To Traffic-related Air Pollution Research Articles

Characterizing the distribution pattern of traffic-related air pollutants in near-road neighborhoods.

In near-road neighborhoods, residents are more frequently exposed to traffic-related air pollution (TRAP), and they are increasingly aware of pollution levels. Given this consideration, this study adopted portable air pollutant sensors to conduct a mobile monitoring campaign in two near-road neighborhoods, one in an urban area and one in a suburban area of Shanghai, China. The campaign characterized spatiotemporal distributions of fine particulate matter (PM2.5) and black carbon (BC) to help identify appropriate mitigation measures in these near-road micro-environments. The study identified higher mean TRAP concentrations (up to 4.7-fold and 1.7-fold higher for PM2.5 and BC, respectively), lower spatial variability, and a stronger inter-pollutant correlation in winter compared to summer. The temporal variations of TRAP between peak hour and off-peak hour were also investigated. It was identified that district-level PM2.5 increments occurred from off-peak to peak hours, with BC concentrations attributed more to traffic emissions. In addition, the spatiotemporal distribution of TRAP inside neighborhoods revealed that PM2.5 concentrations presented great temporal variability but almost remained invariant in space, while the BC concentrations showed notable spatiotemporal variability. These findings provide valuable insights into the unique spatiotemporal distributions of TRAP in different near-road neighborhoods, highlighting the important role of hyperlocal monitoring in urban micro-environments to support tailored designing and implementing appropriate mitigation measures.

The impact of vegetative and solid roadway barriers on particulate matter concentration in urban settings.

A potentially important approach for reducing exposure to traffic-related air pollution (TRAP) is the use of roadside barriers to reduce dispersion from highway sources to adjacent populated areas. The Trees Reducing Environmental Exposures (TREE) study investigated the effect of vegetative and solid barriers along major controlled-access highways in Atlanta, Georgia, USA by simultaneously sampling TRAP concentration at roadside locations in front of barriers and at comparison locations down-range. We measured black carbon (BC) mass concentration, particle number concentration (PNC), and the size distribution of ultrafine aerosols. Our sample sites encompassed the range of roadway barrier options in the Atlanta area: simple chain-link fences, solid barriers, and vegetative barriers. We used Generalized Linear Mixed Models (GLMMs) to estimate the effect of barrier type on the ratio of particle concentrations at the comparison site relative to the roadside site while controlling for covariates including wind direction, temperature, relative humidity, traffic volume, and distance to the roadway. Vegetative barriers exhibited the greatest TRAP reduction in terms of BC mass concentration (37% lower behind a vegetative barrier) as well as PNC (6.7% lower), and sensitivity analysis was consistent with this effect being more pronounced when the barrier was downwind of the highway. The ultrafine size distribution was comprised of modestly smaller particles on the highway side of the barrier. Non-highway particle sources were present at all sample sites, most commonly motor vehicle emissions from nearby arterials or secondary streets, which may have obscured the effect of roadside barriers.

Traffic Density Exposure, Oxidative Stress Biomarkers and Plasma Metabolomics in a Population-Based Sample: The Hortega Study.

Exposure to traffic-related air pollution (TRAP) generates oxidative stress, with downstream effects at the metabolic level. Human studies of traffic density and metabolomic markers, however, are rare. The main objective of this study was to evaluate the cross-sectional association between traffic density in the street of residence with oxidative stress and metabolomic profiles measured in a population-based sample from Spain. We also explored in silico the potential biological implications of the findings. Secondarily, we assessed the contribution of oxidative stress to the association between exposure to traffic density and variation in plasma metabolite levels. Traffic density was defined as the average daily traffic volume over an entire year within a buffer of 50 m around the participants' residence. Plasma metabolomic profiles and urine oxidative stress biomarkers were measured in samples from 1181 Hortega Study participants by nuclear magnetic resonance spectroscopy and high-performance liquid chromatography, respectively. Traffic density was associated with 7 (out of 49) plasma metabolites, including amino acids, fatty acids, products of bacterial and energy metabolism and fluid balance metabolites. Regarding urine oxidative stress biomarkers, traffic associations were positive for GSSG/GSH% and negative for MDA. A total of 12 KEGG pathways were linked to traffic-related metabolites. In a protein network from genes included in over-represented pathways and 63 redox-related candidate genes, we observed relevant proteins from the glutathione cycle. GSSG/GSH% and MDA accounted for 14.6% and 12.2% of changes in isobutyrate and the CH2CH2CO fatty acid moiety, respectively, which is attributable to traffic exposure. At the population level, exposure to traffic density was associated with specific urine oxidative stress and plasma metabolites. Although our results support a role of oxidative stress as a biological intermediary of traffic-related metabolic alterations, with potential implications for the co-bacterial and lipid metabolism, additional mechanistic and prospective studies are needed to confirm our findings.

