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1.  Living near a Freeway is Associated with Lower Bone Mineral Density among Mexican Americans 
Purpose
Adults residing in rural areas have been linked with higher bone mineral density (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 500m of a freeway were 0.02 g/cm2 and 0.03 g/cm2 lower than participants living greater than 1,500m 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.
doi:10.1007/s00198-015-3051-z
PMCID: PMC4470808  PMID: 25677718
osteopenia; osteoporosis; bone mineral density; BMD; traffic-related pollution; air pollution
2.  COSTS OF CHILDHOOD ASTHMA DUE TO TRAFFIC-RELATED POLLUTION IN TWO CALIFORNIA COMMUNITIES 
The European respiratory journal  2012;40(2):363-370.
Recent research suggests the burden of childhood asthma attributable to air pollution has been underestimated in traditional risk assessments, and there are no estimates of these associated costs. We estimated the yearly childhood asthma-related costs attributable to air pollution for Riverside and Long Beach, California, including: 1) the indirect and direct costs of health care utilization due to asthma exacerbations linked to traffic-related pollution (TRP); and 2) the costs of health care for asthma cases attributable to local TRP exposure.
We estimated these costs using estimates from peer-reviewed literature and the authors' analysis of surveys (Medical Expenditure Panel Survey, California Health Interview Survey, National Household Travel Survey, and Health Care Utilization Project).
A lower-bound estimate of the asthma burden attributable to air pollution was $18 million yearly. Asthma cases attributable to TRP exposure accounted for almost half of this cost. The cost of bronchitic episodes was a major proportion of both the annual cost of asthma cases attributable to TRP and of pollution-linked exacerbations.
Traditional risk assessment methods underestimate both the burden of disease and cost of asthma associated with air pollution, and these costs are borne disproportionately by communities with higher than average TRP.
doi:10.1183/09031936.00157811
PMCID: PMC4396740  PMID: 22267764
asthma burden; vehicle emissions; air pollution; children; burden of disease; economic costs
3.  Predictors of intra-community variation in air quality 
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 NO2, NO, and total oxides of nitrogen (NOx), 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 NOx in large urban areas and 76% in small urban areas. Compared with living at least 1,500m from a freeway, living within 250m 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.
doi:10.1038/jes.2011.45
PMCID: PMC4391642  PMID: 22252279
traffic-related air pollution; nitrogen oxides; exposure assessment; traffic; land-use; spatial random effects
4.  Prenatal Air Pollution Exposure and Ultrasound Measures of Fetal Growth in Los Angeles, California 
Environmental research  2014;130:7-13.
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 <10 μm 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 0.2-0.3 mm. For women residing within 5 km of a monitoring station, we estimated biparietal diameter reductions of 0.9-1.0 mm 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.
doi:10.1016/j.envres.2014.01.006
PMCID: PMC4016959  PMID: 24517884
ambient air pollution; fetal growth; pregnancy; traffic-related air pollution; ultrasound measurements
5.  Determinants of the Spatial Distributions of Elemental Carbon and Particulate Matter in Eight Southern Californian Communities 
Emerging evidence indicates that near-roadway pollution (NRP) in ambient air has adverse health effects. However, specific components of the NRP mixture responsible for these effects have not been established. A major limitation for health studies is the lack of exposure models that estimate NRP components observed in epidemiological studies over fine spatial scale of tens to hundreds of meters. In this study, exposure models were developed for fine-scale variation in biologically relevant elemental carbon (EC). Measurements of particulate matter (PM) and EC less than 2.5 μm in aerodynamic diameter (EC2.5) and of PM and EC of nanoscale size less than 0.2 μm were made at up to 29 locations in each of eight Southern California Children's Health Study communities. Regression-based prediction models were developed using a guided forward selection process to identify traffic variables and other pollutant sources, community physical characteristics and land use as predictors of PM and EC variation in each community. A combined eight-community model including only CALINE4 near-roadway dispersion-estimated vehicular emissions accounting for distance, distance-weighted traffic volume, and meteorology, explained 51% of the EC0.2 variability. Community-specific models identified additional predictors in some communities; however, in most communities the correlation between predicted concentrations from the eight-community model and observed concentrations stratified by community were similar to those for the community-specific models. EC2.5 could be predicted as well as EC0.2. EC2.5 estimated from CALINE4 and population density explained 53% of the within-community variation. Exposure prediction was further improved after accounting for between-community heterogeneity of CALINE4 effects associated with average distance to Pacific Ocean shoreline (to 61% for EC0.2) and for regional NOx pollution (to 57% for EC2.5). PM fine spatial scale variation was poorly predicted in both size fractions. In conclusion, models of exposure that include traffic measures such as CALINE4 can provide useful estimates for EC0.2 and EC2.5 on a spatial scale appropriate for health studies of NRP in selected Southern California communities.
