Traffic Pollution Exposure Research Articles

Prevalence and etiotypes of persistent airflow obstruction in the general population across the lifetime

Background and objectivesDifferent factors (etiotypes) can lead to persistent airflow obstruction (PAO) across the lifetime, including genetic factors, abnormal lung development, cigarette smoking, traffic pollution exposure, respiratory infections and asthma. Here we explore the prevalence of PAO and associated etiotypes in the general population in different age bins. MethodsWe studied 664 individuals with PAO (FEV1/FVC post bronchodilation (post-BD) below the lower limit of normal (LLN)) and 11,522 with normal lung function (FEV1/FVC, FEV1 and FVC ≥ LLN and ≤ upper limit of normal (ULN) post-BD) included in the LEAD Study (NCT01727518), a general population cohort in Vienna (Austria). For analysis, participants were stratified in three age bins (<25, 25-<50 and ≥ 50 years of age). ResultsPAO occurred in 3.8 % in females and 5.6 % in males of the cohort, and it increased with age. Most participants with PAO (57.5 %) reported respiratory symptoms, indicating a high burden of disease. PAO was associated with male sex (25-<50 years), ever smoking (>50 years), increased number of pack years (25-<50 years, >50 years), not being breastfed (<25 years) and ever diagnosis of asthma (in all age bins). Etiotypes varied by age bins with cigarette smoking being the most prevalent one, often in combination with traffic pollution exposure. ConclusionIn the general population PAO occurs in about 5 % of participants with a higher prevalence in older individuals. Etiotypes and associated factors for PAO accumulate with age.

Urban environment exposures, energy balance-related behaviors and their combination in preschoolers from three European countries

BackgroundUrban environments are characterized by many factors that may influence children’s energy balance-related behaviors (EBRBs), but there is limited research on the impact of prospective exposure to multiple urban factors in preschoolers. We evaluated prospective associations between various urban exposures and EBRBs in preschoolers across Europe, with EBRBs considered both individually and combined into lifestyle patterns. MethodsWe used data from 4,073 preschoolers (aged 3–4 years) participating in three European cohorts from the EU Child Cohort Network: BiB (United Kingdom), EDEN (France), and INMA (Spain). Eighteen built and food environment, green spaces, road traffic and ambient air pollution exposures were characterized at residential addresses. Various EBRBs were considered as the outcomes including screen time, sleep duration and diet (fruit, vegetables, discretionary sweet foods, sweet beverages) individually and combined into unhealthy lifestyle patterns, using principal components analysis. Associations between urban exposures and outcomes were estimated using a single-exposure analysis and the deletion-substitution-addition algorithm was used to construct multi-exposure models. ResultsIn multi-exposure models, greater walkability and smaller distance to the nearest road were associated with higher scores on the unhealthy lifestyle patterns. Likewise, greater walkability was associated with higher screen time and more frequent discretionary sweet food consumption. A smaller distance to the nearest road was also associated with lower sleep duration and more frequent sweet beverages consumption. On the other hand, higher levels of street connectivity showed an inverse association with the unhealthy lifestyle patterns. In the same vein, greater street connectivity was associated with decreased screen time. ConclusionThis comprehensive examination of multiple urban exposures indicates that residing in walkable environments and in close proximity to roads in densely-populated areas may not be advantageous for children EBRBs, while residing in neighborhoods with higher street connectivity appears to supposedly be beneficial.

Concurrent exposure to light and traffic noise pollution augments behavioral deficits in rats: Protective effect of curcumin