Traffic-related air pollution, chronic stress, and changes in exhaled nitric oxide and lung function among a panel of children with asthma living in an underresourced community

We examined associations between short-term exposure to traffic-related air pollutants (TRAP) and airway inflammation and lung function in children with asthma, and whether these associations are modified by chronic psychological stress. Residents of underresourced port-adjacent communities in New Jersey were concerned about the cumulative impacts of exposure to TRAP, particularly diesel-engine truck emissions, and stress on exacerbation of asthma among children. Children with asthma aged 9–14 (n = 35) were recruited from non-smoking households. We measured each participant's (1) continuous personal exposure to black carbon (BC, a surrogate of TRAP) at 1-min intervals, (2) 24-h integrated personal exposure to nitrogen dioxide (NO2), (3) daily fractional exhaled nitric oxide (FeNO), and (4) lung function for up to 30 consecutive days. Personal BC was recorded by micro-aethalometers. We measured daily FeNO using the NIOX MINO, forced expiratory volume in one second (FEV1), and forced vital capacity (FVC) using Easy One Frontline spirometers. Chronic stress was measured with the UCLA Life Stress Interview for Children. The association was examined using linear mixed-effect models. In the fully adjusted model, an interquartile range (IQR) increase in BC at lag 0–6 h before the FeNO measurement was associated with 8 % (95 % CI: 3 % - 12 %) increase in FeNO, whereas an IQR increase in BC at lag 7–12 h and lag 0–24 h were associated with 6 % (95 % CI: 2 % - 11 %) and 7 % (2 % - 12 %) FeNO increases, respectively. There were no significant lung function changes per IQR increase in BC. No interactions were observed between chronic stress and BC on FeNO. Chronic stress was negatively associated with individual average FeNO levels. Our findings suggest that higher levels of BC exposure within the prior 24 h increased airway inflammation levels in children with asthma, with the strongest effect observed within the first 6 h.

Impacts of intrauterine and postnatal exposure to air pollution on preschool children's asthma: A key role in cumulative exposure

BackgroundDespite mounting evidence linking asthma to air pollution, it remains unclear which specific pollutant(s) exposure during critical time window(s) plays a pivotal role in the development of asthma. ObjectiveThe objective of this study is to investigate the effects of intrauterine and postnatal air pollution exposure on children's asthma. MethodsFrom 2019 to 2020, a retrospective cohort study was conducted in Changsha, China. The inverse distance weighted (IDW) method was used to estimate each child's personal exposure to outdoor air pollutants at their home address. Associations between personal air pollution exposure and asthma were comprehensively examined. ResultsThe occurrence of children's asthma was found to be linked to exposure to PM2.5 and NO2 during both the intrauterine and current periods, with significant ORs (95% CI) of 1.44 (1.08–1.93) and 1.29 (1.00–1.68) for IQR increase in intrauterine exposure particularly during the 2nd trimester, and 1.26 (1.01–1.57) and 1.26 (1.04–1.51) for exposure in previous year. Post-natal PM10 exposure was linked to asthma, with an OR (95% CI) of 1.28 (1.01–1.62). Higher risks of asthma were associated with intrauterine exposure to PM2.5 and postnatal exposure to PM10. The critical time windows for PM2.5, PM2.5-10, and PM10 exposure were identified as the entire pregnancy, the second trimester, and the entire postnatal period, respectively. Cumulative exposure to PM2.5 and NO2 during gestational weeks had a notable impact on asthma. Additionally, exposure to traffic-related air pollution (TRAP) at all timing stages, as well as PM2.5-10 and SO2 at night, increased the risk of asthma. Certain subgroups were more vulnerable to asthma risk due to air pollution. ConclusionChildren's asthma was predominantly influenced by exposure to particulate matters and TRAP during both the intrauterine and postnatal periods.

