Traffic Pollution Exposure Research Articles

Traffic exposures, air pollution and outcomes in pulmonary arterial hypertension: a UK cohort study analysis.

While traffic and air pollution exposure is associated with increased mortality in numerous diseases, its association with disease severity and outcomes in pulmonary arterial hypertension (PAH) remains unknown.Exposure to particulate matter with a 50% cut-off aerodynamic diameter ≤2.5 μm (PM2.5), nitrogen dioxide (NO2) and indirect measures of traffic-related air pollution (distance to main road and length of roads within buffer zones surrounding residential addresses) were estimated for 301 patients with idiopathic/heritable PAH recruited in the UK National Cohort Study of Idiopathic and Heritable PAH. Associations with transplant-free survival and pulmonary haemodynamic severity at baseline were assessed, adjusting for confounding variables defined a prioriHigher estimated exposure to PM2.5 was associated with higher risk of death or lung transplant (unadjusted hazard ratio (HR) 2.68 (95% CI 1.11-6.47) per 3 μg·m-3; p=0.028). This association remained similar when adjusted for potential confounding variables (HR 4.38 (95% CI 1.44-13.36) per 3 μg·m-3; p=0.009). No associations were found between NO2 exposure or other traffic pollution indicators and transplant-free survival. Conversely, indirect measures of exposure to traffic-related air pollution within the 500-1000 m buffer zones correlated with the European Society of Cardiology/European Respiratory Society risk categories as well as pulmonary haemodynamics at baseline. This association was strongest for pulmonary vascular resistance.In idiopathic/heritable PAH, indirect measures of exposure to traffic-related air pollution were associated with disease severity at baseline, whereas higher PM2.5 exposure may independently predict shorter transplant-free survival.

Prenatal Exposure to Traffic Pollution and Childhood Body Mass Index Trajectory.

Background: Limited evidence suggests an association between prenatal exposure to traffic pollution and greater adiposity in childhood, but the time window during which growth may be most affected is not known.Methods: We studied 1,649 children in Project Viva, a Boston-area pre-birth cohort. We used spatiotemporal models to estimate prenatal residential air pollution exposures and geographic information systems to estimate neighborhood traffic density and roadway proximity. We used weight and stature measurements at clinical and research visits to estimate a BMI trajectory for each child with mixed-effects natural cubic spline models. In primary analyses, we examined associations of residential PM2.5 and black carbon (BC) exposures during the third trimester and neighborhood traffic density and home roadway proximity at birth address with (1) estimated BMI at 6 month intervals through 10 years of age, (2) magnitude and timing of BMI peak and rebound, and (3) overall BMI trajectory. In secondary analyses, we examined associations of residential PM2.5 and BC exposures during the first and second trimesters with BMI outcomes.Results: Median (interquartile range; IQR) concentration of residential air pollution during the third trimester was 11.4 (1.7) μg/m3 for PM2.5 and 0.7 (0.3) μg/m3 for BC. Participants had a median (IQR) of 13 (7) clinical or research BMI measures from 0 to 10 years of age. None of the traffic pollution exposures were significantly associated with any of the BMI outcomes in covariate-adjusted models, although effect estimates were in the hypothesized direction for neighborhood traffic density and home roadway proximity. For example, greater neighborhood traffic density [median (IQR) 857 (1,452) vehicles/day x km of road within 100 m of residential address at delivery] was associated with a higher BMI throughout childhood, with the strongest associations in early childhood [e.g., per IQR increment natural log-transformed neighborhood traffic density, BMI at 12 months of age was 0.05 (−0.03, 0.13) kg/m2 higher and infancy peak BMI was 0.05 (−0.03, 0.14) kg/m2 higher].Conclusions: We found no evidence for a persistent effect of prenatal exposure to traffic pollution on BMI trajectory from birth through mid-childhood in a population exposed to modest levels of air pollution.