doi:10.1016/j.atmosenv.2013.11.077
PMCID: PMC4192647  PMID: 25313293
6.  The Effect of Ambient Air Pollution on Exhaled Nitric Oxide in the Children’s Health Study 
The European respiratory journal  2010;37(5):1029-1036.
We assessed the effect of daily variations in ambient air pollutants on exhaled nitric oxide (FeNO) using data from a cohort of schoolchildren with large differences in air pollutant exposures from the Children’s Health Study.
Based on a cohort of 2240 schoolchildren from 13 Southern California communities, cumulative lagged average regression models were fitted to determine the association between FeNO and ambient air pollution levels from central site monitors with lags of up to 30 days prior to FeNO testing.
Daily 24-hr cumulative lagged averages of PM2.5 (over 1–8 days) and PM10 (over 1–7 days), as well as 10AM–6PM cumulative lagged average of O3 (over 1–23 days) were significantly associated with 17.42% (p<0.01), 9.25% (P<0.05) and 14.25% (p<0.01) higher FeNO levels over the inter-quartile range of 7.5 μg/m3, 12.97 μg/m3, and 15.42 ppb, respectively. The effects of PM2.5, PM10 and O3 were higher in the warm season. The PM effects were robust to adjustments for effects of O3 and temperature and did not vary by asthma or allergy status.
In Summary, short-term increases in PM2.5, PM10, and O3 were associated with airway inflammation independent of asthma and allergy status, with PM10 effects significantly higher in the warm season.
doi:10.1183/09031936.00081410
PMCID: PMC4340653  PMID: 20947676
Air pollution; Airway inflammation; Children’s respiratory health; Environmental epidemiology; Exhaled nitric oxide
7.  Annual Average Ambient Particulate Matter Exposure Estimates, Measured Home Particulate Matter, and Hair Nicotine are Associated with Respiratory Outcomes in Adults with Asthma 
Environmental research  2014;129:1-10.
Background
While exposure to outdoor particulate matter (PM) has been associated with poor asthma outcomes, few studies have investigated the combined effects of outdoor and indoor PM (including secondhand tobacco smoke).
Objective
To examine the associations between PM and asthma outcomes.
Methods
We analyzed data from a cohort of adults with asthma and rhinitis (n=302; 82% both conditions; 13% asthma only; 5% rhinitis alone) including measures of home PM, tobacco smoke exposure (hair nicotine and self-report), ambient PM from regional monitoring, distance to roadway, and season (wet or dry). The outcomes of interest were frequent respiratory symptoms and forced expiratory volume in 1 second (FEV1) below the lower limit of normal (NHANES reference values). Multivariable regression analyses examined the associations (Odds Ratio [OR] and 95% Confidence Interval [95%CI]) between exposures and these outcomes, adjusted by sociodemographic characteristics.
Results
In adjusted analyses of each exposure, the highest tertile of home PM and season of interview were associated with increased odds for more frequent respiratory symptoms (OR=1.64 95%CI: [1.00, 2.69] and OR = 1.66 95%CI: [1.09, 2.51]). The highest tertile of hair nicotine was significantly associated with FEV1 below the lower limit of normal (OR=1.80 95%CI: [1.00, 3.25]). In a model including home PM, ambient PM, and hair nicotine, and season, only two associations remained strong: hair nicotine with FEV1 below the lower limit of normal and season of measurement (dry, April-October) with increased respiratory symptoms (OR=1.85 95%CI: [1.00, 3.41] and OR = 1.54 95%CI: [1.0, 2.37]). When that model was stratified by sex, the highest tertiles of ambient PM and hair nicotine were associated with FEV1 below the lower limit of normal among women (OR=2.23 95%CI: [1.08, 4.61] and OR=2.90 95% CI: [1.32, 6.38]), but not men. The highest tertile of hair nicotine was also associated with increased respiratory symptoms in women but not men (OR=2.38 95% CI: [1.26, 4.49]). When stratified by age, the middle quartile of ambient PM and the highest hair nicotine tertile were associated with increased respiratory symptoms (OR=2.07 95%CI: [1.01, 4.24] and OR=2.55 95%CI: [1.21,5.36]) in those under 55 but not in the older stratum.