The current study was aimed to explore the effect of light and traffic noise pollution exposure on behavioral and neurochemical deficits in adult male Wistar rats. We hypothesized that exposure to these pollutants alone or in combination may cause behavioral deficits in rats. Animals were allocated into different groups and were exposed to either varying light cycles (150 lx-5 lx, 14:10 h) or traffic noise with sound level 100 dBA for 6 h/day or both for 28 days. Concurrently, Curcumin (100 mg/kg; per oral; 28 days) was administered in varying light cycles and noise exposed animal groups to study the preventive effect. After the exposure time, the Morris water maze test, elevated plus maze test, novel object recognition test, locomotor activity test, and forced swimming test were conducted. The neurobehavioral results suggested that only combined exposure of light and noise pollution markedly impaired the learning as well as spatial and reference memory in rats. Furthermore, we found significant anxiety (less no. of open arm entries in EPM) and depressive-like behavior (increased immobility time) in light or/and traffic noise pollution exposed group animals in comparison to normal control groups. Curcumin treatment significantly prevented the behavioral anomalies in combined light and noise exposed rats. Furthermore, our results revealed augmentation of acetylcholinesterase, oxidative stress markers and interleukin (IL)-1β in the hippocampal region of noise and light-exposed groups which were markedly ameliorated by curcumin. In conclusion, our results suggest that curcumin significantly modulates light and noise pollution exposed behavioral and neurochemical anomalies in rats.

Changes in socioeconomic and demographic disparities for traffic-related air pollution exposure during pregnancy over a 20-year period in Texas

Background and Aim: Environmental justice issues surround population exposure to ambient air pollution; however, few studies have specifically examined traffic air pollution (a pollutant with localized concentration patterns) and pregnancy exposures (maternal-infant dyads may be particularly susceptible to air pollution effects). How socioeconomic and demographic disparities may change over time is also unclear but could have important policy implications. Methods: We identified ~ 6.9 million pregnant mothers in Texas from 1996 to 2016 using individual-level vital statistics records. We estimated traffic air pollution exposures using full residential addresses and calculated the total vehicle miles travelled (VMT) within 300 m, assigned nitrogen dioxide (NO2) concentrations from a spatial-temporal land use regression model (an indicator of vehicle tailpipe emissions), and linked the National Air Toxic Agency cancer risk index from vehicles emissions to maternal addresses. From census tract data, we examined median household income. We quantified annual absolute and relative mean percent differences in traffic air pollution across socio-demographic indicators of maternal race and ethnicity, educational attainment, and maternal birthplace. Results: We observed marked differences in traffic air pollution exposures by all socio-demographic variables examined. Overall, the strongest disparities were seen among non-White and foreign-born pregnancies. While the absolute level of disparity shrank from 1996 to 2016 (e.g., in 1996 Black individuals were exposed to NO2 levels 1.8 ppb higher than white individuals, while in 2016 NO2 levels were 1.5 ppb higher among Black compared to white individuals), the relative level of disparity continued to increase. Within census tracts (i.e., neighborhoods), we also observed sizeable disparities among socioeconomic and demographic groups. Conclusion: Despite considerable reductions in traffic-related air pollution, the magnitude of disparity has increased when we compared groups with lower socioeconomic positioning to their higher socioeconomic positioned counterparts. Keywords: traffic-related air pollution, pregnancy, environmental justice

Road traffic noise and incidence of primary hypertension: a prospective analysis in UK Biobank

BACKGROUND AND AIM The quality of evidence regarding the associations between road traffic noise and hypertension is low due to the limitations of cross-sectional study design, with the role of air pollution remains to be further clarified. To evaluate associations of long-term road traffic noise and air pollution exposure with incident primary hypertension, we conducted a prospective population-based analysis in UK Biobank. METHODS Road traffic noise was estimated at baseline residential address using the Common Noise Assessment Method model. Incident primary hypertension (ICD 10: I10) was ascertained through linkage with medical records for ~250 000 participants. Cox proportional hazard models were used to estimate hazard ratios (HRs) for association between road traffic noise and incident primary hypertension, adjusting for covariates determined via directed acyclic graph. RESULTS During a median of 8.1 years follow up, 21 185 incident primary hypertension cases were ascertained. The HR for a 10 dB[A] increase in mean weighted average 24-h road traffic noise level (Lden) exposure was 1.08 [95% confidence interval (CI) 1.02, 1.14]. A dose-response relationship was found, with HRs of 1.14 (95% CI: 1.04, 1.26) for Lden &amp;#x3e; 65dB[A] vs. &amp;#x2264; 55dB[A] (P trend &amp;#x3c;0.05), and HRs of 1.15 (95% CI: 1.04, 1.26) for night-time road traffic noise (Lnight)&amp;#x3e;55 dB[A] vs. &amp;#x2264; 45dB[A] (P trend &amp;#x3c;0.05). The associations were all robust to adjustment for fine particulate matter (PM2.5) and nitrogen dioxide (NO2). Furthermore, the highest incident hypertension risk was seen in the group who were exposed to the highest level of both road traffic noise and air pollution. CONCLUSIONS Long-term exposure to road traffic noise was associated with increased incidence of primary hypertension, and the effect estimates were greater in those with higher air pollution exposure. KEYWORDS road traffic noise; air pollution; primary hypertension; prospective analysis