Traffic-Related Air Pollution, Noise and Infant Mortality in London

BackgroundThere is evidence that ambient air pollution is associated with increased risk of infant mortality. Road traffic is a major contributor to ambient air pollution, but it also generates noise. This study investigates long-term exposure to both traffic-related air and noise pollution and risk of infant mortality. MethodsWe conducted a matched case-control study of infant deaths (deaths occurring in 1st year of life) from singleton births across Greater London from 2003-2010. Controls were singleton births in the study area between 2003-2010 surviving to age 1. Cases were matched to controls (n=29) on birthdate and sex. Monthly concentrations of NO2, NOX, source-specific traffic-related PM2.5, PM2.5, PM10 and ozone were estimated at 20x20m resolution using a dispersion model, and time-weighted averages calculated for pregnancy/trimesters and birth to case death at address-level. Road traffic noise was modelled at address-level. We analysed the relationship between air pollutants/noise and infant mortality using conditional logistic regression, with adjustment for confounding. ResultsThe study population comprises 3390 infant deaths (69% neonatal, 31% postneonatal). Average air pollutant exposures for cases from birth to death were 42μg/m3 NO2, 77μg/m3 NOx, 15μg/m3 PM2.5, 24μg/m3 PM10 and 31μg/m3 O3. Average day- and night-time noise levels were 58 and 53 dB respectively. Higher road traffic air pollution and noise exposures were particularly associated with non-White ethnicity and lower socio-economic status. Preliminary results from adjusted single-pollutant models suggest increased risk of infant mortality associated with higher ozone exposure, but not with other air pollutants or noise. Analyses of joint air pollution–noise exposures are currently underway. ConclusionsTo our knowledge, this is the first epidemiological study to investigate risk of infant mortality in relation to both road traffic air pollution and noise co-exposures.

Use of high-resolution metabolomics for the identification of metabolic signals associated with traffic-related air pollution

BackgroundHigh-resolution metabolomics (HRM) is emerging as a sensitive tool for measuring environmental exposures and biological responses. The aim of this analysis is to assess the ability of high-resolution metabolomics (HRM) to reflect internal exposures to complex traffic-related air pollution mixtures. MethodsWe used untargeted HRM profiling to characterize plasma and saliva collected from participants in the Dorm Room Inhalation to Vehicle Emission (DRIVE) study to identify metabolic pathways associated with traffic emission exposures. We measured a suite of traffic-related pollutants at multiple ambient and indoor sites at varying distances from a major highway artery for 12 weeks in 2014. In parallel, 54 students living in dormitories near (20 m) or far (1.4 km) from the highway contributed plasma and saliva samples. Untargeted HRM profiling was completed for both plasma and saliva samples; metabolite and metabolic pathway alternations were evaluated using a metabolome-wide association study (MWAS) framework with pathway analyses. ResultsWeekly levels of traffic pollutants were significantly higher at the near dorm when compared to the far dorm (p < 0.05 for all pollutants). In total, 20,766 metabolic features were extracted from plasma samples and 29,013 from saliva samples. 45% of features were detected and shared in both plasma and saliva samples. 1291 unique metabolic features were significantly associated with at least one or more traffic indicator, including black carbon, carbon monoxide, nitrogen oxides and fine particulate matter (p < 0.05 for all significant features), after controlling for confounding and false discovery rate. Pathway analysis of metabolic features associated with traffic exposure indicated elicitation of inflammatory and oxidative stress related pathways, including leukotriene and vitamin E metabolism. We confirmed the chemical identities of 10 metabolites associated with traffic pollutants, including arginine, histidine, γ‑linolenic acid, and hypoxanthine. ConclusionsUsing HRM, we identified and verified biological perturbations associated with primary traffic pollutant in panel-based setting with repeated measurement. Observed response was consistent with endogenous metabolic signaling related to oxidative stress, inflammation, and nucleic acid damage and repair. Collectively, the current findings provide support for the use of untargeted HRM in the development of metabolic biomarkers of traffic pollution exposure and response.