Intrauterine and early postnatal exposure to air pollution associated with childhood allergic rhinitis

BackgroundDespite mounting evidence linking allergic rhinitis (AR) to air pollution, it remains unclear which major air pollutant(s) and critical window(s) of exposure play important roles in children's AR. ObjectiveTo examine the effects of intrauterine and early postnatal exposure to outdoor air pollution on children with doctor-diagnosed allergic rhinitis (DDAR). MethodsA retrospective cohort study involving 8689 kindergarten children was conducted in Changsha, China, from 2019 to 2020. A questionnaire survey was conducted to collect information on the health status of children and their family members, as well as their living habits and home environment. Personal exposure to daily outdoor air pollutants (PM2.5, PM2.5-10, PM10, SO2, NO2, and CO) was estimated during 40 gestational weeks, three trimesters, the entire pregnancy, and the first year after birth. Multiple logistic regression models were used to assess the associations between air pollution and children's DDAR. ResultsChildren's DDAR was associated with intrauterine CO exposure, with adjusted ORs (95% CI) of 1.18 (1.03–1.34) for each IQR increase in CO exposure. The second and third trimesters were critical windows for PM2.5 and CO exposure in relation to DDAR. Furthermore, early postnatal exposure to PM2.5-10 and PM10 in first year of life was associated with DDAR development, with adjusted ORs (95% CI) of 1.11 (1.01–1.22) and 1.27 (1.09, 1.47). The entire pregnancy and the first year of life were critical windows for CO and PM10 exposure. Some children were predisposed to DDAR risk due to exposure to traffic-related air pollution (TRAP). ConclusionOur findings support the hypothesis of “fetal origin of allergic rhinitis” by demonstrating that intrauterine and early postnatal exposure to air pollution plays an important role in children's DDAR.

Characterizing Ultrafine Particle Mobile Monitoring Data for Epidemiology.

Mobile monitoring is increasingly used to assess exposure to traffic-related air pollutants (TRAPs), including ultrafine particles (UFPs). Due to the rapid spatial decrease in the concentration of UFPs and other TRAPs with distance from roadways, mobile measurements may be non-representative of residential exposures, which are commonly used for epidemiologic studies. Our goal was to develop, apply, and test one possible approach for using mobile measurements in exposure assessment for epidemiology. We used an absolute principal component score model to adjust the contribution of on-road sources in mobile measurements to provide exposure predictions representative of cohort locations. We then compared UFP predictions at residential locations from mobile on-road plume-adjusted versus stationary measurements to understand the contribution of mobile measurements and characterize their differences. We found that predictions from mobile measurements are more representative of cohort locations after down-weighting the contribution of localized on-road plumes. Further, predictions at cohort locations derived from mobile measurements incorporate more spatial variation compared to those from short-term stationary data. Sensitivity analyses suggest that this additional spatial information captures features in the exposure surface not identified from the stationary data alone. We recommend the correction of mobile measurements to create exposure predictions representative of residential exposure for epidemiology.

A hyperlocal hybrid data fusion near-road PM2.5 and NO2 annual risk and environmental justice assessment across the United States.

Exposure to traffic-related air pollutants (TRAPs) has been associated with numerous adverse health effects. TRAP concentrations are highest meters away from major roads, and disproportionately affect minority (i.e., non-white) populations often considered the most vulnerable to TRAP exposure. To demonstrate an improved assessment of on-road emissions and to quantify exposure inequity in this population, we develop and apply a hybrid data fusion approach that utilizes the combined strength of air quality observations and regional/local scale models to estimate air pollution exposures at census block resolution for the entire U.S. We use the regional photochemical grid model CMAQ (Community Multiscale Air Quality) to predict the spatiotemporal impacts at local/regional scales, and the local scale dispersion model, R-LINE (Research LINE source) to estimate concentrations that capture the sharp TRAP gradients from roads. We further apply the Regionalized Air quality Model Performance (RAMP) Hybrid data fusion technique to consider the model's nonhomogeneous, nonlinear performance to not only improve exposure estimates, but also achieve significant model performance improvement. With a R2 of 0.51 for PM2.5 and 0.81 for NO2, the RAMP hybrid method improved R2 by ~0.2 for both pollutants (an increase of up to ~70% for PM2.5 and ~31% NO2). Using the RAMP Hybrid method, we estimate 264,516 [95% confidence interval [CI], 223,506-307,577] premature deaths attributable to PM2.5 from all sources, a ~1% overall decrease in CMAQ-estimated premature mortality compared to RAMP Hybrid, despite increases and decreases in some locations. For NO2, RAMP Hybrid estimates 138,550 [69,275-207,826] premature deaths, a ~19% increase (22,576 [11,288 - 33,864]) compared to CMAQ. Finally, using our RAMP hybrid method to estimate exposure inequity across the U.S., we estimate that Minorities within 100 m from major roads are exposed to up to 15% more PM2.5 and up to 35% more NO2 than their White counterparts.