988-P: Higher Environmental Pollution Burden Scores Associate with Lower Insulin Sensitivity in Minority Children with Overweight and Obesity

Background: Epidemiological evidence in children suggests that environmental pollution, such as ambient and traffic air pollution exposure, is associated with type 2 diabetes risk; however cumulative exposure to various environmental pollutants has not been well examined. The objective of this study was to determine if cumulative measures of environmental pollutants were associated with insulin sensitivity (SI) , acute insulin response (AIR) and disposition index (DI) in minority children. Methods: Participants (N=135, Mage = 14.4 ± 2.9 years; 59% male; 57% Latinx and 43% Black) had a 13-time point frequently sampled intravenous glucose tolerance test. Glucose and insulin values were used in minimal modelling (MinMod Millennium) for determination of SI, AIR, and DI. Self-reported mailing addresses were geocoded to identify census tract number and associated pollution burden scores (1-10) derived by CalEnviroScreen 3.0 (CES 3.0) . Multivariable linear regression was used to test relationships while considering for age, ethnicity, sex, and total body fat percentage (by DEXA) . Due to positive skewness, SI, AIR and DI were natural log transformed. Results: Higher pollution burden score was associated with lower lnSI, after adjusting for covariates (β= -0.150, 95%CI= -0.280, -0.020, p=0.024) . There was a positive, but non-significant association with pollution burden score and lnAIR (β= 0.114, 95%CI= -0.006, 2.35, p=0.063) . An inverse, but non-significant, association was observed between pollution burden scores and lnDI (β= -0.34, 95%CI= -.140, 0.71, p=0.518) . Conclusion: Using a publicly available environmental pollution risk score, we show that high environmental pollution exposures associated with lower SI, but not AIR or DI. Our findings provide further evidence of the link between ambient environmental factors and type 2 diabetes risk. Disclosure K.Barragan: None. M.Weigensberg: None. C.M.Toledo-corral: None. Funding NIH P60MD00254

Urban road traffic noise monitoring, mapping, modelling, and mitigation: A thematic review

Abstract This article analyses the most recent studies on urban traffic noise. About 67 relevant articles on urban road traffic noise and its mitigation strategies were preferred for a critical review. Only 5.97% of items describe how to monitor and record the noise measurement for urban roads, while 7.46% of articles enumerated urban traffic noise pollution exposure. 29.85% of articles proposed a model to evaluate noise reduction effects and predict the noise level. Also, many articles reported noise map generation and its analysis. 56.71% of articles described the noise mitigation strategies in detail, concerning noise control by green vegetation, land use planning, low noise tire and pavement material, noise reduction through façade shielding. Noise pollution standards are being breached in all areas. There is a need for the proper implementation of rules and regulations. Therefore, noise mitigation strategies such as designing noise barriers and other noise control materials are needed. Finally, it is summarized that economic and low-cost optimized noise pollution mitigation strategies like ingeniously made noise barriers, vegetation and landscaping are need of the hour for urban areas of developing countries.

The mediating role of vascular inflammation in traffic-related air pollution associated changes in insulin resistance in healthy adults.