Conclusions
Exposure to PM from both home and ambient sources is associated with increased symptoms and lower lung function in adults with asthma, although these associations vary by type of PM, the respiratory outcome studied, sex and age.
doi:10.1016/j.envres.2013.12.007
PMCID: PMC4169238  PMID: 24528996
Particulate matter; indoor air quality; outdoor air quality; hair nicotine; asthma; respiratory symptoms; lung function
8.  Longitudinal Effects of Air Pollution on Exhaled Nitric Oxide: The Children’s Health Study 
OBJECTIVES
To assess the effects of long-term variations in ambient air pollutants on longitudinal changes in exhaled nitric oxide (FeNO), a potentially useful biomarker of eosinophilic airway inflammation, based on data from the southern California Children’s Health Study.
METHODS
Based on a cohort of 1,211 schoolchildren from 8 Southern California communities with FeNO measurements in 2006/07 and 2007/08, regression models adjusted for short-term effects of air pollution were fitted to assess the association between changes in annual long-term exposures and changes in FeNO.
RESULTS
Increases in annual average concentrations of 24-hr average NO2 and PM2.5 (scaled to the interquartile range (IQR) of 1.8 ppb and 2.4 μg/m3, respectively) were associated with a 2.29 ppb (CI=[0.36,4.21]; p =0.02) and a 4.94 ppb (CI=[1.44,8.47]; p = 0.005) increase in FeNO, respectively, after adjustments for short term effects of the respective pollutants. In contrast, changes in annual averages of PM10 and O3 were not significantly associated with changes in FeNO. These findings did not differ significantly by asthma status.
CONCLUSIONS
Changes in annual average exposure to current levels of ambient air pollutants are significantly associated with changes in FeNO levels in children, independent of short-term exposures and asthma status. Use of this biomarker in population-based epidemiologic research has great potential for assessing the impact of changing real world mixtures of ambient air pollutants on children’s respiratory health.
doi:10.1136/oemed-2013-101874
PMCID: PMC4310696  PMID: 24696513
Air pollution; chronic exposures; Children’s respiratory health; Environmental epidemiology; Exhaled nitric oxide; Airway inflammation
9.  Components of Air Pollution and Cognitive Function in Middle-aged and Older Adults in Los Angeles 
Neurotoxicology  2013;40:1-7.
While experiments in animals demonstrate neurotoxic effects of particulate matter (PM) and ozone (O3), epidemiologic evidence is sparse regarding the relationship between different constituencies of air pollution mixtures and cognitive function in adults. We examined cross-sectional associations between various ambient air pollutants [O3, PM2.5 and nitrogen dioxide (NO2)] and six measures of cognitive function and global cognition among healthy, cognitively intact individuals (n=1,496, mean age 60.5 years) residing in the Los Angeles Basin. Air pollution exposures were assigned to each residential address in 2000–06 using a geographic information system that included monitoring data. A neuropsychological battery was used to assess cognitive function; a principal components analysis defined six domain-specific functions and a measure of global cognitive function was created. Regression models estimated effects of air pollutants on cognitive function, adjusting for age, gender, race, education, income, study and mood. Increasing exposure to PM2.5 was associated with lower verbal learning (β = −0.32 per 10 ug/m3 PM2.5, 95% CI = −0.63, 0.00; p = 0.05). Ambient exposure to NO2 >20 ppb tended to be associated with lower logical memory. Compared to the lowest level of exposure to ambient O3, exposure above 49 ppb was associated with lower executive function. Including carotid artery intima-media thickness, a measure of subclinical atherosclerosis, in models as a possible mediator did not attenuate effect estimates. This study provides support for cross-sectional associations between increasing levels of ambient O3, PM2.5 and NO2 and measures of domain-specific cognitive abilities.
doi:10.1016/j.neuro.2013.09.004
PMCID: PMC3946571  PMID: 24148924
air pollution; cognitive dysfunction; dementia; particulate matter; ozone; verbal learning
10.  Early-Life Air Pollution and Asthma Risk in Minority Children. The GALA II and SAGE II Studies 
Rationale: Air pollution is a known asthma trigger and has been associated with short-term asthma symptoms, airway inflammation, decreased lung function, and reduced response to asthma rescue medications.
