollution (MESA Air), a prospective cohort study of PM(2.5) exposure, subclinical cardiovascular disease, and clinical outcomes. METHODS: We collected 526 two-week, paired indoor-outdoor PM(2.5) filter samples from a subset of study homes. PM(2.5) elemental composition was measured by X-ray fluorescence, and F(inf) was estimated as the indoor/outdoor sulfur ratio. We regressed F(inf) on meteorologic variables and questionnaire-based predictors in season-specific models. Models were evaluated using the R² and root mean square error (RMSE) from a 10-fold cross-validation. RESULTS: The mean ± SD F(inf) across all communities and seasons was 0.62 ± 0.21, and community-specific means ranged from 0.47 ± 0.15 in Winston-Salem, North Carolina, to 0.82 ± 0.14 in New York, New York. F(inf) was generally greater during the warm (> 18°C) season. Central air conditioning (AC) use, frequency of AC use, and window opening frequency were the most important predictors during the warm season; outdoor temperature and forced-air heat were the best cold-season predictors. The models predicted 60% of the variance in 2-week F(inf), with an RMSE of 0.13. CONCLUSIONS: We developed intuitive models that can predict F(inf) using easily obtained variables. Using these models, MESA Air will be the first large epidemiologic study to incorporate variation in residential F(inf) into an exposure assessment.

Parental stress increases the detrimental effect of traffic exposure on children's lung function.

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.

Carotid artery intima-media thickness in college students: race/ethnicity matters.

OBJECTIVE: Racial/ethnic differences in common carotid artery intima-media thickness (CIMT) and in risk factors associated with CIMT have been predominantly observed in middle-aged and older individuals. We aimed to characterize racial/ethnic differences CIMT and other cardiovascular risk factors in a healthy, young-adult population. METHODS: College students were recruited as part of a study to characterize determinants of atherogenesis. Students were eligible if they were lifetime non-smokers, lived in the United States since six months of age, and attended high school in the United States. Blood pressure, heart rate, height, and weight were measured, B-mode carotid ultrasound was performed, questionnaires were administered and a 12-h fasting blood sample was collected. Associations between CIMT and other variables were assessed in 768 students aged 18-25 years using linear regression analysis. RESULTS: In models adjusted for common cardiovascular risk factors, sex exhibited the strongest influence on CIMT, with men having 15.4 µm larger CIMT compared to women (95%CI 6.6, 24.2). Race/ethnicity was also strongly associated with CIMT. African Americans had 17.3 µm greater CIMT (95%CI -0.3, 34.8) compared to non Hispanic Whites, whereas Asians and Hispanic Whites had 14.3 (95%CI -24.3, -4.4) and 15.4 (95%CI -26.2, -4.7) µm smaller CIMT, respectively. BMI and systolic blood pressure were positively associated with CIMT. CONCLUSION: The risk factors associated with atherogenesis later in life are already present and observable in college-aged young adults, so targeted campaigns to reduce life-long cardiovascular disease burden should be initiated earlier in life to improve public health.

Childhood incident asthma and traffic-related air pollution at home and school.

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.

Global goods movement and the local burden of childhood asthma in southern California.

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.