The precise pathophysiologic pathway linking traffic-related air pollution (TRAP) to diabetes mellitus is not well elucidated. We aimed to investigate whether activation of vascular inflammation can be a mechanistic linkage between ambient TRAP and insulin resistance. Study outcomes were determined by assessing a series of circulating biomarkers indicative of insulin resistance and vascular inflammation among 73 healthy adults who underwent repeated clinical visits in Beijing, China, 2014-2016. Concomitantly, concentrations of ambient TRAP indices, including particulate matter in diameter <2.5μm (PM2.5), particles in size fractions of 5-560nm, black carbon, carbon monoxide, nitrogen dioxide, and oxides of nitrogen, were continuously monitored. Participants experienced extremely high levels of TRAP exposures, with mean (standard deviation) PM2.5 concentrations of 91.8 (48.3) μg/m3, throughout the study. We found that interquartile range increases in exposure to moving average concentrations of various TRAP indices at prior up to 7 days were associated with significant elevations of 8.9-49.6% in insulin levels. Higher pollutant levels were also related to worsening metrics of insulin resistance (soluble insulin receptor ectodomain, adipokines, and homeostasis model assessment of insulin resistance) and heightened vascular inflammatory responses, particularly disruptions of the receptor activator of nuclear factor κB ligand/osteoprotegerin system balance and elevations of monocyte/macrophage and T cell activation markers. Mediation analyses showed that activation of vascular inflammation could explain up to 66% of the alterations in metrics of insulin resistance attributable to air pollution. Our results suggest that ambient traffic pollution exposure was capable of promoting insulin resistance possibly via generating vascular inflammation.

Prenatal and postnatal traffic pollution exposure, DNA methylation in Shank3 and MeCP2 promoter regions, H3K4me3 and H3K27me3 and sociability in rats\u2019 offspring

BackgroundRoad traffic air pollution is linked with an increased risk of autistic spectrum disorder (ASD). The aim of this study is to assess the effect of exposure to prenatal or postnatal traffic-related air pollution combining concomitant noise pollution on ASD-related epigenetic and behavioral alternations on offspring.MethodsA 2 × 2 factorial analysis experiment was designed. Wistar rats were exposed at different sites (L group: green space; H group: crossroads) and timings (E group: full gestation; P group: 21 days after birth) at the same time, and air pollutants of nitrogen dioxide (NO2) and fine particles (PM2.5) were meanwhile sampled. On postnatal day 25, brains from offspring of each group were extracted to determine the levels of DNA methylation in Shank3 (three parts: Shank3_01, Shank3_02, Shank3_03) and MeCP2 (two parts: MeCP2_01, MeCP2_02) promoter regions, H3K4me3 and H3K27me3 after three-chamber social test. Meanwhile, the Shank3 and MeCP2 levels were quantified.ResultsThe concentrations of PM2.5 (L: 58.33 µg/m3; H: 88.33 µg/m3, P < 0.05) and NO2 (L: 52.76 µg/m3; H: 146.03 µg/m3, P < 0.01) as well as the intensity of noise pollution (L: 44.4 dB (A); H: 70.1 dB (A), P < 0.001) differed significantly from 18:00 to 19:00 between experimental sites. Traffic pollution exposure (P = 0.006) and neonatal exposure (P = 0.001) led to lower weight of male pups on PND25. Male rats under early-life exposure had increased levels of Shank3 (Shank3_02: timing P < 0.001; site P < 0.05, Shank3_03: timing P < 0.001) and MeCP2 (MeCP2_01: timing P < 0.001, MeCP2_02: timing P < 0.001) methylation and H3K4me3 (EL: 11.94 µg/mg; EH: 11.98; PL: 17.14; PH: 14.78, timing P < 0.05), and reduced levels of H3K27me3 (EL: 71.07 µg/mg; EH: 44.76; PL: 29.15; PH: 28.67, timing P < 0.001; site P < 0.05) in brain compared to those under prenatal exposure. There was, for female pups, a same pattern of Shank3 (Shank3_02: timing P < 0.001; site P < 0.05, Shank3_03: timing P < 0.001) and MeCP2 (MeCP2_01: timing P < 0.05, MeCP2_02: timing P < 0.001) methylation and H3K4me3 (EL: 11.27 µg/mg; EH: 11.55; PL: 16.11; PH: 15.44, timing P < 0.001), but the levels of H3K27me3 exhibited an inverse trend concerning exposure timing. Hypermethylation at the MeCP2 and Shank3 promoter was correlated with the less content of MeCP2 (female: EL: 32.23 ng/mg; EH: 29.58; PL: 25.01; PH: 23.03, timing P < 0.001; site P < 0.05; male: EL: 31.05 ng/mg; EH: 32.75; PL: 23.40; PH: 25.91, timing P < 0.001) and Shank3 (female: EL: 5.10 ng/mg; EH: 5.31; PL: 4.63; PH: 4.82, timing P < 0.001; male: EL: 5.40 ng/mg; EH: 5.48; PL: 4.82; PH: 4.87, timing P < 0.001). Rats with traffic pollution exposure showed aberrant sociability preference and social novelty, while those without it behaved normally.ConclusionsOur findings suggest early life under environmental risks is a crucial window for epigenetic perturbations and then abnormalities in protein expression, and traffic pollution impairs behaviors either during pregnancy or after birth.