Objectives: To assess a causal relationship between air pollution and childhood asthma using data that address temporality by estimating air pollution exposures before the development of asthma and to establish the generalizability of the association by studying diverse racial/ethnic populations in different geographic regions.
Methods: This study included Latino (n = 3,343) and African American (n = 977) participants with and without asthma from five urban regions in the mainland United States and Puerto Rico. Residential history and data from local ambient air monitoring stations were used to estimate average annual exposure to five air pollutants: ozone, nitrogen dioxide (NO2), sulfur dioxide, particulate matter not greater than 10 μm in diameter, and particulate matter not greater than 2.5 μm in diameter. Within each region, we performed logistic regression to determine the relationship between early-life exposure to air pollutants and subsequent asthma diagnosis. A random-effects model was used to combine the region-specific effects and generate summary odds ratios for each pollutant.
Measurements and Main Results: After adjustment for confounders, a 5-ppb increase in average NO2 during the first year of life was associated with an odds ratio of 1.17 for physician-diagnosed asthma (95% confidence interval, 1.04–1.31).
Conclusions: Early-life NO2 exposure is associated with childhood asthma in Latinos and African Americans. These results add to a growing body of evidence that traffic-related pollutants may be causally related to childhood asthma.
doi:10.1164/rccm.201302-0264OC
PMCID: PMC3778732  PMID: 23750510
air pollution; minority; children; asthma
11.  ASTHMA AND SCHOOL COMMUTING TIME 
Objectives
This study examined associations of asthma with school commuting time.
Methods
Time on likely school commute route was used as a proxy for on-road air pollution exposure among 4741 elementary school children at enrollment into the Children's Health Study. Lifetime asthma and severe wheeze (including multiple attacks, nocturnal or with shortness of breath) were reported by parents.
Results
In asthmatic children, severe wheeze was associated with commuting time (odds ratio (OR) 1.54 across the 9-minute 5%-95% exposure distribution; 95% confidence interval (CI) 1.01,2.36). The association was stronger in analysis restricted to asthmatic children with commuting times five minutes or longer (OR 1.97; 95% CI 1.02,3.77). No significant associations were observed with asthma prevalence.
Conclusions
Among asthmatics, severe wheeze was associated with relatively short school commuting times. Further investigation of effects of on-road pollutant exposure is warranted.
doi:10.1097/JOM.0b013e3181ebf1a9
PMCID: PMC4083079  PMID: 20657304
air pollution; asthma; child; epidemiology; traffic; commuting
12.  Traffic-related air pollution and obesity formation in children: a longitudinal, multilevel analysis 
Environmental Health  2014;13:49.
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.
doi:10.1186/1476-069X-13-49
PMCID: PMC4106205  PMID: 24913018
Childhood obesity; Air pollution; Traffic; California
14.  Traffic Related Air Pollution, Particulate Matter, and Autism 
JAMA psychiatry  2013;70(1):71-77.
Context
Autism is a heterogeneous disorder with genetic and environmental factors likely contributing to its origins. Examination of hazardous pollutants has suggested the importance of air toxics in autism etiology, yet little research has examined local level air pollution associations using residence-specific exposure assignments.
Objective
To examine the relationship between traffic-related air pollution (TRP), air quality, and autism.
Design, Setting and Population
This study includes data on 279 autism cases and 245 typically developing controls enrolled in the Childhood Autism Risks from Genetics and the Environment (CHARGE) Study in California. The mother’s address from the birth certificate and addresses reported from a residential history questionnaire were used to estimate exposure for each trimester of pregnancy and first year of life. TRP was assigned to each location using a line-source air-quality dispersion model. Regional air pollutant measures were based on the Environmental Protection Agency’s Air Quality System data. Logistic regression models compared estimated and measured pollutant levels for autism cases and typically developing controls.