Traffic-related air pollution and supplemental folic acid intake in relation to DNA methylation in granulosa cells

BackgroundHigher exposure to traffic-related air pollution (TRAP) is related to lower fertility, with specific adverse effects on the ovary. Folic acid may attenuate these effects. Our goal was to explore the relation of TRAP exposure and supplemental folic acid intake with epigenetic aging and CpG-specific DNA methylation (DNAm) in granulosa cells (GC). Our study included 61 women undergoing ovarian stimulation at a fertility center (2005–2015). DNAm levels were profiled in GC using the Infinium MethylationEPIC BeadChip. TRAP was defined using a spatiotemporal model to estimate residence-based nitrogen dioxide (NO2) exposure. Supplemental folic acid intake was measured with a validated food frequency questionnaire. We used linear regression to evaluate whether NO2 or supplemental folic acid was associated with epigenetic age acceleration according to the Pan-tissue, mural GC, and GrimAge clocks or DNAm across the genome adjusting for potential confounders and accounting for multiple testing with a false discovery rate < 0.1.ResultsThere were no associations between NO2 or supplemental folic acid intake and epigenetic age acceleration of GC. NO2 and supplemental folic acid were associated with 9 and 11 differentially methylated CpG sites. Among these CpGs, only cg07287107 exhibited a significant interaction (p-value = 0.037). In women with low supplemental folic acid, high NO2 exposure was associated with 1.7% higher DNAm. There was no association between NO2 and DNAm in women with high supplemental folic acid. The genes annotated to the top 250 NO2-associated CpGs were enriched for carbohydrate and protein metabolism, postsynaptic potential and dendrite development, and membrane components and exocytosis. The genes annotated to the top 250 supplemental folic acid-associated CpGs were enriched for estrous cycle, learning, cognition, synaptic organization and transmission, and size and composition of neuronal cell bodies.ConclusionsWe found no associations between NO2, supplemental folic acid, and DNAm age acceleration of GC. However, there were 20 differentially methylated CpGs and multiple enriched GO terms associated with both exposures suggesting that differences in GC DNAm could be a plausible mechanism underlying the effects of TRAP and supplemental folic acid on ovarian function.

98 Inhalation Exposure to Traffic-Related Air Pollution Accelerates Alzheimer’s Disease-like Pathology in a Murine Model

Abstract A growing number of epidemiological studies has linked exposure to traffic-related air pollution (TRAP) to neurological and neurodegenerative diseases. In a previous study, we showed that subchronic inhalation exposure to diesel engine exhaust, as a model of TRAP, aggravates amyloid-β plaque formation and motor function impairment in the 5xFAD transgenic mouse model of Alzheimer’s disease (AD). To further strengthen the epidemiological association between TRAP and AD we exposed 5xFAD and wildtype littermate mice for 5 h/day, 5 days/week during 2 or 4 consecutive weeks at a representative urban traffic-dominated location to: (I) concentrated ambient particles, (II) particle filtered ambient air or (III) clean air (control). Our study revealed that repeated inhalation exposure to TRAP accelerates plaque formation in the 5xFAD mice. Data also indicated that the gaseous fraction of the air pollutant mixture probably plays only a minor role in this effect. The major outcome of this study substantiates the role of air pollution in AD and suggests that long-term exposure to traffic-related air pollution particles is a risk factor for this debilitating disease. Acknowledgements: The work leading to these results has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No 814978 (TUBE) and a cross-border grant awarded by the Alzheimer Forschung Initiative (AFI, Germany) and Alzheimer Nederland.

Urban policy interventions to reduce traffic-related emissions and air pollution: A systematic evidence map