Errors associated with the use of roadside monitoring in the estimation of acute traffic pollutant-related health effects

Near-road monitoring creates opportunities to provide direct measurement on traffic-related air pollutants and to better understand the changing near-road environment. However, how such observations represent traffic-related air pollution exposures for estimating adverse health effect in epidemiologic studies remains unknown. A better understanding of potential exposure measurement error when utilizing near-road measurement is needed for the design and interpretation of the many observational studies linking traffic pollution and adverse health.The Dorm Room Inhalation to Vehicle Emission (DRIVE) study conducted near-road measurements of several single traffic indicators at six indoor and outdoor sites ranging from 0.01 to 2.3 km away from a heavily-trafficked (average annual daily traffic over 350,000) highway artery between September 2014 to January 2015. We examined spatiotemporal variability trends and assessed the potential for bias and errors when using a roadside monitor as a primary traffic pollution exposure surrogate, in lieu of more spatially-refined, proximal exposure indicators.Pollutant levels measured during DRIVE showed a low impact of this highway hotspot source. Primary pollutant species, including NO, CO, and BC declined to near background levels by 20–30 m from the highway source. Patterns of correlation among the sites also varied by pollutant and time of day. NO2, specifically, exhibited spatial trends that differed from other single-pollutant primary traffic indicators. This finding provides some indication of limitations in the use of NO2 as a primary traffic exposure indicator in panel-based health effect studies. Interestingly, roadside monitoring of NO, CO, and BC tended to be more strongly correlated with sites, both near and far from the road, during morning rush hour periods, and more weakly correlated during other periods of the day. We found pronounced attenuation of observed changes in health effects when using measured pollutant from the near-road monitor as a surrogate for true exposure, and the magnitude varied substantially over the course of the day. Caution should be taken when using near-road monitoring network observations, alone, to investigate health effects of traffic pollutants.

Road traffic noise, air pollution and incident cardiovascular disease: A joint analysis of the HUNT, EPIC-Oxford and UK Biobank cohorts

BackgroundThis study aimed to investigate the effects of long-term exposure to road traffic noise and air pollution on incident cardiovascular disease (CVD) in three large cohorts: HUNT, EPIC-Oxford and UK Biobank. MethodsIn pooled complete-case sample of the three cohorts from Norway and the United Kingdom (N = 355,732), 21,081 incident all CVD cases including 5259 ischemic heart disease (IHD) and 2871 cerebrovascular cases were ascertained between baseline (1993–2010) and end of follow-up (2008–2013) through medical record linkage. Annual mean 24-hour weighted road traffic noise (Lden) and air pollution (particulate matter with aerodynamic diameter ≤ 10 μm [PM10], ≤2.5 μm [PM2.5] and nitrogen dioxide [NO2]) exposure at baseline address was modelled using a simplified version of the Common Noise Assessment Methods in Europe (CNOSSOS-EU) and European-wide Land Use Regression models. Individual-level covariate data were harmonised and physically pooled across the three cohorts. Analysis was via Cox proportional hazard model with mutual adjustments for both noise and air pollution and potential confounders. ResultsNo significant associations were found between annual mean Lden and incident CVD, IHD or cerebrovascular disease in the overall population except that the association with incident IHD was significant among current-smokers. In the fully adjusted models including adjustment for Lden, an interquartile range (IQR) higher PM10 (4.1 μg/m3) or PM2.5 (1.4 μg/m3) was associated with a 5.8% (95%CI: 2.5%–9.3%) and 3.7% (95%CI: 0.2%–7.4%) higher risk for all incident CVD respectively. No significant associations were found between NO2 and any of the CVD outcomes. ConclusionsWe found suggestive evidence of a possible association between road traffic noise and incident IHD, consistent with current literature. Long-term particulate air pollution exposure, even at concentrations below current European air quality standards, was significantly associated with incident CVD.

Diesel exhaust particles up-regulate interleukin-17A expression via ROS/NF-κB in airway epithelium

IL-17A is implicated in many aspects of pathogenesis of severe asthma, including inducing neutrophilic inflammation, airway hyperresponsiveness, steroid insensitivity and airway remodeling. Diesel exhaust particles (DEP) emission from vehicles has been shown to expand Th17 cells to increase IL-17A release that contributes to DEP-mediated exacerbation of asthma severity. It is not known whether non-immune cells in airways may also release IL-17A in response to DEP exposure. In this study, We found IL-17A expression was upregulated in the epithelium of severe allergic asthma patients from high road traffic pollution areas compared to those in low. Furthermore, we found DEP concentration-dependently increased IL-17A synthesis and release by 122.3 ± 15.72% and 235.5 ± 18.37%, respectively in primary bronchial epithelial cells (PBEC), accompanied with increased ROS production. Pretreatment of ROS scavenger (NAC) significantly inhibited DEP-induced IL-17A mRNA expression. DEP-induced IκBα degradation can be inhibited by NAC. We also found DEP increased p65 and RelB subunits expression, and pretreatment of NF-κB inhibitor (SN50) also inhibited DEP-induced IL-17A expression. We further found DEP increased NF-κB subunit RelB recruitment to IL-17A promoter in PBEC and airway tissue of severe allergic asthma patients from high road traffic pollution areas. These results indicate DEP stimulates IL-17A expression in airway epithelium through ROS/NF-κB pathway, and provide a possible link between traffic pollution exposure and IL-17A-related responses in severe allergic asthma patients.