Main Outcome Measures
Crude and multivariable-adjusted odds ratios (OR) for autism.
Results
Cases were more likely to live at residences in the highest quartile TRP exposure during pregnancy (OR=1.98, 95%CI 1.20–3.31) and the first year of life (OR=3.10, 1.76–5.57) compared to controls. Regional exposure measures of nitrogen dioxide (NO2) and particulate matter less than 2.5 and 10 microns in diameter (PM2.5 and PM10) were also associated with autism during gestation (NO2 OR=1.81/2SD, 95%CI 1.37–3.09; PM2.5 OR=2.08/2SD, 95%CI 1.93–2.25; PM10 OR=2.17/2SD, 95%CI 1.49–3.16) and the first year of life (NO2 OR=2.06, 95%CI 1.37–3.09; PM2.5 OR=2.12, 95%CI 1.45–3.10; PM10 OR=2.14, 95%CI 1.46–3.12).
Conclusions
Exposure to TRP, NO2, PM2.5, and PM10 during pregnancy and the first year of life was associated with autism. Further epidemiological and toxicological examination of likely biological pathways will help determine whether these associations are causal.
doi:10.1001/jamapsychiatry.2013.266
PMCID: PMC4019010  PMID: 23404082
15.  Interaction of the MET Receptor Tyrosine Kinase Gene and Air Pollution Exposure in Autism Spectrum Disorder 
Background
Independent studies report association of autism spectrum disorder with air pollution exposure and a functional promoter variant (rs1858830) in the MET receptor tyrosine kinase (MET) gene. Toxicologic data find altered brain Met expression in mice after prenatal exposure to a model air pollutant. Our objective was to investigate whether air pollution exposure and MET rs1858830 genotype interact to alter ASD risk.
Methods
We studied 252 cases of autism spectrum disorder and 156 typically developing controls the Childhood Autism Risk from Genetics and the Environment Study. Air pollution exposure was assigned for local traffic-related sources and regional sources (particulate matter, nitrogen dioxide and ozone). MET genotype was determined by direct re-sequencing.
Results
Subjects with both MET rs1858830 CC genotype and high air pollutant exposures were at increased risk of autism spectrum disorder compared with subjects who had both the CG/GG genotypes and lower pollutant exposures. A statistical test of multiplicative interaction identified a statistically significant effect between NO2 and MET CC genotype (p=0.03)
Conclusions
MET rs1858830 CC genotype and air pollutant exposure may interact to increase autism spectrum disorder risk.
doi:10.1097/EDE.0000000000000030
PMCID: PMC4019012  PMID: 24240654
16.  Childhood Obesity and Asthma Control in the GALA II and SAGE II Studies 
Rationale: Obesity is associated with increased asthma morbidity, lower drug responsiveness to inhaled corticosteroids, and worse asthma control. However, most prior investigations on obesity and asthma control have not focused on pediatric populations, considered environmental exposures, or included minority children.
Objectives: To examine the association between body mass index categories and asthma control among boys and girls; and whether these associations are modified by age and race/ethnicity.
Methods: Children and adolescents ages 8–19 years (n = 2,174) with asthma were recruited from the Genes-environments and Admixture in Latino Americans (GALA II) Study and the Study of African Americans, Asthma, Genes, and Environments (SAGE II). Ordinal logistic regression was used to estimate odds ratios (OR) and their confidence intervals (95% CI) for worse asthma control.
Measurements and Main Results: In adjusted analyses, boys who were obese had a 33% greater chance of having worse asthma control than their normal-weight counterparts (OR, 1.33; 95% CI, 1.04–1.71). However, for girls this association varied with race and ethnicity (P interaction = 0.008). When compared with their normal-weight counterparts, obese African American girls (OR, 0.65; 95% CI, 0.41–1.05) were more likely to have better controlled asthma, whereas Mexican American girls had a 1.91 (95% CI, 1.12–3.28) greater odds of worse asthma control.