Long-Term Exposure to Road Traffic Noise and Air Pollution, and Incident Atrial Fibrillation in the Danish Nurse Cohort

Background:Associations between long-term exposure to air pollution and road traffic noise have been established for ischemic heart disease, but findings have been mixed for atrial fibrillation (AF).Objectives:The goal of the study was to examine associations of long-term exposure to road traffic noise and air pollution with AF.Methods:Time-varying Cox regression models were used to estimate associations of 1-, 3-, and 23-y mean road traffic noise and air pollution exposures with AF incidence in 23,528 women enrolled in the Danish Nurse Cohort (age at baseline in 1993 or 1999). AF diagnoses were ascertained via the Danish National Patient Register. Annual mean weighted 24-h average road traffic noise levels () at the nurses’ residences, since 1970, were estimated using the Nord2000 model, and annual mean levels of particulate matter with a diameter () and nitrogen dioxide () were estimated using the DEHM/UBM/AirGIS model.Results:Of 23,528 nurses with no prior AF diagnosis at the cohort baseline, 1,522 developed AF during follow-up. In a fully adjusted model (including ), the estimated risk of AF was 18% higher [hazard ratio (HR); 95% confidence interval (CI): 1.18; 1.02, 1.36] in nurses with residential 3-y mean levels vs. , with similar findings for 1-y mean exposures. A increase in 3-y mean was associated with incident AF before and after adjustment for concurrent exposure to road traffic noise (HR 1.09; 95% CI: 1.00, 1.20 and 1.08; 95% CI: 0.97, 1.19, respectively). Associations with 1-y mean exposures were positive but closer to the null and not significant. Associations with were null for all time periods before and after adjustment for road traffic noise and inverse when adjusted for concurrent .Conclusion:Our analysis of prospective data from a cohort of Danish female nurses followed for up to 14 y provided suggestive evidence of independent associations between incident AF and 1- and 3-y exposures to road traffic noise and . https://doi.org/10.1289/EHP8090

Prevalence of pre-clinical autoimmunity in the normal adult population residing in a metropolitan city of India: A cross-sectional study.

A steep rise in the incidence of autoimmune diseases over the decades has been observed, which is simply not explainable with population-level genetic changes, indicating thereby that environmental factors play an important role in their causation. Then again, how air pollution affects the immune system is still not completely elucidated. This study intends to check the presence of autoantibodies and inflammatory markers in normal adults residing for more than 10 years in a highly polluted region. In this observational cross-sectional study design, 1,500 subjects residing in Delhi, India, for more than 10 years were screened, of whom 500 were recruited for the study. Distance from the main road to an individual's house was calculated, which was taken as a proxy for traffic pollution exposure. These subjects were analyzed for autoantibodies and inflammatory markers. The mean age of our cohort was 31.0±8.3 years. Autoantibody positivity was observed in 18% of the subjects, whereas inflammatory markers were elevated in 68% of the subjects. Subjects residing within 200 m of the main road had a higher prevalence of autoantibodies antinuclear antibody (12.5% vs 6.5% p=0.03) and rheumatoid factor (9.6% vs 4.5% p=0.02) than the subjects residing at or more than 250 m away from the main road. A total of 18% of normal subjects had autoantibody positivity. The odds of developing antinuclear antibodies were twice higher in subjects who resided within 200 m of the main road where the exposure to pollution was higher.