Parental Snoring and Environmental Pollutants, but Not Aeroallergen Sensitization, Are Associated with Childhood Snoring in a Birth Cohort.

The objective of this study was to determine whether atopy and other clinical and environmental variables predict the risk of childhood habitual snoring (HS) in a birth cohort born to atopic parents. Participants completed clinical evaluations and questionnaires at ages 1-4 and age 7. HS was defined as snoring ≥3 nights/week. Traffic-related air pollution (TRAP) exposure was estimated using land-use regression. The association between early (≤age 4) and current (age 7) allergic disease, environmental exposures, and snoring at age 7 was examined using adjusted logistic regression. Of the 609 children analyzed the prevalence of HS at age 7 was 21%. Early tobacco smoke exposure [environmental tobacco smoke (ETS)] [odds ratio (OR) 1.79, 95% CI (confidence interval) 1.12-2.84], rhinitis (OR 1.74, 95% CI 1.06-2.92), wheezing (OR 1.63, 95% CI 1.05-2.53), maternal HS (OR 2.08, 95% CI 1.36-3.18), and paternal HS (OR 1.83, 95% CI 1.14-3.00) were significantly associated with HS at age 7. Current TRAP (OR 1.93, 95% CI 1.13-3.26), respiratory infections (OR 1.16, 95% 1.03-1.35), maternal HS (OR 2.86, 95% CI 1.69-4.84), and paternal HS (OR 3.01, 95% CI 1.82-5.09) were significantly associated with HS at age 7. To our knowledge, this is the largest birth cohort examining longitudinal predictors of snoring in children born to atopic parents. Parental HS was the only variable consistently associated with childhood HS from ages 1 to 7. Early rhinitis, early ETS exposure, and concurrent traffic pollution exposure increased the risk of HS at age 7, while aeroallergen sensitization did not. Children with these characteristics should be considered for screening of sleep disorders.

Traffic Maps and Smartphone Trajectories to Model Air Pollution, Exposure and Health Impact

In this study, we explored to combine traffic maps and smartphone trajectories to model traffic air pollution, exposure and health impact. The approach was step-by-step modeling through the causal chain: engine emission, traffic density versus traffic velocity, traffic pollution concentration, exposure along individual trajectories, and health risk. A generic street with 100 km/h speed limit was used as an example to test the model. A single fixed-time trajectory had maximum exposure at velocity of 45 km/h at maximum pollution concentration. The street population had maximum exposure shifted to a velocity of 15 km/h due to the congestion density of vehicles. The shift is a universal effect of exposure. In this approach, nearly every modeling step of traffic pollution depended on traffic velocity. A traffic map is a super-efficient pre-processor for calculating real-time traffic pollution exposure at global scale using big data analytics.

Hyperspectral leaf reflectance of Carpinus betulus L. saplings for urban air quality estimation