Conclusions: Worse asthma control is uniformly associated with increased body mass index in boys. Among girls, the direction of this association varied with race/ethnicity.
doi:10.1164/rccm.201211-2116OC
PMCID: PMC3678111  PMID: 23392439
obesity; asthma control; race and ethnicity; age; sex
17.  Childhood Air Pollutant Exposure and Carotid Artery Intima-Media Thickness in Young Adults 
Circulation  2012;126(13):1614-1620.
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 2007–2009. Participants attended one 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 socio-demographic characteristics and a 12-hr 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 (AQS) 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) O3 exposure was associated with a 7.8 μm (95% CI −0.3, 15.9) or 10.1 μm (95% CI 1.8, 18.5) higher CIMT, respectively. Lifetime exposure to O3 showed similar but non-significant associations. No associations were observed for PM2.5, PM10 or NO2 although adjustment for these pollutants strengthened the childhood O3 associations.
Conclusion
Childhood exposure to O3 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.
doi:10.1161/CIRCULATIONAHA.112.096164
PMCID: PMC3474843  PMID: 22896588
atherosclerosis; cardiovascular diseases; carotid arteries; epidemiology; pediatrics
18.  The impact of secondhand smoke on asthma control among Black and Latino children 
Background
Among people with asthma, the clinical impact and relative contribution of maternal smoking during pregnancy (in utero smoking) and current secondhand smoke exposure on asthma control is poorly documented, and there is a paucity of research involving minority populations.
Objectives
To examine the association between poor asthma control and in utero smoking and current secondhand smoke exposure among Latino and Black children with asthma.
Methods
Case-only analysis of 2 multi-center case-control studies conducted from 2008–2010 using similar protocols. We recruited 2,481 Latinos and Blacks with asthma (ages 8–17) from the mainland United States and Puerto Rico. Ordinal logistic regression was used to estimate the effect of in utero smoking and current secondhand smoke exposures on National Heart Lung and Blood Institute-defined asthma control.
Results
Poor asthma control among children 8–17 years of age was independently associated with in utero smoking (odds ratio; 95% confidence interval = 1.5; 1.1–2.0). In utero smoking via the mother was also associated with secondary asthma outcomes, including early onset asthma (1.7; 1.1–2.4), daytime symptoms (1.6; 1.1–2.1), and asthma-related limitation of activities (1.6; 1.2–2.2).
Conclusions
Maternal smoking while in utero is associated with poor asthma control in Black and Latino subjects assessed at 8–17 years of age.
doi:10.1016/j.jaci.2012.03.017
PMCID: PMC3367092  PMID: 22552109
Secondhand smoke; prenatal exposure delayed effects; asthma; health status disparities
19.  Genetic and Epigenetic Variations in Inducible Nitric Oxide Synthase Promoter, Particulate Pollution and Exhaled Nitric Oxide in Children 
Background
Inducible nitric oxide synthase (iNOS, encoded by NOS2) is the major enzyme for nitric oxide synthesis in airways. As such, measurement of exhaled nitric oxide (FeNO) provides an in vivo assessment of iNOS activity. Short-term exposure to air pollution, haplotypes and DNA methylation in NOS2 promoter have been associated independently with iNOS expression and/or FeNO.
Objective
We aimed to examine the effects of ambient air pollutants, NOS2 promoter haplotypes and NOS2 promoter methylation on FeNO level in children.
Methods
We selected 940 participants in the Children’s Health Study who provided buccal samples and had undergone FeNO measurement on the same day. DNA methylation was measured using a bisulfite-polymerase chain reaction Pyrosequencing assay. Seven single nucleotide polymorphisms captured the haplotype diversity in the NOS2 promoter. Average particulate matter with aerodynamic diameter ≤2.5μm and ≤10μm (PM2.5 and PM10), ozone and nitrogen dioxide levels 7 days before FeNO measurement were estimated based on air pollution data obtained at central monitoring sites.
Results
We found interrelated effects of PM2.5, NOS2 promoter haplotypes and iNOS methylation on FeNO. Elevated 7-day average PM2.5 exposure was associated with lower iNOS methylation (P=.01). NOS2 promoter haplotypes were globally associated with NOS2 promoter methylation (P=6.2 × 10−8). There was interaction among one common promoter haplotype, iNOS methylation level and PM2.5 exposure on FeNO (Pinteraction=.00007).