Health Impacts of Urban Bicycling in Mexico.

Background: Bicycling has been associated with health benefits. Local and national authorities have been promoting bicycling as a tool to improve public health and the environment. Mexico is one of the largest Latin American countries, with high levels of sedentarism and non-communicable diseases. No previous studies have estimated the health impacts of Mexico’s national bicycling scenarios. Aim: Quantify the health impacts of Mexico urban bicycling scenarios. Methodology: Quantitative Health Impact Assessment, estimating health risks and benefits of bicycling scenarios in 51,718,756 adult urban inhabitants in Mexico (between 20 and 64 years old). Five bike scenarios were created based on current bike trends in Mexico. The number of premature deaths (increased or reduced) was estimated in relation to physical activity, road traffic fatalities, and air pollution. Input data were collected from national publicly available data sources from transport, environment, health and population reports, and surveys, in addition to scientific literature. Results: We estimated that nine premature deaths are prevented each year among urban populations in Mexico on the current car-bike substitution and trip levels (1% of bike trips), with an annual health economic benefit of US $1,897,920. If Mexico achieves similar trip levels to those reported in The Netherlands (27% of bike trips), 217 premature deaths could be saved annually, with an economic impact of US $45,760,960. In all bicycling scenarios assessed in Mexico, physical activity’s health benefits outweighed the health risks related to traffic fatalities and air pollution exposure. Conclusion: The study found that bicycling promotion in Mexico would provide important health benefits. The benefits of physical activity outweigh the risk from traffic fatalities and air pollution exposure in bicyclists. At the national level, Mexico could consider using sustainable transport policies as a tool to promote public health. Specifically, the support of active transportation through bicycling and urban design improvements could encourage physical activity and its health co-benefits.

Traffic-related Air Pollution and Incident Obesity during Ages 10-18 years in the Southern California Children’s Health Study

Childhood obesity is a global public health crisis, often continuing into adulthood and contributing to increased morbidity and mortality. A growing literature suggests traffic pollution may contribute to increased BMI in childhood, but few studies have examined whether this translates to an increased risk of obesity. In this study we evaluated how traffic-related air pollution relates to incident obesity in a prospective study of schoolchildren from ages 10 to 18 years.The study population comprised 3430 children from eight Southern California communities who were not obese at study entry, recruited over three waves in 1992-93, 1995-96, and 2002-03. Children were followed until age 18 or high school graduation, and height and weight measurements were collected longitudinally. Residential traffic pollution exposure at baseline was estimated as nitrogen oxides (NOx) using the California line-source dispersion model. Multilevel Poisson regression models were fitted to estimate incidence rate ratios (IRR) for obesity associated with traffic-related NOx exposure, adjusting for a set of confounding variables selected a priori using a directed acyclic graph.Participants were primarily non-Hispanic White (44%) or Hispanic (40%). At study entry the median age was 9.7 (IQR: 9.3-10.1) and most children were of normal weight (78%). Traffic-related NOx was associated with increased risk of childhood obesity: IRR=1.10 (1.01-1.19) per average standard deviation within community. Further adjustment for baseline body mass index category increased the risk: IRR=1.14 (1.05-1.24).Exposure to traffic was associated with higher obesity risk in childhood. These findings strengthen the scientific evidence linking childhood obesity and air pollution from near-roadway sources, a modifiable risk factor which could be targeted through vehicular emissions reductions and exposure policies.