BackgroundUrban areas are hot spots for human exposure to air pollution, which originates in large part from traffic. As the urban population continues to grow, a greater number of people risk exposure to traffic-related air pollution (TRAP) and its adverse, costly health effects. In many cities, there is a need and scope for air quality improvements through targeted policy interventions, which continue to grow including rapidly changing technologies. ObjectiveThis systematic evidence map (SEM) examines and characterizes peer-reviewed evidence on urban-level policy interventions aimed at reducing traffic emissions and/or TRAP from on-road mobile sources, thus potentially reducing human exposures and adverse health effects and producing various co-benefits. MethodsThis SEM follows a previously peer-reviewed and published protocol with minor deviations, explicitly outlined here. Articles indexed in Public Affairs Index, TRID, Medline and Embase were searched, limited to English, published between January 1, 2000, and June 1, 2020. Covidence was used to screen articles based on previously developed eligibility criteria. Data for included articles was extracted and manually documented into an Excel database. Data visualizations were created in Tableau. ResultsWe identified 7528 unique articles from database searches and included 376 unique articles in the final SEM. There were 58 unique policy interventions, and a total of 1,139 unique policy scenarios, comprising these interventions and different combinations thereof. The policy interventions fell under 6 overarching policy categories: 1) pricing, 2) land use, 3) infrastructure, 4) behavioral, 5) technology, and 6) management, standards, and services, with the latter being the most studied. For geographic location, 463 policy scenarios were studied in Europe, followed by 355 in Asia, 206 in North America, 57 in South America, 10 in Africa, and 7 in Australia. Alternative fuel technology was the most frequently studied intervention (271 times), followed by vehicle emission regulation (134 times). The least frequently studied interventions were vehicle ownership taxes, and studded tire regulations, studied once each. A mere 3 % of studies addressed all elements of the full-chain—traffic emissions, TRAP, exposures, and health. The evidence recorded for each unique policy scenario is hosted in an open-access, query-able Excel database, and a complementary interactive visualization tool. We showcase how users can find more about the effectiveness of the 1,139 included policy scenarios in reducing, increasing, having mixed or no effect on traffic emissions and/or TRAP. ConclusionThis is the first peer-reviewed SEM to compile international evidence on urban-level policy interventions to reduce traffic emissions and/or TRAP in the context of human exposure and health effects. We also documented reported enablers, barriers, and co-benefits. The open-access Excel database and interactive visualization tool can be valuable resources for practitioners, policymakers, and researchers. Future updates to this work are recommended. Protocol RegistrationSanchez, K.A., Foster, M., Nieuwenhuijsen, M.J., May, A.D., Ramani, T., Zietsman, J. and Khreis, H., 2020. Urban policy interventions to reduce traffic emissions and traffic-related air pollution: Protocol for a systematic evidence map. Environment international, 142, p.105826.

Relationship between traffic-related air pollution and inflammation biomarkers using structural equation modeling

BackgroundEvidence suggests that exposure to traffic-related air pollution (TRAP) and social stressors can increase inflammation. Given that there are many different markers of TRAP exposure, socio-economic status (SES), and inflammation, analytical approaches can leverage multiple markers to better elucidate associations. In this study, we applied structural equation modeling (SEM) to assess the association between a TRAP construct and a SES construct with an inflammation construct. MethodsThis analysis was conducted as part of the Community Assessment of Freeway Exposure and Health (CAFEH; N = 408) study. Air pollution was characterized using a spatiotemporal model of particle number concentration (PNC) combined with individual participant time-activity adjustment (TAA). TAA-PNC and proximity to highways were considered for a construct of TRAP exposure. Participant demographics on education and income for an SES construct were assessed via questionnaires. Blood samples were analyzed for high sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), and tumor necrosis factor-α receptor II (TNFRII), which were considered for the construct for inflammation. We conducted SEM and compared our findings with those obtained using generalized linear models (GLM). ResultsUsing GLM, TAA-PNC was associated with multiple inflammation biomarkers. An IQR (10,000 particles/cm3) increase of TAA-PNC was associated with a 14 % increase in hsCRP in the GLM. Using SEM, the association between the TRAP construct and the inflammation construct was twice as large as the associations with any individual inflammation biomarker. SES had an inverse association with inflammation in all models. Using SEM to estimate the indirect effects of SES on inflammation through the TRAP construct strengthened confidence in the association of TRAP with inflammation. ConclusionOur TRAP construct resulted in stronger associations with a combined construct for inflammation than with individual biomarkers, reinforcing the value of statistical approaches that combine multiple, related exposures or outcomes. Our findings are consistent with inflammatory risk from TRAP exposure.

Long-term exposure to traffic-related air pollution and stroke: A systematic review and meta-analysis.

Stroke remains the second cause of death worldwide. The mechanisms underlying the adverse association of exposure to traffic-related air pollution (TRAP) with overall cardiovascular disease may also apply to stroke. Our objective was to systematically evaluate the epidemiological evidence regarding the associations of long-term exposure to TRAP with stroke. PubMed and LUDOK electronic databases were searched systematically for observational epidemiological studies from 1980 through 2019 on long-term exposure to TRAP and stroke with an update in January 2022. TRAP was defined according to a comprehensive protocol based on pollutant and exposure assessment methods or proximity metrics. Study selection, data extraction, risk of bias (RoB) and confidence assessments were conducted according to standardized protocols. We performed meta-analyses using random effects models; sensitivity analyses were assessed by geographic area, RoB, fatality, traffic specificity and new studies. Nineteen studies were included. The meta-analytic relative risks (and 95% confidence intervals) were: 1.03 (0.98-1.09) per 1μg/m3 EC, 1.09 (0.96-1.23) per 10μg/m3 PM10, 1.08 (0.89-1.32) per 5μg/m3 PM2.5, 0.98 (0.92; 1.05) per 10μg/m3 NO2 and 0.99 (0.94; 1.04) per 20μg/m3 NOx with little to moderate heterogeneity based on 6, 5, 4, 7 and 8 studies, respectively. The confidence assessments regarding the quality of the body of evidence and separately regarding the presence of an association of TRAP with stroke considering all available evidence were rated low and moderate, respectively. The available literature provides low to moderate evidence for an association of TRAP with stroke.