In urban areas, the demand for local assessment of air quality is high. The existing monitoring stations cannot fulfill the needs. This study assesses the potential of hyperspectral tree leaf reflectance for monitoring traffic related air pollution. Hereto, 29 Carpinus betulus saplings were exposed to an environment with either high or low traffic intensity. The local air quality was estimated by leaf saturation isothermal remanent magnetization (SIRM). The VIS-NIR leaf reflectance spectrum (350–2500 nm) was measured using a handheld AgriSpec spectroradiometer (ASD Inc.). Secondary, leaf chlorophyll content index (CCI), specific leaf area (SLA) and water content (WC) were determined. To gain insight in the link between leaf reflectance and air quality, the correlation between SIRM and several spectral features was determined. The spectral features that were tested are plain reflectance values, derivative of reflectance, two-band indices using the NDVI formula and PCA components. Spectral reflectance for wavelength bands in the red and short wave IR around the red edge, were correlated to SIRM with Pearson correlations of up to R = −0.85 (R2 = 0.72). Based on the spectral features and combinations thereof, binomial logistic regression models were trained to classify trees into high or low traffic pollution exposure, with classification accuracies up to 90%. It can be concluded that hyperspectral reflectance of C. betulus leaves can be used to detect different levels of air pollution within an urban environment.

Exposure to traffic pollution and increased risk of depressive and anxiety symptoms in older adults

Background: Mental health disorders are the third most costly non-fatal condition in America, and account for &gt;140 million disability-adjusted life years worldwide. While the genetic profile is been major risk factor of mental disorders, recent evidence has suggested a role of traffic-related air pollution in the pathogenesis of mental disorders. Methods: We examined the association of distance to road, a marker of traffic pollution exposure, with depression and anxiety in 4,854 community-dwelling adults (aged ≥57) of the National Social Life, Health and Aging Project, a nationally representative, longitudinal sample of older adults in the US. Depression and anxiety were evaluated using standardized questionnaires, with cases identified by dichotomizing questionnaire scores using well-established cutoffs. As a proxy for traffic exposure, we calculated distance from each residential address to the closest A1–A3 road segments. Generalized linear mixed models were used to assess the association with adjustment of confounders (e.g., socioeconomic status), and to explore effect modification (e.g., by season). Results: In models adjusted for age, gender, race, calendar year, season, day of week, region and individual- and neighborhood-level socioeconomic status, we found 1.38 times the odds of adverse depressive symptoms (95%CI: 1.07, 1.78), and 1.51 times the odds of adverse anxiety symptoms (95%CI: 1.16, 1.96) in individuals living within 50m of a road, compared with those living 200m or farther away. We saw no elevations in odds for adults living 50–200 m from the road. The association remains robust upon adjustment of fine particular matter (PM2.5). Association with other neighborhood characteristics (e.g., crime/foreclosure rate, greenness) will be examined. Conclusions: Distance to road was associated with depression and anxiety, suggesting that pollution from traffic may be a newly identified environmental risk factor for mental health.

Genetic Variants in the Bone Morphogenic Protein Gene Family Modify the Association between Residential Exposure to Traffic and Peripheral Arterial Disease.

There is a growing literature indicating that genetic variants modify many of the associations between environmental exposures and clinical outcomes, potentially by increasing susceptibility to these exposures. However, genome-scale investigations of these interactions have been rarely performed particularly in the case of air pollution exposures. We performed race-stratified genome-wide gene-environment interaction association studies on European-American (EA, N = 1623) and African-American (AA, N = 554) cohorts to investigate the joint influence of common single nucleotide polymorphisms (SNPs) and residential exposure to traffic (“traffic exposure”)—a recognized vascular disease risk factor—on peripheral arterial disease (PAD). Traffic exposure was estimated via the distance from the primary residence to the nearest major roadway, defined as the nearest limited access highways or major arterial. The rs755249-traffic exposure interaction was associated with PAD at a genome-wide significant level (P = 2.29x10-8) in European-Americans. Rs755249 is located in the 3’ untranslated region of BMP8A, a member of the bone morphogenic protein (BMP) gene family. Further investigation revealed several variants in BMP genes associated with PAD via an interaction with traffic exposure in both the EA and AA cohorts; this included interactions with non-synonymous variants in BMP2, which is regulated by air pollution exposure. The BMP family of genes is linked to vascular growth and calcification and is a novel gene family for the study of PAD pathophysiology. Further investigation of BMP8A using the Genotype Tissue Expression Database revealed multiple variants with nominally significant (P < 0.05) interaction P-values in our EA cohort were significant BMP8A eQTLs in tissue types highlight relevant for PAD such as rs755249 (tibial nerve, eQTL P = 3.6x10-6) and rs1180341 (tibial artery, eQTL P = 5.3x10-6). Together these results reveal a novel gene, and possibly gene family, associated with PAD via an interaction with traffic air pollution exposure. These results also highlight the potential for interactions studies, particularly at the genome scale, to reveal novel biology linking environmental exposures to clinical outcomes.