Prenatal exposure to traffic and ambient air pollution and infant weight and adiposity: The Healthy Start study

BackgroundPrenatal exposures to ambient air pollution and traffic have been associated with adverse birth outcomes, and may also lead to an increased risk of obesity. Obesity risk may be reflected in changes in body composition in infancy. ObjectiveTo estimate associations between prenatal ambient air pollution and traffic exposure, and infant weight and adiposity in a Colorado-based prospective cohort study. MethodsParticipants were 1125 mother-infant pairs with term births. Birth weight was recorded from medical records and body composition measures (fat mass, fat-free mass, and adiposity [percent fat mass]) were evaluated via air displacement plethysmography at birth (n = 951) and at ~5 months (n = 574). Maternal residential address was used to calculate distance to nearest roadway, traffic density, and ambient concentrations of fine particulate matter (PM2.5) and ozone (O3) via inverse-distance weighted interpolation of stationary monitoring data, averaged by trimester and throughout pregnancy. Adjusted linear regression models estimated associations between exposures and infant weight and body composition. ResultsParticipants were urban residents and diverse in race/ethnicity and socioeconomic status. Average ambient air pollutant concentrations were generally low; the median, interquartile range (IQR), and range of third trimester concentrations were 7.3 μg/m3 (IQR: 1.3, range: 3.3–12.7) for PM2.5 and 46.3 ppb (IQR: 18.4, range: 21.7–63.2) for 8-h maximum O3. Overall there were few associations between traffic and air pollution exposures and infant outcomes. Third trimester O3 was associated with greater adiposity at follow-up (2.2% per IQR, 95% CI 0.1, 4.3), and with greater rates of change in fat mass (1.8 g/day, 95% CI 0.5, 3.2) and adiposity (2.1%/100 days, 95% CI 0.4, 3.7) from birth to follow-up. ConclusionsWe found limited evidence of an association between prenatal traffic and ambient air pollution exposure and infant body composition. Suggestive associations between prenatal ozone exposure and early postnatal changes in body composition merit further investigation.

Health economic assessment of a shift to active transport

Active transportation (walking or cycling) as a substitute for car trips still represents a small percentage of all daily travels in many European cities. This study aimed to estimate the health and economic co-benefits for the adult population of modal shift from driving to active travel in urban environments. Three scenarios were modelled for the case study, the city of Porto, Portugal, by comparing travel patterns of 2013 to hypothetical scenarios of modal shifts from driving to active transport, namely: i) SC1 - conservative scenario, with a change of 5% from driving to cycling and 10% from driving to walking; ii) SC2 - moderate scenario, with a shift of 10% and 15%, respectively; and iii) SC3 - optimistic scenario, with a shift of 15% and 20%, respectively. The mortality risk reduction for five health outcomes (colon and breast cancers, diabetes, ischemic heart disease, cerebrovascular disease) was assessed, including an estimation of traffic injury and air pollution exposure risks. Results were presented in Disability-Adjusted Life Years (DALYs) avoided. Economic valuation for each scenario was performed using a Willingness-to-Pay approach for morbimortality and a Cost of Illness approach for 2013 hospitalizations and work absenteeism. Significant health benefits were found in all modelled scenarios, ranging from 1657 (16%) to 2881 (28%) DALYs avoided. Total costs averted ranged from €3894 to €6769 million through the scenarios. Cardio and cerebrovascular diseases mortality presented the largest benefit, accounting for about 3/4 of all avoidable DALYs in all scenarios. Reductions in CO2 and PM10 emissions were calculated, showing a decrease from 31.6 to 73.7 kt of CO2 and 7 to 16 t for PM10, respectively. A modal shift towards active transportation could lead to significant health and economic benefits, indicating that the evaluation of health impacts should be included in the analysis of active transport interventions.

Traffic-derived air pollution compromises skin barrier function and stratum corneum redox status: A population study.