Conclusion
Promoter variants in NOS2 and short term PM2.5 exposure affect iNOS methylation. This is one of the first studies showing contributions of genetic and epigenetic variations in air pollution mediated phenotype expression.
doi:10.1016/j.jaci.2011.09.037
PMCID: PMC3487398  PMID: 22055874
air pollution; biomarker; DNA methylation; epigenetics; genetics; gene-environment interaction; nitrosative stress
20.  Asthma Discordance in Twins Is Linked to Epigenetic Modifications of T Cells 
PLoS ONE  2012;7(11):e48796.
T cells mediate the inflammatory responses observed in asthma among genetically susceptible individuals and have been suspected to be prone to epigenetic regulation. However, these relationships are not well established from past clinical studies that have had limited capacity to control for the effects of variable genetic predisposition and early environmental exposures. Relying on a cohort of monozygotic twins discordant for asthma we sought to determine if epigenetic modifications in T cells were associated with current asthma and explored whether such modifications were associated with second hand smoke exposures. Our study was conducted in a monozygotic twin cohort of adult twin pairs (n = 21) all discordant for asthma. Regulatory T cell (Treg) and effector T cell (Teff) subsets were assessed for levels of cellular function, protein expression, gene expression and CpG methylation within Forkhead box P3 (FOXP3) and interferon gamma-γ (IFNγ) loci. Comparisons by asthma and current report of exposure to second hand smoke were made. Treg from asthmatic discordant twins demonstrated decreased FOXP3 protein expression and impaired Treg function that was associated with increased levels of CpG methylation within the FOXP3 locus when compared to their non-asthmatic twin partner. In parallel, Teff from discordant asthmatic twins demonstrated increased methylation of the IFNγ locus, decreased IFNγ expression and reduced Teff function when compared to Teff from the non-asthmatic twin. Finally, report of current exposure to second hand smoke was associated with modifications in both Treg and Teff at the transcriptional level among asthmatics. The results of the current study provide evidence for differential function of T cell subsets in monozygotic twins discordant for asthma that are regulated by changes in DNA methylation. Our preliminary data suggest exposure to second hand smoke may augment the modified T cell responses associated with asthma.
doi:10.1371/journal.pone.0048796
PMCID: PMC3511472  PMID: 23226205
21.  Near-Roadway Pollution and Childhood Asthma: Implications for Developing “Win–Win” Compact Urban Development and Clean Vehicle Strategies 
Environmental Health Perspectives  2012;120(11):1619-1626.
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.
doi:10.1289/ehp.1104785
PMCID: PMC3556611  PMID: 23008270
air pollution; asthma; burden of disease; children; compact urban growth; risk assessment; vehicle emissions
22.  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.
doi:10.1164/rccm.201104-0720OC
PMCID: PMC3208647  PMID: 21700914
parental stress; traffic exposure; lung function; children
23.  Traffic exposure and incident venous thromboembolism in the Atherosclerosis Risk in Communities (ARIC) Study 
Summary
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 about 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 history of DVT or pulmonary embolus (PE) at baseline examination (1987-1989). Geographical Information System (GIS)-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 using proportional hazards regression models.
Results
405 subjects developed VTE through 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%CI 0.88-1.57), 0.99 (95%CI 0.74-1.34) and 1.14 (95%CI 0.86-1.51) (p for trend across quartiles = 0.64). For residents living within 150 meters of major roads compared to 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.
doi:10.1111/j.1538-7836.2011.04210.x
PMCID: PMC3071427  PMID: 21255249
traffic exposure; VTE; air pollution; cohort
24.  Residential Proximity to Freeways and Autism in the CHARGE Study 
Environmental Health Perspectives  2010;119(6):873-877.
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.
doi:10.1289/ehp.1002835
PMCID: PMC3114825  PMID: 21156395
autism; epidemiology; gene-environment interaction; roadway proximity; traffic emissions
25.  Traffic exposure and lung function in adults: the Atherosclerosis Risk in Communities study 
Thorax  2007;62(10):873-879.
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.
doi:10.1136/thx.2006.073015
PMCID: PMC2094260  PMID: 17442705

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