The modifying effect of socioeconomic status on the relationship between traffic, air pollution and respiratory health in elementary schoolchildren

The volume and type of traffic and exposure to air pollution have been found to be associated with respiratory health, but few studies have considered the interaction with socioeconomic status at the household level. We investigated the relationships of respiratory health related to traffic type, traffic volume, and air pollution, stratifying by socioeconomic status, based on household income and education, in 3591 schoolchildren in Windsor, Canada. Interquartile range changes in traffic exposure and pollutant levels were linked to respiratory symptoms and objective measures of lung function using generalised linear models for three levels of income and education. In 95% of the relationships among all cases, the odds ratios for reported respiratory symptoms (a decrease in measured lung function), based on an interquartile range change in traffic exposure or pollutant, were greater in the lower income/education groups than the higher, although the odds ratios were in most cases not significant. However, in up to 62% of the cases, the differences between high and low socioeconomic groups were statistically significant, thus indicating socioeconomic status (SES) as a significant effect modifier. Our findings indicate that children from lower socioeconomic households have a higher risk of specific respiratory health problems (chest congestion, wheezing) due to traffic volume and air pollution exposure.

Changes in Vascular Nitrite and FeNO Following Acute Traffic Pollution Exposure With and Without Oral Nitrate Prophylaxis via Beet Juice

BackgroundCirculating NO2‐represents both a marker of endothelial function and a source of NO during hypoxia. Previously we have shown that healthy subjects display increased plasma NO2‐ in response to an ischemic stimulus and that this increase can be abolished by 2 hours of traffic related air pollution (TRAP), the same time frame by which TRAP exposure is epidemiologically associated with acute adverse outcomes such as MI. We have been exploring underlying mechanisms by which such acute effects of air pollution might occur, with a goal of being able to prevent or mitigate them. Dietary inorganic nitrates enter an enterosalivary circuit in which salivary gland bacteria reduce NO3‐ to NO2‐. This circulating NO2‐ is reduced in hypoxic environments to NO resulting in vasorelaxation. Beetroot is high in inorganic NO3‐. We investigated whether beetroot juice (BJ) can be used to supplement circulating NO2‐ levels, affect blood pressure response, and potentially alter the hypoxia response following exposure to TRAP.Methods20 male and female healthy volunteers participated in a randomized, placebo‐controlled, crossover study of whether BJ could ameliorate the oxidant effects of exposure to TRAP. Volunteers were randomized to receive 500ml of BJ (20 mM NO3‐) or orange juice (OJ, 0.001 mM NO3‐) on their first visit and the other on a second visit one week later. Before and after each ride, blood pressure, FeNO (NIOX MINO), and plasma NO2‐ concentration, and the change in plasma NO2‐ in response to a 5 min ischemic forearm stimulus were measured. Plasma NO2‐ was measured by chemical reduction chemiluminesence using a Sievers NOA. Following before‐ride plasma sampling, subjects consumed the juice and were driven on a 2 hour rush‐hour car ride in the truck lanes of the New Jersey Turnpike.ResultsPrior to the rides/juice, baseline circulating NO2‐ was 186 ±159 nM. The NO2‐concentration fell to 140±152 nM after the OJ ride (NS), whereas, even in the face of oxidant TRAP exposure it rose to 403±315 nM following the BJ/ride. Confirming systemic delivery of the NO2‐, the BJ/ride increased FeNO from 18.3 ppb to 29.6 ppb (p&lt;0.0001), with a smaller increase during the OJ/ride (17.9 to 19.8 ppb; p=0.027). Systolic blood pressure rose an average of 1.5 mm Hg (NS) following the OJ rides, and this was reduced to a rise of 0.23 mm Hg (NS) following BJ rides. The change in hyperemic response (before to after the ride) was greater for BJ (38 nM) than for OJ (7 nM), but the difference was not significant as there was considerable variability in the response to both TRAP and BJ (σ=233 nM).ConclusionsThese data suggest that BJ can effectively supplement circulating NO2‐, despite exogenous oxidative stress from TRAP, representing a nutritional mechanism for supporting endothelial function. BJ also increased delivery of NO2‐ to the airways. We speculate that the increase in FeNO following OJ represents TRAP‐induced airway inflammation. Further investigations of prevention of a TRAP effect by BJ will need to incorporate a physiologic measure of endothelial function such as brachial artery ultrasound or peripheral arterial tonometry.Support or Funding InformationThis study was supported by the NIEHS P30 Center for Environmental Exposures and Disease ES005022