Effects of early life exposure to home environmental factors on childhood allergic rhinitis: Modifications by outdoor air pollution and temperature.

There is growing evidence that allergic rhinitis (AR) is associated with indoor environmental factors, but their role in childhood AR during early life remains unclear. To investigate the association of preconceptional, prenatal, early postnatal, and current exposure to home environmental factors with childhood AR, and to further explore whether this association can be interacted by outdoor air pollution and temperature. A retrospective cohort study of 8689 preschool children was conducted during 2019-2020 in Changsha, China. A standard questionnaire was used to collect data on each family's health outcomes and home environments. We considered home environmental exposures during one year before conception, pregnancy, first year of life, and past year. Associations of indoor air pollution and allergens with AR were assessed by multiple logistic regression models. Pre-birth exposure to indoor air pollution emitted by new furniture or redecoration and dampness related allergen derived from mold/damp stains and mold/damp clothes or bedding during 1 year before conception and pregnancy was significantly associated with increased AR, with adjusted ORs (95% CI) ranging from 1.35 (1.05-1.75) to 1.87 (1.55-2.27). Childhood AR was also significantly related with post-birth exposure to dampness related indoor allergen including mold/damp stains and mold/damp clothes or bedding in first year and past year and pollen allergen including total and nonflowing plants in past year, with a range of ORs (95% CI) from 1.20 (1.01-1.42) to 1.79 (1.42-2.27). We identified that pre-birth, particularly in utero exposure to both indoor air pollution from renovation and dampness related allergens, played a key role in AR development compared to post-birth exposures, and accumulative effect was observed with the highest risk of AR. High exposure to traffic-related air pollution (TRAP) including outdoor PM2.5, NO2, CO, and O3, as well as living near traffic road not only significantly increased adverse effect of home environmental factors but also decreased protective effect of household dogs on childhood AR. Early life exposure to low temperature in pregnancy and high temperature in first year significantly increased AR risk of home environmental exposure. Sensitivity analysis indicated that some sub-groups were more susceptible to AR risk of home environmental exposure. Our study suggests that pre-birth exposure to home environmental factors played an important role in AR development and this effect can be interacted by TRAP and temperature, which supports a hypothesis of "(pre)fetal origin of childhood AR".

Association of Traffic-Related Air Pollution with Newborn’s Anthropometric Indexes at Birth

BACKGROUND AND AIM: The evidence suggested many adverse health effects due to exposure to traffic-related air pollution (TRAP). However, the evidence on neonatal anthropometric measurements (NAPM) in low and middle-income countries is very scarce yet. Therefore, we investigate the association of prenatal exposure to indicators of traffic and ambient particulate matter (PM) with NAPM. METHODS: This cross-sectional study was based on hospital medical records of 4053 mother-neonate pairs (2016-2018). PMs were estimated at residential addresses based on validated spatiotemporal models. Moreover, total street length in 100, 300 and 500m buffers around the home, residential distance to the ring road, major roads, heavy-traffic lights, gas station, motorway junction, bank, square, bus terminal, public parking and industrial land-use were calculated as indicators of traffic. The head circumference (HC), birth weight (BW) and birth length (BL) of neonates were collected as NAPM. Multivariate regression models were applied to evaluate the relationship between PMs and indicators of traffic with NAPM, controlled for relevant covariates. RESULTS: The adjusted models revealed that higher exposure to PM2.5 and PM10 was significantly related with lower BW and BL. Similarity results were observed for total street length in a 100 m buffer around maternal home with BW and BL. Moreover, higher distance to heavy traffic lights was significantly associated with higher BW and BL. An IQR increase in PM10 was significantly related to lower HC (95% CI: -0.11, -0.01, P-value = 0.03). An increase in distance from residential address to heavy traffic lights, ring roads, bus terminal, and transportation land-use was associated with higher HC. CONCLUSIONS: This is the first study on the association of prenatal exposure to ambient PMs and different indicators of traffic with NAPM. Overall, our findings suggested that higher prenatal exposure to TRAP was related with lower BW, BL and HC. Keywords: Infant, Maternal, Neonates