Since air pollution is only one of many environmental stressors that can affect skin, it has been challenging to identify skin appearance or functional features profoundly affected by chronic exposure to traffic-derived air pollution. The current population study focused on taxi drivers working in urban and rural areas in order to take advantage of difference in occupational exposure. The skin conditions of 100 middle-aged male taxi drivers from urban Shanghai and 66 from rural Chongming were measured with facial tape strips were collected for biomarker analyses. Trans-epidermal water loss (TEWL) values before and after tape stripping were considerably higher in urban taxi drivers from Shanghai. Contrary to previous studies, there was no apparent detrimental effect on skin wrinkle or pigmentation from traffic pollution, which might be attributed to the higher than general public level of photo-exposure in this population. At the same time, pollution exposure especially the heavy traffic pollution exposure was found to associate with lower stratum corneum trypsin-like enzyme activity (SCTE), reduced catalase activity and total antioxidant capacity (TAOC) in tape strips. The evidence suggests that traffic-derived air pollution could deteriorate skin's physical and antioxidant barrier, whereas factors like photo-exposure can be overwhelming against appearance aging. Therefore, in addition to photoprotection, skin barrier care should be considered for people with high air pollution exposure.

Traffic exposures, air pollution and outcomes in pulmonary arterial hypertension

TPS 671: Cardiometabolic effects of long-term air pollution exposure, Exhibition Hall, Ground floor, August 26, 2019, 3:00 PM - 4:30 PM Background/Aim: 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. Methods: Exposure to particulate matter ≤2.5μm3 (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 PAH national Cohort study. Associations with transplant-free survival and pulmonary hemodynamic severity at baseline were assessed, adjusting for confounding variables defined a priori. Results: Higher 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 3μg/m3, p=0.028). This association remained similar when adjusted for potential confounding variables (HR 4.38; 95%CI 1.44-13.36 per 3μg/m3, 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 500-1000m buffer zones correlated with the ERS/ESC risk categories as well as pulmonary hemodynamics at baseline. This association was strongest for pulmonary vascular resistance. Conclusions: 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.

Air filtration and building envelop modification reduce traffic pollution exposure and blood pressure

Air filtration and building envelop modification reduce traffic pollution exposure and blood pressure

Reducing Traffic Pollution Exposure Improves Blood Pressure

Reducing Traffic Pollution Exposure Improves Blood Pressure

Perturbations of the arginine metabolome following exposures to traffic-related air pollution in a panel of commuters with and without asthma

BackgroundMechanisms underlying the effects of traffic-related air pollution on people with asthma remain largely unknown, despite the abundance of observational and controlled studies reporting associations between traffic sources and asthma exacerbation and hospitalizations. ObjectivesTo identify molecular pathways perturbed following traffic pollution exposures, we analyzed data as part of the Atlanta Commuters Exposure (ACE-2) study, a crossover panel of commuters with and without asthma. MethodsWe measured 27 air pollutants and conducted high-resolution metabolomics profiling on blood samples from 45 commuters before and after each exposure session. We evaluated metabolite and metabolic pathway perturbations using an untargeted metabolome-wide association study framework with pathway analyses and chemical annotation. ResultsMost of the measured pollutants were elevated in highway commutes (p < 0.05). From both negative and positive ionization modes, 17,586 and 9087 metabolic features were extracted from plasma, respectively. 494 and 220 unique features were associated with at least 3 of the 27 exposures, respectively (p < 0.05), after controlling confounders and false discovery rates. Pathway analysis indicated alteration of several inflammatory and oxidative stress related metabolic pathways, including leukotriene, vitamin E, cytochrome P450, and tryptophan metabolism. We identified and annotated 45 unique metabolites enriched in these pathways, including arginine, histidine, and methionine. Most of these metabolites were not only associated with multiple pollutants, but also differentially expressed between participants with and without asthma. The analysis indicated that these metabolites collectively participated in an interrelated molecular network centering on arginine metabolism, underlying the impact of traffic-related pollutants on individuals with asthma. ConclusionsWe detected numerous significant metabolic perturbations associated with in-vehicle exposures during commuting and validated metabolites that were closely linked to several inflammatory and redox pathways, elucidating the potential molecular mechanisms of traffic-related air pollution toxicity. These results support future studies of metabolic markers of traffic exposures and the corresponding molecular mechanisms.