Traffic pollution exposure is associated with altered brain connectivity in school children

Children are more vulnerable to the effects of environmental elements due to their active developmental processes. Exposure to urban air pollution has been associated with poorer cognitive performance, which is thought to be a result of direct interference with brain maturation. We aimed to assess the extent of such potential effects of urban pollution on child brain maturation using general indicators of vehicle exhaust measured in the school environment and a comprehensive imaging evaluation. A group of 263 children, aged 8 to 12years, underwent MRI to quantify regional brain volumes, tissue composition, myelination, cortical thickness, neural tract architecture, membrane metabolites, functional connectivity in major neural networks and activation/deactivation dynamics during a sensory task. A combined measurement of elemental carbon and NO2 was used as a putative marker of vehicle exhaust. Air pollution exposure was associated with brain changes of a functional nature, with no evident effect on brain anatomy, structure or membrane metabolites. Specifically, a higher content of pollutants was associated with lower functional integration and segregation in key brain networks relevant to both inner mental processes (the default mode network) and stimulus-driven mental operations. Age and performance (motor response speed) both showed the opposite effect to that of pollution, thus indicating that higher exposure is associated with slower brain maturation. In conclusion, urban air pollution appears to adversely affect brain maturation in a critical age with changes specifically concerning the functional domain.

Disrupted Nitric Oxide Metabolism from Type II Diabetes and Acute Exposure to Particulate Air Pollution

Type II diabetes is an established cause of vascular impairment. Particulate air pollution is known to exacerbate cardiovascular and respiratory conditions, particularly in susceptible populations. This study set out to determine the impact of exposure to traffic pollution, with and without particle filtration, on vascular endothelial function in Type II diabetes. Endothelial production of nitric oxide (NO) has previously been linked to vascular health. Reactive hyperemia induces a significant increase in plasma nitrite, the proximal metabolite of NO, in healthy subjects, while diabetics have a lower and more variable level of response. Twenty type II diabetics and 20 controls (ages 46–70 years) were taken on a 1.5hr roadway traffic air pollution exposure as passengers. We analyzed plasma nitrite, as a measure of vascular function, using forearm ischemia to elicit a reactive hyperemic response before and after exposure to one ride with and one without filtration of the particle components of pollution. Control subjects displayed a significant increase in plasma nitrite levels during reactive hyperemia. This response was no longer present following exposure to traffic air pollution, but did not vary with whether or not the particle phase was filtered out. Diabetics did not display an increase in nitrite levels following reactive hyperemia. This response was not altered following pollution exposure. These data suggest that components of acute traffic pollution exposure diminish vascular reactivity in non-diabetic individuals. It also confirms that type II diabetics have a preexisting diminished ability to appropriately respond to a vascular challenge, and that traffic pollution exposure does not cause a further measureable acute change in plasma nitrite levels in Type II diabetics.

Air pollution and allergic diseases.

Exposure to traffic-related air pollutants (TRAPs) has been implicated in asthma development, persistence, and exacerbation. This exposure is highly significant because increasingly large segments of the population worldwide reside in zones that have high levels of TRAP, including children, as schools are often located in high traffic pollution exposure areas. Recent findings include epidemiologic and mechanistic studies that shed new light on the impact of traffic pollution on allergic diseases and the biology underlying this impact. In addition, new innovative methods to assess and quantify traffic pollution have been developed to assess exposure and identify vulnerable populations and individuals. This review will summarize the most recent findings in each of these areas. These findings will have a substantial impact on clinical practice and research by the development of novel methods to quantify exposure and identify at-risk individuals, as well as mechanistic studies that identify new targets for intervention for individuals most adversely affected by TRAP exposure.