Traffic-Related Air Pollution and DNA Methylation of the Follicular Fluid

BACKGROUND AND AIM: Higher exposure to traffic-related air pollution (TRAP) is related to lower fertility, with specific adverse effects on the ovary. Epigenetics, specifically DNA methylation (DNAm), may underlie this association but given its tissue specificity, exploring potential mechanisms in toxicological-relevant target tissues is essential. Our objective was to explore the relation between TRAP exposure and follicular fluid (FF) DNAm. METHODS: Our study included 62 women undergoing in vitro fertilization at a fertility center in Boston, Massachusetts (2005-2015). TRAP exposure was defined using a spatiotemporal model to estimate residence-based daily nitrogen dioxide (NO2) concentrations in the 3 months prior. FF was collected during oocyte retrieval and DNAm levels were profiled using the Infinium MethylationEPIC BeadChip. We estimated epigenetic age via an existing granulosa cell clock and other common epigenetic clocks. We used linear regression to test whether accelerated epigenetic age, or differential DNAm across the genome, was associated with NO2 exposure while adjusting for surrogate variables and other confounders. RESULTS: Epigenetic age as measured using the granulosa cell clock was moderately correlated with reported age (r=0.48,p&amp;#x3c;0.001). Other epigenetic age estimators performed poorly in the FF. There was no association between NO2 exposure and accelerated epigenetic aging (β=-0.05 95%CI -1.20,1.10). NO2 exposure was associated with 8 differentially methylated regions and 22 differentially methylated positions, after adjusting the significance threshold for 704,169 tests. The genes annotated were enriched for GATA1 transcription factor binding and for DNA-methyltransferase activity (q-val&amp;#x3c;0.05). Some of the differentially methylated genes, including KCNQ1, VRK1, GPER, MLH1, and PLET1, have been linked to reproductive and fertility outcomes. CONCLUSIONS: Our study suggests that differences in FF DNAm could be a plausible mechanism potentially linking TRAP exposure to ovarian dysfunction. Future work to improve assessment of epigenetic age in reproductive tissues, such as FF, is warranted. KEYWORDS: Air pollution, Epigenetics, Ovary, Fertility

Traffic-related air pollution and birth weight: the roles of noise, placental function, green space, physical activity, and socioeconomic status (FRONTIER)

Background and aim: FRONTIER aims to study the impact of maternal exposure to traffic-related air pollution (TRAP) on fetal growth while disentangling the effects of noise, elucidating the role of placental function as an underlying mechanism; and exploring the potential of greenspace to mitigate it. Methods: FRONTIER has established a new pregnancy cohort of 1,086 pregnant women in Barcelona (BiSC), Spain. Fetal growth was characterized by anthropometric measures at birth together with ultrasound-based measures of fetal development. We are integrating objective data on time-activity patterns with a hybrid modeling framework combining dispersion and land use regression models and campaigns of personal and home-outdoor air pollution monitoring to estimate maternal exposure level and inhaled dose of NO2, PM2.5, and PM2.5 light absorption and contents at the main microenvironments (home, workplace, and commuting routes). We are assessing maternal exposure to noise by integrating measurements at participants’ home-outdoor using noise monitors together with modeled microenvironmental noise levels and data on noise sensitivity, annoyance, and protections against noise. We will develop single- and multi-pollutant models to evaluate the impact of air pollution exposure and inhaled dose on fetal growth and the mediatory role of placental function. Results: BiSC mothers had an average age of 34.8 years with 31.1% having high school education and less and 73.6% having European origin. The mean (SD) of the first and third trimester measured personal NO2 levels were respectively 31.9(11.7) and 31.0(12.1)&amp;#x3bc;g/m3 for the pre-pandemic period and 26.6(10.9) and 25.1(12.1)&amp;#x3bc;g/m3 for the pandemic period. The mean (SD) of measured home-outdoor noise levels (LAeq,24h) was 61.5 (6.7)dB(A). 49.2% of newborns were girl and the mean (SD) of birthweight was 3276.8 (508.2)g The analyses are still ongoing. Conclusions: FRONTIER will provide a robust and comprehensive evaluation of the impact of TRAP exposure on fetal growth using high-resolution exposure data.

Chronic exposure to traffic-related air pollution reduces lipid mediators of linoleic acid and soluble epoxide hydrolase in serum of female rats

Chronic exposure to traffic-related air pollution (TRAP) is known to promote systemic inflammation, which is thought to underlie respiratory, cardiovascular, metabolic and neurological disorders. It is not known whether chronic TRAP exposure dampens inflammation resolution, the homeostatic process for stopping inflammation and repairing damaged cells. In vivo, inflammation resolution is facilitated by bioactive lipid mediators known as oxylipins, which are derived from the oxidation of polyunsaturated fatty acids. To understand the effects of chronic TRAP exposure on lipid-mediated inflammation resolution pathways, we measured total (i.e. free+bound) pro-inflammatory and pro-resolving lipid mediators in serum of female rats exposed to TRAP or filtered air (FA) for 14 months. Compared to rats exposed to FA, TRAP-exposed rats showed a significant 36–48% reduction in fatty acid alcohols, specifically, 9-hydroxyoctadecadienoic acid (9-HODE), 11,12-dihydroxyeicosatetraenoic acid (11,12-DiHETE) and 16,17-dihydroxydocosapentaenoic acid (16, 17-DiHDPA). The decrease in fatty acid diols (11,12-DiHETE and 16, 17-DiHDPA) corresponded to a significant 34–39% reduction in the diol to epoxide ratio, a marker of soluble epoxide hydrolase activity; this enzyme is typically upregulated during inflammation. The findings demonstrate that 14 months exposure to TRAP reduced pro-inflammatory 9-HODE concentration and dampened soluble epoxide hydrolase activation, suggesting adaptive immune changes in lipid mediator pathways involved in inflammation resolution.

Toxicological effects of traffic-related air pollution on the lungs: Evidence, biomarkers and intervention

BackgroundNumerous epidemiological studies have recently observed that exposure to traffic-related air pollution (TRAP) is associated with increased risk of various respiratory diseases. Major gaps in knowledge remain regarding the toxicological effects. ObjectivesWe examined the toxicological effects of the gasoline exhaust particles (GEP), a paradigm of TRAP, in rats, with an objective to provide the evidence, obtain the biomarkers, and suggest effective intervention measure. MethodsWe measured the airway hyperresponsiveness (AHR), inflammatory cells in the bronchoalveolar lavage (BAL) fluid, histological changes in the lung tissues, and the biomarkers so as to systematically examine the toxicological effects of GEPs at different dose levels (0.5, 2.5, 5 mg/kg BW). The intervention of vitamin E (VE), a natural antioxidant, on the toxicological effects was investigated. ResultsThe lung injury caused by GEP exposure was first indicated by the airway hyperresponsiveness (AHR). Compared with the control group, GEP exposure significantly increased the airway resistances and decreased the lung compliance; the higher the dose of GEP, the more serious the lung injury. Lung injury was also revealed by the increase of inflammatory cells, including the lymphocytes and neutrophils, in the BAL fluid. With the increase of GEP dose, histological changes in the lung tissues were further observed: inflammatory cell infiltration increased and alveolar wall thickened. The toxicology of GEP was demonstrated by the increase of the biomarkers of the oxidative stress, the pro-inflammatory cytokines and the apoptosis cytokine. However, administration of VE was found to be effective in restoring airway injury. ConclusionThe toxicological effects of traffic-related air pollution (TRAP) on rat lungs are supported by evidence and biomarkers, and vitamin E intervention is feasible.

Cardiovascular effects of traffic-related air pollution: A multi-omics analysis from a randomized, crossover trial

A system-wide cardiovascular response to traffic-related air pollution (TRAP) has been rarely described. To systemically understand the mechanisms underlying cardiovascular effects of TRAP, we conducted a randomized, crossover trial in 56 young adults, who engaged in two 4-hour exposure sessions on a main road and in a park, alternately. We measured personal exposures to traffic-related air pollutants (TRAPs), including fine and ultrafine particulate matter, black carbon, nitrogen dioxide, and carbon monoxide. Lipidomics, targeted proteomics, urine metabolomics, targeted biomarkers, ambulatory blood pressure and electrocardiogram were measured. We used linear mixed-effects models to estimate the associations. The exposures to TRAPs except for fine particulate matter in the road session were 2–3 times higher. We observed elevated blood pressure and decreased heart rate variability (HRV) after TRAP exposure, accompanied by dozens of molecular alterations involving systemic inflammation, oxidative stress, endothelial dysfunction, coagulation, and lipid metabolism. Pathways like vascular smooth muscle cell proliferation and biomarkers like trimethylamine N-Oxide might also be disturbed. Some of these TRAP-related molecular biomarkers were also associated with changes of blood pressure or HRV. Our results provided systematical mechanistic profiling for the cardiovascular effects of TRAP using multi omics, which may have implications in TRAP control.