Residential Exposure To Traffic Pollution And Congenital Heart Defects, Preterm Births, And Low Birth Weight In Lanzhou, China

Introduction: Some studies have suggested an association of residence near major roads with adverse birth outcomes. However, little is known about this relationship in large Chinese cities, where intra-urban variation in traffic pollution is high due to crisscross major roads adjacent to residential areas. We investigated this relationship in Lanzhou, an important industrial city in China. Methods: To understand the dispersion patterns of traffic pollution, horizontal profile measurements of Nitrogen Dioxide (NO2) and Black Carbon (BC) were conducted within 200m of selected major roads. The study population is 8,558 pregnant women and their children recruited in a birth cohort study during 2010-2012. Residential exposure to traffic pollution was estimated by proximity to nearest major road, and total length of major roads within 200m of residence. The associations of the exposure metrics with Congenital Heart Defects (CHD), preterm births (PTB), and low birth weight (LBW) were estimated using logistic regression models adjusting for infant characteristics (e.g., gender), maternal demographics (age, education, income), health status and lifestyle choices (e.g., smoking, folate acid intake). Results: Concentrations of NO2 and BC decayed linearly by about 40% and 80% by 100m from the edge of a major road and reached a plateau. Compared to women residing far away from a major road (&gt;500m), women residing closest to a major road (≤ 100m), and close to a major road (100-500m) are more likely to have infants with CHD [OR(≤100m): 3.8, 95%CI: 1.1, 13.8; OR(100-500m): 3.7, 95%CI: 1.1, 12.9], respectively. Positive associations between the three outcomes and total length of major roads near residence are consistent but marginally significant. Discussion: The results indicate potential risks of adverse birth outcomes associated with traffic pollution exposure. This work also calls for more research on this issue, and awareness of traffic control in residential area in China.

Traffic pollution at the home address and pregnancy outcomes in Stockholm, Sweden

BackgroundFor the past two decades, several studies have reported associations between elevated levels of ambient air pollution and adverse pregnancy outcomes, although with varying conclusions.ObjectivesTo examine possible associations between the...

Traffic-Related Air Pollution and Dementia Incidence in Northern Sweden: A Longitudinal Study.

BackgroundExposure to ambient air pollution is suspected to cause cognitive effects, but a prospective cohort is needed to study exposure to air pollution at the home address and the incidence of dementia.ObjectivesWe aimed to assess the association between long-term exposure to traffic-related air pollution and dementia incidence in a major city in northern Sweden.MethodsData on dementia incidence over a 15-year period were obtained from the longitudinal Betula study. Traffic air pollution exposure was assessed using a land-use regression model with a spatial resolution of 50 m × 50 m. Annual mean nitrogen oxide levels at the residential address of the participants at baseline (the start of follow-up) were used as markers for long-term exposure to air pollution.ResultsOut of 1,806 participants at baseline, 191 were diagnosed with Alzheimer’s disease during follow-up, and 111 were diagnosed with vascular dementia. Participants in the group with the highest exposure were more likely than those in the group with the lowest exposure to be diagnosed with dementia (Alzheimer’s disease or vascular dementia), with a hazard ratio (HR) of 1.43 (95% CI: 0.998, 2.05 for the highest vs. the lowest quartile). The estimates were similar for Alzheimer’s disease (HR 1.38) and vascular dementia (HR 1.47). The HR for dementia associated with the third quartile versus the lowest quartile was 1.48 (95% CI: 1.03, 2.11). A subanalysis that excluded a younger sample that had been retested after only 5 years of follow-up suggested stronger associations with exposure than were present in the full cohort (HR = 1.71; 95% CI: 1.08, 2.73 for the highest vs. the lowest quartile).ConclusionsIf the associations we observed are causal, then air pollution from traffic might be an important risk factor for vascular dementia and Alzheimer’s disease.CitationOudin A, Forsberg B, Nordin Adolfsson A, Lind N, Modig L, Nordin M, Nordin S, Adolfsson R, Nilsson LG. 2016. Traffic-related air pollution and dementia incidence in northern Sweden: a longitudinal study. Environ Health Perspect 124:306–312; http://dx.doi.org/10.1289/ehp.1408322